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JC WCS > GI & Hepatology JC067: Chronic Diarrhoea: Irritable Bowel Syndrome And Inflammatory Bowel Disease > Flashcards

GI & Hepatology JC067: Chronic Diarrhoea: Irritable Bowel Syndrome And Inflammatory Bowel Disease Flashcards

1
Q

Definition of Diarrhoea

A
  • Bowel habits vary widely between individuals
  • Must first evaluate patient’s normal bowel patterns (baseline) + nature of symptoms

Diarrhoea:
- ↑ daily stool **volume, **frequency, **fluidity
- stool weight >250g / 24hr
- **>2-3 times / day or liquidity

2 types:
1. Acute
- **Inflammatory
- **Infective / Non-inflammatory

  1. Chronic (***記: OSMMII)
    - Osmotic
    - Secretory
    - Malabsorptive
    - Motility disorders
    - Inflammatory
    - Chronic infection
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2
Q

***Chronic diarrhoea

A
  • Loose stools that last ***>4 weeks (sometimes >2 weeks)
  • Usually means ***>=3 loose stools / day
  1. Osmotic
    - **Lactase deficiency (i.e. Lactose intolerance)
    - **    Laxative abuse (for weight loss)
    - Malabsorption
    —> ***resolves with fasting
  2. Secretory (uncommon)
    - **Endocrine tumours (mostly)
    - **    Bile salt malabsorption (draw water + salt into bowel)
    - Laxative abuse
    —> large volume watery diarrhoea, ***persists in fasting state
  3. Malabsorptive
    - **Small bowel diseases (e.g. Crohn’s)
    - **    Pancreatic diseases (e.g. Pancreatitis, CA pancreas)
    - Previous resection
    - Bacterial overgrowth
    —> weight loss, nutrient deficiency, osmotic diarrhoea, (fatty diarrhoea)
  4. Motility disorders (**most common)
    - **    IBS
  5. Inflammatory
    - Crohn’s
    - UC
    —> **blood + **mucus in stools
  6. Chronic infection (uncommon except in immunocompromised)
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3
Q

***Mechanisms of Diarrhoea

A
  1. Secretory
    - e.g. Endocrine problems (VIPoma (watery diarrhoea), Carcinoid syndrome)
    - persists despite fasting
    - no pus, blood, no excess fat in stools
    - ***watery diarrhoea
  2. Exudative / Inflammatory
    - mucus + blood in stools
    - ***PMN in stools
  3. Decreased absorption (e.g. pancreatic / small bowel diseases)
    - osmotic (stop after fasting)
    - **↓ in absorption surface
    - **    motility disorder
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4
Q

Drug-induced diarrhoea

A
  1. ***Antacid, Acid suppressants (Mg-containing, H2RA, PPI (∵ bacterial overgrowth))
  2. Alcohol
  3. ***Antibiotic
  4. Anti-HT (β blockers)
  5. Anti-inflammatory (NSAID, 5-aminosalicylate)
  6. Colchicine, Misoprostol, Theophylline
  7. Vitamin / Mineral supplements, Herbal products
  8. Coffee, Tea, Cola (caffeine / methylxanthine-induced diarrhoea)
  9. Dietetic foods, gums, mints (sorbitol / mannitol-related osmotic diarrhoea)
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5
Q

***Physical examination of Diarrhoea

A
  1. **Fluid + **Electrolyte status (i.e. extent of fluid + electrolyte depletion)
  2. ***Nutritional status (e.g. malabsorption, maldigestion)
  3. Causes of diarrhoea
    - Skin rash, flushing (e.g. Carcinoid syndrome, IBD)
    - **Thyrotoxicosis (thyroid masses, toxic signs)
    - **    Mouth ulcers (Crohn’s)
    - **Arthritis (IBD)
    - Hepatomegaly
    - **    Anorectal exam (mass, anal tone (overflow incontinence), perianal diseases (e.g. fistula, abscess —> Crohn’s))
  4. Signs of toxicity
    - ***Fever
    - Distended, rigid, tender abdomen
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6
Q

***Investigations / Specific testing

A

Directed by History + P/E

Standard investigations:
1. Blood tests
- CBC
—> Anaemia (GI blood loss, B12 folate deficiency due to malabsorption)
—> **Leukocytosis (inflammation, infection)
—> **Eosinophilia (eosinophilic GE, neoplasms, allergy, collagen vascular diseases, parasites)

  • Inflammatory markers
    —> **ESR (suggestive of chronic inflammation)
    —> **    CRP (more acute)
  • **Electrolytes, RFT
    —> Na, K (can be low in malabsorption)
    —> Ca, PO4 (low in Vit D deficiency)
    —> **    Albumin (low in active IBD / other protein-losing enteropathy)
  • Others
    —> **ANA (+ve in IBD, other autoimmune diseases), **p-ANCA (+ve in UC), serum Ig levels (immunodeficiency)
    —> **HIV (immunodeficiency)
    —> **    TSH
    —> Glucose, Sucrose (DM)
    —> Metformin
    —> ***B12, Folate level
  1. Stool examinations
    - **Culture + Microbiology (rule out infection)
    —> **    C. difficile toxin (pseudomembranous colitis, antibiotic-associated diarrhoea)
    —> Aeromonas, Plesiomonas
    —> Protozoan / Parasitic infection
    —> Giardia
  • ***Leukocytes —> Infective, Inflammatory cause
  • ***Occult blood —> IBD, Cancers, Infective
  • ***Faecal calprotectin —> IBD
  • ***Fat —> Malabsorption, Maldigestion
  • Na, K —> Osmotic diarrhoea (due to non-electrolytes), Secretory diarrhoea (due to electrolytes)
  • pH —> <5.6 carbohydrate malabsorption
  1. Imaging
    - **X-ray —> calcification chronic pancreatitis
    - Barium meal —> non-specific diagnosis
    - **    SB follow through (SBFT) —> SB, ileal abnormalities in Crohn’s (e.g. **fistula, irregularities, **strictures, tumours)
    - Barium enema —> colon cancer, polyp, mucosal diseases like IBD
    - USG —> biliary tract obstruction, pancreatic disease
    - ***CT / MRI Enterography (need to swallow contrast to distend SB) —> IBD complications
  2. Endoscopy
    - **OGD —> duodenal biopsy (Celiac, Whipple, Crohn’s)
    - **    Sigmoidoscopy / Colonoscopy —> obtaining mucosal biopsy —> IBD / opportunistic infections (e.g. CMV) / microscopic colitis
    - SB enteroscopy / Capsule endoscopy (need to make sure patient does not have ***obstruction)
  3. ***Biopsy
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7
Q

Faecal calprotectin

A
  • 24kDa dimer of Ca binding proteins
  • secreted by ***neutrophils
  • indicates ***migration of neutrophils to intestinal mucosa
  • ↑ in:
    —> **Infective: Infectious diarrhoea
    —> **    Inflammatory: Crohn’s disease, UC
    —> Cancer
    —> some drugs (NSAIDs, PPI)
  • stable in room temperature
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8
Q

Stool fat excretion (24 hour)

A

rarely performed now

Normal:
- ***<9% of intake

Malabsorption / Maldigestion:
- >18g fat/day while on standard 100g fat/day diet (i.e. ***>18%)
- Malabsorptive states: <8g / 100g stool
- Maldigestive states: >8g / 100g stool (pancreatic insufficiency / biliary steatorrhoea)

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9
Q

Protein-losing enteropathy

A

Example:
- **IBD
- Tropical sprue
- Whipple’s disease
- **Allergic gastroenteropathy
- **Intestinal lymphangiectasia
- **Constrictive pericarditis (mesenteric congestion)
- Congenital hypogammaglobulinaemia
(Others:
- **Hypertrophic fold
- **Linitis plastica
- SB TB
- Lymphoma
- ***SLE (mucositis) (CL Lai))

Diagnostic workup:
1. ***Labeled human serum albumin scan
- localisation of source (see where protein is leaking from GI tract)

  1. ***Faecal α1-antitrypsin concentration (↑ in protein loss)
    - suggestive of excessive GI protein loss
  2. ***Serum α1-antitrypsin clearance (↑ clearance suggests excessive GI protein loss (Web))
  3. ***Colonoscopy
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10
Q

MR Enterography

A
  • assess SB mucosal **inflammation, **fistula, *abscess, stricture (in IBD)
  • advantage: radiation free (good for young patient)
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11
Q

Management of Chronic diarrhoea

A
  1. Specific treatment
    - direct to cause of disease
  2. Supportive treatment
    - **Anti-diarrhoeals
    - **    Octreotide (for endocrine secreting causes e.g. VIPoma, Carcinoid syndrome) —> Octreotide/Lanreotide inhibit secretion of GI peptide e.g. gastrin, secretin, motilin etc. —> important for digestion + GI movement
    - **Bile acid binding resin (bile salt-associated diarrhoea after cholecystectomy)
    - **    Intraluminal absorbants e.g. Charcoal
    - Bismuth compounds
    - Antibiotics? (sometimes useful, esp in bacterial overgrowth)
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12
Q

Management of Malabsorption / Maldigestion

A
  1. Dietary supplements
    - Ca, Mg, Fe
    - Vit A, D, K, B12, Folate
  2. Anti-diarrhoeal agents
    - **Cholestyramine (bile acid-related diarrhoea)
    - **    Lomotil (Diphenoxylate / Atropine), ***Imodium (Loperamide)
  3. Pancreatic enzymes supplements
    - ***Pancreatin
  4. Enteral / Parenteral supplementation
    - not common except in short bowel syndrome
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13
Q

***Irritable bowel syndrome

A

Clinical features:
1. **Abdominal pain (relieved by defaecation)
2. Change in bowel **frequency
3. Change in ***consistency

Functional disease: no gold standard of diagnosis (no endoscopy / blood test can make diagnosis, only based on ***clinical symptoms)

**Rome IV criteria:
- Recurrent abdominal pain, on average **>=1 day per week in last ***3 months
- Associated with >=2 of following:
1. Related to defaecation
2. Change in frequency of stool
3. Change in form (appearance) of stool
(- For last 3 months with symptom onset >=6 months before diagnosis)

Epidemiology:
- 25% population (Rome 1, 2 criteria)
- 4-5% population (Rome 4 criteria)

Pathophysiological features:
1. Brain-gut axis
2. Autonomic nervous system problem
3. Altered bowel motility (motor)
4. Visceral hypersensitivity (sensory)
5. Psychosocial factors
6. Neurotransmitter imbalance (serotonin)

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14
Q

IBS subtypes

A
  1. IBS with diarrhoea (IBS-D)
    - ***loose / watery stool >=25%
    - hard stool <25%
  2. IBS with constipation (IBS-C)
    - loose / watery stool <25%
    - ***hard stool >=25%
  3. Mixed IBS (IBS-M)
    - hard stool >=25%
    - loose / watery stool >=25%
    - ***alternating
  4. Unsubtyped IBS
    - insufficient abnormality of stool consistency to meet criteria for IBS-C, D, M
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15
Q

Features ***against IBS

A

History
1. **Weight loss
2. Rectal **bleeding
3. Onset in ***older patients
4. Family history of CA colon / IBD

Investigations
1. Positive faecal occult blood
2. Anaemia
3. **↑ WBC
4. **↑ ESR, CRP
5. Abnormal biochemistry (HypoK, HypoCa)

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16
Q

***Management of IBS

A

Multi-faceted approach
1. Education
2. Reassurance
3. Dietary modifications
4. Pharmacotherapy (for refractory case)
5. Psychological treatments

Medical treatment: Targets predominant symptoms of IBS
Abdominal pain
1. **Smooth muscle antispasmodics: Otilonium, Mebeverine
2. Peppermint oil
3. TCA: Amitriptyline, Desipramine
4. **SSRI: Citalopram, Paroxetine, Sertraline (slow onset, symptoms may worsen initially)
5. Chloride channel activator (Lubiprostone)
6. Guanylate cyclase C agonists (Linaclotide)
- Tend not to give Anticholinergic (Hyoscine) (∵ many SE)

Diarrhoea
1. **Opioid agonists (loperamide)
2. **Diet (Low FODMAP (fermentable oligo-, di-, mono- saccharides and polyols))
- FODMAP: ↑ osmotic pressure in gut + cause bacterial overgrowth + bloating + distension + diarrhoea
- avoid excessive fructose, fructans, sorbitol, raffinose
3. ***Bile salt sequestrants (Cholestyramine)
4. Probiotics
5. Antibiotics (Rifaximin) (oral, non-systemic, broad-spectrum antibiotic that targets gut and associated with low risk of bacterial resistance)

Constipation
1. **Psyllium
2. **PEG
3. Chloride channel activators (Lubiprostone)
4. Guanylate cyclase C agonists (Linaclotide)

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17
Q

***Inflammatory bowel diseases

A
  1. Ulcerative colitis (UC)
    - Colon only (start from rectum)
    —> **Proctitis (33%)
    —> **    Left-sided colitis (33%) (higher chance of malignancy)
    —> **Extensive / Pan-colitis (33%) (higher chance of malignancy)
    (- **    Backwash ileitis (BWI): Inflammation in distal terminal ileum: caused by reflux of colonic contents where the entire colon is involved (web))
    - **Continuous lesion
    - **    Mucosa + Submucosa confined (no deep penetration)
  2. Crohn’s disease (CD)
    - Whole GI tract (mouth to anus)
    —> Ileocolonic (40-55%) (SB disease (SpC Medicine))
    —> Colon only (20%)
    —> Anoreactal (30-40%) (anal fistula, anal fissure, periproctitic and other abscesses)
    —> Esophagus, stomach, duodenum (3-5%)
    - **Skipped lesion
    - **    Mucosa to Serosa (full thickness)

(3. Indeterminate colitis (does not fit in UC / CD))

Epidemiology:
- ↑ worldwide incidence
- ↑ CD incidence
- ***unknown reason
—> NSAIDs, Infection, Antibiotics (depend on dose + timing), Western diet, Stress, Smoking (SpC Medicine)

Disease course:
Ongoing inflammatory activity —> Accumulation of ***bowel damage (stricture, abscess etc.)

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18
Q

***UC vs CD

A

UC:
1. Radiological
- Diffuse + Continuous
- **Rectosigmoid always involved (*start from rectum)
- No small bowel involved
- No skip lesion
- No stricture / fistula

  1. Endoscopic
    - Hyperaemic mucosa
    - ***Shallow ulcers
    - Diffusely granular appearance
  2. Histology
    - Superficial inflammation
    - Continuous involvement
    - **Granuloma rarely seen
    - **    Goblet cell depletion

CD:
1. Radiological
- Patchy
- Rectosigmoid involved in 50%
- Usually SB, Terminal ileum involved
- Skip lesion (Regional enteritis (SpC Medicine))
- ***Stricture + Fistula (∵ deep penetration)

  1. Endoscopic
    - Aphthous lesions
    - **Solitary + Deep ulcers
    - **    Cobblestone appearance (scattered)
  2. Histology
    - **Transmural inflammation
    - Patchy involvement
    - **    Granuloma common (DDx: ***TB small bowel)
    - Goblet cells present
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19
Q

IBD patient characteristics

A

UC:
- ***older patients
- M:F = 1:1
- 3% family history
- longer duration of disease since diagnosis (117 months)

CD:
- **younger patients (at least 10 years younger)
- **more male (2:1)
- 3% family history
- shorter duration of disease since diagnosis (84 months)

20
Q

***Causes of IBD

A

Generally unknown
1. Family aggregation of both UC, CD —> suggesting genetic basis in both diseases and partially sharing genetic basis
- cannot identify single gene accounting for IBD
- MHC genes (complicated for UC, CD)
- **NOD2 gene SNP8, 12, 13 (no effect for UC, **↑ for CD)
- other genes by linkage analysis (complicated for UC, CD)

  1. Environmental (diet, infection, antibiotics)
    - smoking (protective for UC, ***↑ for CD (more severe as well))
    - early appendicectomy in childhood (protective for UC, no effect for CD)
  2. Immunological
  3. Gut microbiota (early change in gut microbiota)
21
Q

CD: ***Vienna and Montreal classification

A

Location:
L1: Ileal
L2: Colonic
L3: Ileocolonic
L4: Isolated upper disease

Behaviour:
B1: Non-stricturing, non-penetrating
B2: **Stricturing
B3: **Penetrating (i.e. fistula formation)
p: perianal disease modifier

22
Q

Clinical features of IBD (SpC Surg Interactive tutorial: IBD, SpC Medicine)

A

SpC Medicine:
Inflammation:
1. Abdominal pain, tenderness
2. Diarrhoea
3. Weight loss

Obstruction:
1. Cramps
2. Distension
3. Vomiting

Fistula (Enteroenteric, Enterovesical, Retroperitoneal, Enterocutaneous):
1. Diarrhoea
2. Pain
3. Air / Faeces in urine

SpC Surg:
Related to inflammatory damage in GI tract
1. Diarrhoea
2. Constipation (i.e. UC limited to rectum)
3. Pain / Rectal bleeding with bowel movement
4. Tenesmus
5. Abdominal cramps and pain

23
Q

Extraintestinal manifestations

A

記: Joint, Skin, Eye

  1. **Arthritis, Peripheral arthropathy, **Spondylitis mimicking ankylosing spondylitis
  2. Biliary tract complications
    - **Gallstones (∵ impaired bile salt reabsorption —> easier for cholesterol to precipitate)
    - **    Primary sclerosing cholangitis (PSC) (rare) (if concurrent UC + PSC —> much higher chance of ***malignancy)
  3. Renal complications
    - Kidney stones
  4. Skin complications
    - **Pyoderma gangrenosum (inflammatory skin disease where painful pustules or nodules become ulcers that progressively grow)
    - **    Erythema nodosum (inflammation of fat cells under the skin —> tender red nodules)
    - ***Aphthous ulcers of mouth
  5. Eye complications
    - ***Uveitis
    - Iritis
    - Episcleritis
    - Scleritis
24
Q

Diagnosis of IBD

A

No single test / gold standard (no single endoscopy / blood test / biopsy) —> need combination

Diagnosed by
1. **Endoscopic
+
2. **Radiological
+
3. ***Pathological
+/-
4. Biochemical findings

  • including focal, asymmetric, transmural, ***non-caseating granulomatous features
  • have to rule out infection esp. **TB!!! (∵ can mimic CD; **CMV colitis can mimic UC; HIV can present with colitis features)
25
Q

***Investigations of IBD

A
  1. CBC
    - **anaemia (∵ bleeding, malabsorption)
    - **    ↑ WBC
  2. ***↑ CRP (+ ESR)
  3. Stool (to rule out **infection)
    - WBC
    - bacteria
    - parasites (ova, cysts)
    - **    Faecal calprotectin
  4. Serology
    - CD: **ASCA +ve (Anti-saccharomyces cerevisiae Ab)
    - UC: **    p-ANCA +ve (Perinuclear antineutrophil cytoplasmic Ab)
  5. **Colonoscopy / Sigmoidoscopy + **Biopsy
    - CD: **Granuloma
    - UC: **    Mucosal inflammation
    —> involvement of GI tract, pattern, severity of inflammation, histology (to rule out infection)
    —> chronic changes like glandular distortion + atrophy
  6. Small bowel series
  7. CT / MR **enteroclysis / **enterography
  8. CT scan
    - for diagnosis + complications (e.g. **perforation, **stricture, abscess)
26
Q

***Treatment of IBD

A
  1. Induce remission during acute flare up
  2. Maintenance of remission
  3. Modification of clinical course
    - ↓ Complications
    - ↓ Surgery
    - Improve nutritional status
    - Cancer prevention (UC)
    - Improve QOL

Medications:
1. **5-ASA (5-aminosalicylic acid) (Mesalazine, Sulfasalazine)
2. **Steroid
3. **Immunomodulators (Azathioprine)
4. **Biologics (e.g. Infliximab)

Traditional **Pyramid approach to therapy
Mild:
1. **Aminosalicylate (ASA) (e.g. Mesalazine, Sulfasalazine)
2. **Corticosteroid (Budesonide (suppository))
3. *Antibiotics (Metronidazole (SpC Medicine))

Moderate:
1. Corticosteroids
2. **TNF inhibitors
3. **AZA / 6-MP / *MTX

Severe
1. **TNF inhibitors
2. **Cyclosporine
3. Bowel rest
4. ***Surgery (CD for complications, for refractory UC who developed cancers)

*: CD only

Early intervention to prevent disease progression

27
Q
  1. 5-aminosalicylic acid (5-ASA)
A

Indications:
- mild - moderately severe UC / colonic CD
- maintenance of remission

MOA:
- Local anti-inflammatory action
- NOT absorbed —> Topically active anti-inflammatory agent for inflamed intestinal mucosa (SpC Medicine)

**Sulfasalazine (now rarely used)
- Sulfapyridine + 5-ASA
- break down by colonic bacteria —> active ingredient 5-ASA
- SE (Sulfapyridine): **skin rash, haemolysis, **neutropenia, **male infertility, pancreatitis

5-ASA analogues:
- ***Mesalazine, Olsalazine
- oral / enema / suppository

28
Q
  1. Immunomodulators / Immunosuppressants
A

Azathioprine, 6-Mercaptopurine

Indications
- frequently relapsing disease
- ***steroid sparing effects
- fistulating CD

PK:
- delayed onset 3 months —> **NOT good for induce remission
- well tolerated
- SE 10%: **BM suppression, allergy, ***hepatotoxicity, pancreatitis

29
Q
  1. Biologics
A

New treatment for IBD

Indications:
- **standard treatment not working
- fistulating disease
- **extraintestinal manifestations (e.g. pyoderma gangrenosum, uveitis)

  1. Anti-TNFα
    - ***Infliximab
    - Adalimumab (Humira)
    - Certolizumab Pegol (Cimzia)
  2. Anti-adhesion molecules
    - Vedolizumab
  3. Anti-cytokine molecules
    - Ustekinumab
  4. Blockade of downstream signaling (JAK pathway)
    - ***Tofacitinib (SE: DVT (SpC PP))

Risks of Biologics:
- Infections: reactivation of **latent **TB / viral infection e.g. **Hep B flare
- Malignancy: **lymphoma
- ***Autoimmunity: haemolytic anaemia, lupus-like, anti-dsDNA, anti-ANA

(SpC Medicine:
Infusion Reactions:
- Usually can continue treatment and infuse at slower rate
- Cover with hydrocortisone 100mg iv before infusion
- Less common with Humira and Cimzia
- More injection site pain with Humira)

SE:
- Infection, multiple sclerosis, lupus-like reactions (common to all ant-TNFs)
- Higher risk of common bacterial infections, TB, Fungal infections
- Before commencement check:
1. **HBsAg
2. **QuantiFERON-TB Gold
3. ***CXR
- Treat abscess (antibiotics + drainage), withhold anti-TNF)

30
Q

***Complications of CD

A
  1. ***Malnutrition
    - malabsorption, maldigestion
    - protein, calorie, vitamin deficiency
    - poor intake, protein losing enterography, malabsorption
  2. Abscess, **Fistula
    - extension of mucosal fissure and ulcer through bowel wall into extra-intestinal tissue
    - abscess: peritoneal cavity
    - fistula: adjacent viscera, bladder, vagina, abdominal wall (    *enterocutaneous fistula)
  3. **Stricture, **Obstruction
    - mucosal thickening ∵ active inflammation, scarring, adhesions, food impaction in a long-standing stricture
  4. Perianal disease
    - perianal abscess, perianal fistula, anal fissures

(5. CRC in Colonic CD)

31
Q

***Complications of UC

A
  1. **Toxic megacolon
    - Acute UC
    - Diagnosed by plain AXR: **    thumb printing (large bowel wall thickening)
    - Clinical features of severe UC
    —> **Fever >38oC
    —> **    HR >120
    —> **Anaemia
    —> **    Low albumin
    —> **Abdominal pain
    —> **    Diarrhoea
    - Exclude co-existing **C. difficile / **CMV infection
    - Treatment:
    —> **Bowel rest
    —> **    TPN
    —> **Fluid + electrolyte replacement
    —> **    IV corticosteroid
    —> Close monitoring
    - Outcome: ~50% respond to medical treatment, 50% go to urgent colectomy if not respond in 3-7 days

(Pathophysiology (Web + Davidson):
- NO released by neutrophils paralyse GI tract muscle —> dilatation —> bacterial toxins pass freely across diseased mucosa into portal then systemic circulation)

  1. ***CRC
32
Q

Malignancy

A
  • Moderately ↑ risk of colon cancer in patients with **UC (+ **Colonic CD)
  • Extensive UC: ***8-10 years after onset
  • Limited / Left side UC: ***10-15 years
  • Need regular **endoscopic surveillance in long-standing disease
    —> **    NOT polypoid in appearance
    —> Inflammatory cancers
  • Higher risk in patients with concurrent ***primary sclerosing cholangitis (PSC) (require annual surveillance colonoscopy)
33
Q

Surgical therapy

A
  • > 50% of CD require surgery during life time (e.g. ***abscess drainage, bowel resection)
  • Not curative for CD, disease recurs close to the anastomosis
  • Try to preserve as much gut as possible (to avoid short bowel syndrome)
  • Much lower colectomy rate for UC (4-5% at 10 years, mainly for **toxic megacolon / **CRC)

Indications:
- severe bleed, perforation, stricture, fistula, abscess, failed medical treatment, risk of cancer

  1. Resection of diseased intestine
  2. ***Strictureplasty
  3. ***Colectomy / Proctocolectomy
34
Q

SpC Interactive tutorial (Surg): IBD
Epidemiology of IBD

A
  1. Crohn’s disease (CD): **Patchy + **Transmural inflammation, which may affect any part of GI tract
  2. Ulcerative colitis (UC): **Diffuse + **Mucosal inflammation limited to colon
  3. Indeterminate: Fail to be classified between UC vs CD

Incidence:
1. Age
- CD: in the third decade
- UC: between third and seventh decade

  1. Gender
    - CD: F>M (M>F in East Asia)
    - UC: F=M

Prevalence:
- CD: urban > rural areas, higher socioeconomic classes

East vs West:
- More male prevalence with CD, ileocolonic CD
- Less family clustering
- Lower rates of surgery (5-8%)
- Fewer extraintestinal manifestations
- Less primary sclerosing cholangitis with UC
- Higher rates of penetrating and perianal disease CD

35
Q

History taking, P/E, Investigation in IBD

A

History:
- Bowel symptoms
- **Medications
- **Surgery (esp. in CD)
- Immunization status (e.g. TB, HBV —> for future initiation of immunosuppressants)

P/E:
- General and abdomen
- Perianal region: skin tags, fissures, fistulas, abscess, PR exam (e.g. rectal stricture)
- Extraintestinal inspections: mouth, eyes, skin, joints

Investigations:
Laboratory tests
1. Blood tests: CBP, **CRP, **ESR, albumin, ferritin
2. **p-ANCA (UC)
3. **ASCA (CD)
4. Hepatitis serology, HIV, TB testing (for future initiation of immunosuppressants)
5. Stool examination: culture, **Cl. difficile toxin, **calprotectin

Imaging and endoscopy
1. Contrast study
- Follow through (Serial X-ray): check any obstruction
- Enema: check mucosa appearance

  1. Colonic (UC/CD)
    - ***Colonoscopy
    - Sigmoidoscopy (for severe active disease)
  2. Small bowel (CD)
    - ***MR enterography (MRE) / CT enterography (CTE)
    - Small bowel capsule endoscopy (SBCE)
    - Single or double balloon enteroscopy
  3. Foregut symptoms (CD)
    - ***OGD
  4. Perianal (CD)
    - ***MRI anal canal

(Calprotectin:
- Neutrophil-derived protein, 60% of neutrophil cytosol
- Most sensitive marker of intestinal inflammation in IBD
- Well correlated well with endoscopic disease activity
- Predict disease relapse, postop relapse)

36
Q

Treatment of IBD

A

Medical treatment (Main treatment):
- Induce clinical **remission
- **Prevent complications
- Maintain medically + surgically remission

Surgery for UC:
- ***Cure for disease (∵ UC confined to colon)
- Laparoscopic surgery feasible

Surgery for CD:
- **NOT a cure
- To deal with **complication only
- Conservative + minimum resection
- Extended resection do NOT reduce recurrence

37
Q

Surgery for UC

A

Emergency surgery indications:
1. **Acute severe colitis failing medical treatment
2. **Toxic megacolon >6cm
3. Perforation
4. Severe bleeding

Elective surgery indications:
1. Chronic colitis with severe symptoms
2. Steroid dependent
3. Recurrent attacks
4. ***Dysplasia / Cancer
5. Extra-intestinal manifestation

38
Q

Acute severe colitis in UC / CD

A
  • 20% UC, 5-10% Crohn’s colitis

ECCO and ACG guidelines:
- ***>=6 Bloody stools/day + at least one of the followings:
—> Fever (37.8℃)
—> Tachycardia
—> Anaemia (<10.5g/dl)
—> Raised CRP

Investigation:
- AXR
- CT abdomen + pelvis

Treatment:
1. Steroid +/- anti-TNF (≥ D5)
2. Colectomy (if medical treatment fail)

39
Q

***Colectomy

A

Indication:
1. Failure of toxic dilation to respond to 48 hours therapy
2. Deterioration despite optimal treatment
3. Patient choice

Risk for need of colectomy (w/o 2nd line therapy):
- 24 h stool frequency > 8
- stool frequency 3-8 + CRP > 45 mg/L

Emergency surgery:
1. **Total abdominal colectomy + **End ileostomy
—> Rectum left untouched
—> **2nd stage operation when patients are stable
—> Completion **proctectomy +/- ***IPAA (Ileal pouch-anal anastomosis) (join ileum to anal canal)

Elective surgery:
1. Restorative **proctocolectomy + **IPAA (Ileal pouch-anal anastomosis)
- Laparoscopic / Conventional
- Suitable candidate for laparoscopic surgery
- Need temporary + protective ileostomy (to rest the bowel after surgery)
- Stapled / Hand-sewn
- Pouch complications

  1. **Total colectomy + **IRA (Ileorectal anastomosis)
    - If rectum not inflamed
    - Preserve fertility in female patients (∵ proctectomy can cause adhesion / damage to nerve)
  2. With permanent end ileostomy
    - If short mesentery, CA rectum involving sphincters
40
Q

Surgery for CD

A
  • Rarely curative but lead to long-lasting remissions in some patients

Indications:
1. **Complications treatment
- **Stricture
- **Abscess
- **Fistula
- Perforation / bleeding

  1. Severe CD **refractory to medical treatment
    - **    Crohn’s disease activity index (CDAI) >450
    - ***Harvey Bradshaw Index (HBI) >15
  2. ***Ileocolic CD
    - Low threshold for surgery
41
Q

Small bowel stricture

A

2 types:
1. Inflammatory
- ***Medical therapy

  1. Fibrostenosing (after repeated attacks of inflammation):
    - ***Strictureplasty preferred
    —> Heineke–Mikulicz strictureplasty (for short strictures <10cm)
    —> Finney strictureplasty (intermediate stricture 10-20cm)
    —> Michelassi (side-to-side) strictureplasty (long stricture 20-25cm)
    - Resection (only if suspect malignancy / isolated stricture)
    - Endoscopic dilatation (if can access stricture through enteroscopy)
42
Q

Abdominal fistula

A

2 types:
1. ***Internal fistula
- Entero-enteric: no surgery if asymptomatic
- Entero-colic fistula: diarrhoea (may end up malnutrition)

  1. ***External fistula
    - Entero-cutaneous
    - Entero-vesical: pneumaturia, faecaluria
    - Entero-vaginal

Enterocutaneous fistula: Treatment
**“SNAP”
1. **Sepsis control
- Abscess drainage
- Antibiotics

  1. ***Nutrition support
    - High vs Low output (e.g. High fistula may cause malnutrition)
    - Nutritional assessment + support
  2. ***Anatomy
    - CT / MR enterography
  3. ***Procedure
    - Medication adjustment (e.g. immunosuppressant / biologics may cause surgical wound infection)
    - Closure with biological agents
    - Enbloc resection involved bowel + fistula
43
Q

Ileocaecal CD

A
  • ***80% ileocaecal CD require surgery
  • An alternative to medical Tx in the early disease course

Treatment:
1. Laparoscopic ileocaecal resection
- Technically more difficult
—> adhesion due to inflammation
—> phlegmon (localised inflamed soft tissue)
—> shortened mesentery
- Reduction of adhesive bowel obstruction
- Can consider to stop medical Tx after one year of remission

44
Q

Perianal CD

A
  • 24.5% of patients with Crohn’s disease
  • ***83% required surgery
  • ***More complicated courses of fistula tract (∵ most are extra / suprasphincter fistula)
  • **MRI pelvis + **EAUS (Endoanal Ultrasound) necessary to document before the definite treatment

Treatment:
1. **Anti-TNF (Infliximab) +/- **AZA

Abscess:
2. **Antibiotics
- **Metronidazole/ciprofloxacin
3. ***Abscess drainage

Fistula:
4. Simple fistula (Inter / Low transphincteric) —> **Fistulotomy
5. Complex fistula
- **Seton insertion for drainage
- Azathioprine
- Biologics
6. ***Colostomy / Proctectomy

Algorithm:
Antibiotics + AZA
—> EUA +/- Abscess drainage +/- Seton
—> Infliximab 5mg/kg at 0, 2, 6 weeks
—> Remove Seton at 6 weeks
—> Continue Infliximab 8-weekly
—> MRI pelvis
—> Complete response: Stop Infliximab + Continue AZA
—> Partial response: Continue Infliximab, reassess 6-monthly
—> No response: Surgical intervention

45
Q

Biologics for CD

A

Anti-TNF (may develop resistance after prolonged use —> need to switch to other class):
1. Infliximab (1st gen) (IV)
2. Adalimumab (2nd geb) (SC (i.e. can do at home by patient))
3. Certolizumab pegol (SC)

Anti-integrin:
1. Vedolizumab (IV)

Anti-IL12/23 Ab:
1. Ustekinumab (IV then SC)

46
Q

IBD-associated CRC

A
  • Incidence of CRC in IBD: 18% after 30 years of colitis

Pathogenesis:
- Colitis —> Dysplasia —> Carcinoma

Risk factors:
1. Patient
- History of **PSC
- History of **colorectal neoplasia
- Family history of CRC
- Smoking

  1. Disease
    - Duration
    - Extent
    - Cumulative inflammatory burden
    - Active inflammation endoscopically / histologically
  2. Endoscopic features
    - Stricture
    - Shortened tubular colon
    - Pseudopolyps

∵ The cancer do not develop from polyp —> only develop from flat lesion —> need dye to coat dysplastic mucosa

***Chromoendoscopy:
- SCENIC endoscopic classification of superficial colorectal dysplasia in IBD
- Visible dysplasia 90%
- Invisible dysplasia 10%
(Even if no visible dysplasia —> still take biopsy to rule out Invisible dysplasia)

Management of dysplasia:
1. Endoscopically visible dysplasia
- Polypoid: **polypectomy
- Non-polypoid: **endoscopic resection (EMR / ESD) if complete resection possible
- ***Surgery should be considered if not endoscopically feasible

  1. Endoscopically invisible dysplasia
    - Associated with high rate of CRC
    - Referred to an experienced endoscopist
    - If Low grade dysplasia / No dysplasia
    —> 5% LGD changed to HGD or CRC
    —> Surveillance or surgery?
    - If invisible HGD or multifocal LGD —> surgery should be offered

Guideline for surveillance colonscopy:
1. AGA guideline 2010
2. BSG guideline 2010

JC WCS (134 decks)

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