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Dr. Dinesh. M.G
Professor of Surgery
J.J.M.M.C.
Davangere
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
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
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
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)
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
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
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
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
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
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
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
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
Spread
 Direct spread
 Lymphatic spread
 Blood spread
 Trans-coelomic spread
Staging
Modified Duke’s staging
TNM staging
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
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
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
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)
Investigations
 Endoscopy
 Flexible sigmoidoscopy
 Colonoscopy
 CT virtual colonoscopy
Colon cancer on
colonoscopy Normal colonoscopy Virtual colonoscopy
CT virtual colonoscopy(video)
Investigations
 Barium enema and double contrast barium enema
Barium enema
Apple core deformity
Double contrast barium enema
Apple core deformity
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
Treatment
Right hemicolectomy Extended right hemicolectomy
Transverse colectomy Left hemicolectomy
Treatment of hepatic metastasis
Hepatic resection for colorectal metastasis
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%
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
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
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
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
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
Total mesorectal excision
Anterior resection
Abdominoperineal excision
Hartmann’s operation
Hartmann’s procedure
Prognosis
 Stage I 90%
 Stage II 75%
 Stage III 40%
 Stage IV 5%
Thank you
Thank you

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Tumours of Colon and Rectum

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