This document discusses colorectal cancer. Some key points: - It is the 3rd most common cancer globally and incidence is increasing in developing countries. Risk factors include family history, inflammatory bowel diseases, and diet. - Most cases arise from adenomatous polyps through genetic mutations over many years. Symptoms often only appear once cancer has spread. - Diagnosis is made through colonoscopy and biopsy. Staging involves assessing tumor size, lymph node involvement, and metastasis. - Treatment depends on cancer location and staging, and may include surgery, chemotherapy, and targeted therapies. Screening can detect early-stage cancers when more readily treatable.

1. COLORECTAL CANCER
DR OYINTONBRA KOROYE
Consultant General Surgeon

2. EPIDEMIOLOGY
• 3rd commonest malignancy after lung and
stomach in males and breast and cervix in
women
• Constitutes 8.8% of cancers in males and 9.2%
in females
• In Western communities it’s the 2nd
commonest malignancy
• 10 times commoner in developed countries
• Incidence in black Africa is increasing

3. EPIDEMIOLOGY contd
• Ca rectum is commoner in males 2:1
• Colon cancer is commoner in females 11:7
• Peak age of occurrence is 60-79 years
• Half of the cases occor above 60 years
• 20% occur before 50 years

4. DISTRIBUTION ACCORDING TO SITE
• 12% of large bowel malignancy occurs in the
caecum and ascending colon
• Rectum and pelvirectal junction is commonest
site, 60%
• Descending colon is least affected site, 3%

6. • Rarity of pre cancerous conditions
• The young age of the population
• Transit time of feces and fibre diet

7. AETIOLOGY
• Multifactorial
• Susceptibility is inherited influenced by age,
environment and diet

8.  ADENOMAS
.Established adenoma-carcinoma sequence of 5 to 15 years
.The propensity for development of carcinoma depends on
its size, type and degree of dysplasia
 FAMILIAL ADENOMATOUS POLYPOSIS(FAP)
.Accounts for 1% of colorectal cancer
.75% of pxs with FAP develop carcinoma if left untreated
.Need for screening of relatives with colonoscopy and gene
testing

9. .FAP syndromes include Gardners , Oldfield and Turcot
syndromes
 ULCERATIVE COLITIS; malignancy is more likely to occur
if
.Duration of illness > 10 years
.Pancolonic involvement
.Young age at onset
Patients with ulcerative colitis are 30 times more likely
to develop colorectal cancer

10. • CROHNS DISEASE
.20 fold increase in developing carcinoma
• HEREDITARY NON POLYPOSIS COLORECTAL
SYNDROMES; accounts for 5 to 10% of colorectal
carcinoma
.LYNCH 1 is site specific and predisposes to ca colon
only
.LYNCH 2 aka cancer family syndrome. Patients or their
family members develop carcinoma of the colorectum,
breast, uterus or stomach. Inherited autosomal
dominantly

11. • FIRST DEGREE RELATIVES
.Theres a 3 to 4 times increased risk of developing
colorectal carcinoma
• DIET
.Increased intake of saturated fats
.Increased intake of refined sugars and red meat
.low fibre diet
.Refined diets lack vitamins A, C and E

12. • SPORADIC
• OTHERS eg obesity and inactivity

13. PATHOGENESIS
• Mutation; Kras, APC, P53

15. PATHOLOGY
MACROSCOPICALLY there are 4 variants
.CAULIFLOWER, PROLIFERATIVE or FUNGATING
.MALIGNANT ULCER
.ANNULAR, SCIRRHOUS or STRING STRICTURE
.TUBULAR or INFILTRATIVE
MICROSCOPICALLY ; most are adenocarcinoma.
Others are anaplastic ca and colloid ca

17. tubular

18. SPREAD
• DIRECT
.Commoner with the ulcerative variant
.Transverse or longitudinal spread
.May erode adjacent organs causing fistulae eg
colovesical, colouterine, rectovaginal etc
• LYMPHATIC SPREAD; N1, N2 and N3
.Occurs in 2% of colorectal ca
.Metastasis may lodge in lymph vessels of mesorectum
.Degree of spread correlates with degree of intestinal
wall penetration and histological type

19. SPREAD contd
• BLOOD
.Causes 30 to 40% of late deaths
.Spread is via inf and sup mesenteric and
portal veins
• TRANSPERITONEAL SEEDLING, seedlings may
become implanted on viscera or peritoneum
(car

20. GRADING
• GRADING refers to the degree of
differentiation of the cancer cells ie how much
they resemble normal cells of colorectum. The
better the differentiation, the lower the grade
and less its invasiveness and thus the better
the prognosis
• GRADES 1 to 5

21. STAGING
• DUKES CLASSIFICATION
.A ; confined to the bowel wall
.B ; through bowel wall but not involving free
peritoneal serosal surface
.C ; lymph nodes are involved

22. STAGING contd
• ASTLER-COLLER (MODIFIED DUKES) CLASSIFICATION
.A ;Confined to mucosa
.B1 ;extends to but does not penetrate muscularis
mucosae
.B2 ;penetrates muscularis mucosae but no lymph node
involvement
.C1 ;limited to the bowel but with paracolic lymph node
involvement
.C2 ;growth has spread to lymph nodes at the highest
point of ligature
.D ;there is distant metastasis

23. TNM(Tumour Node Metastasis)

24. • STAGE 1 ; T1-2, N0, M0
• STAGE 2 ; T3-4, N0, M0
• STAGE 3 ; T any, N1-3, M0
• STAGE 4 ; T any, N any, M1

27. COMPLICATIONS
• Acute on chronic intestinal obstruction
• Perforation
• Paracolic abscess
• Bleeding , anaemia
• Internal fistulae

28. SYMPTOMS
• Change in bowel habit
• Abdominal pain
• Spurious diarrhoea
• Change in calibre of stools
• Bleeding per rectum(haematochezia, mixed with
feces)
• Mucus in feces
• Borborygmi ,distension
• Dyspepsia from gastrocolic reflex in ca caecum

29. • Abdominal mass; RIF or epigastrum
• Symptoms of anaemia
• Constitutional symptoms of cancer
• Haemorrhoids
• Symptoms of local spread
• Symptoms of metastasis
• One third of patients present as an emergency

30. DIFFERENTIAL DIAGNOSIS
BASED ON LOCATION OF THE TUMOUR
• CAECAL CARCINOMA
.Amoebiasis
.Tuberculosis
.Actinomycosis
.Appendix mass/ abscess
.schistosomiasis
.Ovarian cyst
.Pedunculated fibroid
.Crohns dx, terminal ileitis

31. • TRANSVERSE COLON
.Gastric tumour
.Pseudocyst of the pancreas
.Renal swellings
.Splenic swellings
.Ca gall bladder

32. • LEFT COLON
.Diverticulitis
.Schistosomiasis
.Amoebiasis
.Ovarian cyst
.Pedunculated fibroid

33. • RECTUM
.Anal ca
.Rectal polyp
.Haemorrhoids
.Rectal prolapse
.Intususception
.Chronic granulomatous conditions

34. INVESTIGATIONS
• GENERAL INVESTIGATIONS TO PREPARE PX FOR
SURGERY OR OTHER TREATMENT MODALITIES
.Urinalysis
.FBC
.E/u/Cr
.CXR, ECG as indicated
.Group and crossmatch blood
.Stool microscopy
.CEA

35. • DIAGNOSTIC INVESTIGATIONS
.Barium enema
.Colonoscopy and biopsy(Gold standard)

38. • INVESTIGATIONS TO DETERMINE EXTENT OF
SPREAD OF THE DISEASE
.Endorectal ultrasound scan
.CXR
.Abdominopelvic Uss
.Intraoperative liver USS
.CT scan
.MRI

39. TREATMENT
• GENERAL SUPPORTIVE MEASURES
.Bowel preparation; diet, whole gut irrigation,
rectal enema/ washout, antibiotics, PEG
.Correction of anaemia
.Improve nutrition
.Prophylactic antibiotics
.DVT prophlaxis
.Anti amoebic therapy
.Planning of colostomy

40. DEFINITIVE TREATMENT
• Depends on location of the tumour, extent of
the tumour and the area of bowel spplied by
the main feeding vessel
• Caecal or right sided tumours; RIGHT
HEMICOLECTOMY
• Transverse colon tuours; TRANSVERSE
COLECTOMY
• Left sided tumours; LEFT HEMICOLECTOMY
• Sigmoid tumours; SIGMOID COLECTOMY

44. RECTAL CA
• Preoperative radiotherapy
• Tumour > 10cm from anal verge( ANTERIOR
RESECTION OF THE RECTUM
• Tumour between 6-10 cm (LOW ANTERIOR
RESECTION)
• Tumour < 6cm from anal verge(
ABDOMINOPERINEAL RESECTION WITH
PERMANENT COLOSTOMY)
• Local excision for T1 tumours

45. COMPLICATIONS

46. TREATMENT OF EMERGENCIES

47. ADJUVANT THERAPY
• Chemotherapy , 5FU, capecitabine, oxaliplatin
and irinotecan, leucovorin
• Regimens include FOLFOX and FOLFIRI
• Targeted therapy eg BEVACIZUMAB and
CETUXIMAB which are monoclonal antibodies
against vascular endothelial growth factor and
epidermal growth factor respectively

48. SCREENING
• FOBT with guiac
• Colonoscopy
• Earlier in high risk patients

49. conclusion

50. OUTLINE