1. Diverticulosis = presence of multiple diverticula (sac-like outpouchings of the colonic wall)
2. These are false diverticula (also called "pseudodiverticula" on the left side): only the mucosa and submucosa herniate through the muscularis propria, unlike true diverticula which involve all layers ^[5][6]
   • Right-sided diverticula (common in Asia) are "true" diverticula (involve all layers) while left-sided are "false" ^[6]
3. Formation mechanism: Bowel wall weakening with ageing + increased intraluminal pressure (e.g. constipation, low-fibre diet) ^[5][6]
   • The sigmoid colon has the narrowest calibre → by Laplace's law (P = T/r, where P = pressure, T = wall tension, r = radius), the narrowest segment generates the highest intraluminal pressure for the same wall tension → sigmoid is most susceptible ^[5]
   • Diverticula form at the weakest point: where vasa recta penetrate the circular muscle layer ^[5][6]
4. Bleeding mechanism: As diverticula form, the vasa recta become draped over the dome of the diverticulum → separated from the bowel lumen by only mucosa → asymmetric rupture of the artery into the lumen → arterial bleeding ^[2]
5. Rectum is NEVER affected — because the outer smooth muscle (longitudinal layer) encompasses the full circumference of the rectum (unlike the colon where the longitudinal muscle is concentrated in three taeniae coli, leaving gaps) ^[5]

• Painless massive haematochezia — the hallmark presentation ^[1][2][3]
  • May have mild abdominal discomfort/cramping from colonic spasm induced by intraluminal blood
  • Colour depends on site: right-sided = darker/maroon; left-sided = bright red
• Self-limiting in 80–85% of cases, but rebleeding rate is 14–38% ^[1]
• Not chronic bleeding — typically presents as acute, profuse episodes ^[3]

• Right-sided diverticula are more common in Asians and carry a higher risk of haemorrhage (the right colonic wall is thinner) ^[2][5][6]
• By age 60, approximately 60% of patients have diverticulosis ^[1], of which ~17% will bleed
• Bleeding is actually a rare complication of diverticular disease, but the extremely high prevalence of diverticulosis explains why it is the number one cause of LGIB ^[2]

Advanced age, obesity, hypertension, hyperlipidaemia, IHD, chronic renal insufficiency, NSAIDs/aspirin ^[2][6]

• Dilated, tortuous submucosal vessels — walls composed of endothelial cells lacking smooth muscle ^[2]
• Acquired degenerative condition: chronic, low-grade, intermittent obstruction of submucosal veins by muscular contractions of the colonic wall → progressive dilation of submucosal veins → loss of pre-capillary sphincter competence → formation of small arteriovenous malformations (AVMs) ^[4]
• Most common site: right colon (caecum and ascending colon) ^[2][3][4]
  • Why right side? The caecum has the largest diameter → by Laplace's law, for the same intraluminal pressure, the wall tension is greatest here → chronic distension more likely compresses submucosal veins

• Heyde's syndrome: LGIB associated with aortic stenosis — the mechanism involves acquired Type 2A von Willebrand disease (high-molecular-weight vWF multimers are cleaved by shear stress through the stenotic aortic valve → impaired platelet adhesion) ^[4]
• Osler-Weber-Rendu disease (hereditary haemorrhagic telangiectasia, HHT): congenital vascular malformations throughout the body ^[1][4]
• ESRD (chronic kidney disease on dialysis): uraemic platelet dysfunction + heparin use ^[4]
• von Willebrand disease ^[4]

• Painless haematochezia of variable severity ^[1][3]
• Bleeding is venous in origin → tends to be less massive than diverticular bleeding (which is arterial) ^[2]
• Often presents as occult bleeding → iron deficiency anaemia, FOBT positive ^[2]
• Can present with overt haematochezia or melaena
• Self-limiting in 85–90% but rebleed rate is high (25–85%) ^[1]
• Tends to be intermittent rather than a single massive bleed ^[3]

• Cherry red spots on colonoscopy ^[4]
• Mother-in-law phenomenon on mesenteric angiography: early filling, delayed emptying (early arterial filling of the AVM, with the contrast "lingering" — like a mother-in-law who arrives early and won't leave!) ^[4]

• Haemorrhoids are dilated submucosal vascular cushions (arterioles, venules, and smooth muscle) in the anal canal
• Internal haemorrhoids: above the dentate line → covered by columnar epithelium → portal venous drainage → painless (visceral innervation) ^[2][8]
• External haemorrhoids: below the dentate line → covered by squamous epithelium → systemic venous drainage → painful if thrombosed (somatic innervation) ^[8]
• Mechanism of bleeding: Straining → engorgement of vascular cushions → erosion of overlying mucosa → arterial bleeding from submucosal arterioles → bright red blood ^[2]

• Low-fibre diet, constipation (chronic straining)
• Increased intra-abdominal pressure: pregnancy, obesity, chronic cough ^[8]
• Family history of haemorrhoids ^[8]
• Prolonged sitting on toilet

• Bright-red painless outlet-type bleeding — blood on toilet paper, dripping into bowl, or coating the surface of stool ^[2][3][8]
• Perianal pruritus (mucous discharge from prolapsed internal haemorrhoids)
• Prolapsing mass
• Pain only if: thrombosed external haemorrhoid, strangulated prolapsed internal haemorrhoid
• ALWAYS exclude other possible sources of PR bleeding before attributing bleeding to haemorrhoids ^[8]

• Bleeding occurs due to overlying erosion or ulceration of the tumour surface ^[2]
• Tumour neovascularisation produces fragile, abnormal blood vessels that are prone to bleeding
• Usually presents as chronic, low-volume bleeding → iron deficiency anaemia rather than massive haematochezia
• However, can occasionally present with significant haematochezia if a large vessel is eroded

• Change in bowel habits (alternating diarrhoea and constipation) ^[3]
• Change in stool calibre (pencil-thin stools — from luminal narrowing) ^[4]
• Tenesmus (feeling of incomplete evacuation — from rectal mass) ^[3][4]
• Constitutional symptoms: weight loss, anorexia, malaise ^[3]
• Passage of mucus ^[3]
• Right-sided CRC: tends to present later with iron deficiency anaemia (large caecal lumen accommodates tumour growth before obstruction occurs)
• Left-sided CRC: earlier presentation with obstructive symptoms (narrower lumen)
• Metastatic symptoms: jaundice (liver), bone pain, SOB (lungs), ascites (peritoneal) ^[3]

50 years old, male, smoker, family history, personal history of IBD or polyps, previous colorectal cancer ^[3]

• Ulcerative colitis: Continuous mucosal inflammation starting from rectum, extending proximally → bloody diarrhoea is the hallmark
• Crohn's disease: Skip lesions, transmural inflammation → can affect any part of GI tract
• Both can present with LGIB, usually as bloody diarrhoea rather than massive haematochezia
• Extra-intestinal manifestations: arthritis, episcleritis/uveitis, erythema nodosum, pyoderma gangrenosum, primary sclerosing cholangitis ^[3]

Commonest form ( > 50%) of ischaemic injury of the GI tract ^[7]

Epidemiology: Common in elderly female (90% occurs in > 60 years) ^[7]

Pathophysiology:

• The colon is the most vulnerable part of the GIT to ischaemia (receives less blood than the rest of the GIT) ^[7]
• Non-occlusive (95%): Due to transient systemic low-flow states (hypotension, cardiac surgery, haemodialysis, sepsis) → characteristically affects the watershed areas (Griffiths' point, Sudeck's point) ^[7]
• Occlusive (5%): Embolic/thrombotic — rarely occurs without concurrent small bowel ischaemia (i.e. SMA occlusion) ^[7]
• Damage is primarily mediated by reperfusion injury in most patients; transmural necrosis occurs in only ~15% when ischaemia is prolonged ^[7]

Risk Factors: Cardiovascular disease (HTN, IHD, AF, HF, PVD), diabetes, recent acute MI, recent cardiovascular surgery, dialysis, hypercoagulable states, vasculitis, cocaine use, medications (vasopressors, digitalis) ^[7]

Clinical Features:

• Sudden onset cramping abdominal pain (milder and more lateral than mesenteric ischaemia, can be associated with urgency to defecate) ^[7]
• Mild-to-moderate rectal bleeding develops ≤ 24 hours after onset of pain (may be fresh or dark, more common with left colonic ischaemia) ^[7]
• Tenderness over affected bowel on examination ^[7]
• Systemic upset: usually associated with ↑ WBC but fever is unusual ^[7]

• Causes: C. difficile, CMV, amoebic colitis, TB colitis ^[1][3]
• Presents with: fever, diarrhoea (may be bloody), abdominal pain, nausea/vomiting
• Important history: TOCC (travel, occupation, contact, clustering), immunosuppression (CMV colitis in HIV/transplant patients), antibiotic history (C. diff), previous TB exposure ^[3]

• Complication of radiation therapy for abdominal/pelvic cancers (e.g. cervical, prostate, bladder cancers) ^[2][3]
• Acute radiation injury: within 6 weeks of therapy — mucosal oedema, inflammation
• Chronic radiation injury: months to years later — radiation telangiectasia (abnormal dilated vessels in irradiated mucosa) → chronic oozing/bleeding
• Important history: history of abdominal/pelvic irradiation ^[3]

The nature and relationship of blood to stool is one of the most important features to characterise:

Colour of blood:

• Bright red: Left colon, rectum, anus (short transit → minimal degradation)
• Dark red/maroon: Right colon, small bowel (longer transit → partial degradation by bacteria and enzymes)
• Melaena (rare in LGIB): Very slow right colonic bleeding with sufficient transit time for complete oxidation

• Alternating diarrhoea and constipation, passage of mucus, tenesmus, pencil-thin stools → red flags for colorectal cancer ^[3][4]
  • Tenesmus = feeling of incomplete evacuation → caused by a rectal mass stimulating stretch receptors
  • Pencil-thin stools → caused by luminal narrowing from an annular tumour
• Diarrhoea with blood and mucus → colitis (IBD, infective)
• Constipation → haemorrhoids, anal fissure (also predisposing factor)

• Weight loss, anorexia, malaise → malignancy alarm features ^[3]
  • Cancer → chronic inflammation → cytokine release (TNF-α, IL-6) → cachexia, anorexia
• Fever, chills, night sweats → infective colitis, complicated diverticulitis, or advanced malignancy

• Symptomatic anaemia (chronic, slow bleeding): fatigue, exertional dyspnoea, dizziness, palpitations, syncope ^[2][3]
  • Mechanism: Chronic blood loss → iron deficiency → ↓ Hb → ↓ O₂ carrying capacity → compensatory ↑ HR and ↑ cardiac output
• Hypovolaemic shock (acute, massive bleeding): extreme thirst, confusion, pallor, oliguria, tachycardia, hypotension ^[3]
  • Mechanism: Acute intravascular volume loss → ↓ preload → ↓ cardiac output → compensatory sympathetic activation → tachycardia, peripheral vasoconstriction, then decompensation

• Should be performed early in the workup to identify anorectal pathology (haemorrhoids, fissures, proctitis, rectal ulcers, low rectal tumours) ^[1]
• Can visualise internal haemorrhoids (which are not palpable on DRE)
• Can assess for rectal inflammation (erythema, friability, ulceration → proctitis)

• Always the first step — before any fancy investigation ^[1][3]
• Proctoscopy, sigmoidoscopy to exclude bleeding from anorectal pathology ^[3]
• DRE findings:
  • Fresh blood on glove → confirms active LGIB
  • Melaena on glove → suggests UGIB or slow proximal colonic bleeding
  • Palpable rectal mass → CRC
  • Anal fissure (usually posterior midline)
  • Haemorrhoids are usually NOT palpable (need proctoscopy to see internal haemorrhoids)
• Proctoscopy allows direct visualisation of the anal canal and low rectum — identifies haemorrhoids, low rectal tumours, proctitis
• Rigid sigmoidoscopy extends this to the rectosigmoid — useful for radiation proctitis, distal UC, rectal varices

• NG tube: bile-stained aspiration → bleeding from upper GI tract excluded ^[3]
• Why: If you get bile-stained aspirate WITHOUT blood, it confirms the tube has reached the duodenum and there is no active bleeding proximal to the ligament of Treitz
• Limitation: A non-bilious aspirate is non-diagnostic (the tube may not have reached the duodenum) — and post-pyloric bleeding can be missed if the pylorus is closed
• Indication: Particularly useful when you suspect UGIB in a patient presenting with haematochezia (e.g. haemodynamically unstable with bright red PR bleeding)

Colonoscopy is the first diagnostic modality for haemodynamically stable patients ^[7]

Diagnostic yield = 75–90%, low complication rate ^[1][3]

Why colonoscopy first?

• Allows direct visualisation of the entire colonic mucosa
• Both diagnostic AND therapeutic (can treat the lesion in the same session)
• Usually also intubate the ileocaecal valve to exclude distal small bowel bleeding ^[3]
• Should be performed early (to obtain a diagnosis before bleeding stops — many causes are intermittent) ^[3]

Bowel preparation:

• Bowel prep: 4–6 L of PEG-based solution ^[7]
• ↑ Diagnostic yield but does not ↑ morbidity ^[3]
• NG tube and antiemetics can be used if needed (to facilitate prep in nauseated patients) ^[7]
• NOT feasible in unstable patients ^[3] — don't delay for bowel prep if the patient is actively exsanguinating

Key colonoscopic findings by aetiology:

Therapeutic modalities at colonoscopy — especially effective in angiodysplasia and diverticular disease ^[3]:

• Generally prefer OGD before colonoscopy in some algorithms ^[3] — especially when UGIB cannot be excluded
• Consider upper endoscopy first if not been performed (before proceeding to surgery) ^[7]
• In haemodynamically unstable patients with haematochezia, up to 10–15% have UGIB ^[1][3] → OGD may identify the source before you commit to colonic investigation
• NG tube aspirate can help triage: bile-stained without blood → UGIB less likely → proceed to colonoscopy

• A wireless camera capsule swallowed by the patient that transmits images as it traverses the GI tract
• Indication: Occult GI bleeding, intermittent bleeding with negative top-and-tail (OGD + CLN both negative) ^[2][4]
  • Also used for: iron deficiency anaemia, follow-up of Crohn's, small bowel tumours, polyposis syndromes ^[2]
• Advantages: Non-invasive; visualises entire small bowel
• Limitations ^[2]:
  • Suboptimal visual clarity due to fluid
  • Possibility of missing lesions
  • Difficult to determine exact site of bleeding
  • Long viewing time of video
  • Slow transit time → incomplete data acquisition
  • Inability to take tissue biopsy
  • Inability to perform therapeutics
• Contraindications: GI obstruction or strictures (capsule retention), implantable pacemakers/defibrillators (relative), swallowing and motility disorders ^[2]
  • Do CT/MR enterography beforehand to rule out strictures before capsule endoscopy ^[4]

• Double balloon enteroscopy (DBE): scope with 2 inflatable balloons that "pleat" the small bowel over the scope, allowing deep intubation from mouth (antegrade) or anus (retrograde) ^[4]
• Single balloon enteroscopy (SBE): similar principle with one balloon
• Advantage: Biopsy and therapeutic interventions possible (has accessory channel and tip deflection) ^[2]
• Indication: Small bowel bleeding source suspected after negative capsule endoscopy, or when therapy is needed
• Limitation: Requires prolonged sedation → seldom done during active ongoing bleeding ^[11]

This is increasingly the go-to first-line investigation for haemodynamically unstable patients ^[7]:

"We recommend that if a patient is haemodynamically unstable or has a shock index (heart rate/systolic BP) of > 1 after initial resuscitation and/or active bleeding is suspected, CT angiography provides the fastest and least invasive means to localise the site of blood loss before planning endoscopic or radiological therapy" — BSG 2019 ^[7]

CTA: Sensitivity 85.2% and specificity 92.1% in a meta-analysis (García-Blázquez 2013) ^[7]

Similar or higher diagnostic yield compared to colonoscopy (Lee 2020, Miyakuni 2020) ^[7]

How it works: Multi-phase CT with IV contrast — arterial phase images acquired during peak contrast opacification → active bleeding appears as contrast extravasation (a "blush" of contrast within the bowel lumen that was not present on the non-contrast phase)

Advantages:

• More widely available ^[7]
• Non-invasive ^[7]
• More precise localisation than RBC scan ^[7]
• Fast — can be done within minutes
• Identifies both the site of bleeding AND potential underlying pathology (mass, diverticula, vascular malformation)
• Does not require bowel preparation
• Can guide subsequent intervention (embolisation or surgery)

Limitations:

• Requires active bleeding at the time of scan — minimum bleeding rate ~0.3–0.5 mL/min
• IV contrast → risk of contrast-induced nephropathy (check creatinine) and allergic reactions
• Radiation exposure

Key CTA findings:

Procedure: selective catheterisation of SMA, IMA and coeliac artery by Seldinger technique ^[3][11]

Interpretation: positive defined by extravasation of contrast ^[3][11]

Performance: detects bleeding at 1–1.5 mL/min, diagnostic yield 27–67% ^[11]

Advantages ^[11]:

• Generally more specific but less sensitive (than RBC scan)
• Can be performed intra-operatively → inject dye to guide surgery
• Typically allows embolisation within the same procedure (therapeutic!)
• Can diagnose non-bleeding lesions, e.g. angiodysplasia (early-filling vein = "mother-in-law phenomenon"), small bowel tumours
• More available → can be done during weekends
• Can specifically pinpoint bleeding vessel (cf RBC scan which only shows region)

Disadvantages ^[11]:

• Not sensitive for slow and intermittent bleeding (needs > 0.5–1 mL/min active bleeding)
• Embolisation carries risk of intestinal ischaemia
• Invasive (arterial puncture → haematoma, pseudoaneurysm, dissection)
• Nephrotoxic contrast

Angiographic findings for angiodysplasia ^[4]:

• "Mother-in-law phenomenon": early filling (contrast appears in the vein during the arterial phase because of the AVM shunt), delayed emptying (contrast pools and lingers in the dilated submucosal vessels)

Transcatheter embolisation within 60 minutes is recommended for unstable patients with CTA-confirmed bleeding ^[7].

Clinical indication: GI bleeding ^[9]

Radiopharmaceutical: 99mTc-pertechnetate ^[9]

Technique: Red cells labelled in vitro by UltraTag kit (labelling efficiency = 98%) → re-injected IV → labelled RBCs leak into bowel lumen at site of bleeding → detected by gamma camera ^[9]

Diagnostic criteria ^[9]:

1. Activity conforms to intestinal anatomy
2. Intensity increases with time
3. Activities move (anterograde or retrograde) within the bowels

Preferred over angiography to detect GI bleeding because ^[9]:

• ↑ Sensitivity: minimum bleeding rate 0.1–0.4 mL/min (cf angiography ≥ 0.5–1 mL/min)
• Delayed images up to 24 hours → can detect intermittent bleeding
• Less invasive

Limitations:

• Non-specific ^[3] — poor anatomical localisation (blood moves intraluminally; bowel is mobile)
• Identifies site of blood pooling, not necessarily site of bleeding ^[2]
• Cannot provide therapy
• Takes more time than angiography ^[11]

Role in the algorithm: Best used when bleeding is intermittent or slow and CTA/angiography is negative or unavailable. It can confirm that bleeding IS occurring and give a rough region (right colon vs left colon) to guide further investigation or surgery.

Clinical indication: children with lower GI bleeding ^[9]

Radiopharmaceutical: 99mTc-pertechnetate ^[9]

Principle: 99mTc-pertechnetate is extracted and secreted by the sodium-iodide symporter (NIS) on gastric mucosal cells → detects ectopic gastric mucosa in Meckel's diverticulum ^[9]

Pre-medication with H2 blocker → ↑ uptake, ↓ release of tracer at gastric mucosa → improves sensitivity ( > 80%) ^[9]

Positive scan: A focus of radiotracer uptake in the RLQ that appears at the same time as gastric uptake (both contain gastric mucosa)

• Cross-sectional imaging of the small bowel with oral contrast (to distend the lumen) ± IV contrast
• Indication: Suspected small bowel pathology (tumour, Crohn's stricture, NSAID ulcers) when capsule endoscopy is contraindicated or inconclusive ^[4]
• Do CT/MR enterography beforehand to rule out strictures before capsule endoscopy ^[4]
• MR enterography preferred in young patients (no radiation) and Crohn's (excellent for assessing transmural disease)

4-quadrant submucosal injection technique: Inject 0.5–1 mL aliquots of 1:10,000 adrenaline around the bleeding point in all four quadrants → creates a tamponade cushion while the vasoconstriction takes effect ^[2]

Why APC is ideal for angiodysplasia: Angiodysplastic lesions are superficial (submucosal vessels) in thin-walled colon (especially caecum). APC delivers energy to a controlled, shallow depth → coagulates the abnormal vessels without burning through the full thickness of the colonic wall.