OVARIAN TUMOURS

III UNIT OG

Jagadeesh

lll OG

Anatomy of ovary

Situated in ovarian fossa near fimbrial end of fallopian tube

Almond shapedPearly grey colourMeasures about 35 mm length 25 mm width 18 mm thickness

OVARY - ANATOMY

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

Consists of 3 regions:1.Hilum:

Through which ovarian vessels,lymphatics & nerves pass into the ovary

Composed of connective tissue and unstriped muscle fibres

PARTS

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

Laterally – ovarian fossa

Medially – fimbria of fallopian tube

Anteriorly – obliterated umbilical artery & fallopian tube

Posteriorly - Ureter

RELATIONS

Ovarian artery:Arise from aorta just below renal arteryEnters hilum through infundibulopelvic

ligamentEnds by anastomosing with terminal part of

uterine artery

Uterine artery also give some branches to ovary

Arterial Supply

Left ovarian vein:Drains into left renal vein

Right ovarian vein:Drain into inferior venacava

Ovarian veins form PAMPINIFORM PLEXUS in infundibulopelvic fold

Venous Drainage

By ovarian plexus:Formed by coeliac,renal and hypogastric

plexusIt contains sympathetic(T10,T11) and

parasympathetic(S2,S3,S4) nerves

Lymphatic drainage:

Drain into lateral aortic and pre-aortic nodes

Nerve Supply:

Ovaries develop from the genital ridge which arise from medial side of mesonephros

Embryology

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 RosenmullerRepresents the cranial end of wolffian bodyConsists of vertical tubules in mesovarium

and mesosalpinx

Paroophoron:Represents the caudal end of wolffian bodyContains vertical tubules

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

Wolffian duct

Consists of 2 layers:

1.Theca interna:

Responsible for production of oestrogen and progesterone

Graffian follicle

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

2.Granulosa cell layer:

1.Steroidal hormones:

OestrogenProgesteroneTestosteroneAndrostenedione

2.Non steroids:InhibinRelaxin

Secretes…

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

Ovarian Tumours

SCREENING METHODS:Transvaginal USG:

Sensitivity - 95%

Tumour marker: CA 125

Sensitivity – 50% improves when combined with transvaginal USG

Surface Enhanced Laser Desorption Ionisation Time Of Flight (SELDI-TOF):

-Uses proteomic patterns to identify tumour

Sensitivity- 100% Specificity- 95%

NEWER METHODS:

-Involves measurement of plasma DNA levels and allelic imbalance

87% sensitive at stage I and II95% sensitive at stage III and IV

Digital Single Nucleotide Polymorphism (SNP) Analysis:

ETIOPATHOGENESIS, CLASSIFICATION AND PATHOLOGY

OF OVARIAN TUMOURS BY K JEEVITHARAJALAKSHMI

ETIOLOGYRISK FACTORS: NulliparityDecreased fertilityDelayed childbearingEarly menarche and late menopauseHeredity BRCA 1 BRCA2 ERB B2 –adenocarcinoma TP53 MutationFamily 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 TUMOURSLow malignant potential10% to 20% of epithelial tumoursMitotic figure-<4/10 high field Characteristics:

High survival rateTypical indolent courseSpontaneous regression of peritoneal implantsDiagnosis 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 tumor

Germ cell tumors

Sex cord tumors

Metastais to ovary

origin Coelomic epithelium

Mullerian epithelium

Germ cells from yolk sac

Sex cord of stroma

Mullerian or extramullerian

Overall frequency

65% to 70% 15 to20%

5 %to10%

5%

Amongmalignancy

8o% to90% 3% to5%

2%to3% 5%

Age group 20+yrs 0-25yrs All ages variable

NORMAL OVARY

Surface epithelial germ cells sex cord

Cells stroma

WHO classificationSURFACE EPITHELIAL STROMAL TUMOURS Serous tumors -cystadenoma -borderline -cystadenocarcinoma Mucinous tumours -benign -borderline -malignant Endometriod tumours -adenosarcoma -mesodermal mixed tumour

Epithelial stromal tumours -benign

-borderline -malignantTransitional cell tumours brenner tumourSEXCORD STROMAL TUMOURS Granulosa stromal cell tumour granulosa cell tumour thecoma cell tumour Sertoli leydig cell tumour Gyndroblastoma Lipid cell tumour

GERM CELL TUMOURTeratoma mature immature monodermalDysgerminoma Yolk sac tumour Mixed germ cell tumourMETASTATIC TUMOURSKrukenberg tumourOthers

TYPES RESEMBLANCESEROUS TUMOUR ENDOSALPHINXMUCINOUS 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

THECOMA TUMOUR THECA LUTEIN CELL OF GRAFFIAN FOLLICLE

PATHOLOGY OF OVARIAN TUMOURSRATIONALE FOR HISTOTYPING: DIAGNOSTIC CRITERIACARCINOMA GRADINGTHERAPEUTIC RELAVANCEPROGNOSTIC SIGNIFICANCE

TUMOURS OF SURFACE EPITHELIUMSEROUS TUMOURS Most common Tall columnar epithelium resemble

endosalphinx 50% bilateralGross: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 tumoursResemble endocervixUsually unilateral,5%bilateral12%-25% of ovarian neoplasmGROSS:Multiple cyst without surface involvementMultiloculated with sticky gelatinous fluidHoney combed appearance

MUCINOUS TYPES

MICROSCOPIC FEATURES

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

EndometrioidResemble endometrium lining10% of ovarian neoplasmGROSS:Partly cystic and partly solid with foci of hemorrhageMICROSCOPIC FEATURE:Typical glandular patternLike endometrium

CLEAR CELL CARCINOMA Highly malignantResemble clear cell carcinoma of endometriumGROSS:Large partly cystic and solid MICROSCOPIC FEATURE: Large cuboidal cell with abudant clear cytoplasmHobnail cells

BRENNER TUMOURResemble transitional cell of urinary tract1%-2% of neoplasmGROSS: Solid yellow grey firm mass90% UnilateralMICROSCOPIC FEATURE:Epithelial cell nest- puffed wheat& Coffee

bean nuclei

GERM CELL TUMOURSTeratoma:MATURE- BENIGN:GROSS:Unilocular cyst with hair and cheesy sebaceous material,teeth,bone…MICROSCOPIC FEATURE:Stratified squamous epithelial with Hairshaft,sebaceous gland &skinAdnexal structureKaleidoscopic appearanceEX:Dermoid cyst

IMMATURE –MALIGNANTGROSS:BULKY solid mass with variegated appearanceMICROSCOPIC FEATURE:Immature tissue differentiating towards gland ,nerve ,muscle ,CartilageStruma ovarii- contain thyroid tissueCarcinoid tumour-argentaffinoma

Dysgerminoma80% 90%-Unilateral GROSS:Solid mass, elastic rubber consistencyPink ,lobulated, soft &fleshyMICROSCOPIC FEATURE:Large cells in bunchesDark staining nuclei, clear translucent cytoplasmLmphocytic infiltration of fibrous stroma

Endodermal sinus tumourGROSS:Solid with cystic degeneration MICROSCOPIC FEATURE:Glomerulus like structureSchiller duval bodies- germ cellsCentral blood vessels

CHORIOCARCINOMAVery vascular, highly malignantMICROSCOPIC APPEARANCE:Dimorphic population of syncytotrophoblast

and cytotrophoblast in necrotic& hemorrhagic pattern

SEX CORD STROMAL TUMOURS- mesenchymomasGRANULOSA TUMOURS:Resemble granulosa cell of graffian follicleGROSS:U/L yellowish brown oval,Soft, lobulatedMICROSCOPIC FEATURE:Rosette like call exner bodies contain Central amphorous pink materialSurronded by granulosa cells

FibrothecomaResemble theca lutein cells of graffian follicleGROSS:U/L Solid white firm massMICROSCOPIC FEATURE:Spindle shaped fibroblast & Collagen with fat laden polyhedral cells

SERTOLI LEYDIG CELLS:GROSS: SOLID grey to golden brownMICROSCOPIC FEATURE: Well differentiated tubules – tubules

composed of sertoli and leydig cells interspesed with stroma

TUMOUR FROM CONNECTIVE TISSUE OF OVARYOVARIAN FIBROMA:3% Of ovarian neoplasmGROSS:Oval with smooth surface with large vein in capsule,Firm and harder in consistencyCalcerous degeneration occursMICROSCOPIC APPEARANCE:Uniform spindle shaped cells inFeather stitched patternResemble ovarian cortexMEIG SYNDROME

KRUKENBERG TUMOUR:

Almost BilateralGROSS:Smooth surfaceSolid waxy consistency with cystic spacesMICROSCOPIC 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 cysts2. Germinal inclusion cysts3. Follicular cysts4. Theca lutein cysts

Atretic cystsGraffian 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 cystsWalthard 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 cystsEnlargement 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 estrogenPolycystic ovaries in PCOD- secrete androgens Triad- anovulation, hirsutism,

Rx- disappear spontaneouslyovulation induction- MDPA, Clomiphene citrateCyst persisting more than 2 months- neoplastic

Theca lutein cystsLess common usually B/L multicystic large upto 25 cm

•Endogenous causes- molar pregnancy, chorioCa, multiple pregnancy•Exogenous causes- ovulation induction

High output of GnIncrease 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 causeIn absence of other disease

•Spontaneous regression•Surgical removal of cystic portion of ovary or whole of ovary.

Corpus luteum cystGreater than 3cm

Corpus luteum of pregnancy- forms cyst- degenerates b/w 2nd n 3rd 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 pregnancyHyperplastic 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.

Occasionally some androgenic action – causes virilisation of mother or her

female child.

BENIGN OVARIAN TUMOURS

M . Kiruthika III OG

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 .

Surface epithelium

Corpus luteumTheca cell

Granulosa cell

Ovum

Germ cell tumours• Benign cy stic teratoma

• S truma ovarii• Gonadoblastoma

Sex cord stromal Tumours• Fibroma• Theca cell tumour

Surface epithelial tumours• Serous cystadenoma• Mucinous cystadenoma

• Endometroid cystadenoma

• Brenner tumour

Classification of benign ovarian tumours

BENIGN SURFACE EPITHELIALTUMOURS

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

Respiratory embarassment

Frequency of micturition Edema

Ovarian Cachexia

ASCITES – MEIG‘ S SYNDROME

Ascites

Hydrothorax

Dull ache lower abdominal pain , low back pain.

Peritonitis, shock due to rupture of large cyst. Dyspareunia

Menstrual disorders

Menorrhagia

Amenorrhoea

Post menopausalBleeding.

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 downwardsCONSISTENCY – tense & cystic fluid thrill elicited

PERCUSSION

AUSCULTATION silent

BIMANUAL EXAMINATION GROOVE’S SIGN

MALIGNANT OVARIAN TUMORs

by

Madhu maetha .R III O & G

SECOND MOST COMMON ( 10-15%) GYNAECOLOGICAL CANCER

HIGH MORTALITY RATE

80-85% WOMEN WITH OVARIAN CANCER DIE

CLASSIFICATION

SEROUS CYSTADENOCARCINOMA MUCINOUS CYSTADENOCARCINOMA ENDOMETROID CYSTADENOCARCINOMA CLEAR CELL CARCINOMA MALIGNANT BRENNER TUMOUR UNDIFFERENTIATED CARCINOMA

DYSGERMINOMAENDODERMAL SINUS

TUMOURCHORIOCARCINOMAMALIGNANT TERATOMAEMBRYONAL CELL

CARCINOMAPOLYEMBRYOMA MIXED TUMOURS

GRANULOSA CELL TUMOR

SERTOLI LEYDIG CELL TUMOR

MALIGNANT GERM CELL TUMOURS

MALIGNANT SEX CORD STROMAL TUMOURS

OVARIAN EPITHELIAL CARCINOMA

Classification

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 ADENOCARCINOMAWhich 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 GERM CELL

TUMORS

MALIGNANT SEX-CORD STROMAL

TUMORS

UNCOMMON OVARIAN TUMORS

Malignant germ cell tumorsINCIDENCE *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 MARKERSDYSGERMINOMA 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 PICTURESYMPTOMS- “SILENT KILLER”EARLY STAGE DISEASE- asymptomatic

Non specific GIT symptoms

PRESSURE SYMPTOMSUrinary 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

Extremes of Age Rapid

growth of tumor

In HISTORY,

Loss of weightPain

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 examinationNodules 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 TUMORS

MALIGNANT TUMORS

unilateral bilateral

cystic solid

mobile fixed

smooth irregular

*Ascites*Cul-de-sac nodules*Rapid growth rate

COMPLICATIONS AND DIFFERENTIAL DIAGNOSIS

COMPLICATIONSTORSIONRUPTUREPSEUDOMYXOMA OF THE PERITONIUM INFECTIONEXTRAPERITONEAL DEVELOPMENTSECONDARY 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.

RUPTURETRAUMATIC SPONTANEOUSDirect violence to

abdomenDuring labour Bimanual

examination

Malignant ovarian tumors-papillomatous type

Pappilomatous serous cystadenomas

Actively growing mucinous cystadenomas

rupture

Tumors Mechanism of ruptureMalignant ovarian tumors Pappillomatous serous tumours

Carcinoma cells infiltrate through the connective tissue capsule to ulcerate into the peritoneal cavity

Actively growing mucinous cystadenomas

The epithelial elements of 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 InfrequentMost 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 MALIGNANCY50% in serous cystadenomas.5% in mucinous cystadenomas.1.7% in dermoid cysts.

Never drive faster than your guardian angel can fly.

DIFFERENTIAL DIAGNOSIS FULL BLADDERPREGNANT UTERUSMYOMAASCITESOTHER ABDOMINAL TUMORS

FULL BLADDERTense 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.

MYOMAUsually hard or firm ,without the tense cystic

consistency of atypical ovarian cystPedunculated 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 TUMOURSA 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.MARIMUTHU

1.ULTRASOUNDTransabdominal ultrasound If tumour is abdominalTransvaginal 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 ecogenicThe 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 dopplerNeovascularisation, Increased blood flow,Low pulsatile index <1 andResistance index <0.4 are suggest

malignancy

Colour doppler

3.X-Ray

Abdomen and pelvis demonstrate soft tissue shadow or teeth in

dermoid cystChest To rule out pulmonary metastasis and Hydrothorax- rt sided in Meigs syndromeBarium 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 markersCA 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

fromPelvic 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.

Caecum

Rt. Paracolic gutter

Ascending Colon

Transverse Colon

Descending Colon

Lt. Paracolic gutter

Recto Sigmoid

Colon

Small intestine

& mesentery

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 – biopsyscrapping 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

I A – 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 washings

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 surgeryTo 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 REGIMENINTRAVENOUS CHEMOTHERAPY

DRUGS DOSE(mg/sq.m)

ROUTE INTERVAL(Weeks)

CYCLES

PACLITAXELCARBOPLATIN

175AUC=5-6

IV 3 6-8

PACLITAXELCISPLATIN

13575

IV 3 6-8

CYCLOPHOSPHAMIDECISPLATIN

75075

IV 3 6-8

DRUGS DOSE(mg/sq.mm)

ROUTE

INTERVAL(Weeks)

DOXORUBICIN,LIPOSOMAL

35-50 IV 3-4

TOPOTECAN 1-1.254

IVIV

13(DAILY*3-5DAYS

ETOPOSIDE 50 PO 3,DAYS 14-21

INTRAPERITONEAL CHEMOTHERAPY

DRUGS DOSE(mg/sq.m)

ROUTE INTERVAL(Weeks)

CYCLES

PACLITAXEL 135 IV 3,DAY 1 6

CISPLATIN 50-100 IP DAY 2

PACLITAXEL 60 IP DAY 8

Platinum Compound

Carboplatin Cisplatin

Taxol (Paclitaxel)

STAGE 1 EPITHELIAL TUMOUREarly stage,low risk NO adjuvant therapy is requiredEarly stage,high risk Adjuvant therapy is required Carboplatin and paclitaxel given for 3-6

cycles

ADVANCED STAGE EPITHELIAL TUMOURAdvanced 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

myelosuppressionFIVE ARM TRIAL Addition of either

gemcitabine,topotecan or doxorubicin to the standard regimen does not enhance survival rate

INTRAPERITONEAL CHEMOTHERAPY

Ideal anticancer agentVery effective systemically against ovarian

cancerPenetrate deep into the tumorStays 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 ovarian cancer patients with optimal debulking

Strengths of Intraperitoneal chemotherapyAchieve 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 CatheterBlockadeLeakageInfectionDiarrheaBowel perforationFistula formation

Patient selection issuesPatient characteristics

eg.: renal function ; neuropathy (DM –associated)

Significant peritoneal adhesionOngoing abdominal infection, or indwelling IP

catheter becomes infected or malfunction, will be unable to treated by this route of drug delivery

NEOADJUVANT CHEMOTHERAPYIn 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

ActinomycinCyclophosphamide

BEP BleomycinEtoposideCisplatin

VBC VincristineBleomycinCisplatin

SIDE EFFECTSWhile 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 IIIcInoperable –

BiopsyNeodjuvant

chemoCisplatin +

PaclitaxelComplete

responseSec.

Cytoreductive surgery done now

Palliative and Adjuvant Therapy

ByR.Pani MalarIII OG MMC

Palliation

From Latin palliare to cloakAny 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

•Opiates – Morphine•Muscle spasm – Diazepam

•Bone pain – NSAIDs•Nerve pain – Sod Valproate

carbamazepine•Bowel and bladder pain –

anticholinergics

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 featuressmall disease volume prior to

surgerysmall residual disease after

surgeryabsence of ascites have good

prognosis

5 yr SurvivalFIGO Staging

5 year survival

Stage 0 90 – 100%

Stage I 70%Stage II 25 – 30%Stage III 10%Stage IV 0 - 5%

OVARIAN TUMOURSAND

PREGNANCY

BYX.A.PRASANNA

III UNIT OG

COMMON TUMOURSDYSGERMINOMAMATURE CYSTIC TERATOMAPARAOVARIAN CYSTSEROUS CYSTADENOMACORPUS LUTEAL CYST OF PREGNANCYFIBROMA

MATURE CYSTIC TERATOMA

Mostly asymptomaticShooting pain down thighs, pain abdomenPressure effects

DyspnoeaPrecordial pain

DyspepsiaFrequency

Constipation

CLINICAL FEATURES

Uterus larger than gestational ageMass pushed behind uterus Or to 1flank

StagingSimilar to non-pregnancy stateUsually stage 1 – low grade

Examination

•INCIDENTAL FINDING•MALIGNANT –IRREGULAR SEPTA,SOLID AREAS,PAPILLARY EXCRESCENCESUSG•USED AS A SCREENING PROCEDURE•NOT SPECIFICCA 125•MATERNAL SERUM•ENDODERMAL SINUS TUMOURAFP

INVESTIGATIONS

DIFFERENTIAL DIAGNOSISUterine leiomyomasPelvic kidneyRetroperitoneal

tumourEctopic pregnancyRetroverted gravid

uterusNon pregnant horn

of bicornuate uterus

HINGORANI SIGN

Effects of pregnancy on tumourTorsion

InfectionIncarceration

Effects of tumour on pregnancyUrinary retention

UTI Malpresentation

Rupture -peritonitis

COMPLICATIONS

TORSION OVARY

Effect of tumour on labourObstructed labour

Uterine inertiaRupture

Effect on tumour in puerperiumTorsion (25%)

Why– Rapid involution of uterusLax abdominal walls

Mobility of abdominal viscera

Large solid massesComplications –torsion, incarceration in cul de sacMore lymphatic spreadTreatment – unilateral oopherectomy

+Ipsilateral pelvic & para aortic node dissection

15% bilateral10% recurs

DYSGERMINOMA

Click icon to add picture

Rare Complicated by

Rupture 19% haemoperitoneum

14% dystocia

Edema ,prominent luteinisation ,lacks recognizable differentiation

SEX CORD STROMAL

Similar to non pregnant casesIndividualize treatment

Total abdominal hysterectomyOR

Cytoreduction

Gestational age , fetal viability ,demand

EPITHELIAL TUMOURS

MANAGEMENTSurgery – II trimesterEven then , risk of preterm labor , IUGR ,IUD common

Chemotherapy – controversial .II , III trimester

Radiotherapy – contraindicated

TIMING OF TUMOR

I TRIMESTER

CYSTECTOMY

OVARIECTOM

Y

> 28 WKS

PTLNORMAL DELIVERY

REMOVE TUMOR 1 WK AFTER DELIVERY

WAIT TILL AAA16 WKS

Complicated tumours

< 10 CM •USG – CYST•LUTEAL CYST –RESOLVES BY 12 -16 WKS•IF NOT ,SURGICAL REMOVAL AFTER PUERPERIUM

OBSTRUCTS LABOR

•CAESARIAN FIRST, •TUMOUR REMOVAL

TORSION •IMMEDIATE SURGERY•LAPAROTOMY

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

POSTOPERATIVE CARE

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 avilablePrognosis poor

HIGHLIGHTS

Mostly resolve spontaneously PCOS - Anovulation, hirsutism

USG findings – ‘Necklace appearance’↑E2, LH, androgens

Treatment – Metformin 500 mg tds./Surgery – Lap. punctures

Non neoplastic enlargements

Commonest 80% - epithelial cell tumours (90 % malignant)

Tumour in adolescent and post menopausal women – more often malignant

Boderline ovarian tumours /LMPDon’t invade stroma

Mitotic figures <4/10 high field

OVARIAN TUMOURS

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

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 .

MALIGNANT TUMOURS

Ascites + mass , bilateral , rapidly growing – malignant

Except – meig’s ,fibroma ,brenner tumour

Complications – TorsionRupture

Pseudomyxoma peritonei Infection

Retroperitoneal haematoma

CLINICAL FEATURES & COMPLICATIONS

GOLD STANDARD - INVESTIGATIONTransvaginal ultrasound

– BENIGN

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

Non -echogenic

malignant – bilateral ,solid tumour

Ascites Septa >5mm

Papillary projections

BENIGN - Total abdominal hysterectomy with bilateral salpingo oopherectomy ,

Unilateral ovariotomyCystectomy

Laparoscopic /USG guided aspiration

Stage I , II – Total abdominal hysterectomy and bilateral salpingo oopherectomy , omentectomy

Stage III,IV –Debulking , postoperative chemotherapy , radiotherapy .

TREATMENT

SCREEN BY TRANSVAGINAL

ULTRASOUND

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