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Surgery - Colorectal Cancer (Tutorial)

Colorectal cancer develops from colonic polyps through accumulation of genetic mutations over 10-15 years. Polyp types with higher villous components have greater malignant potential. Endoscopic resection is preferred for treatable polyps while surgical resection with lymph node assessment may be needed for invasive cancers. Screening and surveillance colonoscopy is based on individual risk factors like family history, polyp findings, and hereditary conditions. Prevention focuses on modifiable lifestyle factors and regular screening to detect and remove precancerous polyps.

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0% found this document useful (0 votes)
49 views9 pages

Surgery - Colorectal Cancer (Tutorial)

Colorectal cancer develops from colonic polyps through accumulation of genetic mutations over 10-15 years. Polyp types with higher villous components have greater malignant potential. Endoscopic resection is preferred for treatable polyps while surgical resection with lymph node assessment may be needed for invasive cancers. Screening and surveillance colonoscopy is based on individual risk factors like family history, polyp findings, and hereditary conditions. Prevention focuses on modifiable lifestyle factors and regular screening to detect and remove precancerous polyps.

Uploaded by

hales
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
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MBBS V Surgery – Colorectal CA (tutorial)

Colorectal cancer
Colonic polyp
 70-80% adenoma-carcinoma sequence
 Developed into carcinoma after 10-15 years
 Accumulation of gene mutation
o Proto-oncogene
o Tumour suppressor gene
 Types  aware of pathology after polypectomy
o Neo-plastic polyp (% of villous component: higher risk feature)
 Tubular adenoma 5% (most common)
 Tubo-villous adenoma 20-25%
 Villous adenoma 35-40% (higher risk of malignant transformation)
o Non-neoplastic
 Inflammatory
 Hyperplastic
 Harmatomatous
 Sequence: Malignant colonic polyp
o Indication of malignancy (require pathology report)
1. Size >1.5cm
2. Histological type (more villous component: higher transformation)
3. Degree of dysplasia (high grade: faster malignant transformation)
4. Confined within muscularis mucosae Tis/submucosal T1
 Tis = No risk of lymph node spread if in muscularis mucosae
 T1 = Breached submucosa
o Classification: Haggitt’s classification (site of cancer cell component)
 0: carcinoma confined to mucosa
 1: head of polyp
 2: neck of polyp
 3: stalk of polyp
 4: submucosa involvement
 Colonic polyp treatment (endoscopy: end view vs side view = ERCP)
o i. Endoscopic resection: haustra fold know colonoscopy
 Polypectomy
 Working channel: snare + hemostasis
 Pathological report
 Retain polyp: depends on size of polyp
o Suction channel
o Working channel: polyp retriever with tripod
 ESD (endoscopic submucosal dissection, en-bloc)
 Indication: very large polyp
 Inject hyaluronic acid to raise the polyp
 Special knife to cut away mucosa and dissect across sub-
mucosal plane
o ii. Formal surgical resection: colectomy
 Endoscopic vs surgical resection
 Endoscopy: no GA, ensure adequate margin
 Laparoscopic resection: GA, achieve negative margin, requires
vessel ligation + lymph nodes resection  may revise staging
and management (e.g. adjuvant chemo)
MBBS V Surgery – Colorectal CA (tutorial)

 Indication for colectomy - absence of any of the following features:


1. Poorly differentiated
2. Vascular or lymphatic
3. Invasion beyond submucosa
4. Positive resection margin
 Surveillance after colonic polyp removal
o Normal colonoscopy: 10 years
o Normal colonoscopy (if 1st relative has CRC): 5 years
o <20 hyperplastic polyps <10mm: 10 years
o Hyperplastic polyps >10mm: 3-5 years
o 1-2 Low risk adenomas (tubulo-adenoma): 7-10 years
o 3-4 low risk adenomas or 1 high risk adenoma: 3 years
o >10 adenoma: 1 year
o Sessile polyposis: 1 year
 High risk adenoma:
o Villous/tubulovillous adenoma
o High grade dysplastia
o Adenoma >10mm

Epidemiology and etiology


 Sporadic: 80%
 Familial: strong fam hx
o More than 2 first degree relatives irrespective of age of onset
 Hereditary: gene mutation
o Familial adenomatous polyposis
 Features
 Autosomal dominant, mutation of APC gene (5q)
 <1% of CA colon (not common)
 100% penetrance at age <30 years  prophylactic colectomy
 Dx: >100 polyps
 Mx
 Endoscopy yearly since 12 years old
 Prophylactic colectomy (until diagnosis of CA colon)
o Hereditary non-polyposis colorectal CA (more common)
 Features
 Autosomal dominant, MMR mismatch repair gene
 Commonest inherited colonic cancer: 5-10% of CA colon  80%
risk for development of CA (not 100% penetrance, not
prophylactic mx)
 Less polyps than FAP
 Right side colon tumour
 Dx at age 45 y/o
 Lower stage, better survival
 Higher occurrence - synchronous/metachronous tumour (20%)
o Synchronous: <6 months, metachronous >6 months
 Lynch syndrome
 Lynch syndrome 1:
o Only early onset CA colon
 Lynch syndrome 2: other cancers
MBBS V Surgery – Colorectal CA (tutorial)

o CA colon, endometrial CA, stomach CA, HBP


system, ureter CA, small bowel, renal pelvis
 Amsterdam diagnostic criteria
 3 family members with colorectal CA or other HNPCC extra-
colonic cancer
 At least 2 generations affected
 At least 1 individual before 50 y/o
 1 affected case is first degree relative f other two
 Excluded FAP
 Bethesda criteria

 Diagnosis: genetic study (young CA colon study) = MSH2, MHL1


 Hereditary gastrointestinal cancer registry
o Any

Clinical presentation of CRC


 Right side CRC (less symptoms)
o Iron deficiency anemia
o Right lower quadrant mass
o Stool FOB positive
o More liquid stool: less likely bowel symptoms
 Left side CRC
o PR bleeding
o Blood mix with stool
o Tenesmus
o Mucus with stool
o Change in bowel habit
o Palpable abdominal or rectal mass
o More solid stool: bowel symptoms more prominent
 Constitutional S/S
o Significant weight loss
o Loss of appetite
 Metastatic
o Supraclavicular LN
o Hepatomegaly
 Emergency presentation
o Intestinal obstruction
o Bowel perforation
 Site of perforation: cecum (esp. closed loop obstruction) (common)
 Tumour perforated
MBBS V Surgery – Colorectal CA (tutorial)

 Infected tumour

Risk factors
 Modifiable
o Diet: low fiber, red processed meat/animal fat
o Smoking
o Alcohol consumption
o Obesity
 Non-modifiable
o Long standing colitis: 8% in 20 years, 20% if 30 years
 Inflammatory bowel disease: ulcerative colitis
 Does not follow adenoma-carcinoma sequence
 Low grade to high grade (much shorter sequence)
 Requires endoscopy follow-up
o Personal hx of colonic polyp or CRC
o Significant family hx
o Hereditary cancer: HNPCC, FAP
 Protective effect (debatable)
o Regular physical exercise
o Increase fiber

Prevention/screening for CRC


 Average risk
o No hx or Fhx of CA colon or
o No 1st degree relative with CA colon or
o One 1st degree relative dx CA colon at age >60 years
o Px: Screening colonoscopy once at 50 years (gov: FOBT with FIT)
 Moderate risk
o One 1st degree relative dx CA colon age <60
o Two 1st degree relative dx CA colon at any age
o Px: 5 yearly colonoscopy from age 40 / 10 years prior to dx of youngest relative
 High risk
o Fam hx of FAP/HNPCC/other polyposis syndrome
o Px: Regular screening, every 1-2 years

Screening methods
 Fecal occult blood (annual or biennial)
o Guaiac test based on pseudoperoxidase activity of hematin
 16% reduction in mortality
 Sensitivity 40%
 3 samples collected (may not continuously bleed)
 Dietary restriction: red meat, vitamin C (reducing agent – false-ve)
 Qualitative test
 Detect upper AND lower GI bleed
o Immunochemical test (FIT)
 Antibodies to detect human hemoglobin
 Quantitative test
 If upper GI bleed: small bowel digestion will NOT detect intact Hb
 If +ve = suggests lower GI bleed
 Flexible sigmoidoscopy +/- double contrast Ba enema
MBBS V Surgery – Colorectal CA (tutorial)

o Advantage: Only food enema bowel prep and no sedation


o Disadvantage: not whole colon (need double Ba enema = need bowel prep)
o Every 5 years
o Accuracy of detecting colonic polyp >1cm = that of colonoscopy
o Need to be confirmed with colonoscopy and biopsy if +ve
o Need sphincter continence (not in very old patients: cannot hold air/contrast
for enema  sub-optimal results)
o Appearance
 Apple core: common GI malignancy
 Pedunculated mass
 Colonoscopy
o Diagnostic AND therapeutic (SNARE of polyp)
o Requires full bowel prep (PEG x3)
o Need sedation (IV diazemul/benzodiazepine, IV pethidine)
 Antidote benzo: flumazenil
 Antidote opioid: naloxone
o Risk:
 Bleeding
 Perforation (1/1000)
 Delayed perforation – transmural necrosis after polypectomy –
intervened with clip of mucosal defect
 Sedation overflow (respi depression) requires monitoring
 CT colonoscopy
o Indication
 Synchronous tumour
o Only diagnostic
o Full bowel preparation

Colonoscopy
 Position: left lateral position
 Confirm end site:
o See ileo-cecal valve
o Intubate terminal ileum (see terminal ileum = small bowel nodula mucosa)

Monitoring CEA (carcinoembryonic antigen)


 Glycoprotein in cell membranes
 Elevated:
o Chronic smoker
o CA lung, stomach, breast, ovary, prostate, bladder, kidney, H&N
 Use
o Follow-up in CRC patients (NOT for screening)  dx relapse
 Non-smoker <4.7; Smoker <6.5 (depending on reference)

Investigations
 Confirm dx
o Endoscopy + biopsy
o CT colonoscopy
 Assess fitness for operation + complications of disease
o CBC
o LFT, RFT, CEA
MBBS V Surgery – Colorectal CA (tutorial)

 Staging dx
o CT thorax, abdomen + pelvis with contrast
o PET (if CT is equivocal for any dissemination)

Duke’s staging (old staging method) (A: early, B: muscle, C: LN, D: distant)
 A: lesion not penetrating submucosa
 B1: lesion not through muscularis propria
 B2: lesion through intestinal wall, no adjacent organ involvement
 B3: lesion involve adjacent organ
 C1: B1 + LN met
 C2: B2 + LN met
 C3: B3 + LN met
 D: distant met

TNM staging

 Stage II: no LN involvement


 Stage III: LN involvement, requires adjuvant chemo, prognosis (relapse, survival)

Prognosis of 5 year survival


 Stage I: 80-95%
 Stage II: 55-80% (heterogeneous spectrum)
 Stage III: 40% (requires adjuvant chemo)
 Stage IV: 10%

Spread of tumour
 Direct spread
o +/- fistulation (colo-vesico fistula  risk of urosepsis)
 Lymphatic
o Pericolic LN
o Regional LN
o Para-aortic LN (usually not removed)
 Blood borne
MBBS V Surgery – Colorectal CA (tutorial)

o Hepatic (porto-venous circulation) (most common liver met)


o Pulmonary (systemic circulation)
 Transcoelomic:
o Peritoneal (carcinomatosis)
o Ovaries (Krukenberg tumour)
Management
 Surgical resection
o Location of tumour
 Surgical resection of involved segment  restoration of GI continuity
by anastomosis
 Except in APR: very low CA rectum/sphincter involved CA anus
o Elective/emergency (obstructing tumour/perforation)
 Cannot create pneumoperitoneum since in IO  edema  open
 Fecal peritonitis/shock  open
o Open/laparoscopic
o Patient’s condition
 Adjuvant treatment by oncology
o Chemotherapy
 High risk stage II:
 Lymphovascular involvement
 Poor differentiation
 Emergency (perforation/obstruction)
 Inadequate number of LN resected (>12 required)
 Stage III
 Stage IV
o Targeted therapy
 Surgical approach
o Elective: resection + anastomosis (except low lying/sphincter rectum)
 Low residue diet (smaller lumen: higher risk of IO)
 Fluid diet day before OT
 Bowel prep with PEG night before
 Antibiotic: Cefuroxime, Metronidazole (Gram –ve, anaerobes)
 Injection of dye during CLN for small tumour
 Polypectomy: to stain serosa
o Emergency: usually IO and hopefully clear tumour
 Right side colon: better blood supply
 Resection + ileocolic anastomosis
o Usually ileocolic anastomosis has better healing
o One stage anastomosis
 Left side: to relieve IO and cut both sides (poorer blood supply due
to one main artery, no bowel prep, hence usu. need stoma)
 Resection + stoma (end/double barrel)
o End stoma: Hartmann
o Double barrel stoma: both ends of colon long enough
 Resection + on table lavage + primary anastomosis +
covering stoma (if good conditions; on table lavage = Foley at
appendix  use normal saline to clean the bowel)
 Unfavourable patient conditions
o Dehydrated
o Bowel edema (from IO)
MBBS V Surgery – Colorectal CA (tutorial)

o Shock
o No bowel prep (different right and left side)

 Inoperable (usually uncommon since imaging is available)


 Indications
o Carcinomatosis
o Retroperitoneal mets/iliac met (invaded to life-
threatening structures)
 Proximal diversion (for distal tumour) or ileocolic bypass
o Loop stoma: proximal diversion at transverse colon (CA
sigmoid/distal tumour)
o Ileo-colic bypass (right side tumour) (loop ileostomy
will be of too high output, no stoma = better QoL)
 Colonic stenting
 X-ray controlled: self-expandable metallic stent at IO site
 Marker to be identified by X-ray
o Distal descending tumour from dilated bowel
o Indentation site = site of tumour (should be central)
o Slowly expand over time  clinical assessment: any
flatus, abdominal distention decrease
 Follow-up:
o If not disseminated can arrange elective op (after
edema subside due to IO) (no need to be GA twice, one
stage operation will be more feasible)
o If metastasis/frail  palliative
 Types of colectomy
o Right hemicoletomy: one stage (primary anastomosis)
o Left hemicolectomy: two stage (end colostomy + rectal stump)
o Transverse colectomy: three stage (rare)
o Hartman’s operation: emergency usually
o Subtotal colectomy
o Anterior resection +/- J pouch
 Staged operations
o One stage: elective procedure (immediate restore GI continuity)
o Two stage: e.g. Hartman: resect tumour and stoma + reversion of stoma
o Three stage: Colostomy + stoma + reverse stoma

XR: risk of closed loop obstruction (competent ileo-cecal valve) = more URGENT
 Dilated large bowel = large bowel obstruction
 No small bowel dilatation
 May present with bowel ischemia + perforation
 No perforation

Vs incompetent ileo-cecal valve (diff S/S)


 Usually present with vomiting, abd. distention

Emergency IO operation
MBBS V Surgery – Colorectal CA (tutorial)

 Identify transition between distended bowel vs collapsed bowel: pathology


 No ischemia
 No perforation
 No serosal tear
 Decompress bowel by suction
 Handle with care

Metastasis (usually perform PET scan to exclude multiple/disseminated disease)


 Hepatic (portal venous circulation)
o Resection: hepatectomy
o Radiofrequency ablation (RFA)
o Chemotherapy
 Pulmonary (systemic circulation)
o Resection: lobectomy
o Chemotherapy

Chemotherapy
 5-Fluorouracil (5-FU)
 Folinic acid
 Oxaliplatin – FOLFOX
 Irinotecan – FOLFIRI
 Capecitabine – Xeloda (oral drug) – converted into 5-FU

Target therapy (for mets disease)


 VEGF (vascular endothelial growth factor): Bevacizumab
 EGFR (epidermal growth factor receptor): Cetuximab

Radi-collaboration project in HK
 CT thorax, abdomen + pelvis to private for free

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