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COLORECTAL CANCER
DR OYINTONBRA KOROYE
Consultant General Surgeon
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
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
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%
• Rarity of pre cancerous conditions
• The young age of the population
• Transit time of feces and fibre diet
AETIOLOGY
• Multifactorial
• Susceptibility is inherited influenced by age,
environment and diet
 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
.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
• 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
• 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
• SPORADIC
• OTHERS eg obesity and inactivity
PATHOGENESIS
• Mutation; Kras, APC, P53
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
tubular
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
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
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
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
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
TNM(Tumour Node Metastasis)
• 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
COMPLICATIONS
• Acute on chronic intestinal obstruction
• Perforation
• Paracolic abscess
• Bleeding , anaemia
• Internal fistulae
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
• 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
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
• TRANSVERSE COLON
.Gastric tumour
.Pseudocyst of the pancreas
.Renal swellings
.Splenic swellings
.Ca gall bladder
• LEFT COLON
.Diverticulitis
.Schistosomiasis
.Amoebiasis
.Ovarian cyst
.Pedunculated fibroid
• RECTUM
.Anal ca
.Rectal polyp
.Haemorrhoids
.Rectal prolapse
.Intususception
.Chronic granulomatous conditions
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
• DIAGNOSTIC INVESTIGATIONS
.Barium enema
.Colonoscopy and biopsy(Gold standard)
• INVESTIGATIONS TO DETERMINE EXTENT OF
SPREAD OF THE DISEASE
.Endorectal ultrasound scan
.CXR
.Abdominopelvic Uss
.Intraoperative liver USS
.CT scan
.MRI
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
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
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
COMPLICATIONS
TREATMENT OF EMERGENCIES
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
SCREENING
• FOBT with guiac
• Colonoscopy
• Earlier in high risk patients
conclusion
OUTLINE
COLORECTAL CANCER by Dr. Oyintonbra Koroye pptx
COLORECTAL CANCER by Dr. Oyintonbra Koroye pptx

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COLORECTAL CANCER by Dr. Oyintonbra Koroye pptx

  • 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%
  • 5.
  • 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
  • 14.
  • 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
  • 16.
  • 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
  • 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
  • 25.
  • 26.
  • 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
  • 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)
  • 36.
  • 37.
  • 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
  • 41.
  • 42.
  • 43.
  • 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
  • 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