This document provides information on benign tumours known as polyps, adenomatous polyps, and familial adenomatous polyposis (FAP). It discusses that adenomatous polyps have malignant potential that increases with size, villous type, and dysplasia. FAP is defined by having 100 or more colorectal adenomas and carries a 100% risk of developing colorectal cancer if left untreated. Treatment options for polyps and FAP include polypectomy, colectomy, and proctocolectomy depending on the severity and extent of lesions.

1. Dr. Dinesh. M.G
Professor of Surgery
J.J.M.M.C.
Davangere

2. Benign tumours
 ‘Polyp’ is a clinical description of any protrusion of the mucosa
 They can be single or multiple as part of a polyposis syndrome
Classification of polyps
Inflammatory Hyperplastic Hamartomatous Neoplastic
Ulcerative colitis
Crohn’s colitis
Diverticulitis
Metaplastic Peutz-Jeghers polyp
Juvenile polyp
Adenomatous
•Tubular
•Tubulovillous
•Villous
Adenocarcinoma
Carcinoid tumour

3. Adenomatous polyp
 Tubular like a berry on a stalk
 Villous ( sessile)
 Found on colonoscopic
examination for features of:
 Rectal bleeding
 Diarrhoea
 Mucous discharge
 Hypokalaemia
 Hypoalbuminaemia

4. Adenomatous polyp
 Significance of adenomatous polyps lie in their malignant
potential
 The risk of malignancy increases with
 Size
 < 1cm 1-5% risk
 1-2 cms 10% risk
 >2 cms 30-50% risk
 Villous type
 Dysplasia

5. Adenomatous polyp
Treatment
 Adenomas larger than 5 mm require polypectomy
 Colonoscopic snare polypectomy
 Endoscopic mucosal resection (EMR)
 Transanal resection
 Transanal endoscopic microsurgery (TEMS)
 Resection of colon/rectum if massive or extensive
Colonoscopic snare polypectomy(video)

6. Familial adenomatous polyposis(FAP)
 FAP is defined clinically by the presence of 100 colorectal
adenomas
 Adenomas can also occur in stomach, duodenum or small
intestine
 Inherited as an autosomal dominant disease due to mutation of
APC gene located on short arm of 5th chromosome
 Occurs in the age group of 15-20 years and in both the sexes
equally

7. Familial adenomatous polyposis(FAP)
 Risk of development of colorectal cancer is 100%
 Can be associated with duodenal or ampullary carcinoma
 Gardner syndrome: desmoid tumours + osteomas +
epidermoid cysts
 Turcot’s syndrome: FAP+brain tumours or sarcoma of bone

8. Familial adenomatous polyposis(FAP)
 Clinical features
 Lower abdominal pain
 Loose stools
 Weight loss
 Blood and mucus in stools
 Investigations
 Colonoscopy and biopsy
 Double contrast barium enema
 Screening of all members of the family by genetic testing or by
regular colonoscopy starting at the age of 10-12 years and
repeated every year till the age of 20
 If there are no polyps at 20 years, colonoscopy is repeated every
5 years until 50 yrs. Still if there are no polyps there is probably
no inherited gene

9. Familial adenomatous polyposis(FAP)
 Treatment
 Aim is to prevent the development of colorectal cancer
 Surgical options are:
 Proctocolectomy with ileal pouch anal anastomosis
 Colectomy with ileorectal anastomosis with regular follow up
endoscopic treatment of new rectal polyp
 Total proctocolectomy with ileostomy
Ileal ‘J’ pouch anal
anastomosis
Colectomy with ileorectal
anastomosis
Proctocolectomy
with ileostomy

10. Carcinoma colon
Aetiology
 Diet
 Red meat
 Low fibre diet
 High animal fat
 Genetic
 FAP
 Gardner’s syndrome
 Turcot’s syndrome
 Inflammatory bowel disease: ulcerative colitis and Crohn’s
 Cholecystectomy
 Smoking
 Alcohol

11. Carcinoma colon
 More in developed countries
 Pathogenesis
 Arises from adenomatous polyps after a sequence of genetic
mutations influenced by environmental factors. This is
called adenoma-carcinoma sequence
 Possible sequence of adenoma-carcinoma is
 Mutation of APC gene –small adenomas- K-ras mutation-larger
adenoma-p53gene mutation- carcinoma

12. Pathogenesis of colonic cancer
 Adenoma- carcinoma sequence
 80% loss of heterzygosity pathway(APC-K ras-P53)
 20% RER pathway(Replication Error Repair) leading to
repeated sequences called microsatellite instability
 Colon cancer can be hereditary or non-hereditary
 Hereditary
 FAP
 HNCC
 Cronkhite – Canada syndrome
 Juvenile polyposis syndrome
 Non- hereditary
 Sporadic
 Familial colonic cancer- in Ashkenazi –Jewish population

13. Types
 Synchronous and metachronous
 Gross types
 Annular
 Tubular
 Ulcerative
 Cauliflower like
 Annular
 Common on left side
 Presents with intestinal obstruction
 Ulcerative
 Common on right side
 Proliferative
 Polypoid and is common on right side

14. Spread
 Direct spread
 Lymphatic spread
 Blood spread
 Trans-coelomic spread
Staging
Modified Duke’s staging
TNM staging

15. Staging
 Duke’s staging
 A: Invasion of but not breaching the muscularis propria
 B: Breaching the muscularis propria but not involving
lymph nodes
 C: Lymph nodes involved
 D: Metastatic disease

16. Staging
 TNM Staging
 T, Tumour stage
 Tis, carcinoma in situ, intraepithelial/invasion into lamina propria
 T1, into submucosa
 T2, into muscularis propria
 T3, into pericolic fat or sub-serosa but not breaching serosa
 T4, breaches serosa or directly involving another organ
 N, Nodal stage
 N0, no nodes involved
 N1, 1-3 nodes involved
 N2, four or more nodes involved
 M, Metastases
 M0, no metastasis
 M1, metastasis

17. Clinical features
 Over 50 years, familial type in younger patients
 Anaemia, loss of appetite and weight, abdominal
discomfort and mass per abdomen
 20% present with intestinal obstruction
 20% present with distant metastasis to liver and other
organs
 Right sided growth: Anaemia and mass
 Left sided growth: Colicky pain, altered bowel habits,
palpable lump, distention of abdomen. Bladder symptoms
may herald colovesical fistula
 Perforation and peritonitis or pericolic abscess may form

18. Investigations
 Screening
 Faecal occult blood test
 Sigmoidoscopy
 Colonoscopy
 Endoscopy
 Flexible sigmoidoscopy
 Colonoscopy
 Radiology
 Double contrast barium enema
 CT virtual colonoscopy
 CT chest and abdomen for staging
 X- ray chest
 USG abdomen
 CEA(carcinoembryonic antigen)

19. Investigations
 Endoscopy
 Flexible sigmoidoscopy
 Colonoscopy
 CT virtual colonoscopy
Colon cancer on
colonoscopy Normal colonoscopy Virtual colonoscopy
CT virtual colonoscopy(video)

20. Investigations
 Barium enema and double contrast barium enema
Barium enema
Apple core deformity
Double contrast barium enema
Apple core deformity

21. Treatment
 Surgical
 Preoperative preparation
 Mechanical bowel preparation
 Prophylactic antibiotics
 DVT prophylaxis
 Operations
 Right radical hemicolectomy
 Extended right radical hemicolectomy
 Transverse colectomy
 Left radical colectomy
 Total colectomy for synchronous lesions
 Hepatic resection for metastasis

22. Treatment
Right hemicolectomy Extended right hemicolectomy
Transverse colectomy Left hemicolectomy

23. Treatment of hepatic metastasis
Hepatic resection for colorectal metastasis

24. Adjuvant therapy
 Chemotherapy
 Indications
 Positive node
 T4 lesions
 Chemotherapy regimes are
 5FU+Folinic acid(leucovorin)
 Folinic acid (LV)/5 FU/oxaliplatin- FOLFOX
 Prognosis
 Stage I 90%
 Stage II 75%
 Stage III 50%
 Stage IV less than 5%
 Overall 5 year survival is about 50%

25. Rectal cancer
 Adenocarcinoma comprise vast majority
 Aetiopathogenesis is same as that of colonic cancer
Spread
 Local spread
 Circumferentially ( 12-18 months)
 Muscular coat and parirectal tissue
 Prostate, bladder, seminal vesicles
 Uterus and vagina
 Sacrum and sacral plexus of nerves and ureters

26. Rectal cancer
Spread
 Lymphatic
 Above peritoneal reflection to lymph nodes along superior
rectal vessels
 In mid rectum to pararectal and mid rectal lymph nodes
 Blood spread
 Liver, lungs and adrenals
 Peritoneal spread

27. Clinical features
 Bleeding per rectum
 Change in bowel habits, tenesmus
 Abdominal pain
 Back pain(late feature)
 Urinary symptoms(invasion of bladder or prostate)
 Pelvic pain
 Peritonitis due to perforation or jaundice due to liver
metastasis
 Examination
 Digital rectal examination

28. Investigations
 Proctoscopy/ sigmoidoscopy and biopsy
 Colonoscopy / barium enema
 Usg abdomen
 CT scan of abdomen and pelvis for staging
 Endorectal ultrasound for staging
 PET scan
 CEA levels

29. Treatment
 Surgery
 Principles
 Total Mesorectal Excision(TME) to reduce local recurrence
 Anterior resection open or laparoscopic
 Low anterior resection (open or laparoscopic)
 Abdomino-perineal excision (open or laparoscopic)
 Hartmann’s resection
 For small lesions local excision by
 Transanal approach
 Transanal endoscopic microsurgery
 Palliative sigmoid colostomy for unresectable growth
 Adjuvant chemotherapy and radiotherapy

30. Total mesorectal excision

31. Anterior resection

32. Abdominoperineal excision

33. Hartmann’s operation
Hartmann’s procedure

34. Prognosis
 Stage I 90%
 Stage II 75%
 Stage III 40%
 Stage IV 5%

35. Thank you
Thank you