Lower GI Surgery Flashcards

1
Q

What are the arterial supplies to the colorectal system

A

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)
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2
Q

What vascular anasomotoses at the watershed area of LB?

A

1) Marginal artery of Drummond
2) Arc of Riolan (aka Meandering artery of Gonzalez)

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3
Q

How to identify IMV

A

To the left of DJ flexure

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4
Q

What parts of GI tract do not have a serosa?

A

1) Esophagus (except the very distal part)
2) Middle and Distal rectum

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5
Q

What are the white lines of Toldt?

A

Lateral peritoneal reflections of the ascending and descending colon

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6
Q

Name the venous drainage of the rectum

A

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

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7
Q

Where is the rectosigmoid junction?

A
  • It is constantly located 15-18cm from the anal verge
  • Found anterior to sacral promontory
  • Where mesocolon and haustra terminates
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8
Q

What ions are absorbed and secreted by the colon?

Where in GI tract does majority of water absorption occurs?

A

Colon preferentially absorbs Na+

Colon preferentially secrets K+ and HCO3-

Most water absorption is by ascending colon

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9
Q

What kind of tumour are colorectal cancer?

A

Majority are endoluminal adenocarcinoma arising from mucosa.

Sometimes carcinoid tumours, lymphomas (MALT lymphoma), and Kaposi sarcoma (in HIV)

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10
Q

CRC site distribution

A

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%)

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11
Q

Risk factors of CRC

A

<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)
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12
Q

Pathogenesis of CRC

A

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)

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13
Q

What is the evidence for adenoma-carcinoma sequence?

A

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

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14
Q

Clinical presentation of Colorectal cancer

A

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

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15
Q

Specific presentation of CRC in different sites

A
  • *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
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16
Q

How does CRC spread?

A

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

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17
Q

Investigations in suspected CA colon

What additional workup if rectal tumour?

A
  • *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)

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18
Q

What is CEA? What’s its role in CRC?

A

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)

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19
Q

What are some causes of CEA elevation?

A

1) Smoking can cause mild increase

  • *2) Aerodigestive tract cancer**
  • CA lung
  • CA stomach
  • CRC

3) CA Pancreas

4) Medullary thyroid CA

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20
Q

What to do if colonoscopy cannot reach ileocecal valve in a CRC patient?

A

Perform other imaging investigations:

1) CT colonoscopy (colonography)

2) Barium enema

3) PET/CT

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21
Q

CRC staging systems

What is the prognosis in the TNM stage?

A

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)

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22
Q

CRC surgical intervention types (generally speaking)

A

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
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23
Q

Curative Treatment flow of CA Colon in general

A
  • *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

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24
Q

Bowel prep for colorectal resection

A

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)

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25
Q

Basic principles to note in curative resection of CRC

A

1) Adequate lymphadenectomy (at least 12)

2) High ligation of arterial pedicle

  • *3) Adequate proximal & distal margin**
  • at least 5cm traditionally for colon cancer
  • 2cm for rectal tumour

4) Segment of resection usually determined by vascular anatomy and lymphatic drainage
5) Restoration of bowel continuity (tension-free anastomosis)

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26
Q

Explain margins and anastomosis in colectomy approaches

A

Right Hemicolectomy

  • Remove: distal 10 cm of terminal ileum to proximal 1/3 transverse colon
  • Anastomosis: ileum to transverse colon
  • Vessels: ileocolic, right colic, and right branch of the middle colic vessel

Extended Right Hemicolectomy

  • Remove: distal 10cm of terminal ileum to proximal descending colon (splenic flexure removed as it is watershed area)
  • Anastomosis: ileum to descending colon
  • Vessels: ileocolic, right colic, middle colic vessels (both branches)

Limited transverse colectomy

  • Remove: middle part of transverse colon (not too much otherwise high tension)
  • Anastomosis: remaining ends of transverse colon

Left hemicolectomy

  • Remove: Splenic flexure to (entire or part of) sigmoid colon
  • Anastomosis: Distal transverse colon to sigmoid colon or rectum

Sigmoidectomy

  • Remove: Sigmoid colon
  • Anastomosis: Descending colon to upper rectum
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27
Q

Elective colectomy selection for colorectal cancers

A

A. Caecum, Ascending Colon
1) Right Hemicolectomy

B. Hepatic Flexure
1) Extended right hemicolectomy

C. Transverse Colon (depends on site)

  • *1) Extended Right Hemicolectomy** (most common)
  • *2) Left Hemicolectomy
    3) Transverse colectomy** if mid-transverse CA without extension to both flexures

D. Splenic Flexure Colon (controversial)

  • *1) Extended Right Hemicolectomy** (most common) if lymphatic drains proximal
  • *2) Left Hemicolectomy** if lymphatic drains distally

E. Descending colon
1) Left hemicolectomy

F. Sigmoid colon
1) Sigmoidectomy

G. High rectum
1) Anterior resection (TME)

H. Low rectum
1) Anterior resection (Low TME)

I. Anal verge or sphincter involvement

  • *1) Abdominoperineal (AP) excision
  • **with end-colostomy or ileostomy
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28
Q

Complications of Colectomy and LAR/APR

A
  • *INTRA-OP**
    1) Bleeding (from splenic injury, vessel injury)
    2) Injury to nearby structures (spleen, duodenum, ureter)

POST-OP
A. General (cardiac, pulmonary, DVT, PE, etc)

B. Specific (EARLY)

1) Wound infection
2) AROU
3) Anastomotic leakage / deshicience
4) Intra-abdominal abscess/collection
5) Prolonged ileus

C. Specific (LATE)

  • *1) Anastomotic stricture
    2) Sexual dysfunction** as a result of damage of the splanchnic nerves (in rectum surgery)
  • *3) Urinary retention
    4) LAR syndrome** (Bowel disturbance)
  • Faecal Incontinence
  • Faecal urgency
  • Frequent bowel movements with clustering
  • Bowel fragmentation
  • *5) Stoma Cx** (Ischaemia, Retraction, Prolapse, stenosis, skin problem, parastomal hernia)
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29
Q

What is Hartmann’s Procedure?

A
  • Rectosigmoidectomy
  • End descending colostomy
  • Blind rectal stump
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30
Q

Surgical management of obstructed CA colon

A

After resuscitation; Drip & suck; rectal tube decompression

Depends on the side of tumour

A) If right side (ascending or transverse)

  • *1) Emergency Resection**
    a) Right / extended right with primary anastomosis if possible
    b) Right / extended right with exteriorization of bowel ends
  • *2) Emergency Non-resection**
    a) Iliocolic bypass
    b) diverting stoma

B) If left side

  • *1) Emergency Resection**
    a) 2-stage procedure e.g. Hartmann Procedure
    b) Segmental resection with on-table irrigation and primary anastomosis (“1-stage procedure”)
    c) Subtotal colectomy if caecal perforation
  • *2) Emergency Non-resection**
    a) Stenting
    b) Bypass surgery
    c) Diverting stoma –> 3-stage approach

b) Hartmann procedure (if sigmoid / high rectum)
- > primary anastomosis later

  • *2) 1-stage procedure (can consider for left side)**
    a) Segmental resection (left hemicolectomy, sigmoid colectomy or anterior resection) with on table irrigation and primary anastomosis

b) Subtotal/total colectomy and primary anastomosis

B) Emergency Surgical Non-resection
1) Endoluminal stenting (usually left side tumour)

  • *2) Diverting stoma**
  • if unresectable
  • as 3-stage approach for left sided obstruction (not preferred)

3) Bypass surgery (e.g. iliocolic bypass in right side tumour)

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31
Q

Compare the emergency surgical resection approaches for left sided CRC (pros & cons)

A

1) 3-stage procedure
+ treatment of choice for patients who are unfit for resection at presentation
+ anastomosis and its attendant risk of failure are avoided in the 1st stage operation

  • decreased long term survival (higher cumulative mortality and morbidity)
  • 50% patients never have colostomy closed
  • out of favour

2) 2-stage procedure e.g. Hartmann (preferred)
+ early removal of tumour, relieve obstruction
+ anastomosis and its attendant risk of failure are avoided in the 1st stage operation

  • reanastomosis can be very difficult, ~10% mortality
  • up to 40% of patients did not have bowel continuity restored due to various reasons

3) 1-stage procedure
+ Single procedure
+ avoidance of stoma

  • higher risk of anastomotic leakage (5-10%)
  • Loop ileostomy can be fashioned to allow the primary anastomosis to heal
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32
Q

Why is primary anastomosis not preferable in emergency management of left sided CRC?

A

When we decide to do an emergency surgery on left sided CRC:

1) Patient is usually weak, malnourished, and dehydrated
2) Proximal colon is usually edematous and unhealthy, with its blood supply easily obliterated
3) Heavy bacterial and faecal load in proximal colon due to obstruction. Without proper bowel preparation, easily cause post-op infection
4) The ileocaecal valve remain competence, thus a close loop obstruction might be formed after surgery, causing perforation of large bowel
- > all these make an anastomosis very risky

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33
Q

Functions of metallic stent in colorectal cancer

A

Inserted under endoscope (sometimes with fluoroscopic guidance), for left sided CRC as:

  • *1) Definitive palliation** in unresectable CRC
  • thus avoid surgery in patients unfit for GA
  • avoid stoma
  • *2) As a bridge to surgery (convert emergency to elective)**
  • Avoids emergency surgery with insufficient bowel preparation; avoid stoma
  • Buys time for Elective operation for better workup, staging, and bowel preparation
  • Lower operative morbidity and mortality
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34
Q

Site of stenting for CRC obstruction

A

Most commonly performed for left sided tumours, at:

  • sigmoid (60%)
  • upper rectal (20%)
  • descending colon (15%)

Technically difficult for proximal (right sided) tumours

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35
Q

Advantage of CRC stenting

A

1) Rapid relief of obstruction

2) More comfortable, less invasive

  • *3) Avoids emergency operation and stoma**, thus lower morbidity & mortality
  • can be definitive palliative or bridge to definitive surgery
  • *4) More cost effective**
  • shorter hospital stay
  • cheaper (cf. stoma care cost)
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36
Q

Complications of stenting in CRC

A
  • *1) Re-obstruction** (15%) from:
  • tumour ingrowth or overgrowth
  • faecal impaction
  • stent migration
  • *2) Stent migration** (10%), presenting as:
  • Re-obstruction
  • Spontaneous expulsion
  • No symptom
  • *3) Bowel perforation** (7%)
  • occur during the procedure or within 3 days post-stenting
  • causes peritonitis
  • Tumour upstaging due to peritoneal met

4) Fistula formation

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37
Q

Management of stent re-obstruction in CRC

A

Depends on the causes:

  • *1) Tumour in- or overgrowth**:
  • laser and restenting
  • *2) Faecal impaction:**
  • enema lavage
  • *3) Migration**
  • mostly do not need intervention
  • Restenting
  • Endoscopic removal
  • Conversion to surgery
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38
Q

Things to avoid in endoluminal stenting of CRC

A

Avoid:

1) Balloon Dilatation of stent (due to perforation risk)

2) Concomittant preoperative Chemo-RT in CA rectum (due to perforation risk)

3) Right sided CA colon due to difficulty of deployment

4) Mid to low CA rectum due to pain and urgency

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39
Q

Adjuvant therapy for CA colon (indication, choice)

A
  • *Indications:**
  • stage III or above (Duke C or above)
  • stage II who have inadequate lymph node retrieval (<12) or with unfavorable characteristics
  • *Choice:**
    1) Chemo
  • XELODA (capecitabine, oxaliplatin)
  • FOLFIRI (Leucovorin, 5-FU, irinotecan)
  • FOLFOX (Leucovorin, 5-FU, oxaliplatin)

2) Targeted therapy (for stage IV)
- VEGF inhibitor (bevacizumab)
- EGFR inhibitor (cetuximab)

+/- 3) RT for rectal CA

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40
Q

Unfavourable characteristics of CA colon

A

Unfavorable characteristics include:

Histology

1) poor differentiation
2) mucinous or signet-ring pathology
3) aneuploid nuclei

Lab Ix
4) Markedly elevated CEA (poor prognosis if >5ng/mL)

Gross behaviour

5) venous or perineural invasion
6) multiple lymph node involvement
7) pericolonic tumor deposits
8) bowel perforation

(If stage II with unfavourable characteristics, then consider adjuvant therapies)

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41
Q

Pros and Cons of pre-op or post-op RT for CRC

A

Radiotherapy for CRC:
+ reduce local recurrence rates
- no survival benefits
- cannot reduce distant mets

Preoperative
+ Can downstage tumour, thus increase curative resection chance
+ High Compliance
+ Irradiated bowel is all resected at surgery

  • patients with earlier disease might be included
  • Makes bowel friable and increases fibrosis in the mesorectum in rectal surgery, making the planes more difficult to dissect and total mesorectal excision more difficult

Postoperative
+ Early disease excluded as pathology known
+ Does not delay surgery
+ Planes easier to dissect in total mesorectal excision

  • Small bowel more likely to be in the field
  • Prolonged course
  • May be delayed by surgical complications
  • Irradiated bowel is left in and may result in radiation colitis
  • Compliance is lower as a result of postoperative morbidity
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42
Q

Follow up after CRC surgery

A

Followup is crucial in the first 2-3 years after surgery, when 90% of recurrences occur:

1) Physical Exam

  • *2) CBC LFT CEA CXR FOBT** monitoring
  • rising CEA levels should prompt a CT T+A+P
  • *3) Surveillance colonoscopy**
  • first year after resection
  • then every 3 years until negative
  • then every 5 years
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43
Q

Principles of CA rectum surgery

A

1) Resection of segment containing the tumour

  • *2) Adequate CRM** (circumferential resection margin) by TME (total mesorectal excision)
  • remove the rectal mesentry
  • because rectal cancer (lower 2/3) spread via lymphatics in the mesorectum
  • *3) Adequate Distal margin**
  • must be negative
  • narrow distal margin (2 cm) is adequate provided mesorectal dissection is performed
  • distal margin can be <2 cm in patients with distal tumors to preserve continence
  • *4) Sphincter & autonomic nerve preservation**
  • preserve continence & urogenital functions

5) Adequate Lymph node clearance

6) High ligation of the arterial pedicle (IMA)

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44
Q

CA rectum surgical approach selection

A

Depends on distance from anal verge & local T stage:

  • *A. 0-5cm (distal third)**
  • *T1:** Local excision
  • *T2:** Local excision + neoChemoRT
  • *T3+:** APR; if >4cm then can consider ultra-LAR + TME & proximal diversion

B. 6-10cm (middle third)
T1N0: Local excision or LAR
T2N0: Local excision + neoChemoRT; or LAR
T3+ or N+: LAR + TME & proximal diversion ± neoChemoRT
if incontinence or sphincter involvement: APR

C. 11-15cm (proximal third)
T1/T2: Local excision
LAR ± proximal diversion ± neoChemoRT
_______________
D. Hartmann’s operation
- Patients with poor sphincter function
- Emergency situation when a primary anastomosis is not safe

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45
Q

Explain the CA rectum surgical approaches

A
  • *Local excision (transanal full thickness excision)**
  • Traditional trans-anal excision or
  • Transanal Endoscopic Microsurgery (TEM) or TransAnal Minimally Invasive Surgery (TAMIS) techniques
  • For T1 lesions (or T2 tgt with neoChemoRT)
  • *Anterior resection**
  • Resection of rectum with colorectal anastomosis
  • *Lower Anterior Resection (LAR)**
  • Resection of rectum with colorectal anastomosis
  • mobilization down to distal rectum and anastomosis at the level below the peritoneal reflexion
  • *Abdominoperineal resection (APR)**
  • Synchronous abdominal and perineal resection
  • Permanent colostomy
  • For distal 1/3 disease or sphincter involvements
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46
Q

How did “anterior resection” get its name?

A

Because the resection of rectum is anterior to the sacral promontory

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47
Q

What should be done for low (e.g. coloproctostomy) or tenuous anastomosis in CA rectum surgery?

A

Proximal diversion by a “defunctioning stoma” (e.g. loop colostomy, loop ileostomy) for high leaking risk anastomosis (e.g. low or tenuous).

If primary anastomosis must be performed, try leak testing in the operating theatre.

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48
Q

Why neo-adjuvant therapy in CA rectum

A

1) Downstage the tumour
2) Reduce local recurrence
3) Preserve sphincter function
4) Preoperative therapy is associated with similar results with significantly less toxicity than postoperative therapy

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49
Q

Contraindications of CRC liver met resection

Resection margin of CRC liver mets?

What is the 3-year survival after resection?

A

Contraindication:

  • more than 5 mets
  • other distant mets
  • positive portal/celiac LNs

Resection margin = 1cm

3-year survival = 33%

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50
Q

What is a diverticulum? How is it classified?

A

A diverticulum is an abnormal outpouching of a hollow viscus into the surrounding tissues. Classified into:

1) True diverticulum: contains all layers of the wall of the viscus, e.g. Meckel’s diverticulum

2) False diverticulum, only some layers present, e.g. colonic diverticulum

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51
Q

Pathogenesis and risk factors of Diverticulosis

A
  • *Pathogenesis:**
  • Increased intraluminal pressure cause inner layer of colon bulge through focal sites of weakness where mesenteric blood vessels pass between muscles of the taeniae coli
  • *Risk factors:**
  • Low-fiber diet
  • Constipation (which increases intraluminal pressure)
  • Positive family history
  • Old age
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52
Q

Common site of diverticulosis in HK

A

Most common location is Sigmoid colon

Righ sided diverticulosis is also common in Asians (therefore colonoscopy is better than sigmoidoscopy to visualise diverticulosis in HK)

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53
Q

Management of uncomplicated diverticulosis

A
  • *1) Dietary advice:**
  • High fiber diet (e.g. bran, psyllium)
  • Low fat diet
  • healthy lifestyle
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54
Q

Complications of diverticulosis (& diverticulitis)

A
  • *1) Painless lower GI Bleeding**
  • due to rupture of vasa recta
  • usually stops spontaneously
  • *2) Diverticulitis**
  • when faeces are impacted in diverticulum, causing inflammation and bacterial overgrowth
  • Acute abdominal pain
  • Constipation or diarrhea, fevers
  • 3) Complications of diverticulitis:*
  • *i) Abscess formation**
  • *ii) Fistulization**
  • Colovescial fistula most common (Pneumaturia or fecaluria)
  • Colovaginal fistula in women (expulsion of gas or feces from the vagina)
  • Rarely, colocutaneous fistula, coloenteric fistula
  • *iii) Stricture +/- Obstruction**
  • due to chronic inflammation and thickening of bowel wall
  • *iv) Colonic perforation**
  • leads to peritonitis
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55
Q

Diverticulosis & Cx investigations

A

Dx of unCx diverticulosis:

  • *1) Barium enema
    2) Colonscopy** (better than sigmoidoscopy as right sided diverticulosis is common in Asian)
  • *3) CT colonoscopy**

Dx of diverticulitis
1) Contrast CT abdomen & pelvis

  • *2) Avoid immediate colonoscopy**
  • colonoscopy 6-8 weeks later to r/o malignancy

Dx for diverticular bleeding:
1) OGD to r/o upper GI bleeding; colonoscopy

  • *2) Mesenteric Angiography, CT angiogram
    3) Tc99m tagged RBC scan
    4) intra-operative endoscopy**
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56
Q

Diverticulitis classifications

A

Hinchey Classification - guides treatment

  • *I - Localised abscess** (para-colonic)
  • Conservative Mx with antibiotics, bowel rest, monitoring
  • even as out-patient
  • *II - Pelvic abscess**
  • IV antibiotics, bowel rest, monitoring
  • Image guided percutaneous drainage
  • consider surgery
  • *III - Purulent peritonitis** (the presence of pus in the abdominal cavity)
  • IV antibiotics, bowel rest, monitoring
  • surgery
  • *IV - Feculent peritonitis**
  • IV antibiotics, bowel rest, monitoring
  • surgery
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57
Q

Management and FU of diverticulitis

A

Depends on clinical status and Hinchey classification

1) Fluid resuscitation if necessary; Bowel rest (NPO) & Monitoring

2) PO or IV antibiotics (Hinchey II)

3) Percutaneous drainage if abscess (Hinchey II)

4) Consider EOT if non-responsive or Hinchey III IV:

i) 1 stage (resection + primary anastomosis)
ii) 2 stage Hartmann: resection + 1 anas + stoma; closure of stoma
iii) 3 stage: diverting stoma; resection; primary anastomosis
iv) or the new Laparoscopic peritoneal lavage (LPL)

5) CLN 6-8 weeks after diverticulitis to r/o cancer

6) Consider elective “Interval colectomy” after diverticulitis

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58
Q

Indications of emergency surgery for diverticulitis with perforation

What types of operations is there? Which one has lowest morbidity

A

First line is resus + IV antibiotics ± drainage. Consider emergency resection (hartmann or 2 or 3 stage) or LPL (lap per lavage) if:

1) Non responsive to antibiotics

2) Clinically unstable

  • *3) Hinchey Class III, IV**
  • generalized purulent peritonitis (III)
  • gneralized faecal peritonitis (IV)

========================
Three types of operation:

1) Diverting colostomy and abscess drainage (first of three-stage approach)
2) Hartmann’s procedure (first of two)
3) Resection with colonic wash-out and primary anastomosis (one stage).

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59
Q

After uncomplicated diverticulitis (unoperated), who should undergo interval colectomy?

A
  • most diverticulitis resolve with IV antibiotics
  • 85% do not recur
  • thus “interval colectomy” is not mandatory, but consider for:

i) complicated disease
ii) Persistent symptom after disease; repeated diverticulitis
iii) Immunocompromised, DM, or young patient

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60
Q

Management of diverticular bleeding

A

1) Resuscitation & transfusion if needed; 85% most spontaneously subsides

  • *2) Colonoscopy hemostasis** with:
  • adrenaline injection
  • endoclips
  • *±3) Further localization of bleeding origin** (when colonoscopy fails)
  • mesenteric angiogram (for >1mL/min)
  • RBC scan (for 0.1mL/min)
  • *±4) Urgent colectomy if life threatening bleeding**
  • subtotal colectomy with ileostomy or
  • total colectomy with ileorectal anastomosis
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61
Q

Indications of urgent colectomy for diverticular bleeding

A
  • Unstable hemodynamic despite adequate resuscitation
  • Excessive blood transfusion (> 6 units)
  • Frequent re-bleeding
  • On anticoagulant
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62
Q

Fistulization in Diverticulitis

A

Often between colon and other organs:

  • *1) Colovesical fistula** (most common)
  • pneumaturia, fecaluria
  • often in women with previous hysterectomy
  • *2) Colovaginal fistula**
  • gas or faeces from vagina
  • ​often in women with previous hysterectomy
  • *3) Colocutaneous fistula** (rare)
  • *4) Coloenteric fistula** (rare - may result in corrosive diarrhoea)
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63
Q

Management of diverticular fistula

A

1) Antibiotics & drainage to control sepsis

2) Elective colon resection & repair of adjacent structure

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64
Q

Which vessel provides blood supply to the appendix?

A

Appendiceal artery which is a branch of the ileocolic artery

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65
Q

Position of appendix

A

1) Retrocecal / retrocolic (60%): behind cecum or even ascending colon (if long enough)

2) Pelvic (30%): suspended over the pelvic brim

4) Subcecal (2%)

4) Pre-ileal (1%)

5) Post-ileal (0.5%)

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66
Q

Appendicitis epidemiology

A

Prevalence: most common urgent surgical procedure

Age: highest incidence in 20-30yo

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67
Q

Pathogenesis of acute appendicitis

A

1) Lumen of appendix is first obstructed by:
- hyperplasia of lymphoid tissue
- fecalith
- foreign body
- rare causes e.g. parasites, carcinoid tumour

2) Obstruction causes stasis of fluid, which promotes bacterial overgrowth and inflammation
3) Distention of inflammed appendix might compromise blood supply, causing ischemia, necrosis, and even perforation

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68
Q

Acute appendictitis presentation

A
  • *Start with Alvarado Score (total 10):**
    1) RLQ Pain & tenderness (2)
    2) Pain migration (from peri-umbilical or even LLQ to RLQ)
    3) Rebound tenderness, tenderness, board like rigidity
    4) Anorexia (& Ketonuria)
    5) Nausea, Vomiting
    6) Fever
    7) Leukocytosis > 10,000 (2)
    8) Neutrophilia, with left shift of leukocytes

Plus extra signs:
+ Rovsing’s sign (press LLQ, pain in RLQ)
+ Obturator sign (pain when internal rotation of the thigh)

Plus specific presentation based on location of appendix:
+ Iliopsoas sign (if retrocecal; pain when right hip extension in left lateral decubitus)
+ Periappendiceal abscess or phlegmon as anterior bulging in PR (if pelvic)
+ Diarrhoea (if pelvic, due to rectal irritation; or retroileal from ileum irritation?)
+ Frequency, pyuria, haematuria, dysuria (if pelvic, due to bladder irritation)

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69
Q

Where is the McBurney’s Point? What is it?

A

It is 2/3 from the umbilicus to right ASIS, indicating the location of the base of the appendix

It is displaced in:
1. Pediatrics (mid point from umbilicus to right ASIS)

  1. Gestational (point shifts upwards and lateral due to displacement by fertile womb)
  2. Situs Inversus
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70
Q

Explain the migration of pain in acute appendicitis

A

Migration of dull peri-umbilical (sometimes even LLQ) pain to sharp RLQ pain

It indicates the change from the midgut visceral pain (sympathetic nerve T10, due to inflammation of the appendix itself), to the peritoneal pain (somatic nerve; i.e. intercostal nerve, due to irritation to visceral peritoneum by continuous distension of appendix)

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71
Q

Diagnosis and Ix in suspected appendicitis

A
  • *1) Clinical diagnosis mostly**
  • likely if Avarado score ≥5
  • definite if Avarado score ≥9

Supportive Lab tests (same for acute abdomen)
2) CBC shows leucocytosis > 10,000 & Left shift (neutrophilia)

  • *3) Urinalysis**
  • rule out UTI or stones or urological causes
  • Pyuria, albuminuria, and hematuria in bladder irritation from appendicitis
  • *4) RFT, electrolyte**
  • note dehydration from vomiting or poor oral intake

Imaging Ix (supportive)

  • *5) US** may be helpful if uncertain about the diagnosis
    6) Consider CT (when US failed e.g. due to obese)
    7) Consider MRI (when US failed e.g. in pregnant lady or child)
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72
Q

Does abnormal urinalysis rule out acute appendicits?

A

No

Mild pyuria and haematuria is common in acute appendicitis from pelvic inflammation which causes ureteric inflammation

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73
Q

US findings of acute appendicitis

A

1) Aperistaltic, noncompressible, distended appendix (7mm or greater outer diameter)
2) Thickened and oedematous appendiceal wall with distinct wall layers (target appearance if axial)
3) Periappendiceal fluid collection
4) Appendicoliths or Fecoliths

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74
Q

Treatment of acute appendicitis

A
  • *0) General support**
  • fluid resuscitation
  • NG tube suction if ileus
  • analgesics

1) Antibiotics
- If uncomplicated, pre-op antibiotics
- if perforated or gangrenous, pre-op until 3-5 days post-op with normal WBC

2) Appendicectomy (laparascopic or open)

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75
Q

What are the open appendicectomy incisions

A
  • *1) Gridiron** or McBurney incision
  • perpendicular to ASIS-umbilical line
  • *2) Lanz incision**
  • along skin tension line, thus better cosmesis
  • *3) Rocker Davis incision**
  • horizontal
  • medial extension: Fowler Weir
  • lateral extension: Rutherford Morrison
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76
Q

Complications of acute appenidicitis

A

1) Gangrenous appendicitis, Perforation, Peritonitis, septic shock

2) Appendicular abscess, appendiceal mass

3) Ileus

4) Pelvic abscess

  • *5) Portal pylethrombophlebitis**
  • septic portal vein thrombosis
  • from E. coli
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77
Q

Complications of appendicectomy

A

General vs Specific

Specific:

1) Surgical site infection (commonest), wound abscess
2) Ileus, increased risk of adhesive SBIO in future
3) Appendiceal stump leak, Enterocutaneous fistula
4) Stump abscess
5) Stump appendicitis
6) Increased incidence of right inguinal hernia (damage to ilioinguinal nerve), incisional hernia
7) Injury to surrounding organs (SB, caecum, fallopian tube)

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78
Q

How would you prepare a patient for an open appendicectomy?

How would you perform an open appendicetomy?

A

1) Informed consent

  • *2) NPO, IVF, IV Antibiotics, foley for U/O if needed**
  • Cefuroxime (broad spectrum) and Flagyl (anaerobe cover)

3) Prophylactic antibiotics

  • *4) GA, supine position, skin cleaned and draped**
  • expose the RLQ including the right ASIS, umbilicus and midline.
  • *5) Lanz incision, layered dissection**
  • centred over McBurney’s point
  • perpendicular to line from umbilicus to ASIS
    (alternative: Gridiron which is less cosmetic but easier to extend)

6) Norfolk and Norwich self-retaining retractor, layered dissection

  • *7) Peritoneum held up with two artery forceps** and divided with a scalpel
  • Care is taken not to damage any underlying loops of bowel
  • Peritoneal swab x microscopy + C/ST (esp if perforated)
  • *8) Inspection to r/o other pathology**
  • caecum, SB for other pathology e.g. caecal neoplasm or Meckel’s
  • ovaries and fallopian tubes to r/o PID, pelvic absvess, ovarian cyst complications
  • *9) Mobilise caecum** to reveal appendix
  • identify by following the taenia coli to base of appendix
  • if retrocecal, may need to divide the lateral peritoneal attachments of caecum
  • confirm appendicitis, look for gangrenous change or perforation

10) Mobilization of appendix. Hold appendix with a pair of Babcock’s forceps and avoid perforating it

11) Mesoappendix is divided between artery forceps and secured with 2/0 Vicryl ties to skeletonize the appendix and free it to its base (anterograde dissection)

12) A straight crushing clamp is applied across the base and replaced 5 mm distally. After applying a 0 Vicryl tie in the form of a surgeon’s knot to the base, divide the appendix flush to the clamp using a scalpel

  • *13) Pouting mucosa edge of the appendix base is cauterised with diathermy**
  • kill mucosal cells to prevent mucocele formation and reduce the bacterial load

14) Abd cavity is then washed out with warm saline

15) Drain if needed, to pelvis
16) Haemostasis
17) Wound closed

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79
Q

How to take out a difficult appendix?

A

Expect a difficult operation if the history is long and if an appendix mass is present. There are several techniques to help:

1) Enlarging and extending the incision
2) Assistant for retraction
3) In a true retrocaecal appendix, the caecum can be mobilized by dividing its lateral peritoneal attachments as for a right hemicolectomy
4) Removing the appendix retrogradely (base first)
5) In the presence of an abscess and being unable to find the appendix, placing a large size Robinson drain into the abscess, washing out the abdomen with saline and closing it

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80
Q

What would you do if the appendix were normal during an EOT for suspected acute appendicitis?

A

If the appendix were normal looking, I would need to search for other possible causes:

1) In a woman, look at the right fallopian tube and ovary
2) Inspect the terminal ileum and palpate for any thickening. This might indicate Crohn’s ileitis or tuberculous ileitis depending on background

3) The small bowel is run to examine for a Meckel’s diverticulum or for any inflamed mesenteric lymph nodes (mesenteric adenitis)
- If there were an inflamed Meckel’s diverticulum this would need to be resected with a short segment of adjacent normal bowel, and a primary interrupted extramucosal anastomosis performed

4) Inspect the large bowel (to look for sigmoid diverticulitis)
5) Palpate posterior abdominal wall, ascending colon, liver edge and gallbladder fundus (for cholecystitis). Look for bile-stained fluid suggesting a perforated duodenal ulcer

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81
Q

What to do if appendix if perforated at its base?

A

1) Limited caecal resection if possible
2) Limited right hemicolectomy

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82
Q

What is an appendiceal mass

A

aka Appendiceal phlegmon:

An appendiceal mass is an inflammatory mass consisting of the inflamed appendix, its adjacent viscera, and the greater omentum. (cf. abscess is pus containing).

It often presents as a palpable mass days following the onset of symptoms

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83
Q

Management of appendiceal mass

When would EOT be needed?

A

An appendix mass is usually treated conservatively:

  • Bed rest
  • IV antibiotics
  • Serial examination to monitor clinical response
  • Interval appendicectomy at 6 weeks

EOT is indicated if:

1) The mass becomes tender or enlarges
2) Uncontrolled Sepsis
3) Development of complication e.g. peritonitis, ileus, obstruction

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84
Q

DDx of appendiceal tumour

A

1) Carcinoid tumour (most common)

2) Adenocarcinoma
3) Malignant mucoid adenocarcinoma (may cause pseudomyxoma peritonei if the appendix ruptures)

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85
Q

What is a carcinoid tumour?

What are the common sites

A

Carcinoid is a tumour that arises from neuroendocrine cells i.e. Kulchistsky cells –> Secretes serotonin

Common sites “AIR”:

1) Appendix (most common)
2) Ileum
3) Rectum
4) Bronchus
5) Other sites e.g. stomach, duodenum, jejnum, colon, pancreas, thymus, ovary, testis

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86
Q

Clinical features of carcinoid tumour

A

Depends on position of tumor:

1) Mostly asymptomatic

  • *2) Abdominal pain, GI bleeding
    3) SBO** due to severe mesenteric fibrosis
  • *4) Intussuception**
  • *5) Carcinoid syndrome** from serotonin and vasoactive peptides
  • Bronchospasm
  • Flushing of skin
  • Diarrhoea
  • Right side heart failure, TR, PS (as lung filtes the vasoactive peptides)
  • *6) Pellagra-like symptoms** from decreased niacin production
  • Diarrhoea
  • Dermatitis
  • Dementia
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87
Q

Wht does carcinoid syndrome not seen in all carcinoid tumours?

What does it indicate?

A

Carcinoid syndrome (“Be FRD”) = bronchospasm, flushing, right heart failure, diarrhoea due to serotonin released from carcinoid tumour

However the liver degrades serotonin to 5-HIAA if the tumour drains into the portal vein.

Therefore, presence of carcinoid tumour indicates possible:

  • liver mets
  • retroperitoneal disease draining into paravertebral veins
  • primary tumour outside the GI tract
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88
Q

Management of carcinoid tumour

A
  • *1) Surgical excision** of primary tumour and liver metastasis
  • right hemicolectomy if tumour >1.5cm
  • appendicectomy if appendicular tumour <1.5cm, with no serosal or cecal involvement

2) Chemotherapy for advanced disease

  • *3) Medical therapy** for palliation of carcinoid syndrome
  • Octreotide (somatostatin analogue)
  • Anti-serotonin drug
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89
Q

DDx of severe anal pain

A

1) Fissure in ano
2) Perianal haematoma
3) Strangulated or thrombosed internal haemorrhoids
4) Perianal and ischiorectal abscess
5) IBD
6) Rectal or anal tumours

90
Q

What is an anal fissure?

A

An anal fissure is a longitudinal tear in the mucosa and skin of the lower third of the anal canal.

91
Q

Etiology and pathophysiology of fissure-in-ano

A

If typical (i.e. posterior midline), then:

  • *1) Hard stool in constipation
  • > Local trauma
  • > internal and external anal sphincter dysfunction
  • > ischaemia**of the overlying anoderm at the posterior midline (due to poor blood supply over the area)

if atypical position and multiple in number, then suspect:**n

1) Inflammatory bowel disease (Crohn’s disease)
2) tuberculosis
3) syphilis, HIV, CMV infection**

92
Q

Site of Fissure-in-ano

A
  • 90% at posterior midline
  • 10% at anterior midline (more common in women), especially after vaginal delivery
  • Think about secondary causes if at atypical sites
93
Q

Chronic anal fissure features

A

Associated with:

1) sentinel pile

2) hypertrophic papilla

3) internal sphincter muscles visualisation at the base of the fissure

94
Q

What is a sentinel pile?

A

It is thickened mucosa / skin tag at the distal end of an anal fissure, indicative of chronic anal fissure

(often confused with a small haemorrhoid)

95
Q

Anal fissure:

  • epidemiology
  • symptoms
  • clinical exam findings
  • diagnosis methods
A
  • *Epidemiology**
  • usually 20-30yo male > female
  • *Clinical feature:**
    1) Anal pain during or immediately after defecation
  • as a result of sphincter spasm
  • can persist for up to an hour

2) Fresh PRB, watery anus discharge
3) Pruritus Ani
4) Constipation

  • *Physial Exam:**
  • fissure usu concealed by anal spasm -> need to spread the buttock to reveal the fissure by visual examination
  • see the white circular fibres of internal sphincter muscle at the base of fissure
  • potentially see small anal skin tag at the superficial end of the fissure
  • DRE and proctoscopy are painful and not indicated
96
Q

Fissure-in-ano management

A

Non-operative treatment successful in >50%
A. Reduce internal sphincter spasm by:
1) LA anaesthetic gel (e.g. Xylocaine jelly)
2) GTN ointment cream 0.2% TDS (2 courses 4-6/52)
- local vasodilator effect, and allow healing
3) Diltiazem cream 2% BD (Topical Ca channel blocker)
4) Botulinum toxin injection

B. Manage constipation & hard stool

  • *1) Lifestyle modification** with hydration and high fibre diet
  • *2) Laxatives**
  • Senna, lactulose

==================

_Surgical treatment (if failed conservative therapy)_
**1) Lateral internal sphincterotomy**
97
Q

How to perform Lateral internal sphincterotomy

(indication and procedure)

A

Indication: Anal fissure with failed medical therapy (usually 2 courses of GTN ointment 0.2% TDS x 6/52)

Procedure:

  • Under GA or SA
  • Lithotomy position
  • EUA with DRE / proctoscopy / RS -> confirm diagnosis, rule out synchronous pathology
  • Examine with Eisenhammer’s or Park’s retractor
  • Develop submucosal plane with LA injection -> identify internal sphincter muscle
  • Insert metzenbaum scissors into the intersphincteric space and enlarge
  • Internal sphincter muscle fibres are usually cut to dentate line, away and lateral to fissure
98
Q

What are the complications of lateral sphincterotomy?

A

General

Specific:

1) Treatment failure in 5%
2) Faecal or flatus incontinence (permanent in 5%)

99
Q

What is the difference between fistula and sinus?

A
  • *Fistula**:
  • a communication between 2 epithelial-lined surfaces
  • always abnormal
  • *Sinus**:
  • a blind-ending tract communicating with 1 epithelial-lined surface
  • could be normal (e.g. carotid sinus) or abnormal (pilonidal sinus)
100
Q

Anal fistula definition and etiology

A
**_Definition:_**
Abnormal tracts (usu lined with granulation tissue) communicating between the rectum/anal canal with perineal skin
  • *Etiology:**
    1) From perianal abscess, due to crypt or gland infection

2) Crohn’s disease
3) Tuberculosis, HIV infection
4) Foreign body, Trauma
5) Carcinoma

101
Q

Clinical features of anal fistula

A
  • Perianal pain, associated with AROU or constipation
  • Perianal swelling
  • Recurrent peri-anal/rectal abscess
  • Perianal drainage, External opening with discharge
  • “diaper rash”
  • Pruritus ani
102
Q

Classification of anal fistula

A

i. e. the Parks Classification
1) intersphincteric
2) transphincteric
3) suprasphincteric
4) extrasphincteric

103
Q

What is the law on fistula-in-ano

A

Goodsall’s law:
- imagine a transverse line through the anus, with patient in lithotomy position

1) If external opening lies anterior to the line
- the course of the fistula is straight (i.e. pass directly into anal canal)

2) If external opening lies posterior to the line
- the course of the fistula is curve in a horseshow manner and enter anal canal in the posterior midline

104
Q

Aim of management for anal fistula

A
  • *1) Define Anatomy**
  • to identify the internal opening is the most important determinant

2) Effective drainage of sepsis

3) Eradication of source of sepsis

4) Preservation of sphincter function

5) Wound care

105
Q

Management of anal fistula

A

A. First delineate the anatomy first
1) EUA and Rigid Sigmoidoscopy

B. Depends on location (Parks classification)

  • *1) Superficial, Intersphincteric, and low trans-sphincteric (below puborectalis)**
  • Marsupialization of fistula tract (laid opened and packed)
  • Followed by routine Sitz baths, and dressing and packing
  • *2) High trans-sphincteric (above puborectalis) and suprasphincteric**
  • Seton suture (because immediate laying open has a high risk of faecal incontinence)
  • *3) Extrasphincteric**
  • Endorectal advancement flap
  • Laparatomy & resection & fistula curettage
106
Q

Procedure of surgery for anal fistula

A

1) Patient under GA, lithotomy position

  • *2) EUA + RS to inspect** internal opening of the fistula
  • can consider inject H2O2 or methylene blue to observe bubbling or blue dye

2) Lockhart-Mummery Probe inserted into the external opening to note direction and depth, use the Goodsall’s law

SUPERFICIAL FISTULA

3) If the probe passes superficially then the tract is excised with knife or diathermy
- excision by directly cutting down on to the probe
- if necessarym divide the superficial fibres of the internal sphincter

  • *4) Excise any overhanging skin** on either side of the fistula
  • to encourage healing by granulation

5) Curette granulation tissue
6) Send excised tissue for pathology to look for cause

===============================
DEEP FISTULA
3) Seek help if complex, if no help available, then insert a nylon seton to aid drainage and allow re-assessment at a later date

4) For trans-sphincteric fistula
- identify internal opening with proctoscope, usually at level of anal valves
- Probe the external opening
- Open the anal canal epithelium to level of internal opening
- If internal tracts open below the anal valves, divide the muscle
- If internal tracts open above the anal valves, insert seton

107
Q

What is a seton?

What is its function?

A

A seton is a thick thread or suture that is placed along the fistula tract

  • *Loose seton**
  • tied loosely to act as an effective drain, thus allowing healing (in 50%)
  • *Tight cutting seton**
  • tied tightly, so it will slowly cut through the sphincter muscle
  • subsequently tightened every 2 weeks under LA
  • allows fibrosis to take place behind, thus maintaining sphincter integrity and allow continence after transection
108
Q

Features of a complex fistula

A

1) Recurrent episodes post-surgery
2) Multiple external opening
3) Induration felt above puborectalis muscle
4) Probe from external opening passes upwards instead of to the anus
5) Associated with Crohn’s disease

109
Q

Anorectal abscess clinical features

A
  • Pain
  • Swelling
  • Drainage, pus
  • Constipation and urinary difficulties due to associated pain
110
Q

Anorectal abscess etiology

A
  • *1) cryptoglandular infection**
  • crypt or gland abscess in dentate line with spread

2) specific infections (esp when multiple abscesses)
• inflammatory bowel disease
• tuberculosis
• actinomycosis
• foreign body
• surgery
• malignancies

111
Q

Site of anorectal abscess

A

1) Ischiorectal 60%
2) Perianal 20%
3) Intersphincteric 18%
4) Supralevator 2%

112
Q

Anorectal abscess management

A
  • *1) EUA + Incision and drainage**
  • insertion of drain if deep abscess
  • post-op wound care (dressing and packing) and Sitz bath, analgesics
  • *2) Antibiotics** in selected patients:
  • cellulitis
  • immunosuppressed patient, DM
  • heart valve abnormality
113
Q

What is the indication for post-op IV antibiotics after I&D of anorectal abscess?

A

1) Cellulitis
2) Immunosuppressed patient, DM
3) Heart valve abnormality

114
Q

What percentage of patients will develop fistula-in-ano during the 6 months after I&D for anorectal abscess?

A

Around 50%

115
Q

What is a pilonidal cyst / sinus

What is its aetiology

A

Pilonidal cyst

  • A cyst or abscess near or on the natal cleft of the buttocks that often contains hair and skin debris
  • pilonidal sinus = a sinus tract with opening to the surface of the skin

Aetiology has 2 schools of hypothesis:

  • *1) Acquired** (the more popular view)
  • ingrown hair causes it (risk factors being chronic sitting, deep natal cleft, obesity)
  • chronic trauma allows hair tip to penetrate the skin, rolling motion of buttocks causes the hair to burrow in
  • *2) Congenital** (dated view)
  • a nest of hairs is enclosed as the skin closes
  • however does not explain why the hairs found at the bottom of pilonidal abscess are “scalp type” hair
116
Q

Management of pilonidal disease

A

A. Conservative management

  • observe if asymptomatic or minimal symptoms
  • good personal hygiene, regular removal of hairs

B. Surgical management
1) Incision and drainge if infection or abscess

  • *2) Wide excision and lay open** if persistent sinus
  • completely excise puts and lateral tracks with elliptical excision
  • wound should be laid opened, packed with ribbon gauze
  • can consider marsupialization
  • *3) Primary closure e.g. Karydakis Procedure**
  • Z-plasty or advancement flap is created to bring away the wound from the midline without tension, thus allowing primary closure
  • Karydakis procedure also renders the natal cleft shallow
117
Q

Pre-op, intra-op, post op care of pilonidal disease (excision of pilonidal sinus)

Explain the procedure

A

Pre-op

1) Fleet enema to prevent early post-op defaecation
2) IV antibiotics on induction

Intra-op (Karydakis Procedure)

1) Patient under GA
2) Prone position, buttocks strapped apart
3) Natal cleft is shaved, prepared and draped
4) Asymmetrical (D-shape) elliptical incision marking
- encompass both midline pits and lateral sinus
5) Skin incised with diathermy, deepen to pre-sacral fascia. The block of tissue is excised
6) Restraining tapes are removed, skin flaps are created to approximate both edges
7) Haemostasis
8) Interrupted 1/0 vicryl to fat, interrupted 1/0 nylon to skin
9) Mini-vac placed and secured to help close down the dead space

Post-op

1) Drain reviewed and normally taken out at 24 hours
2) Oral antibiotics for 5-7 days
3) No sitting for at least 5 days to prevent tension; to lie on his side

118
Q

What is the anatomy of haemorrhoids? What are their functions?

A
  • *Anatomy**:
  • Engorged vascular cushions found within the submucosa of anal canal
  • Formed of a sacculated venous plexus with rich arterial supply supported by a fibromuscular connective tissue
  • forms three columns (3, 7, 11):

1) Left lateral
2) Right antero-lateral
3) Right postero-lateral

  • *Function** being:
    i) Aid in continence(act as a plug)
    ii) Protect sphincters/anus from the trauma of defecation
119
Q

How to differentiate anal haemorrhoids from anal varices?

A

We can differentiate the two by the color of the blood:

Haemorrhoids: Fresh, bright red blood

Varices: Dark coloured blood

120
Q

Compare internal and external haemorrhoids

A
  • *External haemorrhoids**
  • Distal to the dentate line
  • from ectoderm
  • covered by squamous epithelium
  • innervated by pudendal nerve & sacral plexus, thus causes pain
  • drains by inferior rectal vein into IVC
  • *Internal haemorrhoids**
  • Proximal to dentate line
  • from endoderm
  • covered by columnar epithelium of anal mucosa
  • Not supplied by somatic sensory nerve, thus usually do not cause pain
  • drains by superior rectal vein into portal system
121
Q

How does internal haemorrhoids cause pain?

A

Internal haemorrhoids are not supplied by somatic sensory nerves, and therefore cannot cause pain per se.

However, prolapse of internal haemorrhoid will cause spasm of sphincter, thus causing perianal pain. Incarceration and strangulation of an internal haemorrhoid will cause pain too.

122
Q

Etiology of pathological haemorrhoids

A

1) Constipation, low fibre diet
- shearing forces -> fragmentation of the supporting fibromuscular matrix

2) Prolonged strainign
- due to engorgement of the anal cushions

3) Pregnancy
4) Internal sphincter dysfunction

123
Q

Classifications of internal haemorrhoids

A

Goligher Classification:
For internal haemorrhoids only!!

  • *1st degree:**
  • not prolapse out of anal canal
  • *2nd degree:**
  • prolapse out of anal canal (usu during straining) and reduce spontaneously
  • *3rd degree:**
  • requires manually reduction
  • *4th degree:**
  • cannot be manually reduced & thus remain out of anal canal (due to considerable swelling preventing back flow of blood)
  • result in thrombosis, prolpase, and ulcer
124
Q

Symptoms of haemorrhoids

A

1) Anal mass, prolapse
2) PRB (bright red fresh blood, coated or dripping from faeces, but not mixed with stool)
3) Mucus discharge -> pruritus ani
4) Pain occurs only when complications are present (thrombosis, incarceration, strangulation)

125
Q

Treatment strategy for haemorrhoids

A
  • *1) Non-operative**
  • diet modification with high fibre diet
  • sitz bath: for prolapsed haemorrhoids
  • *2) Office procedures (if symptomatic first or second degree)**
  • rubber band ligation
  • injection sclerotherapy
  • *3) Surgical Hemorrhoidectomy**
  • Excision (conventional haemorrhoidectomy)
  • Stapled hemorrhoidopexy
126
Q

How do you inject haemorrhoid?

A

Out-patient setting

  • *1) Informed consent**
  • warn that the procedure is painful
  • may notice significant blood loss for ~48 hours
  • repeat injections may be required

2) Left lateral position

  • *3) Proctoscopy and injection**
  • direct vision of the haemorrhoids
  • inject 5% phenol in almond oil into the bases (start with lowest haemorrhoid first so bleeding won’t obscure view)
  • avoid the dentate line due to severe pain

4) Watch till the superficial tissue blanch and swell (indication of correct plane)
5) Review in 6 weeks

127
Q

Indications of haemorrhoidectomy

A

1) 3rd or 4th degree haemorrhoid

2) Mixed internal and external

3) Failure of other treatment

4) Patient preference

5) In conjunction with another procedure

128
Q

Open vs Closed haemorrhoidectomy

A
  • *1) Open haemorrhoidectomy**
  • “Milligan-Morgan”
  • leaves the mucosa “open”
  • *2) Closed haemorrhoidectomy**
  • “Ferguson”
  • Closes the mucosa with sutures after removal of haemorrhoid tissue
129
Q

Procedure of haemorrhoidectomy

A

1) Pre-operative fleet
2) Patient under GA or SA
3) Lithotomy position of jack-knife position, head-down
4) EUA with DRE, proctoscopy, RS
5) Inject LA into each skin bridge and external components of each haemorrhoid
6) Apply Spencer-Wells forceps to perianal skin outside the mucocutaneous junction -> retract to bring out the harmorrhoid
7) Start with inferior haemorrhoid to prevent blood from obscuring the view
8) Scoring with cutting diathermy to mark amount of excision (V-shape in the skin)
9) Excise external components with coagulation diathermy
10) Extend dissection from the anal canal under tension, thus separating haemorrhoid from the internal sphincter white fibres (blunt and sharp)
11) Can consider transfixing the vascular pedicle with Vicryl (however might cause post-operative pain), after which transect the pedicle
12) Repeat same procedure to other haemorrhoids, leaving enough skin and mucosal bridges to avoid stenosis
13) Haemostasis
14) Xylocaine jelly to anal canal; some surgeons like to insert Flagyl 500mg, diclofenac suppository, along with gauze into the anal canal to keep mucocutaneous bridges flat against internal sphincter

130
Q

Complications of haemorrhoidectomy

A

General from anaesthesia risks

Specific (early)

  • *1) Pain ++, AROU, constipation, faecal impaction
    2) Reactionary haemorrhage** (within 24 hours)
  • may cause exanguination with blood pooling peoximally
  • *3) Secondary haemorrhage** (POD 7-8) from infection
    4) Infection, pelvic infection

Specific (late)

  • *5) Faecal or flatus incontinence** (damage to sphincter)
  • *6) Anal stenosis
    7) Perianal fistula
    8) Recurrence of haemorrhoid**
131
Q

What structures are being examined during DRE?

A

1) Intra-luminally:
- rectal mass, anal mass
- blood, stool

2) Anteriorly
- Male: prostate, rectovesical pouch, vas, seminal vesicles, bimanual palpable of bladder
- Female: pouch of Douglas, uterus and vagina (posterior fornix)

3) Posteriorly
- Male: sacrum, coccyx, sympathetics and splanchnic vessels
- Female: sacrum, coccyx

4) Laterally
- Male: ischial spines, obturator internus, Alcock’s canal
- Female: ischial spines

132
Q

What to note in physical examination in an Enterocutaneous fistula case

A

1) Describe the fistula
- size
- location
- nature of discharge (?bile ?faeces)

2) Surrounding skin
- any hints of previous irradiation
- if irritated skin -> could hint small bowel contents

3) Presence of scars suggestive of previous surgery
- could hint on previous anastomotic leak or malignancy
- presence of stoma, healed stoma, or drain sites

4) IBD signs

133
Q

What is the etiology of enterocutaneous fistula?

A
  • *1) Inflammation**
  • IBD esp Crohn’s
  • Diverticular disease
  • Tuberculosis
  • infection with abscess
  • *2) Malignancy**
  • following spontaneous rupture and abscess formation by the tumour
  • *3) Trauma**
  • penetrating wound to the abd, esp involving perforation of several separate loops of bowels
  • *4) Iatrogenic**
  • RT e.g. pelvic irradiation
  • Anastomotic leak after primary anastomosis
134
Q

How to classify enterocutaneous fistula?

A

By Anatomy:

  • *1) High enterocutaneous fistula**
  • involves stomach, duodenum, jejenum, or ileum
  • usually associated with high output
  • *2) Low enterocutaneous fistula**
  • involves large intestine
  • usually lower fluid loss

By Output

  • *1) High output fistula** (>500ml daily)
  • *2) Low output fistula** (<500ml daily)
135
Q

What investigations in suspected enterocutaneous fistula

A

A. Blood tests

1) CBC, CRP
2) RFT and electrolytes to check hydration
3) Albumin to review nutrition status

B. Radiological exam

  • *1) CT with IV and oral contrast**
  • reveal site of fistula
  • demonstrate any obstruction
  • intra-abdominal collections and underlying bowel pathology

2) Barium follow-through or enema

  • *3) Fistulogram**
  • show where the fistula connects to the bowel
136
Q

Principles of enterocutaneous fistula treatment

A

A. 50% will close with conservative management:

  • *1) Sepsis control**
  • open or percutaneous drainage of collection/abscess
  • antibiotics if needed
  • avoid early surgical intervention to close fistula due to higher morbidity
  • *2) Nutritional optimisation**
  • may need parenteral nutrition (PPN, TPN)
  • replace fluids, K (electrolyte lost)

3) Skin protection

4) Decrease output e.g. NPO if high output >500, loperamide

  • *5) Delineate anatomy with Ix**
  • CT, barium follow-through or enema, fistulogram

B. Surgical management if unhealed with conservative management (usu >3 to 6 months)
1) Resection of the involved segment

137
Q

Predisposing factors of fistula patency

A

Factors affecting fistula healing:

1) High output (>500ml daily)
2) Intestinal destruction (>50% circumference)
3) Short segment fistula <2.5cm

4) Foreign body e.g. drain
5) Radiation
6) infection
7) Epithelialization (e.g. colostomy)
8) Neoplasm
9) Distal obstruction

138
Q

Population based Screening of CRC

(i.e. asymptomatic patients!!)

A

Starts at 50yo
Screen till at least 75yo
Individualise after 75yo based on 10-year survival

1) Colonoscopy every 10 years

2) CT colonography every 5 years

  • *3) Faecal sample tests
  • FIT**every 1 year
  • Multitarget stool DNA testing every 3 years if a/v
  • Other options based on resource limitation or patient preference:*
  • Sigmoidoscopy (5-10 year) + annual FIT
  • Sigmoidoscopy (5-10 year)
  • gFOBT annually (if FIT not a/v)
139
Q

Screening of CRC for high risk patients

A

i.e. for patients who are:

  • *1) Positive Family History**
  • Colonoscopy every 5 years
  • Initiate @ 40yo or 10 years before youngest relative diagnosis
  • *2) FAP**
  • Flexible Sigmoidoscopy every year; consider surgery
  • Initiate @ 12yo
  • *3) HNPCC**
  • Colonoscopy every 1-2 years
  • Initiate @ 20yo or 10 years before youngest relative diagnosis
  • *4) IBD**
  • Colonoscopy with random biopsies every 1-2 years
  • 8 years after diagnosis of pan-colitis or 12 years after left sided colitis
140
Q

What are the available FOBT types?

What are their principles?

Pros and Cons?

A

1) Guaiac FOBT (gFOBT)

  • Looks for heme of hemoglobin
  • Heme contains pseudo-peroxidase, which will convert colourless guaiac into blue color

+ Examine entire GI tract
+ Cheap, simple
+ Home, out-patient
+ Extensively validated
+ Non-invasive

  • low sensitivity & specificity (cannot pinpoint LGIB)
  • Need diet prep (high fibre diet; avoid the following 3 days ago)
  • Affected by red meat, fruits, veggies, medication (NSAIDs, aspirin, vitamin C)
  • 3 stool samples required
  • manual testing

2) Immunochemical FOBT (iFOBT) aka Fecal Immunochemical Test (FIT)

  • Looks for globin
  • antibodies detect globin from haemoglobin

+ Not affected by diet or medication (thus no diet prep)
+ Higher sensitivity and specificity (can differentiate LGIB from UGIB as globin from UGI are digested)
+ Continuously released, thus 1 sample is enough (cf. 3 in gFOBT)
+ Automated
+ Non-invasive

  • More expensive
  • Large volume of fecal sample required
141
Q

Advantage of FIT over gFOBT

A

1) Higher sensitivity and specificity -> currently FIT preferred over gFOBT

2) FIT is not affected by diet or medication, thus do not require diet or med restriction before test

3) FIT only requires 1 sample (cf. 3 samples for gFOBT)

4) FIT is an automated test; FOBT is manual

5) FIT has an easy one-step closed system for specimen collection; cf. gFOBT’s specimen collection is an open system prone to exposure and patient error

142
Q

Pre-colonoscopy preparations and precaution afterwards

A

<strong>1) Confirm Patient identity<br></br>2) Obtain Written informed consent</strong><br></br>- 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

143
Q

What gas is used for insufflation in colonoscopy? Why?

A

CO2, easily absorbed thus not there won’t be extensive distension, esp afterwards

144
Q

How to know the completion of colonoscopy?

A

Visualisation of the ileocecal valve in colonoscopy, using the “Bow & Arrow sign”:

Bow = curvature of appendiceal orifice
Arrow = general direction of location of ileocecal valve
145
Q

Complications of Colonoscopy (& risk statistics)

A

Risk level depends on whether therapeutic procedure or not:

1) Sedation complications

  • *2) Bowel Preparation Complications**
  • N+V+, abd bloating, abd pain
  • aspiration, esophageal tear from vomiting
  • *3) PR Bleeding**
  • usually associated with polypectomy, ~1-2%

4) Perforation caused by:

  • mechanical trauma from pressure exerted by the colonoscope (usu rectosigmoid)
  • barotrauma (usu caecum)
  • electrocautery injury during polypectomy
  • 0.1% if just screening
  • 0.2% if polypectomy
  • 0-6% if anastomotic stricture dilatation
  • 0-18% if Crohn’s stricture dilatation
  • *5) Post-polypectomy syndrome**
  • results from electrocoagulation injury to the bowel wall, creating a transmural burn and focal peritonitis without frank perforation
  • managed with IVF, bowel rest, antibiotics
146
Q

Colorectal adenoma endoscopic classifications (based on endoscopic appearance)

A

Paris Classification

**_I = Protruded Lesion_ (polyp)**
p = pedunculated (base is narrow with mucosal stalk)
sp = subpedunculated
s = sessile (base and the top of the lesion have the same diameter)
**_II = Flat lesion (height less than one-half the diameter of the lesion)_**
a = flat elevated
b = flat
c = mucosal depression
IIa/IIc = flat elevated with central depression
IIc/IIa = depression with elevated edge

-> depressed lesion particularly likely to harbor high-grade dysplasia or be malignant

147
Q

What are the main types of colonic polyps? (histological)

A

Firstly A. Malignant (i.e. Tis CRC) vs B. Non-malignant;

For non-malignant polyps, further classified as:

  • *I. Non-adenomatous polyps**
    1) Hyperplastic polyps
  • most common, 90%
  • serrated polyps
  • if small distal then no malignant potential, routine CLN 10yr
  • if 1cm or >20, then repeat CLN 3-5yr as natural history still unclear

2) Hamartomatous polyps
- tissue that are normally found at that site but in disorganized manner

  • Juvenile polyp
  • more common in childhood
  • solitary does not increase CRC risk
  • Juvenile polyposis syndrome (CRC and CA stomach risk)
  • Peutz Jehgers polyps
  • usually benign, but may grow progressively and produce symptoms or undergo malignant transformation
  • a/w PJS, which increase GI and breast malignancy risk

3) Inflammatory pseudo-polyps
- non-neoplastic intraluminal projections of mucosa consisting of stromal and epithelial components and inflammatory cells
- associated with ulcerative colitis –> look for abnormal underlying mucosa
- no risk of malignancy

  • *II. Adenomatous Polyps**
    1) Tubular adenoma (>75% tubular features)
  • low risk of malignancy
  • most common of adenomatous polyps

2) Tubulovillous adenoma (if 25-75% villous features)
- intermediate risk of malignancy

3) Villous adenoma
- greatest risk of malignancy (>75% villous features)

-> Also need to look for low-grade or high-grade dysplasia

148
Q

Management of colonic adenoma (polyp)

A

1) Endoscopic resection i.e. Polypectomy
- if 2mm or smaller, can completely remove with Bx forceps
- snare resection (Cold snaring to avoid full thickness injury, and minimize delayed post-polypectomy bleeding)
- Large sessile adenomas often require piecemeal resection

2) Advanced endoscopic resection for larger lesion
- EMR
- ESD

+/- 3) Surgical excision if endoscopically not feasible

4) Surveillance (see next card)

149
Q

CLN follow-up in patients with tubular adenoma

A

Depends on histology, size, number

A. If cancer with adequate resection

  • Surveillance CLN in 3 months

B. If advanced adenoma

  • if up to 1cm
  • villous histology
  • high grade dysplasia
  • First surveillance CLN in 3 years (if piecemeal for 2cm, then 6 month)
  • If normal first re-scope or just 1-2 TA, then 5 yearly CLN
  • If first re-scope 3-4 TA, then 3-5 yearly CLN
  • If first re-scope 5-10 TA, then 3 yearly CLN

C. If >10 non-advanced adenoma

  • First surveillance CLN in 1 year

D. If 3-4 non-advancaed adenoma

  • First surveillance CLN in 3-5 years

E. If 1-2 non-advanced adenoma

  • First surveillance CLN in 7-10 years
150
Q

Staging of Malignant Colorectal Polyps (i.e. T1 CRC)

A

Hagitt classification & Kudo classification; for Hagitt 0-III, LN met risk is <1%; but if Hagitt IV, then LN met risk up to 25%:

Hagitt (T1):
0 = non-invasive
I = invasive, @ head of pedunculated
II = invasive, @ neck of pedunculated
III = invasive, @ stalk of pedunculated
IV = invasive, @ base; or all malignant Sessile polyps (see Kudo)

Kudo (T1):
SM1 = superficial 1/3 submucosa
SM2 = up to middle 1/3 of submucosa
SM3 = up to deep 1/3 of submucosa

151
Q

Managemnt of Malignant Colorectal polyps

A

Depends on stage & site:

Hagitt I to III, SM1-2
- Endoscopic polypectomy with ≥2mm margin

SM3 (sessile with lower 1/3 submucosa involved)
- Segmental colectomy (same as CRC of same site)

If @ distal 1/3 rectum any stage, lesions may have an increased risk of lymph node metastasis, thus perform transanal full thickness excision via:

  • traditional transanal excision
  • TEM (Transanal Endoscopic Microsurgery)
  • TAMIS (Transanal Minimally Invasive Surgery)
152
Q

When to consider surgery after polypectomy of malignant colorectal polyp?

A

When risk factors for residual cancer and/or nodal metastases:

  • *1) Inadequate resection margin (or positive margin)**
  • 2mm is considered adequate

2) T2 disease i.e. invasion into the muscularis propria

3) Kudos 3 i.e. lower 1/3 submucosal penetration in a sessile polyp

  • *4) Unfavourable Histology**
  • Poorly-differentiated histology.
  • Lymphovascular permeation
  • Peri-neural invasion
153
Q

Classification of intestinal ischemia

A

Colonic ischemia = large bowel ischemia
Mesenteric ischemia = small bowel ischemia

1) Acute mesenteric ischemia

  • sudden onset of SB hypoperfusion
  • caused by:
  • Arterial embolism (50%) usu SMA
  • usually cardioembolism
  • AF, MI, valvular disorder
  • Arterial thrombosis (25%) usu SMA
  • Acute occlusion from plaque rupture over pre-existing atherosclerotic disease
  • Concurrent atherosclerotic disease in other site (e.g. CAD, stroke, PVD)
  • Non-occlusive mesenteric ischemia (20%)
  • Splanchnic vasocontriction due to low cardiac output or use of vasopressors
  • often seen in critically ill elderly patients
  • Venous thrombosis (less than 10%)
  • e.g. SMV / IMV / PV / splenic vein
  • thrombophilia, COC, malignancy, infection

2) Chronic mesenteric ischemia
- patients with mesenteric atherosclerosis causing episodic intestinal hypoperfusion related to eating.

154
Q

Clinical presentation of acute mesenteric ischemia

A
  • Symptoms*
  • *1) Severe abdominal pain**
  • aka “abdominal angina”, periumbilical or generalised
  • Sudden onset, severe, constant of arterial embolism or thrombosis
  • Background of chronic post-prandial pain if arterial thrombosis
  • insidious onset of abdominal pain that can wax and wane if venous occlusion

2) Anorexia, nausea, vomiting

  • *3) If intestinal infarction** occured:
  • Blood in stool
  • peritoneal signs (rebound tenderness, guarding)
  • shock (hypotension, tachycardia)
  • Sepsis (lactic acidosis, fever, confusion)
  • Physical Examination:*
  • *1) Abdominal pain is out of proportion** to their physical exam initially

2) Peritonism & Blood in stool if complicated with perforation and peritonitis

155
Q

Investigations of suspected acute mesenteric ischemia

A
  • *1) Blood results**
  • ABG and lactate
  • non-specific, normal results does not exclude bowel ischemia
  • *2) CXR (E), AXR (E+S)**
  • could be normal
  • may note ileus, pneumatosis intestinalis, free gas if perforated
  • *3) Computed tomographic (CT) angiography**
  • if relatively stable
156
Q

Management of acute mesenteric ischemia

A
  • *1) Supportive therapy**
  • NPO, NGT decompression, foley
  • IV resuscitation, electrolyte resuscitation
  • broad spectrum antibiotics (Zinacef + Flagyl)
  • Analgeics

2) Consider systemic anticoagulation to prevent thrombus formation and propagation

  • *3) Avoid vasoconstricting** agents and digitalis
  • If vasopressors are needed, dobutamine, low-dose dopamine, or milrinone are preferred
  • *4) Exploration Laparotomy +/- Bowel resection +/- Stoma**
  • if peritoneal signs
  • embolectomy if solitary, proximal SMA embolus
157
Q

Name of polyposis syndrome and explain

A

Mostly Autosomal Dominant!

  • *1) Familial adenomatous polyposis (FAP)**
  • hereditary APC gene mutation (AD)
  • hundreds of polyps in colon, duodenum is also involved in 90%
  • risk of CRC is 100% around 40yo
  • *2) Gardner syndrome**
  • variant of FAP (AD)
  • with extra symptoms i.e. osteomas, dental abnormalities, benign soft tissue tumours, desmoid tumours, sebaceous cysts
  • risk of CRC is 100% around 40yo
  • *3) Turcot syndrome**
  • AD or AR
  • polyps
  • plus cerebellar medulloblastoma or glioblastoma multiforme
  • *4) Peutz-Jeghers syndrome**
  • AD
  • Single of multiple harmatomas scattered through GI tract mainly in small bowels (80%), but also colon (60%) and some in stomach (30%)
  • harmatomas have very low malignant potential
  • hyperpigmentation spots around lips, oral mucosa, face, genitals, palmar surface
  • Slight increased incidence in other carcinomas (stomach, ovary, breast, cervix, testicle, lungs)
  • causes intussusception or GI bleeding
  • *5) Family juvenile polyposis coli**
  • rare, presents in childhood
  • small risk of CRC
  • present with 10-hundreds of colon harmatomatous polyps

6) PTEN harmatoma tumour syndrome (PHTS)
7) MEN 2b
8) NF1

158
Q

FAP and HNPCC genetics

A
  • *FAP:**
  • APC mutation
  • Autosomal dominant
  • *HNPCC:**
  • defective mismatch repair genes (MMR), e.g. MSH2 or MLH1
  • Autosomal Dominant
159
Q

Clinical Presentation of FAP

esp Extra-colonic manifestation

A

1) Colonoscopy shows >100 adenomatous polyps (mostly colon, present in duodenum & stomach too)
2) 100% CRC before 40yo

Esp Gardner syndrome:

3) Benign extra-colonic manifestation
- Desmoid tumour in abd wall or cavity
- Skull Osteoma
- Epidermoid cyst
- Congenital Hyperplasia of Retina Pigment Epithelium (CHRPE)

4) Malignant extra-colonic manifestation
- CA Pancreas (peri-ampullary)
- Hepatoblastoma in childhood
- Thyroid cancer, Brain cancer

160
Q

FAP management

A

A. Surgical Prophylaxis

  • *1) Total** proctocolectomy
  • with end ileostomy (or ileal-pouch anal anastomosis)
  • *2) Total Colectomy with removal of rectal mucosa (mucosal protectomy)**
  • if rectum is relatively spared
  • with ileorectal anastomosis
  • need lifelong surveillance

2) Surveillance

  • Start yearly screening colonoscopy/sigmoidoscopy @ 12yo
  • Start 5-yearly OGD for Periampullary Cancer @ 25yo

3) Genetic testing of at-risk family members

161
Q

Tell me about HNPCC

A

Hereditary nonpolyposis colorectal cancer, is an autosomal dominant condition:

Also known as Lynch syndrome:

  • *1) Lynch syndrome I** (i.e. site specific CRC)
  • early onset CRC
  • no antecedent adenomatous polyposis
  • *2) Lynch syndrome II** (i.e. cancer family syndrome)
  • same as Lynch syndrome I, but with:
  • increased number and early onset of other cancers (i.e. brain, skin, stomach, pancreas, biliary tract, breast, female genital tract)
162
Q

Diagnosis of HNPCC

A

Amsterdam II criteria: “3-2-1 rule”

i) 3 relatives with associated cancer (CRC, SB, endometrial, renal pelvis & ureter)
ii) 2 generations affected by cancer
iii) 1 relative diagnosed before 50yo

(FAP excluded)
(1 should be a first-degree relative of the other two)

163
Q

Radiation proctocolitis pathogenesis and presentation

A

Pelvic radiotherapy for malignancy might damage the rectal mucosa, leading to formation of vascular telengiectasis:

  • *Early phase** (days to weeks)
  • mucosal damage, oedema, ulceration
  • Nausea, vomiting, diarrhoea, tenesmus
  • *Late phase** (weeks to years)
  • Bowel thickening and fibrosis
  • tenesmus, haematochezia
  • ulceration with bleeding, stricture, fistula
164
Q

Radiation proctocolitis Risk factors

A

Risk factors:

1) high dose irradiation to pelvis (>6000cGy)
2) vascular diseasse
3) DM, HTN
4) previous low anterior resection
5) Old age

165
Q

Radiation proctocolitis management

A
  • *1) Endoscopic Haemostasis**
  • Infrared coagulation
  • Argon beam coagulation
  • Laser
  • *2) Medical treatment for mild cases**
  • Stool softeners
  • Steroid enemas
  • Topical 5-aminosalicylic acid

3) Transanal 4% formalin when (2) fails

  • *4) Surgery** if bleeding is unstoppable
  • Diverting colostomy
  • Proctectomy
166
Q

Common antibiotics that causes pseudomembranous colitis

A

Overgrowth of Clostridium difficile can be seen after use of:

1) Clindamycin, Ampicillin

2) Cephalosporin

But almost all antibiotics can be associated

167
Q

Clinical presentation of pseudomembranous colitis

A

Usually begin during 1st week of antibiotics (but may happen up to 6 weeks after stopping antibiotics):

1) Profuse watery diarrhoea (can be bloody or mucus)

2) Crampy abdominal pain
If severe
3) Toxic megacolon
4) Colonic perforation
5) Anasarca with electrolyte disturbances

168
Q

Ix for suspected pseudomembranous colitis

A
  • *POCT, Lab tests**
    1) Vital signs (to make sure no dehydration)
    2) CBC (to note leukocytosis of infection)
  • *Imaging**
    1) CXR, AXR (erect, supine)
  • look for megacolon & perforation
  • *Diagnostic Tests**
  • *1) Detection of Toxin A**
  • at least 1 out of 3 stool sample
  • PCR for toxin genes
  • *2) Stool culture** of C difficile
  • if toxin A not found
  • *3) Proctoscopy** or flexible sigmoidoscopy
  • visualise sloughing colonic mucosa
  • pseudomembranes
  • *4) CT if peritonism etc**
  • transmural colonic thickening
169
Q

Treatment of pseudomembranous colitis

A

1) Stop unnecessary antibiotics

2) PO or IV metronidazole
(alt: oral vancomycin)
If severe and cannot tolerate oral:
3) Vancomycin enema
<u>If complicated with toxic megacolon or perforation:</u>
4) Emergency Surgery
- emergency laparotomy with total colectomy and end-ileostomy

170
Q

Compare the different inflammatory bowel diseases

A

Ulcerative Colitis vs Crohn’s Disease:

  • *1) Clinical Course**
  • Remissions & flares VS smoldering
  • *2) Clinical presentation**
  • more commonly bleeds VS less common
  • less common abdominal pain VS more
  • no strictures, fistula VS more
  • Some different extraintestinal manifestations
  • *3) Depth**:
  • UC is confined to mucosa and submucosa (this shallow ulcers)
  • CD extends from mucosa to serosa (i.e. transmural; deep ulcers)
  • *4) Site**:
  • UC is confined to colon & rectum (rectosigmiod lesion always present!)
  • CD extends along the entire GI tract (commonly terminal ileum; only 50% involves rectosigmoid)
  • Rare perianal or SB disease in UC; common in CD
  • UC is continuous while CD are skipped lesions
  • *5) Endoscopic appearance**
  • UC: Granularity, shallow ulcers, pseudopolyps
  • CD: Longitudinal deep ulcers, fissure, cobblestone
  • *6) Histology**
  • no Granuloma in UC VS yes in CD
  • depletion of Goblet cell (thus low mucus) in UC VS increased mucus
  • Reactive LN in UC; granulomatous LN in CD
  • *7) Malignancy risk**
  • Higher in UC than CD
171
Q

Epidemiology of IBD

A
  • *Sex:**
  • UC: more male
  • CD: more female
  • *Age:**
  • Bimodal distribution
  • Peak around 25-35 and 50-65
172
Q

Some risk factors for IBD

A
  • *1) Genetics** (Family History)
  • Family aggregation of both UC and CD, suggesting genetic basis in both diseases and partially sharing the genetic basis
  • MHC gene, NOD2 gene
  • *2) Environmental factors**
    i) smoking (for CD; in fact protective for UC)
    ii) appendicectomy
    iii) Infection
    iv) Oral contraceptives
  • *3) Immunological**
  • Presence of other autoimmune disorders
173
Q

Hx to clarify in IBD

A

1) GI symptoms
2) Extra-colonic symptoms
3) Risk factors (Family, smoking, appendiectomy); causes of flares

4) Past Med Hx:
- TB & HBV status -> for consideration of biological agents
- G6PD deficiency -> cannot use sulfasalazine

5) Psychosocial history -> disabling socially, and might cause depression

174
Q

Clinical features of IBD in general

A

1) diarrhoea (more likely with blood in UC, but not CD)
2) Hematochezia (more common in UC)
3) abdominal pain, nausea, vomiting
4) Absent bowel sounds in flare

5) Anorexia, malabsorption, weight loss
6) fever
7) anaemia
8) extraintestinal manifestations
- look at next

175
Q

Extraintestinal manifestation of IBD

A
  • *1) Eye lesion**
  • Episcleritis
  • Anterior Uveitis
  • *2) Mucocutaneous**
  • Oral aphthous ulcers
  • Pyoderma gangrenosum (especially UC)
  • Erythema nodosum (especially CD)
  • *3) Arthropathy**
  • Enteropathic arthropathy (migratory oligoarthropathy mainly affecting joints of lower limbs)
  • UC patients have greater incidence of ankylosing spondylitis
  • Bilateral symmetrical Sacroilitis, dactylitis, heel ethesitis
  • *4) Bone**
  • Osteoporosis
  • *5) Hepatobiliary**
  • Primary sclerosing cholangitis in UC
  • Gallstones in CD
  • *6) Renal**
  • Renal & bladder stones
  • Ureteral obstruction in CD
  • *7) Secondary amyloidosis**
  • in CD
  • *8) Hematological**
  • Hypercoagulable state (precipitates DVT, PE, stroke etc)
  • Idiopathic thrombocytopenic purpura
176
Q

Investigations in suspected IBD

A

Confirm the diagnosis by:
<strong>0. Bowel prep</strong> (should avoid vigorous cleansing agent)
1. Endoscopy with biopsy
- UC: Flexible sigmoidoscopy (esp during flare) or colonoscopy with random biopsies at multiple levels
- CD: OGD, push enteroscopy, colonoscopy with random biopsies

  • *2. Barium contrast studies**
  • UC: Barium enema
  • CD: Barium meal, barium follow through, barium SB enema, barium enema (esp look for fistula, stricture)
  • *3. CT scan, MRI**
  • in CD for abscess, fistula, mass

4. Fecal leucocytes (in UC)

5. p-ANCA in UC; ASCA in CD

  • ***) Screen for:**
  • TB (tuberculin & CXR; as biological agents may cause relapse)
  • HBV status (as biological agents may cause relapse)
  • G6PD (sulphasalazine may lead to attack)

____
Investigations to be done is same as chronic diarrhoea Ix:

  • *1) Blood test**
  • CBC (anemia? leucocytosis? eosinophilia? neutrophilia for infection?)
  • ESR, CRP (CRP higher in inflammatory diarrhoea)
  • Serum electrolyte panel (Na, K, Ca, albumin)
  • Thyroid function test (TSH)
  • RFT (baseline for contrast, sometimes ARF causes vomiting, also for electrolytes)
  • ANF, p-ANCA, ASCA (for Crohn’s disease, ulcerative colitis)
  • *2) Stool test**
  • FOBT
  • Fecal Leucocyte (indicates inflammtory)
  • Na & K concentration (if secretory, then very high)
  • Fat content (malabsorptive or maldigestion)
  • alpha-1 antitrypsin concentration (high = excessive GI protein loss)
  • pH (if <5.6, then consider carbohydrate malabsorption)
  • Culture and stain (bacteria)
  • ova and parasites (O&P) test
  • C diffcile toxin (pseudomembraneous colitis)
  • *3) Imaging**
  • AXR
  • Barium follow through, barium enema (IBD)
  • CT abdomen
  • Labeled human serum scan (to localise source of protein losing enteropathy)

4) Endoscopy
Take biopsy too
- EGD, push enteroscopy
- Sigmoidoscopy
- Colonoscopy
- Capsule enteroscopy
- DB or SB enteroscopy
- etc

177
Q

Causes of IBD flares

A

Remissions and flares usually occur in UC (CD is smouldering)

1) Stress
2) Durg non-compliance
3) NSAIDs
4) Smoking
5) Infection
6) Specific food
7) Idiopathic

178
Q

Gross & pathological appearance of IBD

A
  • *UC:**
  • Continuous lesion
  • mucosal ulcers, crypt abscesses, mucosal oedema, pseudopolyps
  • no Goblet cell no granuloma
  • *CD:**
  • Skip lesion (perianal disease, ileal inflammation)
  • aphthous ulcers, fistula, strictures, cobblestone appearance, pseudopolyps
  • Fat wrapping, bowel wall thickening, shortened thickened mesentery
  • Goblet cell, granuloma
179
Q

Classifications of Crohn’s Disease

A

Based on the Vienna and Montreal classification for CD:

Location:
L1 = ileal
L2 = colonic
L3 = ileocolonic
L4 = isolated upper disease

Behaviour
B1 = non-stricturing, non-penetrating
B2 = stricturing
B3 = penetrating

Modifier:
p = perianal disease modifier

180
Q

Complications of IBD

A
  • *Ulcerative Colitis**
    1) GI haemorrhage with iron deficiency anemia

2) Toxic Megacolon (leading cause of death)
3) Electrolyte disturbances, dehydration, hypotension secondary to diarrhoea
4) Colorectal cancer & cholangiocarcinoma
5) Primary sclerosing cholangitis
6) Growth retardation

  • *Crohn’s Disease**
    1) Fistula
  • enteroenteral
  • enterovescial
  • enterovaginal
  • enterocutaneous

2) Abscess

3) Stricture, SBO
- oedema and spasm of bowel causes transient obstruction
- scarring and thickening of bowel wall cause chronic obstruction

4) Malnutrition and Malabsorption
- protein losing enteropathy
- lack of calorie, protein, Vitamin B12 and bile acid

5) Perianal disease
- perianal fistula
- anal fissures
- perianal abscess

6) Toxic megacolon (less common than UC)
7) Gallstone and renal stone
8) Growth retardation

181
Q

Distribution of IBD

A

Ulcerative Colitis:
- Rectum is always involved, while colon is involved partially or completely in a continuous manner:

  • *1) Proctitis, proctosigmoiditis** (10%)
  • only rectum
  • *2) Left sided Colitis** (40%)
  • rectum plus descending colon

3) Extensive colitis, pancolitis

4) Rarely, the distal ileum might be involved, aka “Backwash ileitis

B. Crohn’s DIsease:
Skip lesions that could involve the entire GI tract; 40% rectal sparing, anal involvement is common

1) Ileocolic (most common)

2) Small bowel

3) Colonic

4) Pan-enteric (from mouth to anus)

182
Q

Peri-anal disease in Crohn’s Disease

A

Can be first manifestation in CD:

  • anal skin tags
  • anal fissures
  • anal abscess
  • anal fistula
  • Anal canal: stenotic, fibrotic & thicken
  • Rectovaginal fistula
183
Q

How to determine severity of Ulcerative Colitis?

A

Truelove and Witts’ severity index:

  • Haematochezia
  • Diarrhoea
  • Fever, ESR, tachycardia, anaemia
  • *-> Classified into mild / moderate / severe
  • > determines treatment**
184
Q

Why not full colonoscopy in UC flare

A

Because colonoscopy during flare will:

1) Precipitate toxic megacolon

2) Higher risk of peforation

3) Difficulty of advancement of scope

185
Q

Management of non-acute IBD

A

Step up approach:

  • *1) Local Medical therapy for UC**
  • 5-ASA suppository, enema
  • prednisolone enema
  • steroid retention foam
  • *2) Systematic Medical therapy for UC and CD**
  • 5-ASA (sulfasalazine)
  • Steroid (Prednisolone course for UC flare; Budesonide continuous low dose steroid therapy for CD)
  • PO Metronidazole and Ciprofloxacin (if anal or perianal disease in CD)
  • *3) Immunosuppressants** (for steroid dependent or resistant UC; moderate disease)
  • 6-MP, MTX, Cyclosporin
  • Azathioprine (delay onset of action for 3 months, so not good for initiation of therapy)

4) Biological agents if severe
basically anti-TNF agents: “Ada Inflicts Ethan Seto”
- Adalimumab (human, better)
- Infliximab (chimeric, more allergy)
- Etanercept
- Certolizumab

  • *5) Endoscopic management for CD complications**
  • balloon dilatation of Crohn’s stricture

6) Surgery (curative UC, palliative CD)

  • Curative elective surgery for UC
  • Total proctocolectomy with
    i) IPAA (J pouch) for stable patients
    ii) continent ileostomy (Kock Pouch)
    iii) end ileostomy (if old, poor sphincter, CA rectum)
  • Palliative elective surgery for CD complications
  • Strictureplasty, bypass surgery for strictures
  • Anorectal abscess and fistula drainage
186
Q

Surgical therapy indications in IBD

A

Different for UC or CD

  • UC: usually with curative intent
  • CD: usually palliative intent to solve complications

UC can be elective or emergency:

  • *Elective for UC**
    1) Possible malignant transformation
    2) intractable symptoms with failed medical therapy
    3) In children, to prevent growth retardation
    4) Severe extra-colonic manifestation
  • *Emergency for UC**
    1) Perforation
    2) Life threatening Haemorrhage
    3) Toxic megacolon

CD usually for complications:

1) Obstruction
2) Perforation
3) Toxic megacolon
4) Abscess, Fistula

187
Q

Emergency Management of UC

e.g. severe colitis, flare, Toxic megacolon

A

Admit the patient, followed by:

1) General measures
- Dietary restriction ± parenteral nutrition
- IV fluid resuscitation (sometimes blood transfusion)
- protein replacement
(NPO, NG tube)
(Decompression by flatus tube, colonoscopy etc)
(Close clinical monitor, serial AXR)

  • *2) Medical therapy**
  • Systemic steroid (IV prednisolone)
  • Immunosuppressants
  • Broad spectrum antibiotics
  • *3) Surgery** (mostly for Toxic megacolon)
  • Subtotal colectomy with end ileostomy (Rectum preserved to be removed electively later)
188
Q

Indications of different medical therapy in IBD

A
  • *1) 5-ASA agents**
  • Mild to moderately severe CD & UC
  • Maintenance of remission
  • Local anti-inflammatory action
  • *2) Steroids**
  • Frequently relapsing disease
  • *3) Immunosuppressants**
  • Frequently relapsing disease
  • Steroid sparing effects
  • Fistulating CD
  • *4) Biological agents**
  • only drug that can induce mucosal healing whilst improving symptoms
  • standard treatment not working
  • extra-intestinal manifestations
  • fistulising CD
189
Q

5-ASA route of IBD medications

A

Multiple routes are prescribed simultaneously:

  • *1) Suppository**
  • more localised to procto-anal region
  • *2) Enema** (always after suppository)
  • more localised, up to rectum
  • *3) Per-oral**
  • for more proximal disease
190
Q

Compare 5-ASA and its analogues

A

Sulfasalazine (5-aminosalycylic acid) VS mesalazine (5-ASA analogue)

  • *1) Reduce SB absorption** to increase delivery by:
  • Sulphur moiety (sulphpyridine) VS
  • enteric coating
  • *2) More side effects** due to Sulphur moiety VS less
  • e.g. allergy

3) Cheaper VS more expensive

191
Q

ADR of anti-TNF agents

A
  • *1) Infection**:
  • reactivation of latent TB & latent viral e.g. HBV
  • *2) Malignancy:**
  • Lymphoma
  • *3) Autoimmunity:**
  • hemolytic anaemia
  • lupus-like, anti-dsDNA, ANA
192
Q

What increases risk for CRC in IBD?

A

Higher risk for “Colitic Cancer” of colorectum in IBD if:

  • *1) UC > CD**
  • Overal increased risk in CD, but about half that of UC
  • *2) Extent of disease**
  • pancolitis
  • left sided colitis

3) Prolonged duration of illness (cumulative risk)
30 years = 35%
40 years = 65%

193
Q

Features of Colitic CRC

A
  • Multicentric
  • Infiltrative & scirrhous
  • Highly aggressive & poorly differentiated
  • Relatively asymptomatic
  • Same survival, Poorer overall outcome
194
Q

Screening for CRC in IBD patients

A

Colonoscopy with random biopsies every 1-2 years, which start:

  • 8 years after onset of pan-colitis or;
  • 12 years after onset of left sided colitis
195
Q

Toxic megacolon aetiology

A

Complications of:

1) Ulcerative Colitis, rarely Crohn’s Disease

2) Pseudomembranous colitis

3) Amoebic colitis, CMV colitis, bacterial colitis (Shigella)

196
Q

Toxic megacolon clinical features

A
  • *Clinical features:**
  • Diarrhoea (increase in frequency, blood and mucus)
  • Dehydration, electrolyte imbalance, mental changes
  • Abdominal distension
  • Fever, anaemia, low albumin
  • hypotension, tachycardia, Shock
197
Q

Toxic megacolon Ix (and findings)

A
  • *1) AXR** for diagnosis
  • ≥6cm @ transverse colon
  • Assess extent of disease by looking for segments without fecal materials
  • Thumbprinting

2) Ix for IBD, pseudomembranous colitis, CMV infection

198
Q

Toxic megacolon Mx

A
  • *1) General measures**
  • Dietary restriction ± parenteral nutrition
  • IV fluid resuscitation & electrocyte (sometimes blood transfusion)
  • protein replacement
  • NPO, NG tube
  • Decompression by flatus tube, colonoscopy etc
  • Close clinical monitor, serial AXR
  • *2) Medical therapy**
  • Systemic steroid
  • Immunosuppressants
  • Broad spectrum antibiotics
  • *3) Surgery** (if no response to medical therapy in 24 hours)
  • Subtotal colectomy with end ileostomy (Rectum preserved to be removed electively later)
199
Q

Colonic obstruction clinical presentation

A

Presentation of IO:

1) Colicky abdominal pain
2) Abdominal distension
3) Constipation, even obstipation
4) Visible peristalsis, hyperactive borborygmi

5) Some presentation more suggestive of SBO: Vomiting (Feculent), dehydration, electrolyte disturbances

200
Q

Etiology of colonic mechanical obstruction

A

Usually at sigmoid colon:

  • INTRAMURAL*
  • *1) CRC (90%)**
  • left sided > right > rectum
  • *2) Strictures**
  • anastomotic stricture
  • radiation
  • chronic intestinal ischemia
  • IBD (esp CD)

3) Diverticular disease

4) Intussusception

  • EXTRINSIC*
  • *5) Volvulus**
  • sigmoid volvulus (in old, common)
  • caecal volvulus (in young, less common)
  • *6) External compression**
  • extraperitoneal tumours e.g. pelvic met
  • INTRALUMINAL:*
  • *7) Fecal impaction**
  • OTHERS:*
  • *8) “Pseudo-obstruction” i.e. Ogilvie Syndrome**
201
Q

Investigation for colonic obstruction

A

Very similar to SBO investigations
Lab tests:
1) CBC (look for leucocytosis if sepsis or peritonitis)

  • *2) Fluid status**
  • Urine output (Foley catheter to assess dehydration status)
  • BP, pulse rate, respiratory rate
  • BUN:Creatinine ratio

3) ABG (volume contraction -> metabolic alkalosis; if with necrotic bowels, there might be metabolic acidosis)

4) LFT, RFT (for baseline; electrolyte for hypokalemia, hypochloremia)

5) Serum amylase (if pancreatitis) or lactate (increased if strangulated)

6) Type and Screen (to prepare for surgery)

Imaging studies & endoscopy
1) CXR: exclude perforation and pneumoperitoneum; note aspiration pneumonia or atelectasis, lung met

  • *2) AXR** (supine & erect)
  • Distended large bowel ± small bowel (depending on competence of ileocaecal valve)
  • Colonic cut off point at level of obstruction
  • Multiple air fluid levels
  • also look for signs of perforation and pneumoperitoneum signs
  • *3) CT scan with contrast**
  • IV contrast to note critical ischemia or strangulation
  • localize and characterize the obstruction
  • staging
  • *4) Colonoscopy**
  • Colonoscopic decompression
  • Localization of obstructive tumour
  • Exclude synchronous tumour or polyps distal to level of obstruction
  • Stenting
202
Q

What to comment on AXR for colonic obstruction?

A
  • *1) Distended large bowels; look for cut off point of gas**
  • Large intestine >6cm; caecum >9cm
  • note haustra; multiple air-fluid levels
  • cut-off (distally no gas) means site of obstruction
  • *2) Look for distended small bowels (valvulae conneventes)**
  • if present, incompetent ileocecal valve, lower risk of perforation
  • if no SB gas, competent IC valve, high risk of perforation

3) Look for signs of perforation and pneumoperitoneum signs

203
Q

What is the most likely site of perforation in colonic obstruction? Why is that?

A

Caecum. Due to the LaPlace Law:

LaPlace Law states that in a long pliable tube, the site of largest diameter requires the least pressure to distend. With a competent ileocecal valve, caecum has the largest diameter, and therefore will distend the most, and more likely to perforate.

204
Q

How common is acute obstruction in CRC? Where is the site?

A
  • Acute obstruction is presented in 10% of CRC patients
  • *Site:**
  • Most commonly left sided (sigmoid, descending colon)
  • Secondly right sided (ascending & transverse)
  • Rectum quite uncommon
205
Q

Mx of IO caused by faecal impaction

A

1) Digital evacuation

  • *2) Prevent future episodes by:**
  • lifestyle modification
  • laxatives
206
Q

Ogilvie Syndrome (definition, presentation, etiology)

A

Definition:
Signs, symptoms, and radiographic evidence of large bowel obstruction are present, but there is no mechanical obstruction

Presentation:
- Massive colon dilatation in the absence of mechanical obstruction
- No colicky pain
- Hypoactive bowel sounds

  • *Etiology**:
    1) recent surgery or trauma (esp pelvic surgery)

2) severe extracolonic medical illnesses (e.g., sepsis, cardiac disease, pulmonary disease, malignancy, hyponatremia)
3) medications (e.g., narcotics, psychotropic drugs, anticholinergics)

207
Q

Diagnosis of Ogilvie Syndrome

A
  • *Diagnosis**:
  • By exclusion (until mechanical obstruction and volvulus are ruled out)
  • Gastrografin enema (both diagnostic and therapeutic)
208
Q

Ogilvie syndrome Management

A

0) Stop offending agents (narcotics, other drugs)

  • *1) General therapy**
  • NPO, fluid/electrolyte resuscitation, parenteral nutrition, NG tube feeding

2) Decompression by:

  • colonoscopic decompression
  • rectal tube (malecot cath as flatus tube)
    ± NG tube suction
    ± aggressive enema regimen (cottonseed and docusate sodium enema)

3) Adrenergic blocker (guanethidine)

4) IV Neostigmine infusion (parasympathomimetic)

  • *5) Surgical decompression** with:
  • cecostomy or colostomy
  • Total colectomy with end ileostomy (EI) lastly
209
Q

What types of colonic volvulus are there? What are their pathogenesis?

A
  • *1) Sigmoid volvulus**
  • 60%
  • common in elderly
  • acquired due to sigmoid redundancy with narrowing of mesenteric pedicle
  • *2) Caecal volvulus**
  • 30%
  • common in younger population
  • due to congenital failure of appropriate cecal tethering
  • *3) Transverse**, splenic flexure, ileosigmoid knotting
  • very rare
  • presentation similar to sigmoid volvulus
210
Q

Risk factors for volvulus

A

Different for Sigmoid vs Caecal Volvulus

  • *SIGMOID**
    1) Sigmoid redundancy with narrowed mesocolon pedicle

2) Previous abdominal surgery
3) Old age, chronic illness, bed-ridden, institutionalisation, CNS disease

4) Chronic constipation (High-residue diet), antimotility drugs, laxative abuse
- > faecal loaded sigmoid colon

5) Pregnancy

  • *CAECAL**
    1) Congenital lack of caecal tethering

2) Previous abdominal surgery

211
Q

Diagnosis and findings in volvulus

A
  • *A. Sigmoid volvulus**
    1) AXR will show:
  • Omega loop sign (inverted U)
  • “Bent inner tube sign” which points towards RUQ
  • Gas bubbles along the large intestines before sigmoid colon

2) Gastrografin enema show:
- “bird’s beak sign” at the obstructed junction
- aka “ace of spade sign”

3) CT will show:
- “Whirlpool sign”

4) Confirmed with sigmoidoscopy

  • *B. Caecal volvulus**
    1) AXR will show:
  • “Coffee bean sign”
  • extends to LUQ

2) Water soluble contrast enema show:
- “bird’s beak sign” at the obstructed junction
- aka “ace of spade sign”

3) CT
- “Whirlpool sign”

212
Q

Treatment of volvulus

A
  • *Depends on sigmoid VS caecal**
  • *SIGMOID**
  • *0) General therapy**
  • NPO, TPN, oxygen

1) Start with Sigmoidoscopy decompression
± Placement of rectal tube (flatus tube) for decompression

  • *2) If uncomplicated:**
  • Discuss early elective sigmoidectomy (redundant part) with primary anastomosis
  • aim at preventing recurrence
  • *3) If complicated** with peritonitis, bowel ischemia (or failed sigmoidoscopic decompression)
  • emergency Hartmann procedure (rectosigmoid colectomy, end descending colostomy, blind rectal stump)
  • *CAECAL**
  • *1) Emergency surgical reduction** required:
  • Right hemicolectomy with primary anastomosis or ileostomy
213
Q

Cecal volvulus anatomy

A

Cecal volvulus occurs as either a:

1) true axially rotated volvulus (90%) or

2) antero-superior folding in “cecal bascule” (10%).

214
Q

Definition of lower GI bleeding

Defintino of massive LGIB

A

LGIB: Bleeding distal to the ligament of Treitz

Massive LGIB: defined as LGIB that requires >2 Units of RBC transfusion within 24-hour

215
Q

How to differentiate GI tract bleeding and anorectal bleeding by stool examination & history?

A

Lower GI tract bleeding:
Hematochezia with blood mixed with stool

Anorectal bleeding:
Hematochezia with blood separated from stool (dripping to toilet bowl or on toilet paper)

216
Q

Investigations in lower GI tract bleeding

A
  • *1) POCT & Lab Tests**
  • Vitals; Haemodynamic status (blood pressure, pulse, respiratory rate, capillary refill)
  • Hemocue
  • CBC (Hb is usually not as low as in UGIB)
  • Clotting profile (platelet, PT, aPTT)
  • LFT
  • RFT (BUN: creatinine ratio might not be raised, unlike UGIB)
  • Type and screen (to prepare transfusion)
  • Proctoscopy, PR exam (to rule out anorectal causes)

2) Cause investigation
i) OGD, NG tube to rule out massive UGIB
ii) Colonoscopy, sigmoidoscopy
<u>If still unidentified, proceed to second line Ix:</u>
iii) Small Bowel “Push” enteroscopy, Single balloon enteroscopy, double balloon enteroscopy
iv) Capsule enteroscopy
v) Nuclear scan
- Tc-99m sulfur colloid scan
- Tagged RBC Scan
vi) Mesenteric Angiography (for patients with positive nuclear scan)
vii) Last resort
- Exploratory laparoscopy
- explorative laparotomy
- Intraoperative endoscopy

  • *3) Specific tests**
  • e.g. CT or PET when suspecting malignancy
  • biopsy from endoscopy
  • serum tumour markers
  • etc.
217
Q

Common causes of Lower GI tract bleeding

A
  • NADIR*
  • *N) Neoplasm**
  • Colorectal cancer (4th common)
  • Colorectal polyps (3rd common)
  • post polypectomy
  • *A) AVMs**
  • aka angiodysplasia, vascular ectasia
  • common in 60+
  • *D) Diverticulosis** (most common!)
  • note LGIB is rare in diverticulitis

I) Inflammatory Bowel Disease (more in UC)

  • *I) (Infective) colitis**
  • infective colitis
  • Radiation proctocolitis
  • from IBD
  • idiopathic
  • *I) Ischemia**
  • Acute mesenteric ischemia
  • Chronic mesenteric ischemia
  • *R) ‘Rhoids** (Anorectal sources)
  • haemorrhoids (second common)
  • rectal varices (related to portal hypertension)
  • anal or rectal ulcer
  • fissure-in-ano

____

  • beware that massive UGIB might mimic LGIB:*
    1) Duodenal or gastric ulcer
    2) Esophageal or gastric varices
    3) Aortoduodenal fistula
    4) Dieulafoy’s lesion
218
Q

Surgical management of massive LGIB without localisation

A

1) Exploration laparotomy with Intraoperative endoscopy:

Route:

  • Via enterotomy
  • can be transanal, peroral (too long), laparoscopic assisted

Support with on-table antegrade irrigation:

  • Foley catheter inserted through appendicotomy or enterotomy
  • Bowel preparation by on table antegrade irrigation
  • Effluent from anus

2) Total colectomy as last resort

219
Q

What side do tumours form in Lynch Syndrome?

A

Right

220
Q

Waht needs to be divided to gain access to coeliac axis during radical gastrectomy?

A

Lesser Omentum