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CARCINOMA ENDOMETRIUM
Dr saeed ur rehman wazir
PG trainee officer(NORI)
INTRODUCTION
Most frequently encountered gynaecologic
cancer in western countries because of decline
in Ca Cx
 Account for 7.0%of all cancers in women
Peak incidence is in the age group of 55 to
69 years.
Over three-fourth of these women are
diagnosed when the disease is still localized and
surgery offers satisfactory results.
PREDISPOSING FACTORS
1. Unsupervised administration of ERT in
menopausal women.
2. Women suffering from Hyperestrogenic
states i.e. Endometrial hyperplasia as cases
of DUB.
3. Familial predisposition to it and may be due
to genetic factors or dietary habits.
4. Tamoxifen prescribed to women with breast
cancer.
PREDISPOSING FACTORS OLD AUNT
O=Obesity
L=Late menopause
D=Diabetes mellitus
A=cAncer: ovarian, breast, colon
U=Unopposed estrogen: PCOS, anovulation, HRT
N=Nulliparity
T=Tamoxifen, chronic use
CONTN..
5. OCPs containing only estrogen while OCPs
with E & P have protective effect.
6. Obesity, HT, Diabetes, Infertility, nulliparity
are associated with endometrial cancer in
30% cases.
7. PCOD patients are more prone to this
disease.
CAUSES OF HIGH UNOPPOSED ESTROGEN
 Exogenous Estrogen: Estrogen Replacement Therapy in
postmenopausal women.
 Endogenous Estrogen:
 Increased secretion : e.g. feminizing ovarian tumors
(granulose cell tumor).
 Increased androgen precursors: e.g. androgen secreting
tumors, liver diseases, chronic an-ovulation (PCOS), or
stress.
 Increased aromatization: e.g. obesity, liver diseases, or
hyperthyroidism.
 Increased free estrogen due to decreased level of SHBG.
PATHOLOGY
 Uterus is enlarged and Endometrial cancer may
be localized or diffuse.
 Localized form may appear as a nodule or polyp
or localized carcinomatous patch.
 Diffuse form may be involving the entire uterine
cavity stopping short of internal os.
 It may infiltrate uterine myometrium and remain
restricted to its boundaries for a long time.
 In advanced stages growth may directly spread
beyond uterine body to cervix, vagina, adnexa
and may metastesize into nodes and distant
THIS ADENOCARCINOMA OF THE ENDOMETRIUM IS MORE OBVIOUS. IRREGULAR
MASSES OF WHITE TUMOR ARE SEEN OVER THE SURFACE OF THIS UTERUS THAT
HAS BEEN OPENED ANTERIORLY. THE CERVIX IS AT THE BOTTOM OF THE PICTURE.
THIS ENLARGED UTERUS WAS NO DOUBT PALPABLE ON PHYSICAL EXAMINATION.
SUCH A NEOPLASM OFTEN PRESENT WITH ABNORMAL BLEEDING.
THE ENDOMETRIAL ADENOCARCINOMA IS PRESENT ON THE LUMENAL
SURFACE OF THIS CROSS SECTION OF UTERUS. NOTE THAT THE
NEOPLASM IS SUPERFICIALLY INVASIVE. THE CERVIX IS AT THE RIGHT.
This uterus is not enlarged, but there is an irregular mass in the upper
fundus that proved to be endometrial adenocarcinoma on biopsy.
Such carcinomas are more likely to occur in postmenopausal women.
Thus, any postmenopausal bleeding should make you suspect that
this lesion may be present.
THE ENDOMETRIAL ADENOCARCINOMA IN THE POLYP AT THE LEFT
IS MODERATELY DIFFERENTIATED, AS A GLANDULAR STRUCTURE
CAN STILL BE DISCERNED. NOTE THE HYPERCHROMATISM AND
PLEOMORPHISM OF THE CELLS, COMPARED TO THE UNDERLYING
ENDOMETRIUM WITH CYSTIC ATROPHY AT THE RIGHT.
HISTOPATHOLOGY
 It is adeno carcinoma
 Grading of these tumors is based on
differentiation and ability to maintain gland
formation, morphology and anaplasia of the
tumour lining cells and presence of infiltration
in stroma
 Tumor grading affects the prognosis of the
disease in any individual case
THIS IS ENDOMETRIAL ADENOCARCINOMA WHICH CAN BE SEEN INVADING
INTO THE SMOOTH MUSCLE BUNDLES OF THE MYOMETRIAL WALL OF THE
UTERUS. THIS NEOPLASM HAS A HIGHER STAGE THAN A NEOPLASM THAT
IS JUST CONFINED TO THE ENDOMETRIUM OR IS SUPERFICIALLY INVASIVE.
SYMPTOMS
1. May be asymptomatic to begin with.
2. Menometrorrhagia in perimenopausal
women
3. Post menopausal bleeding.
SIGNS
1. Per vaginal examination: may or may not
reveal a bulky uterus.
2. Enlarged uterus may be associated with Ca
endometrium along with fibroid or pyometra
3. Sub-urethral Vaginal metastatic growth may be
noted in advanced cases.
4. When adnexa is involved in late stages
enlarged uterus with unilateral or bilateral
adnexal enlargement and fixed nodules in
Pouch of Douglas may be present.
INVESTIGATIONS
1. Routine Haematogram and blood chemistry, urine
examination, X-ray chest and ECG should be done.
2. USG- often reveals thickened and hyperplastic,
polyp in uterine cavity.
Post menopausal endometrial thickness >4mm is
abnormal
3. Endometrial cell sampling by aspiration cytology.
4. Diagnostic hysteroscopy followed by selective
biopsy of suspected area.
5. Fractional curettage and histopathological
examination- this will help in differentiating whether
Ca endometrium is involving cervical canal or not.
6. CT/MRI help in defining the extent of disease into
the myometrium , nodes and distant organs.
DIFFERENTIAL DIAGNOSIS
1. Senile endometritis
2. Genital tuberculosis
3. Atypical endometrial hyperplasia
4. Any other cause of post menopausal
bleeding like senile vaginitis, foreign body,
ERT abuse, cervical polyp, urethral
caruncle, Ca cervix and ovarian carcinoma
etc
SCREENING OF ENDOMETRIAL CARCINOMA
1. Routine screening of all asymptomatic
women on HRT and tamoxifen therapy
2. Perimenopausal women with
menometrorrhagia should be investigated
and screened to exclude endometrial
carcinoma.
3. All women with postmenopausal bleeding
should be screened by pv examination,
TVS, Pipelle aspiration cytology.
4. Fractional curettage along with diagnostic
hysteroscopy.
• DESCRIPTIONSTAGE
• Cancer confined to corpus uteri
• 1A- Tumor limited to endometrium
• 1B- Tumor involving half or less than half the
myometrial thickness
• 1C – Tumor involves more than half the
myometrial thickness
1
• Tumor involves cervix but does not extend
beyond uterus
• 2A- Endocervical gland involvement only.
• 2B- Cervical stromal invasion
2
• Local and/or regional spread
• 3A-Tumor involves serosa, spreads to adnexae,
positive peritoneal cytology.
• 3B- Presence of vaginal metastasis
• 3C- Node metastasis to pelvis and para aortic
nodes.
3
• Tumour Widespread
• 4A Tumor involves bladder and /or
bowel mucosa
• 4B Tumor shows distant metastasis (
intra-abdominal and inguinal nodes)
4
SURGICAL STAGING
 Hysterectomy
 Bilateral Salpingo-oopherectomy
 Biopsy of all metastatic deposits
 Peritoneal fluid cytology
 Cytology in clockwise fashion
 Pelvic and para-aortic lymph node dissection
ROLE OF LYMPHADENECTOMY
 Patients with grade 1–2 endometrioid tumors, less than
50%myometrium invasion, and tumor of 2 cm or less seem
to be at low risk for recurrence and may not require a
surgical lymphadenectomy (level of evidence: B).
 Lymphadenectomy may alter or eliminate the need for
adjuvant therapy and its associated morbidity (level of
evidence: B).
 Sentinel lymph node dissection may reduce the morbidity
associated with standard lymphadenectomy and may
enhance the therapeutic benefit of surgical staging in early
endometrial cancer (level of evidence: I).
TREATMENT
 cases of simple hyperplasia develop in
malignancy in 10-20%
60-70% cases of atypical hyperplasia
develop into malignancy.
Stage 0-(Endometrial hyperplasia)-
Abdominal Pan Hysterectomy is the ideal
treatment.
Young women may be kept under
observation and 30-40 mg
medroxyprogesterone daily therapy may be
offered for 6-12 months.
RX CONTN..
 Stage IA & IB: Observation, or if grade 2–3
and adverse features present (age >60
years, LVSI, large tumor size, lower uterine
involvement), pelvic RT and/or vaginal cuff
brachytherapy (VC)
 Stage IC: Observation, or if other adverse
features present (grade 2–3, advanced age
>50–70 years, LVSI, large tumor size, lower
uterine segment involvement) pelvic RT
and/or vaginal cuff brachytherapy (VC).
Consider chemotherapy for grade 3
RX: CONTN..
 Stage IIA & IIB: Consider pelvic RT ±VC.
Consider chemotherapy for grade 3
 Stage IIIA: Positive cytology only:
Observation for grade 1–2, chemotherapy for
grade 3. Consider pelvic RT and/or VC. All
other IIIA: Chemotherapy and/or
tumordirected RT
 Stage III-IV: Surgery → chemotherapy and/or
tumor-directed RT
 Medically Inoperable: Tumor-directed EBRT
to uterus, cervix, upper vagina, pelvic LN,
and other involved areas (~45–50.4 Gy),
followed by intracavitary brachytherapy boost
(e.g.,6 Gy × 3 HDR to uterine serosal
surface). Consider dose-escalation to gross
disease using image-guided brachytherapy
or IMRT with CT or MRI planning
RECURRENCE
 If no prior RT → EBRT and IC or IS
brachytherapy boost to total dose 60–70 Gy.
Consider IS salvage brachytherapy for select
previously irradiated patients
PAPILLARY SEROUS/CLEAR CELL
 Surgery. For stage IA, consider
chemotherapy and/or tumor-directed RT. For
stage IB, IC, II, and debulked stage III-IV,
give chemotherapy ± tumordirected RT.
SARCOMAS, CARCINOSARCOMA MALIGNANT
MIXED MESODERMAL (MULLERIAN) TUMOR
 Surgery. Post-op RT for high-grade
sarcomas, Leiomyosarcomas, and
carcinosarcomas to improve LC. Pelvic RT ±
VC for stages I–II and tumor-directed RT for
stages III–IV. Consider chemotherapy for
high grade undifferentiated sarcoma and
leiomyosarcoma
RADIATION TECHNIQUES
 Simulate patient supine with CT planning; administer
presimulation
 enema.
 J WP borders: superior = L5-S1; inferior = below obturator
canal
 and including upper 1/2–2/3 of vagina; lateral = 2 cm
lateral to
 pelvic brim; posterior = split sacrum to S3; anterior =
pubic
 symphysis. Consider using IMRT (Fig. 30.1)
 J EFRT borders: Extend superior border to top of L1 with
CT
 planning to avoid kidneys. Recommend IMRT.
BRACHYTHERAPY
 Vaginal brachytherapy: Place two marker seeds J in
vaginal cuff at
 both ends of hysterectomy scars. Use largest vaginal
cylinder possible
 (2.5–3.5 cm). Target upper two-third of vaginal cuff.
Consider
 CT planning. We recommend prescribing dose to vaginal
surface
 because it represents the Dmax of normal tissue.
However, some
 institutions prescribe to 0.5 cm, and dose and
fractionation
 should be modified based on institutional their
experience.
 Brachytherapy for intact uterus: Use
Martinez-Y applicator or
 combination of tandem and cylinder with
interstitial catheters.
 Consider using US guidance and 3D image-
guided brachytherapy.
 Use tandem with ring or ovoids for pre-op
stage II.
DOSE PRESCRIPTIONS
 Post-op
 J WP: 1.8 Gy/fx to 45–50.4 Gy.
 J VC boost: 6 Gy × 3 at vaginal surface (HDR) or 20
Gy at vaginal
 surface (LDR).
 J VC alone: 6 Gy × 5–6 or 10–10.5 Gy × 3 at vaginal
surface
 (HDR) or 50–60 Gy at vaginal surface (LDR).
 J Pre-op: WP 1.8 Gy/fx to 45 Gy and T&R or T&O 6
Gy × 3
 (HDR).
 Vaginal extension: WP 45 Gy plus interstitial implants 6–7
Gy × 3
 (HDR).
 J Paraaortic LN+: EFRT to 45–50 Gy, enlarged
unresectable
 nodes should be boosted to 60 Gy. IMRT recommended.
 Consider IORT at surgery.
 J WART: 1.5 Gy/fx to 30 Gy to whole abdomen → boost
paraaortic
 LN and WP to 45 Gy. Consider IMRT to improve target
coverage
 and marrow sparing.
 J Inoperable: WP 45–50 Gy and 6–7 Gy × 3 (HDR).
SURVIVAL RATE
 Stage I 75 %
 Stage II 55 %
 Stage III 30%
 Stage IV 10%

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Ca endometrium

  • 1. CARCINOMA ENDOMETRIUM Dr saeed ur rehman wazir PG trainee officer(NORI)
  • 2. INTRODUCTION Most frequently encountered gynaecologic cancer in western countries because of decline in Ca Cx  Account for 7.0%of all cancers in women Peak incidence is in the age group of 55 to 69 years. Over three-fourth of these women are diagnosed when the disease is still localized and surgery offers satisfactory results.
  • 3. PREDISPOSING FACTORS 1. Unsupervised administration of ERT in menopausal women. 2. Women suffering from Hyperestrogenic states i.e. Endometrial hyperplasia as cases of DUB. 3. Familial predisposition to it and may be due to genetic factors or dietary habits. 4. Tamoxifen prescribed to women with breast cancer.
  • 4. PREDISPOSING FACTORS OLD AUNT O=Obesity L=Late menopause D=Diabetes mellitus A=cAncer: ovarian, breast, colon U=Unopposed estrogen: PCOS, anovulation, HRT N=Nulliparity T=Tamoxifen, chronic use
  • 5. CONTN.. 5. OCPs containing only estrogen while OCPs with E & P have protective effect. 6. Obesity, HT, Diabetes, Infertility, nulliparity are associated with endometrial cancer in 30% cases. 7. PCOD patients are more prone to this disease.
  • 6. CAUSES OF HIGH UNOPPOSED ESTROGEN  Exogenous Estrogen: Estrogen Replacement Therapy in postmenopausal women.  Endogenous Estrogen:  Increased secretion : e.g. feminizing ovarian tumors (granulose cell tumor).  Increased androgen precursors: e.g. androgen secreting tumors, liver diseases, chronic an-ovulation (PCOS), or stress.  Increased aromatization: e.g. obesity, liver diseases, or hyperthyroidism.  Increased free estrogen due to decreased level of SHBG.
  • 7. PATHOLOGY  Uterus is enlarged and Endometrial cancer may be localized or diffuse.  Localized form may appear as a nodule or polyp or localized carcinomatous patch.  Diffuse form may be involving the entire uterine cavity stopping short of internal os.  It may infiltrate uterine myometrium and remain restricted to its boundaries for a long time.  In advanced stages growth may directly spread beyond uterine body to cervix, vagina, adnexa and may metastesize into nodes and distant
  • 8. THIS ADENOCARCINOMA OF THE ENDOMETRIUM IS MORE OBVIOUS. IRREGULAR MASSES OF WHITE TUMOR ARE SEEN OVER THE SURFACE OF THIS UTERUS THAT HAS BEEN OPENED ANTERIORLY. THE CERVIX IS AT THE BOTTOM OF THE PICTURE. THIS ENLARGED UTERUS WAS NO DOUBT PALPABLE ON PHYSICAL EXAMINATION. SUCH A NEOPLASM OFTEN PRESENT WITH ABNORMAL BLEEDING.
  • 9. THE ENDOMETRIAL ADENOCARCINOMA IS PRESENT ON THE LUMENAL SURFACE OF THIS CROSS SECTION OF UTERUS. NOTE THAT THE NEOPLASM IS SUPERFICIALLY INVASIVE. THE CERVIX IS AT THE RIGHT.
  • 10. This uterus is not enlarged, but there is an irregular mass in the upper fundus that proved to be endometrial adenocarcinoma on biopsy. Such carcinomas are more likely to occur in postmenopausal women. Thus, any postmenopausal bleeding should make you suspect that this lesion may be present.
  • 11.
  • 12.
  • 13. THE ENDOMETRIAL ADENOCARCINOMA IN THE POLYP AT THE LEFT IS MODERATELY DIFFERENTIATED, AS A GLANDULAR STRUCTURE CAN STILL BE DISCERNED. NOTE THE HYPERCHROMATISM AND PLEOMORPHISM OF THE CELLS, COMPARED TO THE UNDERLYING ENDOMETRIUM WITH CYSTIC ATROPHY AT THE RIGHT.
  • 14.
  • 15.
  • 16.
  • 17. HISTOPATHOLOGY  It is adeno carcinoma  Grading of these tumors is based on differentiation and ability to maintain gland formation, morphology and anaplasia of the tumour lining cells and presence of infiltration in stroma  Tumor grading affects the prognosis of the disease in any individual case
  • 18.
  • 19. THIS IS ENDOMETRIAL ADENOCARCINOMA WHICH CAN BE SEEN INVADING INTO THE SMOOTH MUSCLE BUNDLES OF THE MYOMETRIAL WALL OF THE UTERUS. THIS NEOPLASM HAS A HIGHER STAGE THAN A NEOPLASM THAT IS JUST CONFINED TO THE ENDOMETRIUM OR IS SUPERFICIALLY INVASIVE.
  • 20. SYMPTOMS 1. May be asymptomatic to begin with. 2. Menometrorrhagia in perimenopausal women 3. Post menopausal bleeding.
  • 21. SIGNS 1. Per vaginal examination: may or may not reveal a bulky uterus. 2. Enlarged uterus may be associated with Ca endometrium along with fibroid or pyometra 3. Sub-urethral Vaginal metastatic growth may be noted in advanced cases. 4. When adnexa is involved in late stages enlarged uterus with unilateral or bilateral adnexal enlargement and fixed nodules in Pouch of Douglas may be present.
  • 22. INVESTIGATIONS 1. Routine Haematogram and blood chemistry, urine examination, X-ray chest and ECG should be done. 2. USG- often reveals thickened and hyperplastic, polyp in uterine cavity. Post menopausal endometrial thickness >4mm is abnormal 3. Endometrial cell sampling by aspiration cytology. 4. Diagnostic hysteroscopy followed by selective biopsy of suspected area. 5. Fractional curettage and histopathological examination- this will help in differentiating whether Ca endometrium is involving cervical canal or not. 6. CT/MRI help in defining the extent of disease into the myometrium , nodes and distant organs.
  • 23. DIFFERENTIAL DIAGNOSIS 1. Senile endometritis 2. Genital tuberculosis 3. Atypical endometrial hyperplasia 4. Any other cause of post menopausal bleeding like senile vaginitis, foreign body, ERT abuse, cervical polyp, urethral caruncle, Ca cervix and ovarian carcinoma etc
  • 24. SCREENING OF ENDOMETRIAL CARCINOMA 1. Routine screening of all asymptomatic women on HRT and tamoxifen therapy 2. Perimenopausal women with menometrorrhagia should be investigated and screened to exclude endometrial carcinoma. 3. All women with postmenopausal bleeding should be screened by pv examination, TVS, Pipelle aspiration cytology. 4. Fractional curettage along with diagnostic hysteroscopy.
  • 25. • DESCRIPTIONSTAGE • Cancer confined to corpus uteri • 1A- Tumor limited to endometrium • 1B- Tumor involving half or less than half the myometrial thickness • 1C – Tumor involves more than half the myometrial thickness 1 • Tumor involves cervix but does not extend beyond uterus • 2A- Endocervical gland involvement only. • 2B- Cervical stromal invasion 2
  • 26. • Local and/or regional spread • 3A-Tumor involves serosa, spreads to adnexae, positive peritoneal cytology. • 3B- Presence of vaginal metastasis • 3C- Node metastasis to pelvis and para aortic nodes. 3 • Tumour Widespread • 4A Tumor involves bladder and /or bowel mucosa • 4B Tumor shows distant metastasis ( intra-abdominal and inguinal nodes) 4
  • 27.
  • 28. SURGICAL STAGING  Hysterectomy  Bilateral Salpingo-oopherectomy  Biopsy of all metastatic deposits  Peritoneal fluid cytology  Cytology in clockwise fashion  Pelvic and para-aortic lymph node dissection
  • 29. ROLE OF LYMPHADENECTOMY  Patients with grade 1–2 endometrioid tumors, less than 50%myometrium invasion, and tumor of 2 cm or less seem to be at low risk for recurrence and may not require a surgical lymphadenectomy (level of evidence: B).  Lymphadenectomy may alter or eliminate the need for adjuvant therapy and its associated morbidity (level of evidence: B).  Sentinel lymph node dissection may reduce the morbidity associated with standard lymphadenectomy and may enhance the therapeutic benefit of surgical staging in early endometrial cancer (level of evidence: I).
  • 30. TREATMENT  cases of simple hyperplasia develop in malignancy in 10-20% 60-70% cases of atypical hyperplasia develop into malignancy. Stage 0-(Endometrial hyperplasia)- Abdominal Pan Hysterectomy is the ideal treatment. Young women may be kept under observation and 30-40 mg medroxyprogesterone daily therapy may be offered for 6-12 months.
  • 31. RX CONTN..  Stage IA & IB: Observation, or if grade 2–3 and adverse features present (age >60 years, LVSI, large tumor size, lower uterine involvement), pelvic RT and/or vaginal cuff brachytherapy (VC)  Stage IC: Observation, or if other adverse features present (grade 2–3, advanced age >50–70 years, LVSI, large tumor size, lower uterine segment involvement) pelvic RT and/or vaginal cuff brachytherapy (VC). Consider chemotherapy for grade 3
  • 32. RX: CONTN..  Stage IIA & IIB: Consider pelvic RT ±VC. Consider chemotherapy for grade 3  Stage IIIA: Positive cytology only: Observation for grade 1–2, chemotherapy for grade 3. Consider pelvic RT and/or VC. All other IIIA: Chemotherapy and/or tumordirected RT  Stage III-IV: Surgery → chemotherapy and/or tumor-directed RT
  • 33.  Medically Inoperable: Tumor-directed EBRT to uterus, cervix, upper vagina, pelvic LN, and other involved areas (~45–50.4 Gy), followed by intracavitary brachytherapy boost (e.g.,6 Gy × 3 HDR to uterine serosal surface). Consider dose-escalation to gross disease using image-guided brachytherapy or IMRT with CT or MRI planning
  • 34. RECURRENCE  If no prior RT → EBRT and IC or IS brachytherapy boost to total dose 60–70 Gy. Consider IS salvage brachytherapy for select previously irradiated patients
  • 35. PAPILLARY SEROUS/CLEAR CELL  Surgery. For stage IA, consider chemotherapy and/or tumor-directed RT. For stage IB, IC, II, and debulked stage III-IV, give chemotherapy ± tumordirected RT.
  • 36. SARCOMAS, CARCINOSARCOMA MALIGNANT MIXED MESODERMAL (MULLERIAN) TUMOR  Surgery. Post-op RT for high-grade sarcomas, Leiomyosarcomas, and carcinosarcomas to improve LC. Pelvic RT ± VC for stages I–II and tumor-directed RT for stages III–IV. Consider chemotherapy for high grade undifferentiated sarcoma and leiomyosarcoma
  • 37. RADIATION TECHNIQUES  Simulate patient supine with CT planning; administer presimulation  enema.  J WP borders: superior = L5-S1; inferior = below obturator canal  and including upper 1/2–2/3 of vagina; lateral = 2 cm lateral to  pelvic brim; posterior = split sacrum to S3; anterior = pubic  symphysis. Consider using IMRT (Fig. 30.1)  J EFRT borders: Extend superior border to top of L1 with CT  planning to avoid kidneys. Recommend IMRT.
  • 38. BRACHYTHERAPY  Vaginal brachytherapy: Place two marker seeds J in vaginal cuff at  both ends of hysterectomy scars. Use largest vaginal cylinder possible  (2.5–3.5 cm). Target upper two-third of vaginal cuff. Consider  CT planning. We recommend prescribing dose to vaginal surface  because it represents the Dmax of normal tissue. However, some  institutions prescribe to 0.5 cm, and dose and fractionation  should be modified based on institutional their experience.
  • 39.  Brachytherapy for intact uterus: Use Martinez-Y applicator or  combination of tandem and cylinder with interstitial catheters.  Consider using US guidance and 3D image- guided brachytherapy.  Use tandem with ring or ovoids for pre-op stage II.
  • 40. DOSE PRESCRIPTIONS  Post-op  J WP: 1.8 Gy/fx to 45–50.4 Gy.  J VC boost: 6 Gy × 3 at vaginal surface (HDR) or 20 Gy at vaginal  surface (LDR).  J VC alone: 6 Gy × 5–6 or 10–10.5 Gy × 3 at vaginal surface  (HDR) or 50–60 Gy at vaginal surface (LDR).  J Pre-op: WP 1.8 Gy/fx to 45 Gy and T&R or T&O 6 Gy × 3  (HDR).
  • 41.  Vaginal extension: WP 45 Gy plus interstitial implants 6–7 Gy × 3  (HDR).  J Paraaortic LN+: EFRT to 45–50 Gy, enlarged unresectable  nodes should be boosted to 60 Gy. IMRT recommended.  Consider IORT at surgery.  J WART: 1.5 Gy/fx to 30 Gy to whole abdomen → boost paraaortic  LN and WP to 45 Gy. Consider IMRT to improve target coverage  and marrow sparing.  J Inoperable: WP 45–50 Gy and 6–7 Gy × 3 (HDR).
  • 42. SURVIVAL RATE  Stage I 75 %  Stage II 55 %  Stage III 30%  Stage IV 10%