"Haemorrhoids: abnormal engorgement and prolapse of the anal vascular cushions" ^[3]

Pathophysiology:

• Degeneration of supporting fibroelastic tissues and smooth muscles → anal cushions are displaced caudally → dilation and engorgement of the arteriovenous plexuses → prolapse ^[3].
• This is a degenerative sliding theory — not simply venous congestion.
• Acute thrombosis can occur: the prolapsed, engorged tissue becomes incarcerated → venous outflow obstruction → thrombosis → painful, large, swollen, irreducible mass with marked anal sphincter contraction ^[3].

Risk factors:

• Aging (degeneration of connective tissue)
• Sitting on the toilet for prolonged periods
• Increased intra-abdominal pressure: constipation, chronic cough, ascites, pregnancy, obesity ^[1][3]
• Genetic predisposition ^[3]
• Low-fibre diet ^[1]

Types:

Grading of Internal Haemorrhoids:

Definition: A tear in the anoderm distal to the dentate line — one of the most common anorectal conditions ^[1][7].

Pathophysiology:

1. Stretching of anal mucosa beyond its normal capacity (e.g. passage of hard stool, prolonged diarrhoea, vaginal delivery, anal intercourse) ^[1]
2. Repeated injury → spasm of the exposed internal sphincter muscle beneath the tear
3. Spasm pulls the edges of the fissure apart → impairs healing
4. Ischaemia secondary to reduced perfusion — the anoderm at the posterior midline has the poorest blood supply of any quadrant in the anal canal (this is why > 90% of fissures are posterior) ^[1]
5. Increased anal pressure from sphincter spasm → further reduces perfusion → a vicious cycle of ischaemia, pain, spasm, and failed healing

Aetiology:

• Primary: Local trauma — hard stools, prolonged diarrhoea, vaginal delivery, anal sex ^[1]
• Secondary: IBD (especially Crohn's), granulomatous disease (TB, sarcoidosis), malignancy (SCC of anus, leukaemia), STDs (HIV, syphilis, chlamydia) ^[1]

Why are lateral or multiple fissures a red flag? A typical (primary) fissure is single and posterior midline because of the poor blood supply posteriorly. If the fissure is lateral, anterior, or multiple → suspect a secondary cause (Crohn's disease, TB, anal cancer, HIV).

Clinical features:

• Pain on defaecation — tearing pain with passage of bowel movements ^[1][7]
• Fresh rectal bleeding — limited to a small amount on toilet paper or surface of stool ^[1][7]
• Perianal pruritus or skin irritation
• Diagnosis is by spreading the buttocks to reveal the fissure ^[7]
• Rectal examination and proctoscopy are painful and not indicated in the acute setting ^[7]

Acute vs Chronic:

• Acute: Typically heals within 6 weeks with conservative management
• Chronic: Fails conservative management; may show a sentinel pile (skin tag at the external end) and hypertrophied anal papilla at the internal end; requires more aggressive approach (GTN, diltiazem, botox, lateral internal sphincterotomy)

Pathology:

• Squamous cell carcinoma — below dentate line (80%) ^[3]
  • Anal intraepithelial neoplasia (AIN) is the pre-malignant lesion
• Adenocarcinoma — above dentate line (10%) ^[3]
• Others: melanoma

Risk factors:

• HPV infection (90%): especially HPV-16 and HPV-18 ^[3][7]
• HIV infection ^[3]
• Anal intercourse, sexually transmitted diseases ^[7]
• Smoking, immunocompromised states, Crohn's disease ^[3]

Clinical features:

• Painful PR bleeding ^[3][7]
• Presented with bleeding, pain and anal mass ^[7]
• Pruritus
• Signs: palpable mass and its distance from anal verge, lymphadenopathy (superficial inguinal LN if tumour below dentate line because lymphatic drainage below the dentate line goes to inguinal nodes) ^[3]

• Definition: Protrusion of the rectal wall through the anus — complete (all layers) or partial (mucosa only) ^[1]
• More common in elderly women ^[1]
• Risk factors: chronic straining/constipation/diarrhoea, pelvic floor dysfunction, multiparity, prior pelvic surgery, dementia, stroke ^[1]
• Can cause PR bleeding (from mucosal trauma/ulceration), mucus discharge, faecal incontinence (75%), and incomplete evacuation ^[1]
• Must differentiate from prolapsed internal haemorrhoids (haemorrhoids have radial folds; prolapse has concentric circular folds)

• Acute haemorrhagic rectal ulcer — more common in Asia ^[5]
• Typically in elderly, critically ill, and bedridden patients ^[5]
• Presents with sudden severe painless bleeding ± shock ^[5]
• Bedside proctoscopy may reveal bleeding ulcer ^[5]
• Treatment: packing of adrenaline-soaked gauze, suture plication, endoscopic electrocoagulation ^[5]

Also includes solitary rectal ulcer syndrome (SRUS) — associated with rectal prolapse and straining; chronic, often with mucus and blood on the stool surface.

• Due to portal hypertension — portosystemic shunt between superior rectal veins (portal) and inferior rectal veins (systemic) ^[2][6]
• Not the same as haemorrhoids (which are submucosal arteriovenous cushions)
• Often presents with severe bleeding ^[2][6]
• Management: injection sclerotherapy (local), TIPS if uncontrolled ^[2][6]

"Commonest cause of LGIB" ^[2][5][8]

• ~17% of patients with diverticulosis will bleed ^[2][5][8]
• Ruptured vasa recta into the diverticulum ^[5][8]
• Bleeding usually from a single diverticulum ^[5]

Pathophysiology of diverticulosis:

1. Bowel wall weakening with aging + increased intraluminal pressure (e.g. constipation) ^[3]
2. The sigmoid colon has the narrowest lumen → highest wall pressure due to Laplace's law (Pressure = Tension / Radius; smaller radius = higher pressure for same wall tension) ^[3]
3. The colon wall has only one layer of full-thickness longitudinal muscle arranged in three taeniae coli → the weakest point is where vasa recta penetrate the circular muscle ^[3]
4. Mucosa and submucosa herniate through these weak points → false diverticula (true diverticula involve all layers; colonic diverticula are almost always false)
5. The rectum is never affected because its outer smooth muscle layer encompasses the full circumference ^[3]

Site:

• Right-sided in Asia, sigmoid in Western countries ^[1][3]
• Right-sided diverticula have a higher risk of haemorrhage (thinner wall of caecum/ascending colon → more vulnerable vasa recta) ^[1]

Clinical features:

• Painless massive PR bleeding (painless haematochezia of variable severity) ^[2][3][5][8]
• Bleeding stops spontaneously in 80–85% but rebleeding ~20–30% ^[5][8]
• The blood may be bright red (left-sided source) or dark/maroon-coloured mixed with stool (right-sided source)

Risk factors for diverticular disease:

• Age (rare before 30y) ^[3]
• Low-fibre diet ^[1][3]
• Obesity ^[1][3]
• Increased intraluminal pressure: constipation ^[3]
• Drugs: NSAIDs, steroids, opiates ^[1][3]
• Decreased physical activity ^[1]
• Connective tissue disease (e.g. Marfan's, Ehlers-Danlos) ^[3]

"Most common vascular cause of LGIB; most common in age > 65" ^[1][2]

Pathophysiology:

• Dilated, tortuous submucosal vessels ^[1][2]
• Walls composed of endothelial cells lacking smooth muscle ^[1]
• Acquired degenerative condition — thought to arise from chronic, low-grade obstruction of submucosal veins where they penetrate the muscle layers of the colon → progressive dilation → incompetent precapillary sphincters → arteriovenous communications ^[1]
• Most commonly found in the caecum or ascending colon ^[1][2]

Associations:

• Osler-Weber-Rendu disease (Hereditary Haemorrhagic Telangiectasia, HHT) — autosomal dominant, mucocutaneous telangiectasias + visceral AVMs ^[2]
• Aortic stenosis (Heyde syndrome) — acquired von Willebrand factor type 2A deficiency due to shear-induced degradation of high-molecular-weight vWF multimers across the stenotic valve → ↑bleeding from angiodysplastic lesions ^[2]

Clinical features:

• Usually painless haematochezia of variable severity ^[2]
• Bleeding is venous in origin → tends to be less massive than diverticular bleeding ^[1]
• Mostly self-limiting (85–90%) but rebleeds in 25–85% ^[2]
• Often occult, manifesting as FOBT +ve stools or iron deficiency anaemia ^[1]

"~10% of PR bleed in > 50y" ^[2]

Epidemiology in Hong Kong:

• 1st most common cancer overall (and in males), 2nd in females ^[4]
• Incidence: 74.1/100,000/year; mortality: 28.5/100,000/year ^[4]
• M:F = 1.6:1; peak incidence 60–70y ^[4]
• Rectosigmoid most common site (~70% left-sided) ^[4]

Pathophysiology of bleeding:

• Tumour outgrows its blood supply → central necrosis → overlying erosion or ulceration → exposed vessels bleed ^[2]
• Usually low-grade, intermittent bleeding — may present with iron-deficiency anaemia or FOBT +ve ^[2]

Risk factors (abbreviated):

• Non-modifiable: Age > 50, male, family history, polyposis syndromes (FAP, HNPCC/Lynch), IBD, prior CRC or polyps ^[4]
• Modifiable: Red/processed meat, animal fat, obesity, smoking, alcohol, physical inactivity ^[4]
• Protective: High-fibre diet, NSAIDs/aspirin, physical activity, calcium/vitamin D ^[4]

Clinical features suggesting CRC (red flags):

• Change in bowel habit (alternating diarrhoea and constipation) ^[3][5]
• Change in stool calibre (pencil-thin stools) ^[3]
• Tenesmus (feeling of incomplete evacuation — suggests rectal mass) ^[3]
• Constitutional symptoms: loss of appetite, loss of weight, malaise ^[2]
• Blood mixed with stool ^[5]
• Family history of CRC ^[3][5]
• Metastatic symptoms: jaundice, bone pain, dyspnoea ^[2]

• Fresh outlet-type bleed, perianal mass / pain, constipation, risk factors (e.g. pregnancy) ^[3]
• Distinguishing features: Blood is bright red, drips into toilet bowl or stains tissue paper, typically occurs during or immediately after defaecation. Internal haemorrhoids → painless; thrombosed external → painful blue/purple perianal mass ^[3][9]
• Why it bleeds: Engorgement of anal vascular cushions → arterial bleeding from the arteriolar component of the cushion (this is why the blood is bright red, not dark venous blood) ^[3]
• Trap: Haemorrhoids are so common (4.4% prevalence) that they may coexist with a more sinister pathology. Never attribute PR bleeding solely to haemorrhoids without excluding other sources, especially in patients with red flags ^[1][3]

• History of constipation; severe sharp pain upon defecation ^[9]
• Distinguishing features: The key discriminator is pain — tearing, burning pain that occurs during and may persist for hours after defaecation. Blood is typically a small amount, bright red, on paper or stool surface ^[1]
• Why it hurts so much: The tear is below the dentate line → somatic innervation (inferior rectal nerve) → exquisite pain. Internal sphincter spasm perpetuates the cycle ^[1]
• Typical vs atypical: Single posterior midline fissure = typical/primary. Multiple, lateral, or anterior fissures → think secondary causes (Crohn's, TB, HIV, anal SCC) ^[1]

• Presented with bleeding, pain and anal mass ^[5]
• Risk factors: anal intercourse, sexually transmitted diseases, infection with HPV ^[5]
• Distinguishing features: Persistent, progressive symptoms. A palpable mass on DRE. Inguinal lymphadenopathy (lymphatic drainage below dentate line → superficial inguinal LN). Usually in patients with risk factors (HPV, HIV, immunosuppression) ^[3][5]

• More common in Asia; elderly, critically ill, bedridden patients ^[5]
• Sudden severe painless bleeding ± shock ^[5]
• Distinguishing features: The clinical context is key — this is a patient in ICU or nursing home, not an ambulatory outpatient. Diagnosis made by bedside proctoscopy revealing a bleeding ulcer ^[5]
• Also consider solitary rectal ulcer syndrome (SRUS) — associated with rectal prolapse and chronic straining; presents with mucus, blood, and tenesmus

• Due to portal hypertension → portosystemic shunt between superior and inferior rectal veins ^[2]
• Distinguishing features: Clinical context of chronic liver disease (jaundice, spider naevi, ascites, splenomegaly). Often presents with severe bleeding ^[2]. Must differentiate from haemorrhoids — rectal varices are submucosal venous channels in the rectum proper, whereas haemorrhoids are vascular cushions in the anal canal
• Why it bleeds: High portal pressure → distension of collateral veins → thin-walled varices → rupture

• Prolapsing mass with concentric circular folds (cf. haemorrhoids which have radial folds)
• Can cause PR bleeding from mucosal trauma/ulceration
• Usually in elderly women with pelvic floor dysfunction ^[1]

• Painless, usually profuse haematochezia (not chronic) ^[2][9]
• DDx: angiodysplasia, severe colitis, rectal ulcer, small bowel bleeding, UGIB ^[8]
• Distinguishing features: Sudden onset of painless, often profuse bleeding in an elderly patient. No preceding change in bowel habit, no constitutional symptoms, no fever (diverticular bleeding ≠ diverticulitis) ^[1][2]
• Blood may be dark/maroon-coloured if right-sided (common in Asia) or bright red if left-sided ^[1][9]
• Bleeding stops spontaneously in 80–85% but rebleeding ~20–30% ^[2][5][8]
• ~17% of patients with diverticulosis will bleed ^[2][8]
• Key differentiator from angiodysplasia: Diverticular bleeding is arterial (from ruptured vasa recta) → tends to be more profuse. Angiodysplasia is venous → tends to be less severe but more intermittent ^[1][2]

• Usually in elderly, may be associated with vascular malformations (e.g. HHT) and aortic stenosis ^[2][9]
• Painless, less severe than diverticular but tends to be intermittent ^[2][9]
• Distinguishing features: Recurrent episodes of painless bleeding in an elderly patient; often presents as occult bleeding with iron-deficiency anaemia and FOBT +ve rather than massive haematochezia ^[1]
• Associations to look for:
  • Aortic stenosis (Heyde syndrome) — acquired type 2A vWD from shear-induced degradation of high-MW vWF multimers across the stenotic valve ^[2][3]
  • Hereditary Haemorrhagic Telangiectasia (Osler-Weber-Rendu) — look for telangiectasias on lips, oral mucosa, fingertips ^[2]
  • ESRD, von Willebrand disease ^[3]
• Colonoscopy appearance: cherry red spots ^[3]
• Angiography appearance: "mother-in-law phenomenon" (early filling, delayed emptying — the lesion fills quickly and empties slowly, like a mother-in-law who comes early and stays late) ^[3]

• > 50y, male, smoker, FHx, Hx of IBD, polyps and colorectal CA ^[2][9]
• Alternating diarrhoea and constipation, pencil-thin stools, tenesmus ^[2][9]
• Loss of appetite, loss of weight, malaise ^[2][9]
• Intractable pain, jaundice/LUQ pain, dyspnoea, bone pain (metastatic features) ^[9]
• Distinguishing features: PR bleeding that is low-grade and intermittent (not massive and acute), associated with progressive change in bowel habit and constitutional symptoms ^[2]. May present with iron-deficiency anaemia or FOBT +ve only. This is the one you must not miss ^[2][9]

Right-sided vs Left-sided CRC — different presentations:

^[4][10]

The mnemonic "Right side bleeds, Left side blocks" captures this nicely ^[10].

All forms of colitis can cause PR bleeding, but they have distinct patterns:

• Iatrogenic — occurs after colonoscopic polypectomy ^[5]
• Can be immediate (during procedure) or delayed (up to 2 weeks post-procedure)
• Important to ask about recent endoscopy/polypectomy in the history ^[2][5]
• Usually self-limiting but may require endoscopic re-intervention

• The absolute first "investigation" — costs nothing, takes 30 seconds
• Confirm haematochezia; look for anorectal pathologies ^[9]
• What you can find: stool colour (fresh blood, melena, normal), palpable mass (rectal CA — note distance from anal verge), anal tone assessment, prostate/rectovaginal septum, tenderness, induration ^[3]

• Exclusion of bleeding from anorectal disorders ^[1][2]
• Visualises the anal canal and lower rectum (~7–8 cm)
• Best way to diagnose internal haemorrhoids (1st/2nd degree may not be palpable on DRE) at 3, 7, 11 o'clock positions ^[3]
• Bedside proctoscopy may reveal bleeding ulcer in acute haemorrhagic rectal ulcer ^[5]
• For intermittent/episodic PR bleeding: bedside examination with proctoscopy for anorectal pathology ^[5]

• Bile-stained aspiration without blood → bleeding from upper GI tract excluded ^[2][9]
• Why bile must be present: if the aspirate is clear (no bile), it may mean the tube tip is not in the duodenum — a duodenal source could still be bleeding distally without refluxing into the stomach
• A bloody aspirate = UGIB confirmed → proceed to OGD
• Limitation: Cannot definitively exclude a duodenal source if aspirate is non-bilious and non-bloody

This is the cornerstone investigation for PR bleeding in haemodynamically stable patients.

Advantages ^[1]:

• Localisation of bleeding is accurate regardless of the aetiology or rate of bleeding
• Ability to collect pathological specimens for diagnosis (biopsy)
• Ability for therapeutic intervention

Disadvantages ^[1]:

• Requires bowel preparation and has poor visualisation in unprepared colon
• Risks of sedation in an acutely bleeding patient
• Low diagnostic yield in massive bleeding (poor visualisation from blood obscuring the field) ^[3]

Key Endoscopic Findings by Diagnosis:

Endoscopic therapeutic modalities (especially effective for angiodysplasia and diverticular disease) ^[2][5][9]:

Stigmata of recent haemorrhage (SRH) — endoscopic findings that indicate the diverticulum or lesion has recently bled and may re-bleed ^[3]:

• Active bleeding (spurting or oozing)
• Non-bleeding visible vessel
• Adherent clot

These are the same Forrest classification concepts used in UGIB, adapted for LGIB.

• Indicated if bleeding source is not identified on colonoscopy ^[1]
• Generally prefer OGD before colonoscopy if there is any clinical suspicion of UGIB ^[2][9]
• In the lecture algorithm: for unstable patients, consider UGI endoscopy unless CTA has already located the site of bleeding ^[5]
• Critical in patients with haemodynamic instability + haematochezia (10–15% will have UGIB source)

Why CTA before colonoscopy in unstable patients? An unstable patient cannot tolerate bowel preparation or the prolonged sedation required for colonoscopy. CTA is fast (minutes), requires no bowel prep, and can be done simultaneously with resuscitation. It provides a "roadmap" for subsequent transcatheter embolisation or surgery.

Two main techniques — both are screening tools to confirm and localise bleeding, particularly useful for intermittent or obscure bleeding ^[1][13]:

Diagnostic criteria for a positive RBC scan ^[13]:

• Activity conforms to intestinal anatomy
• Intensity increases with time
• Activities move (anterograde or retrograde) within the bowels

Why is the RBC scan preferred over angiography for initial detection? Because it is more sensitive (0.1–0.4 mL/min vs 0.5–1.0 mL/min), less invasive, and can image over 24 hours to catch intermittent bleeding ^[13]. However, its poor localisation means that if positive, you often still need angiography or colonoscopy to pinpoint the exact source.

Rubber Band Ligation (RBL) ^[3]:

• Apply rubber bands to strangulate the pile by Barron's bander → ischaemic necrosis of piles → slough off within 10 days
• Efficacy: 70% resolve, 30% recur
• Administration: up to 3 bandings at ≥ 1 cm above dentate line (must be above dentate line because below = somatic innervation = excruciating pain)
• Indication: symptomatic Grade II/III internal haemorrhoids
• Complications: pain, bleeding (7–10 days post-banding due to sloughing of ligated haemorrhoids)
• Contraindications: anticoagulant use, immunocompromised (risk of post-banding sepsis)

Sclerotherapy ("Mitchell") ^[3]:

• 5% phenol in almond oil injected submucosally → creates fibrosis → obliterates vascular channels and fixes position
• Largely abandoned now: risk of allergy to nuts and intraprostatic injection ^[3]

Haemorrhoidal Artery Ligation Operation (HALO) ^[3]:

• May be Doppler-guided (DG-HALO) to identify feeding vessels
• Mainly for bleeding symptoms, indicated for Grade II/III haemorrhoids
• Lowest post-op complications, but highest recurrence rate ^[3]

Indications:

• Grade III/IV internal haemorrhoids
• Symptomatic internal/external haemorrhoids refractory to other treatments

Approaches:

• 3-leaf clover excision pattern: avoid circumferential excision — prone to stenosis ^[3]
• Efficacy: 95% resolve ^[3]
• Pre-op preparation: stool softener, enema ^[3]
• Position: prone jackknife or lithotomy ^[3]
• Anaesthesia: perianal / spinal / general ^[3]

Complications:

• Pain (~100% due to internal anal sphincter spasm) ^[3]
• Urinary retention — caused by pain and anal spasm, fluid overload, rectal packing, drugs (narcotics, anticholinergics), pre-existing outflow tract obstruction ^[3]
• Faecal incontinence, anal fissure, anal stenosis ^[3]