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Ovarian carcinoma
By
Dr. Khattab KAEO
Prof. and Head of Obstetrics & Gynaecology
Department
Faculty of Medicine, Al-Azhar University,
Damietta
Incidence: 1/10 000;
1.35/10 000 among
Ashkenazi Jews born in
Europe & America. Ovarian
cancer = 4% of cancer in
women. 25% of all ovarian
neoplasms are malignant.
The incidence is high in
developed countries.
Prognosis: 2/3 of cases are diagnosed in
stage III or IV. This could be attributed
to the facts of vague symptoms and lack
of adequate screening.
1/3 of stage I cases are upgraded to
stage III.
All these facts explain the poor survival rate.
Ovarian carcinoma is the 4th most
common cause of death in women in
Western countries.
In the USA ovarian cancer is the 5th most
common cancer & is the 4th most
common cause of death due to cancer.
Epithelial ovarian carcinoma is the most
frequent cause of death from
gynaecological malignancy.
Risk factors:
- Age: Incidence peaks between ages of 65
and 75 years (1 in 400; at the age of 50,
the prevalence is 1:1500). Ovarian neoplasms occurring in the childhood up to the
early twenties are probably malignant
(non-epithelial). Germ cell tumour is the
most frequent malignant tumor in children.
-Nulliparity.
- History of breast or endometrial cancer.
- Higher consumption of animal fat,
proteins and whole milk.
- The use of infertility drugs for >1 y. The
use of CC for >1 year carries a 10-x risk.
- Family history: Only 5% are due to hereditary factors
(30% among Ashkenazi Jews for ex). It is an autosomal dominant disease. Syndromes include BRCA1
or 2 mutation & Hereditary NonPolyposis Colorectal
Cancer Syndrome (HNPCC, Lynch Syndrome of
familial breast, colo-rectal & ovarian cancer).
BRCA1 gene is on 17q.
Ovarian tumors, not epithelial, arise in some other rare
syndromes e.g. Peutz-Jagher syndrome (granulosa
cell tumours, Brenner tumours & dysgerminoma),
Gorlin syndrome (fibromas) & gonadal dysgenesis
(gonadoblastoma).
Hereditary ovarian or breast cancer = ≥2 affected 1st
degree relatives or a family pedigree indicative of
autosomal inheritance. One affected relative = 2-3x increase in relative risk. 2 affected 1st degree
relatives = chance increases from 1:70 to 1:40.
BRCA1 is found in almost all families with both
breast & ovarian cancer & in 40% of families with
breast cancer alone. 80% of affected individuals
develop malignancy.
The mean age of onset (50y) in BRCA1 mutations is 5
years younger (risk begins to rise in the late 30s).
Protective factors:
1- Parity.
2- There is inverse association with age at first
birth!
3- The use of COCs (≥5y) substantially reduces
the risk of sporadic & hereditary ovarian
carcinoma.
4- Tubal ligation or hysterectomy  reduced risk
through reduced contamination of peritoneum
& ovary and possibly through decreased ovul.
5- Breast feeding suppresses ovulation.
6- Higher consumption of dietary fibres, vit A & C
7- Infection with mumps virus!
Hypotheses:
Fathalla postulated repeated minor trauma to the
epithelial surface. In animals, proliferations of
epithelium after ovulation and mitotic figures near
the site of ovulation have been shown. Factors that
suppress ovulation reduce the risk of ovarian cancer
Risk is increased with fertility drugs.
The Gn hypothesis postulates exposure of the ovary to
continuous high levels of Gn. Parity & COCs have a
protective effect Risk is increased with fertility drugs
The pelvic contamination theory postulates that pathogens may contaminate the ovary after passage
through the genital tract.
BRCA1 & 2 function as tumour suppressor genes. They
encode proteins necessary for repair of DNA damage
Mutations  uncontrolled cell growth  cancers in
the breast, tubes, ovary & peritoneum.
STAGING: FIGO.
Stage I
Ltd to the ovary.
IA Ltd to 1 ovary; no tumor on the surf.; no ascites;
cap. is intact.
IB Ltd to both ovaries + same conditions.
IC Either IA or IB with tumour on the surface, ruptured cap or malign. ascites/+ve peritoneal washing.
Stage II
Pelvic extension.
IIA Extension to the uterus or tubes.
IIB Other pelvic extensions.
IIC Either IIA or IIB with tumour on the surf; ruptured cap or malign ascites /+ve peritoneal washing.
Stage III Peritoneal implants outside the pelvis
+ve LN; &/or superf. liver M
IIIA Microscopic seeding of peritoneal surfaces.
IIIB Histological implants of peritoneal surfaces <2cm
IIIC Same implants >2cm.
Stage IV Distant metastasis including liver
parenchyma, pleural effusion, etc.
WHO Histological Classification:
I- Epithelial tumours:
Serosal tumours: Serous cyst adenocarcinoma.
Constitutes 50% of all epithelial malignancy &
40% of malignant ovarian tumours (the com
monest ovarian carcinoma). Bilateral in 50%
of cases Presents as stage III in 50% of cases
Ascites is always present. Psammoma bodies
are encountered in >30% of serous tumours
(characteristic). They are microcrystals of
bone similar to calcium phosphate crystals
formed intracellularly and are consequences
of dystrophic calcification. Usually endophytic
Most are partially cystic & partially solid.
Either smooth or with papillary projections.
Mucinous carcinoma: Bilateral in 5-10%.
Clear cell carcinoma: Characterised by Hobnail cells (polygonal cells with clear cytoplasm).
It contains tubules, glands, papillae & cysts.
Bilateral in 40%. 50% are stage I.
Endometrioid carcinoma: Up to 30%
coexist with endometrial adenocarcinoma & closely resembles it.
10% coexist with endometriosis
and arises in endometrioma. The
vast majority are unilateral &
almost always stage I. Attacks of
pain, unusual with ovarian cancer,
are common. Usually cystic and
chocolate brown in colour If such a
cyst ruptures spontaneously,
malignancy should be suspected.
Brenner tumours arise in epithelial
cells of Wolffian origin.
Transitional cell carcinoma: Brenner tumour
closely resembles low-grade transitional cell
carcinoma. Transitional cell carcinoma differs
in lacking the benign Brenner component,
are more likely to spread beyond the ovary
and more likely to result in death even if
confined to the ovary. It also lacks the prominent stromal calcifications present in most
malignant Brenner tumours. In spite of that
transitional cell carcinoma is more sensitive
to chemotherapy and has a more favourable
survival than serous carcinoma.
Mixed epithelial tumours.
Undifferentiated tumours.
Unclassified epithelial tumours.
II- Stromal gonadal (Sex cord stromal) tumours
Previously called mesenchymoma. 90% are
thecoma and granulosa cell tumours. Inhibin
(particularly  unit) distinguishes them from
non-sex cord tumours.
Granulosa cell tumours constitute 10% of all solid
malignant ovarian tumours and 70% of sex cordstromal tumours. They have a good prognosis, but
0.6-6% of cases is associated with endometrial
adenocarcinoma. It is a hormonally active tumour
(most tumours secrete oestrogen; few produce androgen), may be malignant or semi-malignant.
Sertoli-Leydig cell tumour (Androblastoma): Rare
and occurs in young adult females. The well-differen
tiated tumour may be of the Sertoli cell type, Leydig
cell type, Sertoli-Lydig cell type or Sertoli cell type
with lipid storage Moderately & poorly-differentiated
types also exist. The tumour may contain cartilage &
GIT epithelium (heterogenous type). It may secrete
testosterone (rarely oestrogen) in 25% of cases The
androgen-secreting tumor is called arrhenoblastoma
The tumour usually appears small white or yellowish
It is usually of low-grade malignancy. The tumour is
mainly composed of tubules lined by cuboidal cells
with interstitial cells of Leydig (containing the rodshaped structures, crystalloids of Reinke) inbetween
the tubules.
Gynandroblastoma
III- Germ cell tumours
Constitute 10% of ovarian tumours with
4% are malignant. They are more prevalent in children & adolescents. Under
the age of 20, germ cell tumours = 6070% of ovarian tumours with 33% are
malignant (under the age of 20, 85%
are malignant). Secrete AFP & hCG.
Either dysgerminoma or embryonal carcin.
The latter is either embryonic (polyembryoma or teratoma) or extra-embryonic (chorio
carcinoma or endodermal sinus tumour).
The following is the WHO histologic
classification of germ cell tumours:
i- Teratoma.
A- Immature teratomas may be solid &/ or cystic. It is
composed of both embryonal & adult tissues from all
3 germ layers. Mesodermal elements often predomin
depending on maturity of the tumor. Endodermal
elements may be represented by tubules lined with
columnar epithelium. Ectodermal elements usually
consist of hair, teeth & neural tissue, contained
within loose stroma.
It is reported in ages ranging from 14 months to 40 y
80% presents as a palpable pelvic/abdominal mass,
mostly unilateral, firm, irregular, 5-35 cm with multi
ple cystic spaces 0.5-10 cm diameter each with areas
of haemorrhage & necrosis. Neural tissue may be
visible grossly. Fever & leukocytosis are noted in
25% of cases. Haematogenous metastases are rare.
Malignant teratoma is unilateral.
Unilateral salpingo-oophorectomy may be sufficient
for stage I tumors; VAC chemotherapy, (over a 12month period) is added for grade 3 and stage II or
III tumours Rupture before or during surgery carries
an 80% risk of recurrence.
B- Mature teratomas may be solid (grade 0) or cystic.
a- >95% of teratomas are mature (adult) cystic teratomas (dermoids).
Epidermal elements often predominate. It may be found in neo
nates, but predominates in the reproductive years. Size ranges
from 4 mm to 15 cm, usually unilocular with thick greasy fluidy
sebum & desquamated cells (mucinous intestinal or clear watery
brain cells). There may be laminated pellets of lipids. Teeth in
30%. Bilateral in 12%. It tends to have a long pedicle (torsion
is the most common complication). The pedicle may dissolute
( parasitic dermoid). Wall is thick and gray, lined by stratified
squamous epithelium. There may be a projecting area in the
cavity known as Rokitansky's protuberance or the dermoid process. Strange contents include rudimentary fetal tissue such as
cranium & brain, mandible, arm & forearm, ribs, pelvic bones,
vertebrae & phalanges (complex dermoid). Cystic teratomas
tend to be asymptomatic; however, 47% of patients complains
of pain, while 15% complains of a mass & 15% complains of
bleeding. Rupture is rare; chemical peritonitis may occur which
may be catastrophic Peculiarly, rupture may result in expulsion
of teeth, bones and hair from the rectum or bladder. A small
defect may result in chronic or intermittent abdominal pain and
granulomatous reaction with lipid-laden macrophages, lymphocytes, plasma cells & foreign body giant cells.
b- Dermoid cyst with malignant transformation; 2% of benign cys
tic teratomas contain a malignant component Extirpation of the
tumor with conservation of the ovary or hysterectomy with uni
lateral or BSO may be chosen according to patient's age & fert.
C- monodermal (highly specialised) teratoma.
a- struma ovarii. 5-10% of cystic teratomas. Diagnosis is made if thyroid tissue occupies all or
most of the tumour or if thyroid tissue is recog
nised grossly. The tumor is smooth, rounded &
the cut surface has a glistening amber appearance
b- carcinoid (argentaffinoma) is a serotonin-prod
ucing tumour arises in association with dermoid.
The typical carcinoid syndrome consists of patchy cyano
sis, flushing, diarrhea, colic, oedema, hypertension & car
diac failure due to tricuspid valve lesion. Most ovarian
carcinoids are of the insular type (= those derived from
the mid-gut; solid islands of cells separated by a dense
fibrous stroma Trabecular carcinoids are also reported (=
those derived from the fore & hind gut; longway ribbons
of cells separated by loose fibrous stroma). The larger
the carcinoid component, the more solid is the
tumor. The median age for the insular & the tra
becular types is 57 & 47 y (well above that for
dermoid. The median diameter is 10 cm. Symptoms regress after removal of the tumor. The
optimal ttt is TAHBSO. In the childbearing period however, a unilateral SO may suffice, but
the contralateral ovary should be biopsed.
c- struma ovarii and carcinoid (commonly of the trabecular type). d- others.
ii- Dysgerminoma: The commonest malignant germ cell neoplasm
(=48%) Solid, usually ovoid or lobular, of rubbery consistency
& greyish colour. Morphologically, it is identical to testicular
seminoma (both arise from the primordial germ cells of the indefferent stage of gonadogenesis). About 15 cm (ranges from
3 cm to a size filling the abdomen), with a smooth cap, with
necrosis & hage in 50% It secretes hCG, but may be estrogenic
less commonly androgenic. It is bilateral in 15% of cases Micro
scopically, it consists of masses of large clear epithelial cells
separated by fine connective tissue infiltrated by lymphocytes.
The cells are arranged in cords or in an alveolar pattern. The
majority of cases are diagnosed before the age of 30. Many
appear relatively benign and do not recur. It is both radio- &
chemo-sensitive. The optimal therapy must be based on the
operative findings and a histologic examination. Unilateral SO
can be adopted to unilateral cases in young nullipara, but only
in conjunction with peritoneal saline irrigation for cytologic
study, wedge biopsy of the contralateral ovary, omental biopsy
and aortic node sampling at the level of the duodenum. Any
palpable nodes should be removed. Bilaterality does not affect
survival, while marked lymphocytic infiltration or a granulomat
ous response are associated with a favourable outcome. The
most important microscopic determinant of survival is the presence of other germ cell elements. If >1/3 of a stage I t is com
posed of endodermal sinus tumour, choriocarcinoma or G 3 im-
iii Endodermal sinus tumor: = 20% of germ cell t
It is highly malignant and affects children & young
adults (14 mo to 45 y. It is 2nd to dysgerminoma before
the age of 20y). Pain is present in 77% of cases, abdom.
mass in 27% & fever in 24%. Average size is 10-20
cm, unilateral, the cut surface is yellowish tan
or gray with areas of necrosis or hage & Swiss
cheese small cysts. It may be found as a broad
ligament tumor when some germ cells did not
complete migration from the y s to the gonadal
site The classic microscopic pattern is reticular
(consists of a network of sinuses lined by cuboidal cells with scanty cytoplasm & occasional
hobnail cells). The characteristic appearance is
Schiller Duval body, found in 75% of the t; it is
villus-like structure with central bl v (y s endoderm surrounding a capillary). There ± intra &
intercellular hyaline droplets (with AFP found
in them The tumor produces AFP Although very chemo
sensitive, prognosis is poor (fatality rate = 90% & peritoneal metastasis is encountered after removal of a well
encapsulated tumor. At the best, survival rate is 17%,
and that is when the tumor is <10 cm, confined to the
ovary & paradoxically if ruptured!) ttt is unilat. SO
iv- Choriocarcinoma. Extremely rare. Highly malignant
Most commonly associated with dysgerminoma. It is
thought that the presence of chorionic villi, establishes
the origin of the tumour from an ovarian pregnancy!
Diagnosis of pure non-gestational choriocarcinoma
can only be made with certainty prebubetal (the high
hCG levels stimulates ovarian stroma  precocious
puberty or IUB. Also, the rapidly enlarging tumour is
often aggravated by ascites. Rupture  peritoneal
haemorrhage and acute surgical emergency).
Choriocarcinoma is always unilateral. The opposite
ovary is frequently enlarged by theca-lutein cysts or
shows marked stromal luteinisation. The surface is
nodular with haemorrhagic tissue within a thin caps.
The tumor is extremely friable with areas of necrosis
and cavitation. Microscopically, it is composed of syn
cytiotrophoblasts lining blood-filled spaces or cover
islands of cytotrophoblasts The tumor secretes hCG,
oestrogen and other trophoblastic products. It does
not respond well to conventional treatment of gestational choriocarcinoma; responds better to MAC.
Endodermal sinus tumour and choriocarcinoma are
called tumours of extra-embryonic tissues.
v- Embryonic carcinoma: Rare. Reported in
ages from 4-28 y. Unilateral, 10-25 cm in dia
meter. Smooth and the cut section is yellow
to gray with occasional cysts, necrosis & hage
Sheets/nests of pleomorphic cells with round
vesicular nuclei containing prominent nucleoli
Syncytiotrophoblastic giant cells are scattered
in the periphery or throughout the stroma.
Hyaline droplets characteristic of endodermal
sinus tumor and AFP are found in these cells
and in the mononuclear embryonal cells.
Secretes hCG and causes precocious puberty
in 50% of cases. IUB & amenorrhoea are reported too. ttt is unilateral SO with adjuvant
chemotherapy (MAC or VAC).
vi- Polyembryoma.
vii- Mixed tumours.
IV- Mixed gonadal stromal & germ
cell tumour (Gonadoblastoma): It
is composed of large primitive
germ cells & small granulosa cells.
The latter may form Call-Exner
bodies (small rosettes) Stroma
may contain Leydig-like cells.
Gonadoblastoma almost always
occurs in gonads of inter-sexual
patients Y chromosome is detected
in >90% of cases. 80% of patients
are phenotypically females.
V- Lipoid cell tumours: Rare tumors
causing masculinisation and signs
of hypercorticoidism such as striae,
obesity, polycythaemia, diabetes
and hypertension. The tumour is
commonly large & yellowish with
cells containing a high amount of
lipid The 17-ketosteroid output is
greatly increased and the excretion
of 17-hydroxycorticosteroids is
also raised.
VI- Unspecified CT tumours: Fibro-sarcoma.
Often occurs in postmenopausal women.
Usually lobulated, 10cm in average & the cut
surface shows focal necrosis & cystic degene
ration. Leiomyosarcoma and myxosarcoma.
VII- Unclassified tumours. lymphocytic, histo
cytic & Hodgkin's lymphomas. Diffuse or
localised. Characteristically, lymphomatous
tissue, does not destroy the normal architecture & this differentiates it from carcinomas.
Anaemia is out of proportion of vaginal
bleeding which occurs in 20-30% of cases.
VIII- Metastatic tumours: Constitute 10%-20%
of ovarian tumours.
Secondary
carcinoma
of thetract,
ovary
1ry tumour may
be in the genital
breast,
stomach or large intestine. The meta static
growths reach a large size while the 1ry growth is small. Krukenburg's tumors are most
commonly due to lymphatic spread from endo
metrial carcinoma. The ovarian tumours are
bilateral, of equal size, smooth & lobulated.
They remain freely mobile. The cut surface
typically exhibits gelatinous necrosis & mucin
-filled spaces of variable size. There are very
cellular (hyperplastic) stroma, in which there
are large epithelial cells lying singly or in alv.
The epithelial cells have a crescentic nucleus
pushing a clear cytoplasm full of mucin (signet
ring appearance). The patient is usually between
30 & 40 y of age with a typical presentation
of a large cystic mass and the majority of
Spread
IMPLANTATION. Involvement of the
omentum occurs in >80% of cases.
The major route of spread is along
the right paracolic gutter to the
undersurface of the right hemidaiaphragm, leading to obstruction
of diaphragmatic lymphatics and
early onset of ascites. Lymphatic
spread occurs mainly to the paraaortic glands, sometimes to the
pelvic and even inguinal groups.
Presentation
- Family history
of ovarian, breast or colorectal
carcinoma. Ask of which histologic type? Ask
about the ethnic origin.
- Early symptoms are often non-specific such
as abdominal discomfort, nausea, gas, etc.
- As the tumor enlarges it causes compression
symptoms such as constipation, urinary freq,
pelvic pressure, etc.
- The tumour itself may undergo complications
of torsion, rupture, haemorrhage, etc.
- Although weight loss is occasionally seen with
anorexia & intestinal obstruction, weight GAIN
is much more common!
- Pelviabdominal mass in most patients Benign
masses tend to be unilateral, cystic, mobile
& smooth, while a malignant mass tends to
be solid, nodular & immobile. A huge mass is
often benign or of low-grade malignancy
- Amenorrhoea is much more likely to occur
with functioning tumours.
- Oestrogen-producing tumours accounts for
3% of all solid tumours of the ovary. Estrogen excess causes hyperplasia of the myometrium ( enlarged uterus); hyperplasia
of the endometrium ( IUB or amenorrhea
if the level of oestrogen does not fluctuate)
hyperplasia of the mammary gland tissue
( enlarged tender breasts) & precocious
puberty. 60% of estrogen-producing tumors
occur in the childbearing period ( IUB);
30% occur in postmenopausal women (
postmenopausal bleeding) & 10% occur in
children ( precocious puberty). In childhood and early adulthood the tumours are
mainly granulosa cells, and should be considered as carcinoma In later life the tumors
are usually thecoma. In 14% of cases endo
metrial hyperplasia becomes atypical & car-
- Androgen-producing tumours are
of three types: Sertoli-Leydig cell
tumour (arrhenoblastoma), hillar
cell tumour and lipoid cell tumour.
Hillar cell tumour is very rare and
occurs in post-menopausal women.
Defeminsation occurs followed by
mild virilism... It is a small brown
tumour in the ovarian hilum
consisting of Leydig cells with
crystalloids of Reinke
- It should be noted that non-functioning ovarian tumours may result in hormone production
The presence of tumour growth in the ovary
occasionally induces a thecal transformation o
the ovarian stroma which in turn produces ste
roids, sometimes androgenic but more commo
nly oestrogenic. This has been reported with
benign and malignant cysts, Brenner tumours,
fibroma and secondary carcinoma of the ovary
- Disordered small bowel motility secondary to
adhesions and interference with neural transmisssion through the mesenteric plexus is a
prominent feature and may simulate smallbowel obstruction. Colonic obstruction occurs
due to compression by the mass, less
commonly due to invasion.
CA 125: 80%Investigations
of patients with epithelial cancer
has abnormal values (N: <35IU/ml).
X-ray may distinguish a benign cystic teratoma
Psammoma bodies of serous tumors or
ascites and dilated loops of intestine.
CXR: Effusion or, rarely, metastases.
IVU: Ureteric displacement obstruction or
cystic kidney.
Barium enema ( sigmoidoscopy): Diverticulae
cancer colon, inflammatory bowel disease or
metastases. However, cystoscopy is not a
routine because involvement of bladder
mucosa is exceedingly rare.
Ultrasonography: Malignant tumor is generally
multi loculated, more solid, >5 cm with thick
septa & solid nodules Ascites is easily detect-
Differential diagnosis
Ascites.
Retroperitoneal tumour.
A functional cyst is suspected if unilateral & of a diameter <8-10 cm.
The likelihood of ovarian masses to
be malignant is 50% in the prepube
rtal and postmenopausal women;
10% in women of the reproductive
period.
Screening
CA 125 is present in serum, semen, bronchial secre
tion, cervical mucus and amniotic fluid It is intensely
expressed in >80% of epithelial ovarian cancers (>65
IU/L). It is used in: ovarian screening (detects only 
50% of stage 1 disease); preoperative evaluation of
benign vs. malignant neoplasms; and follow-up of
patients with ovarian cancer As a test for ovarian
cancer, it has a sensitivity of 80% & a specificity of
>95%. CA 125 is less likely to be raised in mucinous
than in serous tumours. Other sources of increased
CA125 include active endometriosis, abdominal TB
with ascites and tumours from the GIT Metastatic GI
tumours can be differentiated from metastatic ovarian tumours by other investigations; serum SEA &/
or CA19-9 will be abnormal with the former but normal with the latter.
Women with 2 first-degree relatives with ovarian
cancer should have annual recto-vaginal exam, CA
125 evaluation and TVS from their mid 20s or when
they are 5 years younger than the youngest affected
member of the family, whichever is sooner.
AFP: For teratomas. (N: <15ng/ml).
Screening could save 3 y of life and is po
tentially cost-effective. CA 125 + TVS
 +ve predictive value of 20%. 5 ope
rations for each cancer found are acce
ptable. Deaths in the screened group
= ½ that of the controls with significant
improvement in survival (73mo vs 42)
However, no test(s) has proved practical! On the other hand, screening of
women with +ve family history carries
a substantial risk of false +ve results.
Prognosis: High mortality rate; >75%
of cases are diagnosed in stages III
and IV. Staging is the best indicator
of prognosis. 5-year survival rate for
stage I = 90%. 5-year survival rate
for stage IV = <5%.
Management
In BRCA1 & BRCA2 +ve women, prophylactic bilateral SO reduces the rates of ovarian (up to 12%),
tube & breast cancer. Individuals with a history of
hereditary ovarian or breast cancer should be advised to have prophylactic oophorectomy once their
family is completed or at the age of 35 (ovarian carcinoma is rare <45) However the risks of premature
menopause outweigh the benefits of a reduction in
in the risk of ovarian carcinoma. If only 1 relative is
affected, the advice is to have oophorectomy at
hysterectomy indicated for other reasons.
Malignant tumours are staged surgically through a
vertical incision laparotomy Ascitic fluid or peritoneal
saline washings & smears from the underside of the
diaphragm are collected before handling the t. Liver,
subdiaphragm, bowel & mesenteries, omentum &
aortic nodes are, then, inspected and palpated.
Suspicious areas are biopsied Since 5% are metastatic from the stomach & pancreas, these organs
must be carefully palpated.
This is followed by removal of as much malignant
tissue as possible (surgical debulking or cytoreductive treatment). Masses need not be transected,
since peritoneal lines of cleavage are usually found.
The following organs are removed in addition: the
uterus, tubes, appendix & omentum. If cancer
extends to the bladder & bowel, epithelial cancer
tends to spread over, rather than penetrate these
organs, and a plane of cleavage can often be found.
Excision is facilitated by a retroperitoneal dissection
along the iliac vessels and ureters from the pelvic
brim to the lower limit of the tumor. This retropeiton
eal access is very helpful and mostly safe, but it can
lead to major vascular injury. The pelvic veins are
especially vulnerable.
This is followed by chemotherapy in advanced cases.
Taxanes + platinum = appropriate first choice. It
induces complete remission in 45% of patients with
residual masses <2 cm; the percent is reduced to
the half in larger masses.
Second look procedures can exclude recurrent tumors
and thence allow discontinuing treatment with alky-
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