Lower Gi Bleed
Lower gastrointestinal bleeding is hemorrhage originating distal to the ligament of Treitz, most commonly from colonic sources such as diverticulosis, angiodysplasia, or colorectal neoplasms.
Lower gastrointestinal bleeding (LGIB) refers to bleeding originating from the gastrointestinal tract distal to the ligament of Treitz (the duodenojejunal flexure) [1][2][3]. In practice, LGIB encompasses bleeding from the jejunum, ileum, colon, rectum, and anus — though the vast majority arises from colonic sources.
The ligament of Treitz ("Treitz" = named after Czech anatomist Václav Treitz) is the suspensory ligament/muscle that fixes the duodenojejunal junction to the diaphragm. It serves as the anatomical landmark dividing upper GI bleeding (proximal) from lower GI bleeding (distal).
Key Terminology
| Term | Definition | Mechanism / Notes |
|---|---|---|
| Haematochezia | Passage of bright red blood or blood clots per rectum | Blood has not been significantly altered by digestive enzymes; implies a distal or rapidly bleeding source |
| Melaena | Black, tarry, foul-smelling stool | Blood oxidised by gastric acid and bacterial degradation over time; typically from UGIB but can rarely occur with slow right-sided colonic bleeding |
| Occult bleeding | Not visible to the naked eye; detected by FOBT or iron deficiency anaemia | Chronic, low-volume ooze |
| Overt bleeding | Visible blood in stool (haematochezia or melaena) | Higher volume or more acute source |
- Bright red blood → usually left colon, rectum, or anus (short transit time, minimal degradation)
- Dark/maroon blood mixed with stool → usually right colon or small bowel (longer transit, partial degradation)
- Haematochezia can occur in massive UGIB — when bleeding rate is so high that blood transits the entire bowel before it can be degraded [2][3]
- Annual incidence: 20–27 per 100,000 population [1][3]
- Age: Predominantly affects the elderly, with incidence increasing significantly with age (the majority of cases occur in patients > 60 years old) [1][3]
- Why? The two most common causes — diverticular disease and angiodysplasia — are degenerative conditions that accumulate with age
- Sex: Slight male predominance overall
- Mortality: Lower than UGIB (2–4% vs 6–10% for UGIB), but can be significant in elderly patients with comorbidities
- Self-limiting: Approximately 80–85% of LGIB episodes stop spontaneously [1], but rebleeding rates are significant (14–38% for diverticular bleeding)
- Hospitalisation trend: Increasing due to ageing population and rising use of antithrombotic agents
Hong Kong–Specific Epidemiology
- In Hong Kong (and Asia generally), diverticulosis has a significantly higher proportion of right-sided disease compared to Western countries where left-sided (sigmoid) predominates [2][5][6]
- Right-sided diverticula carry a higher risk of haemorrhage (thinner wall on the right side of the colon) [1][3]
- Right-sided diverticular disease in Asian patients is often confused with acute appendicitis when it presents with RLQ pain [5][6]
- Colorectal cancer remains a top 2 cancer in Hong Kong — always consider malignancy in any patient with LGIB, especially if > 50 years old
- Prevalence of H. pylori infection in Hong Kong is falling but still relevant (some LGIB patients actually have a missed UGIB from peptic ulcer disease)
| Risk Factor | Mechanism / Relevance |
|---|---|
| Advanced age ( > 60) | Degenerative vascular changes (angiodysplasia), increased prevalence of diverticulosis, higher use of anticoagulants |
| NSAIDs / Aspirin | Inhibit COX → ↓ prostaglandins → ↓ mucosal protection + impaired platelet function → ↑ bleeding risk. Can also cause small bowel ulcers (NSAID enteropathy) [3][7] |
| Anticoagulants / Antiplatelets | Warfarin, DOACs, clopidogrel — impair haemostasis, prolong bleeding from any lesion [3] |
| Obesity | ↑ intra-abdominal pressure → promotes diverticular formation; also associated with chronic inflammation |
| Hypertension, IHD, Hyperlipidaemia | Vascular risk factors predispose to angiodysplasia and ischaemic colitis [2] |
| Chronic kidney disease / ESRD | Associated with angiodysplasia (uraemic platelet dysfunction), also associated with heparin use during dialysis [4] |
| Low-fibre diet | ↑ intraluminal pressure → promotes diverticular formation (Laplace's law) [5][6] |
| Constipation | Straining → ↑ intraluminal pressure → diverticula; also worsens haemorrhoids |
| Previous radiation therapy (abdominal/pelvic) | Radiation proctitis/colitis — damages endothelium, causes telangiectasia [2][3] |
| History of IBD | Chronic mucosal inflammation → friable, ulcerated mucosa → bleeding |
| Connective tissue disease (e.g. Marfan's, Ehlers-Danlos) | Weakened colonic wall → ↑ diverticular formation [5] |
| Steroids | Impair wound healing, thin mucosa [5][6] |
| Portal hypertension / Liver disease | Rectal varices, coagulopathy, thrombocytopaenia |
Anatomy and Function
Understanding the vascular anatomy of the colon is essential for understanding why certain locations bleed and why certain areas are vulnerable to ischaemia.
| Segment | Arterial Supply | Origin |
|---|---|---|
| Caecum, ascending colon, proximal 2/3 transverse colon | Superior mesenteric artery (SMA) → ileocolic, right colic, middle colic arteries | Midgut |
| Distal 1/3 transverse colon, descending colon, sigmoid colon | Inferior mesenteric artery (IMA) → left colic, sigmoid arteries, superior rectal artery | Hindgut |
| Rectum | Superior rectal (IMA), middle rectal (internal iliac), inferior rectal (internal pudendal) | Dual supply |
- Marginal artery of Drummond: Continuous anastomotic arcade along the mesenteric border of the colon connecting SMA and IMA territories [7]
- Arc of Riolan (meandering mesenteric artery): A more proximal anastomosis between SMA and IMA — variable presence
- Griffiths' point (splenic flexure): Junction between SMA (middle colic artery) and IMA (left colic artery) territories — the collateral here via the marginal artery can be tenuous [7]
- Sudeck's point (rectosigmoid junction): Junction between the last sigmoid artery (IMA) and the superior rectal artery — poor collateral flow [7]
These watershed areas are clinically important because they are most susceptible to ischaemic colitis during low-flow states (e.g. hypotension, cardiac surgery, aortic surgery).
- The vasa recta ("straight vessels") are the terminal arteries that penetrate the circular muscle layer of the colonic wall to supply the mucosa and submucosa
- Diverticula form where vasa recta penetrate the muscularis propria — this is the weakest point of the colonic wall [5][6]
- As diverticula herniate outward, the vasa recta become draped over the dome of the diverticulum, separated from the bowel lumen only by a thin layer of mucosa → predisposes to arterial rupture into the lumen = diverticular bleeding [2]
| Region | Venous Drainage |
|---|---|
| Above dentate line | Portal venous system (superior rectal veins → inferior mesenteric vein → portal vein) |
| Below dentate line | Systemic venous system (middle and inferior rectal veins → internal iliac vein → IVC) |
This dual venous drainage explains why portal hypertension can cause rectal varices (not haemorrhoids — rectal varices and haemorrhoids are distinct entities) via engorgement of the portosystemic anastomosis at the rectum.
The dentate line divides the anal canal into upper 2/3 and lower 1/3 — this is a critical landmark:
| Feature | Above Dentate Line | Below Dentate Line |
|---|---|---|
| Embryology | Endoderm | Ectoderm |
| Epithelium | Columnar (→ adenocarcinoma) | Stratified squamous (→ SCC) |
| Nerve supply | Autonomic (visceral — dull, poorly localised pain) | Somatic (inferior rectal nerve — sharp, well-localised pain) |
| Venous drainage | Portal system (superior rectal veins) | IVC system (middle & inferior rectal veins) |
| Lymphatic drainage | Internal iliac / inferior mesenteric LN | Superficial inguinal LN |
Clinical Pearl
This is why internal haemorrhoids (above the dentate line) are typically painless (visceral innervation) while external haemorrhoids and anal fissures (below the dentate line) are exquisitely painful (somatic innervation).
Etiology (with Focus on Hong Kong)
The causes of LGIB can be organised anatomically:
| Source | Cause | Approx. Frequency |
|---|---|---|
| Massive UGIB | Peptic ulcer, variceal bleed | < 10% [1][3] |
| Large bowel (vast majority) | Diverticular disease | 17–40% (most common) |
| Angiodysplasia | 2–30% | |
| Colitis (infective, inflammatory, ischaemic, radiation) | 9–21% | |
| Neoplasm (carcinoma, large polyps, post-polypectomy) | 7–33% | |
| Small bowel (~5%) | Meckel's diverticulum, angiodysplasia, small bowel tumours, NSAID-induced ulcers, Crohn's, TB enteritis, aortoenteric fistula | ~5% |
| Anorectal (~10%) | Haemorrhoids, fissure-in-ano, anal/rectal ulcers, rectal varices | ~10% |
Sources marked with asterisks in senior notes can present with heavy/massive bleeding [1][3]
Now let's go through each cause in detail:
1. Diverticular Bleeding (Most Common Cause of LGIB Overall)
"Diverticulum" → Latin: di- (apart) + vertere (to turn) = "a turning aside" — an outpouching of the bowel wall.
- Diverticulosis = presence of multiple diverticula (sac-like outpouchings of the colonic wall)
- 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]
- 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]
- 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]
- 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]
2. Angiodysplasia (Most Common Cause in Age > 65)
"Angiodysplasia" → angio- (vessel) + dys- (abnormal) + -plasia (formation) = abnormal formation of blood vessels.
- 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]
3. Haemorrhoids (Most Common Cause in Age < 50)
"Haemorrhoid" → Greek: haima (blood) + rhoos (flowing) = "blood flow" — dilated vascular cushions.
- 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]
| Grade | Description |
|---|---|
| 1st degree | Bleeding only, no prolapse |
| 2nd degree | Prolapse at defecation, reduces spontaneously |
| 3rd degree | Prolapse requires manual reduction |
| 4th degree | Permanently prolapsed, cannot be reduced |
- 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]
4. Colorectal Cancer (CRC)
- 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]
5. Colitis (Multiple Types)
"Colitis" → colon + -itis (inflammation) = inflammation of the colon.
- 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]
Important
IBD should NOT be misdiagnosed as infectious or ischaemic colitis — the management is fundamentally different (immunosuppression vs antibiotics vs supportive care) [2].
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]
| Cause | Notes |
|---|---|
| Meckel's diverticulum | Remnant of omphalomesenteric (vitelline) duct; "Rule of 2s": ~2% population, ~2 feet from ileocaecal valve, ~2 inches long, 2% symptomatic; 50% contain ectopic gastric mucosa (approaches 100% if bleeding); most common cause of LGIB in children [9] |
| Angiodysplasia | Can occur in small bowel as well as colon |
| Small bowel tumours | GISTs, lymphoma, adenocarcinoma, carcinoid |
| NSAID-induced small bowel ulcers | NSAID enteropathy — separate mechanism from peptic ulcers [3][7] |
| Crohn's disease | Transmural inflammation → ulceration → bleeding |
| TB enteritis | Important in HK endemic setting |
| Aortoenteric fistula | Communication between aortic graft (after AAA repair) and duodenum/small bowel → "herald bleed" followed by massive exsanguination — a surgical emergency [1][3] |
Meckel's Diverticulum
Meckel's scan uses 99mTc-pertechnetate which is taken up by ectopic gastric mucosa via the sodium-iodide symporter (NIS). Pre-medication with an H2 blocker increases uptake but decreases release of the tracer from gastric mucosa → improves sensitivity ( > 80%) [9].
| Cause | Features |
|---|---|
| Haemorrhoids | Most common anorectal cause (see above) |
| Fissure-in-ano | Longitudinal tear in anoderm below dentate line → severe sharp pain on defecation + small amount bright red blood; usually posterior midline; associated with constipation [3] |
| Anal/rectal ulcers | Solitary rectal ulcer syndrome (from rectal prolapse/straining), stercoral ulcers (from faecal impaction) |
| Rectal varices | Associated with portal hypertension — engorged portosystemic collaterals at the rectum; can present with heavy bleeding [1][3] |
| Dieulafoy's lesion | Abnormally large submucosal artery that erodes through the mucosa → massive bleeding from a tiny mucosal defect; can occur in the rectum [2] |
| Post-polypectomy bleeding | Iatrogenic — occurs after colonoscopic polypectomy; early (within 24h) or delayed (up to 2 weeks) |
Classification
| Type | Definition |
|---|---|
| Acute LGIB | Recent onset ( < 3 days) of visible blood per rectum ± haemodynamic compromise |
| Chronic LGIB | Slow, intermittent passage of blood over days to weeks |
| Occult LGIB | No visible bleeding; detected by FOBT positivity or iron deficiency anaemia |
| Severity | Features |
|---|---|
| Mild | Usually mixed with stool; haemodynamically stable; anorectal pathologies, CRC, mild colitis |
| Moderate | Significant bleeding requiring fluid resuscitation; tachycardia but responsive |
| Massive/Severe | Haemodynamic instability (hypotension, tachycardia, altered consciousness); often from diverticular disease, angiodysplasia, ischaemic colitis, rectal varices, Meckel's diverticulum [1][3] |
| Source | Approximate % | Common Causes |
|---|---|---|
| Large bowel | ~85% | Diverticular disease, angiodysplasia, colitis, CRC |
| Anorectal | ~10% | Haemorrhoids, fissures, rectal varices |
| Small bowel | ~5% | Meckel's, angiodysplasia, Crohn's, NSAID ulcers |
| UGIB presenting as haematochezia | < 10% | Peptic ulcer, variceal bleed |
Clinical Features
Symptoms (with Pathophysiological Basis)
The nature and relationship of blood to stool is one of the most important features to characterise:
| Pattern | Likely Source | Mechanism |
|---|---|---|
| Blood mixed with stool | Proximal to sigmoid colon (right colon, transverse colon) | Blood is mixed during colonic transit and formed into stool |
| Blood on surface of stool / separate from stool | Rectum or anus (outlet-type) | Blood is added after stool is formed |
| Blood on toilet paper only | Near anal margin (fissure, low haemorrhoid) | Minimal bleeding from superficial source |
| Blood after defecation / dripping into toilet | Haemorrhoids | Straining → engorgement → mucosal erosion → arterial ooze that continues after passage of stool |
| Blood by itself (torrential) | Diverticular disease, angiodysplasia, Meckel's diverticulum | Brisk arterial (diverticular) or venous (angiodysplasia) bleeding overwhelms stool formation |
| Bloody diarrhoea | Colitis (IBD, infective, ischaemic) | Mucosal inflammation → impaired absorption → diarrhoea + mucosal erosion → bleeding |
| Cyclical pattern | GI endometriosis | Ectopic endometrial tissue in bowel wall bleeds with menstrual cycle [4] |
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
| Pain Pattern | Likely Cause | Mechanism |
|---|---|---|
| Painless massive haematochezia | Diverticular bleeding, angiodysplasia | Vasa recta rupture or AVM bleeding does not involve inflammation of the bowel wall |
| Cramping/colicky pain relieved by defecation | Symptomatic uncomplicated diverticular disease (SUDD) | Muscular spasm of the thickened colonic wall |
| Sudden cramping abdominal pain followed by rectal bleeding ≤ 24h | Ischaemic colitis | Ischaemia → mucosal injury → pain → reperfusion → mucosal sloughing → bleeding |
| Severe sharp pain on defecation | Anal fissure | Tearing of anoderm (somatic innervation below dentate line) |
| Lower abdominal pain + fever + leucocytosis (clinical triad) | Diverticulitis (usually NOT a cause of major LGIB) | Faecolith obstruction → bacterial overgrowth → inflammation [5] |
| Diffuse abdominal pain with bloody diarrhoea | IBD, infective colitis | Widespread mucosal inflammation |
| Intense pain out of proportion to findings | Mesenteric ischaemia | Intestinal infarction with visceral peritoneal involvement; initially poorly localised |
- 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
| Symptom | Suggests | Why |
|---|---|---|
| Perianal mass/pain | Haemorrhoids (thrombosed), perianal abscess | Thrombosis triggers acute inflammation (somatic nerve territory) |
| Pruritus ani | Haemorrhoids (mucous discharge) | Prolapsed internal haemorrhoids secrete mucus → irritates perianal skin |
| Extra-intestinal manifestations (arthritis, uveitis, skin lesions) | IBD | Immune-mediated systemic inflammation |
| Jaundice, ascites, peripheral oedema | Liver disease → rectal varices/coagulopathy | Portal hypertension + synthetic failure |
| Recurrent dysuria, pneumaturia, faecaluria | Colovesical fistula (from diverticulitis) | Fistula between colon and bladder → air and faeces in urine [5] |
| Previous aortic graft surgery | Aortoenteric fistula | Graft erodes into adjacent duodenum/small bowel |
| History of pelvic/abdominal radiation | Radiation proctitis/colitis | Endothelial damage → telangiectasia |
Signs (with Pathophysiological Basis)
| Sign | Significance | Mechanism |
|---|---|---|
| Pallor (conjunctival, palmar crease) | Anaemia from chronic or acute blood loss | ↓ Hb → ↓ red colouration of skin/mucosae |
| Tachycardia | Early sign of hypovolaemia OR chronic anaemia | Compensatory sympathetic activation to maintain cardiac output |
| Hypotension (SBP < 90 or postural drop > 20 mmHg) | Significant hypovolaemia (class II-III haemorrhagic shock) | ≥ 15–30% blood volume lost → inadequate preload → ↓ stroke volume |
| Prolonged capillary refill ( > 2 sec) | Peripheral vasoconstriction | Sympathetic response to hypovolaemia redirects blood to vital organs |
| Altered mental status | Severe hypovolaemia / shock | ↓ Cerebral perfusion |
| Koilonychia (spoon nails) | Iron deficiency anaemia (chronic LGIB) | Iron required for nail matrix keratin formation |
| Angular stomatitis, glossitis | Iron deficiency anaemia | Rapidly dividing epithelial cells are sensitive to iron deprivation |
| Sign | Significance | Mechanism |
|---|---|---|
| Palpable mass | CRC (caecum/ascending colon mass on the right; sigmoid mass on the left) | Tumour large enough to be palpable through abdominal wall |
| Tenderness (localised) | Diverticulitis (LLQ in Western, RLQ in Asia [5]), ischaemic colitis (over affected segment), infective colitis | Inflammation of the bowel wall → irritation of visceral/parietal peritoneum |
| Hepatomegaly | Liver metastases from CRC, or chronic liver disease (portal hypertension) | Tumour deposits expand the liver; cirrhosis may cause hepatomegaly initially |
| Ascites | Peritoneal carcinomatosis or portal hypertension | Malignant seeding → exudative ascites; portal HTN → transudative ascites |
| Stigmata of chronic liver disease (spider naevi, caput medusae, jaundice) | Liver disease → coagulopathy, portal hypertension → rectal varices | Hepatocyte failure → ↓ clotting factor synthesis; portal hypertension → collateral formation |
| Abdominal distension | Intestinal obstruction (from CRC stricture or diverticular stricture) | Mechanical obstruction → proximal dilation with air and fluid |
Never Forget the DRE
A digital rectal examination is mandatory in every patient presenting with LGIB. It can identify rectal masses (CRC), assess stool colour, detect haemorrhoids, anal fissures, rectal tenderness (proctitis), and assess for blood on the glove.
| Finding | Significance |
|---|---|
| Fresh blood on glove | Confirms active lower GI bleeding |
| Melaena on glove | Suggests UGIB or slow proximal colonic bleed |
| Palpable rectal mass | Rectal carcinoma (hard, irregular, fixed) |
| Anal fissure (usually posterior midline) | Source of painful bleeding, especially with constipation history |
| Internal haemorrhoids | Not typically palpable (soft vascular cushions); assess with proctoscopy |
| Anal canal tenderness | Fissure, thrombosed haemorrhoid, abscess |
| Prostatic abnormalities (in men) | Incidental finding; does not cause LGIB but important for general assessment |
- 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)
Approach to History Taking for LGIB
This is the systematic clinical approach — essentially asking "5 key questions" [3]:
- Presentation: Acute vs chronic? Overt vs occult?
- How is the blood found? Mixed with stool / on surface / on paper / after defecation / by itself
- How heavy? Mild (mixed with stool) vs heavy (by itself)
- Colour? Bright red vs dark red/maroon vs melaena
- Previous episodes? Duration, frequency, previous investigations
- Frequency, consistency, colour
- Mucus → colitis or CRC
- Anorectal symptoms (pain, pruritus) → anorectal pathology
- Red flags for CRC: alternating diarrhoea/constipation, pencil-thin stools, tenesmus, passage of mucus [3]
- Signs of UGIB? (haematemesis, coffee ground vomitus, melaena)
- Abdominal pain? → which painful pathologies?
- Risk factors: > 50y, male, smoker, family history, IBD, polyps [3]
- Bowel habits: as above
- Constitutional symptoms: weight loss, anorexia, malaise
- Signs of spread: intractable pain (sacral nerve invasion), irritative urinary symptoms (bladder invasion), ascites (peritoneal carcinomatosis), jaundice (liver metastases), bone pain, SOB (lung metastases) [3]
- Comorbidities: Cardiopulmonary disease (susceptible to hypoxaemia), HF/RF (fluid overload risk), liver disease (coagulopathy), bleeding disorders [3]
- Drug history: NSAIDs, antiplatelets, anticoagulants, steroids [2][3]
- TOCC: For infective colitis
- Previous radiation: Radiation proctitis
- Previous surgery: Aortic graft (aortoenteric fistula), polypectomy (post-polypectomy bleed)
- Family history: CRC, IBD, bleeding disorders
Nuclear Medicine Imaging for LGIB
Two important nuclear medicine techniques are worth highlighting for LGIB localisation:
- Principle: Patient's own red blood cells are labelled with 99mTc-pertechnetate in vitro (UltraTag kit, labelling efficiency 98%) → re-injected → if there is GI bleeding, labelled RBCs leak into the intestinal lumen → detected on gamma camera
- Diagnostic criteria: (1) Activity conforms to intestinal anatomy, (2) Intensity increases with time, (3) Activities move (anterograde or retrograde) within bowels [9]
- Preferred over angiography for GI bleeding because:
- Limitation: Poor anatomical localisation (bowel is mobile, blood moves intraluminally)
- Principle: 99mTc-pertechnetate is taken up by gastric mucosa (via NIS) → detects ectopic gastric mucosa in Meckel's diverticulum
- Pre-medication with H2 blocker → ↑ uptake, ↓ release → improves sensitivity ( > 80%) [9]
- Clinical indication: Children with LGIB [9]
High Yield Summary
Definition: LGIB = bleeding distal to ligament of Treitz. Presents primarily with haematochezia but 10% of haematochezia is actually from massive UGIB.
Epidemiology: 20–27/100k/year; mainly elderly; 80–85% self-limiting.
Most Common Causes by Age:
- Overall: Diverticular disease (17–40%)
- Age > 65: Angiodysplasia
- Age < 50: Haemorrhoids
- Children: Meckel's diverticulum
Hong Kong Focus: Right-sided diverticula more common in Asia → higher bleeding risk → can mimic appendicitis.
Key Pathophysiology:
- Diverticular bleeding = arterial (vasa recta rupture) → painless, massive, self-limiting (80–85%)
- Angiodysplasia = venous (degenerative AVM) → painless, less massive, intermittent, high rebleed rate
- Ischaemic colitis = watershed area hypoperfusion → cramping pain → bleeding ≤ 24h → non-occlusive (95%)
Blood-Stool Relationship: Mixed with stool = proximal to sigmoid; separate/on surface = outlet; by itself = torrential (diverticular, angiodysplasia).
Red Flags for CRC: > 50y, family history, alternating bowel habits, pencil-thin stools, tenesmus, constitutional symptoms, passage of mucus.
Never forget: DRE in every patient; exclude UGIB (NG tube/OGD) in severe haematochezia; always consider CRC.
Watershed areas: Griffiths' point (splenic flexure), Sudeck's point (rectosigmoid) — vulnerable to ischaemic colitis.
RBC scan: Sensitivity 0.1–0.4 mL/min, delayed imaging up to 24h, detects intermittent bleeding.
Active Recall - Lower GI Bleed (Definition, Epidemiology, Etiology, Clinical Features)
[1] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.3.6 Lower GI Bleeding, p281–285) [2] Senior notes: felixlai.md (Lower GI bleeding section) [3] Senior notes: Ryan Ho GI.pdf (Section 3.1.2 Lower GI Bleeding, p106–109) [4] Senior notes: maxim.md (Section 4.2 LGIB) [5] Senior notes: maxim.md (Diverticular disease section) [6] Lecture slides: Diverticular diseases - Dr. J Tsang.pdf [7] Senior notes: Ryan Ho GI.pdf (Ischaemic Colitis, p146) [8] Senior notes: felixlai.md (Hemorrhoids / Anatomy of anal canal section) [9] Senior notes: Ryan Ho Diagnostic Radiology.pdf (Red Blood Cell Scan p62, Meckel's Scan p63)
Differential Diagnosis of Lower GI Bleeding
The differential diagnosis of LGIB is best approached by thinking systematically about where the blood is coming from (anatomical source) and what is making it bleed (pathological process). Let me walk you through this the way you'd think at the bedside: a patient walks in with blood per rectum — what's on your list, and how do you tell them apart?
Before you dive into colonic causes, remember this:
Do NOT Forget UGIB
Up to 10–15% of patients presenting with haematochezia actually have a massive upper GI source [1][2][3]. A briskly bleeding duodenal ulcer or variceal bleed can transit the entire bowel so fast that blood comes out bright red per rectum. Always consider UGIB in any patient with severe haematochezia, especially if haemodynamically unstable. An NG tube aspirate showing bile confirms the aspirate has reached the duodenum — if it's bile-stained without blood, UGIB is less likely (but not excluded). If non-bilious, it's non-diagnostic [3].
The table below organises every cause you need to know, grouped by anatomical source, with the key distinguishing clinical features and the pathophysiological reason for bleeding [1][2][3][4][5]:
| Anatomical Source | Cause | Approx. % | Key Distinguishing Features | Why It Bleeds (Mechanism) |
|---|---|---|---|---|
| Massive UGIB | Peptic ulcer, variceal bleed | < 10% | Melaena, haematemesis, coffee ground vomitus; consider in severe haematochezia | Arterial erosion (ulcer) or rupture of high-pressure portosystemic collateral (varix) |
| Large bowel | Diverticular disease | 17–40% | Painless, usually profuse haematochezia (not chronic) | Rupture of vasa recta draped over diverticulum dome → arterial bleeding |
| Angiodysplasia | 2–30% | Painless, less severe than diverticular but tends to be intermittent; elderly; may be associated with HHT and aortic stenosis | Degenerative AVM; venous bleeding from dilated submucosal vessels lacking smooth muscle | |
| Colitis — Inflammatory (IBD) | 9–21% (all colitis) | Usually bloody diarrhoea; extra-intestinal manifestations: arthritis, episcleritis/uveitis, erythema nodosum | Chronic immune-mediated mucosal inflammation → friable, ulcerated mucosa | |
| Colitis — Ischaemic | CVS risk factors, acute MI, stroke; sudden cramping pain → bleeding ≤ 24h | Hypoperfusion of watershed areas → mucosal ischaemia → reperfusion injury → sloughing | ||
| Colitis — Infective | Fever, chills, rigors, night sweats, nausea/vomiting, diarrhoea, pain; TOCC, immunosuppression (CMV colitis); previous TB exposure/infection, BCG vaccination status | Pathogen invasion → mucosal destruction → bleeding | ||
| Colitis — Radiation | Hx of abdominal irradiation | Endothelial damage → telangiectasia → chronic oozing | ||
| Colorectal carcinoma (CRC) | 7–33% | *** > 50y, male, smoker, FHx, Hx of IBD, polyps and colorectal CA***; alternating diarrhoea and constipation, pencil-thin stools, tenesmus; loss of appetite, loss of weight, malaise; intractable pain, jaundice/RUQ pain, dyspnoea, bone pain | Tumour neovascularisation + overlying mucosal erosion/ulceration | |
| Post-polypectomy bleeding | Variable | History of recent colonoscopy with polypectomy (within 2 weeks) | Iatrogenic — arterial bleeding from polypectomy stalk | |
| Small bowel (~5%) | Meckel's diverticulum | Painless, massive altered blood (maroon-coloured); most common cause of LGIB in children; "Rule of 2s" | Ectopic gastric mucosa secretes acid → peptic ulceration of adjacent ileal mucosa → arterial bleeding | |
| Angiodysplasia | Similar to colonic — painless, intermittent | Same degenerative AVM mechanism | ||
| Small bowel tumours (GIST, lymphoma, carcinoid) | Constitutional symptoms, possible palpable mass, obstruction | Tumour erosion into vessels or mucosal ulceration | ||
| NSAID-induced small bowel ulcers | History of chronic NSAID use | NSAID enteropathy (distinct from gastric PUD): direct mucosal toxicity + ↓ prostaglandins → mucosal disruption [3] | ||
| Crohn's disease / TB enteritis | Abdominal pain, diarrhoea, weight loss; TB: endemic exposure | Transmural inflammation → deep ulceration → vessel erosion | ||
| Aortoenteric fistula | Previous aortic graft surgery; "herald bleed" followed by massive exsanguination | Graft erodes into adjacent duodenum → initially self-tamponades (herald bleed) → then catastrophic rupture | ||
| Anorectal (~10%) | Haemorrhoids | Blood coating stools or bleeding following defecation; may note perianal prolapsing mass, pruritus (mucus secretion) ± pain (if thrombosed) | Engorged vascular cushions → mucosal erosion → arteriolar bleeding | |
| Anal fissure | Hx of constipation; severe sharp pain upon defecation | Tear in anoderm below dentate line (somatic territory) → exposed vessels in fissure base | ||
| Rectal varices | Stigmata of chronic liver disease, portal hypertension | Portosystemic collateral (superior ↔ middle/inferior rectal veins) engorgement and rupture | ||
| Rectal/anal ulcers | Solitary rectal ulcer (straining/prolapse), stercoral ulcer (faecal impaction) | Mucosal ischaemia from prolapse or pressure necrosis from impacted faeces | ||
| Dieulafoy's lesion | Massive bleeding from a tiny mucosal defect; recurrent | Abnormally large submucosal artery fails to taper → erodes through overlying mucosa |
Differentiating by Clinical Pattern — A Practical Framework
The key to narrowing the differential at the bedside is to ask four pattern-recognition questions [1][3][4]:
| Pattern | Most Likely Diagnosis | Reasoning |
|---|---|---|
| Blood mixed with stool | Proximal colonic source (right colon, transverse colon) — CRC, proximal colitis | Blood enters lumen proximally and is incorporated during stool formation |
| Blood on surface / separate from stool | Outlet-type — haemorrhoids, anal fissure, low rectal lesion | Blood added after stool is already formed |
| Blood by itself (torrential) | Diverticular disease, angiodysplasia, IBD, bleeding CA [4] | Brisk bleeding overwhelms stool formation |
| Blood after defecation | Anorectal — haemorrhoids [4] | Straining during defecation → engorgement → mucosal erosion → arterial ooze continues after stool passes |
| Cyclic manner | GI endometriosis [4] | Ectopic endometrial tissue in bowel wall bleeds synchronously with menstrual cycle |
| Melaena | UGIB [4] | Slow bleeding oxidised by gastric acid + bacterial degradation over transit |
| Painful | Painless |
|---|---|
| Anal fissure (severe sharp pain on defecation) | Diverticular bleeding |
| Ischaemic colitis (cramping → then bleeding ≤ 24h) | Angiodysplasia |
| IBD (diffuse abdominal pain + bloody diarrhoea) | Haemorrhoids (unless thrombosed) |
| Infective colitis (fever, abdominal pain, diarrhoea) | CRC (usually painless unless advanced/complicated) |
| Thrombosed external haemorrhoid | Meckel's diverticulum (painless massive altered blood) [10] |
| Complicated diverticulitis (NB: diverticulitis ≠ diverticular bleeding) | Post-polypectomy bleeding |
This distinction is clinically very useful. The painless massive bleeders are diverticular disease, angiodysplasia, and Meckel's diverticulum. The painful bleeders involve inflammation or ischaemia.
| Age Group | Top Differentials | Reasoning |
|---|---|---|
| Children | Meckel's diverticulum, intussusception, juvenile polyps, anal fissure | Congenital or age-specific pathologies; Meckel's = most common congenital GI anomaly [10] |
| Young adults ( < 50) | Haemorrhoids (most common), IBD, infectious colitis, anal fissure | Inflammatory conditions peak in young adults; haemorrhoids from straining/pregnancy |
| Elderly ( > 65) | Diverticular disease, angiodysplasia, CRC, ischaemic colitis | Degenerative vascular and structural changes accumulate with age; CRC incidence rises |
This is a common exam question — all four present with bloody diarrhoea and abdominal pain, but the clinical context, timing, and associated features differ [2][3]:
| Feature | Inflammatory (IBD) | Ischaemic | Infective | Radiation |
|---|---|---|---|---|
| Age | Young adults (UC: 20–40; Crohn: 15–35) | Elderly ( > 60y, 90%) | Any age | Any age (post-treatment) |
| Key Hx | Chronic relapsing course; family history | CVS risk factors, recent MI, stroke, recent surgery | TOCC, immunosuppression, antibiotic use | Hx of abdominal/pelvic irradiation |
| Pain | Variable; may be diffuse | Sudden cramping, lateral | Diffuse, colicky | Rectal discomfort |
| Bleeding | Bloody diarrhoea with mucus | Mild–moderate, ≤ 24h after pain onset | Variable — may be bloody diarrhoea | Chronic ooze or intermittent |
| Fever | Variable | Unusual (but ↑WBC) | Usually present | Unusual |
| Distribution | UC: continuous from rectum; Crohn: skip lesions | Watershed areas (splenic flexure, rectosigmoid) | Diffuse or segmental | Irradiated field |
| Extra-GI features | Arthritis, uveitis, erythema nodosum, PSC | None specific | None specific | None specific |
| Key investigation | Colonoscopy + biopsy; faecal calprotectin | CT angiography; colonoscopy (thumbprinting → segmental inflammation) | Stool culture + C. diff toxin | Colonoscopy (telangiectasia in irradiated field) |
Management Implication
IBD should NOT be misdiagnosed as infectious or ischaemic colitis since the therapy is fundamentally different — IBD requires immunosuppression, infective colitis requires antimicrobials, and ischaemic colitis is mostly supportive. Misdiagnosis can be dangerous [2].
These are the two most common causes of significant LGIB in the elderly, and exams love to compare them [1][2][3]:
| Feature | Diverticular Bleeding | Angiodysplasia |
|---|---|---|
| Mechanism | Rupture of vasa recta into diverticulum | Degenerative AVM (dilated submucosal vessels lacking smooth muscle) |
| Type of bleeding | Arterial → tends to be more profuse | Venous → tends to be less profuse |
| Severity | Can be massive | Usually moderate; often occult (IDA, FOBT +ve) |
| Pattern | Acute, self-limiting in 80–85%; rebleed 14–38% | Intermittent; self-limiting in 85–90%; rebleed 25–85% |
| Pain | Painless | Painless |
| Most common site | Right colon (in Asia); sigmoid (in West) | Right colon (caecum, ascending colon) |
| Age | Usually > 60 (60% have diverticulosis by age 60) | Usually > 70 (2/3 at > 70y) |
| Associations | Obesity, HTN, NSAIDs, low-fibre diet | Aortic stenosis (Heyde syndrome), HHT (Osler-Weber-Rendu), ESRD, vWD |
| Colonoscopy | Active bleeding from diverticulum / adherent clot | Cherry red spots |
| Angiography | Active contrast extravasation | "Mother-in-law phenomenon" (early filling, delayed emptying) |
| Treatment | Endoscopic (clips, injection) → angiographic embolisation → segmental resection after 2nd bleed | Argon plasma coagulation (APC) → angiographic embolisation → right hemicolectomy |
In children, the differential for LGIB is quite different from adults [10]:
| Cause | Key Features | Mechanism |
|---|---|---|
| Anal fissure | Painful defecation, outlet-type, Hx of constipation | Tear in anoderm from passage of hard stool |
| Colonic polyp (90% juvenile polyps) | Painless, usually single, pedunculated | Torsion/erosion of polyp surface → bleeding |
| Meckel's diverticulum | Painless, large amount, altered blood (maroon) | Ectopic gastric mucosa → acid secretion → peptic ulceration of adjacent ileal mucosa |
| Intussusception | Painful, small amount, mucus ("redcurrant jelly" stool) | Telescoping bowel → venous congestion → mucosal ischaemia → bloody mucus |
| IBD | Bloody diarrhoea, weight loss, growth failure | Chronic mucosal inflammation |
| Intestinal duplication cyst | Variable; may present with obstruction or bleeding | Ectopic gastric mucosa (similar to Meckel's) |
| Small bowel ischaemia (e.g. volvulus) | Acute abdomen, bilious vomiting | Vascular compromise → ischaemic necrosis → bloody stool |
Meckel's Diverticulum — Rule of 2s (Must Know!)
2% of the population, 2% symptomatic, often by age of 2, 2:1 male-to-female ratio, 2 inches in length, found within 2 feet of the ileocaecal valve, 2 types of ectopic tissue: gastric (60%) and pancreatic (6%) [10]. It is a true congenital diverticulum (all layers) at the anti-mesenteric aspect of the small intestine, from incomplete obliteration of the vitelline duct (omphalomesenteric duct).
This is a rapid-fire clinical decision table for the ward [3][4]:
| Presentation | Think About | Key Discriminating Feature |
|---|---|---|
| Painless profuse haematochezia (acute, not chronic) | Diverticular bleeding | Self-limiting; no inflammation; often right-sided in HK |
| Painless intermittent haematochezia in elderly + anaemia | Angiodysplasia | Intermittent; associated with aortic stenosis; cherry red spots on CLN |
| Outlet-type bright red blood + prolapsing mass | Haemorrhoids | Blood on toilet paper / dripping after defecation; perianal pruritus |
| Sharp pain on defecation + streak of blood | Anal fissure | History of constipation; pain inhibits further examination |
| Bloody diarrhoea + mucus + chronic relapsing course | IBD | Extra-intestinal manifestations; young patient |
| Sudden cramping pain → bleeding within 24h | Ischaemic colitis | CVS risk factors; elderly; watershed distribution |
| Change in bowel habit + constitutional symptoms + bleeding | CRC | Pencil-thin stools; tenesmus; family history; > 50y |
| Fever + diarrhoea + blood + travel/antibiotics | Infective colitis | TOCC; C. diff after antibiotics; immunosuppression (CMV) |
| Bleeding + history of pelvic radiation | Radiation proctocolitis | Temporal relationship to radiotherapy |
| Massive painless altered blood in a child | Meckel's diverticulum | Rule of 2s; Meckel's scan |
| "Herald bleed" then massive exsanguination + previous aortic surgery | Aortoenteric fistula | Surgical emergency; previous aortic graft |
| Bleeding + signs of chronic liver disease | Rectal varices | Portal hypertension; portosystemic collateral at rectum |
When standard "top and tail" endoscopy (OGD + colonoscopy) fails to identify the source, we enter the territory of GI bleeding of obscure origin [5]:
- Definition: Bleeding of unknown origin after negative upper endoscopy and colonoscopy
- Most found in the small bowel eventually [5]
- Common small bowel sources: angiodysplasia, Meckel's diverticulum, small bowel tumours (GIST, carcinoid, lymphoma), NSAID ulcers, Crohn's disease, Dieulafoy's lesion, aortoenteric fistula
- This category is important because it reminds you that a negative colonoscopy does not mean there is no significant pathology — you must pursue small bowel investigation
When a patient with known liver disease presents with GI bleeding, the differential is broader than just varices [6]:
| Cause | Notes |
|---|---|
| Varices (50–90%): oesophageal or gastric | Most common — high-pressure portosystemic collaterals; usually bleeding from varices ≤ 3–5 cm of GEJ |
| Portal hypertensive gastropathy (PHG) | Very common in cirrhotics but bleeding is uncommon; friable "snake-skin" mucosa → diffuse oozing [6] |
| Peptic ulcer disease | Still common in cirrhotics |
| Generalised bleeding tendency | Thrombocytopaenia (hypersplenism), ↓ production of clotting factors, ↑ fibrinolysis |
| Rectal varices | Portosystemic collateral at rectum → LGIB |
| Mallory-Weiss tears | Especially in alcoholic cirrhosis (repeated retching) |
The key point: variceal bleeding is NOT the only cause of GI bleeding in a cirrhotic patient [6]. Always keep an open differential.
High Yield Summary
Approach to DDx of LGIB:
- Always exclude massive UGIB (10–15% of haematochezia is from upper GI)
- Characterise the bleeding: relationship to stool, severity, colour, pain
- Consider the patient's age and risk factors
Most Common Causes by Frequency: Diverticular disease (17–40%) > Angiodysplasia (2–30%) > Colitis (9–21%) > CRC (7–33%) > Anorectal (~10%) > Small bowel (~5%)
The Two Big Painless Bleeders: Diverticular (arterial, more profuse, self-limiting 80–85%) vs Angiodysplasia (venous, less profuse, intermittent, high rebleed)
Four Types of Colitis: Inflammatory (IBD — young, relapsing, extra-intestinal features), Ischaemic (elderly, CVS RFs, watershed areas), Infective (fever, TOCC, C. diff), Radiation (Hx of irradiation)
Red Flags for CRC: > 50y, FHx, alternating bowel habits, pencil-thin stools, tenesmus, constitutional symptoms, passage of mucus
Children: Meckel's (painless massive altered blood), intussusception (painful + redcurrant jelly), juvenile polyps (painless), anal fissure (painful)
Cirrhotic Patient: Not just varices — also PHG, PUD, generalised bleeding tendency, rectal varices, Mallory-Weiss
Obscure GI Bleeding: Negative top and tail → think small bowel (angiodysplasia, Meckel's, GIST, NSAID ulcers, Crohn's, aortoenteric fistula)
Active Recall - Differential Diagnosis of Lower GI Bleed
References
[1] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.3.6 Lower GI Bleeding, p281–285) [2] Senior notes: felixlai.md (Lower GI bleeding section) [3] Senior notes: Ryan Ho GI.pdf (Section 3.1.2 Lower GI Bleeding, p107–111) [4] Senior notes: maxim.md (Section 4.2 LGIB) [5] Senior notes: maxim.md (Section 3.3 UGIB — definitions of obscure GI bleeding) [6] Senior notes: Ryan Ho GI.pdf (Variceal Haemorrhage, p324) [7] Lecture slides: GC 186. Lower and diffuse abdominal painfresh blood in stool.pdf (p38) [10] Senior notes: maxim.md (Paediatric GI bleed / Meckel diverticulum section)
The diagnostic approach to LGIB follows three overarching principles — think of them as the "3S framework" [3][1]:
- Save the patient — resuscitation and haemodynamic stabilisation
- Search for the bleeding — localisation of the bleeding site
- Stop the bleeding — endoscopic, radiological, or surgical haemostasis
The investigations you choose and the order you pursue them depend entirely on haemodynamic stability and bleeding severity. Let's build this from first principles.
Before any investigation, you must assess how bad things are. The lecture slides emphasise a structured bleeding severity assessment [7]:
History: When did the bleeding start? First episode? Haematochezia? Melaena? Recent endoscopy? [7]
Physical examination (vital signs, cardiopulmonary and abdominal examinations, including DRE): tachycardia? hypotension? syncope? gross blood on DRE? recurrent/ongoing haematochezia? [7]
Laboratory tests (FBC, serum electrolytes, coagulation tests, type and cross match): Hb? ↓ Albumin? ↑ INR? ↓ PLT? ↑ creatinine [7]
Co-morbidities: Older age? Need for RBC transfusion? [7]
Concomitant medications: NSAIDs? antiplatelet agents? anticoagulants? [7]
Oakland Score
The Oakland score is mentioned in the BSG 2019 guidelines cited in the lecture slides [7]: if Oakland score < 8, consider safe hospital discharge and outpatient evaluation in haemodynamically stable patients. This score incorporates age, sex, prior LGIB admission, DRE findings, heart rate, SBP, and Hb.
Haemodynamic Classification of Blood Loss
Understanding why we classify by haemodynamic status:
| Class | Blood Loss | Heart Rate | SBP | Clinical Features | What's Happening Physiologically |
|---|---|---|---|---|---|
| I | < 15% (~750 mL) | < 100 | Normal | Minimal symptoms | Compensatory vasoconstriction maintains BP |
| II | 15–30% (~750–1500 mL) | 100–120 | Normal or mildly ↓ | Anxiety, ↓ pulse pressure, postural drop | Baroreceptor-mediated ↑ sympathetic tone; cardiac output maintained by ↑ HR |
| III | 30–40% (~1500–2000 mL) | 120–140 | ↓ (SBP < 90) | Confusion, oliguria, pallor | Decompensation begins; CO falls despite maximal sympathetic response |
| IV | > 40% ( > 2000 mL) | > 140 or bradycardic | Profoundly ↓ | Lethargy, anuria, imminent arrest | Cardiovascular collapse; paradoxical bradycardia from vagal response |
75% of LGIB stops spontaneously [1][3] — but you still need to prepare for the worst.
These are your first-line laboratory tests — ordered immediately on presentation alongside resuscitation [1][3][7]:
| Investigation | What You're Looking For | Interpretation / Why |
|---|---|---|
| CBC (Hb, haematocrit) | Severity of blood loss; baseline for serial monitoring | Hb usually ↓ after 48 hours (because haemodilution takes time — in acute bleeding, you lose whole blood proportionally, so initial Hb may be falsely normal) [3][11]. ↓ MCV suggests chronic bleeding (iron deficiency) vs normal MCV in acute bleeding |
| RFT (U&E, creatinine) | Hydration status, pre-renal failure, electrolyte imbalance | ↑ Urea:Creatinine ratio > 100:1 suggests UGIB (digested blood protein is absorbed and converted to urea in the liver) OR dehydration (pre-renal) [11]. Creatinine also assesses suitability for contrast scans |
| LFT | Underlying liver disease → coagulopathy, portal hypertension | ↑ bilirubin, ↓ albumin, ↑ NH₃ suggest cirrhosis → think varices, PHG, coagulopathy |
| Clotting profile (PT/INR, aPTT) | Coagulopathy | ↑ INR on warfarin; liver failure; DIC. ↓ Body temperature can cause ↓ efficiency of clotting factors [1][3] — keep the patient warm |
| Type and screen / cross-match | Prepare for transfusion | Cross-match 2–4 units packed RBCs at minimum [1][3] |
| Lactate + ABG | Tissue perfusion, acid-base status | Metabolic acidosis + ↑ lactate → poor tissue perfusion (shock) or intestinal ischaemia [4][12] |
Transfusion Thresholds (from Lecture Slides)
If Hb < 7 g/dL, transfuse: target Hb 7–9 g/dL post-transfusion if no CVD [7]
If Hb ≥ 8 g/dL and CVD present, transfuse: target Hb ≥ 10 g/dL [7]
Why the restrictive strategy? Over-transfusion in GI bleeding is associated with ↑ mortality — likely because ↑ intravascular volume → ↑ portal/splanchnic pressure → promotes rebleeding.
Investigation Modalities in Detail
1. Bedside Investigations
- 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)
2. Endoscopy — The Workhorse
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:
| Cause | Colonoscopic Appearance | Why It Looks Like This |
|---|---|---|
| Diverticular bleeding | Active bleeding from diverticulum, adherent clot, visible vessel in diverticulum | Arterial bleed from ruptured vasa recta |
| Angiodysplasia | Cherry red spots — small, flat, bright red lesions typically in right colon [4] | Dilated submucosal vessels visible through thin mucosa |
| CRC | Exophytic/polypoid mass, may be friable, ulcerated, necrotic, ± circumferential [13] | Tumour neovascularisation with abnormal, fragile surface vessels |
| UC | Continuous erythema, friability, ulceration starting from rectum, loss of vascular pattern, pseudopolyps | Immune-mediated mucosal inflammation with crypt abscesses |
| Crohn's | Patchy "skip" lesions, aphthous ulcers, cobblestoning, strictures | Transmural granulomatous inflammation |
| Ischaemic colitis | Segmental oedema, petechial haemorrhage, thumbprinting (submucosal oedema/haemorrhage), cyanotic mucosa, ulceration in watershed areas | Mucosal ischaemia → oedema → haemorrhage → necrosis |
| C. difficile colitis | Pseudomembranes (yellow-white adherent plaques) | Toxin-mediated epithelial necrosis with fibrinous exudate |
| Radiation proctitis | Telangiectasias, pale/friable mucosa in irradiated field | Radiation-induced endothelial damage → neovascularisation of fragile vessels |
Therapeutic modalities at colonoscopy — especially effective in angiodysplasia and diverticular disease [3]:
| Modality | Mechanism | Best For |
|---|---|---|
| Epinephrine injection (1:10,000) | Local vasoconstriction + tamponade; not used alone [4] | Adjunct to other methods; buys time |
| Through-the-scope (TTS) clips / Cap-mounted clips | Mechanical compression of bleeding vessel | Diverticular bleeding [7] |
| Endoscopic band ligation (EBL) | Strangulates tissue around bleeding point → ischaemic necrosis → haemostasis | Diverticular bleeding [7] |
| Argon plasma coagulation (APC) | Non-contact thermal coagulation using ionised argon gas | Angiodysplasia, radiation proctitis [4][7] |
| Monopolar electrocautery / heat probe | Contact thermal coagulation | Angiodysplasia |
| Hemostatic topical agents | Haemostatic powder (e.g. TC-325) sprayed onto bleeding site | Salvage treatment for delayed post-polypectomy bleeding [7] |
Endoscopic Haemostasis Indications
Stigmata of recent haemorrhage warrant endoscopic treatment: active bleeding, non-bleeding visible vessel, adherent clot [4]. A clean base (no stigmata) generally does not require endoscopic therapy.
- 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]
3. Radiological Investigations
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:
| Finding | Interpretation |
|---|---|
| Contrast extravasation into bowel lumen | Active bleeding at that site |
| "Blush" conforming to a diverticulum | Diverticular bleeding |
| Hypervascular lesion in bowel wall | Tumour or AVM |
| Bowel wall thickening + pericolonic stranding | Colitis or diverticulitis |
| Non-tapering vessel (Dieulafoy's) | Aberrant submucosal artery |
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]:
- Activity conforms to intestinal anatomy
- Intensity increases with time
- 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)
| Modality | Min. Bleeding Rate | Sensitivity | Specificity | Therapeutic? | Best For |
|---|---|---|---|---|---|
| Colonoscopy | N/A (visualisation) | 75–90% diagnostic yield | High (direct visualisation + biopsy) | Yes (clips, APC, EBL, injection) | First-line in stable patients |
| CTA | ~0.3–0.5 mL/min | 85.2% | 92.1% | No (but guides embolisation/surgery) | First-line in unstable patients |
| Mesenteric angiography | 0.5–1 mL/min | Lower (27–67% yield) | More specific | Yes (embolisation) | Active brisk bleeding; when CTA positive → proceed to embolise |
| Tc-99m RBC scan | 0.1–0.4 mL/min | Most sensitive | Low (non-specific) | No | Intermittent/slow bleeding |
| Capsule endoscopy | N/A | Moderate (but good for SB) | Moderate | No | Occult/obscure bleeding, negative top-and-tail |
| Meckel's scan | N/A | > 80% (for EGM) | High | No | Children with LGIB |
Surgery is required in ~15–20% of patients with acute LGIB [3]
- For relatively stable patients, persistent bleeding after exhausting endoscopic and radiological interventions [7]
- For patients who don't respond to initial resuscitation [7]
- Haemodynamic instability despite adequate resuscitation [3]
- Massive blood transfusion ( > 6 units) [3]
- Frequent rebleeding [3]
- On anticoagulants/antiplatelets (higher bleeding risk) [3]
Operative approach [7]:
- Consider upper endoscopy first if not been performed [7]
- Palpation of small bowel (tumour, diverticulum) [7]
- On-table upper endoscopy and colonoscopy [7]
- On-table enteroscopy (diagnostic yield of 80–92%) [7]
- Clamping of bowel segments (to determine which segment is accumulating blood) [7]
- Segmental resection if bleeding source identified → rebleeding rate 0–15% [7]
- If no source of bleeding identified, and probable colonic cause → subtotal or total colectomy (rebleeding rate of 10–20%) [7]
Why Subtotal Colectomy?
If you can't localise the bleeding and the patient is exsanguinating, a subtotal colectomy with ileostomy removes the entire colon (the most likely source of massive LGIB). This is a last-resort procedure because it carries significant morbidity, but it is lifesaving when localisation has failed and the patient is bleeding to death. The rebleeding rate is 10–20% (because small bowel sources may still be present).
When standard "top and tail" endoscopy (OGD + colonoscopy) are both negative [3]:
- Repeat upper endoscopy or colonoscopy → can identify 35% of bleeding lesions that were missed on the first pass [3]
- Look for small bowel sources by:
- For children/young patients: Meckel's scan [11]
- For older patients: Contrast CT abdomen → exclude ALL solid organ malignancies first → then enteroscopy if negative [11]
| Clinical Scenario | First-Line Investigation | Rationale |
|---|---|---|
| Haemodynamically unstable, active bleeding | CTA → then transcatheter embolisation or surgery [7] | Fastest, non-invasive localisation; guides intervention |
| Haemodynamically stable, significant bleeding | Colonoscopy (with bowel prep) [7] | Diagnostic + therapeutic in one procedure |
| Stable, low-risk (Oakland < 8) | Outpatient colonoscopy [7] | Safe discharge; colonoscopy when electively prepared |
| Suspect UGIB in haematochezia | OGD (± NG tube aspirate) [3] | 10–15% of haematochezia is UGIB; must exclude |
| Negative top-and-tail, ongoing bleeding | CTA or mesenteric angiography [4] | Localise active bleeding for embolisation |
| Negative top-and-tail, intermittent bleeding | Capsule endoscopy, double balloon enteroscopy [4] | Visualise small bowel; therapeutic with DBE |
| Child with painless massive LGIB | Meckel's scan [9] | Detects ectopic gastric mucosa with > 80% sensitivity |
| Failed all localisation, ongoing massive bleeding | Emergency laparotomy with on-table enteroscopy [7] | Last resort; on-table dx yield 80–92% |
High Yield Summary
Bleeding severity assessment: History + P/E (vitals, DRE) + Labs (FBC, RFT, LFT, clotting, T&S, lactate/ABG). Oakland score < 8 → safe outpatient evaluation.
Transfusion targets: Hb < 7 → transfuse to 7–9 g/dL; if CVD + Hb ≥ 8 → transfuse to ≥ 10 g/dL.
First investigation depends on stability:
- Unstable → CTA (BSG 2019: shock index > 1 → CTA first)
- Stable → Colonoscopy (first diagnostic modality, diagnostic yield 75–90%)
CTA: Sensitivity 85.2%, specificity 92.1%; fastest non-invasive localisation; needs active bleeding (~0.3–0.5 mL/min).
Colonoscopy: Diagnostic + therapeutic; bowel prep ↑ yield but not feasible in unstable patients; intubate ileocaecal valve to exclude distal SB source.
RBC scan: Most sensitive (0.1–0.4 mL/min); delayed imaging up to 24h; detects intermittent bleeding; but non-specific localisation.
Mesenteric angiography: More specific; allows embolisation; needs active bleeding ≥ 0.5–1 mL/min.
Surgery (15–20%): After exhausting endoscopic + radiological options; segmental resection if localised (rebleed 0–15%); subtotal colectomy if not localised (rebleed 10–20%).
Obscure GI bleeding: Repeat top-and-tail (finds 35%); then capsule endoscopy / DBE / Meckel's scan / CT enterography.
Failure to localise: 8–12% of cases.
Active Recall - Diagnosis and Investigation of Lower GI Bleed
[1] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.3.6 Lower GI Bleeding, p281–285) [2] Senior notes: felixlai.md (Lower GI bleeding section; Capsule endoscopy section) [3] Senior notes: Ryan Ho GI.pdf (Section 3.1.2 Lower GI Bleeding, p108–111) [4] Senior notes: maxim.md (Section 4.2 LGIB; Angiodysplasia section) [7] Lecture slides: GC 186. Lower and diffuse abdominal painfresh blood in stool.pdf (p6, p33, p35, p38, p40, p48) [9] Senior notes: Ryan Ho Diagnostic Radiology.pdf (Red Blood Cell Scan p62; Meckel's Scan p63) [11] Senior notes: Ryan Ho GI.pdf (Mesenteric angiography p48; UGIB investigations p43; Meckel's diverticulum p162) [12] Senior notes: Ryan Ho GI.pdf (Investigations for acute abdomen, p105) [13] Senior notes: Ryan Ho GI.pdf (Colonoscopy + Bx for CRC, p166)
Step 1: Initial Resuscitation and Stabilisation
This is the "Save the patient" phase. Every LGIB patient gets this regardless of severity [1][2][3][4]:
| Component | Action | Rationale |
|---|---|---|
| A — Airway | Intubate if decompensated (confused) or massive haematemesis [3] | Altered consciousness → loss of airway protective reflexes → aspiration risk |
| B — Breathing | O₂ on nasal cannula [3] | ↑ O₂ carrying capacity of remaining blood; compensate for ↓ Hb |
| C — Circulation | 2× large-bore IV cannula (14/16G at antecubital vein) [3][14] → crystalloid (NS or Hartmann's) full rate | Large-bore cannulae allow rapid volume infusion (flow rate ∝ r⁴ by Poiseuille's law — a 14G cannula delivers fluid ~4× faster than an 18G). Crystalloids restore intravascular volume quickly |
- Nil by mouth (NPO) — in case endoscopy or surgery is needed [2]
- Withhold anticoagulants and antiplatelet drugs [2]
- But weigh against thrombotic risk of the individual patient before reversing anticoagulation [2]
- Close monitoring [1][3]:
- Shock chart hourly
- Vitals: BP/P, RR, body temperature (↓ body temperature can cause ↓ efficiency of clotting factors — keep the patient warm) [1][3]
- Foley's catheter: urine output ≥ 0.5 mL/kg/h [1][3]
- Cardiac monitor, pulse oximetry [1][3]
- ± CVP line for PAWP (in ICU setting to guide resuscitation without fluid overload) [1][3]
- Cardiac monitor especially important to prevent volume overload in patients with congestive heart failure during fluid resuscitation/blood transfusion [2]
Give rapid fluid challenge: 500 mL (or 1000 mL) of crystalloid solution over 5–10 min → reassess BP/P every 5 min → repeat if not responding [14]
| Fluid | When to Use | Mechanism |
|---|---|---|
| Isotonic crystalloid (NS 0.9% or Hartmann's/Ringer's lactate) | First-line for all patients | Expands intravascular volume; distributes across ECF; cheap, readily available |
| Colloid (e.g. gelatin, albumin) | Acceptable alternative | Stays intravascular longer (larger molecules → higher oncotic pressure) but no proven mortality benefit over crystalloid |
| Packed RBCs | See transfusion thresholds below | Restores oxygen-carrying capacity |
From the BSG 2019 guidelines cited in lecture slides [7]:
If Hb < 7 g/dL → transfuse: target Hb 7–9 g/dL post-transfusion if no CVD [7]
If Hb ≥ 8 g/dL and CVD present → transfuse: target Hb ≥ 10 g/dL [7]
Indications for transfusion [3]:
- Profuse ongoing bleeding
- Persistent haemodynamic instability despite crystalloid resuscitation
- Symptomatic anaemia
- Acute MI / unstable angina with low Hb
Why Restrictive Transfusion?
Restrictive transfusion strategy (targeting Hb 7–9 rather than higher) is associated with ↓ mortality in GI bleeding. Over-transfusion raises intravascular volume and pressure → ↑ splanchnic blood flow → can promote rebleeding, especially from varices and arterial sources. Also avoids transfusion-related complications (TRALI, volume overload, immunosuppression).
| Product | Indication | Mechanism |
|---|---|---|
| Fresh frozen plasma (FFP) | Coagulopathy (↑ INR/PT from liver disease, warfarin, DIC) [2] | Contains all clotting factors |
| Platelets | Platelet dysfunction or thrombocytopaenia ( < 50 × 10⁹/L in active bleeding) [2] | Direct replacement of platelet mass |
| Vitamin K (IV) | Warfarin over-anticoagulation | Cofactor for hepatic synthesis of factors II, VII, IX, X; takes 6–24h to work |
| Prothrombin complex concentrate (PCC) | Urgent warfarin reversal | Concentrated factors II, VII, IX, X; acts within minutes (faster than FFP) |
| Idarucizumab | Dabigatran reversal | Monoclonal antibody fragment that binds and neutralises dabigatran |
| Andexanet alfa | Factor Xa inhibitor reversal (rivaroxaban, apixaban) | Recombinant modified factor Xa decoy that binds anti-Xa drugs |
| Tranexamic acid | Adjunct antifibrinolytic | Inhibits plasmin → stabilises clots. Used in some centres as adjunct for LGIB [4] |
Step 2: Endoscopic Therapy (First-Line Definitive Treatment)
Endoscopic therapy is the cornerstone of LGIB management once the patient is stabilised. It allows simultaneous diagnosis and treatment [1][3][7].
Stigmata of recent haemorrhage: active bleeding, non-bleeding visible vessel, adherent clot [4]
Endoscopic Treatment Modalities
The lecture slides and BSG guidelines specify which modality for which pathology [7]:
| Agent | Mechanism | Important Caveat |
|---|---|---|
| Epinephrine (adrenaline) injection (1:10,000) | Local tamponade effect (volume of injected fluid compresses the vessel) + vasoconstriction (α₁ adrenergic agonism) + platelet aggregation promotion | Not used alone [4] — stops bleeding in 90–95% initially but often rebleeds within 1 hour after the adrenaline is absorbed [15]. Must be combined with a second modality |
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]
| Modality | Mechanism | Best For | Risk |
|---|---|---|---|
| Argon plasma coagulation (APC) | Non-contact thermal coagulation using ionised argon gas; ↓ energy depth than heat probe → ↓ risk of perforation | Angiodysplasia [4][7], radiation proctitis [15] — ideal for thin-walled structures and diffuse superficial oozing | Perforation (rare due to limited depth) |
| Heat probe (bipolar coagulation) | Contact thermal coagulation — literally "melts" the vessel wall shut | Visible vessel in ulcer base | Perforation (deeper energy penetration) |
| Laser coagulation | Photocoagulation | Rarely used now; superseded by APC | Cost, availability |
| Monopolar electrocautery | Contact thermal | Angiodysplasia (alternative to APC) [4] | Perforation |
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.
| Modality | Mechanism | Best For |
|---|---|---|
| Through-the-scope (TTS) clips | Metallic clip deployed through the endoscope channel; physically compresses the bleeding vessel against underlying tissue | Diverticular bleeding [7]; large visible vessels; post-polypectomy bleeding |
| Cap-mounted clips | Clip device mounted on the tip of the endoscope; allows en face application | Diverticular bleeding [7] — can grasp the bleeding diverticulum en bloc |
| Endoscopic band ligation (EBL) | Rubber band placed around the tissue containing the bleeding vessel → strangulation → ischaemic necrosis → haemostasis | Diverticular bleeding [7]; analogous to variceal banding |
| Over-the-scope clip (OTSC / Ovesco) | Large clip that can grasp a wide area of tissue; deployed over the scope tip | Larger defects; can even treat GI perforation, leakage, fistula [4] |
| Agent | Mechanism | Role |
|---|---|---|
| Haemostatic topical agent (e.g. TC-325 Hemospray) | Nanopowder sprayed onto bleeding site → absorbs moisture → creates a mechanical barrier → activates clotting cascade | Salvage treatment [7] — used when other modalities fail; particularly useful for delayed post-polypectomy bleeding [7] |
Endoscopic Therapy Summary by Aetiology (from Lecture Slides)
- Suspected perforation (gas insufflation → pneumoperitoneum → abdominal compartment syndrome → ↓ venous return and death, plus splinting of diaphragm compromising ventilation) [3][15]
- Unstable cardiac/pulmonary status (anaesthetic risk)
- Unable to achieve adequate bowel preparation (unstable patients — proceed to CTA instead)
- Uncooperative patient without sedation
- Anaesthetic risk: respiratory depression, MI, CVA
- Procedure-related: aspiration, bleeding (worsening), perforation, failure of haemostasis, incomplete scope
Step 3: Interventional Radiology — Transcatheter Embolisation
When endoscopy fails or is not feasible (e.g. massive bleeding with poor visualisation), interventional radiology is the next step [2][4][7].
Procedure: Selective catheterisation of SMA, IMA, and coeliac artery by Seldinger technique → identification of active extravasation → super-selective catheterisation of the bleeding vessel → deployment of embolic agents [3][11]
Embolic agents [16]:
- Gelfoam (absorbable gelatin sponge) — temporary occlusion
- PVA particles (polyvinyl alcohol) — permanent small-vessel occlusion
- Coils (metallic) — permanent occlusion of named vessels
- Glue (cyanoacrylate) — for AVMs and emergencies
From lecture slides: Transcatheter embolisation within 60 minutes is recommended for haemodynamically unstable patients with CTA-confirmed bleeding [7]
| Indication | Rationale |
|---|---|
| Failed endoscopic haemostasis | Escalation to next treatment tier |
| Brisk bleeding with CTA-confirmed extravasation | Direct access to bleeding vessel for embolisation |
| Bleeding source identified on angiography (even without prior CTA) | Therapeutic opportunity during diagnostic procedure |
| Patient unfit for surgery [15] | TAE is less invasive; equally effective as surgery for failed endoscopy with fewer complications [2] |
| Recurrent bleeding despite endoscopy | Re-endoscopy may not succeed |
- Equally effective compared to surgery in patients who failed therapeutic endoscopy with fewer complications [2]
- Reduces the need for surgery without increasing overall mortality [2]
- Can be performed under local anaesthesia (no GA required)
- Can specifically pinpoint the bleeding vessel [11]
- Can be performed intra-operatively to guide surgery [11]
- Embolisation carries risk of intestinal ischaemia [11] — the colon has less collateral circulation than the stomach/duodenum; super-selective catheterisation minimises this risk
- Not sensitive for slow/intermittent bleeding (requires active extravasation ≥ 0.5–1 mL/min)
- Nephrotoxic contrast
- Access site complications (haematoma, pseudoaneurysm, dissection)
- Non-target embolisation
- Injection of intra-arterial vasopressin via the angiography catheter [2]
- MoA: Potent mesenteric vasoconstriction → ↓ blood flow to bleeding site → haemostasis
- Largely superseded by embolisation (vasopressin has systemic side effects — cardiac ischaemia, hypertension, bowel ischaemia — and high rebleeding rate after cessation)
- Rarely used in modern practice
Step 4: Surgical Management (Last Resort)
For relatively stable patients, persistent bleeding after exhausting endoscopic and radiological interventions [7]
For patients who don't respond to initial resuscitation [7]
Additional indications [1][3]:
- Haemodynamic instability despite adequate resuscitation
- Massive blood transfusion ( > 6 units)
- Frequent rebleeding
- On anticoagulants or antiplatelets (higher bleeding tendency)
- Consider surgery for patients with LGIB due to pathology not amenable to being treated endoscopically or radiologically [7]
Consider upper endoscopy first if not been performed [7]
The systematic intra-operative assessment [7]:
- Palpation of small bowel (tumour, diverticulum) — run the entire length of small bowel between fingers feeling for masses, thickening, or diverticula
- On-table upper endoscopy and colonoscopy — the surgeon can observe the bowel both luminally (via endoscope) and serially (via direct observation)
- On-table enteroscopy (diagnostic yield of 80–92%) [7] — scope inserted through an enterotomy at the mid-small bowel and advanced in both directions
- Clamping of bowel segments — sequential clamping to isolate the segment that is accumulating blood
| Scenario | Procedure | Outcome |
|---|---|---|
| Bleeding source localised | Segmental resection (resect the affected segment + primary anastomosis) | Rebleeding rate 0–15%, mortality 0–13% [1][3] |
| Bleeding source NOT localised, probable colonic cause | Subtotal or total colectomy (remove entire colon with ileostomy or ileorectal anastomosis) | Rebleeding rate 10–20% [7]; mortality 0–40% [1] |
| Blind segmental resection (without localisation — AVOID) | Segmental resection based on guess | Rebleeding rate up to 75% [1] — this is why pre-operative localisation is so important |
Never Do a Blind Segmental Resection
Blind segmental resection has a rebleeding rate of up to 75% [1]. This is because you may be resecting the wrong segment while the actual bleeding source remains in situ. Always attempt to localise the bleeding before committing to segmental resection. If localisation fails and the patient is exsanguinating, a subtotal colectomy (which removes the entire colon) is safer than guessing.
Aetiology-Specific Management
Now let's integrate the above framework with management tailored to each specific cause:
| Step | Treatment | Details |
|---|---|---|
| Spontaneous resolution | Observation | 50% of bleeding stops spontaneously [5]; 80–85% overall [1] |
| Conservative | Lifestyle modification | High-fibre diet, bulk laxatives (e.g. methylcellulose), weight reduction [5]; avoid stimulant laxatives and NSAIDs [5] |
| Endoscopic | TTS/cap-mounted clip or EBL [7] | 4-quadrant submucosal injection of adrenaline in bleeding diverticular vessel; bipolar coagulation for visualised non-bleeding vessel [2] |
| Radiological | Embolisation or infusion of vasopressin via angiography [2] | Alternative when colonoscopy fails to identify/treat the source |
| Surgical | Segmental colectomy (with localisation) or subtotal colectomy (without localisation) | Semi-elective resection after 2nd bleeding episode [1]; reserved for failed endoscopic/angiographic therapy [2] |
Localisation of diverticular bleeding follows a stepwise approach [5]: Colonoscopy → angiography → on-table lavage and colonoscopy → subtotal colectomy and ileostomy if bleeding source still cannot be identified
| Step | Treatment | Details |
|---|---|---|
| Conservative | Bed rest, tranexamic acid [4] | Antifibrinolytic stabilises clots; most bleeding is venous and self-limiting |
| Endoscopic | Argon plasma coagulation (APC) [4][7] or monopolar electrocautery [4] | APC is preferred: non-contact, controlled depth, ideal for thin-walled right colon |
| Radiological | Mesenteric angiogram for super-selective catheterisation and embolisation [4] | When CLN inconclusive or endoscopic therapy fails |
| Surgical | Resection (right hemicolectomy) with anastomosis [4] | Only for selected patients — high mortality. Indications: (1) failed endoscopic and angiographic treatment, (2) severe acute life-threatening GIB, (3) multiple angiodysplastic lesions that cannot be managed otherwise [4] |
| Grade | Management | Mechanism |
|---|---|---|
| Grade 1 | Conservative: high-fibre diet, adequate hydration, stool softeners, avoid straining | ↓ intra-abdominal pressure → ↓ venous engorgement |
| Grade 1–2 | Rubber band ligation [1] | Strangulates the haemorrhoidal tissue above dentate line → ischaemic necrosis → scarring → fixation |
| Grade 2–3 | Injection sclerotherapy (5% phenol in almond oil) | Chemical inflammation → fibrosis → shrinkage |
| Grade 3–4 | Haemorrhoidectomy (excisional: Milligan-Morgan open or Ferguson closed) [1] | Surgical excision of haemorrhoidal tissue |
| Thrombosed external | Incision and evacuation if < 72h; otherwise conservative | Evacuation provides immediate pain relief; after 72h, clot is organising and pain is improving |
- Definitive management: Surgical resection (type depends on tumour location — right hemicolectomy, left hemicolectomy, anterior resection, abdominoperineal resection)
- Acute LGIB from CRC is rarely massive; usually managed with colonoscopic biopsy → staging → planned surgical resection
- If presenting with obstructing CRC + bleeding → consider endoscopic stenting as bridge to surgery [17]
| Type | Management | Key Points |
|---|---|---|
| IBD (UC/Crohn's) | Immunosuppression: 5-ASA, steroids, azathioprine, biologics (anti-TNF, vedolizumab) | Treat the underlying inflammation → bleeding resolves |
| Ischaemic colitis | Majority resolve with supportive care [17]: NPO, IV fluids, broad-spectrum antibiotics, ± rectal tube decompression | Surgery (emergency laparotomy + resection) for infarction/necrosis, perforation, peritonitis, haemodynamic instability [17] |
| Infective colitis | Antibiotics targeted to organism (e.g. metronidazole/vancomycin for C. diff); supportive | Identify the pathogen; stool culture + C. diff toxin |
| Radiation proctitis | APC (endoscopic) is first-line; also formalin application, sucralfate enemas | APC coagulates the telangiectatic vessels in the irradiated mucosa |
| Scenario | Management |
|---|---|
| Symptomatic | Resection [4][10] |
| Symptomatic, narrow base | Simple diverticulectomy (excision at the base + suture closure) [4] |
| Symptomatic, broad base / ulceration at margin / mesenteric border | Segmental bowel resection + primary anastomosis [4] |
| Asymptomatic, detected on imaging | Not resect [4] |
| Asymptomatic, detected during surgery | Depends on age: Child → resect; Adult < 50y → resect if palpable, length > 2 cm and broad base > 2 cm; Adult > 50y → not resect [4] |
| Treatment | Details |
|---|---|
| Injection sclerotherapy (local) [1] | Direct injection into the varix → thrombosis |
| TIPS (if uncontrolled bleeding) [1] | Transjugular intrahepatic portosystemic shunt → decompresses portal system → ↓ variceal pressure |
| Band ligation | Analogous to oesophageal variceal banding |
| Treat underlying portal hypertension | Non-selective β-blockers (propranolol/nadolol) for secondary prophylaxis |
Post-Bleeding Management
After achieving haemostasis, several important steps follow:
| Cause | Secondary Prevention |
|---|---|
| Diverticular disease | High-fibre diet; avoid NSAIDs; semi-elective resection after 2nd bleeding episode [1] |
| Angiodysplasia | No proven pharmacological prophylaxis; consider APC if recurrent; address Heyde syndrome (aortic valve replacement) |
| Haemorrhoids | Dietary fibre, hydration, stool softeners, avoid straining |
| CRC | Surveillance colonoscopy post-resection; adjuvant chemotherapy if indicated |
| IBD | Maintenance immunosuppressive therapy |
| Drug-related bleeding | Review and rationalise NSAIDs, antiplatelets, anticoagulants — weigh thrombotic risk vs bleeding risk |
This is a common clinical dilemma. The general principle:
- Antiplatelets (e.g. aspirin for secondary CVD prevention): Restart as soon as haemostasis is achieved (usually within 1–3 days), as the thrombotic risk typically outweighs the rebleeding risk
- Anticoagulants (e.g. warfarin, DOACs): Restart when haemostasis is secure and the indication is strong (e.g. mechanical valve, high-risk AF) — usually within 7 days
- Always involve the relevant specialty (cardiology, haematology) in shared decision-making
| Severity | Management |
|---|---|
| Mild, self-limiting, low-risk (Oakland < 8) | Outpatient colonoscopy; conservative management |
| Moderate, stable | Inpatient colonoscopy with bowel prep → endoscopic therapy |
| Severe, stable | Urgent colonoscopy → endoscopic therapy → if fails → CTA/angiography + embolisation |
| Massive, unstable | Resuscitate → CTA → transcatheter embolisation within 60 min → if fails → emergency surgery |
| Exsanguinating, all modalities failed | Emergency laparotomy → on-table enteroscopy → segmental resection or subtotal colectomy |
High Yield Summary
Resuscitation: ABC; 2× large-bore IV; crystalloid bolus; target Hb 7–9 (no CVD) or ≥ 10 (CVD); correct coagulopathy (FFP, platelets, vitamin K); stop anticoagulants; keep patient warm (hypothermia impairs clotting).
Endoscopic therapy (first-line definitive):
- Diverticular bleeding → TTS/cap-mounted clip or EBL
- Angiodysplasia → APC
- Post-polypectomy bleeding → mechanical therapy or thermal; hemostatic topical agent as salvage
- Adrenaline injection is adjunct only — never monotherapy (rebleeds within 1h)
Transcatheter embolisation: Within 60 minutes for unstable patients with CTA-confirmed bleeding. Equally effective as surgery for failed endoscopy with fewer complications. Risk: intestinal ischaemia.
Surgery (15–20%):
- After exhausting endoscopic + radiological interventions
- OR for patients not responding to initial resuscitation
- On-table enteroscopy (dx yield 80–92%)
- Segmental resection if localised (rebleed 0–15%)
- Subtotal colectomy if not localised (rebleed 10–20%)
- NEVER do blind segmental resection (rebleed up to 75%)
Aetiology-specific:
- Diverticular: spontaneous resolution 50–85%; semi-elective resection after 2nd bleed
- Angiodysplasia: APC first-line; surgery (right hemicolectomy) only after failed endoscopic + angiographic Tx
- Ischaemic colitis: mostly supportive; surgery for necrosis/perforation
- Meckel's: symptomatic → resect; asymptomatic found on imaging → do NOT resect
Active Recall - Management of Lower GI Bleed
[1] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.3.6 Lower GI Bleeding, p281–286) [2] Senior notes: felixlai.md (Lower GI bleeding — Treatment section) [3] Senior notes: Ryan Ho GI.pdf (Section 3.1.2 Lower GI Bleeding, p110–111) [4] Senior notes: maxim.md (LGIB acute management; Angiodysplasia; Meckel diverticulum) [5] Senior notes: maxim.md (Diverticular disease management) [7] Lecture slides: GC 186. Lower and diffuse abdominal painfresh blood in stool.pdf (p38, p40) [10] Senior notes: maxim.md (Meckel diverticulum section) [11] Senior notes: Ryan Ho GI.pdf (Mesenteric angiography, p48) [14] Senior notes: Ryan Ho Critical Care.pdf (Management of Hypovolemic Shock, p21) [15] Senior notes: Ryan Ho GI.pdf (Endoscopic Tx modalities, p45; UGIB management, p43) [16] Senior notes: Ryan Ho Diagnostic Radiology.pdf (Transcatheter Embolization, p85) [17] Senior notes: Ryan Ho GI.pdf (Ischaemic colitis management, p147; LBO management, p139)
Complications of LGIB arise from three overlapping domains: (A) complications of the bleeding itself (the physiological consequences of blood loss), (B) complications of the underlying aetiology (what happens if the causative disease progresses), and (C) complications of the treatments (endoscopic, radiological, and surgical). Understanding each from first principles helps you anticipate, prevent, and manage them.
A. Complications of the Bleeding Itself
These are the direct physiological consequences of losing blood into the GI tract. They apply regardless of aetiology.
"Hypovolaemia" → hypo- (under) + vol- (volume) + -aemia (blood) = insufficient blood volume.
Pathophysiology: Acute blood loss → ↓ intravascular volume → ↓ preload → ↓ stroke volume → ↓ cardiac output → compensatory sympathetic activation (tachycardia, peripheral vasoconstriction) → if blood loss exceeds ~30% of total blood volume, the compensatory mechanisms are overwhelmed → decompensated shock → multi-organ failure [1][3]
- Shock: extreme thirst, confusion, pallor, oliguria [3]
- Tachycardia (earliest sign — the heart tries to compensate for ↓ stroke volume by ↑ rate)
- Hypotension (SBP < 90 mmHg — a late sign indicating > 30% volume loss)
- Cold, clammy extremities (sympathetic vasoconstriction redirects blood to vital organs)
- Prolonged capillary refill ( > 2 seconds)
- Altered mental status → obtundation → cardiac arrest if untreated
Why this matters: Hypovolaemic shock is the most immediate life-threatening complication of massive LGIB. It is the reason resuscitation must precede all diagnostic efforts. Mortality is directly proportional to the duration and severity of shock.
Pathophysiology: Chronic or subacute blood loss → progressive depletion of red cell mass → ↓ haemoglobin → ↓ oxygen-carrying capacity of blood → tissue hypoxia → compensatory cardiovascular responses (↑ heart rate, ↑ stroke volume, ↑ 2,3-DPG to improve O₂ offloading)
- Symptomatic anaemia: SOB on exertion, postural dizziness, syncope, chest pain, palpitation, lethargy or fatigue [3]
- In chronic LGIB (e.g. from angiodysplasia, CRC, slow diverticular ooze): iron deficiency anaemia develops → koilonychia (spoon nails), angular stomatitis, glossitis, pica
Why some patients present with anaemia rather than acute shock: In chronic, slow bleeding, the body has time to compensate by expanding plasma volume (haemodilution) and increasing erythropoiesis. Hb drops gradually and the patient may tolerate remarkably low Hb levels (e.g. Hb 5–6 g/dL) if the decline is slow enough. They present with fatigue and exertional dyspnoea rather than acute collapse.
When shock is prolonged or severe, individual organs fail:
| Organ | Complication | Mechanism |
|---|---|---|
| Kidney | Acute kidney injury (pre-renal → intrinsic ATN) | ↓ Renal perfusion pressure → ↓ GFR → oliguria; if prolonged, tubular ischaemic necrosis |
| Heart | Myocardial ischaemia / acute MI | ↓ O₂ delivery to myocardium + ↑ myocardial O₂ demand (tachycardia) → supply-demand mismatch; especially dangerous in patients with pre-existing coronary artery disease |
| Brain | Confusion, syncope, hypoxic-ischaemic encephalopathy | ↓ Cerebral perfusion and oxygenation |
| Liver | "Shock liver" (ischaemic hepatitis) | Hepatic ischaemia → massive ↑ transaminases (ALT/AST), ↑ LDH [14] |
| Gut | Non-occlusive mesenteric ischaemia | Compensatory splanchnic vasoconstriction to preserve vital organs → paradoxically worsens gut ischaemia → can exacerbate bleeding or cause new ischaemic colitis |
Vicious Cycle
Shock from LGIB can cause non-occlusive mesenteric ischaemia (especially at watershed areas like the splenic flexure and rectosigmoid junction) → which causes more bleeding from the ischaemic colonic mucosa → which worsens the shock. This vicious cycle makes aggressive resuscitation critical.
- Mechanism: Massive haematochezia with haemodynamic instability → altered consciousness → loss of airway protective reflexes → aspiration of gastric contents or blood into the lungs
- Particularly relevant if there is concurrent UGIB with haematemesis
- Prevention: Early intubation in patients who are confused or have massive bleeding [1][3]
"Coagulopathy" → coagul- (clotting) + -pathy (disease) = disordered clotting.
- Dilutional coagulopathy: Massive crystalloid/colloid resuscitation without balanced blood product replacement → dilution of clotting factors and platelets → ↑ bleeding tendency
- Hypothermic coagulopathy: ↓ Body temperature can cause ↓ efficiency of clotting factors [1][3] — enzymatic reactions of the coagulation cascade are temperature-dependent; even mild hypothermia (35°C) significantly impairs clot formation
- Consumptive coagulopathy (DIC): In severe shock, tissue factor release and endothelial damage can trigger disseminated intravascular coagulation → simultaneous microvascular thrombosis and bleeding
- Acidotic coagulopathy: Metabolic acidosis from poor tissue perfusion inhibits clotting factor activity
The "lethal triad" of trauma surgery — hypothermia, acidosis, coagulopathy — applies equally to massive GI bleeding. Each element worsens the others in a self-perpetuating cycle. This is why keeping the patient warm, correcting acidosis, and replacing blood products (not just crystalloid) are essential.
- Rebleeding is one of the most feared complications and a major determinant of morbidity/mortality
- Rates vary by aetiology:
- Signs of rebleeding: ↑ pulse rate, haematemesis, fresh blood from NGT, fresh melaena, sudden ↓ Hb [15]
- Note: melaena can last 3–5 days after major bleeding → look for fresh melaena (jet-black, tarry) as opposed to stale (dull grey-black, mixed with normal stool) [15]
- Risk factors for recurrent bleeding [15]:
- Blood loss: shock on presentation, Hb < 8 on presentation, need for blood transfusion
- Patient profile: age > 60y, comorbidities, coagulopathy, already hospitalised for other conditions
- Disease: diverticular bleeding (inherently recurrent), angiodysplasia (intermittent by nature)
- Over-aggressive fluid resuscitation, especially in patients with HF or RF (who are predisposed to fluid overload) [3], can cause pulmonary oedema
- This is why CVP monitoring (± PAWP via Swan-Ganz catheter) is recommended in patients with cardiac comorbidities [1][3]
- Also relevant: over-transfusion is associated with ↑ mortality in GI bleeding (↑ intravascular volume → ↑ splanchnic pressure → promotes rebleeding)
B. Complications of Underlying Aetiologies
Each cause of LGIB carries its own set of complications if the disease progresses untreated:
| Complication | Mechanism | Clinical Features |
|---|---|---|
| Recurrent bleeding | Same vasa recta vulnerability persists; rebleeding rate 14–38% [1] | Recurrent episodes of painless haematochezia |
| Diverticulitis (distinct from bleeding) | Faecolith obstruction → bacterial overgrowth → inflammation | Clinical triad: lower abdominal pain (RLQ in Asia) + fever + leucocytosis [5] |
| Perforation | Inflammation erodes through diverticular wall → free perforation | Acute abdomen, generalised peritonitis, free gas under diaphragm on CXR |
| Abscess (pericolic, psoas, hepatic) | Contained perforation → walled-off collection | Persistent fever/pain despite antibiotics ± tender mass on PR [5] |
| Fistula formation | Inflammatory process erodes into adjacent organ | MC colovesical fistula: recurrent dysuria, pneumaturia, faecaluria [5] |
| Intestinal obstruction | Fibrosis and stricture from repeated inflammation → LBO; adhesions to inflamed bowel → SBO | Abdominal distension, vomiting, constipation, colicky pain [5] |
Hinchey classification for complicated diverticulitis [5]:
| Stage | Description | Mortality | Treatment |
|---|---|---|---|
| I | Localised pericolic abscess | 0% | IV antibiotics ± drainage |
| II | Distant abscess (retroperitoneal/pelvic) | 5% | IV antibiotics + drainage |
| III | Generalised suppurative peritonitis | 25% | Hartmann's operation / one-stage resection |
| IV | Faecal peritonitis (bowel wall perforation) | 50% | Hartmann's operation |
| Complication | Mechanism |
|---|---|
| Intestinal obstruction | Annular tumour narrows lumen → LBO; more common in left-sided CRC (narrower lumen) |
| Perforation | Tumour necrosis → full-thickness wall breach; or proximal perforation from closed-loop obstruction (competent ileocaecal valve) |
| Iron deficiency anaemia | Chronic occult bleeding from tumour surface → gradual Hb decline |
| Metastatic disease | Liver (portal venous drainage), lung, peritoneum, bone → organ-specific symptoms |
| Malignant fistula | Tumour invades adjacent organ (bladder → colovesical fistula; vagina → colovaginal fistula) |
| Complication | Mechanism | Details |
|---|---|---|
| Fulminant colitis | Severe inflammation extends beyond mucosa to muscle layers | > 10 stools/day, continuous bleeding, abdominal pain, distension, fever, anorexia [2] |
| Toxic megacolon | Non-obstructive colonic dilatation ≥ 6 cm (or caecum > 9 cm) with systemic toxicity | Fever, tachycardia, hypotension, dehydration, electrolyte disturbances, mental changes; diagnosed by plain AXR [2] |
| Perforation | Most commonly as consequence of toxic megacolon | Perforation with peritonitis = high mortality [2] |
| Stricture | Repeated inflammation → fibrosis or muscle hypertrophy → luminal narrowing | Should be considered malignant until proven otherwise by endoscopy with biopsy [2] |
| Colorectal cancer | Chronic inflammation → dysplasia → carcinoma sequence | Risk increases with disease duration and extent; regular endoscopic surveillance required [2] |
| Complication | Mechanism |
|---|---|
| Transmural necrosis / Gangrene | Prolonged ischaemia (15% of cases) → full-thickness bowel wall infarction → perforation → faecal peritonitis; mortality up to 50–75% [17] |
| Stricture | Fibrosis during healing phase → chronic narrowing |
| Persistent colitis | Some patients develop chronic segmental colitis resembling IBD |
| Complication | Mechanism |
|---|---|
| Haemorrhage | Ectopic gastric mucosa → acid secretion → peptic ulceration of adjacent ileal mucosa |
| Meckel's diverticulitis | Mimics appendicitis (RLQ pain); often only diagnosed intra-operatively [4] |
| Intestinal obstruction | Intussusception (Meckel's as lead point), volvulus, Littre's hernia (hernia containing Meckel's diverticulum) [4] |
C. Complications of Treatment
Colonoscopy is the most frequently performed investigation/therapy for LGIB. Complications are rare but important (overall morbidity ~0.28%, mortality ~0.007%) [18]:
| Complication | Mechanism | Prevention / Management |
|---|---|---|
| Perforation | Mechanical (scope tip pressure against thin wall) or thermal (electrocautery/APC extending into muscularis and serosa) → pneumoperitoneum and peritonitis | Careful technique; use CO₂ insufflation (absorbed faster than air); diagnosed by free gas on AXR/CT; management: small contained perforation → endoscopic clips (OTSC) + antibiotics + NPO; large/diffuse peritonitis → emergency surgery [2][18] |
| Bleeding (post-polypectomy) | Immediate: involvement of an underlying artery or inadequate coagulation of polyp stalk; Delayed (typically 5–7 days): sloughing of the coagulated eschar that was covering a blood vessel [2][18] | Prevention: adequate coagulation of stalk before cutting; use prophylactic clips on large stalks. Management: re-endoscopy with clips/thermal/topical haemostatic agent [7] |
| Post-polypectomy syndrome | Electrocoagulation injury to bowel wall creating a transmural burn and focal peritonitis without frank perforation [2][18] | Presents with fever, focal abdominal tenderness and leukocytosis 1–5 days following polypectomy [2]; management is conservative (NPO, IV antibiotics, observation) — no surgery needed as there is no free perforation |
| Sedation-related | Respiratory depression (opioids + benzodiazepines), MI, CVA, aspiration, hypoxaemia, arrhythmia, hypotension [15][18] | Appropriate monitoring (pulse oximetry, BP, ECG); have reversal agents ready (naloxone for opioids, flumazenil for benzodiazepines) |
| Preparation-related | Fluid and electrolyte disturbance (from 4–6 L PEG prep); nausea, vomiting, bloating, abdominal discomfort [18] | Ensure adequate hydration; monitor electrolytes in elderly/renal patients; split dosing regimen improves tolerance |
Post-polypectomy Syndrome vs Perforation
These two are commonly confused. Post-polypectomy syndrome = transmural burn WITHOUT perforation → focal peritonitis, fever, leucocytosis, but NO free gas on imaging → managed conservatively. Perforation = full-thickness breach → free gas on imaging → usually requires surgery or endoscopic clip closure. The distinction is made by imaging (AXR or CT looking for pneumoperitoneum).
| Complication | Mechanism | Incidence / Notes |
|---|---|---|
| Bowel ischaemia and infarction | Occlusion of end-artery → downstream tissue ischaemia; risk ~20% (decreases to 3–4% for super-selective embolisation) [7] | The colon has less collateral supply than the stomach/duodenum; super-selective catheterisation targets only the bleeding branch → minimises ischaemic territory |
| Contrast allergy | Hypersensitivity to iodinated contrast | Pre-medication with steroids/antihistamines in known allergy |
| Renal failure (contrast-induced nephropathy) | Contrast media → renal tubular toxicity + renal vasoconstriction | Risk factors: pre-existing CKD, diabetes, dehydration; prevention: adequate hydration, use low-osmolar contrast [11] |
| Bleeding from puncture site | Arterial puncture (femoral/radial) → haematoma, pseudoaneurysm, AV fistula, retroperitoneal bleeding | Careful technique; post-procedure compression; monitor for groin swelling/hypotension [11] |
| If resection is subsequently required, the anastomosis may not heal | Embolisation compromises blood supply to the segment that may later need surgical resection → ischaemic anastomosis → leak | This is a critical consideration: embolisation may "burn bridges" for future surgery [1] |
| Rebleeding | Incomplete embolisation; collateral vessel reconstitution | May require repeat embolisation or surgery |
| Non-target embolisation | Embolic material migrates to unintended vessels | Ischaemia of non-target organs; minimised by super-selective technique |
3. Complications of Surgery
| Complication | Mechanism |
|---|---|
| Surgical site infection | Contamination of wound by bowel flora (especially in unprepared bowel — common in emergency LGIB surgery) |
| Postoperative ileus | Surgical manipulation of bowel → reflex inhibition of peristalsis by sympathetic nervous system; electrolyte disturbances (↓ K⁺, ↓ Ca²⁺); opioid use |
| Venous thromboembolism (DVT/PE) | Virchow's triad: stasis (immobility post-op), endothelial injury (surgery), hypercoagulability (stress response, dehydration) |
| Complication | Details |
|---|---|
| Injury to adjacent structures | Left ureter and gonadal vessels (during left-sided resection); iliac artery; spleen (during splenic flexure mobilisation in TME); GB/D2 (right hemicolectomy); seminal vesicles (LAR) [18] |
| Autonomic nerve injury (especially in rectal surgery) | Sympathetic damage → urinary incontinence, impaired ejaculation; Parasympathetic damage → urinary retention, erectile dysfunction [18] |
| Complication | Timing | Mechanism | Clinical Features | Management |
|---|---|---|---|---|
| Anastomotic bleeding | Early ( < 30 days) | Bleeding from suture line or staple line | Fresh PR blood post-operatively | Blood transfusion, correction of coagulopathy; rarely requires re-operation [2] |
| Anastomotic leak | Early (typically apparent 5–7 days post-op) [2] | Failure of tissue healing at anastomotic site → spillage of bowel contents | Pain, fever, tachycardia, feculent or purulent drainage; radiological signs: fluid or gas-containing collections [2] | Fluid resuscitation, broad-spectrum IV antibiotics, bowel rest, image-guided percutaneous drainage, temporary faecal diversion or drainage, or resection of the anastomosis [2] |
| Anastomotic stricture | Late ( > 30 days) | Fibrosis during healing | Obstructive symptoms, difficulty with bowel movements | Finger dilatation for low anastomosis; endoscopic balloon dilatation for high anastomosis [2]; majority do not require intervention |
| Fistula | Late ( > 30 days) | Breakdown of anastomosis → abnormal communication | Enterocutaneous (colocutaneous) → managed conservatively (most close spontaneously); Rectovaginal, rectourinary → require proximal faecal diversion [2] |
| Timing | Complication | Mechanism |
|---|---|---|
| Early ( < 30 days) | Stomal bleeding | Mucocutaneous junction haemorrhage |
| Stomal necrosis | Ischaemia from inadequate blood supply to the exteriorised bowel | |
| Stomal retraction | Tension on the stoma due to thick abdominal wall / inadequate mobilisation | |
| Mucocutaneous separation | Breakdown of the junction between stoma and skin | |
| Skin irritation and dermatitis | Most common in end and loop ileostomy due to high-output and high alkaline enzymatic effluent [2] — the small bowel contents are more corrosive than colonic contents | |
| Late ( > 30 days) | Parastomal hernia | Weakness in the fascial aperture through which the stoma is brought out |
| Stomal prolapse | Intussusception of bowel through the stoma | |
| Stomal stenosis | Fibrosis at the fascial or skin level |
| Complication | Mechanism |
|---|---|
| Rectal stump leak/abscess/fistula | Closed rectal stump can break down → pelvic sepsis |
| Ureteric injury | Close proximity of left ureter to sigmoid colon |
| Stoma complications | As above (end colostomy at LIF) |
| Reversal-related morbidity | Re-anastomosis (Hartmann's reversal) at 2–3 months is itself a significant operation with its own complication rate |
| Category | Complications |
|---|---|
| Bleeding itself | Hypovolaemic shock, symptomatic anaemia, end-organ damage (AKI, MI, ischaemic hepatitis), aspiration pneumonia, acquired coagulopathy (dilutional, hypothermic, DIC), rebleeding, fluid overload |
| Underlying disease | Diverticulitis → perforation → abscess → fistula → obstruction; CRC → obstruction → perforation → metastasis; IBD → fulminant colitis → toxic megacolon → perforation → CRC; Ischaemic colitis → gangrene → perforation |
| Endoscopy | Perforation, post-polypectomy bleeding (immediate or delayed at 5–7 days), post-polypectomy syndrome, sedation-related (respiratory depression, aspiration), preparation-related (electrolyte disturbance) |
| Embolisation | Bowel ischaemia (20% → 3–4% if super-selective), contrast allergy, CIN, puncture-site bleeding, non-target embolisation, compromised future anastomosis |
| Surgery | SSI, ileus, VTE, organ injury (ureter, spleen, autonomic nerves), anastomotic leak/bleed/stricture/fistula, stoma complications |
High Yield Summary
Complications of LGIB itself: Hypovolaemic shock (most immediately life-threatening); symptomatic anaemia (chronic LGIB); end-organ damage (AKI, MI, shock liver); acquired coagulopathy (the "lethal triad" of hypothermia + acidosis + coagulopathy); rebleeding (14–38% diverticular, 25–85% angiodysplasia).
Signs of rebleeding: ↑ pulse rate, fresh PR blood, fresh melaena, sudden ↓ Hb. Melaena can persist 3–5 days after a bleed — look for FRESH melaena.
Post-polypectomy syndrome vs perforation: Both present with fever, pain, leucocytosis post-colonoscopy. Key difference: post-polypectomy syndrome = NO free gas (transmural burn without perforation → conservative Mx). Perforation = free gas on imaging → surgery/endoscopic closure.
Embolisation risk: Bowel ischaemia ~20% (↓ to 3–4% with super-selective technique). If subsequent surgical resection needed, compromised blood supply → anastomosis may not heal.
Anastomotic leak: Apparent 5–7 days post-op; pain + fever + tachycardia + purulent drainage. Mx: resuscitation, antibiotics, bowel rest, drainage ± re-operation.
Stoma dermatitis: Worst with ileostomy (high-output alkaline enzymatic effluent). Late complications: parastomal hernia, prolapse, stenosis.
Diverticulitis complications (Hinchey): Stage I-II = abscess (conservative/drainage); Stage III-IV = peritonitis (Hartmann's operation). Mortality reaches 50% in Stage IV.
Active Recall - Complications of Lower GI Bleed
[1] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.3.6 Lower GI Bleeding, p281–286) [2] Senior notes: felixlai.md (Lower GI bleeding section; Colonoscopy complications; Colorectal surgery complications; UC complications) [3] Senior notes: Ryan Ho GI.pdf (Section 3.1.2 Lower GI Bleeding, p109–111) [4] Senior notes: maxim.md (Angiodysplasia; Meckel diverticulum) [5] Senior notes: maxim.md (Diverticulitis and complications; Hinchey classification; Hartmann's operation) [7] Lecture slides: GC 186. Lower and diffuse abdominal painfresh blood in stool.pdf (p36, p40) [11] Senior notes: Ryan Ho GI.pdf (Mesenteric angiography complications, p48) [14] Senior notes: Ryan Ho Critical Care.pdf (Management of Hypovolemic Shock, p21) [15] Senior notes: Ryan Ho GI.pdf (Endoscopic Tx modalities and rebleeding monitoring, p45) [17] Senior notes: Ryan Ho GI.pdf (Ischaemic colitis management/prognosis, p147) [18] Senior notes: Ryan Ho GI.pdf (Colonoscopy complications, p180; Post-operative complications of colorectal surgery, p169); Senior notes: maxim.md (Post-operative complications section); Senior notes: felixlai.md (Colorectal surgery complications section)
History Taking: Lower GI Bleed (LGIB)
This is the one complaint where you might need to resuscitate before you history-take. A patient passing large-volume bright red blood per rectum can be in hypovolaemic shock. Your first job is a quick "eyeball" assessment. [1][2]
- Is the patient haemodynamically stable? (BP, pulse, conscious level, capillary refill)
- Very severe: hypotension, tachycardia, agitation, confusion, drowsiness, coma [2]
- Moderate to severe: postural hypotension (indicates ≥20% reduction in blood volume) [2]
In your OSCE, you won't literally resuscitate the mannequin, but you should verbalise that you would assess haemodynamic stability first. This scores marks.
Cantonese phrasing:
- "你而家覺得頭暈嗎？企起身會唔會暈？" (Do you feel dizzy? Dizzy when standing up?)
- "你隻手腳有冇凍？" (Are your hands and feet cold?)
1. Characterise the Bleeding
This is the most important part of your history. The way blood appears tells you roughly where it comes from. [1][2][3]
| Finding | Likely Source | Cantonese |
|---|---|---|
| Blood mixed with faeces | Proximal to sigmoid (right colon) — faeces still fluid so blood mixes in [1][2] | 血同大便撈埋一齊 |
| Blood on surface of stools / streaking | Left colon / rectum — faeces already solid [1] | 血喺大便外面 |
| Blood on toilet paper only | Anorectal conditions — mild, close to anal margin [1][2] | 抹嘅時候先見到血 |
| Blood after defecation | Anus, e.g. haemorrhoids [2] | 屙完之後先滴血 |
| Blood by itself (torrential) | Diverticular disease, angiodysplasia, rectal varices [2] | 淨係出血，冇大便 |
| Melena (黑色、臭、稀) | Upper GI or right colon [2] | 大便黑色好似芝麻糊，好臭 |
Practical phrasing:
- "你見到嘅血係咩顏色？鮮紅色定暗紅色定黑色？" (What colour is the blood? Bright red, dark red, or black?)
- "血係混喺大便入面，定喺大便外面，定抹嘅時候先見到？" (Is the blood mixed in the stool, on the surface, or only on wiping?)
- "有冇試過淨係出血冇大便？" (Have you ever passed blood by itself without stool?)
Why the relationship of blood to stool matters
This single question narrows your differential enormously. Blood mixed with stool = proximal source (cancer, IBD, diverticular disease). Blood separate from stool = outlet-type (haemorrhoids, fissure). Blood by itself in large volume = vascular cause (diverticular, angiodysplasia). Examiners love this distinction. [1][2]
- "每次出幾多血？好似幾多？有冇成廁所都係血？" (How much blood each time? Has the toilet bowl been full of blood?)
- "出咗幾多次？幾時開始？" (How many times? When did it start?)
- "係持續出血定間歇性？" (Continuous or intermittent?)
Why this matters: Diverticular bleeding is classically painless, profuse haematochezia that stops spontaneously in 80–85% of cases but can be massive. [1][2] Angiodysplasia tends to be intermittent and less severe (venous bleeding). [1][2] Colorectal cancer tends to be low-grade, intermittent and may present with iron-deficiency anaemia rather than frank haematochezia. [4]
2. Associated GI Symptoms
- "你大便習慣有冇改變？有冇試過肚屙同便秘輪住嚟？" (Any change in bowel habits? Alternating diarrhoea and constipation?)
- "有冇痾黏液？" (Any mucus in stools?)
- "大便嘅粗幼有冇變？" (Has the calibre of your stool changed?)
- Why: Change in stool calibre is a red flag for obstructing colorectal lesion. [3]
- "肛門有冇痛？痕？有冇嘢突出嚟？" (Any pain/itchiness at the anus? Any lump coming out?)
- Perianal mass/pain → haemorrhoids (especially if thrombosed), perianal abscess [3]
- Pruritus → haemorrhoids (mucus secretion), threadworms
- Sense of prolapse → haemorrhoids
- "有冇嘔血？嘔啡色嘢？" (Any vomiting blood? Coffee-ground vomitus?)
- Why: 10–15% of haematochezia is actually from a massive upper GI bleed. Always consider this, especially if the patient is haemodynamically unstable. [2]
These are the questions examiners specifically look for. [3][5]
- Change in bowel habit (alternating diarrhoea/constipation) [3][5]
- Tenesmus [3][5]
- Mucus per rectum [3][5]
- Duration of bleeding [5]
- Blood mixed with stool [5]
- Melaena / altered blood / dark red / maroon-coloured [5]
- Older age (>50) [5]
- Constitutional symptoms: weight loss (體重有冇輕咗?), loss of appetite (冇胃口?), fatigue (成日好攰?) [2][3]
- Family history of colorectal cancer or polyposis syndromes [3][5]
- Symptoms of metastatic spread: jaundice (skin/eyes yellow), bone pain, persistent cough/SOB, intractable sacral pain [2]
Red Flag Checklist for PR Bleeding
If a patient is >50 years old with any change in bowel habit, weight loss, blood mixed with stool, or family history of CRC — this is a two-week-wait referral for colonoscopy. Students commonly forget to ask about family history and constitutional symptoms. Don't lose these easy marks. [5]
This is where you earn extra marks — showing the examiner you're thinking about specific diagnoses. [1][2][3]
| Differential | Key Differentiating Questions | Why It Matters |
|---|---|---|
| Diverticular disease (憩室病) | Painless profuse haematochezia? Self-limiting? Previous episodes? [1][2][3] | Commonest cause of LGIB (17–40%). Painless. Stops spontaneously 80–85%. Right-sided diverticula commoner in Asians. [1] |
| Angiodysplasia | Elderly? Hx of aortic stenosis? Hereditary haemorrhagic telangiectasia? CKD? [1][2] | Degenerative, venous bleeding, intermittent. Associations: Heyde syndrome (aortic stenosis), Osler-Weber-Rendu. [1][2] |
| Colorectal carcinoma | >50y? Change in bowel habit? Pencil-thin stools? Tenesmus? Weight loss? FHx? Smoker? Previous polyps? [2][3] | ~10% of PR bleed in >50y. Low-grade, intermittent bleeding. May present as iron-deficiency anaemia. [4] |
| IBD | Young patient? Bloody diarrhoea? Mucus? Extra-intestinal features (joint pain, skin rash, eye symptoms)? [2] | UC more commonly causes bleeding than Crohn's. Ask about extra-intestinal manifestations. [4] |
| Ischaemic colitis | CVS risk factors? Acute MI? Stroke? AF? Abdominal pain post-prandially? [2] | Classically LIF pain with bloody diarrhoea in elderly with vascular risk factors. |
| Infective colitis | Fever? Recent travel (TOCC)? Antibiotics (C. difficile)? Food history? Contacts? Immunosuppression (CMV)? [2][6] | Must exclude infectious causes before diagnosing IBD. |
| Haemorrhoids | Outlet-type bleeding? Blood on wiping/dripping after defecation? Constipation? Pregnancy? Perianal lump? [1][2][3] | Most common cause of LGIB in < 50y. Painless unless thrombosed. |
| Anal fissure | Severe sharp pain on defecation? Hx of constipation? [2] | Classic triad: pain, spasm, bleeding on defecation. |
| Radiation proctocolitis | Previous pelvic RT (cervical, prostate, rectal cancer)? Timing of symptoms relative to RT? [1][4] | Acute (< 6 weeks) or delayed ( > 9 months, can be >10 years). [4] |
| Post-polypectomy | Recent colonoscopy or polypectomy? [1][5] | Acute (arterial) or delayed (eschar slough) bleeding. Always ask! [1] |
| Meckel's diverticulum | Young patient? Painless bleeding? [1] | Rule of 2s. Important in paediatric/young adult LGIB. |
| Rectal varices | Known liver disease? Portal hypertension? [4] | Portosystemic shunt between superior and inferior rectal veins. Severe bleeding. [4] |
| GI endometriosis | Cyclical bleeding pattern? Young female? [3] | Bleeding in a cyclical manner → pathognomonic. [3] |
5. Targeted Systems Review
- AF, IHD, heart failure, aortic stenosis (Heyde syndrome), peripheral vascular disease
- Why: CVS risk factors → ischaemic colitis; HF → susceptible to fluid overload during resuscitation; aortic stenosis → angiodysplasia [2]
- SOB at rest or on exertion
- Why: Anaemia symptoms; cardiopulmonary disease → more susceptible to hypoxaemia [2]
- Easy bruising, prolonged bleeding from cuts, heavy periods
- Why: Underlying bleeding disorder may be the reason bleeding is disproportionate [7]
- Previous bleeding episodes — When? What investigation? What treatment? [5]
- Peptic ulcer disease — Could this be an upper GI source? [1]
- IBD — Known diagnosis? On treatment?
- Previous colonoscopy / polypectomy — When? Findings? [5]
- Chronic liver disease — Coagulopathy, varices [1]
- Heart failure or renal failure — Fluid management implications [2]
- Hereditary haemorrhagic telangiectasia — Angiodysplasia [1]
- Connective tissue disorders — Ehler-Danlos [7]
- Abdominal aortic aneurysm (AAA) repair with graft → DDx: aorto-enteric fistula (herald bleed → massive exsanguination) [1]
- Gastroenteric anastomosis → DDx: marginal ulcers [1]
- Previous colorectal surgery → anastomotic bleeding, altered anatomy
- Previous pelvic surgery → adhesions, radiation history
Don't Forget the Aorto-Enteric Fistula
Any patient with a history of AAA repair presenting with GI bleeding must be considered to have an aorto-enteric fistula until proven otherwise. This is a life-threatening emergency. Students almost always miss this. A "herald bleed" (small initial bleed) can precede catastrophic haemorrhage. [1]
This is consistently highlighted across all lecture slides and notes. [1][2][5]
| Drug Class | Relevance | Cantonese |
|---|---|---|
| NSAIDs | Peptic ulcers, small bowel ulcers, colitis [2][6] | 你有冇食止痛藥？ |
| Aspirin | ↑ bleeding risk, peptic ulcers [1] | 你有冇食薄血丸或者阿士匹靈？ |
| Antiplatelets (clopidogrel) | ↑ bleeding risk [1][2] | |
| Anticoagulants (warfarin, DOACs) | ↑ bleeding risk [1][2][5] | |
| Iron supplements | Can cause black stool (must distinguish from melena) [1] | 你有冇食鐵丸？ |
| Antibiotics | C. difficile-associated colitis [6] | 最近有冇食過抗生素？ |
| Traditional Chinese medicine | May contain steroids → GI ulceration [1] | 有冇食中藥？ |
| Steroids | ↑ ulcer risk |
- Allergies: "你有冇對咩藥物敏感？" (Any drug allergies?)
- Colorectal cancer — First-degree relative with CRC → significantly elevated risk [3][5]
- Familial polyposis syndromes (FAP, Lynch syndrome)
- IBD — Family predisposition
- Bleeding disorders — Haemophilia, von Willebrand disease [7]
"你屋企人有冇人試過大腸癌或者腸瘜肉？" (Has anyone in your family had bowel cancer or polyps?)
| Domain | Questions | Why It Matters |
|---|---|---|
| Smoking | 你有冇食煙？食咗幾耐？每日幾多支？ | Risk factor for CRC and peptic ulcers [1] |
| Alcohol | 你飲唔飲酒？飲幾多？ | Chronic liver disease → varices, coagulopathy [1] |
| Diet | High red/processed meat, low fibre | CRC risk factors |
| Sexual history | If appropriate — MSM, receptive anal intercourse | Proctitis (gonorrhoea, HSV, chlamydia) [6] |
| Travel history (TOCC) | 最近有冇去旅行？去邊度？ | Endemic areas for parasitic infections (amebiasis) [6] |
| Occupation | Prolonged sitting/standing | Haemorrhoid risk |
| Functional baseline | ADLs, mobility, exercise tolerance | Pre-morbid fitness affects surgical candidacy |
These findings should prompt immediate escalation to a senior clinician/surgeon:
- Haemodynamic instability — Hypotension (SBP < 90), tachycardia (> 100), confusion, syncope [2]
- Massive ongoing haematochezia — Not settling, requiring transfusion
- Suspected aorto-enteric fistula — History of AAA graft + GI bleed [1]
- Signs of peritonism — Guarding, rebound tenderness → perforation/ischaemic bowel
- Massive transfusion requirement — >6 units pRBC [2]
- Anticoagulant use with uncontrolled bleeding [2]
- Suspected upper GI source — Haematemesis, coffee-ground vomitus, haemodynamic instability disproportionate to PR bleeding [2]
Common Student Mistakes
- Forgetting to exclude upper GI bleed — 10–15% of haematochezia is from massive UGIB. Always ask about haematemesis, coffee-ground vomitus, and melena. [2]
- Not asking about the relationship of blood to stool — This is the single most localising question and students routinely skip it.
- Ignoring drug history — NSAIDs, antiplatelets, and anticoagulants are consistently tested. [1][2][5]
- Not asking about recent procedures — Post-polypectomy bleeding is an important and easily missed cause. [1][5]
- Forgetting iron supplements — Black stool from iron ≠ melena. Ask specifically. [1]
- Not asking about AAA repair — Aorto-enteric fistula is rare but lethal and always asked in exams. [1]
- Skipping constitutional symptoms and family history — These are the CRC red flags examiners specifically look for. [5]
- Assuming haemorrhoids in a young patient without exclusion of other causes — Haemorrhoids are common but should be a diagnosis of exclusion in someone with red flags.
- Not checking haemodynamic status first — In an OSCE, verbalise: "Before taking a detailed history, I would assess haemodynamic stability."
- "75% of lower GI bleeding stops spontaneously" [2] — This is a favourite exam fact. It means that most LGIB is self-limiting, but you still need to find the cause.
- Right-sided diverticula are more common in Asians (cf. left-sided in Western populations) and have a higher risk of haemorrhage. [1] — HKU loves this.
- Hb does NOT reflect acute blood loss — It takes ≥24 hours for haemodilution to occur. A normal Hb in the ED does NOT mean the patient hasn't bled significantly. [2]
- Colour of blood is a rough guide only — Fresh PR blood (鮮紅色) = distal to splenic flexure; Dark PR blood (暗紅色) = proximal to splenic flexure. [3]
- Diverticular bleeding occurs in the absence of diverticulitis — A common misconception. Bleeding and inflammation are separate complications. [1]
- Colonoscopy diagnostic yield = 75–90% and should be performed early. [2]
- 99mTc-labelled RBC scan is more sensitive than angiography for GI bleeding (min bleeding rate 0.1–0.4 vs ≥0.5–1 mL/min) and can detect intermittent bleeding with delayed images up to 24h. [8]
Mr Chan is a 68-year-old gentleman who presented 2 days ago to Queen Mary Hospital with a 3-day history of painless, profuse, bright red per-rectal bleeding. He describes passing large volumes of fresh blood by itself without stool on approximately 6 occasions. He denies any abdominal pain, change in bowel habit, tenesmus, mucus per rectum, or constitutional symptoms such as weight loss or loss of appetite. There is no haematemesis or coffee-ground vomitus. He reports feeling light-headed on standing and has had one syncopal episode.
His past medical history is significant for hypertension, hyperlipidaemia, and type 2 diabetes mellitus. He had a right hemicolectomy 5 years ago for a benign adenomatous polyp. He has no history of inflammatory bowel disease, liver disease, or previous GI bleeding.
His past surgical history includes the right hemicolectomy as mentioned, and an open appendicectomy in childhood. He has had no aortic surgery.
His regular medications include aspirin 80 mg daily, atorvastatin 40 mg daily, metformin 500 mg BD, and amlodipine 5 mg daily. He has no known drug allergies.
His family history is notable for a brother diagnosed with colorectal carcinoma at age 72. There is no family history of inflammatory bowel disease or polyposis syndromes.
Socially, Mr Chan is a retired bus driver. He is an ex-smoker with a 30 pack-year history, having quit 10 years ago. He drinks alcohol socially, approximately 2 units per week. He is independent in all activities of daily living and has a good exercise tolerance, able to climb 2 flights of stairs without limitation.
In summary, Mr Chan is a 68-year-old gentleman with cardiovascular risk factors, on aspirin, presenting with acute, painless, profuse haematochezia with haemodynamic compromise including syncope. The leading differential diagnosis is diverticular bleeding given the painless, profuse nature and his age. However, given his family history of colorectal carcinoma and personal history of adenomatous polyp, malignancy must be excluded. I would like to discuss his resuscitation plan, the need for urgent colonoscopy, and whether we should consider a CT angiogram given his haemodynamic instability.
Active Recall - History Taking
High Yield Summary
Lower GI bleed = bleeding distal to ligament of Treitz. Most common presentation is haematochezia. 75% stops spontaneously.
Key history framework: (1) Assess haemodynamic stability FIRST. (2) Characterise the bleeding — nature, colour, relationship to stool, volume, timing. (3) Associated GI symptoms — bowel habit change, pain, anorectal symptoms. (4) Red flags for CRC — age >50, change in bowel habit, constitutional symptoms, family history. (5) Always exclude UGIB (10–15% of haematochezia). (6) Drug history — NSAIDs, antiplatelets, anticoagulants, iron, antibiotics, TCM. (7) Surgical history — AAA repair (aorto-enteric fistula), recent polypectomy. (8) Comorbidities — liver disease (varices/coagulopathy), CKD (platelet dysfunction), CVS disease (ischaemic colitis), HF/RF (fluid overload risk).
Top differentials by age: < 50y = haemorrhoids, IBD, Meckel's. >50y = diverticular disease, angiodysplasia, colorectal carcinoma. All ages = infectious colitis, ischaemic colitis, post-procedure bleeding.
Three things students always forget: (1) Asking about relationship of blood to stool. (2) Excluding UGIB. (3) AAA graft history.
[1] Senior notes: felixlai.md (Lower GI bleeding, sections on differential diagnosis and history taking) [2] Senior notes: Ryan Ho GI.pdf (pp. 107–111, Approach to Lower GI Bleeding — History Taking, Causes, Investigations) [3] Senior notes: maxim.md (Section 4.2 LGIB, DDx table and Section 4.8 Diseases of anal canal) [4] Senior notes: Ryan Ho Fundamentals.pdf (pp. 281–286, Lower GI Bleeding causes and approach) [5] Lecture slides: GC 186. Lower and diffuse abdominal painfresh blood in stool.pdf (pp. 3, 4, 19, 38) [6] Senior notes: felixlai.md (Ulcerative colitis section — differential diagnosis including infectious colitis, radiation colitis, sexual history) [7] Senior notes: Ryan Ho Haemtology.pdf (p. 114, Approach to Bleeding Disorders — history taking) [8] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p. 62, Red Blood Cell Scan for GI bleeding)
Llq Pain
Left lower quadrant pain is discomfort localized to the lower left abdomen, commonly associated with diverticulitis, ovarian pathology, or sigmoid colon disorders.
Obstructive Jaundice
Obstructive jaundice is a condition caused by blockage of the bile ducts, preventing bile drainage into the intestine and resulting in conjugated hyperbilirubinemia, dark urine, pale stools, and pruritus.