1. Inflammatory Bowel Disease

1.1 Epidemiology

• Crohn’s Disease (CD): Incidence ~7/100,000 (increasing); prevalence ~70/100,000.
  • Common in developed countries, highest reported in New Zealand.
• Ulcerative Colitis (UC): Incidence ~12/100,000 (stable); prevalence ~120/100,000.
• Both exhibit bimodal age peaks: 3rd–4th decade and 6th–7th decade of life.
• More common in Ashkenazi Jews and 2nd-generation Asians in developed nations.
• Also includes indeterminate colitis (features overlap UC and CD) and microscopic colitis.

1.2 Aetiology

1. Genetic Factors
   • Polygenic traits, up to 160+ associated genes identified.
   • Crohn’s has stronger concordance in twins (~50%) vs. ~10% in UC.
   • CARD15/NOD2 gene on chromosome 16 linked to CD → alters bacterial antigen handling.
2. Environmental Factors
   • Highest prevalence in developed countries with improved sanitation.
   • Dietary shift towards animal fat (less oily fish) linked to rising IBD incidence.
   • Smoking: Worsens Crohn’s risk/activity, but reduces risk in UC.
3. Immunological Factors
   • Gut microbiome interplay: certain bacterial profiles may trigger or protect from mucosal inflammation.
   • No single agent firmly identified; likely a result of microbial interactions with susceptible mucosa.

1.3 Pathophysiology

1. Mucosal Barrier Breach
   • Antigens (dietary or bacterial) breach the intestinal mucosa, prompting an immune response.
2. Immune Activation
   • Specialised antigen-presenting cells (APCs) release pro-inflammatory cytokines (e.g. TNF-α, IL-12).
   • CD4+ T-cells become activated:
     • Crohn’s often associated with Th1 response → TNF-α, IFN-γ.
     • UC often associated with Th2 response → IL-5.
   • Growing recognition of Th17/IL-23 involvement, plus T regulatory cells.
3. Inflammation and Tissue Damage
   • Recruitment of neutrophils, lymphocytes → chronic inflammation of bowel wall.
   • Additional activation of mast cells, fibroblasts → further mucosal injury and compromised barrier.
   • Extraintestinal manifestations from circulating inflammatory mediators.

1.4 Clinical Features

1.4.1 Crohn’s Disease

• Distribution: Can affect any part of GI tract, often skip lesions; 40% ileocolic, 30% small intestine only, 20% colon only, 10% perianal.
• Transmural inflammation → deep ulcers, “cobblestone” mucosa, fistulae, strictures.
• Symptoms:
  • Ileal CD → postprandial pain, non-bloody diarrhoea, malabsorption (B12, folate), weight loss.
  • Colonic CD → bloody diarrhoea, constitutional symptoms.
  • Perianal CD → fistulae, abscesses, anal tags.
• Histology: Non-caseating granulomas in ~50%.

1.4.2 Ulcerative Colitis

• Distribution: Always rectum ± continuous proximal spread. Proctitis, left-sided, or pancolitis.
• Mucosal-only inflammation, continuous involvement.
• Symptoms:
  • Proctitis → fresh rectal bleeding, mucus, tenesmus.
  • Extensive/pancolitis → bloody diarrhoea, abdominal pain, systemic upset.
• Histology: Mucosal crypt abscesses, inflammatory infiltrate, risk of dysplasia/carcinoma over time.

1.4.3 Extraintestinal Disease

• Occurs in ~35% of patients; includes:
  • Arthritis (large joints, ankylosing spondylitis).
  • Skin: Erythema nodosum, pyoderma gangrenosum.
  • Eyes: Uveitis, episcleritis.
  • PSC (primary sclerosing cholangitis).

1.5 Diagnostic Approach

1. Blood Tests
   • FBC, ESR, CRP, ferritin, B12, folate.
   • Faecal calprotectin: sensitive marker of GI inflammation.
   • LFTs to check for PSC.
2. Stool Analysis
   • Culture + C. difficile toxin to exclude infective causes.
3. Endoscopy
   • Flexible sigmoidoscopy for initial diagnosis (especially if severe).
   • Full colonoscopy for extent staging in stable disease. Biopsies essential.
4. Imaging
   • AXR: toxic megacolon, obstruction.
   • CT/MRI: evaluate small bowel (Crohn’s), complications (abscess, fistula).
   • Capsule endoscopy: occasionally to detect subtle small bowel lesions.

1.6 Complications

• Toxic Megacolon: Colonic diameter >6 cm with signs of severe colitis, risk of perforation. More frequent in UCbut can occur in Crohn’s.
• Strictures, Fistulae: Mostly in Crohn’s → can lead to obstruction, abscess, sepsis.
• Malnutrition: Common in Crohn’s if extensive small bowel disease.
• Colorectal Carcinoma: Risk increases with disease extent, duration (>8 yrs), PSC coexisting, and severity. Surveillance colonoscopy is crucial.

1.7 Management Overview

1.7.1 Inducing Remission

• Crohn’s:
  • Mild–moderate: Budesonide or prednisolone, ± enteral nutrition.
  • Severe/refractory: IV steroids, anti-TNF (infliximab, adalimumab), immunomodulators (azathioprine, methotrexate).
• Ulcerative Colitis:
  • Distal mild: 5-ASA suppositories/enema.
  • Extensive moderate: Oral 5-ASA ± oral prednisolone.
  • Severe: IV steroids ± IV cyclosporin or infliximab rescue.
• Address infection (e.g. C. difficile), correct fluid/electrolyte imbalances.

1.7.2 Maintaining Remission

• Crohn’s: Avoid prolonged steroids; typical choices are azathioprine/6MP or methotrexate. Anti-TNF or other biologics if refractory.
• Ulcerative Colitis: 5-ASA for mild disease; azathioprine or biologics if severe/refractory.
• Nutrition: Monitor for deficiencies (iron, B12, folate, vitamin D, etc.).

1.7.3 Surgery

• Crohn’s: Not curative. Indications: perforation, obstruction, fistula, abscess, or intractable disease. Minimally resect to preserve bowel length.
• UC: Proctocolectomy ± ileal pouch may be curative. Indications include medical failure, toxic megacolon, or dysplasia/cancer.

1.8 Prognosis

• Life expectancy now near normal due to improved medical/surgical treatments.
• Crohn’s: ~90% need at least one operation (especially ileal disease).
• UC: ~90% relapsing–remitting, ~10% chronic active requiring possible colectomy.

2. Microscopic Colitis

2.1 Epidemiology

• Combined incidence of microscopic colitis (MC) is ~5–10 per 100,000 annually.
• More common in individuals with coeliac disease, autoimmune disorders, and those taking certain drugs (especially PPIs, NSAIDs).
• Typically presents in 60–70-year-olds; female preponderance in collagenous colitis.

2.2 Aetiology

1. Likely Multifactorial
   • Represents mucosal immune response to unknown luminal agents in predisposed hosts.
   • No clear genetic link identified; possibly triggered by certain medications.
2. Smoking
   • Risk factor for MC (contrasting with the protective effect in UC or harmful effect in Crohn’s).
3. Drug Associations
   • Common implicated agents: PPIs, NSAIDs, ranitidine, sertraline, aspirin and others.

2.3 Pathophysiology

1. Uncontrolled Immune Response
   • In susceptible individuals, a dysregulated mucosal immune reaction to luminal antigens leads to chronic inflammation in the colonic epithelium.
2. Distinct Histological Subtypes
   • Collagenous colitis: thickened subepithelial collagen layer with inflammatory infiltrates.
   • Lymphocytic colitis: significant increase in intraepithelial lymphocytes; no collagen band thickening.
3. Normal-Looking Colon Endoscopically
   • Despite ongoing microscopic inflammation, macroscopic mucosal appearance is often normal or near-normal.

2.4 Clinical Features

• Characterised by watery, non-bloody diarrhoea (chronic or intermittent).
• Often accompanied by abdominal pain and variable weight loss.
• Endoscopic examination is typically normal; diagnosis relies on colonic biopsies.

2.5 Investigations

1. Colonoscopy with Biopsy
   • Essential to detect histological changes.
   • Right colon biopsies more likely to detect the typical pathological findings.
   • Collagenous colitis → subepithelial collagen thickening.
   • Lymphocytic colitis → increased intraepithelial lymphocytes.
2. Exclude Other Conditions
   • Coeliac disease, bile acid malabsorption, lactose intolerance, or iatrogenic causes (e.g. offending drugs).
3. Faecal Calprotectin
   • May be normal or mildly elevated; not reliable for confirming or excluding microscopic colitis.

2.6 Management

1. Remove Potential Triggers
   • Discontinue or reduce suspicious medications (e.g. PPIs, NSAIDs).
   • Advise smoking cessation.
2. Pharmacotherapy
   • Mild disease: loperamide as needed.
   • Moderate to severe: budesonide is first choice for inducing remission (9 mg daily).
     • Budesonide can also maintain remission at lower doses (4.5–6 mg daily).
   • Alternative immunosuppressives (azathioprine, anti-TNF therapies) used only if refractory to budesonide.
3. Long-Term Considerations
   • Relapses are common after budesonide withdrawal.
   • Provide bone protection (calcium, vitamin D) if on prolonged budesonide.

2.7 Prognosis

• No impact on overall survival compared to the general population.
• Health-related quality of life can be significantly reduced if frequent watery stools persist.
• Adequate therapy (budesonide) and removal of triggers usually restore a near-normal quality of life.

3. Functional Gastrointestinal Disorders

3.1 Epidemiology

• Functional gastrointestinal disorders (FGIDs)—now often called disorders of gut–brain interaction—are extremely common.
• Overall prevalence: up to 20% of people meet diagnostic criteria, but only around 10% seek medical help.
• Gender & age: more frequent in women; can manifest at any age but typically in the childbearing years.
• Overlap with other functional disorders (eg, chronic fatigue syndrome, functional back pain) is common.

3.2 Aetiology

1. Psychosocial Factors
   • Psychological aspects (stress, depression, anxiety) influence both perception of gut stimuli and gut motility.
   • Chronic distress can alter the hypothalamic–pituitary–adrenal (HPA) axis and impact GI functioning.
2. Visceral Hypersensitivity
   • Heightened perception of pain/pressure in the GI tract.
   • Modulated by both neural and immune factors (eg, mast cells, cytokines).
3. Abnormal Gut Motility
   • Disordered motor patterns (accelerated or slowed transit, altered reflexes).
   • Influenced by central and peripheral signals, neurotransmitters (serotonin, dopamine), and local mediators.
4. Mucosal Immune Activation
   • Low-grade inflammation post gut infections or from subclinical triggers.
   • ~25% of irritable bowel syndrome (IBS) onset is postinfectious, accompanied by mild immunological changes in the mucosa.
5. Dietary Components
   • Fermentable carbohydrates (FODMAPs) can exacerbate IBS.
   • Some FGIDs may be triggered by immunological or non-immunological responses to certain foods.

3.3 Pathophysiology

1. Neural–Immune Axis
   • Enteric neurons and immune cells (eg, mast cells, eosinophils) communicate bidirectionally.
   • Psychological stress, food antigens or dysbiosis can drive mild mucosal activation, causing release of pronociceptive mediators (histamine, proteases).
   • These mediators sensitise visceral afferent pathways (eg, via TRP channels), heightening pain signals.
2. Visceral Hypersensitivity Mechanisms
   • Peripheral: mast cells, eosinophils and local mediator excess (histamine, tryptase) → lowered thresholds for pain.
   • Central: emotional states (anxiety/depression) modulate spinal cord and brain responses → amplifying sensory input from the gut.
3. Abnormal Motor Function
   • Stress, inflammation, or luminal triggers can disrupt normal gut reflexes, causing accelerated or slowed transit and altered reflex patterns.
   • Subsequent bloating, diarrhoea or constipation can reinforce discomfort and pain.
4. Gut Barrier and Microbiome
   • Subtle increases in intestinal permeability allow more luminal antigens/bacteria to contact local immune cells.
   • Perturbed microbiome (due to diet, antibiotics, etc.) can produce or degrade mediators (short-chain fatty acids, histamine) influencing motility, sensation and local immunological tone.
5. Psychological Influences
   • Chronic stress or anxiety leads to persistent upregulation of HPA axis and CRH-mediated mast cell activation → further sensitisation.
   • Cognitive processes, including catastrophising or hypervigilance, intensify perceived symptom severity.

3.4 Clinical Syndromes and Features

1. Functional Heartburn
   • Retrosternal burning in the absence of pathological reflux.
   • Non-erosive on endoscopy, unresponsive or only partly responsive to antireflux measures.
2. Functional Dyspepsia (FD)
   • Subclassified into:
     • Postprandial distress syndrome: post-meal fullness, early satiety, bloating.
     • Epigastric pain syndrome: upper abdominal pain or burning, less meal related.
   • Endoscopy is typically normal or near-normal.
3. Irritable Bowel Syndrome (IBS)
   • Characterised by abdominal pain plus altered bowel habit (diarrhoea, constipation or mixed).
   • Rectal mucus discharge and incomplete evacuation sensations are frequent.
   • Symptoms typically do not disturb sleep.
4. Functional Constipation
   • Infrequent defaecation, straining, passage of hard stools, sense of incomplete voiding.
   • Slow transit constipation: decreased colonic motility, especially in younger women; unresponsive to high-fibre diets.
   • Defaecation disorder: impaired rectal evacuation (rectocoele, pelvic floor dyssynergia).

3.5 Management

1. Reassurance & Explanation
   • Emphasise benign nature once serious pathology is excluded.
   • A positive, not purely exclusion-based, diagnosis is often preferred.
2. Dietary Adjustments
   • Functional Dyspepsia: small meals, avoidance of aggravating foods; limited evidence for major dietary exclusion.
   • IBS:
     • FODMAP-restricted diets can alleviate diarrhoea/bloating.
     • Care with extremes (low or high fibre) in IBS subtypes.
   • Functional Constipation: balanced fibre approach; osmotic or stimulant laxatives if required.
3. Pharmacological Therapy
   • Antispasmodics (eg, mebeverine, hyoscine) reduce postprandial cramping in some IBS patients.
   • Loperamide helps diarrhoea in IBS but less on pain.
   • Tricyclic antidepressants (low-dose) can relieve chronic pain in IBS and functional dyspepsia.
   • PPIs can be tried in functional heartburn or FD, but often less effective than in GORD.
4. Psychological and Behavioural
   • Cognitive behavioural therapy or hypnotherapy beneficial in IBS, FD or refractory functional heartburn.
   • Stress management, mindfulness-based approaches and coping strategies improve health-related quality of life.
5. Other Approaches
   • Prokinetics have limited evidence in functional dyspepsia.
   • Biofeedback helps pelvic floor dyssynergia in defaecation disorders.
   • Avoid anti-reflux surgery in functional heartburn; typically no proven benefit.

3.6 Prognosis

• No increased mortality: FGIDs do not lead to structural organ damage or reduce longevity.
• Chronic or relapsing pattern is common, significantly impacting quality of life.
• Good management (education, diet, psychosocial support, tailored pharmacotherapy) can lessen symptom burden and healthcare costs, though complete resolution of symptoms is variable.

4.1 Overview of Gut Ischaemia

• Gut ischaemia arises from compromised blood flow to the gastrointestinal tract. The watershed regions, especially around the splenic flexure between the superior mesenteric artery (SMA) and inferior mesenteric artery (IMA), are notably vulnerable.

• Key causes:
  • Arterial thromboembolism (most common)
  • Venous outflow obstruction (mesenteric venous thrombosis)
  • Low-flow states / profound hypotension (e.g. shock, heart failure)
  • Vasculitis (less frequent)

The following sections discuss three distinct clinical conditions:

1. Acute Mesenteric Ischaemia (principally small bowel)
2. Chronic Mesenteric Ischaemia (commonly called ‘intestinal angina’)
3. Ischaemic Colitis (large bowel involvement)

4.2 Acute Mesenteric Ischaemia (Small Bowel)

4.2.1 Epidemiology

• Relatively rare but highly lethal; mortality exceeds 80%.
• Often occurs in older patients with cardiovascular risk factors, such as atrial fibrillation or atherosclerotic disease.
• True incidence is low, but suspicion must be high in atrial fibrillation or diffuse atherosclerosis if acute severe abdominal pain is present.

4.2.2 Aetiology

• Arterial occlusion:
  • Embolic (from the heart in atrial fibrillation or mural thrombi).
  • Thrombotic (on pre-existing mesenteric arterial plaques).
• Venous thrombosis (~5%): associated with hypercoagulable states (e.g. malignancy, hereditary thrombophilia).
• Hypoperfusion / low-flow states (~20%): severe hypotension, shock.
• Vasculitis and rarer mechanisms (trauma to vessels, strangulating obstruction).

4.2.3 Pathophysiology

• Abrupt cessation of blood supply → transmural small bowel infarction.
• Early changes: mucosal barrier breakdown → bacterial translocation → sepsis, peritonitis.
• Ongoing ischaemia leads to necrosis of the entire bowel wall → perforation, shock.

4.2.4 Signs and Symptoms (Clinical Features)

• Severe, acute abdominal pain that is classically out of proportion to minimal findings on examination.
• Early physical signs can be deceptively mild: slight distension, reduced bowel sounds.
• Later: peritonism, rectal bleeding, shock (hypotension, tachycardia).
• Blood tests: leucocytosis, raised lactate (metabolic acidosis), often mildly raised amylase.

4.2.5 Complications

• Perforation and septic peritonitis.
• Progression to multi-organ failure (via SIRS).
• Short-bowel syndrome if extensive resection is required in survivors.
• Mortality is high (~80%).

4.2.6 Immediate Management

• Urgent resuscitation:
  • IV fluids, correct metabolic acidosis, broad-spectrum IV antibiotics (e.g. piperacillin/tazobactam).
  • Anticoagulation (e.g. IV heparin) if mesenteric arterial/venous occlusion is confirmed or strongly suspected.
• Emergency imaging:
  • CT/MR angiography to locate occlusion (though not to delay surgery if the clinical diagnosis is certain).
• Emergency laparotomy:
  • Resection of infarcted bowel.
  • Attempt embolectomy or localised infusion of thrombolytics if feasible.
  • Second-look laparotomy sometimes required.

4.2.7 Long-Term Management

• In survivors with large resections, parenteral nutrition may be needed long-term (short-bowel syndrome).
• Risk factor modification: manage atrial fibrillation, use prophylactic anticoagulation if indicated, treat atherosclerosis.

4.3 Chronic Mesenteric Ischaemia (a.k.a. “Intestinal Angina”)

4.3.1 Epidemiology

• Uncommon, typically in older patients with extensive atherosclerotic disease (e.g. aortic or other major vessel plaques).
• Often under-recognised due to its insidious, non-specific features.

4.3.2 Aetiology

• Generally arises from atherosclerotic stenosis in two or three of the major mesenteric vessels (coeliac axis, SMA, IMA), leading to insufficient postprandial blood supply.
• Chronic low-flow state in a setting of decreased mesenteric reserve.

4.3.3 Pathophysiology

• Partial arterial lumen compromise due to plaques → reduced mesenteric arterial flow.
• After meals, intestinal demand increases (for digestion/absorption) → further mismatch → ischaemic pain.
• Over time, fear of pain → reduced food intake → malnutrition, weight loss.

4.3.4 Signs and Symptoms (Clinical Features)

• Postprandial colicky epigastric pain typically 30 minutes after eating, lasting ~2–4 hours.
• Anorexia, often severe weight loss or “food fear.”
• Abdominal bruit (rare).

4.3.5 Complications

• Escalation to acute mesenteric infarction.
• Progressive weight loss, malnutrition.

4.3.6 Immediate Management

• Analgesia and basic supportive measures (IV fluids if needed).
• Imaging:
  • CT or MR angiography, or conventional angiography, to define mesenteric vessel lesions.

4.3.7 Long-Term Management

• Diet: small, frequent meals may ease postprandial demand.
• Revascularisation (percutaneous angioplasty ± stenting, or surgical bypass) can relieve symptoms and prevent infarction—but often high surgical risk due to comorbidities.
• Ongoing management of atherosclerotic risk factors (smoking cessation, statins, antiplatelet therapy).

4.4 Ischaemic Colitis

4.4.1 Epidemiology

• Commonly affects older patients with arterial disease, often in the IMA territory.
• Incidence is higher in individuals with known atherosclerosis, heart failure or other vascular compromise.

4.4.2 Aetiology

• Non-occlusive low-flow states in the inferior mesenteric artery distribution.
• May also involve atheromatous or thrombotic occlusion, vasculitis or arrhythmias.
• The splenic flexure (a watershed) is frequently involved.

4.4.3 Pathophysiology

• Reduced colonic perfusion → mucosal/submucosal necrosis or, in severe cases, transmural infarction.
• The colon’s watershed regions are susceptible.
• In milder forms, partial mucosal damage; in fulminant forms, gangrene or toxic dilatation can result.

4.4.4 Signs and Symptoms (Clinical Features)

• Sudden onset abdominal pain, typically left-sided.
• Rectal bleeding or bloody diarrhoea, occasionally watery diarrhoea.
• More severe “fulminant” form → toxic megacolon, gangrenous bowel, sepsis.

4.4.5 Complications

• Toxic megacolon with risk of perforation.
• Stricture formation during healing.
• Gangrenous colitis → septic shock, high mortality.

4.4.6 Immediate Management

• Resuscitation: IV fluids, correct electrolyte imbalance, analgesia.
• Assessment for severity: abdominal X-ray or CT to detect colonic dilatation, necrosis or perforation.
• Gentle limited colonoscopy (if stable) to confirm diagnosis (oedematous ulcerated mucosa, “thumb-printing” on imaging).
• IV broad-spectrum antibiotics if concern for necrosis/perforation.
• Surgery (subtotal colectomy ± stoma) if gangrenous or perforated.

4.4.7 Long-Term Management

• Supportive: many mild–moderate cases resolve spontaneously.
• Monitor for stricture: repeated colonoscopy if necessary.
• Risk factor reduction for vascular disease (e.g. manage atherosclerosis).

5. Radiation Enterocolitis

5.1 Epidemiology

• Frequency
  • Acute radiation enteritis: Affects up to 70% of patients within weeks of starting abdominal or pelvic radiotherapy.
  • Chronic radiation enteritis/enterocolitis: Occurs in ~15% of patients (though some literature quotes up to 40–50% in certain cohorts).
• Factors influencing risk
  • Radiotherapy dose (cumulative dose, total field size, fractionation protocols).
  • Concomitant treatments (e.g. chemotherapy).
  • Patient comorbidities (e.g. diabetes, hypertension).
  • Previous abdominal/pelvic surgery.

5.2 Aetiology

• Direct effect of ionising radiation on bowel tissue as part of cancer radiotherapy, commonly for:
  • Pelvic tumours (e.g. cervical, prostate, rectal cancer).
  • Abdominal tumours (e.g. pancreatic, gastric lymphoma).
• Unavoidable collateral damage to adjacent healthy bowel when radiation is aimed at a localised tumour region.

5.3 Pathophysiology

1. Acute radiation damage
   • Injury to rapidly dividing mucosal epithelial cells causes crypt cell apoptosis, mucosal barrier disruption, and local inflammatory mediator release.
   • Typically arises within days/weeks of initial exposure.
2. Chronic radiation enteritis
   • Develops months to years (occasionally decades) after therapy.
   • Key pathology: obliterative endarteritis (damage to small arterioles) → progressive ischaemia + secondary fibrosis.
   • End result: poor vascular supply → mucosal ulceration, strictures, fistulae, perforation.
3. Common final pathways
   • Fibrosis: A hallmark of chronic stage, triggered by TGF-β and other cytokine signals.
   • Ischaemia: Bowel wall thinning and necrosis predispose to fistula, perforation or bleeding.

5.4 Signs and Symptoms (Clinical Features)

5.4.1 Acute Radiation Enteritis

• Usually starts during the early weeks of radiotherapy.
• Common symptoms:
  • Diarrhoea (often watery, may have mucus).
  • Abdominal pain, cramping.
  • Nausea, vomiting.
• Typically self-limiting once radiotherapy completes or is paused.

5.4.2 Chronic Radiation Enteritis

• May first appear 6–12 months after therapy, occasionally many years later.
• Symptom patterns vary with location and extent of bowel involved:
  • Small bowel involvement:
    • Chronic diarrhoea, bloating, malabsorption (steatorrhoea, vitamin deficiencies).
    • Strictures → partial obstruction (pain, distension).
    • Fistulae → discharge, local sepsis.
  • Colonic/Rectosigmoid involvement (radiation proctitis/proctocolitis):
    • Rectal bleeding (often from telangiectasias in the mucosa).
    • Tenesmus, urgency, mucus discharge.
    • Chronic diarrhoea or constipation.
    • Incontinence if anal sphincter is damaged.
    • Rectal pain or ulceration.
• Symptoms can be progressive over months/years, often intermittent or relapsing.

5.5 Complications

1. Ulcers → recurrent bleeding, chronic blood loss → anaemia.
2. Fistula formation (e.g. enterocutaneous, entero-vesical, rectovaginal).
3. Strictures → partial or complete bowel obstruction.
4. Perforation → peritonitis, sepsis, surgical emergency.
5. Malabsorption → weight loss, malnutrition (especially if extensive small bowel involvement).
6. Faecal incontinence → if rectum or anal sphincters are damaged (internal anal sphincter particularly radiosensitive).
7. Rare: Secondary malignancies in the irradiated field (long-term risk).

5.6 Immediate Management

5.6.1 Acute Radiation Enteritis

• Supportive: Usually self-limiting, but mainstays are:
  • Antiemetics (e.g. metoclopramide, ondansetron) for vomiting.
  • Antidiarrhoeals (e.g. loperamide).
  • Adequate fluid and electrolyte replacement.
  • Occasionally dose modification or temporary pause in radiotherapy if symptoms severe.

5.6.2 Severe Bleeding or Obstruction (Acute on Chronic)

• Stabilise: IV fluids, correct anaemia if indicated, broad-spectrum antibiotics if perforation suspected.
• Endoscopic therapy: For rectal bleeding, argon plasma coagulation or endoscopic thermal coagulation.
• Surgical intervention is typically avoided unless perforation, uncontrollable haemorrhage, or complete obstruction are present.

5.7 Long-Term Management

1. Dietary modifications
   • Low-residue diet may help reduce chronic diarrhoea.
   • Correct nutritional deficiencies with vitamins, minerals, or enteral support as needed.
2. Medications for Chronic Symptoms
   • Rectal bleeding:
     • Argon plasma coagulation or endoscopic approaches for telangiectatic bleeds.
     • Topical therapies: 5-ASA enemas, sucralfate enemas, corticosteroid enemas for mild haemorrhage.
     • Hyperbaric oxygen therapy can benefit refractory rectal bleeding.
   • Faecal incontinence:
     • Loperamide or codeine phosphate to reduce stool frequency and liquidity.
     • Anal plugs or pelvic floor rehabilitation for sphincter dysfunction.
   • Chronic diarrhoea:
     • Antimotility agents (loperamide).
     • Consider bile salt sequestrants (e.g. cholestyramine) if bile acid malabsorption is suspected.
     • Antibiotics (e.g. metronidazole) if bacterial overgrowth is demonstrated.
   • Fistula:
     • Low-output fistula → conservative management: nutritional support, possible somatostatin analogues (octreotide).
     • High-output or complicated fistula → possible surgical resection or bypass if feasible.
3. Surgical
   • Indicated only for intractable complications: persistent obstruction, non-healing fistula with sepsis, or massive haemorrhage.
   • High risk of postoperative morbidity (poor healing in irradiated tissues).
4. Prevention
   • Careful radiation planning: limiting dose, using conformal or intensity-modulated techniques to spare healthy bowel.
   • Surgical displacement of bowel loops out of radiation field when feasible.
   • Effective prophylaxis with supportive measures (e.g. nutritional interventions, prophylactic medication trials).
5. Monitoring and Follow-up
   • Surveillance for strictures, new or recurrent bleeding.
   • Assess nutritional status regularly.
   • Check for rare secondary malignancies over time.