1. COLORECTAL CANCER
DR BASHIR BIN YUNUS (MBBS,MWACS)
GENERAL SURGERY LECTURE SERIES

2. OUTLINE
• INTRODUCTION
• ANATOMY
• RISK FACTORS
• PATHOLOGY
• CLINICAL PRESENTATION
• INVESTIGATIONS
• TREATMENTS
• FOLLOW UP
• PROGNOSIS

3. INTRODUCTION
• It is the 3rd commonest malignancy after cancer of the lungs and
stomach in males and after breast and cervix in the females.
• Accounts for 10% of cancers in males, 9.4% in females. Cancer
mortality of 8%
• Worldwide incidence is 1.2million annually and half die of the
disease.
• In the western world it is next to only bronchogenic carcinoma.
• Within the colon, about 50% of cancers arise in the left side and 25%
in the right.

4. INTRODUCTION
• In Africans incidence is increasing due to urbanization even though
the overall incidence is low.
• Attributed to;
• The young age of the population
• Transit time of faeces and fibre diet
• Rarity of precancerous conditions

5. ANATOMY
• The large intestine starts at the ileocecal junction and extends to the anus.
• It is about 5–6 ft (125–150 cm) long and can be divided into the cecum
with the appendix, the ascending colon, the transverse colon, the
descending colon, the sigmoid colon, and the rectum.
• The rectum is 12–15 cm above the anal verge as measured by rigid
sigmoidoscopy.
• The arterial blood supply to the colon comes from the superior mesenteric
artery (SMA) and the inferior mesenteric artery (IMA), which communicate
in a watershed area in the splenic flexure.
• This arcade is complete in only 15% to 20% of people.

7. • Iliocolic, right colic, and middle colic arteries which are branches of
superior mesenteric artery supply the colon from caecum to splenic
flexure.
• Left colic, sigmoid, superior rectal arteries which are branches of
inferior mesenteric artery supply the descending and sigmoid colon
• The anastamotic arcade formed between the branches of superior
and inferior mesenteric arteries is called ‘arc of Riolan’
• The rectum has additional branches from the internal iliac vessels

8. • The middle rectal arteries arise from the internal iliac arteries and
supply the distal rectum and upper anal canal. The inferior rectal
arteries, branches from the internal pudendal arteries, cross the
ischiorectal fossae to supply the anal sphincters.
• Sudeck critical point; at the rectosigmoid junction, the last sigmoid
arterial branch of the inferior mesenteric artery, it usually forms an
anastomosis with a branch of the superior rectal artery. The
anastomosis is small and often only singular. A watershed area.

9. • Venous drainage occurs into superior mesenteric vein (which joins the
splenic vein to form the portal vein) and inferior mesenteric vein
(drains into the splenic vein).
• Mucosa contains no lymph channels, so mucosal cancers rarely
metastasize.
• Nodes are epicolic (located in the colonic wall), paracolic(located
along the inner margin), intermediate (located near mesenteric
vessels), principal (located near main mesenteric vessels).

10. RISK FACTORS
• PRE-CANCEROUS
• ADENOMAS
• POLYPOSIS SYNDROMES
• INFLAMMATORY BOWEL DISEASES
• HEREDITARY NON-POLYPOSIS COLORECTAL CANCER (HNPCC)
• DIET
• RADIATION OF PROSTATE CANCER
• ALCOHOL AND CIGARETTE SMOKING
• PREVIOUS SURGIERIES; cholecystectomy, ileal resection,
ureterosigmoidostomy
• SPORADIC- 85-90 %

11. RISK FACTORS
1. PRE-CANCEROUS CONDITIONS
a. Conventional Adenomas;
85% of colorectal adenocarcinoma arise from conventional adenomas. It may
take 5-15years. The risks include sessile adenomas > 2cm with villous
pathology.

12. ADENOMA-CARCINOMA SEQUENCE
• This is a multistep model that describes the carcinogenesis as an
accumulation of genetic events, uninhibited cell growth, proliferation and
clonal development.
• It involves several mutations and deletions.
• APC gene (adenoma-polyposis coli)- a tumour suppressor gene. The
gatekeeper of colonic neoplasm. Its mutation is the initial step of
carcinogenesis. Present in 60-80% of sporadic colorectal cancer.
• MCC gene (mutated in colon cancer)
• K-ras (an oncogene). Present in 30-50% of colorectal cancer
• DCC (deleted in colonic cancer)- a tumour suppressor gene. Loss of DCC is
important from progression of benign polyp to malignant conditions.
• P53. a tumour suppressor, present in 75% of colorectal cancer.

13. Normal epithelium
↓ initiation; loss of APC(adenomatous
polyposis coli) gene on chromosome 5q
Dysplasia
↓
DNA methylation
↓
Early adenoma
↓ activation of K-ras on chromosome 12p
Intermediate adenomas
↓ loss of DCC on chromosome 18q
Late adenoma
↓ loss of p53 on 17q
Carcinoma
↓
Spread

14. b. Serrated adenoma/polyps;
• Give rise to about 15 % of colorectal carcinoma
• Cancers are usually proximal in location
• The pathway is usually shorter than tha adenoma-carcinoma sequences
c. Polyposis syndromes;
FAP- familial adenomatous polyposis syndrome
• Autosomal dominant on chromosome 5q21
• It account for less than 1% of colorectal cancer
• Characterized by more than 100 polyps
• 75-100% of patients develop carcinoma of the rectum and sigmoid at a mean
age of 40 years if untreated.
• The cancer may be multiple.
• Variants; Gardner’s syndrome, Turcot’s, oldfields syndrome

15. Familial adenomatous polyposis

16. Hamartomatous polyposis syndromes
• They are autosomal dominant;
• Juvenile polyposis syndrome
• Peutz-Jeghers syndrome
• Cowden syndrome
• Banayan-Riley-Ruvalcaba syndrome
• Cronkite- Canada syndrome

17. Juvenile polyposis
syndrome
Juvenile polyposis syndrome (JPS) is
a hereditary condition identified by
the presence of benign polyps in
the gastrointestinal tract, most
commonly in the colon. In addition
to polyps, people with juvenile
polyposis syndrome are at an
increased risk(9-50%) for
developing specific types of cancer,
including: Colorectal cancer, Gastric
cancer, Pancreatic cancer.

18. Peutz- Jeghers
sydrome
• 2-3 % develop GI and extraintestinal
malignancy
• 2nd most common harmatoma after
jeuvenile polyposis syndrome
• Harmatomas in the upper Gi especially
the jejunum.
• Skin pigment(melanin) – most frequently
perioral or bucal mucosa
• Have risk of intussciception

19. COWDEN SYNDROME
These growths are most commonly
found on the skin and mucous
membranes (such as the lining of the
mouth and nose), but they can also
occur in the intestine and other parts of
the body. The growth of hamartomas on
the skin and mucous membranes
typically becomes apparent by a person's
late twenties.
Increased risk of developing several
types of cancer, particularly cancers of
the breast, thyroid, and endometrium.
Other cancers that have been identified
in people with Cowden syndrome
include colorectal cancer, kidney cancer,
and a form of skin cancer called
melanoma

20. d. Inflammatory bowel disease;
Ulcerative colitis. Psuedopolyp of ulcerative colitis may become malignant if ;
• The duration of the disease is over 10 years
• The whole large bowel is involved
• The disease start at young age
The carcinoma is often multiple, and 8 times. Colorectal cancer is 30 times
commoner in patients with ulcerative colitis.
Crohn’s disease of the colon; 20 times risk of developing cancer.

21. 2. HEREDITARY NON POLYPOSIS COLON CANCER SYNDROME;
• 5-10 % of colorectal cancer are due to HNPCC
• Autosomal dominance with 70-85 % penetrance
• Manifest at mean age of 44 years
• Two main syndromes; Lynch I and Lynch II syndromes
• Lynch I is site-specific which predispose to colorectal only, commonly right
side, occurs in early age, and 40 % are metachronous.
• Lynch II. Cancer family syndrome. Patients or their family developes
colorectal, ovarian, breast, endometrial, stomach proximal ureters and biliary
tree

22. Criteria for diagnosis of HNPCC
• Amsterdam criteria
• Modified Amsterdam criteria
• Bethesda criteria

23. Amsterdam criteria
• At least 3 relatives of common cancer
• One affected person is 1st degree relative of other two affected persons
• Two successive generations affected
• At least one case of colon cancer diagnosed before the age of 50 years
• FAP excluded
Modified Amsterdam criteria;
• Same as Amsterdam except cancer must be associated with HNPCC
(colon, endometrium, small intestine, renal pelvis and ureter) instead of
specifically colon cancer
• Tumour should be verified by pathologist

24. Bethesda criteria
Amsterdam criteria or one of the following;
• 2 cases of HNPCC associated cancer in one patient including
synchronous or metachronous cancer.
• Colon cancer and 1st degree relative with HNPCC associated cancer
and or colonic adenoma
• Colon or endometrial cancer diagnosed before the age of 45
• Right sided colon cancer that has an undifferentiated pattern or
signet cell type before the age of 45
• Adenoma diagnosed before 45

25. 3. DIET;
Red meat, high intake of fat (saturated), increase the risk of colorectal
cancer.
Saturated fat increases the tumour-promoting arachidonic acid and its
metabolites on cell membrane.
Increased fat/meat content of diet enhances the activity of certain
anaerobic organisms which encourage degradation of primary bile
(cholic acid and chenodeoxycholic acids) acids into secondary bile
acids (lithocholic and deoxycholic acids) which are carcinogenic.

26. • Fibre- (vegetable, fruits and whole grain cereals), calcium, vitamin A,
C, E, zinc and fish are protective.
• Fruits and vegetables depresses the faecal bacterial enzyme activity
and thereby reduces the concentration of faecal bile acids (FBA).
• There is positive association between colorectal cancer and the level of
FBA. High FBA is correlated to adenoma size and severity of epithelial
dyspepsia.
• Calcium combine with bile salt and fatty in the stole to insoluble
complexes that are less likely to attack the colonic mucosa. Calcium
also acts on the colonic mucosal cell to reduce the proliferative
potential.

27. 4. Radiation; Radiation treatment of prostates cancer moderately
increases the risk of rectal cancer in radiated sites with time. (mucinous
carcinoma).
5. Surgeries; cholecystectomy, ileal resection, ureterosigmoidostomy,
gastrectomies
Cholecystectomy, alters the enterohepatic cycle of bile acids, there is
increase bile acid pool in the large bowel. The bile acids induces
hyperproliferation of intestinal mucosa via several intracellular
mechanisms.
Ureterosigmoidostomy increase the risk by 100-500 times, after
cholecystectomy and ileal resection, there is increase bile salt which is
carcinogenic.

28. 6. OTHERS;
• Lack of physical activity
• Diabetes
• Cigarette smoking (esp. after > 35 years of use )
• Acromegaly; increase risk of circulating insulin-like growth factors
• obesity

29. PATHOLOGY
• MACROSCOPICALLY; there are 4 types ; “CUTA”
• C – cauliflower
• U- ulcerative
• T- annular
• A- tubular

30. • Cauliflower or proliferative type is a bulky fungating tumour which
project into the lumen of the gut. As it grow it may become necrotic
and ulcerates. They are usually tumours of the right side.
• Malignant ulcers has raised, irregular, everted edges and a sloughing
floor. It grows in the transverse axis of the bowel. Commonly on the
right side
• Annular (stenosing); common on the left side. It is circumferential
≤2cm. Present with intestinal obstruction.
• Tubular or infiltrative; when annular spread longitudinally to involve
segment 5cm and above.

31. • 5-10 % of colon cancer are synchronous i.e multiple primary tumours
at different part of the colon at the same time.
• 10-20 % are metachronous; growth in different part at different
period.

32. Histological types
• Adenocarcinoma—90%.
• Mucinous adenocarcinoma—5-10%.
• Signet ring cell carcinoma.
• Small cell/oat cell carcinoma—rare—extremely poor prognosis.
• Squamous cell carcinoma.
• Undifferentiated carcinoma.

33. STAGING
• DUKE’S
• A- Confined to bowel wall, mucosa and submucosa
• B- Extends across the bowel wall to the muscularis propria with no lymph
nodes involved
• C- Lymph nodes are involved

34. STAGING
• MODIFIED DUKE’S
• A. Growth limited to rectal wall
• B. Growth extending into extrarectal tissues but no lymph node spread
• B1: Invading muscularis mucosa
• B2: Invading into or through the serosa
• C. Lymph node secondaries
• D. Distant spread

35. STAGING
• ASTLER COLLER MODIFICATION OF DUKE’S
• A- Confined to the mucosa
• B1- extent to but does not penetrate the muscularis mucosae
• B2- penetrates the muscularis mucosa, but lymph nodes are not involved
• C1- limited to the bowel wall with paracolic lymph node involvement
• C2- spread to the lymph node at the highest point of ligation
• D – distant metastasis

36. STAGING
• MODIFIED ASTLER COLLER (MAC)
• TNM

37. TNM Classification of Colon ca
Primary tumour
 Tx- primary tumour cannot be assessed
 To –No evidence of primary tumour
 Tis- Carcinoma in situ
 T1- Tumour invades the submucosa
 T2- Tumour invades the muscularis propria
 T3- Tumour invades into the subserosa
 T4 –Tumour breaches the visceral peritoneum and/or
invades other organs

38. Regional lymph node
 Nx- Regional lymph nodes cannot be assessed
 No- No regional lymph node metastasis
 N1-Metastasis in 1 to 3 regional LN
 N2-Metastasis in 4 or more regional lymph nodes
Distant metastasis
 Mx- Distant metastasis cannot be assessed
 Mo- No distant metastasis
 M1- Distant metastasis

39. Stage T N M Dukes MAC
0 Tis N0 M0 - -
I T1 N0 M0 A A
T2 N0 M0 A B1
IIA T3 N0 M0 B B2
IIB T4 N0 M0 B B3
IIIA T1-T2 N1 M0 C C1
IIIB T3-T4 N1 M0 C C2/C3
IIIC Any T N2 M0 C C1/C2/C3
IV Any T Any N M1 - D

40. SPREAD
• 1. Direct spread
• 2. Via lymphatic vessels
• 3. via the blood stream
• 4. Transperitoneal seedling

41. • Direct infiltration; In the bowel it spread transversely to encircle it.
Spread in longitudinal axis is limited. Microscopically it does not
spread beyond 5cm. It spread through all layer to involve the adjacent
structures. Invasion may lead to formation of internal fistulae.

42. • Growth through lymphatics spreads to paracolic nodes, intermediate and
principal group of lymph nodes.
• Groups of lymph nodes draining colon
• N1: Nodes immediately adjacent to bowel wall.
• N2: Nodes along ileocolic/right colic/middle colic/ left colic/sigmoid
arteries.
• N3: Nodes near the origin of SMA and IMA.
• Nodal spread in carcinoma colon is sequential from N1 → N2 → N3
• However, and in about 30% of cases nodal involvement can skip a tier of
glands.

43. • Blood spread:
• 33- 40% of carcinoma colon spreads to liver via portal veins.
• Secondaries may be either solitary or multiple, present as liver with
hard, umbilicated nodules.
• It spread to the lungs (22%), adrenals(11%), kidneys, bones (10%) and
the brain.

44. • Transperitoneal seedling.
• When tumour has spread to the peritoneal surface, they drop as
seedlings. Ascites may result.

45. CLINICAL PRESENTATION
• Occurs usually after 50 years. Usually in the 6th and 7th decades.
Familial type can present in younger age group.
• Rectal cancer is commoner in males. Colonic commoner in females.
• Presentation maybe insidious (75%) or urgent as intestinal
obstruction (18%) or perforation (7%)
• The commonest and important symptom is change in bowel habits
and abdominal pain. Change in bowel habits maybe constipation,
diarrhea or alternating constipation and diarrhea.
• Passage of blood or mucus in the faeces , noises in the abdomen
(audible borborygmi from increasing obstruction), abdominal pain,
distension and dyspepsia are other presenting symptoms.

46. • The patient often notices a lump in the abdomen especially in
carcinoma of the caecum
• Right sided growth commonly presents with anaemia,asthenia and
anorexia. Palpable mass in the right iliac fossa, which is not moving
with respiration, mobile, non-tender, hard, well-localized with
impaired resonant note.
• Left sided growth presents with colicky pain, altered bowel habits
(alternating constipation and diarrhea), palpable lump, distension of
abdomen due to sub acute/chronic obstruction. Later may present like
complete colonic obstruction. Tenesmus, with passage of blood and
mucus, with alternate constipation and diarrhea, is common.

47. • Sigmoid colon and rectum;
• most important symptoms is rectal bleeding. The blood is bright red
and either mixed with faeces and mucus or passed alone.
• Tenesmus; frequent urge to defecate which is fruitless
• Spurious diarrhea
• Haemorrhoids ; Obstruction to superior rectal veins. So any patient
above 40 years with haemorrhoid should be properly evaluated.

48. • Involvement of adjacent structures; sacral pain when sacral plexus is
invaded, recto-vaginal fistulae. Recto-vesical fistula presenting with
faecoluria and pneumaturia. Compression of the ureters give
hydroureters and hydronephrosis. Tumour of the transverse colon can
invade the stomach giving gastro-colic fistula.

49. • Examination may reveal distension, ascites, lump, hepatomegaly.
• Tumours in rectum if less than 10 cm from the anal verge is felt by
rectal examination. It may be a hard tumour encircling the lumen and
narrowing it. Or a raised ulcer.
• It takes upto 6months for a tumour to occupy ¼ of the circumference
and hence 2 years to be completely circumferential

50. Emergency presentations
• Acute on chronic intestinal obstruction
• Perforation
• Paracolic abscess
• Acute bleeding

51. INVESTIGATIONS
• Double contrast Barium enema: Shows irregular filling defect and
‘apple core’ deformity (in left sided carcinoma). It also helps in finding
colonic polyps (Air-contrast barium enema). Can serve as a road map
for colonoscopy.
• Colonoscopy and biopsy confirms the diagnosis. Synchronous
tumours looked for.
• Transrectal uss; depth of invasion, lymph node. 5 year survival: 90%,
70%, and 30% for Duke A, B, C respectively.
• Abdominal uss; To see secondaries in liver, peritoneum, lymph node
status, rectovesical secondaries. Presence of hydronephrosis.

52. INVESTIGATIONS
• IVU ; when hydroureters and hydronephrosis is peaked by uss, ivu is
done to check the site of obstruction.
• CEA (Carcinoembryonic antigen): cell surface glycoprotein, a tumour
marker. CEA is primarily associated with colorectal cancers, however
non specific. Uses in colorectal cancers are:
• Preoperative levels >7.5 ng/ml signifies poor prognosis.
• If postoperative level does not fall, it indicates either incomplete resection, or
occult metastasis elsewhere.
• Increase CEA during follow-up indicates recurrence or secondaries.
• A slow rise indicates loco regional disease.
• A rapid rise signifies metastasis.

53. • Base line investigations to prepare for treatment;
• FBC, U/ECR, LFT, FBS, ECG, GXM

54. DIFFERENTIAL DIAGNOSIS
• Carcinoma of the caecum; appendix abscess,amoeboma,crohn’s
disease, hyperplastic ileocecal TB, actinomycosis, renal swelling,
ovarian cyst, pedunculated myoma of the uterus.
• Left sided; diverticulitis,amoeboma, schistosomiasis,
• Transverse colon; gastric ca, gall bladder ca, secondary deposite on
the omentum, hepatic, splenic or renal enlargement.

55. BOWEL PREPARATION
• To reduce the bacterial and faecal load of the colon before operation
to reduce infection and anastomotic leakage.
• Mechanical Bowel prep
• Dietary Restriction-
• Cathartics
• Enemas
• PEG
• Antibiotic bowel prep
• Neomycin
• metronidazole

56. TREATMENT OPTIONS
• SURGERY
• CHEMOTHERAPY
• TARGETED THERARY
• RADIOTHERAPY

57. TREATMENT
Mainly surgery.
• Colonic tumours;
• Caecum, ascending colon, Rt hemicolectomy
• Hepatic flexure – extended Rt hemicoloctomy
• Transverse colon- Transverse colectomy including both flexure
• Splenic flexure; Left hemicoloctomy.
• Desending colon; left hemicolectomy
• Signal colon – sigmoid colectomy

58. • Rectal cancer
• Rectal cancer should be preceded by neoadjuvant chemotherapy, plus
radiotherapy to down stage before surgery.
• Duke A – wide local excision. Wide local excision with 2cm margin for
tumour <10cm from anal verge, <3cm in diameter, mobile, well
differentiated, exophytic- polypoid or sessile and no lymph nodes
involved.
• Tumour >10cm from anal verge Anterior resection
• Tumour 6 – 10 cm from anal verge low anterior resection using
stapler

59. • Tumours < 6cm Abdomino perineal resection (synchronous combine
AP resection by two surgeons – abdominal or perineal)
• Note; margin of the normal tissues should be at least 2.5cm – 5 cm
from the anal verge and must not be breached for continent surgery.

60. ADJUVANT THERAPY
• 1. Radiotherapy – Reduce incidence of local recurrence
• 2. Cytotoxic therapy ↓ recurrence and improve overall survival by 30%
• Cyclic 5 FU and levamisole (stimulate immune function)
• Mayo’s regimen – 5 FU & lecovurine
• 5 FU + α inteferone
• Flox – 5 FU, oxaliplatin
• FOLFOX4, FOLFOX6, mFOLFOX; folinic acid, 5FU and Oxaliplatin
• FOLFIRI – Folinic acid (leucovorin), 5 FU, Irinotican.
• FOLFIRINOX

61. • FOLFOX
• LEUCOVORINE; it increases the intracellular concentration of
methylene tetrahydrofolate, thus stabilizing the ternary complex
formed between fluorodeoxyuridine monophosphate (FdUMP) and
the thymidylate synthase (TS), improving the cytotoxic activity of 5FU.
• FLOX; 5-fu 500mg/mg² iv weekly plus leucovorin 500mg/m² iv
weekly for 6weeks( days 1, 8, 15, 22, 29, and 36) of each 8weekly
plus oxaliplatin 85mg/m² iv administered on day 1, 15, and 29 of
each 8-wk cycles

62. • mFOLFOX6 ; Day 1: Oxaliplatin 85mg/m2 IV over 2 hrs + leucovorin
400mg/m2 IV over 2 hrs, followed by 5-FU 400mg/m2 IV bolus,
followed by 5-FU 1,200mg/m2 /day IV x 2 days (total 2,400mg/m2 )
as a 46–48 hr continuous infusion. Repeat every 2 weeks.
• CapeOX; Day 1: Oxaliplatin 130mg/m2 IV. Days 1–14: Capecitabine
1,000mg/m2 orally twice daily. Repeat every 3 weeks for 8 cycles.
• FOLFIRI; Day 1: Irinotecan 180mg/m2 IV + leucovorin 400mg/m2 IV,
followed by 5-FU 400mg/m2 IV bolus, followed by 5-FU 1,200mg/m2
/day IV x 2 days (total 2,400mg/m2 ) as a 46–48 hr continuous
infusion. Repeat every 2 weeks.

63. METASTATIC DISEASE
• Bevacizumab; inhibit VEGF plus chemotherapy (used in metastatic disease)
• Bevacizumab (Avastin), cetuximab (Erbitux), panitumumab (Vectibix), or
irinotecan should not be used in the adjuvant setting for Stage II or III
patients outside a clinical trial setting
• Cetuximab or panitumumab ; inhibit EGFR
• In patients with metastatic colon cancer, testing of the tumor
for KRAS mutations at exons 2, 3, and 4; NRAS mutations at exons 2, 3, and
4 and BRAF V600E mutation should guide the decision whether to use
biologic agents that target epidermal growth factor receptor (EGFR).
• Patient with mutated K-Ras are unlikely to benefit from anti-EGFR
therapy
• Patients with wild-type K-RAS and no BRAF V600E typically respond to
anti-EGFR therapy.

64. • Patients with right sided tumors are less likely to respond to EGFR
therapy with cetuximab or panitumumab.
• BRAF V600E mutation makes response to anti-EGFR therapy less
likely.
• Choice of initial therapy for advanced disease is based on goals of
treatment, location of tumor, mutational profile, toxicity profile of the
drugs, and patient's performance status.
• mFOLFOX6, FOLFIRI, CapeOx, FOLFOXIRI, capecitabine, and infusional
5FU/LV with or without targeted agents are all considered
appropriate first-line agents.

65. • Note in emergency presentation, there is need for resuscitation and
faecal diversion before later giving a definitive treatment.

66. FOLLOW UP
1. Serum CEA – 2 monthly.
2. Fecal occult blood testing – 3 days every 6 months.
3. Colonoscopy – done 1 year after operation, and every 2 – 3 years
thereafter.

67. RECTUM
• GOALS FOR SURGERY
• The primary goal of surgical treatment for rectal cancer is
complete eradication of the primary tumor along with the
adjacent mesorectal tissue and the superior hemorrhoidal artery
pedicle

68. • RESECTION MARGIN;
• The use of APR for low rectal cancers traditionally has been based on
the need for a 5-cm distal margin of normal tissue.
• Distal intramural spread usually is limited to within 2.0 cm of the
tumor unless the lesion is poorly differentiated or widely metastatic.
• Therefore, a 2-cm distal margin is acceptable for resection of rectal
carcinoma, although a 5-cm proximal margin is still recommended

69. • RADIAL MARGIN;
• The length of mesorectum beyond the primary tumor that needs to
be removed is thought to be between 3 and 5 cm because tumor
implants usually are seen no further than 4 cm from the distal edge of
the tumor within the mesorectum.
• Therefore, in proximal rectal cancers, distal mesorectal excision 5 cm
below the lower border of the tumor should be the goal.

70. CHARACTERISTICS OF TUMORS AMENABLE TO LOCAL EXCISION
• T1N0 or T2N0 lesion
• <4 cm in diameter
• <40% circumference of the lumen
• <10 cm from dentate line
• Well- to moderately diff erentiated histology
• No evidence of lymphatic or vascular invasion on biopsy
• Patients with extensive metastatic disease and poor prognosis who
• require local control
• Adjuvant treatment for patients with lymphatic invasion, T1 with
• poor prognosis features, T2 lesions

71. TECHNIQUES FOR LOCAL RESECTION
• There are four approaches to local excision:
• Transsphincteric,
• Transanal,
• Transcoccygeal,
• TEM (transanal endoscopic microsurgery)

72. TRANS ANAL EXCISION
Under general or regional anesthesia, often with
a pudendal block for analgesia and sphincter
relaxation.
Retractors or an operating anoscope is used for
exposure, and electrocautery is used to excise a
full thickness section of the rectum.
The tumor, attached mesorectal fat, and a
margin of normal tissue are removed.
The rectum is then closed transversely.

73. Trans coccygeal
The incision is made in
the intergluteal fold
over the sacrum and
coccyx
After division of the skin
and subcutaneous
tissue, the coccyx is
removed by cauterizing
its attachments
The levator ani muscles
are separated in the
midline, rectum can be
completely mobilized
The tumour is excised
with 1cm margin of
normal rectum

74. Total endoscopic
microsurgery
Dr. Gehard Buess - 1980s.
Requires rectal insufflation, 3D visualization and
magnification through a stereoscope and binocular
eyepiece, and instrumentation via
an operating rectoscope.
It allows for full thickness resection
in the extraperitoneal rectum, including perirectal
fat and, if necessary, circumferential resection and
anastomosis
In the intraperitoneal rectum, only mucosectomy is
possible

75. • Trans anal minimally invasive surgery
• A single incision laparoscopic surgery (SILS) apparatus and standard
laparoscopic surgical instruments are used.
• Relatively small case series describe the safety and feasibility of TAMIS for
resection of adenomas and early rectal cancers

76. INTERSPHINCTERIC RESECTION
• Schiessel – 1994
• It exploits the plane between internal and external sphincters to achieve a balance between
adequate oncologic resection and continence preservation
• Combination of abdominal and perineal approaches.
• Proctectomy and TME are combined with resection of all or part of the internal anal
sphincter and creation of a handsewn transanal anastomosis
• The abdominal approach consists of a proper TME as described previously.
• The perineal approach then allows for identification of the mass.
• Coloanal anastomosis after the resection

77. • Indication
• T1-3 tumors located within 3-3.5 cm from the anal verge, with or without internal
anal sphincter invasion
• Contraindications
• T4 tumors
• invasion of external anal sphincter
• fixed tumors in digital examination (indication that the tumor has broken through the
intersphincteric plane)
• poorly differentiated tumor
• poor preoperative sphincter function
• distant metastases

78. ABDOMINOPERINEAL
RESECTION WITH
PARMANENT
COLOSTOMY
T3 or T4 tumor in the involving the levator
ani/external sphincter muscle.
Patients with impaired continence; previous
obstetric, traumatic, or iatrogenic injury to
the sphincters;
chronic diarrheal diseases such as
Inflammatory bowel diseases
patient’s preference for a stoma

79. PROGNOSIS
• Depends on:
• Site—left sided tumours has got better prognosis as they present early.
• Type—colloid carcinoma has got poorer prognosis.
• Size of the tumour.
• Lymph nodes status: Number of lymph nodes involved decides the prognosis.
• Liver secondaries has poor prognosis.
• Age of the patient; younger patients have poorer prognosis.
• Associated diseases like HIV.
• Stage of the tumour.
• Presence of complications, perforation, peritonitis.
• On the whole, it is a curable malignancy with proper surgery and adjuvant therapy.

80. PREVENTION AND SCREENING
• Screening of population at risk is recommended in asymptomatic
adults at age 50 years.
• First base-line colonoscopy is done, and if no pathology is found,
repeated every 10 years
• FOBT should be done on annual bases, positive result should
precipitate a full colonic evaluation. Every 5 years, a flexible
sigmoidoscopy is done. If a precursor lesion is found, they should be
removed and colonoscopy performed 1-3years to detected missed
(20%) or recurrent polyps.
• Individuals at increased risk, screening starts earlier. 45 years.
• Screening have shown to reduce colorectal cancer incidence by 76-
90%.