Per Rectal Bleeding
Per rectal bleeding is the passage of blood through the anus, originating from the rectum, colon, or other parts of the gastrointestinal tract, indicating conditions ranging from hemorrhoids to colorectal malignancy.
Per Rectal Bleeding (PR Bleeding)
Per rectal (PR) bleeding — also termed rectal bleeding or haematochezia in its overt form — refers to the passage of blood through the anus. The term is broad and encompasses a spectrum from a tiny streak on toilet paper to massive, life-threatening haemorrhage with haemodynamic compromise.
Key terminology to get straight from the start:
| Term | Meaning |
|---|---|
| Haematochezia | Passage of bright red blood or blood clots per rectum — implies a source relatively close to the anus (left colon, rectum, anus) or a very brisk upper GI bleed |
| Melena | Black, tarry, offensive-smelling stools — implies blood that has been digested (usually > 50 mL originating proximal to the ligament of Treitz, but can occur with right-sided colonic lesions if transit is slow) |
| Occult bleeding | Bleeding not visible to the naked eye — detected by faecal occult blood test (FOBT) or faecal immunochemical test (FIT), or presenting with iron-deficiency anaemia |
| Outlet-type bleeding | Blood separate from stool, dripping into the toilet bowl or on tissue paper — suggests an anorectal source |
Why does the colour matter? Haemoglobin is degraded by gut bacteria and gastric acid into haematin (black) during transit. The longer blood sits in the GI tract, the darker it gets. Bright red = short transit / distal source. Dark red / maroon = proximal colonic or small bowel source with moderate transit. Melena = prolonged transit / upper GI source.
- Incidence: Annual incidence of significant lower GI bleeding (LGIB) is approximately 20–27 per 100,000 in Western populations, with incidence rising markedly with age [2].
- Age distribution:
- Haemorrhoids are the most common cause in patients < 50 years [1][3].
- Diverticular disease and angiodysplasia predominate in patients > 60 years [1][2].
- Colorectal cancer should be considered in anyone > 50 (some guidelines now say > 45) with new PR bleeding, or younger if red-flag features are present.
- Sex: Overall slight male predominance for LGIB; CRC is M:F ≈ 1.6:1 in Hong Kong [4].
- Hong Kong-specific considerations:
- Colorectal cancer is the most common cancer overall and 2nd most common cause of cancer death in Hong Kong (incidence 74.1/100,000/year) [4].
- Diverticular disease in Asia is more commonly right-sided (ascending colon/caecum), unlike the left-sided (sigmoid) predominance in Western populations — and right-sided diverticula carry a higher risk of haemorrhage [1][3].
- Rectal ulcer (acute haemorrhagic rectal ulcer) is more common in Asia — typically in elderly, critically ill, and bedridden patients [5].
3. Anatomy and Function
Understanding the anatomy is critical because the source site determines the clinical presentation, investigation strategy, and management.
- The ligament of Treitz (suspensory muscle of the duodenum) is the peritoneal fold at the duodenojejunal flexure.
- By convention:
- Some authors further subdivide LGIB into small bowel bleeding (mid-GI) and colonic/anorectal bleeding (true lower GI).
| Artery | Territory | Notes |
|---|---|---|
| Superior Mesenteric Artery (SMA) | Caecum → proximal 2/3 of transverse colon | Ileocolic, right colic, middle colic arteries |
| Inferior Mesenteric Artery (IMA) | Distal 1/3 of transverse colon → upper rectum | Left colic, sigmoid arteries, superior rectal artery |
| Internal Iliac Artery (IIA) | Mid and lower rectum, anal canal | Middle rectal artery, inferior rectal artery (via pudendal) |
Collateral circulation:
- Marginal artery of Drummond — connects SMA and IMA territories along the mesenteric border of the colon.
- Arc of Riolan (meandering mesenteric artery) — a more central collateral between SMA and IMA.
Watershed areas (vulnerable to ischaemia):
- Griffiths' point — at the splenic flexure, where the ascending branch of the left colic artery communicates with the marginal artery of Drummond. This is the junction between SMA and IMA territories [3][6].
- Sudeck's point — at the rectosigmoid junction, where the descending branch of the left colic artery anastomoses with the superior rectal artery [3][6].
Why do watershed areas matter for PR bleeding? These areas receive the least robust blood supply. In low-flow states (e.g. shock, heart failure, post-cardiac surgery), they are the first to become ischaemic → ischaemic colitis → bloody diarrhoea = a cause of PR bleeding.
- The vasa recta are the terminal straight arteries that penetrate the circular muscle layer of the colon to supply the mucosa and submucosa.
- Diverticula form at the points where vasa recta penetrate the muscular wall — this is the weakest point in the colonic wall [1][3][5].
- When a diverticulum herniates, the vasa recta are draped over the dome of the diverticulum and are separated from the bowel lumen only by mucosa → vulnerable to erosion and rupture → diverticular bleeding [1].
The anal canal is approximately 4 cm long from the anal verge. The dentate (pectinate) line divides it into an upper 2/3 and lower 1/3, and this boundary is one of the most important anatomical landmarks in surgery [1][3].
| Feature | Above Dentate Line | Below Dentate Line |
|---|---|---|
| Embryology | Endoderm (hindgut) | Ectoderm (proctodeum) |
| Epithelium | Columnar → adenocarcinoma | Stratified squamous → SCC |
| Nerve supply | Autonomic (inferior hypogastric plexus) → painless | Somatic (inferior rectal nerve via pudendal nerve) → painful |
| Venous drainage | Superior rectal vein → portal system | Middle & inferior rectal veins → IVC (systemic) |
| Lymphatic drainage | Internal iliac & inferior mesenteric LN | Superficial inguinal LN |
Why is this table clinically important?
- Internal haemorrhoids arise above the dentate line → covered by columnar epithelium with autonomic innervation → classically painless bleeding (unless they strangulate or thrombose).
- External haemorrhoids arise below the dentate line → somatic innervation → painful, especially when thrombosed.
- Anal fissures involve the anoderm below the dentate line → somatic nerve supply → intensely painful on defaecation.
- The venous drainage explains why internal haemorrhoids are part of the portosystemic anastomosis — in portal hypertension, blood is shunted from the superior rectal veins (portal) to the middle/inferior rectal veins (systemic), forming rectal varices (not the same as haemorrhoids!).
- Anal vascular cushions are clusters of vascular tissue, smooth muscle, and connective tissue located in the submucosa of the anal canal [3].
- They are composed of branches of the superior rectal artery and superior rectal veins, covered by a mucosal layer.
- Function: They assist the anal sphincter in maintaining continence by forming a "seal" — they contribute ~15–20% of resting anal pressure.
- Classically found at the 3, 7, and 11 o'clock positions (in the lithotomy position) [3].
- Haemorrhoids represent abnormal engorgement and prolapse of these anal vascular cushions — not simply "varicose veins" [3].
4. Aetiology (with Focus on Hong Kong) and Pathophysiology
The causes of PR bleeding can be organised anatomically, from the anus upwards, or by the nature of the pathology (anatomical, vascular, inflammatory, neoplastic). Below is a comprehensive breakdown.
4.1 Anorectal Causes (~10% of LGIB)
"Haemorrhoids: abnormal engorgement and prolapse of the anal vascular cushions" [3]
Pathophysiology:
- Degeneration of supporting fibroelastic tissues and smooth muscles → anal cushions are displaced caudally → dilation and engorgement of the arteriovenous plexuses → prolapse [3].
- This is a degenerative sliding theory — not simply venous congestion.
- Acute thrombosis can occur: the prolapsed, engorged tissue becomes incarcerated → venous outflow obstruction → thrombosis → painful, large, swollen, irreducible mass with marked anal sphincter contraction [3].
Risk factors:
- Aging (degeneration of connective tissue)
- Sitting on the toilet for prolonged periods
- Increased intra-abdominal pressure: constipation, chronic cough, ascites, pregnancy, obesity [1][3]
- Genetic predisposition [3]
- Low-fibre diet [1]
Types:
| Feature | Internal Haemorrhoids | External Haemorrhoids |
|---|---|---|
| Origin | Above dentate line (columnar epithelium) | Below dentate line (squamous epithelium) |
| Innervation | Autonomic → painless | Somatic → painful |
| Venous drainage | Superior rectal vein → portal system | Inferior rectal vein → IVC |
| Clinical features | Painless bright red PR bleeding (outlet-type), prolapse, anal itching, mucous discharge | Pain after defecation → severe perianal pain if thrombosed, perianal swelling/skin tags |
Grading of Internal Haemorrhoids:
| Grade | Description |
|---|---|
| 1st degree | Bleeding only without prolapse |
| 2nd degree | Prolapse at defecation but reduces spontaneously |
| 3rd degree | Prolapse requiring manual reduction |
| 4th degree | Permanently prolapsed (irreducible) |
Always Exclude Other Causes
ALWAYS exclude other possible sources of PR bleeding before attributing symptoms to haemorrhoids. Haemorrhoids are so common that they can coexist with colorectal cancer. A patient with haemorrhoids and red-flag features (change in bowel habit, weight loss, age > 50, family history) must have further investigation (colonoscopy). [1][3]
Definition: A tear in the anoderm distal to the dentate line — one of the most common anorectal conditions [1][7].
Pathophysiology:
- Stretching of anal mucosa beyond its normal capacity (e.g. passage of hard stool, prolonged diarrhoea, vaginal delivery, anal intercourse) [1]
- Repeated injury → spasm of the exposed internal sphincter muscle beneath the tear
- Spasm pulls the edges of the fissure apart → impairs healing
- Ischaemia secondary to reduced perfusion — the anoderm at the posterior midline has the poorest blood supply of any quadrant in the anal canal (this is why > 90% of fissures are posterior) [1]
- Increased anal pressure from sphincter spasm → further reduces perfusion → a vicious cycle of ischaemia, pain, spasm, and failed healing
Aetiology:
- Primary: Local trauma — hard stools, prolonged diarrhoea, vaginal delivery, anal sex [1]
- Secondary: IBD (especially Crohn's), granulomatous disease (TB, sarcoidosis), malignancy (SCC of anus, leukaemia), STDs (HIV, syphilis, chlamydia) [1]
Why are lateral or multiple fissures a red flag? A typical (primary) fissure is single and posterior midline because of the poor blood supply posteriorly. If the fissure is lateral, anterior, or multiple → suspect a secondary cause (Crohn's disease, TB, anal cancer, HIV).
Clinical features:
- Pain on defaecation — tearing pain with passage of bowel movements [1][7]
- Fresh rectal bleeding — limited to a small amount on toilet paper or surface of stool [1][7]
- Perianal pruritus or skin irritation
- Diagnosis is by spreading the buttocks to reveal the fissure [7]
- Rectal examination and proctoscopy are painful and not indicated in the acute setting [7]
Acute vs Chronic:
- Acute: Typically heals within 6 weeks with conservative management
- Chronic: Fails conservative management; may show a sentinel pile (skin tag at the external end) and hypertrophied anal papilla at the internal end; requires more aggressive approach (GTN, diltiazem, botox, lateral internal sphincterotomy)
Pathology:
- Squamous cell carcinoma — below dentate line (80%) [3]
- Anal intraepithelial neoplasia (AIN) is the pre-malignant lesion
- Adenocarcinoma — above dentate line (10%) [3]
- Others: melanoma
Risk factors:
- HPV infection (90%): especially HPV-16 and HPV-18 [3][7]
- HIV infection [3]
- Anal intercourse, sexually transmitted diseases [7]
- Smoking, immunocompromised states, Crohn's disease [3]
Clinical features:
- Definition: Protrusion of the rectal wall through the anus — complete (all layers) or partial (mucosa only) [1]
- More common in elderly women [1]
- Risk factors: chronic straining/constipation/diarrhoea, pelvic floor dysfunction, multiparity, prior pelvic surgery, dementia, stroke [1]
- Can cause PR bleeding (from mucosal trauma/ulceration), mucus discharge, faecal incontinence (75%), and incomplete evacuation [1]
- Must differentiate from prolapsed internal haemorrhoids (haemorrhoids have radial folds; prolapse has concentric circular folds)
- Acute haemorrhagic rectal ulcer — more common in Asia [5]
- Typically in elderly, critically ill, and bedridden patients [5]
- Presents with sudden severe painless bleeding ± shock [5]
- Bedside proctoscopy may reveal bleeding ulcer [5]
- Treatment: packing of adrenaline-soaked gauze, suture plication, endoscopic electrocoagulation [5]
Also includes solitary rectal ulcer syndrome (SRUS) — associated with rectal prolapse and straining; chronic, often with mucus and blood on the stool surface.
- Due to portal hypertension — portosystemic shunt between superior rectal veins (portal) and inferior rectal veins (systemic) [2][6]
- Not the same as haemorrhoids (which are submucosal arteriovenous cushions)
- Often presents with severe bleeding [2][6]
- Management: injection sclerotherapy (local), TIPS if uncontrolled [2][6]
4.2 Colonic Causes (Vast Majority of LGIB)
"Commonest cause of LGIB" [2][5][8]
- ~17% of patients with diverticulosis will bleed [2][5][8]
- Ruptured vasa recta into the diverticulum [5][8]
- Bleeding usually from a single diverticulum [5]
Pathophysiology of diverticulosis:
- Bowel wall weakening with aging + increased intraluminal pressure (e.g. constipation) [3]
- The sigmoid colon has the narrowest lumen → highest wall pressure due to Laplace's law (Pressure = Tension / Radius; smaller radius = higher pressure for same wall tension) [3]
- The colon wall has only one layer of full-thickness longitudinal muscle arranged in three taeniae coli → the weakest point is where vasa recta penetrate the circular muscle [3]
- Mucosa and submucosa herniate through these weak points → false diverticula (true diverticula involve all layers; colonic diverticula are almost always false)
- The rectum is never affected because its outer smooth muscle layer encompasses the full circumference [3]
Site:
- Right-sided in Asia, sigmoid in Western countries [1][3]
- Right-sided diverticula have a higher risk of haemorrhage (thinner wall of caecum/ascending colon → more vulnerable vasa recta) [1]
Clinical features:
- Painless massive PR bleeding (painless haematochezia of variable severity) [2][3][5][8]
- Bleeding stops spontaneously in 80–85% but rebleeding ~20–30% [5][8]
- The blood may be bright red (left-sided source) or dark/maroon-coloured mixed with stool (right-sided source)
Risk factors for diverticular disease:
- Age (rare before 30y) [3]
- Low-fibre diet [1][3]
- Obesity [1][3]
- Increased intraluminal pressure: constipation [3]
- Drugs: NSAIDs, steroids, opiates [1][3]
- Decreased physical activity [1]
- Connective tissue disease (e.g. Marfan's, Ehlers-Danlos) [3]
Diverticular Bleeding ≠ Diverticulitis
Diverticular bleeding typically occurs in the ABSENCE of diverticulitis. The mechanism is different: bleeding = vasa recta rupture (arterial); diverticulitis = obstruction of diverticulum by faecolith → stasis → bacterial overgrowth → inflammation. A patient with acute diverticular bleeding usually does NOT have fever, peritonism, or leucocytosis (unless there is concomitant diverticulitis). [1]
"Most common vascular cause of LGIB; most common in age > 65" [1][2]
Pathophysiology:
- Dilated, tortuous submucosal vessels [1][2]
- Walls composed of endothelial cells lacking smooth muscle [1]
- Acquired degenerative condition — thought to arise from chronic, low-grade obstruction of submucosal veins where they penetrate the muscle layers of the colon → progressive dilation → incompetent precapillary sphincters → arteriovenous communications [1]
- Most commonly found in the caecum or ascending colon [1][2]
Associations:
- Osler-Weber-Rendu disease (Hereditary Haemorrhagic Telangiectasia, HHT) — autosomal dominant, mucocutaneous telangiectasias + visceral AVMs [2]
- Aortic stenosis (Heyde syndrome) — acquired von Willebrand factor type 2A deficiency due to shear-induced degradation of high-molecular-weight vWF multimers across the stenotic valve → ↑bleeding from angiodysplastic lesions [2]
Clinical features:
"~10% of PR bleed in > 50y" [2]
Epidemiology in Hong Kong:
- 1st most common cancer overall (and in males), 2nd in females [4]
- Incidence: 74.1/100,000/year; mortality: 28.5/100,000/year [4]
- M:F = 1.6:1; peak incidence 60–70y [4]
- Rectosigmoid most common site (~70% left-sided) [4]
Pathophysiology of bleeding:
- Tumour outgrows its blood supply → central necrosis → overlying erosion or ulceration → exposed vessels bleed [2]
- Usually low-grade, intermittent bleeding — may present with iron-deficiency anaemia or FOBT +ve [2]
Risk factors (abbreviated):
- Non-modifiable: Age > 50, male, family history, polyposis syndromes (FAP, HNPCC/Lynch), IBD, prior CRC or polyps [4]
- Modifiable: Red/processed meat, animal fat, obesity, smoking, alcohol, physical inactivity [4]
- Protective: High-fibre diet, NSAIDs/aspirin, physical activity, calcium/vitamin D [4]
Clinical features suggesting CRC (red flags):
- Change in bowel habit (alternating diarrhoea and constipation) [3][5]
- Change in stool calibre (pencil-thin stools) [3]
- Tenesmus (feeling of incomplete evacuation — suggests rectal mass) [3]
- Constitutional symptoms: loss of appetite, loss of weight, malaise [2]
- Blood mixed with stool [5]
- Family history of CRC [3][5]
- Metastatic symptoms: jaundice, bone pain, dyspnoea [2]
4.2.4 Colitis (Inflammatory, Ischaemic, Infective, Radiation)
- Bleeding more commonly associated with UC than Crohn's disease [2]
- Usually presents as bloody diarrhoea (mucoid loose stools) [2]
- Rarely life-threatening but can require emergency colectomy if massive or refractory [2]
- Extra-intestinal manifestations: arthritis, episcleritis/uveitis, erythema nodosum, pyoderma gangrenosum
"Commonest form ( > 50%) of ischaemic injury of GI tract" [6]
Epidemiology: Common in elderly females (90% occur in > 60y) [6]
Pathophysiology:
- Non-occlusive (95%): transient systemic low-flow states → hypoperfusion of watershed areas [6]
- Occlusive (5%): arterial embolism (e.g. from AF), arterial thrombosis, venous thrombosis [3][6]
- Colon is most vulnerable to ischaemia as it receives less blood than the rest of the GIT [6]
- Majority are transient — damage mediated by reperfusion injury (transmural necrosis only in 15% when ischaemia is prolonged) [6]
Risk factors: CVS disease, AF, recent cardiac surgery, hypotension/shock, vasopressor use, atherosclerosis, hypercoagulable states [6]
Clinical features:
- Sudden onset cramping abdominal pain (milder and more lateral than mesenteric ischaemia) [6]
- Mild-to-moderate rectal bleeding developing ≤ 24h of onset of abdominal pain [6]
- May be fresh or dark blood, more common with left colonic ischaemia [6]
- Tenderness over affected bowel on palpation [6]
- ↑WCC but fever unusual [6]
- Clostridium difficile, CMV, amoebic dysentery, TB, Salmonella, Shigella, E. coli O157:H7
- History: fever, travel, immunosuppression, recent antibiotics (C. diff)
- May present with bloody diarrhoea
"Radiation damage to rectal mucosa → formation of vascular telangiectasia" [5][2]
- Due to epithelial atrophy and fibrosis associated with obliterative endarteritis → chronic mucosal ischaemia [2]
- Timing: acute (< 6 weeks) or delayed ( > 9 months, can be > 10 years) [2]
- Cause: RT for pelvic malignancies (cervical, prostate, bladder cancer) [1][2]
- Clinical features: diarrhoea, rectal urgency/tenesmus, bleeding [2]
- Treatment: [5]
- Blood transfusion
- Sucralfate enema
- Steroid enema
- Argon plasma coagulation (APC)
- RFA
- Formalin
- Laser / infrared
- Stoma diversion [5]
| Cause | Notes |
|---|---|
| Meckel's diverticulum | Most common congenital anomaly of GI tract; "Rule of 2's" — 2% of population, 2 feet from ileocaecal valve, 2 inches long, 2 types of ectopic mucosa (gastric, pancreatic); gastric mucosa secretes acid → ulceration of adjacent ileal mucosa → painless PR bleeding; most common in children/young adults |
| Angiodysplasia / haemangioma | Similar pathophysiology to colonic angiodysplasia |
| Small bowel tumours | Carcinoid, GIST, lymphoma, adenocarcinoma |
| Small bowel ulcers (NSAID-related) | NSAID-induced enteropathy — topical mucosal injury + COX inhibition → reduced mucosal prostaglandins → reduced mucosal blood flow and bicarbonate secretion → ulceration |
| Crohn's disease | Transmural inflammation, can affect any part of GI tract (but terminal ileum most common) |
| Aortoenteric fistula | Communication between aorta and duodenum (or other small bowel); classically post-aortic graft surgery; "herald bleed" followed by massive haemorrhage — a surgical emergency |
- Up to 10–15% of patients presenting with haematochezia actually have an upper GI source [2][5]
- Occurs with massive UGIB where transit time is rapid → blood passes through before being fully degraded
- Common culprits: peptic ulcer, variceal bleeding
- Always consider UGIB in haemodynamically unstable patients with bright red PR bleeding — an NG tube aspirate or urgent upper endoscopy (OGD) may be needed
5. Classification
| Category | Definition |
|---|---|
| Acute overt LGIB | Visible bleeding of recent onset (haematochezia, maroon stools, melena from a colonic source) ± haemodynamic compromise |
| Chronic overt LGIB | Visible bleeding over days to weeks without haemodynamic compromise |
| Occult LGIB | No visible bleeding; detected by FOBT/FIT or iron-deficiency anaemia |
| Level | Examples |
|---|---|
| Anorectal | Haemorrhoids, fissures, rectal ulcer, rectal varices, anal cancer, rectal prolapse |
| Colonic | Diverticular disease, angiodysplasia, CRC, polyps, colitis (IBD, ischaemic, infective, radiation), post-polypectomy |
| Small bowel | Meckel's diverticulum, angiodysplasia, tumours, NSAID ulcers, Crohn's, aortoenteric fistula |
| Upper GI (presenting as PR bleed) | Peptic ulcer, variceal bleeding |
| Severity | Features |
|---|---|
| Minor | Self-limiting, haemodynamically stable, no significant Hb drop |
| Major | Ongoing bleeding requiring transfusion, Hb drop ≥ 2 g/dL, or haemodynamic compromise |
| Massive / Life-threatening | Shock (HR > 100, SBP < 90), requires > 4 units pRBC in 24h, ongoing active bleeding despite resuscitation |
The lecture slides distinguish this as a separate clinical pattern:
- Haemorrhoid
- Anal fissures
- Polyps
- Proctitis
- Rectal ulcers
- Cancers
6. Clinical Features
6.1 Symptoms (with Pathophysiological Basis)
| Symptom | Description | Pathophysiological Basis |
|---|---|---|
| Bright red blood on toilet paper / dripping into bowl | Outlet-type bleeding | Blood from an anorectal source (below or near dentate line) has minimal transit → no time for degradation → bright red; somatic innervation below dentate line makes the patient aware of the bleeding |
| Bright red blood coating the stool surface | Outlet-type or low rectal source | Blood applied to the exterior of formed stool as it passes through the anal canal/rectum |
| Blood separate from stool (outlet-type) | Suggests anorectal source | Blood is passed after the stool or between bowel movements; not mixed because the lesion is distal to where stool is formed |
| Blood mixed with stool | Proximal to sigmoid colon | Bleeding occurs at a level where stool is still being formed or mixing occurs during colonic transit [3] |
| Dark red / maroon-coloured stools | Right colonic or small bowel source | Longer transit → partial degradation of haemoglobin by colonic bacteria |
| Melena (black tarry stool) | Usually UGIB, but can be right colonic | Haemoglobin is oxidised to haematin (black) by gastric acid/bacterial enzymes; requires > 50 mL blood and prolonged transit |
| Mucus mixed with blood | Suggests mucosal inflammation or tumour | Goblet cell hypersecretion from inflamed/neoplastic mucosa (IBD, CRC, proctitis) |
| Cyclic pattern of bleeding | GI endometriosis | Ectopic endometrial tissue in bowel wall bleeds in synchrony with menstrual cycle [3] |
| Symptom | Likely Source | Pathophysiological Basis |
|---|---|---|
| Pain on defaecation (tearing pain) | Anal fissure | Somatic innervation of anoderm below dentate line → acute stretching of a fissure + internal sphincter spasm → severe pain [7] |
| Painless bleeding | Haemorrhoids (internal), diverticular, angiodysplasia | Internal haemorrhoids: autonomic innervation (painless); diverticular/angiodysplasia: no mucosal inflammation → no pain receptors stimulated |
| Severe perianal pain (not related to defaecation) | Thrombosed external haemorrhoid, perianal abscess | Acute thrombosis in external haemorrhoid → distension of the somatic-innervated perianal skin → severe pain [3] |
| Profuse painless haematochezia | Diverticular bleeding | Arterial bleeding from ruptured vasa recta — arterial pressure causes profuse bleeding but there is no surrounding inflammation to cause pain [5][8] |
| Change in bowel habit (alternating diarrhoea/constipation) | CRC (red flag) | Tumour obstructs lumen → faecal impaction proximal to tumour → overflow diarrhoea alternating with obstructive constipation [3][5] |
| Change in stool calibre (pencil-thin stools) | Left-sided CRC (red flag) | Annular, constricting tumour in the narrower left colon → reduced luminal diameter → "ribbon-like" stools [3] |
| Tenesmus | Rectal mass (CRC, polyp) (red flag) | Mass in rectum stimulates stretch receptors → sensation of incomplete evacuation → repeated urge to defaecate [3][5] |
| Constitutional symptoms (weight loss, fatigue, loss of appetite) | CRC, lymphoma (red flag) | Malignancy → cachexia mediated by TNF-α, IL-6 → anorexia and catabolism [5] |
| Bloody diarrhoea | IBD, infective colitis, ischaemic colitis | Mucosal inflammation → impaired absorption + hypersecretion + bleeding from friable inflamed mucosa |
| Sudden cramping abdominal pain → bleeding within 24h | Ischaemic colitis | Mucosal ischaemia → pain; reperfusion or mucosal sloughing → haemorrhage [6] |
| Diarrhoea, rectal urgency, tenesmus + bleeding post-RT | Radiation proctitis | Radiation-induced obliterative endarteritis → chronic mucosal ischaemia → telangiectasia → friable vessels → bleeding [2] |
| Intermittent perianal discharge + pain until pus discharges | Anal fistula | Chronic infection from obstructed anal gland → abscess → tracks to skin surface → intermittent discharge [3] |
| Symptom | Significance | Mechanism |
|---|---|---|
| Dizziness, light-headedness, syncope | Hypovolaemia | Blood loss → ↓circulating volume → ↓cerebral perfusion |
| Palpitations, tachycardia | Hypovolaemia / anaemia | Sympathetic compensation for ↓stroke volume |
| Dyspnoea on exertion | Anaemia | ↓O₂-carrying capacity → tissue hypoxia → compensatory hyperventilation |
| Chest pain | Anaemia-related demand ischaemia | ↓O₂ delivery to myocardium + ↑heart rate → supply-demand mismatch |
| Extreme thirst | Hypovolaemia | Activation of renin-angiotensin-aldosterone system + ADH → thirst centre stimulation |
| Oliguria | Shock / hypovolaemia | ↓Renal perfusion → ↓GFR → reduced urine output |
| Confusion | Shock | Severe ↓cerebral perfusion → impaired cognition |
6.2 Signs (with Pathophysiological Basis)
| Sign | Significance | Mechanism |
|---|---|---|
| Pallor (conjunctivae, palmar creases) | Anaemia | ↓Haemoglobin → reduced colour of perfused tissues |
| Tachycardia (HR > 100) | Haemodynamic compromise | Baroreceptor reflex → sympathetic activation → ↑HR to maintain cardiac output |
| Hypotension (SBP < 90) / postural drop | Significant blood loss ( > 30% circulating volume) | Loss of intravascular volume → ↓venous return → ↓cardiac output → ↓BP |
| Cold, clammy extremities | Shock | Sympathetic vasoconstriction redirects blood to vital organs |
| Prolonged capillary refill time ( > 2 sec) | Peripheral hypoperfusion | Sympathetic vasoconstriction |
| Koilonychia (spoon nails) | Chronic iron-deficiency anaemia | Iron deficiency → impaired nail matrix keratinisation |
| Angular stomatitis, glossitis | Chronic iron-deficiency anaemia | Iron is a cofactor for epithelial cell turnover |
| Sign | Significance | Mechanism |
|---|---|---|
| Abdominal mass | CRC, diverticular abscess | Tumour growth / walled-off collection |
| Hepatomegaly | CRC with liver metastases, chronic liver disease | Metastatic deposits / portal hypertension |
| Splenomegaly | Portal hypertension | Splenic congestion from ↑portal venous pressure |
| Ascites | Portal hypertension, peritoneal carcinomatosis | Portal HTN → ↑splanchnic hydrostatic pressure + ↓oncotic pressure (↓albumin) → fluid shifts into peritoneum |
| Tenderness (localised) | Diverticulitis (RLQ in Asia), ischaemic colitis, IBD | Inflammation of parietal peritoneum overlying affected bowel |
| Peritonism (guarding, rigidity, rebound) | Perforation (diverticulitis, ischaemic bowel) | Free bowel content in peritoneal cavity → chemical + bacterial peritonitis → parietal peritoneal irritation |
| Sign | Finding | Significance |
|---|---|---|
| Inspection | Perianal skin tags, excoriation | Chronic haemorrhoids, fissure |
| Visible fissure (on spreading buttocks) | Anal fissure [7] | |
| External swelling, blue/purple tense lump | Thrombosed external haemorrhoid | |
| Prolapsing mass — radial folds | Prolapsed haemorrhoids | |
| Prolapsing mass — concentric circular folds | Rectal prolapse | |
| Sinus opening with discharge | Anal fistula, pilonidal sinus | |
| Condylomata (warts) | HPV — risk factor for anal SCC | |
| Palpation (DRE) | Pain, induration, lesion | Fissure (pain), abscess, tumour |
| Tone assessment — ask patient to squeeze | Assesses internal anal sphincter (resting tone) and external anal sphincter (voluntary squeeze) | |
| Palpable mass + distance from anal verge | Rectal cancer (staging, surgical planning) | |
| Prostate / rectovaginal septum assessment | Rule out prostate pathology / gynaecological mass | |
| Blood on glove — nature (fresh, dark, melena) | Confirms PR bleeding and gives clue to source | |
| Proctoscopy | Haemorrhoids at 3, 7, 11 o'clock | Internal haemorrhoids (may not be palpable on DRE — especially 1st/2nd degree) |
| Mucosal ulceration, telangiectasia | Proctitis, radiation changes, rectal ulcer | |
| Bleeding ulcer in elderly/bedridden | Acute haemorrhagic rectal ulcer — bedside proctoscopy may reveal bleeding ulcer [5] |
| Sign | Suggests |
|---|---|
| Oral ulcers, perianal skin tags/fistulae, erythema nodosum | Crohn's disease |
| Pyoderma gangrenosum, episcleritis | IBD (especially UC) |
| Telangiectasias on lips, oral mucosa, fingertips | Osler-Weber-Rendu disease (HHT) → GI angiodysplasia |
| Aortic stenosis murmur + GI bleeding in elderly | Heyde syndrome |
| Spider naevi, jaundice, palmar erythema, gynaecomastia | Chronic liver disease → portal HTN → rectal varices |
| Virchow's node (left supraclavicular), Sister Mary Joseph nodule | Metastatic GI malignancy |
The lecture slides emphasise these red flags for intermittent/episodic PR bleeding: [5]
- Change of bowel habit
- Tenesmus
- Mucus
- Duration of bleeding
- Blood mixed with stool
- Melena / altered blood / dark red / maroon-coloured
- Older age ( > 50? or > 40?)
- Constitutional symptoms
- Family history
→ Digital rectal examination & proctoscopy [5]
| Cause | Typical Age | Pain? | Bleeding Pattern | Key Associated Features |
|---|---|---|---|---|
| Haemorrhoids | Any (peak < 50) | Painless (internal) / Painful (thrombosed external) | Bright red, outlet-type, on paper/coating stool | Prolapse, pruritus, mucous discharge |
| Anal fissure | Young adults | Severe tearing pain on defaecation | Small amount bright red on paper/stool surface | Posterior midline tear, constipation history |
| Diverticular disease | > 60 | Painless | Profuse, may be maroon (right-sided) | Self-limiting in 80%, recurrent |
| Angiodysplasia | > 65 | Painless | Variable, often occult/intermittent | Aortic stenosis, HHT |
| CRC | > 50 (usually) | Usually painless | Intermittent, mixed with stool, occult | Change in bowel habit, weight loss, FHx |
| IBD | 15–40 (bimodal) | Cramping abdominal pain | Bloody diarrhoea | Extra-intestinal manifestations |
| Ischaemic colitis | > 60 | Cramping pain → bleeding within 24h | Moderate, often dark | CVS risk factors, watershed area involvement |
| Radiation proctitis | Post-RT | Tenesmus, urgency | Chronic, intermittent | History of pelvic RT |
| Rectal ulcer | Elderly/bedridden | Painless (acute haemorrhagic type) | Sudden, severe, ± shock | More common in Asia, critically ill |
| Anal cancer | Any (risk: HPV, HIV) | Painful | Intermittent | Palpable mass, inguinal LN |
High Yield Summary
-
Definition: PR bleeding = passage of blood through the anus; ranges from occult (FOBT+) to massive haemorrhage.
-
Always consider upper GI source in brisk haematochezia — up to 10–15% of apparent LGIB is actually UGIB.
-
Anatomy essentials: Dentate line divides pain vs painless pathology; watershed areas (Griffiths' point, Sudeck's point) explain ischaemic colitis distribution; vasa recta penetration sites explain diverticular location and bleeding.
-
Most common causes by age: < 50 → haemorrhoids; > 60 → diverticular disease and angiodysplasia.
-
Diverticular bleeding: Commonest cause of LGIB. Painless. Right-sided in Asia. Stops in 80-85%. Recurs 20-30%.
-
Red flags (must investigate for CRC): Change in bowel habit, tenesmus, blood mixed with stool, weight loss, family history, age > 50.
-
DRE and proctoscopy are mandatory for every patient with PR bleeding.
-
Haemorrhoids = engorgement and prolapse of anal vascular cushions (not "varicose veins"). Graded 1–4 by degree of prolapse.
-
Anal fissure: Posterior midline (poor blood supply), tearing pain + spasm → vicious cycle of ischaemia and failed healing.
-
Ischaemic colitis: Cramping pain → bleeding within 24h; watershed areas; non-occlusive (95%) in elderly with CVS disease.
-
In Hong Kong: CRC is the #1 cancer. Diverticular disease is right-sided. Acute haemorrhagic rectal ulcer is more common in Asia.
Active Recall - Per Rectal Bleeding
[1] Senior notes: felixlai.md (Lower GI Bleeding, Hemorrhoids, Anal Fissures, Rectal Prolapse, Diverticular Disease sections) [2] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.3.6 Lower GI Bleeding, p281–282) [3] Senior notes: maxim.md (LGIB, Haemorrhoids, Diverticular Disease, Anal Fistula, Anal Carcinoma sections) [4] Senior notes: Ryan Ho GI.pdf (Section 3.3.6 Colorectal Tumours, p163) [5] Lecture slides: GC 186. Lower and diffuse abdominal painfresh blood in stool.pdf (p8, p9, p12, p13, p18, p19) [6] Senior notes: Ryan Ho GI.pdf (Section B. Ischaemic Colitis, p146) [7] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p46, p73) [8] Lecture slides: Diverticular diseases - Dr. J Tsang.pdf (p8)
Differential Diagnosis of Per Rectal Bleeding
The differential diagnosis of PR bleeding is one of those topics where a structured approach pays enormous dividends. You need a mental framework — think anatomically from bottom (anus) upwards, or think by pathological mechanism (anatomical/structural, vascular, inflammatory, neoplastic, iatrogenic). Both work; the key is being systematic so you never miss a diagnosis.
Let me walk you through this the way I'd think on a ward round: "Where is the blood coming from, and what's the mechanism?"
The causes can be grouped by anatomical level and by pathological mechanism. The following table integrates both, and I've included approximate proportions to give you a sense of the clinical landscape [1][2][9].
| Anatomical Level | Category | Cause | Approximate Proportion of LGIB |
|---|---|---|---|
| Upper GI (proximal to lig. of Treitz) | — | Peptic ulcer, variceal bleed | < 10% (but must always consider!) |
| Small bowel | Anatomical | Meckel's diverticulum, jejunoileal diverticula | ~5% total |
| Vascular | Angiodysplasia, haemangioma | ||
| Neoplastic | Small bowel tumours (GIST, carcinoid, lymphoma) | ||
| Inflammatory | Crohn's disease, TB enteritis | ||
| Drug-related | NSAID-induced small bowel ulcers | ||
| Vascular | Aortoenteric fistula | ||
| Large bowel (colon) | Anatomical | Diverticular bleeding (17–40%) | Vast majority |
| Vascular | Angiodysplasia (2–30%) | ||
| Neoplastic | Colorectal carcinoma, large polyps, post-polypectomy bleeding | 7–33% | |
| Inflammatory | IBD (UC > Crohn's), infective colitis (C. diff, CMV, amoebic, TB), ischaemic colitis, radiation proctocolitis | 9–11% | |
| Anorectal | Structural | Haemorrhoids, anal fissure, rectal prolapse | ~10% |
| Vascular | Rectal varices (portal HTN) | ||
| Neoplastic | Anal carcinoma | ||
| Ulcerative | Rectal ulcer (acute haemorrhagic) |
Items marked with * can present with heavy bleeding [2]
Never Forget Upper GI Bleeding
Up to 10–15% of patients presenting with apparent haematochezia actually have a massive upper GI source [2][9]. In any haemodynamically unstable patient with PR bleeding, you MUST consider UGI bleeding and have a low threshold for upper endoscopy (OGD) or at least NG tube aspiration (bile-stained aspirate without blood → UGI bleed less likely). This is perhaps the single most important point in the differential diagnosis of PR bleeding.
The following mermaid diagram walks through the clinical reasoning when a patient presents with PR bleeding, helping you narrow the differential based on key discriminating features:
3. Detailed Differential Diagnosis by Cause
I'm going to walk through each differential systematically, focusing on the distinguishing features that help you tell them apart at the bedside. Think of this as "What would make me suspect Diagnosis X over Diagnosis Y?"
3.1 Anorectal Causes
- Fresh outlet-type bleed, perianal mass / pain, constipation, risk factors (e.g. pregnancy) [3]
- Distinguishing features: Blood is bright red, drips into toilet bowl or stains tissue paper, typically occurs during or immediately after defaecation. Internal haemorrhoids → painless; thrombosed external → painful blue/purple perianal mass [3][9]
- Why it bleeds: Engorgement of anal vascular cushions → arterial bleeding from the arteriolar component of the cushion (this is why the blood is bright red, not dark venous blood) [3]
- Trap: Haemorrhoids are so common (4.4% prevalence) that they may coexist with a more sinister pathology. Never attribute PR bleeding solely to haemorrhoids without excluding other sources, especially in patients with red flags [1][3]
- History of constipation; severe sharp pain upon defecation [9]
- Distinguishing features: The key discriminator is pain — tearing, burning pain that occurs during and may persist for hours after defaecation. Blood is typically a small amount, bright red, on paper or stool surface [1]
- Why it hurts so much: The tear is below the dentate line → somatic innervation (inferior rectal nerve) → exquisite pain. Internal sphincter spasm perpetuates the cycle [1]
- Typical vs atypical: Single posterior midline fissure = typical/primary. Multiple, lateral, or anterior fissures → think secondary causes (Crohn's, TB, HIV, anal SCC) [1]
- Presented with bleeding, pain and anal mass [5]
- Risk factors: anal intercourse, sexually transmitted diseases, infection with HPV [5]
- Distinguishing features: Persistent, progressive symptoms. A palpable mass on DRE. Inguinal lymphadenopathy (lymphatic drainage below dentate line → superficial inguinal LN). Usually in patients with risk factors (HPV, HIV, immunosuppression) [3][5]
- More common in Asia; elderly, critically ill, bedridden patients [5]
- Sudden severe painless bleeding ± shock [5]
- Distinguishing features: The clinical context is key — this is a patient in ICU or nursing home, not an ambulatory outpatient. Diagnosis made by bedside proctoscopy revealing a bleeding ulcer [5]
- Also consider solitary rectal ulcer syndrome (SRUS) — associated with rectal prolapse and chronic straining; presents with mucus, blood, and tenesmus
- Due to portal hypertension → portosystemic shunt between superior and inferior rectal veins [2]
- Distinguishing features: Clinical context of chronic liver disease (jaundice, spider naevi, ascites, splenomegaly). Often presents with severe bleeding [2]. Must differentiate from haemorrhoids — rectal varices are submucosal venous channels in the rectum proper, whereas haemorrhoids are vascular cushions in the anal canal
- Why it bleeds: High portal pressure → distension of collateral veins → thin-walled varices → rupture
- Prolapsing mass with concentric circular folds (cf. haemorrhoids which have radial folds)
- Can cause PR bleeding from mucosal trauma/ulceration
- Usually in elderly women with pelvic floor dysfunction [1]
3.2 Colonic Causes
- Painless, usually profuse haematochezia (not chronic) [2][9]
- DDx: angiodysplasia, severe colitis, rectal ulcer, small bowel bleeding, UGIB [8]
- Distinguishing features: Sudden onset of painless, often profuse bleeding in an elderly patient. No preceding change in bowel habit, no constitutional symptoms, no fever (diverticular bleeding ≠ diverticulitis) [1][2]
- Blood may be dark/maroon-coloured if right-sided (common in Asia) or bright red if left-sided [1][9]
- Bleeding stops spontaneously in 80–85% but rebleeding ~20–30% [2][5][8]
- ~17% of patients with diverticulosis will bleed [2][8]
- Key differentiator from angiodysplasia: Diverticular bleeding is arterial (from ruptured vasa recta) → tends to be more profuse. Angiodysplasia is venous → tends to be less severe but more intermittent [1][2]
Diverticular Bleeding vs Diverticulitis
Diverticular bleeding and diverticulitis rarely coexist [9]. Bleeding = arterial (vasa recta rupture into diverticulum). Diverticulitis = obstruction by faecolith → bacterial overgrowth → inflammation. A patient presenting with PR bleeding + fever + LLQ/RLQ pain + leucocytosis is more likely to have diverticulitis (which may cause minor bleeding) or another diagnosis, not "diverticular bleeding" in the classic sense.
- Usually in elderly, may be associated with vascular malformations (e.g. HHT) and aortic stenosis [2][9]
- Painless, less severe than diverticular but tends to be intermittent [2][9]
- Distinguishing features: Recurrent episodes of painless bleeding in an elderly patient; often presents as occult bleeding with iron-deficiency anaemia and FOBT +ve rather than massive haematochezia [1]
- Associations to look for:
- Aortic stenosis (Heyde syndrome) — acquired type 2A vWD from shear-induced degradation of high-MW vWF multimers across the stenotic valve [2][3]
- Hereditary Haemorrhagic Telangiectasia (Osler-Weber-Rendu) — look for telangiectasias on lips, oral mucosa, fingertips [2]
- ESRD, von Willebrand disease [3]
- Colonoscopy appearance: cherry red spots [3]
- Angiography appearance: "mother-in-law phenomenon" (early filling, delayed emptying — the lesion fills quickly and empties slowly, like a mother-in-law who comes early and stays late) [3]
- > 50y, male, smoker, FHx, Hx of IBD, polyps and colorectal CA [2][9]
- Alternating diarrhoea and constipation, pencil-thin stools, tenesmus [2][9]
- Loss of appetite, loss of weight, malaise [2][9]
- Intractable pain, jaundice/LUQ pain, dyspnoea, bone pain (metastatic features) [9]
- Distinguishing features: PR bleeding that is low-grade and intermittent (not massive and acute), associated with progressive change in bowel habit and constitutional symptoms [2]. May present with iron-deficiency anaemia or FOBT +ve only. This is the one you must not miss [2][9]
Right-sided vs Left-sided CRC — different presentations:
| Feature | Right (proximal) colon | Left (distal) colon / Rectosigmoid |
|---|---|---|
| Bleeding | Occult bleeding → iron-deficiency anaemia (4× higher mean daily blood loss) | Haematochezia with altered blood |
| Bowel habit | Less commonly changes (liquid stools, spacious lumen) | Alternating diarrhoea and constipation; pencil-thin stools |
| Obstruction | Less common | More common (narrower lumen, harder stools) |
| Mass | Right-sided abdominal mass | Less likely palpable |
| Other | Late presentation | Tenesmus (rectal tumours), mucus, early morning bloody diarrhoea |
The mnemonic "Right side bleeds, Left side blocks" captures this nicely [10].
All forms of colitis can cause PR bleeding, but they have distinct patterns:
| Type | Key Distinguishing Features | Mechanism of Bleeding |
|---|---|---|
| IBD | Usually bloody diarrhoea; extra-intestinal manifestations (arthritis, episcleritis, erythema nodosum); bleeding more common in UC than Crohn's [2][9] | Chronic mucosal inflammation → friable, ulcerated mucosa |
| Infective | Fever, chills, rigors, N/V, diarrhoea, pain; TOCC history; immunosuppression (CMV colitis); previous TB exposure/infection, BCG vaccination status [9]; recent antibiotics (C. difficile) | Mucosal invasion by pathogen → ulceration |
| Ischaemic | CVS risk factors, acute MI, stroke [9]; sudden cramping pain → bleeding within 24h; watershed area involvement (splenic flexure, rectosigmoid) | Mucosal ischaemia → necrosis → reperfusion haemorrhage |
| Radiation | Hx of abdominal irradiation [9]; delayed onset (months to years after RT); telangiectasia on endoscopy | Obliterative endarteritis → chronic mucosal ischaemia → telangiectasia formation |
IBD vs Infective Colitis
IBD should not be misdiagnosed as infectious or ischaemic colitis since therapy is different [1]. IBD requires immunosuppressive therapy (steroids, azathioprine, biologics), whereas infective colitis requires antimicrobials, and ischaemic colitis is largely supportive. Always send stool cultures and C. difficile toxin before committing to a diagnosis of IBD.
These account for ~5% of LGIB but are important to consider when upper and lower endoscopy are negative ("obscure GI bleeding") [2].
| Cause | Distinguishing Features |
|---|---|
| Meckel's diverticulum | Young patient (usually < 30y); painless PR bleeding (often maroon/dark red); contains ectopic gastric mucosa → acid secretion → ulceration of adjacent ileum; diagnosed by Tc-99m pertechnetate scan ("Meckel's scan" — detects ectopic gastric mucosa) [2] |
| Angiodysplasia / haemangioma | Similar to colonic angiodysplasia; diagnosed by capsule endoscopy or double-balloon enteroscopy |
| Small bowel tumours | GIST, carcinoid, lymphoma, adenocarcinoma; may present with obscure bleeding or intermittent obstruction |
| NSAID-induced small bowel ulcers | History of chronic NSAID use; NSAID-induced enteropathy is a separate phenomenon from peptic ulcers and causes mucosal disruption by a different mechanism (direct topical injury + COX inhibition → reduced mucosal prostaglandins) [9] |
| Crohn's disease / TB enteritis | Small bowel Crohn's → skip lesions, strictures; TB → ileocaecal involvement, caseating granulomas |
| Aortoenteric fistula | Surgical emergency. History of prior aortic graft surgery. "Herald bleed" (self-limiting small bleed) followed by catastrophic haemorrhage. Communication between aorta and duodenum (most common) or jejunum [2] |
- Melena, haematemesis, coffee ground vomitus [9]
- Should be considered especially in severe haematochezia (10–15% from UGI) [2][9]
- Common culprits: peptic ulcer disease (commonest cause of UGIB), variceal bleeding (in the context of chronic liver disease)
- Key discriminators for UGIB: Preceding epigastric pain (PUD), history of GERD, liver disease stigmata, NSAID/anticoagulant use, preceding forceful vomiting (Mallory-Weiss), raised BUN/creatinine ratio (digested blood = protein load → ↑urea production)
4. History-Taking Framework for the Differential Diagnosis
To systematically work through the differential at the bedside, here is a structured approach based on the lecture slides and senior notes [2][5][9]:
| Question | What It Differentiates |
|---|---|
| When did it start? First episode? | Acute vs chronic; recurrent diverticular bleeding vs new CRC |
| Amount and colour? | Bright red outlet = anorectal; dark/maroon mixed = right colon/SB; melena = UGIB/right colon |
| Haematochezia? Melena? | Determines level of source |
| Blood relationship to stool? | Separate/outlet → anorectal; mixed → proximal to sigmoid; cyclic → endometriosis [3] |
| Recent endoscopy / polypectomy? | Post-polypectomy bleeding [5] |
| Symptom Cluster | Likely Diagnosis |
|---|---|
| Pain on defaecation + small bright red bleed | Anal fissure |
| Painless profuse haematochezia, elderly | Diverticular disease / angiodysplasia |
| Change in bowel habit + tenesmus + mucus | CRC (red flag) [5] |
| Bloody diarrhoea + extra-intestinal manifestations | IBD |
| Fever + diarrhoea + TOCC | Infective colitis |
| Cramping pain → bleeding within 24h, CVS risk factors | Ischaemic colitis |
| Post-pelvic RT | Radiation proctitis |
| Constitutional symptoms (wt loss, fatigue, anorexia) | Malignancy [5] |
| Portal HTN stigmata + severe bleeding | Rectal varices |
| Risk Factor | Points Towards |
|---|---|
| Older age ( > 50? or > 40?) [5] | CRC, diverticular disease, angiodysplasia, ischaemic colitis |
| Family history [5] | CRC (especially HNPCC/Lynch, FAP) |
| NSAIDs / antiplatelets / anticoagulants | Drug-related bleeding (peptic ulcer, NSAID enteropathy), ↑severity of any bleeding source [9] |
| Pregnancy, constipation, chronic cough | Haemorrhoids |
| HPV, HIV, anal intercourse | Anal carcinoma |
| Chronic liver disease, alcohol | Rectal varices, coagulopathy |
| Prior pelvic RT | Radiation proctitis |
| CVS disease, AF, recent MI/surgery | Ischaemic colitis |
| Immunosuppression | CMV colitis, opportunistic infections [9] |
The lecture slides present a clear algorithm for the patient presenting with acute LGIB [5]:
Key points from the lecture algorithm [5]:
- Haemodynamically unstable → CTA before any treatment (to localise the bleeding source)
- Consider UGI endoscopy unless CTA has already located the bleeding site
- Reserve emergency laparotomy for patients in whom endoscopy and radiology have failed
- Transcatheter embolisation within 60 minutes for unstable patients
- Haemodynamically stable → consider safe hospital discharge if Oakland score < 8
- Colonoscopy as first diagnostic modality for stable patients
- Bowel preparation: 4–6L PEG-based solution; NG tube and antiemetics can be used if needed
- Transfusion targets: Hb < 7 g/dL → transfuse to target 7–9 g/dL; if Hb ≥ 8 g/dL with CVD → target ≥ 10 g/dL
- Endoscopic treatment: diverticular → TTS/cap-mounted clip or EBL; angioectasia → APC; post-polypectomy → mechanical or thermal therapy; salvage → hemostatic topical agent
| Feature | Diverticular | Angiodysplasia | CRC | Haemorrhoids | Fissure | Ischaemic Colitis | IBD |
|---|---|---|---|---|---|---|---|
| Age | > 60 | > 65 | > 50 | Any (< 50 most common) | Young adults | > 60 | 15–40 |
| Pain | Painless | Painless | Usually painless | Painless (internal) | Severe tearing | Cramping | Cramping |
| Volume | Profuse | Moderate / occult | Low-grade, intermittent | Small, outlet | Small | Moderate | Variable |
| Colour | Bright or maroon | Variable | Dark or occult | Bright red | Bright red | Fresh or dark | Bloody mucus |
| Stool relationship | Separate | Separate or mixed | Mixed | Separate / coating | On paper | With diarrhoea | With diarrhoea |
| Key association | Diverticulosis on imaging | Aortic stenosis, HHT | FHx, polyps, IBD | Constipation, pregnancy | Constipation | CVS disease, AF | Extra-intestinal |
| Natural history | Self-limiting 80–85% | Self-limiting 85–90% | Progressive | Chronic / recurrent | Heals (acute) or chronic | Usually transient | Chronic relapsing |
A few important traps to be aware of:
- Haemorrhoids masking CRC: As stated above, never stop at haemorrhoids. If the patient has any red flags → colonoscopy [1][3]
- UGIB presenting as haematochezia: In a shocked patient with brisk PR bleeding, the source may be a bleeding peptic ulcer or ruptured oesophageal varix. The NG tube aspirate trick: if it returns bile without blood, UGIB is less likely (but not excluded — a duodenal ulcer can bleed without refluxing into the stomach) [2][9]
- Diverticulitis vs Diverticular bleeding: These are different pathological processes that rarely coexist [1][9]
- IBD misdiagnosed as infective colitis: Always send stool cultures first, but therapy is fundamentally different — immunosuppression for IBD vs antimicrobials for infection [1]
- Right-sided CRC missed because no obvious PR bleeding: Right-sided tumours present with occult bleeding and anaemia rather than visible haematochezia — a normal-looking stool doesn't exclude CRC [4][10]
High Yield Summary
-
Structure your differential anatomically: Anorectal → Colonic → Small bowel → Upper GI.
-
Always consider UGIB in severe haematochezia — 10–15% of apparent LGIB is from upper GI source.
-
Commonest cause of massive LGIB = diverticular bleeding (painless, profuse, self-limiting in 80–85%, arterial from ruptured vasa recta).
-
Angiodysplasia = venous, less profuse, more intermittent, elderly, associations with aortic stenosis (Heyde syndrome) and HHT.
-
CRC red flags: Change in bowel habit, tenesmus, pencil-thin stools, constitutional symptoms, FHx, age > 50. "Right side bleeds, left side blocks."
-
Haemorrhoids: Most common cause < 50y. Outlet-type bright red bleeding. Internal = painless; thrombosed external = painful. Always exclude coexisting CRC.
-
Anal fissure: Severe tearing pain on defaecation. Posterior midline. Atypical location → think secondary cause.
-
Ischaemic colitis: Cramping pain → bleeding within 24h. Watershed areas. Non-occlusive (95%) in elderly with CVS disease.
-
For unstable patients: CTA → consider UGI endoscopy → transcatheter embolisation → emergency laparotomy as last resort.
-
For stable patients: Oakland score assessment → colonoscopy (with bowel prep) as first diagnostic modality.
Active Recall - Differential Diagnosis of PR Bleeding
References
[1] Senior notes: felixlai.md (Lower GI Bleeding, Hemorrhoids, Anal Fissures, Diverticulitis sections) [2] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.3.6 Lower GI Bleeding, p281–285) [3] Senior notes: maxim.md (LGIB, Haemorrhoids, Angiodysplasia, Anal Carcinoma sections) [4] Senior notes: Ryan Ho GI.pdf (Section 3.3.6 Colorectal Tumours, p163–165) [5] Lecture slides: GC 186. Lower and diffuse abdominal painfresh blood in stool.pdf (p8, p9, p12, p13, p18, p19, p38) [8] Lecture slides: Diverticular diseases - Dr. J Tsang.pdf (p8) [9] Senior notes: Ryan Ho GI.pdf (Section B. Approach to Lower GI Bleeding, p107–111) [10] Senior notes: Ryan Ho GI.pdf (p165 — Clinical features: right side bleeds, left side blocks)
PR bleeding is not a single diagnosis — it's a presentation. There is no single "diagnostic criterion" the way you have for, say, rheumatic fever. Instead, the diagnostic approach is about systematically localising the source and identifying the underlying pathology. Think of it as a three-step mission that the senior notes describe perfectly [2][9]:
1. Save the patient (resuscitation and stabilisation) 2. Find the bleeding (localisation of bleeding site) 3. Stop the bleeding (endoscopy, angiography, surgery)
Let me walk you through each component of the diagnostic workup from first principles.
1. Initial Assessment and Severity Stratification
Before you reach for any investigation, you need to answer one critical question: Is this patient haemodynamically stable? This determines your entire diagnostic pathway.
This was covered in detail in the DDx section, but the key diagnostic history points are [1][9]:
| History Element | Diagnostic Implication |
|---|---|
| Nature of blood and relationship to stool | Blood mixed with faeces = above sigmoid; blood on surface = anus/rectum; blood on toilet paper = anal margin; blood after defaecation = anus (haemorrhoids); blood by itself = torrential (diverticular, angiodysplasia) [9] |
| Colour of blood | Bright red = distal source; dark/maroon = proximal colon or SB; melena = UGIB or right colon with slow transit [1][9] |
| Hx of recent endoscopy / polypectomy | Post-polypectomy bleeding [1] |
| Red flags | Change in bowel habit, tenesmus, mucus, constitutional symptoms, FHx, age > 50 → investigate for CRC [5] |
| Component | What You're Looking For | Why |
|---|---|---|
| Vitals: BP/P, RR, postural BP | Tachycardia, hypotension, postural drop | Quantify blood loss — Class II shock (15–30% blood loss) shows tachycardia before hypotension; Class III ( > 30%) shows both [2][9] |
| Temperature | Fever → infective/inflammatory colitis. ↓ Body temperature can cause ↓ efficiency of clotting factors — prevent hypothermia [2][9] | |
| General examination | Pallor, tachycardia (anaemia); dehydration (CRT, dry tongue); extra-abdominal manifestations of IBD [2][9] | |
| Abdominal examination | Mass, tenderness — usually normal in LGIB [9] | |
| Digital rectal examination + proctoscopy | Confirm haematochezia; look for anorectal pathologies (haemorrhoids, fissure-in-ano, masses) [2][5][9] |
The lecture slides reference the Oakland score for risk stratification of stable patients [5]:
The Oakland Score predicts the probability of safe discharge in patients with acute LGIB. It uses 7 variables:
| Variable | Points |
|---|---|
| Age | 0–2 |
| Sex | 0–1 |
| Previous LGIB hospitalisation | 0–1 |
| DRE findings | 0–2 |
| Heart rate | 0–2 |
| Systolic BP | 0–2 |
| Haemoglobin | 0–6 |
- Oakland score < 8 → consider safe hospital discharge and outpatient evaluation [5]
- Oakland score ≥ 8 → warrants inpatient investigation and management
Why does this matter? Many patients with PR bleeding (e.g. young patient with a small amount of bright red blood on paper from an obvious fissure) do NOT need admission. The Oakland score helps you formalise that clinical judgement.
2. Laboratory Investigations
| Test | What It Tells You | Interpretation Pearls |
|---|---|---|
| CBC: Hb, haematocrit | Baseline Hb; severity of blood loss | Hb will often be at normal baseline initially — the patient is losing whole blood (both plasma and cells in proportion). Hb declines as blood is diluted by fluid during resuscitation (haemodilution). So an initial "normal" Hb does NOT exclude significant bleeding [1][9] |
| Type and cross-match | Indicated for haemodynamically unstable patients — prepare blood products [1][9] | |
| Clotting profile (PT/INR, aPTT) | Look for coagulopathy — liver disease, warfarin use, DIC [1][9] | |
| LFT | Look for chronic liver disease (portal HTN → rectal varices) and liver metastasis; albumin to assess nutritional status [1][9] | |
| RFT | Hydration status, pre-renal failure, electrolyte imbalance. Chronic renal disease → low Hb at baseline (↓ erythropoietin), interpret CBC with caution [1][9] | |
| BUN-to-creatinine ratio (or urea-to-creatinine ratio) | Normal ratio ( < 20:1 for BUN:Cr; < 100:1 for urea:Cr) in acute LGIB with normal renal perfusion. An elevated ratio suggests UGIB — because digested blood is a protein load → bacteria convert it to urea → ↑ BUN/urea disproportionately to creatinine [1] | |
| Lactate, ABG | Assess tissue perfusion and acid-base status in shock [3] |
The BUN:Cr Ratio Trick
An elevated BUN-to-creatinine ratio ( > 20:1) in a patient with apparent PR bleeding is a clue that the source may actually be upper GI. The mechanism: blood is digested → amino acids are absorbed → hepatic conversion to urea → ↑BUN. Creatinine is unaffected. This is a simple, cheap bedside clue that the "lower GI bleed" may actually be an upper GI bleed presenting with haematochezia [1].
| Test | Purpose |
|---|---|
| CEA | Low sensitivity (~30%) for colorectal cancer [5][11]. NOT a diagnostic test for CRC — its main roles are prognostication, treatment monitoring, and detection of recurrence post-operatively. An elevated CEA in PR bleeding may prompt further investigation but a normal CEA does NOT exclude cancer [11] |
| Stool tests | Amoeba histolytica (amoebic dysentery); Clostridium difficile toxin (pseudomembranous colitis); stool culture for bacterial pathogens (Salmonella, Shigella, Campylobacter); FOBT/FIT for occult bleeding [1] |
| Iron profile | Iron-deficiency anaemia pattern (↓ ferritin, ↓ serum iron, ↑ TIBC, ↓ transferrin saturation) → suggests chronic occult bleeding (right-sided CRC, angiodysplasia) [11] |
The following comprehensive algorithm integrates the lecture slide algorithm [5] with the senior notes approach [2][3][9]. The fundamental branch point is haemodynamic stability.
Key Algorithm Principles from Lecture Slides
For UNSTABLE patients [5]:
- CTA before any treatment to localise source
- Consider UGI endoscopy unless CTA has already located the site
- Reserve emergency laparotomy for patients in whom endoscopy and radiology have failed
- Transcatheter embolisation within 60 minutes
For STABLE patients [5]:
- Consider safe hospital discharge if Oakland score < 8
- Colonoscopy as the first diagnostic modality
- Prepare with 4–6L of PEG-based solution; NG tube and antiemetics if needed
- Transfusion: Hb < 7 g/dL → target 7–9 g/dL; Hb ≥ 8 g/dL + CVD → target ≥ 10 g/dL
4. Investigation Modalities — Detailed Breakdown
4.1 Bedside Investigations
- The absolute first "investigation" — costs nothing, takes 30 seconds
- Confirm haematochezia; look for anorectal pathologies [9]
- What you can find: stool colour (fresh blood, melena, normal), palpable mass (rectal CA — note distance from anal verge), anal tone assessment, prostate/rectovaginal septum, tenderness, induration [3]
- Exclusion of bleeding from anorectal disorders [1][2]
- Visualises the anal canal and lower rectum (~7–8 cm)
- Best way to diagnose internal haemorrhoids (1st/2nd degree may not be palpable on DRE) at 3, 7, 11 o'clock positions [3]
- Bedside proctoscopy may reveal bleeding ulcer in acute haemorrhagic rectal ulcer [5]
- For intermittent/episodic PR bleeding: bedside examination with proctoscopy for anorectal pathology [5]
| Feature | Detail |
|---|---|
| Reach | Up to sigmoid colon (~25 cm from anal verge) |
| Indications | Anorectal pathology (biopsy within reach), assess true height of rectal tumour, lower resection margin planning, conservative treatment of sigmoid volvulus [3] |
| Advantages | No sedation required, quick, office procedure |
| Limitations | Limited reach, cannot assess proximal colon |
- Bile-stained aspiration without blood → bleeding from upper GI tract excluded [2][9]
- Why bile must be present: if the aspirate is clear (no bile), it may mean the tube tip is not in the duodenum — a duodenal source could still be bleeding distally without refluxing into the stomach
- A bloody aspirate = UGIB confirmed → proceed to OGD
- Limitation: Cannot definitively exclude a duodenal source if aspirate is non-bilious and non-bloody
4.2 Endoscopic Investigations
This is the cornerstone investigation for PR bleeding in haemodynamically stable patients.
| Aspect | Detail |
|---|---|
| Diagnostic yield | 75–90% [2][9] |
| Timing | Should be performed early (to obtain a diagnosis before bleeding stops) [2][9]. For acute LGIB in stable patients, aim for colonoscopy within 24 hours of presentation |
| Bowel preparation | 4–6L of PEG-based solution [5]; ↑ diagnostic yield but does not ↑ morbidity [2][9]; NG tube and antiemetics can be used if needed [5]; NOT feasible in unstable patients [9] |
| Scope | Usually also intubate the ileocaecal valve to exclude distal small bowel bleeding [9] |
| Failure to localise | 8–12% failure rate [2][9] |
Advantages [1]:
- Localisation of bleeding is accurate regardless of the aetiology or rate of bleeding
- Ability to collect pathological specimens for diagnosis (biopsy)
- Ability for therapeutic intervention
Disadvantages [1]:
- Requires bowel preparation and has poor visualisation in unprepared colon
- Risks of sedation in an acutely bleeding patient
- Low diagnostic yield in massive bleeding (poor visualisation from blood obscuring the field) [3]
Key Endoscopic Findings by Diagnosis:
| Diagnosis | Endoscopic Appearance |
|---|---|
| Diverticular bleeding | Active bleeding, non-bleeding visible vessel, or adherent clot located in a diverticulum (but definite diverticular sources only identified in ~21% [9]); multiple diverticula visible |
| Angiodysplasia | Cherry red spots — flat or slightly raised, well-demarcated, red vascular lesions typically in caecum/ascending colon [3] |
| CRC | Endoluminal mass (exophytic or polypoid), may have bleeding (oozing/frank) from friable, necrotic, or ulcerative surface; may be circumferential ("apple-core") [11] |
| UC | Extensive ulceration of mucosa; surface is irregular, friable, erythematous, with loss of normal vascular markings; continuous involvement starting from rectum [1] |
| Crohn's colitis | Skip lesions, aphthous ulcers, cobblestone mucosa, strictures |
| Ischaemic colitis | Segmental involvement (watershed areas); oedematous folds, ischaemic ulcers, necrosis of colonic wall; submucosal haemorrhage ("thumbprinting" appearance) [1] |
| Radiation proctitis | Vascular telangiectasia on mucosal surface; pallor, friability [2] |
| Polyps | Pedunculated or sessile mucosal projections; post-polypectomy sites may show ulcer base with visible vessel |
Endoscopic therapeutic modalities (especially effective for angiodysplasia and diverticular disease) [2][5][9]:
| Therapy | Best Used For | Mechanism |
|---|---|---|
| TTS / cap-mounted clip | Diverticular bleeding [5] | Mechanical compression of bleeding vessel |
| Endoscopic band ligation (EBL) | Diverticular bleeding [5] | Band strangulates tissue containing bleeding vessel |
| Argon plasma coagulation (APC) | Angioectasia (angiodysplasia) [3][5] | Non-contact thermal coagulation using ionised argon gas — ablates superficial vascular malformations |
| Adrenaline injection (1:10,000) | Initial haemostasis (any source) | Vasoconstricton + tamponade effect; not used alone [3] |
| Bipolar diathermy / heat probe | Visible vessel | Thermal coagulation of vessel wall |
| Mechanical or thermal therapy | Delayed post-polypectomy bleeding [5] | |
| Haemostatic topical agent | Salvage treatment [5] | Haemostatic powder (e.g. TC-325/Hemospray) applied to bleeding surface |
Stigmata of recent haemorrhage (SRH) — endoscopic findings that indicate the diverticulum or lesion has recently bled and may re-bleed [3]:
- Active bleeding (spurting or oozing)
- Non-bleeding visible vessel
- Adherent clot
These are the same Forrest classification concepts used in UGIB, adapted for LGIB.
- Indicated if bleeding source is not identified on colonoscopy [1]
- Generally prefer OGD before colonoscopy if there is any clinical suspicion of UGIB [2][9]
- In the lecture algorithm: for unstable patients, consider UGI endoscopy unless CTA has already located the site of bleeding [5]
- Critical in patients with haemodynamic instability + haematochezia (10–15% will have UGIB source)
| Feature | Detail |
|---|---|
| Reach | Up to descending colon (~60 cm) [3] |
| Indications | Fresh PR bleed without alarming symptoms; may be considered for patients < 40y as initial investigation [3] |
| Preparation | Low residue diet 3 days before, clear fluid diet 1 day before, Fleet enema ×2 [3] |
| Advantages | No sedation required, quick (~10 min), can do polypectomy |
| Limitations | Cannot visualise proximal colon (misses right-sided pathology); considered inadequate for diagnosis alone with gradual shift towards proximal tumours [11] |
Why Full Colonoscopy Over Flexible Sigmoidoscopy?
Right-sided colonic pathology (diverticular disease in Asia, right-sided CRC — which is becoming more common worldwide, caecal angiodysplasia) will be MISSED by flexible sigmoidoscopy. Synchronous tumours occur in 3–5% of CRC patients (30% for polyps) [11], so you need to scope the entire colon. Flexible sigmoidoscopy alone is only appropriate for low-risk patients (young, no red flags, typical outlet-type bleeding).
4.3 Radiological Investigations
| Feature | Detail |
|---|---|
| Principle | IV contrast-enhanced CT with arterial phase timing; extravasation of contrast into bowel lumen indicates active bleeding |
| Indication | Haemodynamically unstable patient — CTA before any treatment [5]; or when colonoscopy is non-diagnostic/not feasible |
| Sensitivity | Detects bleeding rates as low as 0.3–0.5 mL/min (better than conventional angiography) |
| Advantages | Widely available, fast, minimally invasive [1]; can localise bleeding to guide subsequent intervention (embolisation or surgery); also shows non-vascular pathology (tumour, diverticulitis, etc.) |
| Disadvantages | Lacks therapeutic capability [1]; requires radiation exposure and IV contrast (risk of contrast nephropathy and allergy) [1] |
| Key finding | Active contrast extravasation into bowel lumen = positive CTA |
Why CTA before colonoscopy in unstable patients? An unstable patient cannot tolerate bowel preparation or the prolonged sedation required for colonoscopy. CTA is fast (minutes), requires no bowel prep, and can be done simultaneously with resuscitation. It provides a "roadmap" for subsequent transcatheter embolisation or surgery.
| Feature | Detail |
|---|---|
| Principle | Selective catheterisation of SMA, IMA, and coeliac artery by Seldinger technique; look for extravasation of contrast [2][9][12] |
| Sensitivity | Detects bleeding rate of 0.5–1.0 mL/min [1]; diagnostic yield 27–67% [12] |
| Advantages | Localisation of bleeding site is very accurate [1]; allows therapeutic embolisation (injection of intra-arterial vasopressin or transcatheter embolisation) [1]; can diagnose non-bleeding lesions (angiodysplasia, SB tumours) [12]; can be done intra-operatively to guide surgery [12]; can specifically pinpoint the bleeding vessel (cf RBC scan) [12] |
| Disadvantages | Not sensitive for slow or intermittent bleeding [12]; embolisation carries risk of intestinal ischaemia [12]; invasive; requires interventional radiology expertise |
| Key findings | Contrast extravasation = active bleeding; early-filling vein with delayed emptying ("mother-in-law phenomenon") = angiodysplasia [3]; anomalous vitelline artery branch of SMA = Meckel's diverticulum [9] |
Two main techniques — both are screening tools to confirm and localise bleeding, particularly useful for intermittent or obscure bleeding [1][13]:
| Feature | 99mTc Sulphur Colloid Scan | 99mTc-Labelled RBC Scan |
|---|---|---|
| Principle | IV injection of radionuclide-labelled colloid; extravasation into bowel lumen detected | IV injection of 99mTc-labelled autologous RBCs; serial imaging over hours for extravasation |
| Sensitivity | Requires active bleeding; cannot detect intermittent bleeding | Detects intermittent bleeding at 0.1–0.4 mL/min [1][13] — more sensitive than angiography |
| Delayed imaging | Not possible (colloid is rapidly cleared by RES) | Delayed images up to 24h → can detect intermittent bleeding [13] |
| Localisation | Poor localisation of bleeding site [1] | Poor localisation (blood moves within bowel lumen between images) [1] |
| Therapeutic capability | No therapeutic value [1] | No therapeutic value [1] |
| Main role | Rapid screening | Preferred over angiography for initial detection of GI bleeding due to higher sensitivity and less invasiveness [13] |
Diagnostic criteria for a positive RBC scan [13]:
- Activity conforms to intestinal anatomy
- Intensity increases with time
- Activities move (anterograde or retrograde) within the bowels
Why is the RBC scan preferred over angiography for initial detection? Because it is more sensitive (0.1–0.4 mL/min vs 0.5–1.0 mL/min), less invasive, and can image over 24 hours to catch intermittent bleeding [13]. However, its poor localisation means that if positive, you often still need angiography or colonoscopy to pinpoint the exact source.
| Feature | Detail |
|---|---|
| Principle | 99mTc-pertechnetate is taken up by gastric mucosa (both orthotopic and ectopic). Ectopic gastric mucosa in a Meckel's diverticulum will accumulate the tracer |
| Indication | Young patients with suspected Meckel's diverticulum as cause of PR bleeding [9][12] |
| Sensitivity | ~85% in children, lower in adults |
| Key finding | Focal uptake in the right lower quadrant that appears simultaneously with gastric uptake |
| Feature | Detail |
|---|---|
| Principle | Spiral CT with IV contrast + air insufflation + intraluminal (enema) contrast → computer-generated 3D "fly-through" of the colon simulating colonoscopy [11] |
| Indication | When caecum cannot be reached by colonoscopy (incomplete colonoscopy due to obstruction/intolerance) [11] |
| Advantages | Non-invasive, similar diagnostic accuracy for tumours > 1 cm, provides extraluminal information [11] |
| Disadvantages | High radiation dose, not therapeutic (still needs colonoscopy for biopsy), requires mechanical bowel prep (stools can simulate polyps) [11] |
| Feature | Detail |
|---|---|
| Principle | Barium + air insufflation → double contrast outlines mucosal surface |
| Classic finding | "Apple-core" lesion — near-circumferential involvement of bowel walls by CRC [11] |
| Status | Largely superseded by CT colonography — risk of barium peritonitis if perforation; lower diagnostic accuracy [11] |
| Film | Findings and Significance |
|---|---|
| AXR | Dilated bowel loops (obstruction from CRC); thumbprinting (submucosal haemorrhage/oedema in ischaemic colitis); pneumatosis intestinalis (advanced ischaemia — gas in bowel wall); free air (perforation) |
| CXR | Free gas under diaphragm (perforation — e.g. perforated diverticulitis); lung metastases (CRC staging) |
When "top and tail" (OGD + colonoscopy) are both negative, the bleeding is termed obscure GI bleeding — and the source is most commonly in the small bowel [2][3][9].
| Investigation | Indication | Key Features |
|---|---|---|
| Wireless capsule endoscopy | Intermittent/stopped SB bleeding | Swallowed camera capsule transmits images; non-invasive; contraindicated if intestinal obstruction — do CT/MR enterography beforehand [3]; diagnostic yield ~60% for obscure OGIB |
| Double-balloon enteroscopy (DBE) | Intermittent SB bleeding, therapeutic intent | Scope with 2 inflated balloons, advances into SB from mouth or anus [3]; allows biopsy and therapy; more invasive |
| CT / MR enterography | SB pathology (tumour, Crohn's, radiation enteritis) | Non-invasive; good for mural and extramural lesions; segmental inflammation, bowel thickening, mucosal hyperenhancement [9] |
| Enteroclysis | SB neoplasm detection | Intubation of DJ flexure under fluoroscopy → injection of barium, methylcellulose, and water (double contrast) [3]; low yield (~10%), cannot detect vascular lesions [9] |
| Meckel's scan | Young patients | As above — 99mTc pertechnetate for ectopic gastric mucosa [12] |
| Intra-operative enteroscopy | Last resort, ongoing bleeding | Enteroscope through enterotomy at middle of SB → go both directions → plicate or excise lesions seen [12] |
Approach to obscure bleeding [9][12]:
| Clinical Scenario | Approach |
|---|---|
| Ongoing bleeding + unstable | Emergency exploratory laparotomy + on-table inspection/enteroscopy [12] |
| Ongoing bleeding + stable | Mesenteric angiogram (faster) or RBC scan (more sensitive); enteroscopy seldom done in ongoing bleeding (risk of prolonged sedation) [12] |
| Stopped bleeding | Meckel's scan (young); CT abdomen (older → exclude solid organ malignancies first); capsule endoscopy / enteroscopy if above negative [12] |
| Clinical Scenario | First-Line Investigation | Second-Line | Third-Line |
|---|---|---|---|
| Stable, intermittent outlet-type bleeding, young | DRE + Proctoscopy [5] → Flexible sigmoidoscopy | Colonoscopy if red flags | — |
| Stable, LGIB with red flags | Colonoscopy (with bowel prep) [5] | OGD if CLN negative | SB investigations |
| Unstable, massive haematochezia | CTA [5] → transcatheter embolisation | OGD (if UGIB suspected) | Emergency laparotomy |
| Suspected UGIB presenting as PR bleed | OGD (or NG aspirate first) [2][9] | CTA if OGD negative | — |
| Occult bleeding / IDA | Colonoscopy + OGD ("top and tail") | Capsule endoscopy / CT enterography | DBE / enteroscopy |
| Recurrent SB bleeding | Capsule endoscopy / DBE [3] | Mesenteric angiography | On-table enteroscopy [12] |
| Young patient, suspected Meckel's | Meckel's scan [12] | Mesenteric angiography | Laparoscopic exploration |
| Diagnosis | Key Investigation | Diagnostic Finding |
|---|---|---|
| Haemorrhoids | Proctoscopy | Engorged vascular cushions at 3, 7, 11 o'clock |
| Anal fissure | Inspection (spread buttocks) | Visible tear in posterior midline anoderm |
| Diverticular bleeding | Colonoscopy (+ angiography) | Active bleeding / visible vessel / adherent clot in diverticulum |
| Angiodysplasia | Colonoscopy | Cherry red spots (flat, well-demarcated, red vascular lesions) |
| Mesenteric angiography | "Mother-in-law phenomenon" (early filling, delayed emptying) | |
| CRC | Colonoscopy + biopsy (gold standard) [11] | Endoluminal mass, friable/necrotic/ulcerative; biopsy for histology |
| DCBE | "Apple-core" lesion | |
| UC | Colonoscopy + biopsy | Continuous inflammation from rectum, loss of vascular markings, friable mucosa, pseudopolyps |
| Ischaemic colitis | Colonoscopy; AXR | Segmental involvement at watershed areas; thumbprinting (AXR); oedematous folds with ischaemic ulcers |
| Radiation proctitis | Colonoscopy + biopsy | Vascular telangiectasia; segmental pallor with friability |
| Meckel's diverticulum | Meckel's scan | Focal RLQ uptake synchronous with gastric uptake |
| Active GI bleeding | RBC scan | Activity conforming to intestinal anatomy, increasing with time, moving within bowels [13] |
| Active GI bleeding | CTA / Mesenteric angiography | Contrast extravasation into bowel lumen |
High Yield Summary
-
Three principles: Save the patient → Find the bleeding → Stop the bleeding.
-
Haemodynamic status is the primary branch point — unstable → CTA first; stable → colonoscopy first.
-
Oakland score < 8 → consider safe discharge with outpatient evaluation.
-
Initial bloods: CBC (Hb may be falsely normal initially), clotting, LRFT, T&S. BUN:Cr ratio > 20:1 suggests UGIB.
-
DRE + proctoscopy are mandatory bedside investigations for every patient with PR bleeding.
-
Colonoscopy = first-line diagnostic modality for stable LGIB (yield 75–90%); requires bowel prep (4–6L PEG); should be done early.
-
OGD must be considered when colonoscopy is negative or when UGIB is suspected (10–15% of haematochezia is UGIB).
-
CTA for unstable patients — fast, no prep needed, localises source for subsequent embolisation.
-
RBC scan > angiography for sensitivity (0.1–0.4 vs 0.5–1.0 mL/min) and can detect intermittent bleeding over 24h, but poor localisation and no therapeutic capability.
-
Obscure GI bleeding (negative top-and-tail): Capsule endoscopy → DBE → CT/MR enterography → Meckel's scan (young) → on-table enteroscopy (last resort).
-
CEA has low sensitivity (~30%) for CRC — NOT a screening/diagnostic test; used for monitoring and recurrence detection.
Active Recall - Diagnosis of PR Bleeding
[1] Senior notes: felixlai.md (Lower GI Bleeding sections — History, Physical examination, Biochemical tests, Radiological tests) [2] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.3.6 Lower GI Bleeding, p281–285) [3] Senior notes: maxim.md (LGIB, Angiodysplasia, Haemorrhoids, Flexible/Rigid Sigmoidoscopy sections) [5] Lecture slides: GC 186. Lower and diffuse abdominal painfresh blood in stool.pdf (p19, p20, p38) [9] Senior notes: Ryan Ho GI.pdf (Section B. Approach to Lower GI Bleeding, p108–111) [11] Senior notes: maxim.md (CRC Investigations section); Senior notes: Ryan Ho GI.pdf (p166 — Diagnostic investigations for CRC) [12] Senior notes: Ryan Ho GI.pdf (p48 — Mesenteric angiography; p162 — Meckel's diverticulum investigations) [13] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p62 — Red Blood Cell Scan)
The management of PR bleeding follows the same three principles we established in the diagnostic section [2][9]:
1. Save the patient — resuscitation and haemodynamic stabilisation 2. Find the bleeding — localisation (covered in Dx section) 3. Stop the bleeding — endoscopic, radiological, or surgical haemostasis
The specific therapeutic approach then depends on two things: (a) the haemodynamic status of the patient, and (b) the underlying cause of the bleeding. Let me walk you through this systematically.
1. Resuscitation — "Save the Patient"
This is universal for all causes and must happen simultaneously with diagnostic workup in any significant bleed. You don't wait for a diagnosis to start resuscitation.
| Step | Action | Rationale |
|---|---|---|
| A — Airway | Intubate if decompensated (confused) or massive haematemesis [2][9] | Protects airway from aspiration of blood/vomitus; a confused patient has lost airway protective reflexes |
| B — Breathing | O₂ cannula to ↑ O₂-carrying capacity of blood [2][9] | Even with reduced Hb, maximising the O₂ saturation of remaining haemoglobin improves tissue oxygen delivery |
| C — Circulation | Large-bore IV cannula (14/16G at antecubital vein) with colloid/crystalloid infusion ± blood transfusion [2][9][14] | Large bore = faster flow rate (flow rate ∝ r⁴ by Hagen-Poiseuille equation — a 14G cannula delivers fluid ~4× faster than an 18G). Two access points ensure redundancy |
- NPO (nil by mouth) — in case OGD or surgery is needed [1][3]
- Set up 2 large-bore IV access and give 2L IV NS full rate [3]
- Stop all anticoagulants [3] — but weigh against the thrombotic risk of the individual patient before complete reversal of anticoagulation [1]
- Monitor vitals — cardiac monitor, pulse oximetry [1][2]
| Parameter | Target / Action | Why |
|---|---|---|
| Shock chart hourly | BP/P, RR, body temperature | ↓ Body temperature can cause ↓ efficiency of clotting factors — actively prevent hypothermia [2][9] |
| Foley's catheter | Urine output ≥ 0.5 mL/kg/h [2][9] | UO is the best real-time marker of end-organ perfusion (renal perfusion reflects cardiac output) |
| Cardiac monitor, pulse oximetry | Continuous | Detect arrhythmias from electrolyte imbalance or myocardial ischaemia from anaemia |
| ± CVP line | For PAWP monitoring | Consider if history of cardiac failure — to guide fluid resuscitation without causing pulmonary oedema [2][9] |
Transfusion triggers and targets from the lecture algorithm [5]:
| Clinical Scenario | Transfusion Trigger | Target Hb |
|---|---|---|
| No cardiovascular disease (CVD) | Hb < 7 g/dL | 7–9 g/dL |
| CVD present | Hb ≥ 8 g/dL | ≥ 10 g/dL |
| Profuse / ongoing bleeding | Transfuse regardless of Hb [2][9] | — |
| Persistent haemodynamic instability despite crystalloid | Transfuse [2][9] | — |
| Symptomatic anaemia | Transfuse [2][9] | — |
| Acute MI / unstable angina with low Hb | Transfuse [2][9] | — |
Correction of coagulopathy [1]:
- Fresh frozen plasma (FFP) for coagulopathy (INR > 1.5)
- Platelets for platelet dysfunction or thrombocytopenia (platelets < 50 × 10⁹/L in active bleeding)
- Vitamin K if warfarin-related coagulopathy (but takes 6–12h for effect)
- Prothrombin complex concentrate (PCC) for urgent warfarin reversal
- Tranexamic acid (antifibrinolytic) — may be considered although evidence in LGIB is limited [3]
Restrictive vs Liberal Transfusion
Why target Hb 7–9 rather than higher? The TRIGGER trial and subsequent evidence showed that a restrictive transfusion strategy (Hb 7 g/dL trigger) in GI bleeding reduces mortality compared to liberal transfusion (Hb 9 g/dL trigger). Over-transfusion can raise portal pressure (→ ↑risk of variceal rebleeding), cause volume overload (especially in cardiac patients), and has immunomodulatory effects. The exception is patients with active CVD who need higher Hb to maintain myocardial oxygen delivery.
3. Cause-Specific Management
"Treatment: endoscopic vs surgical resection" [5][8]
The management follows a stepwise escalation:
Step 1: Conservative / Supportive
- 50% of diverticular bleeding stops spontaneously [3]; 80–85% overall stop spontaneously [5][8]
- Fluid resuscitation and blood transfusion as needed [1]
- Lifestyle modification: high-fibre diet, bulk laxatives (e.g. methylcellulose), weight reduction [3]
- Avoid stimulant laxatives and NSAIDs (NSAIDs ↑ risk of diverticular bleeding via impaired platelet function and mucosal injury) [3]
Step 2: Endoscopic Therapy (colonoscopy to identify and treat)
- Indication: stigmata of recent haemorrhage (active bleeding, non-bleeding visible vessel, adherent clot) [3]
- Modalities [1][3][5]:
- TTS / cap-mounted clip — mechanical compression of bleeding vessel [5]
- Endoscopic band ligation (EBL) [5]
- Adrenaline injection (1:10,000) — not used alone (temporary effect only; rebleeds after absorption ~1h) [3][9]
- 4-quadrant submucosal injection of adrenaline in bleeding diverticular vessel [1]
- Bipolar coagulation for non-bleeding visible vessel [1]
- Localisation of bleeding: colonoscopy → angiography → on-table lavage and colonoscopy → subtotal colectomy if source still unidentified [3]
Step 3: Angiographic Therapy (if endoscopy fails or is not feasible)
- Embolisation or infusion of vasopressin by localising the site of bleeding [1]
- Transcatheter embolisation within 60 minutes for unstable patients [5]
- Risk: Intestinal ischaemia from embolisation (occluding blood supply to bowel wall) [12]
Step 4: Surgical Resection (last resort) [1][5][9]
- Reserved for patients in whom bleeding does not stop spontaneously and cannot be controlled with endoscopic or angiographic therapy [1]
- Indications for surgery (laparotomy) [1][2][9]:
- Haemodynamic instability despite adequate resuscitation
- Massive blood transfusion ( > 6 units)
- Frequent re-bleeding
- On anticoagulant or antiplatelets (higher risk of ongoing bleeding)
- Procedures [2][9]:
- Semi-elective resection after 2nd bleeding episode should be considered for recurrent diverticular bleeding [2]
Operative approach for acute LGIB (from lecture slides) [5]:
- For relatively stable patients, persistent bleeding after exhausting endoscopic and radiological interventions
- For patients who don't respond to initial resuscitation
- Consider upper endoscopy first if not been performed
- Palpation of small bowel (tumour, diverticulum)
- On-table upper endoscopy and colonoscopy
- On-table enteroscopy (diagnostic yield 80–92%) [5]
- Clamping of bowel segments (to isolate bleeding segment)
- Segmental resection if bleeding source identified, rebleeding rate 0–15% [5]
- If no source identified and probable colonic cause, subtotal or total colectomy (rebleeding rate 10–20%) [5]
Why Not Blind Segmental Resection?
Blind segmental resection (without pre-operative localisation) has a rebleeding rate of up to 75% [2]. This is because you may resect the wrong segment — the remaining colon still harbours the bleeding source. Always attempt to localise the bleeding before surgery. If you cannot localise it, a subtotal colectomy is safer than guessing.
| Step | Modality | Details |
|---|---|---|
| Conservative | Bed rest, tranexamic acid [3] | Most episodes (85–90%) self-limiting |
| Endoscopic | Argon plasma coagulation (APC) or monopolar electrocautery [3][5] | APC is the treatment of choice — delivers non-contact thermal energy via ionised argon gas; has lower energy depth than heat probe → lower risk of perforation → ideal for thin-walled vascular lesions [9][15] |
| Interventional Radiology | Mesenteric angiogram for super-selective catheterisation and embolisation [3] | When colonoscopy is non-diagnostic or endoscopic haemostasis fails |
| Surgical | Right hemicolectomy (most angiodysplasia is caecal/ascending colon) [3] | Only in selected patients due to high mortality; indications: failed endoscopic + angiographic treatment; severe acute life-threatening GI bleed; multiple lesions that cannot be managed otherwise [3] |
Why APC for angiodysplasia? Angiodysplasia lesions are superficial (submucosal), thin-walled vessels lacking smooth muscle. APC delivers controlled, shallow thermal energy → ablates the superficial malformation without burning deep into the bowel wall → minimises perforation risk. This is why it's specifically recommended for angiodysplasia over deeper thermal modalities [9][15].
3.3 Haemorrhoids
Management is guided by the Goligher grading of internal haemorrhoids [3]:
| Grade | Description | Management |
|---|---|---|
| I | Palpable, non-prolapsing, bleeding only | Lifestyle + medical |
| II | Prolapse with straining, spontaneous reduction | Lifestyle + medical + RBL |
| III | Prolapse requiring manual reduction | Lifestyle + medical + RBL + consider surgery |
| IV | Chronic prolapse, irreducible ± strangulated | Surgery |
| Measure | Rationale |
|---|---|
| High-fibre diet, increase fluid intake | Softens stool → reduces straining → reduces engorgement of anal cushions |
| Avoid prolonged sitting on toilet, avoid prolonged straining | Straining ↑ intra-abdominal pressure → ↑ venous congestion of haemorrhoidal plexus |
| Exercise, weight loss | ↓ chronic ↑ intra-abdominal pressure |
| Avoid spicy food | Reduces anal irritation |
| Agent | Mechanism |
|---|---|
| Stool softeners, bulking agents (e.g. Metamucil / psyllium) | ↑ stool bulk and softness → ↓ straining |
| Topical antiseptic (KMnO₄ sitz bath) | Reduces local infection/irritation |
| Topical haemostatic (e.g. Faktu) | Local haemostasis |
| Topical astringent (e.g. Anusol — contains zinc oxide, bismuth) | Shrinks swollen tissue, reduces mucous discharge |
| Topical analgesics | Pain relief |
Rubber Band Ligation (RBL) [3]:
- Apply rubber bands to strangulate the pile by Barron's bander → ischaemic necrosis of piles → slough off within 10 days
- Efficacy: 70% resolve, 30% recur
- Administration: up to 3 bandings at ≥ 1 cm above dentate line (must be above dentate line because below = somatic innervation = excruciating pain)
- Indication: symptomatic Grade II/III internal haemorrhoids
- Complications: pain, bleeding (7–10 days post-banding due to sloughing of ligated haemorrhoids)
- Contraindications: anticoagulant use, immunocompromised (risk of post-banding sepsis)
Sclerotherapy ("Mitchell") [3]:
- 5% phenol in almond oil injected submucosally → creates fibrosis → obliterates vascular channels and fixes position
- Largely abandoned now: risk of allergy to nuts and intraprostatic injection [3]
Haemorrhoidal Artery Ligation Operation (HALO) [3]:
- May be Doppler-guided (DG-HALO) to identify feeding vessels
- Mainly for bleeding symptoms, indicated for Grade II/III haemorrhoids
- Lowest post-op complications, but highest recurrence rate [3]
Indications:
- Grade III/IV internal haemorrhoids
- Symptomatic internal/external haemorrhoids refractory to other treatments
Approaches:
| Approach | Description | Best For |
|---|---|---|
| Conventional haemorrhoidectomy | For internal ≥ grade III or external | Most cases requiring surgery |
| Open (Milligan-Morgan) | Open wound, heal by secondary intention | Preferred for acute gangrenous haemorrhoids (prevents further tissue oedema and necrosis) |
| Closed (Ferguson) | Close wound by continuous suture | More commonly used |
| Stapled haemorrhoidopexy | For internal only, stapler excises ring of prolapsing mucosa | Less painful but higher recurrence rate; less favoured now due to poorer long-term outcomes |
- 3-leaf clover excision pattern: avoid circumferential excision — prone to stenosis [3]
- Efficacy: 95% resolve [3]
- Pre-op preparation: stool softener, enema [3]
- Position: prone jackknife or lithotomy [3]
- Anaesthesia: perianal / spinal / general [3]
Complications:
| Timing | Management |
|---|---|
| Presents within 72h | Excision under local anaesthesia (excise the entire thrombosed haemorrhoid — NOT just incision and drainage, which leads to recurrence) |
| Presents after 72h | Conservative management (sitz baths, analgesics, stool softeners) — the thrombus is already organising and will resolve spontaneously (leaving a skin tag) |
| Phase | Treatment | Mechanism |
|---|---|---|
| Acute (< 6 weeks) | Supportive: ↑ dietary fibre and water, stool softeners/laxatives, warm sitz baths (relax sphincter + ↑ blood flow to anal mucosa), topical analgesics (lidocaine jelly) [1] | Softens stool → ↓ trauma to anoderm; sitz bath → ↓ sphincter spasm → ↓ ischaemia → promotes healing |
| Chronic ( > 6 weeks) / Failed conservative | Topical vasodilators: topical nifedipine ointment or topical nitroglycerin (GTN) ointment [1] | Chemical sphincterotomy — relaxes internal anal sphincter smooth muscle → ↓ resting anal pressure → ↑ blood flow to ischaemic posterior midline → promotes healing |
| Botulinum toxin type A injection [1] | Chemical denervation of internal anal sphincter → ↓ spasm for ~3 months → allows healing | |
| Lateral internal sphincterotomy [1] | Definitive surgical treatment — divides the internal anal sphincter (partially) → permanently ↓ resting anal tone → ↑ perfusion → heals the fissure. Risk: minor faecal incontinence |
Why lateral internal sphincterotomy is so effective: The root cause of chronic fissure is internal sphincter spasm creating a vicious cycle of ischaemia and failed healing. By dividing part of the sphincter, you break this cycle. The operation has a > 95% healing rate. The trade-off is a small risk (~5–8%) of minor incontinence to flatus.
Treatment [5]:
- Packing of adrenaline-soaked gauze — direct tamponade + local vasoconstriction
- Suture plication — surgical closure of the bleeding ulcer
- Endoscopic electrocoagulation — thermal haemostasis of the bleeding vessel
- Blood transfusion (for anaemia from chronic bleeding)
- Sucralfate enema — cytoprotective; forms a barrier over ulcerated mucosa, promotes healing
- Steroid enema — reduces inflammation
- Argon plasma coagulation (APC) — ablates telangiectatic vessels (first-line endoscopic therapy)
- RFA (radiofrequency ablation)
- Formalin (4% formalin application) — causes chemical cauterisation of telangiectatic tissue
- Laser / infrared coagulation
- Stoma diversion — diverting proximal stoma to defunctionalise the rectum (last resort for intractable cases) [5]
- Proctectomy — rarely done, reserved for truly refractory cases [2]
- Endoscopic treatment has limited role for bleeding CRC [2] — the bleeding is from friable tumour surface, not a discrete vessel
- Definitive management is oncological treatment (surgical resection ± chemo/radiotherapy) — this is a separate major topic
- In the acute setting: supportive care, transfusion, and expedited staging workup
- Mostly supportive: IV fluids, bowel rest, broad-spectrum antibiotics (to prevent secondary bacterial translocation)
- Surgery indicated for: peritoneal signs (transmural necrosis/perforation), persistent bleeding, stricture formation
- Treat underlying cause (optimise cardiac output, hold vasopressors if possible)
| Cause | 1st Line | 2nd Line | 3rd Line / Surgical |
|---|---|---|---|
| Diverticular bleeding | Endoscopic: TTS/cap clip or EBL [5] | Transcatheter embolisation [5] | Segmental colectomy (with localisation) or subtotal colectomy (without) [5] |
| Angiodysplasia | APC [3][5] | IR: super-selective embolisation [3] | Right hemicolectomy (selected cases only) [3] |
| Haemorrhoids (I–II) | Lifestyle + medical + RBL [3] | — | — |
| Haemorrhoids (III–IV) | Haemorrhoidectomy [3] | — | — |
| Anal fissure (acute) | Fibre, sitz bath, topical analgesics [1] | Topical GTN/nifedipine [1] | Lateral internal sphincterotomy [1] |
| Rectal ulcer | Adrenaline gauze packing [5] | Suture plication [5] | Endoscopic electrocoagulation [5] |
| Radiation proctitis | Sucralfate/steroid enema [5] | APC, formalin, laser [5] | Stoma diversion [5] |
| Rectal varices | Sclerotherapy [2] | TIPS [2] | — |
| CRC | Supportive + staging | Surgical resection ± chemo/RT [2] | — |
| IBD | Medical (5-ASA, steroids, biologics) [2] | Emergency colectomy if life-threatening [2] | — |
| Post-polypectomy | Mechanical (TTS/cap clip or EBL) or thermal treatment [5] | Haemostatic topical agent as salvage [5] | — |
Since endoscopic haemostasis is the cornerstone of LGIB management for many causes, here's a comprehensive breakdown of the modalities [3][9][15]:
| Modality | Mechanism | Best Indication | Key Points |
|---|---|---|---|
| Adrenaline injection (1:10,000) | Volume tamponade effect + vasoconstriction + platelet attraction for thrombosis [15] | Initial haemostasis (any bleeding source) | Stops bleeding in 90–95% but often rebleeds ~1h after absorption; NOT used alone [3][15] |
| APC | Non-contact thermal coagulation via ionised argon gas; superficial energy delivery | Angiodysplasia, radiation proctitis [5][15] | ↓ Energy depth than heat probe → ↓ risk of perforation → ideal for thin-walled structures [15] |
| Heat probe / bipolar diathermy | Contact thermal coagulation melting vessel wall | Visible vessel in diverticulum or ulcer | Higher energy depth → ↑ risk of perforation cf APC |
| TTS clip / cap-mounted clip | Mechanical compression of bleeding vessel | Diverticular bleeding [5] | Through-the-scope (TTS) clips are standard; cap-mounted clips (e.g. Ovesco) are larger and can close bigger defects |
| Endoscopic band ligation (EBL) | Band strangulates tissue containing bleeding vessel → ischaemic necrosis | Diverticular bleeding [5] | Same principle as rubber band ligation for haemorrhoids/varices |
| Haemospray / haemostatic topical agent | Nanopowder with large surface area → contact activation of clotting cascade → haemostasis [15] | Salvage treatment when other modalities fail [5] | Temporary measure; powder washes off with ongoing bleeding |
| Sclerotherapy | Chemical thrombosis and fibrosis of vessels | Rectal varices, haemorrhoids (largely historical) | — |
| Laser coagulation | Focused thermal energy | Radiation telangiectasia | Less commonly used now (APC preferred) |
Transcatheter embolisation within 60 minutes for haemodynamically unstable patients [5]:
| Aspect | Detail |
|---|---|
| Principle | Selective catheterisation (Seldinger technique) → identify bleeding vessel by contrast extravasation → occlude vessel with embolic agents |
| Embolic agents | Gelfoam (temporary), PVA particles (permanent), coils (permanent), glue (permanent) [14] |
| Indication | Failed endoscopic haemostasis; unstable patient not amenable to colonoscopy; management of acute visceral bleeding [14] |
| Advantage | Can be done without bowel prep; definitive in many cases; avoids general anaesthesia of surgery |
| Risk | Intestinal ischaemia (occluding mesenteric vessel → downstream bowel wall necrosis); contrast nephropathy; access site haematoma [12] |
| Contraindication | Severe contrast allergy (relative); severe peripheral vascular disease precluding catheter access |
Why preferred over surgery in some cases? Embolisation is less invasive, avoids general anaesthesia, preserves bowel length, and can be done rapidly in the angiography suite. However, it carries a risk of ischaemia, and if it fails, surgery is still needed.
7. Surgical Management — Indications and Procedures
- Haemodynamic instability despite adequate resuscitation
- Massive blood transfusion ( > 6 units)
- Frequent re-bleeding
- On anticoagulant or antiplatelets (higher risk of uncontrollable bleeding)
- Patients with LGIB due to pathology not amenable to endoscopic or radiological treatment [5]
- Patients who don't respond to initial resuscitation [5]
| Step | Action |
|---|---|
| 1 | Consider upper endoscopy first if not been performed |
| 2 | Palpation of small bowel (looking for tumour, diverticulum) |
| 3 | On-table upper endoscopy and colonoscopy |
| 4 | On-table enteroscopy (diagnostic yield 80–92%) |
| 5 | Clamping of bowel segments (to isolate the bleeding segment) |
| 6a | Segmental resection if bleeding source identified — rebleeding rate 0–15% |
| 6b | If no source identified and probable colonic cause → subtotal or total colectomy — rebleeding rate 10–20% |
| Procedure | Rebleeding Rate | Mortality |
|---|---|---|
| Segmental resection with localisation | 0–15% | 0–13% |
| Blind segmental resection | Up to 75% | Higher |
| Subtotal colectomy | 10–20% | 0–40% |
8. Special Scenarios
| Agent | Action in Acute Bleeding | Considerations |
|---|---|---|
| Warfarin | Hold; give IV Vitamin K ± FFP ± PCC for urgent reversal | Weigh thrombotic risk (mechanical valve, recent PE) against bleeding risk |
| DOACs (dabigatran, rivaroxaban, apixaban) | Hold; dabigatran → idarucizumab for reversal; factor Xa inhibitors → andexanet alfa (if available) or PCC | Short half-lives (12–17h); holding for 24–48h often sufficient |
| Aspirin | Generally continue in active CVD; may hold if bleeding is life-threatening and no recent coronary stent | Irreversible COX-1 inhibition → platelet dysfunction lasts 7–10 days; platelet transfusion if critical |
| Clopidogrel / Dual antiplatelet therapy | Discuss with cardiology; hold if life-threatening bleed; platelet transfusion if needed | Recent coronary stent ( < 6 months) → high risk of stent thrombosis if stopped |
Endoscopic treatment:
- Mechanical therapy (TTS/cap-mounted clip or EBL) or thermal treatment
- Haemostatic topical agent as salvage treatment
| Clinical Status | Management |
|---|---|
| Symptomatic (bleeding) | Resect |
| Narrow base → simple diverticulectomy (excision + suture at base) | |
| Broad base / ulceration at margin → segmental bowel resection + primary anastomosis | |
| Asymptomatic, found on imaging | Do NOT resect |
| Asymptomatic, found during OT | Depends on age: child → resect; adult < 50y → resect if palpable, length > 2 cm, broad base > 2 cm; adult > 50y → do not resect [3] |
High Yield Summary
-
Resuscitation is simultaneous with diagnosis: ABC, 2× large-bore IV, NPO, stop anticoagulants, O₂, monitor UO ≥ 0.5 mL/kg/h.
-
Transfusion targets: Hb < 7 → target 7–9 g/dL (no CVD); Hb ≥ 8 + CVD → target ≥ 10 g/dL. Correct coagulopathy with FFP/platelets.
-
Unstable patient: CTA → transcatheter embolisation within 60 min → emergency laparotomy if all else fails.
-
Stable patient: Oakland < 8 → discharge + outpatient. Oakland ≥ 8 → inpatient colonoscopy as first diagnostic/therapeutic modality.
-
Endoscopic therapy by cause: Diverticular → TTS/cap clip or EBL; Angiodysplasia → APC; Post-polypectomy → mechanical/thermal; Salvage → haemostatic topical agent.
-
Diverticular bleeding escalation: Conservative (80–85% self-limiting) → endoscopic → embolisation → segmental resection (with localisation) or subtotal colectomy (without).
-
Haemorrhoids by grade: I–II → lifestyle + medical ± RBL; III–IV → haemorrhoidectomy. RBL ≥ 1 cm above dentate line. Open Milligan-Morgan for gangrenous; Closed Ferguson for routine.
-
Anal fissure: Fibre + sitz bath → topical GTN/nifedipine → botox → lateral internal sphincterotomy.
-
Surgery for LGIB (~15–20%): Segmental resection with localisation (rebleed 0–15%) >> blind resection (rebleed 75%) >> subtotal colectomy without localisation (rebleed 10–20%).
-
On-table enteroscopy has diagnostic yield 80–92% — invaluable when all else fails intra-operatively.
Active Recall - Management of PR Bleeding
[1] Senior notes: felixlai.md (Lower GI Bleeding Treatment, Anal Fissure Treatment, Diverticulitis Treatment sections) [2] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.3.6 Lower GI Bleeding — Resuscitation and Management, p282–286) [3] Senior notes: maxim.md (LGIB Acute Management, Haemorrhoids Management, Angiodysplasia Management, Diverticular Disease Management, Meckel's Diverticulum sections) [5] Lecture slides: GC 186. Lower and diffuse abdominal painfresh blood in stool.pdf (p9, p12, p13, p38, p40) [8] Lecture slides: Diverticular diseases - Dr. J Tsang.pdf (p7, p8) [9] Senior notes: Ryan Ho GI.pdf (Section B. Approach to Lower GI Bleeding — Investigations and Management, p110–111) [12] Senior notes: Ryan Ho GI.pdf (p48 — Mesenteric angiography, Operative approach; p162 — Meckel's diverticulectomy) [14] Senior notes: Ryan Ho Critical Care.pdf (p21 — Management of Hypovolemic Shock); Senior notes: Ryan Ho Diagnostic Radiology.pdf (p85 — Transcatheter Embolization) [15] Senior notes: Ryan Ho GI.pdf (p45 — Endoscopic Tx modalities); Senior notes: Ryan Ho Fundamentals.pdf (p255 — Endoscopic Tx modalities)
Complications of PR bleeding can be divided into two broad categories: (A) complications of the bleeding itself (i.e., what happens to the patient because of blood loss), and (B) complications of the treatments used to manage the bleeding (endoscopic, radiological, surgical). Both are clinically important and frequently tested.
A. Complications of PR Bleeding Itself
These are direct consequences of intravascular volume depletion from blood loss. The severity depends on the rate and total volume of bleeding.
| Complication | Mechanism | Clinical Features |
|---|---|---|
| Hypovolaemic shock | Loss of circulating blood volume → ↓ venous return → ↓ cardiac output → ↓ tissue perfusion. Classified by ATLS haemorrhage classes (I–IV) based on % blood volume lost | Extreme thirst, confusion, pallor, oliguria [2]; tachycardia, hypotension, cold clammy extremities, delayed CRT |
| Pre-renal acute kidney injury | ↓ Renal perfusion pressure → ↓ GFR → ↓ urine output; if prolonged → acute tubular necrosis (ischaemic injury to renal tubular epithelium) | ↑ Creatinine, ↑ urea (disproportionately if UGIB), oliguria < 0.5 mL/kg/h |
| Myocardial ischaemia / infarction | ↓ O₂-carrying capacity (anaemia) + ↑ heart rate (compensatory tachycardia) → supply-demand mismatch in coronary circulation, especially in patients with pre-existing coronary artery disease | Chest pain, ECG changes (ST depression/elevation), ↑ troponin |
| Cerebral hypoperfusion | ↓ Cardiac output → ↓ cerebral perfusion pressure | Confusion, agitation, syncope, seizures (in severe shock) |
| Multi-organ dysfunction syndrome | Prolonged shock → global tissue ischaemia → organ failure cascade (kidneys, liver, lungs, coagulation) | ARDS, DIC, hepatic dysfunction, metabolic acidosis |
Why does tachycardia precede hypotension? The baroreceptor reflex detects falling arterial pressure → activates the sympathetic nervous system → ↑ heart rate and ↑ systemic vascular resistance (vasoconstriction) to maintain blood pressure. Hypotension only manifests when compensatory mechanisms are overwhelmed (typically at > 30% blood volume loss / Class III haemorrhage). This is why tachycardia is an earlier and more sensitive marker of blood loss than hypotension.
| Complication | Mechanism | Clinical Features |
|---|---|---|
| Symptomatic anaemia | ↓ Haemoglobin → ↓ O₂ delivery to tissues | SOB on exertion, postural dizziness, syncope, chest pain, palpitation, lethargy or fatigue [2] |
| Iron-deficiency anaemia (chronic occult bleeding) | Chronic blood loss → depletion of body iron stores → insufficient iron for haemoglobin synthesis → microcytic hypochromic anaemia | Fatigue, koilonychia, angular stomatitis, glossitis, pica, Plummer-Vinson syndrome (oesophageal web) |
| High-output cardiac failure | Severe chronic anaemia → compensatory ↑ cardiac output (↑ heart rate + ↑ stroke volume) → eventually myocardial fatigue → heart failure | Dyspnoea, peripheral oedema, raised JVP — usually only in very severe, prolonged anaemia (Hb < 5–6 g/dL) |
| Complication | Mechanism |
|---|---|
| Dilutional coagulopathy | Massive crystalloid/colloid resuscitation dilutes clotting factors and platelets → impaired coagulation → worsening bleeding → vicious cycle |
| Hypothermia-induced coagulopathy | ↓ Body temperature can cause ↓ efficiency of clotting factors [2][9] — clotting enzymes are temperature-dependent serine proteases; hypothermia slows their catalytic activity. Massive transfusion of cold blood products exacerbates this |
| Disseminated intravascular coagulation (DIC) | Prolonged shock → massive tissue factor release → widespread microvascular thrombosis → consumption of clotting factors and platelets → paradoxical bleeding |
The Lethal Triad of Trauma/Massive Haemorrhage
Hypothermia + Acidosis + Coagulopathy = the "lethal triad" or "triad of death." Each component worsens the others: hypothermia impairs clotting enzyme function; acidosis impairs platelet aggregation and clotting factor activity; coagulopathy causes more bleeding → more volume loss → more hypothermia and acidosis. This is why preventing hypothermia during resuscitation of massive PR bleeding is critical — warm IV fluids, warm blood products, warm the patient.
Some of the conditions causing PR bleeding have their own natural history complications that worsen outcomes:
| Underlying Cause | Complications Unique to the Condition |
|---|---|
| Diverticular bleeding | Recurrent bleeding (rebleeding ~20–30% [5][8]); need for emergency surgery if uncontrolled |
| CRC | Bowel obstruction (annular tumour), perforation, metastasis (liver, lung, peritoneal), fistula formation |
| IBD (UC) | Fulminant colitis → toxic megacolon (colonic dilatation ≥ 6 cm with systemic toxicity) → perforation → peritonitis (high mortality) [1]; CRC risk (long-standing disease) [1] |
| Ischaemic colitis | Transmural necrosis (15% of cases) → perforation → peritonitis; stricture formation (chronic fibrosis) |
| Haemorrhoids | Strangulation and thrombosis, gangrene, ulceration, fibrosis, portal pyaemia [1] |
B. Complications of Treatment
B1. Complications of Endoscopy (Colonoscopy / OGD)
Endoscopy is the workhorse of PR bleeding management but carries its own risks. These can be divided by timing [1][9]:
| Complication | Mechanism |
|---|---|
| Hypoxaemia / respiratory depression | Sedation (benzodiazepines ± opioids) → central respiratory drive depression → hypoventilation → ↓ SpO₂ |
| Aspiration pneumonia | Sedated patient with ↓ airway reflexes + blood/gastric contents in upper GI tract → aspiration into lungs |
| Hypotension / cardiac arrhythmia / AMI | Sedation-induced vasodilation + myocardial depression; compounded by pre-existing hypovolaemia from bleeding |
| Preparation-related | Bowel prep (4–6L PEG) → fluid and electrolyte disturbance, N/V, bloating, abdominal discomfort [9] |
| Complication | Incidence | Mechanism | Management |
|---|---|---|---|
| Perforation | ~0.1–0.3% (diagnostic); ↑ with therapeutic procedures | Gas insufflation during endoscopy can cause pneumoperitoneum → abdominal compartment syndrome → ↓ venous return → death; also splinting of diaphragm compromising ventilatory movement [9][15]. Direct mechanical trauma from scope or polypectomy | Surgery (laparotomy/repair) for free perforation; conservative for contained micro-perforation |
| Bleeding | ~1–2% after polypectomy [9] | Disruption of vessels at polypectomy site; inadequate coagulation of stalk | Endoscopic haemostasis (clip, coagulation); rarely surgery |
| Complication | Timing | Mechanism | Features |
|---|---|---|---|
| Delayed bleeding | 5–7 days post-procedure [1][9] | Sloughing of an eschar covering a blood vessel or extension of thermal necrosis zone to non-injured tissue → vessel exposure | Fresh PR bleeding days after polypectomy; usually self-limiting; may require repeat endoscopy |
| Post-polypectomy syndrome | 1–5 days [1][9] | Electrocoagulation injury to bowel wall creating a transmural burn and focal peritonitis WITHOUT frank perforation | Fever, focal abdominal tenderness, and leucocytosis following polypectomy; usually managed conservatively (bowel rest, antibiotics); CT shows localised thickening without free air |
Perforation During Endoscopy — Why It Matters
Endoscopy is contraindicated if there is known perforation [15]. Gas insufflation during endoscopy in a perforated bowel → free gas enters peritoneal cavity → pneumoperitoneum → ↑ intra-abdominal pressure → abdominal compartment syndrome (compressed IVC → ↓ venous return → cardiovascular collapse; splinted diaphragm → respiratory failure). This is a life-threatening scenario.
From the lecture slides [7]:
Complications of haemorrhoidectomy:
- Bleeding
- Urine retention
- Pain
- Faecal impaction
- Infection
- Anal tags
- Anal stenosis
- Incontinence
Let me explain each:
| Complication | Mechanism | Notes |
|---|---|---|
| Pain | ~100% due to internal anal sphincter (IAS) spasm [3] | The operated area is below the dentate line (somatic innervation). Sphincter spasm is reflexive and persistent. Managed with analgesics, sitz baths, topical GTN/nifedipine |
| Urinary retention | Multifactorial: pain and anal spasm → reflex inhibition of detrusor; fluid overload; rectal packing; drugs (narcotics → ↑ bladder sphincter tone; anticholinergics → ↓ detrusor contraction); pre-existing outflow tract obstruction [3] | Management: leave urinary catheter in situ for 24h [3] |
| Bleeding (early/reactionary) | Slippage of ligature or disruption of cauterised vessel in the first 24h; or secondary haemorrhage at 7–10 days from infection eroding vessels | May require return to theatre for haemostasis |
| Faecal impaction | Post-op pain → patient avoids defaecation → stool accumulates → impaction | Prevented by stool softeners; treated with enemas/manual disimpaction |
| Infection | Surgical wound contamination in a bacterially-rich environment (perineum) | Antibiotics; rare but can lead to severe pelvic sepsis |
| Anal stenosis | Circumferential excision removes too much anoderm → scarring → stenosis → this is why the 3-leaf clover excision pattern is used (leaves mucosal bridges between excision sites) [3] | Prevented by technique; treated with finger dilation or anoplasty |
| Incontinence | Damage to internal or external anal sphincter during dissection → ↓ resting tone (IAS) or ↓ squeeze pressure (EAS) | Risk minimised by careful dissection; more common with open techniques |
| Anal tags | Residual redundant skin at excision margins | Usually cosmetic; can be excised if symptomatic |
Outcomes of stapled haemorrhoidopexy (from lecture slides) [7]:
- Less pain, less analgesic requirement, quicker recovery and shorter hospital stay
- Higher patient's satisfaction
- Less postoperative bleeding, wound complications
- Complications can be serious: rectal perforation, severe pelvic sepsis, rectovaginal fistula
- More recurrence than conventional haemorrhoidectomy
Why does stapled haemorrhoidopexy have a higher recurrence rate? The stapler resects a circumferential ring of mucosa/submucosa above the haemorrhoids and pulls them back into position, but it doesn't actually remove the haemorrhoidal tissue. Over time, the vascular cushions can re-engorge and re-prolapse. Conventional haemorrhoidectomy physically excises the cushion tissue — more definitive but more painful.
| Complication | Mechanism |
|---|---|
| Pain | Band placed too close to (or below) the dentate line → somatic nerve territory → pain |
| Bleeding (7–10 days post-banding) | Sloughing of ligated haemorrhoids exposes underlying vessels; contraindicated in patients on anticoagulants or immunocompromised [3] |
| Post-banding sepsis | Rare but potentially fatal; mucosal breach → bacterial translocation; presents with fever, perineal pain, urinary retention (triad) → necrotising fasciitis risk |
| Complication | Mechanism | Risk Factor |
|---|---|---|
| Intestinal ischaemia / infarction | Occluding a mesenteric vessel deprives the downstream bowel wall of blood supply → mucosal ischaemia → transmural necrosis if collateral circulation is insufficient | Watershed areas; atherosclerotic disease; non-selective embolisation |
| Access site complications | Femoral artery puncture (Seldinger technique) → haematoma, pseudoaneurysm, AV fistula, dissection | Anticoagulation, obesity, repeated punctures |
| Contrast-related | Contrast nephropathy (direct tubular toxicity + renal vasoconstriction); allergic reaction | Pre-existing renal impairment, dehydration, iodine allergy |
| Non-target embolisation | Embolic particles travel to unintended vessels → ischaemia of non-target organs | Reflux of particles during injection |
B5. Complications of Colorectal Surgical Resection
These are relevant when surgery is required for bleeding that cannot be controlled by endoscopic or radiological means. The complications mirror those of any major colorectal surgery [1][3][16]:
| Complication | Mechanism | Key Points |
|---|---|---|
| Surgical site infection (5–15%) | Bacterial contamination of wound from colonic flora; risk factors: malnutrition, DM, immunosuppression, age > 60, faecal contamination, extensive surgery [16] | Superficial (wound) or deep (intra-abdominal abscess) |
| Postoperative ileus | Handling of bowel + peritoneal irritation + opioid use → disruption of normal coordinated peristalsis | Abdominal distension, N/V, absent bowel sounds; usually self-limiting (3–5 days); managed conservatively (NGT, IV fluids, ambulation) |
| Anastomotic leak | Failure of healing at the surgical join → bowel content leaks into peritoneal cavity or surrounding tissue. Classically on day 4–7 [16]. Incidence 1–5% overall but up to 10% in low anterior resection (ileoanal > colocolic > ileocolic) [16] | Diffuse feculent peritonitis + septic shock if free leak; abscess or enterocutaneous fistula if contained [16]. Risk factors: liver/renal impairment, steroid use, suboptimal bowel condition (emergency surgery), tension on anastomosis, poor blood supply |
| Anastomotic bleeding | Bleeding from staple/suture line | Usually self-limiting; managed with transfusion and correction of coagulopathy [1] |
| Injury to neighbouring structures | Left ureter and gonadal vessels (left-sided resections); iliac artery; duodenum/GB (right hemicolectomy); spleen (splenic flexure mobilisation in TME); seminal vesicles (LAR); bladder; urethra [3][16] | — |
| Autonomic nerve injury (especially rectal surgery) | Damage to hypogastric nerves (sympathetic) or pelvic splanchnic nerves (parasympathetic) during mesorectal excision | Sympathetic injury → urinary incontinence, impaired ejaculation; parasympathetic injury → urinary retention, erectile dysfunction [3]. Risk reduced by low tie (distal to left colic artery) which avoids damage to the hypogastric nerve [3] |
| Complication | Mechanism | Management |
|---|---|---|
| Anastomotic stricture | Fibrosis and scarring at the anastomotic site → luminal narrowing | Finger dilation for low anastomosis; endoscopic balloon dilation for high anastomosis [1][3] |
| Fistula | Failed healing of anastomosis → abnormal communication between bowel and adjacent structure | Enterocutaneous → conservative (most close spontaneously); rectovaginal/rectourinary → proximal faecal diversion [1][3] |
| Incisional hernia | Failure of fascial closure → bowel herniates through abdominal wall defect | Surgical repair (mesh) |
| Parastomal hernia, stomal prolapse, stomal stenosis | Fascial defect around stoma → hernia; excessive bowel mobility → prolapse; scarring → stenosis | Revision of stoma; local repair |
| Timing | Complication | Mechanism |
|---|---|---|
| Early | Stomal bleeding | Inadequate haemostasis at stoma site |
| Stomal necrosis | Compromised blood supply to terminal bowel brought through abdominal wall → ischaemic necrosis | |
| Stomal retraction | Inadequate bowel mobilisation or tension on bowel → stoma pulls below skin level → difficulty with appliance fitting | |
| Mucocutaneous separation | Failure of mucosal-skin junction to heal → gap between stoma and surrounding skin | |
| Skin irritation and dermatitis | Most common in end and loop ileostomy due to high-output and high alkaline enzymatic effluent [1] — small bowel effluent contains active pancreatic enzymes (lipase, protease) that digest skin | |
| Late | Parastomal hernia | Most common late stoma complication; fascial defect around stoma widens over time |
| Stomal prolapse | Excessive bowel length or inadequate fixation → bowel telescopes through stoma | |
| Stomal stenosis | Scarring at skin or fascial level → narrowed stoma opening |
A particularly important complication of rectal surgery:
- S/S: change in bowel movement (ranging from constipation to faecal urgency, faecal incontinence) that persists ≥ 1 month after surgery [3]
- Pathophysiology: colonic dysmotility + neorectal reservoir dysfunction + anal sphincter dysfunction [3]
- Prevention: post-op pelvic floor muscle exercise, anterograde colonic irrigation via stoma/enema, faecal diversion [3]
- Management: antidiarrhoeal, transanal irrigation, pelvic floor rehab, sacral nerve stimulation [3]
Why does LAR syndrome occur? The rectum normally acts as a compliant reservoir that stores stool and allows controlled evacuation. When you resect the rectum and create a neo-rectum (from colon or a J-pouch), this new reservoir is smaller and less compliant → reduced capacity → ↑ frequency and urgency. Additionally, the surgical dissection can damage the autonomic nerves and internal anal sphincter → ↓ continence. The result is a frustrating constellation of symptoms that significantly impacts quality of life.
| Complication | Mechanism | Incidence |
|---|---|---|
| Minor faecal incontinence (mainly to flatus) | Division of internal anal sphincter → ↓ resting anal pressure → impaired fine control of anal continence | ~5–8% |
| Keyhole deformity | Excessive sphincter division → gutter-like deformity in anal canal → mucous soiling | Rare with modern technique |
| Bleeding / wound infection | Minor surgical complications | Rare |
| Category | Complications |
|---|---|
| Bleeding itself | Hypovolaemic shock, pre-renal AKI, myocardial ischaemia, cerebral hypoperfusion, MODS, dilutional/hypothermic coagulopathy, DIC, chronic IDA |
| Endoscopy | Sedation-related (respiratory depression, aspiration, hypotension, arrhythmia); perforation; bleeding (immediate or delayed at 5–7d); post-polypectomy syndrome |
| Haemorrhoidectomy | Bleeding, urinary retention, pain, faecal impaction, infection, anal tags, anal stenosis, incontinence [7] |
| Stapled haemorrhoidopexy | Rectal perforation, severe pelvic sepsis, rectovaginal fistula; higher recurrence [7] |
| RBL | Pain, delayed bleeding (7–10d), post-banding sepsis |
| Embolisation | Intestinal ischaemia, access site complications, contrast nephropathy, non-target embolisation |
| Colorectal surgery | SSI, ileus, anastomotic leak (day 4–7), anastomotic bleeding, organ injury (ureter, nerves), DVT/PE; late: stricture, fistula, hernia, stoma complications, LAR syndrome |
High Yield Summary
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Hypovolaemic shock is the most immediate life-threatening complication — tachycardia precedes hypotension (compensatory sympathetic response fails at > 30% blood loss).
-
Hypothermia → ↓ clotting factor efficiency — actively warm patients during massive resuscitation (part of the "lethal triad": hypothermia + acidosis + coagulopathy).
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Symptomatic anaemia: SOB on exertion, postural dizziness, syncope, chest pain, palpitations, fatigue. Chronic occult bleeding → iron-deficiency anaemia.
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Complications of haemorrhoidectomy (must know): bleeding, urinary retention, pain, faecal impaction, infection, anal tags, anal stenosis, incontinence.
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Stapled haemorrhoidopexy: Less pain/faster recovery but higher recurrence and risk of serious complications (rectal perforation, pelvic sepsis, rectovaginal fistula).
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Anastomotic leak: Classically day 4–7 post-op; up to 10% in LAR; presents with peritonitis/sepsis (free leak) or abscess (contained leak).
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Post-polypectomy syndrome: Transmural burn WITHOUT perforation → fever + focal tenderness + leucocytosis 1–5 days post-polypectomy. Usually managed conservatively.
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Delayed post-polypectomy bleeding: 5–7 days post-procedure from eschar sloughing.
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LAR syndrome: Faecal urgency/incontinence/frequency ≥ 1 month post rectal surgery due to neorectal dysfunction + autonomic nerve damage.
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Embolisation risk: Intestinal ischaemia from non-target or over-aggressive embolisation — always balance haemostasis against ischaemic risk.
Active Recall - Complications of PR Bleeding
[1] Senior notes: felixlai.md (Hemorrhoids Complications, Colorectal Surgery Complications, Colonoscopy Complications, Anal Fissure, UC Complications sections) [2] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.3.6 Lower GI Bleeding, p283 — Complications of bleeding) [3] Senior notes: maxim.md (Haemorrhoids Complications, Haemorrhoidectomy Complications, Colorectal Surgery Post-op Complications, LAR Syndrome, RBL sections) [5] Lecture slides: GC 186. Lower and diffuse abdominal painfresh blood in stool.pdf (p9 — diverticular bleeding rebleeding rate) [7] Lecture slides: GC 179. Anal pain perianal lesions and sepsis.pdf (p35 — Complications of haemorrhoidectomy; p40 — Outcomes of stapled haemorrhoidopexy) [8] Lecture slides: Diverticular diseases - Dr. J Tsang.pdf (p8 — rebleeding rate) [9] Senior notes: Ryan Ho GI.pdf (p110–111 — Monitoring, hypothermia and clotting; p180 — Colonoscopy complications) [15] Senior notes: Ryan Ho GI.pdf (p45 — Endoscopic complications, perforation contraindication) [16] Senior notes: Ryan Ho GI.pdf (p175 — Complications of colorectal resection)
High Yield Summary
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Definition: PR bleeding = passage of blood through the anus; ranges from occult (FOBT+) to massive haemorrhage.
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Always consider upper GI source in brisk haematochezia — up to 10–15% of apparent LGIB is actually UGIB.
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Anatomy essentials: Dentate line divides pain vs painless pathology; watershed areas (Griffiths' point, Sudeck's point) explain ischaemic colitis distribution; vasa recta penetration sites explain diverticular location and bleeding.
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Most common causes by age: < 50 → haemorrhoids; > 60 → diverticular disease and angiodysplasia.
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Diverticular bleeding: Commonest cause of LGIB. Painless. Right-sided in Asia. Stops in 80-85%. Recurs 20-30%.
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Red flags (must investigate for CRC): Change in bowel habit, tenesmus, blood mixed with stool, weight loss, family history, age > 50.
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DRE and proctoscopy are mandatory for every patient with PR bleeding.
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Haemorrhoids = engorgement and prolapse of anal vascular cushions (not "varicose veins"). Graded 1–4 by degree of prolapse.
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Anal fissure: Posterior midline (poor blood supply), tearing pain + spasm → vicious cycle of ischaemia and failed healing.
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Ischaemic colitis: Cramping pain → bleeding within 24h; watershed areas; non-occlusive (95%) in elderly with CVS disease.
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In Hong Kong: CRC is the #1 cancer. Diverticular disease is right-sided. Acute haemorrhagic rectal ulcer is more common in Asia.
High Yield Summary
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Structure your differential anatomically: Anorectal → Colonic → Small bowel → Upper GI.
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Always consider UGIB in severe haematochezia — 10–15% of apparent LGIB is from upper GI source.
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Commonest cause of massive LGIB = diverticular bleeding (painless, profuse, self-limiting in 80–85%, arterial from ruptured vasa recta).
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Angiodysplasia = venous, less profuse, more intermittent, elderly, associations with aortic stenosis (Heyde syndrome) and HHT.
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CRC red flags: Change in bowel habit, tenesmus, pencil-thin stools, constitutional symptoms, FHx, age > 50. "Right side bleeds, left side blocks."
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Haemorrhoids: Most common cause < 50y. Outlet-type bright red bleeding. Internal = painless; thrombosed external = painful. Always exclude coexisting CRC.
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Anal fissure: Severe tearing pain on defaecation. Posterior midline. Atypical location → think secondary cause.
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Ischaemic colitis: Cramping pain → bleeding within 24h. Watershed areas. Non-occlusive (95%) in elderly with CVS disease.
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For unstable patients: CTA → consider UGI endoscopy → transcatheter embolisation → emergency laparotomy as last resort.
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For stable patients: Oakland score assessment → colonoscopy (with bowel prep) as first diagnostic modality.
High Yield Summary
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Three principles: Save the patient → Find the bleeding → Stop the bleeding.
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Haemodynamic status is the primary branch point — unstable → CTA first; stable → colonoscopy first.
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Oakland score < 8 → consider safe discharge with outpatient evaluation.
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Initial bloods: CBC (Hb may be falsely normal initially), clotting, LRFT, T&S. BUN:Cr ratio > 20:1 suggests UGIB.
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DRE + proctoscopy are mandatory bedside investigations for every patient with PR bleeding.
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Colonoscopy = first-line diagnostic modality for stable LGIB (yield 75–90%); requires bowel prep (4–6L PEG); should be done early.
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OGD must be considered when colonoscopy is negative or when UGIB is suspected (10–15% of haematochezia is UGIB).
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CTA for unstable patients — fast, no prep needed, localises source for subsequent embolisation.
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RBC scan > angiography for sensitivity (0.1–0.4 vs 0.5–1.0 mL/min) and can detect intermittent bleeding over 24h, but poor localisation and no therapeutic capability.
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Obscure GI bleeding (negative top-and-tail): Capsule endoscopy → DBE → CT/MR enterography → Meckel's scan (young) → on-table enteroscopy (last resort).
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CEA has low sensitivity (~30%) for CRC — NOT a screening/diagnostic test; used for monitoring and recurrence detection.
High Yield Summary
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Resuscitation is simultaneous with diagnosis: ABC, 2× large-bore IV, NPO, stop anticoagulants, O₂, monitor UO ≥ 0.5 mL/kg/h.
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Transfusion targets: Hb < 7 → target 7–9 g/dL (no CVD); Hb ≥ 8 + CVD → target ≥ 10 g/dL. Correct coagulopathy with FFP/platelets.
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Unstable patient: CTA → transcatheter embolisation within 60 min → emergency laparotomy if all else fails.
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Stable patient: Oakland < 8 → discharge + outpatient. Oakland ≥ 8 → inpatient colonoscopy as first diagnostic/therapeutic modality.
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Endoscopic therapy by cause: Diverticular → TTS/cap clip or EBL; Angiodysplasia → APC; Post-polypectomy → mechanical/thermal; Salvage → haemostatic topical agent.
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Diverticular bleeding escalation: Conservative (80–85% self-limiting) → endoscopic → embolisation → segmental resection (with localisation) or subtotal colectomy (without).
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Haemorrhoids by grade: I–II → lifestyle + medical ± RBL; III–IV → haemorrhoidectomy. RBL ≥ 1 cm above dentate line. Open Milligan-Morgan for gangrenous; Closed Ferguson for routine.
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Anal fissure: Fibre + sitz bath → topical GTN/nifedipine → botox → lateral internal sphincterotomy.
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Surgery for LGIB (~15–20%): Segmental resection with localisation (rebleed 0–15%) >> blind resection (rebleed 75%) >> subtotal colectomy without localisation (rebleed 10–20%).
-
On-table enteroscopy has diagnostic yield 80–92% — invaluable when all else fails intra-operatively.
High Yield Summary
-
Hypovolaemic shock is the most immediate life-threatening complication — tachycardia precedes hypotension (compensatory sympathetic response fails at > 30% blood loss).
-
Hypothermia → ↓ clotting factor efficiency — actively warm patients during massive resuscitation (part of the "lethal triad": hypothermia + acidosis + coagulopathy).
-
Symptomatic anaemia: SOB on exertion, postural dizziness, syncope, chest pain, palpitations, fatigue. Chronic occult bleeding → iron-deficiency anaemia.
-
Complications of haemorrhoidectomy (must know): bleeding, urinary retention, pain, faecal impaction, infection, anal tags, anal stenosis, incontinence.
-
Stapled haemorrhoidopexy: Less pain/faster recovery but higher recurrence and risk of serious complications (rectal perforation, pelvic sepsis, rectovaginal fistula).
-
Anastomotic leak: Classically day 4–7 post-op; up to 10% in LAR; presents with peritonitis/sepsis (free leak) or abscess (contained leak).
-
Post-polypectomy syndrome: Transmural burn WITHOUT perforation → fever + focal tenderness + leucocytosis 1–5 days post-polypectomy. Usually managed conservatively.
-
Delayed post-polypectomy bleeding: 5–7 days post-procedure from eschar sloughing.
-
LAR syndrome: Faecal urgency/incontinence/frequency ≥ 1 month post rectal surgery due to neorectal dysfunction + autonomic nerve damage.
-
Embolisation risk: Intestinal ischaemia from non-target or over-aggressive embolisation — always balance haemostasis against ischaemic risk.
Hematuria
Hematuria is the presence of red blood cells in the urine, which may be visible (gross) or detectable only microscopically, indicating potential urinary tract pathology.
Polycystic Kidney Disease
Polycystic kidney disease is a genetic disorder characterized by the progressive development of multiple fluid-filled cysts in the kidneys, leading to renal enlargement and eventual loss of kidney function.