Carcinoma Endometrium DR H.K.Cheema Professor-OBG,PIMS Jalandhar

1. CARCINOMA OF THE
ENDOMETRIUM
Dr. H.K.CHEEMA
M.D.A.C.M.E
FAIMER FELLOW (2019)
Professor-OBG
PIMS-Jalandhar

2. CARCINOMA OF ENDOMETRIUM:
 One of the commonest Gynecological cancers especially in
developed countries.
 It is a disease of postmenopausal women with a peak incidence
in the 6th & 7th decade of life
 It occurs most often in postmenopausal women ( up to 80％ of
cases )with less than 5 ％ diagnosed under 40 years of a g e ．
Injudicious use of
Oestrogen in post
menopausal women-
commonest cause
5 year survival rate
stage I=>90%
Diagnosis-early

3. Risk Factors
Mnemonic-Family has OLD AUNTI
Family Family History
Has- -- Hypertension
O-- Obesity
L-- Late menopause/early menarche
D----- Diabetes
A-- atypical endometrial hyperplasia
U- unopposed oestrogen in body
N- Nulliparity
T- Therapy (Tamoxifen & radiation)
I- Infertility

4. RISK FACTORS OF ENDOMETRIAL CARCINOMA.
 The actual cause of this cancer is unknown (idiopathic).
 -Early menarche < 12 Y
 Late menopause > 52 Y
 Estrogen
 If oestrogen is given alone as postmenopausal hormone
replacement therapy .
 Estrogen secreting tumors of the ovary are associated with
an increased incidence of endometrial carcinoma．

5. RISK FACTORS:
4. Nulliparity and PCOS syndrome（with defective
progesterone synthesis）carry an increased risk．
5. Corpus cancer syndrome=
Obesity，diabetes and hypertension in women
6. Risk in women with breast, ovarian,(endometrial type) &
colorectal Ca.
7.Previous pelvic radiation therapy
8.Family History of endometrial Ca-5% Lunch II or Hereditary
Non Polyposis colo rectal cancer(HNPCC syndrome)

6. RISK FACTORS:
 6. The endometrial hyperplasia induced by Tamoxifen
,produces endometrial polyp suggested a four-fold increase in
endometrial carcinoma．
 7.( Oral contraception，especially after long term
use.reduces incidence of both endometrial and ovarian
carcinomas).Risk decreases by 40%even after 15 yrs of
discontinuation of therapy.
 8. Endometrial hyperplasia preceeds Endometrial carcinoma in
25% cases.

7. SYMPTOMS
The usual presenting symptom of endometrial carcinoma is
 1.Postmenopausal bleeding which carries a 10％ risk of
associated malignancy in the absence of hormone replacement
therapy. Curettage，or endometrial sampling is mandatory.
 Postmenopausal discharge from pyometra carries a 50％
risk of associated malignancy.
 Pain (colicky) may occur with pyometra or metastatic spread．

9. SCREENING:
 There is no effective screening programme.
 but occasionally cervical smears contain endometrial cancer
cells in 50% cases , so not used in routine but can’t ignore the
presence of malignant endometrial cells in Pap smear.
 Endometrial ultrasonic thickness (double thickness of) 4mm or
more in post menopausal women and women on Tamoxifen
therapy indicates a need for endometrial sampling．

10. Diagnosis Of Endometrial Carcinoma
 A case of Post menopausal bleeding should be considered as a case of
Endometrial carcinoma until unless proved otherwise.
 History & Clinical Examination
 Tumour marker-CA 125 Raised in late stages
 Pap Smear-not a reliable method.
 Endometrial Biopsy-using Sharman curette or soft, flexible, plastic
suction cannula-Pipelle
 This is done as OPD procedure. Histology-definitive diagnosis

11. Pipelle Endometrial Cannula
Plastic long disposable cannula- used as OPD procedure

12. DIAGNOSIS
Ultra-sound & colour Doppler study
Findings
1. Endometrial thickness > 4mm.
2. Hyper-echoic endometrium with irregular lining
3. ↑ vascularity with ↓ vascular resistance
4. Intra-cavitary fluid +
Hysteroscopy is beneficial as endometrial biopsy is taken under
direct vision.
Fractional Curettage-definite method of diagnosis

13. DIAGNOSIS
 Steps of Fractional Curettage
 Done under short G/A in O.T
 Endo-cervical curettage
 Now insert Uterine sound to know the length of utero-cervical canal.
 Dilate the internal os with Hegar’s dilator.
 Uterine curettage at Fundus & lower part of body,
 Polyp forceps introduced to remove endometrial polyp, if any.
 Specimens put in separate containers with separate labels, for HPE in
formalin.
 If Pyometra-withhold Curettage for one week. Put antibiotics to avoid
systemic infection & perforation.

14. Further Investigations
 X-ray Chest
 CT-Scan to detect lymph node involvement.
 MRI-Detects myometrial invasion and endo-cervical spread.
 Positron Emission Tomography ( PET Scan)

15. 2003-10-27
1
0
Carcinoma of the Endometrium

16. 2003-10-27
1
1
Carcinoma of the Endometrium
Naked Eye
examination
Small/normal/enlarg
ed/fibroid/
Pyometra
Two Varieties
1.Localized growth
2. Diffused growth
Signs
1.P/S exam
2. Bimanual P/V
exam
3.P/R exam

17. Types Of Endometrial Carcinoma

18. HISTOPATHOLOGY
 1-Adenocarcinomas 60 – 70 %.
 2- Adenosquamous Ca 10-20%
 3- Papillary Serous Ca 10%.
 4- Clear cell Ca 4%.
 5- Mucinous Ca 9%.
 6- Secretory Ca 1-2%.
 7- Squamous cell Ca extremely rare

19. Histo-Pathological Types

21. SPREAD
 In general this cancer is slow to spread from the
uterine cavity, probably because the endometrium
lacks lymphatics.
 A chest X-ray helps detect lung metastases.
 Magnetic resonance imaging is preferable to
ultrasound for detection of myometrial invasion and
pelvic spread.

22. LOCAL SPREAD
 Local Spread
 Slow invasion of the myometrium is the commonest
spread.
 Itmay produce considerable uterine enlargement;
 or spread may involve the vaginal vault.

23. VENOUS SPREAD
 Venous Spread
 This pathway might account for the occasional
appearance of a low vaginal metastasis; but
venous spread is not a common feature of
uterine cancer.

24. LYMPHATIC SPREAD
 Lymphatic Spread
 The incidence of this seems to be between 10
 and 30%.
 All pelvic nodes, including the internal iliacs, the parametrium,
the ovaries, and the vagina may be involved, probably with
equal frequency.
 Lymphatic spread is more likely to occur when the tumour is
anaplastic and the uterine wall is deeply invaded.

25. 2003-10-27
2
4
Carcinoma of the Endometrium
Lymphatic Spread of Endometrial Carcinoma

26. TUBAL SPREAD:
 Tubal Spread
 Malignant cells can pass along the tube in the same
way that peritoneal spill may occur during
menstruation.
 This may account for isolated ovarian metastases.

27. Stage 0
Endometrial Hyperplasia

29. Stage I A & I B

30. Stage II

31. Protective Factors
Weight reduction
Exercise
Long term use of COCs (50%)
Use of progestins
LNG-IUS
Smoking

32. Treatment of Carcinoma
Endometrium

33. Primary Prevention
1.Strict weight Control
2.To restrict oestrogen in menopausal
stage
3.If oestrogen required, add
Progesterone along to prevent
Endometrial hyperplasia.
4. Prophylactic surgery in Lynch
syndrome(HNPCC)
TAH (60% prevention)
B/L S.O ( 10-12% prevention of ovarian
cancer)
Secondary Prevention
1.Screening of High Risk women in
menopause. Annual scanning of High
Risk women> 35 yrs. Is recommended.
2. No role of routine screening.
3.Education regarding irregular
menstruation in pre-menopausal and
post menopausal bleeding is a must.
4.Presence of malignant cells in
vaginal pool requires diagnostic
curettage.
Management Of Endometrial Carcinoma

34. Curative treatment of Endometrial Carcinoma
Various treatment Modalities ;
1. Surgery
2. Radiotherapy
3. Chemotherapy
4. Combined therapy

35. Pre-operative Evaluation
 Blood examination-CBC, RBS, RFT, LFT, S.TSH,
electrolytes
 Urine routine exam, c/s
 ECG, X-Ray chest(P-A view)
 Abdominal & Pelvic USG- for ascites, metastasis,
pelvic/para-aortic lymph node involvement
 MRI/CT-Scan-to assess extra-uterine spread of disease
 Steroid receptor status

36. PROGNOSIS OF ENDOMETRIAL CARCINOMA
 With the exception of stage 1 tumors of histological grades I
and II, the prognosis is less favourable than many
gyaecologists believe，with an overall 5 year survival of
70％ approximately．
 Fortunately over 80％of cases are diagnosed at
stage 1 ．

37. PROGNOSTIC FACTORS
 Age at diagnosis-old age
 Stage of disease-
 Histologic type- papillary,clear cell-bad prognosis
 Histologic grading- grade 3 bad prognosis
 Myometrial penetration
 Lymph node metastasis
 Extension to cervix

38. TREATMENT OF ENDOMETRIAL CARCINOMA
 This is essentially surgical with postoperative radiotherapy
added when :
 1.unfavourable prognostic features are found at surgery ,
 2.Pre-operative clinical Staging is inaccurate．
 Progestogen therapy is probably only of value in recurrent
disease.
 ．Surgery= (Extra fascial) Hystrectomy
 (Removal of Uterus+Cervix+B/L/Tubes+B/L Ovaries +
removal of vaginal cuff (Optional)

39. Surgery (Laprotomy/ Laproscopic/Assisted Robotic surgery
 Surgical Staging, laprotomy, Peritoneal washings
 Abdominal Hysterectomy
 Bilateral salpingo-oopherectomy
 Omentectomy
 Pelvic and para-aortic lymph node sampling.

40.  - Peritoneal washings: subdiaphragmatic
area, paracolic gutters and pelvis, for
cytology.
 - Open uterus and assess for tumor size,
myometrial invasion and cervical
extension. Frozen section preferred.

41. Stage IB and IC
 Post operative pelvic radiotherapy.
 - 4000-5000 cGy over 5-6 weeks.
 Vaginal vault radiotherapy.

42. Stage II
 Tumour involves cervix but does not extend
beyond uterus.
 Brachytherapy followed 1 to 6 weeks later by
Surgery and External Radiotherapy.
 Alternately, Wertheim’s hysterectomy.

43. Stage III
 Local and/or regional spread
 IIIA- serosa, adnexa, peritoneal spread.
 IIIB- Vaginal metastasis.
 IIIC- Para-aortic/ Pelvic Lymph nodes.

44. Stage III
 INOPERABLE.
 Adjuvant chemotherapy followed by pelvic irradiation.
 Doxorubicin 60 mg per sq. meter
 Cisplatin and Paclitaxel.
 Medroxyprogesterone acetate.
 Whole abdomen irradiation 3000 cGy with Kidney
shielding.
 1500 cGy and 2000 cGy para-aortic nodes and pelvic
irradiation.

45. Stage IV-Tumour widespread.
 Palliative radiotherapy, chemotherapy and
progestrogen may prolong life.
 Progestrogens:
 MDPA 1g weekly or 200 mg OD.
or
 Norethisterone 1g IM weekly.
 Tamoxifen 10 mg BD reduces oestrogen receptors.

46. Recurrent growth
 Vaginal vault, Lateral pelvic wall, lymph
nodes, lungs, liver, brain, bones.
 Tamoxifen 20-40 mg daily.

47. 5-year survival rate
Stage Overall survival rate (%)
I >90
II 65-80
III 35-45
IV 5-20

48. WOMEN UN FIT FOR OPERATION:
 Few women are unfit for surgery， and caesium
insertion radioactive therapy may be employed for
these
 but radiation alone is less effective than combined
surgical and radiation treatment．

49. CARCINOMA OF THE ENDOMETRIUM COMPARED
WITH CA CERVIX:
 The overall results are better than for carcinoma of
the cervix，not because it is less malignant tumour，
but because treatment is usually given earlier．
 Post－menopausal bleeding ismuch more difficult
to ignore than the irregular bleeding of the younger
woman．

50. RECURRENCE OF ENDOMETRIAL CARCINOMA
 The incidence of recurrence within 5years is in the region of
30％and is accepted along with the 5-year survival rate as a
measure of the effectiveness of the various systems of
treatment．
 The majority recurrences appear within 3 years
of treatment. Early recurrence has a poor
Prognosis.

51. Hormone therapy
 PROGESTOGENS Many endometrial carcinomata are
hormone dependent and progestogens have been used as
part of a combined primary treatment , recurrent or
metastatic growths．
 Between 15％and 50％of recurrences will respond．
Medroxyprogesterone acetate， 400 mg to 600 mg daily
 Tamoxifen
 Anti-oestrogenic non steroidal agent
 Dosage= 10 mg B.D. with progestrone therapy.
 Very effective when used with Progestrone therapy.

52. Follow up
 After initial therapy
 Examine after every 4 months—2 years
 Then every 6 months---3 years.
 Then every year ( ACOG Guidelines)
 Evaluation of symptoms, clinical examination, X-Ray chest-
essential.
 Doubt of recurrence-CT-Scan/MRI
 CA 125- in papillary serous endometrial carcinoma