OVARIAN TUMOURS

III UNIT OG
Anatomy
of
ovary

Jagadeesh
lll OG
 OVARY - ANATOMY

Situated in ovarian fossa near fimbrial end of

fallopian tube
Almond shaped
Pearly grey colour
Measures about 35 mm length
25 mm width
18 mm thickness
Attached to lateral pelvic wall by
INFUNDIBULOPELVIC LIGAMENT

Inner pole of ovary is attached to cornua of

uterus by OVARIAN LIGAMENT

Attached to posterior surface of broad ligament

by MESOVARIUM
 PARTS
Consists of 3 regions:
1.Hilum:

Through which ovarian vessels,lymphatics &

nerves pass into the ovary

Composed of connective tissue and

unstriped muscle fibres
2.Cortex:
Outer layer, contains graffian follicles

Lined by a single layer of germinal

epithelium

3.Medulla:

Central portion composed of connective

tissue and blood vessels
 RELATIONS

Laterally – ovarian fossa

Medially – fimbria of fallopian tube

Anteriorly – obliterated umbilical artery &

fallopian tube

Posteriorly - Ureter
 Arterial Supply

Ovarian artery:
Arise from aorta just below renal artery
Enters hilum through infundibulopelvic
ligament
Ends by anastomosing with terminal part of
uterine artery

 Uterine artery also give some branches to ovary

 Venous Drainage

Left ovarian vein:

Drains into left renal vein

Right ovarian vein:

Drain into inferior venacava

Ovarian veins form PAMPINIFORM PLEXUS in

infundibulopelvic fold
Nerve Supply:
By ovarian plexus:
Formed by coeliac,renal and hypogastric plexus
It contains sympathetic(T10,T11) and
parasympathetic(S2,S3,S4) nerves

Lymphatic drainage:

Drain into lateral aortic and pre-aortic

nodes
 Embryology
Ovaries develop from the genital ridge which
arise from medial side of mesonephros
Primordial germ cells that are formed migrate
to region of developing ovary
Sex cords proliferate from the germinal epithelium

Cords then surrounds primordial germ cell to form

primordial follicle.
Epoophoron:
Known as organ of Rosenmuller
Represents the cranial end of wolffian body
Consists of vertical tubules in mesovarium and
mesosalpinx

Paroophoron:
Represents the caudal end of wolffian body
Contains vertical tubules
 Wolffian duct
Its remnant Known as Gartner’s duct

Runs below and parallel to fall tube in

mesosalpinx

Runs by the side of uterus upto internal os and

enters the cervix

Then runs forwards to reach vaginal wall and

hymen
 Graffian follicle

Consists of 2 layers:

1.Theca interna:

Responsible for production of oestrogen and

progesterone
2.Granulosa cell layer:

These cells form projection into the cavity of

graffian follicle called CUMULUS OOPHORUS

Spherical bodies scattered among the

granulosa cells are called CALL EXNER BODIES

These cells secrete liquor folliculi and

contains oestrogen
Secretes…

1.Steroidal hormones:
Oestrogen
Progesterone
Testosterone
Androstenedione

2.Non steroids:
Inhibin
Relaxin
 Ovarian Tumours
SCREENING: done for women with
• Low parity
• Low fertility
• Delayed childbearing
• Familial predisposition
• BRCA-1 & BRCA-2 genes
• Mumps prior to menarche
• Multiple ovulation in IVF
SCREENING METHODS:
Transvaginal USG:

Sensitivity - 95%

Tumour marker: CA 125

Sensitivity – 50% improves when

combined with transvaginal USG
NEWER METHODS:

Surface Enhanced Laser Desorption Ionisation

Time Of Flight (SELDI-TOF):

-Uses proteomic patterns to identify tumour

Sensitivity- 100%
Specificity- 95%
Digital Single Nucleotide Polymorphism (SNP)
Analysis:

-Involves measurement of plasma DNA levels

and allelic imbalance

87% sensitive at stage I and II

95% sensitive at stage III and IV
 ETIOPATHOGENESIS,
CLASSIFICATION AND PATHOLOGY
OF OVARIAN TUMOURS
BY K JEEVITHARAJALAKSHMI
ETIOLOGY
RISK FACTORS:
 Nulliparity
 Decreased fertility
 Delayed childbearing
 Early menarche and late menopause
 Heredity

BRCA 1 BRCA2
ERB B2 –adenocarcinoma
TP53 Mutation
 Family history
 Multiple ovulation in IVF programme
OTHER FACTORS
 Environmental factors:
high fat diet
use of talc on perineum
industrial pollution
 White race and increasing age
 mumps prior to menarche

PROTECTIVE FACTORS:
 Multiparity
 breast feeding
 anovulation
 OCP’S
PATHOGENESIS
 Incessant ovulation theory: Repetitive ovulation
cyclic repair of ovarian surface epithelium p53
mutation carcinogenesis
 5% to 10%- inherited predisposition loss of
BRCA and P53 function
Benign cyst

Low malignant potential tumours

Invasive carcinoma
BORDERLINE OVARIAN
TUMOURS
Low malignant potential
10% to 20% of epithelial tumours
Mitotic figure-<4/10 high field

Characteristics:
 High survival rate
 Typical indolent course
 Spontaneous regression of peritoneal implants
 Diagnosis based on examination
 Multiple section examination
CRITERIA:
 Epithelial proliferation with papillary
formation and pseudostratification
 Nuclear atypia and increase mitotic
activity
 Absence of stromal invasion
serous borderline tumor
 Surface epithelial Germ Sex cord Metastais to
tumor cell tumors ovary
tumors
origin Coelomic Germ Sex cord Mullerian or
epithelium cells of stroma extramulleria
from n
Mullerian yolk sac
epithelium
Overall 65% to 70% 15 5 %to10% 5%
frequency to20%
Among 8o% to90% 3% to5% 2%to3% 5%
malignancy
Age group 20+yrs 0-25yrs All ages variable
NORMAL OVARY

Surface epithelial germ cells sex

cord
Cells
stroma
WHO classification
SURFACE EPITHELIAL STROMAL TUMOURS
 Serous tumors
-cystadenoma
-borderline
-cystadenocarcinoma
 Mucinous tumours
-benign
-borderline
-malignant
 Endometriod tumours
-adenosarcoma
-mesodermal mixed tumour
Epithelial stromal tumours

-benign
-borderline
-malignant
Transitional cell tumours
brenner tumour
SEXCORD STROMAL TUMOURS
 Granulosa stromal cell tumour
granulosa cell tumour
thecoma cell tumour
 Sertoli leydig cell tumour
 Gyndroblastoma
 Lipid cell tumour
GERM CELL TUMOUR
Teratoma
mature
immature
monodermal
Dysgerminoma
Yolk sac tumour
Mixed germ cell tumour
METASTATIC TUMOURS
Krukenberg tumour
Others
TYPES RESEMBLANCE
SEROUS TUMOUR ENDOSALPHINX
MUCINOUS TUMOUR ENDOCERVIX

ENDOMETRIOIDTUMOUR ENDOMETRIUM

CLEAR CELL TUMOUR CLEAR CELL CA OF

ENDOMETRIUM
BRENNER TUMOUR URINARY TRACT

GERM CELL TUMOUR GERM CELL

ENDODERMAL SINUS TUMOUR EMRYONAL TISSUE OF

YOLK SAC
GRANULOSA TUMOUR GRANULOSA CELL OF
GRAFFIAN FOLLICLE
PATHOLOGY OF OVARIAN TUMOURS
RATIONALE FOR HISTOTYPING:
DIAGNOSTIC CRITERIA
CARCINOMA GRADING
THERAPEUTIC RELAVANCE
PROGNOSTIC SIGNIFICANCE
TUMOURS OF SURFACE EPITHELIUM
SEROUS TUMOURS
Most common
Tall columnar epithelium resemble
endosalphinx
50% bilateral
Gross:
Cystic lesions-intracystic or papillary projections
from surface
TYPE GROSS

Benign smooth glistening wall with no

or less papillary projection

Borderline more papillary projections

malignant Irregular large solid mass with

nodularity and fixation
SEROUS -TYPES MICROSCOPIC
FEATURE
BENIGN Columnar epithelium
with abudant cilia
and microscopic
papillae

BORDERLINE More complexity of

stromal papillae with
stratification and
nuclear atypia

MALIGNANT More complexity and

stromal infiltration
Mucinous tumours

Resemble endocervix

Usually unilateral,5%bilateral

12%-25% of ovarian neoplasm

GROSS:
Multiple cyst without surface involvement
Multiloculated with sticky gelatinous fluid
Honey combed appearance
MUCINOUS MICROSCOPIC FEATURES
TYPES

BENIGN Tall columnar epithelium

with mucin and absence of
cilia

BORDERLINE Abudant gland like with

stratification without
stromal invasion

MALIGNANT More solid growth

,Epithelial cell atypia, loss
of gland like, necrosis
,stromal invasion
Endometrioid
Resemble endometrium lining
10% of ovarian neoplasm
GROSS:
Partly cystic and partly solid
with foci of hemorrhage
MICROSCOPIC FEATURE:
Typical glandular pattern
Like endometrium
CLEAR CELL CARCINOMA
Highly malignant
Resemble clear cell carcinoma
of endometrium
GROSS:
Large partly cystic and solid
MICROSCOPIC FEATURE:
Large cuboidal cell with
 abudant clear cytoplasm
Hobnail cells
BRENNER TUMOUR
Resemble transitional cell of urinary tract
1%-2% of neoplasm
GROSS:
Solid yellow grey firm mass
90% Unilateral
MICROSCOPIC FEATURE:
Epithelial cell nest- puffed wheat& Coffee bean
nuclei
GERM CELL TUMOURS
Teratoma:
MATURE- BENIGN:
GROSS:
Unilocular cyst with hair and cheesy
sebaceous material,teeth,bone…
MICROSCOPIC FEATURE:
Stratified squamous epithelial with
Hairshaft,sebaceous gland &skin
Adnexal structure
Kaleidoscopic appearance
EX:Dermoid cyst
IMMATURE –MALIGNANT
GROSS:
BULKY solid mass with
variegated appearance
MICROSCOPIC FEATURE:
Immature tissue differentiating
towards gland ,nerve ,muscle ,
Cartilage
Struma ovarii- contain thyroid
tissue
Carcinoid tumour-argentaffinoma
Dysgerminoma
80% 90%-Unilateral
GROSS:
Solid mass, elastic rubber
consistency
Pink ,lobulated, soft &fleshy
MICROSCOPIC FEATURE:
Large cells in bunches
Dark staining nuclei, clear
translucent cytoplasm
Lmphocytic infiltration
of fibrous stroma
Endodermal sinus tumour
GROSS:
Solid with cystic degeneration
MICROSCOPIC FEATURE:
Glomerulus like structure
Schiller duval bodies- germ cells
Central blood vessels
CHORIOCARCINOMA
Very vascular, highly malignant
MICROSCOPIC APPEARANCE:
Dimorphic population of syncytotrophoblast
and cytotrophoblast in necrotic& hemorrhagic
pattern
SEX CORD STROMAL
TUMOURS- mesenchymomas
GRANULOSA TUMOURS:
Resemble granulosa cell of graffian
follicle
GROSS:
U/L yellowish brown oval,
Soft, lobulated
MICROSCOPIC FEATURE:
Rosette like call exner bodies contain
Central amphorous pink material
Surronded by granulosa cells
Fibrothecoma
Resemble theca lutein cells of graffian follicle
GROSS:
U/L Solid white firm mass
MICROSCOPIC FEATURE:
Spindle shaped fibroblast &
Collagen with fat laden polyhedral cells
SERTOLI LEYDIG CELLS:
GROSS:
SOLID grey to golden brown
MICROSCOPIC FEATURE:
Well differentiated tubules – tubules
composed of sertoli and leydig cells interspesed
with stroma
TUMOUR FROM CONNECTIVE TISSUE
OF OVARY
OVARIAN FIBROMA:
3% Of ovarian neoplasm
GROSS:
Oval with smooth surface with large vein in capsule,
Firm and harder in consistency
Calcerous degeneration occurs
MICROSCOPIC APPEARANCE:
Uniform spindle shaped cells in
Feather stitched pattern
Resemble ovarian cortex
MEIG SYNDROME
KRUKENBERG TUMOUR:

Almost Bilateral
GROSS:
Smooth surface
Solid waxy consistency with cystic spaces
MICROSCOPIC FEATURE:
Mucin producing large signet ring cells in cellular
stroma
BENIGN OVARIAN
ENLARGEMENTS

- KARTHIK. M
Causes of ovarian enlargement:
• Retention cysts- distention cysts
• Lutein cysts
• Endometriosis
•Hypertrophy- cong. & acquired
•Corpus luteum hematoma
•Ovarian pregnancy
•Oophoritis- acute, chronic
•Luteoma of pregnancy
•1ᵒ neoplasm- benign, malignant
•2ᵒ neoplasm
 Retention cysts:
Cystic changes greater than normal range.
1. Atretic cysts
2. Germinal inclusion cysts
3. Follicular cysts
4. Theca lutein cysts
 Atretic cysts
Graffian follicle, corpus luteum,
corpus albicans, corpus fibrosum.

All these may remain cystic prior to

replacement by fibrous tissue.

Cysts- small and multiple

Lined by granulosa cells, granulosa

lutein, theca lutein, connective
tissue or hyaline tissue.
Germinal inclusion cysts
Walthard inclusions

Microscopic cysts found in ovaries of

older women.

Importance- origin of cystadenoma,

Brenner tumor

It is lined by epithelium similar to

that on surface of ovary.
 Follicular cysts
Enlargement of immature unruptured
graffian follicle.
Anovulation.
Ovum degenerates but granulosa and
theca cell layer may persist.
Single or multiple size-3 to 5cm

Due to accumulation of more follicular

fluid, follicles increase in size lining
epithelium flattens and disappear.
• Excessive normal Gn stimulus- ovulation of other
follicles not arrested
 Abnormal Gn stimulus- ovulation arrested

 Single follicular cyst- secrete estrogen

 Polycystic ovaries in PCOD- secrete androgens
 Triad- anovulation, hirsutism,

 Rx- disappear spontaneously

 ovulation induction- MDPA, Clomiphene citrate
 Cyst persisting more than 2 months- neoplastic
 Theca lutein cysts
Less common usually B/L
multicystic large upto 25 cm

•Endogenous causes- molar pregnancy,

chorioCa, multiple pregnancy
•Exogenous causes- ovulation induction
High output of Gn
Increase in hCG

Excessive leutinisation

Rx- disappears spontaneously when cause is

removed
 Symptoms
•POLYMENNORHEA, POLYMENNORHAGIA - multiple
small cysts ass. with condns causing ovarian
hyperemia.

•AMENNORHEA OR OLIGOMENNORHEA - when

cystic ovaries are androgenic.

•INFERTILITY - anovulation or decreased ovulation.

•PAIN - in iliac fossa
When associated with Hemorrhage, pelvic
adhesions.
Tunica albuginea of ovary ill defined and
nonresistant to distension.
Pain arises only when blood leaks into
peritoneum from hematoma.
Cystic ovaries that are buried in
peritoneal adhesions – resistant to
enlargement – pain.
 Treatment

If associated with PID- treat the cause

In absence of other disease
•Spontaneous regression
•Surgical removal of cystic portion of
ovary or whole of ovary.
 Corpus luteum cyst
Greater than 3cm

Corpus luteum of pregnancy- forms cyst-

degenerates b/w 2 nd n 3 rd month, it is
symptomless

Corpus luteum of menstruation- may become

cystic.

Lining layers of granulosa lutein and paraleutin

continuously produces progesterone and
estradiol.

Endometrium is in secretory phase.

Excretion of pregnanediol is increased.

• Symptoms- delayed menstruation,
pain, adnexal mass.

• Complications- rupture, torsion

• Rx- if ruptured, it leads to

hemoperitoneum. It requires
surgical treatment.
 Luteoma of pregnancy
Hyperplastic conditions

8 to 20cm large cut section- orange

yellow in color

Solid multiple foci of luteal tissue- in one

or both the ovaries during pregnancy.
Usually asymptomatic.
Arises from theca or stromal cells.
Due to the action of hCG.

It disappears spontaneously after

pregnancy.
BENIGN OVARIAN TUMOURS

M . Kiruthika
BENIGN OVARIAN TUMOURS

 Predominantly occur in premenopausal women.

 Benign neoplastic cystic tumours of germ cell origin are
most common in young women.
 Benign ovarian tumours are usually slow growing .
Classification of benign ovarian tumours
Germ cell tumours
• Benign cy stic teratoma
Ovum
• S truma ovarii
• Gonadoblastoma
Granulosa cell

Theca cell
Corpus luteum
Sex cord
stromal
Tumours Surface epithelium
• Fibroma Surface epithelial tumours
• Theca cell • Serous cystadenoma
tumour • Mucinous cystadenoma
• Endometroid cystadenoma
• Brenner tumour
BENIGN SURFACE EPITHELIAL
TUMOURS
Serous cystadenoma
• Women aged between 30 – 50 years.
• 30 % Bilateral.
• Moderate sizes ranging from 10 – 15 cm.
• Clear yellow fluid present.
• TYPES
Simple serous cysts.
Multilocular serous cysts.
Papillary serous cystadenoma.
• No specific symptoms.
Mucinous cystadenoma
 Common in 30 – 50 age group.
 Unilateral.
 May reach huge size & Multilocular.
 Bluish or yellowish transparent colour.
 Filled with mucinous material which is sticky,
slimy, viscid.
 Rupture may cause pseudomyxoma peritoni.
Endometroid cystadenoma

 Rare tumour
 Median age of occurrence 57 years
 Usually unilateral , 17 % Bilateral
 Median diameter – 10 cm
 External surface – smooth,
 Cyst contains clear or yellowish fluid.
Brenner tumour

Rare tumour
 Prevalent in women > 40 years.
 Usually small ( < 2 cm ) to moderate size.
 Solid in consistency.
 Probably arise from Wollfian metaplasia of surface
ovarian epithelium
BENIGN GERM CELL TUMOURS
Benign cystic teratoma

• Common.
• Encountered below 20 years, during pregnancy & during
child bearing period.
• Usually of moderate size ( 8 – 10 cm ) & bilateral.
• Most have a long pedicle.
• Greyish in colour
• Mostly unilocular.
• Consists of combination of well differentiated ectoderm,
mesodermal & endodermal elements.
Skin & skin appendages
Sebaceous glands
Sweat glands
Hair follicles
Muscle fibers
Cartilage, bone ,teeth
Respiratory & gastrointestinal epithelium.
• 50 % asymptomatic
STRUMA OVARI

Monodermal teratoma composed of harmonally active

thyroid tissue.
1 – 4 % of cystic teratomas.
 Only 5 % produce sufficient thyroid harmone to produce
symptoms.
GONADOBLASTOMA

 Composed of germ cells mixed with other cells

resembling granulosa & sertoli cells.
 Patients have an abnormal gonad with a Y chromosome
in 90 % of cases.
 Predispose to development of dysgerminoma or other
malignant germ cell tumours..
BENIGN SEX CORD STROMAL
TUMOURS
FIBROMA

 Around age of 50 years.

 Usually mobile with a long pedicle.
 Lobulated glistening white surface.
 Firm ,hard tumour .
 Associated with ascites and hydrothorax
MEIG’S SYNDROME
THECA CELL TUMOUR
( THECOMA)

Occurs in postmenopausal women.

 unilateral
 encapsulated tumour
 Many are functioning tumours producing oestrogen.
CLINICAL FEATURES
SYMPTOMS

ABDOMINAL
SWELLING
 Pressure symptoms

Frequency of micturition Ovarian Cachexia

Edema

Respiratory
embarassment
ASCITES – MEIG‘ S SYNDROME

Hydrothorax

Ascites
 Dull ache lower abdominal pain , low back pain.
 Peritonitis, shock due to rupture of large cyst.
 Dyspareunia
Menstrual disorders

Menorrhagia

Amenorrhoea

Post menopausal
Bleeding.
PHYSICAL SIGNS
INSPECTION
• Abdominal swelling.
• Symmetrical enlargement of abdomen.
• On deep inspiration the abdominal wall can be seen to
move over the swelling.
PALPATION
• Mass – central or to one side.
• Well defined upper & lateral border.
• Smooth or lobulated surface
MOBILE from above downwards
CONSISTENCY – tense & cystic
fluid thrill elicited

PERCUSSION
AUSCULTATION
 silent

BIMANUAL EXAMINATION
GROOVE’S SIGN
MALIGNANT OVARIAN TUMORs

by

Madhu
maetha .R
SECOND MOST COMMON ( 10-15%)
GYNAECOLOGICAL CANCER

HIGH MORTALITY RATE

80-85% WOMEN WITH OVARIAN CANCER DIE

  DYSGERMINOMA
 ENDODERMAL SINUS
TUMOUR MALIGNANT GERM CELL
CLASSIFICATION
 CHORIOCARCINOMA
 MALIGNANT TERATOMA
TUMOURS
 EMBRYONAL CELL
CARCINOMA
 POLYEMBRYOMA
MALIGNANT SEX TUMOURS
 MIXED
CORD STROMAL
TUMOURS
Classification
 GRANULOSA CELL TUMOR
 SERTOLI LEYDIG CELL
TUMOR

 SEROUS CYSTADENOCARCINOMA
 MUCINOUS CYSTADENOCARCINOMA
 ENDOMETROID CYSTADENOCARCINOMA
OVARIAN EPITHELIAL  CLEAR CELL CARCINOMA
CARCINOMA  MALIGNANT BRENNER TUMOUR
 UNDIFFERENTIATED CARCINOMA
EPITHELIAL OVARIAN
CANCER
 INCIDENCE

*60-70% of all Ovarian Tumors

*90% of all Ovarian Malignances

 AETIOLOGY

*Nulliparous or Infertile women

*Hereditary genetic factors

-5-10% genetic predisposition
-younger age
-defective BRCA 1 and BRCA 2
Macroscopically
Microscopically
ADENOCARCINOMA
Which might be, commonly

 SEROUS ADENOCARCINOMA (75%)

 MUCINOUS ADENOCARCINOMA(20%)
 ENDOMETROID ADENOCARCINOMA(2%)
Serous cystadenocarcinoma
Mucinous cystadenocarcinoma
Endometroid carcinoma
Clear cell carcinoma
 RARELY,
 malignant brenner tumor

 Transitional cell carcinoma

 SMALL CELL CARCINOMA

 NON-EPITHELIAL
OVARIAN CANCER

MALIGNANT MALIGNANT SEX- UNCOMMON

GERM CELL CORD STROMAL OVARIAN
TUMORS TUMORS TUMORS
 Malignant germ cell tumors
INCIDENCE

*20-30% of all ovarian tumors

*5% of germ cell tumors- MALIGNANT

CLASSIFICATION
SPECIAL FEATURES OF GERM CELL
TUMORS
 Lower age incidence

 Tends to grow rapidly

Most tumors produce TUMOR MARKERS

TUMOR MARKERS
DYSGERMINOMA ALKALINE

PHOSPHATASE &
LACTATE DEHYDROGENASE

ENDODERMAL SINUS TUMOR ALPHA

FETOPROTEIN

CHORIO CARCINOMA HUMAN

CHORIONIC
GONADOTROPIN
DYSGERMiNOMA
 Commonest Malignant Germ cell tumor

 Younger age (10-20 years)

 secretes ALKALINE PHOSPHATASE &

LACTATE DEHYDROGENASE
dysgerminoma
MALIGNANT TERATOMA
 2nd commonest Germ Cell Malignancy

 contains elements resembling tissues derived from Embryo

- ABNORMAL MATURATION producing Undisciplined
growth

 occur in combination with other Germ cell tumors-

MIXED GERM CELL TUMOR

 Malignant change in Benign cystic teratoma-0.5% to 2%-

commonly Squamous cell carcinoma
ENDODERMAL SINUS TUMOR
 from Multipotent Embryonal tissue –
SELECTIVE DIFFERENTIATION OF YOLK
SAC STRUCTURES

Young age ( 16-18 years)

secretes ALPHA FETOPROTEIN

clinical presentation- Abdominal pain & Pelvic

mass
endodermal sinus tumor
Chorio carcinoma
 Rarely occurs in Pure form, generally it is a part of Mixed Germ Cell
Tumor

 its origin as a Teratoma- confirmed in Pre- pubertal girls

 secretes HUMAN CHORIONIC GONADOTROPIN

 Highly malignant- metastasis to Liver, Lungs, Brain,Bones and other

viscera
choriocarcinoma
MALIGNANT SEX CORD STROMAL TUMORS
arises from Functioning or Non-Functioning stroma of ovary
 Functioning sex cord tumors may be

* Estrogenic- GRANULOSA CELL TUMOR

* Androgenic- SERTOLI-LEYDIG CELL TUMOR
* Both Estrogenic and Androgenic(very rare)
- GYNANDROBLASTOMA

 Non-functioning stroma may very rarely give rise to

Fibrosarcoma of ovary
Granulosa cell tumor
 functioning- secrete ESTROGEN

 associated with Endometrial carcinoma in 5-10%

of cases & with Endometrial hyperplasia in 25-
50% of cases

 causes Irregular bleeding, Precocious puberty,

menstrual irregularities, postmenopausal bleeding
Granulosa cell tumor
Sertoli leydig cell tumors
 many are Functioning- secrete ANDROGENS

Defeminisation followed by masculinisation

Primary modes of spread of ovarian
cancer
DIRECT
EXTENSION

TRANSCOELOMIC
SPREAD

LYMPHATIC
SPREAD

HEMATOGENOUS
SPREAD
METASTATIC OVARIAN
CANCER
 5-6% of Ovarian tumors
PRIMARY

GENITAL EXTRA GENITAL

KRUKERNBERG TUMOR
 accounts for 30-40% of Metastatic cancers of
ovary

 Bilateral solid ovarian tumor

Microscopically- SIGNET RING CELLS

 CEA markers increase

 arise by RETROGRADE LYMPHATIC SPREAD

KRUKERNBURG TUMOR
CLINICAL PICTURE
SYMPTOMS- “SILENT KILLER”
EARLY STAGE DISEASE- asymptomatic

Non specific
GIT symptoms
PRESSURE SYMPTOMS
Urinary frequency

Constipation
  ABDOMINAL PAIN

 ABDOMINAL SWELLING

 ABNORMAL UTERINE
BLEEDIND especially

POST-MENOPAUSAL
BLEEDING
 PHYSICAL SIGNS
 Palpation of a
Pelvic mass

 Bilateral Solid
Fixed masses
suggest
MALIGNANCY
 CLINICAL FEATURES SUGGESTING
malignancy in ovarian tumors
In HISTORY,
 Extremes of Age
 Rapid growth
of tumor

 Loss of weight
Pain
Post menopausal bleeding
&
symptoms of Virilisation
On general examination,
 Malignant Cachexia

 Palpable
Supraclavicular
nodes

Pleural Effusion

Any asssociated Breast mass

On abdominal examination,
INSPECTION
Abdominal
enlargement

PALPATION
 Bilateral solid
fixed mass
PERCUSSION

Presence of
Ascites
On pelvic examination
Nodules in the
Pouch of Douglas

Frozen Pelvis
At laparotomy
 Ascites especially if
altered blood stained
ascites

Bilaterality,fixation
& invasion of capsule

Extracystic papillae &

ADHESION to
surrounding
structures
Peritoneal nodules or
Secondary deposits in
omentum, intestine or liver

Variable consistency
of tumor & cut
section showing
Haemorrhage and
Necrosis
OMENTAL
DEPOSITS
BENIGN MALIGNANT
TUMORS TUMORS
unilateral bilateral

cystic solid

mobile fixed

smooth irregular
*Ascites
*Cul-de-sac nodules
*Rapid growth rate
COMPLICATIONS AND
DIFFERENTIAL DIAGNOSIS
 COMPLICATIONS
 TORSION
 RUPTURE
 PSEUDOMYXOMA OF THE PERITONIUM
 INFECTION
 EXTRAPERITONEAL DEVELOPMENT
 SECONDARY MALIGNANCY
 TORSION
 It occurs
• commonly in ovarian cyst.
• when size of the cyst is 10 cm or more in
diameter.
 As a result of rotation
• anterior surface of tumor turns towards the
patient’s right side.
•the veins in pedicle becomes occluded.
 The increased tension causes severe abdominal pain
and peritoneal irritation.
 Rotation of an ovarian cyst is hemodynamic.
 Rare in chocolate cysts and malignant ovarian tumors.
torsion
Ordinary people
think merely of
spending time,
great people
think of using
it.
 RUPTURE
TRAUMATIC SPONTANEOUS
 Direct violence to  Malignant ovarian
abdomen tumors-
 During labour papillomatous type
 Bimanual examination  Pappilomatous
serous cystadenomas
 Actively growing
mucinous
cystadenomas
rupture
Tumors Mechanism of rupture
Malignant ovarian tumors Carcinoma cells infiltrate
through the connective
Pappillomatous serous tissue capsule to ulcerate
tumours into the peritoneal cavity

Actively growing mucinous The epithelial elements of

cystadenomas the growth grow so rapidly
that the connective tissue
of the capsule are unable
to keep up with them.
First thing in the
human personality
that dissolves in
alcohol is dignity.
 PSEUDOMYXOMA OF PERITONEUM
 Coagulated mucinous material adherent to
omentum and intestines.
 Boiled sago pudding.
 At operation , the material cannot be removed
completely.
 Usually occurs with mucinous cystadenoma and
also reported in mucocele of appendix and
carcinoma of large intestine.
 Mesothelium of peritoneum secretes mucinous
material because of its conversion into columnar
cells.
 Bad prognosis.
Pseudomyxoma of peritoneum
 INFECTION
 Infrequent
 Most cases follow acute salpingitis and torsion.
 Uncommon through bloodstream.
 Infected ovarian tumors are always adherent to
adjacent viscera.
 EXTRAPERITONEAL DEVELOPMENT
 Burrow extraperitoneally during their
development.
 It may spread upwards into the perinephric
region.
 Removal-extremely difficult ,
•danger of injuring the ureter.
•large vessels may be torn.
 SECONDARY MALIGNANCY
 50% in serous cystadenomas.
 5% in mucinous cystadenomas.
 1.7% in dermoid cysts.
Never drive
faster than your
guardian angel
can fly.
 DIFFERENTIAL DIAGNOSIS
FULL BLADDER
PREGNANT UTERUS
MYOMA
ASCITES
OTHER ABDOMINAL TUMORS
 FULL BLADDER
 Tense and tender ,fixed in position ,anterior to
the uterus ,projecting anteriorly more than an
ovarian cyst.
 A catheter should be passed to establish the
diagnosis.
 PREGNANT UTERUS
 It should be thought of whenever a tumour
is found arising from the pelvis.
 Exclude pregnancy by
•careful bimanual examination
•signs of pregnancy
•ultrasonic examination and
pregnancy tests
 Mistakes-unmarried girl who denies history
of amenorrhoea.
 MYOMA
 Usually hard or firm ,without the tense cystic
consistency of atypical ovarian cyst
 Pedunculated and degenerated fibroid may
however mistaken for an ovarian cyst.
Don’t dig ur grave
with ur own knife
and fork
 ASCITES
 Sometimes , it is difficult to distinguish between a
large ovarian cyst and ascites.
 With a large ovarian cyst
• percussion note over the tumour is dull
•both flanks are resonant
 In ascites
•note is dull over the flanks
•abdomen is tympanitic in the midline
•physical signs of shifting dullness may
be
obtained.
 OTHERS TUMOURS
 A large hydronephrosis
•penetrates back into the loin and
situated high
up in the abdomen ,well above the
pelvis.
•intravenous or retrograde pyelography
will
establish the diagnosis.
 Enlarged spleen , mesenteric cyst , mucocele of
appendix or gallbladder , hydatid cysts and
pancreatic cysts should be considered if
physical signs of an ovarian cysts are atypical.
INVESTIGATIONS

M.MARIMUTH
U
1.ULTRASOUND
 Transabdominal ultrasound
If tumour is abdominal
 Transvaginal ultrasound
It gives more details about the
tumour(>95%sensitivity)
 Normal size of ovary is 2*1.5*1cm
volume is 8.8ml. More than this is suspicious of an
ovarian growth.
Normal ovary
In benign lesions-

 The tumour is mostly unilateral , unilocular or

multilocular with septa is <5mm in thick.
 The cavity is non ecogenic
 The dermoid cyst shows solid areas in cystic tumour
occasional presence of a tooth
Benign solid mass
Benign cystic ovarian mass
In malignant lesions –

 The tumour is bilateral or may be unilateral and

multiloculated with septa is greater than 5mm thickness
 Solid tumours with echogenic or cystic area
 In Meigs syndrome ascites is characteristic of benign
tumour
 The endometrial lining more than 4mm in thickness with
papillary projections in a perimenopausal women is seen
in feminizing tumour and if endometrial secondaries are
present
Malignant ovary
Malignant ovarian mass
2.Colour doppler
 Neovascularisation,
 Increased blood flow,
 Low pulsatile index <1 and
 Resistance index <0.4 are suggest malignancy
Colour doppler
3.X-Ray

 Abdomen and pelvis

demonstrate soft tissue shadow or teeth in dermoid cyst
 Chest
To rule out pulmonary metastasis and
Hydrothorax- rt sided in Meigs syndrome
 Barium meal
To exclude a GI primary carcinoma
4.Breast examination
To rule out pregnancy and primary growth
5.CT and MRI
To identifying a dermoid cyst , haemorrhagic cyst ,
fibroma , endometriosis, hydro salpinx
In malignant tumour – to rule out the spread of tumour ,
enlargement of pelvic and para aortic lymph nodes >1cm
to planning surgery , post operative radiotherapy and
chemotherapy .
MRI malignant ovary
MRI malignant ovary
6.Tissue markers
 CA 125
It is a glycoprotein
More than 30 U/ml suggest malignant
Not produced by normal ovarian epithelium may be
produced by both benign and malignant ovarian tumour
It is synthesized within affected ovarian epithelial
cells and secreted in to the cysts.
 In benign tumours , excess antigen is released in to
and may accumulate within cyst fluid.
Hypothetically , abnormal tissue architecture
associate with malignant tumours may allow antigen
release into the vascular circulation .
90% of women presenting with malignant non
mucinous tumours , CA125 levels are elevated .
 FALSE NEGATIVE :
Half of stage 1 ovarian cancers will have a normal
CA 125 measurement

 FALSE POSITIVE :
Pelvic inflammatory disease, endometriosis,
leiomyomas, abdominal TB, pregnancy and even
menstruation
 CEA(Carcino Embryonic Antigen)
CEA more than 5ng/ml (normal 2.5-5ng/ml) is reported
in endometrioid, brenner tumour, mucinous tumour,
colonic, liver, breast and lung metastasis.
 Alpha fetoprotein, hCG, NB/70k, placental alkaline
phosphatase and lactate dehydrogenase are tissue markers
for germ cell tumours.
 In mucinous tumour –
Tumour marker is CA 19-9
CEA may be better indicators of disease than CA125
7.Cytological study
 Ascitic fluid or aspirated cystic fluid may reveal
malignancy. False negative is high.
 STAGING LAPAROTOMY

AND

SURGERY FOR OVARIAN CANCER

- MURUGESAN. V
WHAT IS

STAGING
LAPAROTOMY ?
STAGING LAPARATOMY:
FIGO staging of ovarian cancer

TECHNIQUE:
Incision – Midline or Paramedian
abdominal incision.

If Ovarian malignancy is present and

the tumor is apparently confined to the
ovaries or the pelvis, thorough surgical
staging to be done.
STAGING STEPS:

Any free fluid in the pelvic cul-de-sac -

Cytological evaluation.

If no free fluid-Peritoneal washing

Peritoneal washing:
Instilling and recovering 50 – 100ml of saline
from
Pelvic cul-de-sac,

Right and left paracolic gutter and

 Beneath each hemi-diaphragm

Then send it for Cytological evaluation

A systematic exploration of all intra
abdominal surfaces and viscera – clockwise
fashion.
Transverse Colon

Ascending Descending
Colon Colon

Small
Rt. Paracolic Lt. Paracolic
intestine
gutter gutter
&
mesentery
Recto Sigmoid
Caecum Colon
Any suspicious areas or adhesions on the
peritoneal surfaces - sampled for biopsy.

Eg: peritoneum over the bladder,

peritoneum of the pelvic cul-de-sac and
both the paracolic gutters and intestinal
mesenteries.

The diaphragm –
 biopsy
scrapping with a tongue
depressor
Infra colic omentectomy-
Omentum is resected from the
transverse colon, after ligating the branches
of gastro epiploic vessels that feed the infra
colic omentum.
If the Gastrocolic ligament is palpably
normal, it does not need to be resected.

Exploration of retroperitoneal spaces-

Pelvic and para aortic lymph nodes.
Enlarged lymph nodes should be resected
and sent for frozen section.
FIGO STAGING
FOR
Ca OVARY
STAGE I – Tumour restricted to one or
both ovaries

IA
 – Tumour restricted to one ovary
No tumour on external surface
Capsule intact, no Malignant
ascites
I B – Tumour limited to both ovaries

No tumour on external surface
Capsule intact, no Malignant
ascites
I C – Tumour IA or IB

Positive for surface malignant
growth
Capsule ruptured
Malignant ascites or positive peritoneal
washings
STAGE II – Tumour involves one or both
ovaries with pelvic extensions

 II A – Extension/Metastasis to uterus,
fallopian tubes or pelvic extensions.
No Malignant cells in
ascites/washings.
 II B – Extension to other pelvic organs
No Malignant cells in
ascites/washings.
 II C - Tumour II A or II B with surface
growth
Capsule ruptured at/or prior to
surgery.
Malignant ascites/positive peritoneal
STAGE III –
Tumour involving one/both ovaries
with microscopic implants outside
the pelvis with positive
nodes(inguinal, retroperitoneal)

Tumour limited to true pelvis but

with histological evidences of
spread to bowel, omentum,
presence of superficial
metastasis on the liver.
 III A – Tumour grossly limited to the pelvis
Nodes negative, but microscopic
seedlings of peritoneum of the
abdominal wall.

 III B – Tumour with abdominal peritoneal

implants of less than 2cm size and
nodes negative.

 III C – Abdominal implants of more than 2cm

size and positive nodes.
STAGE IV – Growth involving one or both
ovaries with distant
metastasis in liver, lungs and
pleura.

Tap fluid for cytology.

SURGERY
Early stage disease
( STAGE I AND II)
 Post menopausal women:
Total Abdominal Hysterectomy with
Bilateral Salphingo-oophorectomy with
Infracolic Omentectomy.
 Reproductive Age group:
Unilateral Oophorectomy
Preserve Uterus and contralateral ovary

Follow up with CA-125

After completion of child bearing, other

ovary and uterus should be removed.

ADVANCED STAGE DISEASE
(STAGE III AND IV)
 Cyto Reductive Surgery:
Removal of as much of the tumour and its
metastasis as possible.
 Debulking Surgery:
Total Abdominal Hysterectomy with
Bilateral Salphingo- Oopherectomy
Omentectomy
Resection of metastatic lesions from the
peritoneal surfaces or the intestines.
Second look surgery
To detect presence of any residual tumor
following a planned course of chemotherapy.

Following a 3 to 6 months of chemotherapy, in

an inoperable case- Total abdominal
hysterectomy with Bilateral salpingo
oophorectomy or debulking procedure.
CHEMOTHERAPY

N.NIRANJANA JOY
Prolongs remission and survival

Also used for palliative treatment in

advanced and recurrent disease

Administered in all cases beyond stage Ia

Earlier single agents were used, nowadays

combination therapy is favoured
No chemotherapeutic agent kills all cancer cells in
one treatment , treatment needs to be repeated
several times

All agents used should be active against that

particular tumor

should have different modes of action to avoid drug

resistance and should have different mechanisms of
toxicity.
Drugs are given at 3 weeks intervals
TYPES OF CHEMOTHERAPY

Intravenous chemotherapy

Intraperitoneal chemotherapy

Neoadjuvant chemotherapy
 RECOMMENDED REGIMEN
INTRAVENOUS CHEMOTHERAPY

DRUGS DOSE ROUTE INTERVAL CYCLES

(mg/sq.m) (Weeks)

PACLITAXEL 175 IV 3 6-8

CARBOPLATIN AUC=5-6
PACLITAXEL 135 IV 3 6-8
CISPLATIN 75

CYCLOPHOSPH 750 IV 3 6-8

AMIDE 75
CISPLATIN
DRUGS DOSE ROUTE INTERVAL
(mg/sq.mm) (Weeks)

DOXORUBICIN, 35-50 IV 3-4

LIPOSOMAL

TOPOTECAN 1-1.25 IV 1
4 IV 3(DAILY*3-5DAYS

ETOPOSIDE 50 PO 3,DAYS 14-21

 INTRAPERITONEAL
CHEMOTHERAPY
DRUGS DOSE ROUTE INTERVAL CYCLES
(mg/sq.m) (Weeks)
PACLITAXEL 135 IV 3,DAY 1 6

CISPLATIN 50-100 IP DAY 2

PACLITAXEL 60 IP DAY 8
Platinum Compound

Carboplatin Cisplati
n
Taxol (Paclitaxel)
STAGE 1 EPITHELIAL TUMOUR
Early stage,low risk
NO adjuvant therapy is required
Early stage,high risk
Adjuvant therapy is required
Carboplatin and paclitaxel given for 3-6
cycles
ADVANCED STAGE EPITHELIAL
TUMOUR
Advanced epithelial ovarian cancer is very
sensitive to chemotherapy with responses in
the range of 70-80% to first-line
chemotherapy. The majority, however,
relapse and ultimately die of chemotherapy-
resistant disease.
Major advance in the treatment of advanced
stage tumour is the introduction of paclitaxel as
one of the chemotherapeutic agents
Carboplatin has less toxicity compared with
cisplatin
Preferred regimen carboplatin and paclitaxel
DOCETAXEL AND CARBOPLATIN
Docetaxel has efficacy similar to
paclitaxel
regimen produced significant
myelosuppression
FIVE ARM TRIAL
Addition of either
gemcitabine,topotecan or doxorubicin to the
standard regimen does not enhance survival
rate
INTRAPERITONEAL CHEMOTHERAPY
Ideal anticancer agent
Very effective systemically against ovarian
cancer
Penetrate deep into the tumor
Stays in the peritoneal cavity for prolonged
period
Low incidence of systemic adverse effect but
providing satisfactory drug concentrations in
the inner core of tumor
Cisplatin

The peritoneal lining had 2.5-8 times

higher levels of drug after IP
administration

Intraperitoneal chemotherapy might

increase the therapeutic index for small
tumors confined to the peritoneal cavity

IP cisplatin-based chemotherapy has been

shown to have a survival benefit over IV
cisplatin-based chemotherapy for advance
Strengths of Intraperitoneal
chemotherapy
Achieve dose intensification (as ‘high-dose’)

Treats both intraperitoneal tumor bed and

extraperitoneal tumor via systemic
recirculation

Reaches sites that may not be reached by

Intravenous route.
Toxicity

More bonemarrow suppressions,

Gastrointestinal effects, neurologic
symptoms, and infections
Complications of Catheter
Blockade
Leakage
Infection
Diarrhea
Bowel perforation
Fistula formation
Patient selection issues
Patient characteristics
 eg.: renal function ; neuropathy (DM –associated)
Significant peritoneal adhesion
Ongoing abdominal infection, or indwelling IP
catheter becomes infected or malfunction, will
be unable to treated by this route of drug
delivery
NEOADJUVANT CHEMOTHERAPY
In stage 3 and stage 4 disease chemotherapy
can be given to ‘downstage the disease’ prior to
chemotherapy
Helpful in patients with massive ascitis ,pleural
effusion.
 REGIMEN FOR NON-EPITHELIAL
TUMORS
 Germ cell tumors are treated with surgery and
multi-agent chemotherapy in most cases
VAC Vincristine
Actinomycin
Cyclophosphamide
BEP Bleomycin
Etoposide
Cisplatin
VBC Vincristine
Bleomycin
Cisplatin
SIDE EFFECTS
 While chemotherapy drugs kill cancer cells, they
also damage some normal cells, causing side
effects. These side effects will depend on the
type of drugs given, the amount taken, and how
long treatment lasts. Temporary side effects
might include the following:
• nausea and vomiting
• loss of appetite
• hair loss
• hand and foot rashes
• kidney or nerve damage
• mouth sores
bleeding or bruising after minor cuts
(from a shortage of platelets)

an increased chance of infection (from a

shortage of white blood cells)
tiredness (from low red blood cell counts)
Ca Ovary IIIc
Inoperable –
Biopsy
Neodjuvant chemo
 Cisplatin +
Paclitaxel
Complete response
Sec. Cytoreductive
surgery done now
Palliative and Adjuvant
Therapy

By
R.Pani Malar
III OG MMC
 Palliation

From Latin palliare to cloak

Any form of medical care or
treatment that concentrates on
reducing the severity of disease
symptoms, rather than striving to
halt, delay, or reverse progression
of the disease itself or provide a
cure.
Palliative Radiotherapy
•In advanced ovarian cancer
shrinks the tumor and
reduces the symptoms
•Dysgerminoma
•Nodal metastasis
 Intra peritoneal
radiotherapy
•Provides local radioactivity
•Treats all peritoneal surfaces
•Uses Au-198 and P-32
 Method
•10 – 15 mCi of P-32 mixed
with 1 to 2 L of saline injected
intra peritonealy
•Positional changes every 15 to
30 min
 External radiation
MOVING STRIP TECHNIQUE

•Hypofractionation technique
•12 to 14 strips of 2.5 cm height
are marked
•Treated for 5 - 6 weeks
•180 to 200 cGy
Open Field Technique
•Larger treatment field of 45
cm
•Treated daily
•Liver and kidneys shielded
•25 to 45 Gy
 Nutrition
•Calories 2000-2400
kcal/day
•Adequate protein vitamins
and minerals
•Fluid intake 1500 – 2000 ml
•Blood transfusion for anemia
Relief of Pain
 Steroids
•Promotes the feeling of well
being
•Increases appetite
•Relieves the pressure of
metastasis in brain and liver
•Also effective in bladder and
bowel pain
 Relief of symptoms
•Vomiting - Haloperidol
Metoclopramide
•Cerebral vomiting - Cyclizine

Domperidone

•Constipation - laxatives
•Thrush - fluconazole
 •Ascites - tapping
•Pleural effusion -
pleurodesis

thoracocentesis
•Intestinal obstruction –
Surgery
 Psychological Impact
•Decreased sex libido
•Dyspareunia
•Menopausal symptoms – HRT
•Mental depression due to oestrogen
deficiency
 Follow up
•Clinical Examination
•Radiological – USG
•Serology – tumor markers
 Prognostic factors
•Pathology -Histology
-grade- well
differentiated - good
poorly
differentiated - bad
•Biology -Low stage - diploid-good
High stage-aneuploid-bad
•Clinical features
5 yr Survival
FIGO 5 year
Staging survival
Stage 0 90 –
100%
Stage I 70%
Stage II 25 – 30%
Stage III 10%
Stage IV 0 - 5%
 OVARIAN TUMOURS BY
X.A.PRASANNA
AND III UNIT OG
PREGNANCY
 COMMON TUMOURS
 DYSGERMINOMA
 MATURE CYSTIC TERATOMA
 PARAOVARIAN CYST
 SEROUS CYSTADENOMA
 CORPUS LUTEAL CYST OF
PREGNANCY
 FIBROMA
MATURE CYSTIC TERATOMA
 CLINICAL FEATURES
Mostly asymptomatic
Shooting pain down thighs, pain abdomen
Pressure effects
Dyspnoea
Precordial pain
Dyspepsia
Frequency
Constipation
 Examination
Uterus larger than
gestational age
Mass pushed behind uterus
Or to 1flank

Staging
Similar to non-pregnancy state
Usually stage 1 – low grade
INVESTIGATIONS

USG
●
INCIDENTAL FINDING
●
MALIGNANT –IRREGULAR SEPTA,SOLID
AREAS,PAPILLARY EXCRESCENCES

CA 125 USED AS A SCREENING PROCEDURE

●

●
NOT SPECIFIC

AFP MATERNAL SERUM

●

●
ENDODERMAL SINUS TUMOUR
DIFFERENTIAL DIAGNOSIS
Uterine leiomyomas
Pelvic kidney
Retroperitoneal tumour
Ectopic pregnancy
Retroverted gravid HINGORANI SIGN
uterus
Non pregnant horn
of bicornuate uterus
COMPLICATIONS
Effects of pregnancy on tumour
Torsion
Infection
Incarceration

Effects of tumour on pregnancy

Urinary retention
UTI
Malpresentation
Rupture -peritonitis
TORSION OVARY
Effect of tumour on labour
Obstructed labour
Uterine inertia
Rupture

Effect on tumour in puerperium

Torsion (25%)
Why– Rapid involution of uterus
Lax abdominal walls
Mobility of abdominal viscera
 DYSGERMINOMA
 Large solid masses
 Complications –torsion, incarceration in cul de sac
 More lymphatic spread
 Treatment – unilateral oopherectomy
+
Ipsilateral pelvic & para aortic node dissection
 15% bilateral
 10% recurs
Click icon to add picture
 SEX CORD STROMAL
 Rare
 Complicated by
Rupture
19% haemoperitoneum
14% dystocia

 Edema ,prominent luteinisation ,lacks recognizable

differentiation
 EPITHELIAL TUMOURS
 Similar to non pregnant cases
 Individualize treatment
Total abdominal hysterectomy
OR
Cytoreduction

 Gestational age , fetal viability ,demand

 MANAGEMENT
 Surgery – II trimester
Even then , risk of preterm labor , IUGR ,IUD common

 Chemotherapy – controversial .
II , III trimester

 Radiotherapy – contraindicated
 TIMING OF TUMOR

WAIT TILL AAA

16 WKS

I TRIMESTER > 28 WKS

 USG – CYST

< 10 CM
●

●
LUTEAL CYST –RESOLVES BY 12 -16 WKS
●
IF NOT ,SURGICAL REMOVAL AFTER
PUERPERIUM

Complicated tumours

OBSTRUCTS ●
CAESARIAN FIRST,
LABOR ●
TUMOUR REMOVAL

IMMEDIATE SURGERY
TORSION
●

●
LAPAROTOMY
 POSTOPERATIVE CARE
1. Sedatives – 48 to72 hours

2. 25 mg progesterone –parenterally 1 week

3. Gentle & minimal handling of pregnant uterus

Survival not different from non pregnant cases

 HIGHLIGHTS
Ovarian enlargements, solid/cystic may occur at any
age
Functional and inflammatory enlargements develop
during child bearing years
Second most common site for development of
gynaecological malignancy (10-15% gynaecological
cancers)
Easy screening methods not avilable
Prognosis poor
Non neoplastic
enlargements
Mostly resolve
spontaneously
PCOS - Anovulation,
hirsutism
USG findings – ‘Necklace appearance’
↑E2, LH, androgens
Treatment – Metformin 500 mg tds./
Surgery – Lap. punctures
OVARIAN TUMOURS
Commonest 80% - epithelial cell tumours (90 % maligna

Tumour in adolescent and post menopausal women –

more often malignant

Boderline ovarian tumours /LMP

Don’t invade stroma
Mitotic figures <4/10 high field
ORIGIN OF TUMOURS TUMOURS

ENDOSALPINX SEROUS EPITHELIAL CELL TUMOUR

ENDOCERVIX MUCINOUS EPITHELIAL TUMOUR

ENDOMETRIUM ENDOMETRIOID TUMOUR

TRANSITIONAL CELL BRENNER TUMOUR

CLEAR CELL Ca ENDOMETRIUM CLEAR CELL CARCINOMA

TOTIPOTENT CELLS TERATOMA

MESENCHYMAL CELLS GRANULOSA CELL TUMOUR

MALIGNANT TUMOURS
 BRCA 1 ,BRCA 2 mutations in 5 – 10%

 Yolk sac tumour -↑ AFP , ↑ alpha 1 antitrypsin

 Choriocarcinoma - ↑ hCG

 Embryonal cell carcinoma - ↑ AFP ,↑hcg

 Metastasis – pylorus

 Krukenburg’s tumour – myxomatous stroma ,signet ring cells,

retrograde lymphatic spread .
CLINICAL FEATURES &
COMPLICATIONS
 Ascites + mass , bilateral ,
rapidly growing – malignant

 Except – meig’s ,fibroma ,brenner tumour

 Complications – Torsion
Rupture
Pseudomyxoma peritonei
Infection
Retroperitoneal haematoma
GOLD STANDARD - INVESTIGATION
Transvaginal ultrasound –
BENIGN

Unilateral , unilocular
,thin wall, thin septa
<5mm

Non -echogenic
 malignant – bilateral
,solid tumour

Ascites

Septa >5mm

Papillary projections
 TREATMENT
 BENIGN - Total abdominal hysterectomy with
bilateral salpingo oopherectomy ,
Unilateral ovariotomy
Cystectomy
Laparoscopic /USG guided aspiration

 Stage I , II – Total abdominal hysterectomy and

bilateral salpingo oopherectomy , omentectomy

 Stage III,IV –Debulking , postoperative

chemotherapy , radiotherapy .
SCREEN BY TRANSVAGINAL

ULTRASOUND
THANK YOU