Lower GI Surgery Flashcards
What are the arterial supplies to the colorectal system
The colon is supplied by the SMA and IMA, and the rectum supplied by 3 arterial supplies:
1) Branches of SMA include
- Ileocolic artery
- Right colic artery
- Middle colic artery
2) Branches of IMA include:
- Left colic artery
- Sigmoid branches
- Superior rectal artery
3) Rectum is further supplied by:
- Middle rectal artery from internal iliac artery
- Inferior rectal artery from internal pudendal artery (from internal iliac)
What vascular anasomotoses at the watershed area of LB?
1) Marginal artery of Drummond
2) Arc of Riolan (aka Meandering artery of Gonzalez)
How to identify IMV
To the left of DJ flexure
What parts of GI tract do not have a serosa?
1) Esophagus (except the very distal part)
2) Middle and Distal rectum
What are the white lines of Toldt?
Lateral peritoneal reflections of the ascending and descending colon
Name the venous drainage of the rectum
1) Proximal rectum drains to IMV to splenic vein to portal vein
2) Middle rectum drains to iliac vein to IVC
3) Distal rectum drains to iliac vein to IVC
Where is the rectosigmoid junction?
- It is constantly located 15-18cm from the anal verge
- Found anterior to sacral promontory
- Where mesocolon and haustra terminates
What ions are absorbed and secreted by the colon?
Where in GI tract does majority of water absorption occurs?
Colon preferentially absorbs Na+
Colon preferentially secrets K+ and HCO3-
Most water absorption is by ascending colon
What kind of tumour are colorectal cancer?
Majority are endoluminal adenocarcinoma arising from mucosa.
Sometimes carcinoid tumours, lymphomas (MALT lymphoma), and Kaposi sarcoma (in HIV)
CRC site distribution
Depends on the locality, majority are on the left side
Up to 70% of colonic cancers occur in the sigmoid colon and upper rectum
However in Asian population, more right side
In Hong Kong:
1) Ascending colon (30%)
2) Sigmoid (25%)
3) Rectum (20%)
4) Descending colon (15%)
5) Transverse colon (10%)

Risk factors of CRC
<strong><em>Modifiable VS non-modifiable </em></strong>
Modifiable:
1) Diet & Lifestyle
- Smoking (higher risk for rectal cancer)
- Alcohol
- high red & processed meat (12 portion)
- high fat, low fibre
- low physical activity
2) Obesity
Non-modifiable
3) Male
4) Age >50yo (thus start screening)
- *5) Past history** of CRC or adenomatous polyps
- villosity, high grade dysplasia
- higher risk if larger polyps, plenty number
- *6) Family History (Genetics)**
- 1 first degree relatives with CRC or adeno polyp
- 2 second degree relatives with CRC
- esp diagnosed under 60yo
- *7) IBD**
- Ulcerative colitis poses more risk than Crohn Disease
- *8) Major polyposis syndromes**
- FAP
- Gardner syndrome
- Turcot syndrome
- Peutz-Jeghers
- Familial juvenile polyposis coli
- *9) Hereditary nonpolyposis CRC**
(i. e. Lynch syndrome I & II)
Pathogenesis of CRC
Two molecular pathways:
1) Chromosomal instability pathway (i.e. adenoma-carcinoma sequence)
2) Microsatellite instability pathway (i.e. Lynch syndrome)
_____________
1) Adenoma-carcinoma sequence & Knudson’s multi-hit Hypothesis
- *Normal Mucosa**
- (hyperproliferation, DNA hypomethylation)
- *-> Adenoma**
- (oncogene mutation)
- *-> Severe dysplasia**
- (allelic deletion, aneuploidy)
-> Colorectal carcinoma
Transition from normal mucosa to carcinoma is due to accumulated abnormalities of particular genes. Mutations in mismatch-repair genes cause microsatellite instability and the successive mutation of target cancer genes.
APC allele is often inherited (first hit). Hypomethylation may inactivate the normal tumour suppressor APC allele (second hit). Subsequent changes include oncogen mutation (K-ras), tumour suppressor gene inactivation (p53, LOH)
What is the evidence for adenoma-carcinoma sequence?
1) Distribution of cancers is similar to polyps
2) FAP always proceeds to cancer
3) Adenocarcinoma is seen histologically in adenomatous polyps
4) Systematic removal of polyps reduces lifetime cancer risk
5) Age incidence peaks for polyps about 5 years before carcinoma
Clinical presentation of Colorectal cancer
It may present in 3 ways:
A) Asymptomatic discovered by screening
B) Suspicious symptoms and signs
1) Constitutional Sx
2) Altered bowel habits (more common left), mucus in stool
3) Anaemia, occult blood (right side)
4) Haematochezia (left side)
5) Rectal mass or abdominal mass
6) Tenesmus, rectal pain, pencil stool (rectal)
7) Abdominal pain
8) Symptoms due to metastasis e.g. bone pain, jaundice, pleural effusion
C) Emergency Admission
1) Colonic obstruction (usually left side)
2) Perforation with peritonitis
3) Acute massive lower GI bleeding
Specific presentation of CRC in different sites
- *Right sided tumours**
- occult blood with anaemia, altered blood more common
- triad of anemia, weakness, RLQ mass
- less common obstruction or altered bowel habits due to larger luminal diameter in caecum, also more liquid stool
- *Left sided tumours**
- Hematochezia more common
- Crampy abdominal pain associated with defaecation
- common present with change in bowel habits, i.e. alternating diarrhoea and constipation
- common with narrowing of stool (“pencil stool”)
- more likely to present with colonic obstruction (due to small luminal diameter), thus distention, obstipation
- *Rectal cancer**
- Hematochezia more common
- Pencil stool
- Tenesmus, rectal pain
- Rectal mass
How does CRC spread?
Colorectal cancer spread by:
- *1) Direct extension**
- first circumferentially
- then through the bowel wall
- later invade adjacent peritoneal organs
- *2) Hematogenous**
- via portal circulation to liver (most common)
- via lumbar or vertebral veins to lungs
- also bone, adrenal mets
- *3) Lymphatics**
- regional LN (e.g. para-aortic LN)
- Virchow’s node if advanced
4) Transcoelomic
Investigations in suspected CA colon
What additional workup if rectal tumour?
- *A. Blood tests**
1) CBC - for anaemia
2) LFT, RFT (liver met)
3) CEA (for pre-op level)
4) Clotting profile, type & screen (pre-op) - *B. Complete Colonoscopy (Gold Standard)**
- Diagnosis of tumour with biopsy (genetic testing for VEGF and EGFR mutation)
- Removal of synchronous polyps
- Detection of synchronous cancer (5%)
- *C. Imaging**
1) CXR (Lung met), AXR
2) CT T+A+P or PET-CT for M staging - *D. Additional for Rectal Tumour**
1) Rigid sigmoidoscopy for accurate assessment of distance of rectal tumour from anal verge
2) Rectal protocol MRI (some uses trans-rectal USG)
- good for local staging of rectal carcinoma (T & N stage)
- assessing depth of invasion into the mesorectal fat surrounding the rectum
- determine circumferential resection margin (CRM)
What is CEA? What’s its role in CRC?
Carcinoembryonic antigen (CEA) is a glycoprotein present in primitive endoderm. Serum CEA raised in advanced CRC.
Role of CEA in CRC:
★ NOT for screening or diagnosis
i) For prognosis
ii) For baseline and recurrence surveillance after curative resection; allows early detection & thus treatment of recurrence (no proven survival benefit)
What are some causes of CEA elevation?
1) Smoking can cause mild increase
- *2) Aerodigestive tract cancer**
- CA lung
- CA stomach
- CRC
3) CA Pancreas
4) Medullary thyroid CA
What to do if colonoscopy cannot reach ileocecal valve in a CRC patient?
Perform other imaging investigations:
1) CT colonoscopy (colonography)
2) Barium enema
3) PET/CT
CRC staging systems
What is the prognosis in the TNM stage?
A) Dukes’ staging (ABCD)
- Dukes’ A: tumor within the wall of the bowel
- Dukes’ B: invades through the wall of the bowel
- Dukes’ C: regional lymph node mets
- Dukes’ D: distant mets
B) TNM staging (I to IV)
- Tis: in-situ i.e. intra-mucosa
- T1: submucosa
- T2: muscularis propria
- T3: invades through MP to subserosa
- T4: through serosa to surroundings
- N1: 1-3
- N2: 4 or more
- M1: distant met
- Stage I: T1-2, N0, M0 (90% 5-year)
- Stage II: T3-4, N0, M0 (70% 5-year)
- Stage III: N1-2, M0 (50% 5-year) = Duke C
- Stage IV: M1 (10% 5-year) = Duke D
3) Haggitt classification & Kudo classification for Tis & T1 disease (i.e. malignant polyps)
CRC surgical intervention types (generally speaking)
Curative vs Palliative
- *CURATIVE RESECTION**
1) Resection of the bowel segment with tumor
2) Adequate lymphadenectomy (12+)
3) Resection of distant metastasis (e.g. solitary liver metastasis) - *PALLIATIVE RESECTION** (when removal of all cancer tissue not possible)
1) Palliation of symptoms such as obstruction and bleeding - *PALLIATIVE NON-RESECTION**
1) Diverting Stoma
2) Bypass surgery for palliation
3) Stenting
Curative Treatment flow of CA Colon in general
- *1) Staging** via colonscopy, biopsy, CXR, AXR, PET/CT
- also do genetic testing for VEGF and EGFR mutation
2) Serum CEA level used to establish baseline
- *3) Pre-operative preparation**
- ERAS protocol
- Oral antibiotic bowel prep
- Mechanical bowel prep
- 24-hr IV antibiotics prophylaxis
- NPO to reduce stool volume and facilitate colonic manipulation
- Type and screen
- *4) Specific surgical resection** depending on the lesion
- Based on sites of CRC
- Adequate lymphadenectomy (at least 12)
- *5) Post surgical** routine management
- Pain Mx e.g. epidural
- LMWH for DVT prophylaxis
- *6) Adjuvant therapy (for stage III, IV)**
- Chemotherapy FOLFIRI (leucovorin, 5-FU, irinotecan) or FOLFOX (leucovorin, 5-FU, oxaliplatin)
- Radiotherapy
- Targeted therapy with VEGF inhibitor (bevacizumab) an EGFR inhibitor (cetuximab)
7) Follow-up surveillance
Bowel prep for colorectal resection
Preoperative “bowel prep”:
1) Golytely colonic lavage or Fleets Phospho-Soda until clear effuent per rectum
2) PO antibiotics
3) Pre-op 24-hr IV antibiotics (Zinacef, Flagyl)



2) Obtain Written informed consent
- Indication, Procedure, Alternative, Possible Outcomes, Complications * *3) Preparations** i) Low residual diet 2 days before (i. e. no fruit, brans, vegetables and dairy products) ii) Fluid diet night before and day of procedure (rice water, clear water) iii) Purgative the night or morning of procedure (clear bowel) - Isoosmolar agent like Polyethylene glycol - e.g. PEG-ELS or SF-PEG-ELS (more palatable) * *4) After procedure** i) resume diet normally after 1 hour ii) not to drive car or machinery after the procedure


