Rectal Bleeding
Rectal bleeding is the passage of blood through the anus, originating from the rectum or lower gastrointestinal tract, which may indicate conditions ranging from hemorrhoids to colorectal malignancy.
Rectal Bleeding — Clinical Approach (Definition through Clinical Features)
Rectal bleeding (also termed per-rectal (PR) bleeding or haematochezia) refers to the passage of blood through the anus. It encompasses a spectrum from bright-red blood on toilet paper to massive, haemodynamically significant haemorrhage. Although the term is often used interchangeably with "lower GI bleeding," it is important to understand the distinction:
- Lower GI bleeding (LGIB) = bleeding from the gut distal to the ligament of Treitz (the duodenojejunal flexure) [1][2][3]. The ligament of Treitz is the anatomical landmark that suspends the duodenojejunal junction — anything proximal is "upper GI," anything distal is "lower GI."
- Rectal bleeding is the presenting symptom; the source may be anywhere from the duodenum (in a massive upper GI bleed) to the anal margin.
"Haematochezia" → Greek: haima = blood + chezein = to defecate. Literally "bloody defecation."
"Melaena" → Greek: melaina = black. Tarry black stools from degraded haemoglobin (upper GI source, rarely right colon).
Key Conceptual Point
- Annual incidence of LGIB: approximately 20–27 per 100,000 [2][3].
- Incidence increases with age — most cases occur in the elderly. The median age of presentation is > 60 years [2].
- In younger adults (< 50 years), haemorrhoids and anal fissures are the most common causes [1][4].
- New bleeding in patients age > 55 years demands colonic investigation to exclude malignancy [1].
- In Hong Kong, colorectal cancer (CRC) is the 1st most common cancer overall and in males, 2nd most common in females, with an incidence of ~74.1/100,000/year [5]. This makes excluding CRC a top priority in any patient presenting with PR bleeding in the local context.
- Diverticular disease prevalence increases with age (~60% by age 60), and in Asian populations, right-sided diverticula predominate (unlike the left-sided/sigmoid predominance in Western countries) [2][4].
3. Anatomy and Function
Understanding the anatomy is essential because it directly determines:
- The character of the bleeding (colour, relationship to stool)
- The pain or lack thereof
- The physical examination findings
- The investigation of choice
The colon receives blood from the superior mesenteric artery (SMA) and inferior mesenteric artery (IMA), with the rectum also receiving supply from the internal iliac artery (IIA):
| Segment | Arterial Supply | Key Collateral |
|---|---|---|
| Caecum → transverse colon | SMA (ileocolic, right colic, middle colic aa.) | Marginal artery of Drummond |
| Splenic flexure → sigmoid | IMA (left colic, sigmoid aa.) | Marginal artery of Drummond |
| Rectum (upper) | Superior rectal artery (terminal IMA) | — |
| Rectum (middle/lower) | Middle & inferior rectal aa. (from IIA) | — |
Watershed areas — zones between two arterial territories with limited collateral supply — are most vulnerable to ischaemia:
- Griffiths' point (splenic flexure): junction of middle colic artery territory (SMA) and ascending left colic artery (IMA) at the marginal artery of Drummond [4][6].
- Sudeck's point (rectosigmoid junction): junction of the last sigmoid artery and the superior rectal artery [4][6].
Why does this matter clinically? Ischaemic colitis characteristically affects these watershed areas. A patient presenting with sudden cramping left-sided abdominal pain followed by bloody diarrhoea within 24 hours — think splenic flexure or rectosigmoid ischaemia [6].
| Region | Venous Drainage | System |
|---|---|---|
| Above dentate line | Superior rectal vein → IMV → portal system | Portal |
| Below dentate line | Middle & inferior rectal veins → internal iliac vein → IVC | Systemic |
This dual drainage explains:
- Rectal varices in portal hypertension: the superior rectal veins (portal) communicate with the middle/inferior rectal veins (systemic). When portal pressure rises, these porto-systemic anastomoses dilate → varices → potentially severe bleeding [2][3][4].
- Haemorrhoids are NOT varices — they are dilated anal vascular cushions (submucosal arteriovenous plexuses), though portal hypertension can worsen them.
The anal canal is approximately 4 cm long from the anal verge. The dentate (pectinate) line divides the upper two-thirds from the lower one-third and is a crucial landmark [4]:
| Feature | Above Dentate Line | Below Dentate Line |
|---|---|---|
| Embryology | Endoderm | Ectoderm |
| Epithelium | Columnar (→ adenocarcinoma) | Stratified squamous (→ SCC) |
| Nerve supply | Autonomic (inferior hypogastric plexus) — visceral, poorly localised sensation | Somatic (inferior rectal nerve ← pudendal nerve) — sharp, well-localised pain |
| Venous drainage | Superior rectal vein → portal system | Middle/inferior rectal veins → IVC |
| Lymphatic drainage | Internal iliac & inferior mesenteric LNs | Superficial inguinal LNs |
Clinical Relevance of the Dentate Line
- Internal haemorrhoids (above dentate line) = painless bleeding, because they are innervated by autonomic nerves that do not carry somatic pain fibres.
- External haemorrhoids / thrombosed haemorrhoids (below dentate line) = very painful, because somatic nerves (inferior rectal nerve) provide exquisite pain sensation.
- Anal fissures typically occur below the dentate line → tearing pain on defecation.
- The lymphatic drainage dictates metastatic patterns: anal SCC below the dentate line → inguinal lymph nodes (palpable on examination!).
Normal anal cushions are clusters of:
- Branches of the superior rectal artery
- Superior rectal veins (forming an arteriovenous plexus)
- Smooth muscle and connective tissue covered by mucosa
They sit at the 3, 7, and 11 o'clock positions (in lithotomy position) and contribute to fine continence (~15% of resting anal tone) by forming a soft, compressible seal [4][7].
- Colonic diverticula are false (pseudo-) diverticula: only mucosa and submucosa herniate through the muscularis propria [4][8].
- They form at points of weakness where the vasa recta penetrate the circular muscle layer [4][8].
- The sigmoid colon has the narrowest lumen → by Laplace's law (Wall tension = Pressure × Radius / Wall thickness), for a given contractile force, the narrowest segment generates the highest intraluminal pressure → most common site in Western populations [8].
- In Asia, right-sided diverticula predominate — and the right colon has a thinner wall, making diverticular bleeding more common on the right [2][4][8].
- The rectum is never affected because its outer longitudinal smooth muscle layer encompasses the full circumference (unlike the colon, which has three taeniae coli with gaps between them) [8].
4. Etiology (Focused on Hong Kong Context)
The following classification by anatomical source is fundamental [2][3]:
| Source | Causes | Approximate % of LGIB |
|---|---|---|
| Massive Upper GI (< 10%) | Peptic ulcer, variceal bleed | < 10% |
| Large Bowel (vast majority) | Diverticular disease* (17–40%), Angiodysplasia (2–30%), Colitis (9–11%), Neoplasm (7–33%) | ~80–85% |
| Small Bowel (~5%) | Meckel's diverticulum, angiodysplasia, small bowel tumours, NSAID-induced ulcers, Crohn's/TB enteritis, aortoenteric fistula | ~5% |
| Anorectal (~10%) | Haemorrhoids, fissure-in-ano, anal/rectal ulcers, rectal varices | ~10% |
* Causes marked with asterisk can present with heavy, life-threatening bleeding [2][3].
These are the most common causes you should consider first:
- Haemorrhoids / perianal haematoma
- Anal fissure
- Colorectal polyp
- Diverticulitis (though note: diverticular bleeding and diverticulitis rarely coexist)
- Excoriated skin (anal pruritus)
| Category | Conditions |
|---|---|
| Vascular | Ischaemic colitis, angiodysplasia (vascular ectasia), anticoagulant therapy |
| Infection | Enteritis (e.g. Campylobacter, Salmonella) |
| Cancer/Tumours | Colorectal cancer, caecal cancer, lymphoma, villous adenoma |
| Other | Inflammatory bowel disease (colitis/proctitis), intussusception |
- Rectal prolapse
- Anal trauma (accidental / non-accidental)
- Villous adenoma
- Meckel diverticulum
- Solitary ulcer of rectum
Exam Tip — Murtagh's Framework
Murtagh's diagnostic strategy is a favourite framework in HKUMed exams. Be able to recall the probability diagnosis, serious disorders not to be missed, pitfalls, and rarities for rectal bleeding. It structures your differential neatly.
5. Detailed Etiology with Pathophysiology
Most common cause of LGIB (17–40%) [2][3][5]. 60% of patients have diverticulosis by age 60, of whom ~17% will bleed [3].
Pathophysiology:
- As diverticula form, the vasa recta (small arteries that normally penetrate the bowel wall to supply the mucosa) become draped over the dome of the diverticulum [2][4].
- These arteries are separated from the bowel lumen by only a thin layer of mucosa (no muscularis propria protection).
- Over time, the arterial wall weakens (asymmetric thinning of the media and intimal thickening from chronic mechanical injury).
- Rupture of the vasa recta into the diverticulum → arterial bleeding → painless, often profuse haematochezia [2][3][4].
- Diverticular bleeding typically occurs in the ABSENCE of diverticulitis — the two conditions rarely coexist [2][4][5]. This is a common exam pitfall.
Key Features:
- Painless haematochezia of variable severity — can be massive [2][3]
- Stops spontaneously in 80–85% but 14–38% rebleeding rate [3]
- Right-sided bleeding more common (even though in Western populations diverticula are mostly left-sided — the right colon wall is thinner) [2][3]
- In Asia: right-sided diverticula are more common anyway, making right-sided diverticular bleeding even more relevant in Hong Kong [4][8]
Risk Factors: Advanced age, obesity, hypertension, hyperlipidaemia, IHD, chronic renal insufficiency, NSAIDs, aspirin [2][4].
Pathophysiology:
- Acquired degenerative condition: repeated peristaltic contraction → intermittent obstruction of submucosal veins as they pass through the muscularis propria → chronic venous congestion → loss of pre-capillary sphincter competence → formation of small arteriovenous malformations (AVMs) [4][8].
- The walls are composed of thin endothelial cells lacking smooth muscle → fragile and prone to bleeding [2].
- Most common site: caecum and ascending colon (right-sided) [2][3][4].
- Bleeding is venous in origin → tends to be less massive than diverticular bleeding but more intermittent and recurrent [2][3].
Associations:
- Heyde syndrome: association with aortic stenosis — the shear stress through a stenotic valve causes acquired von Willebrand factor (vWF) type 2A deficiency (large vWF multimers are cleaved by ADAMTS13 under high shear) → bleeding tendency from angiodysplastic lesions [3][4][8].
- Osler-Weber-Rendu disease (Hereditary Haemorrhagic Telangiectasia / HHT): autosomal dominant condition with widespread vascular malformations [3][4].
- ESRD (end-stage renal disease) — platelet dysfunction from uraemia [4][8].
Key Features:
- Painless haematochezia, variable severity, mostly self-limiting (85–90%) but rebleeds in 25–85% [3]
- May present as occult GI bleeding with iron deficiency anaemia and FOBT-positive stools [2]
- Colonoscopy: "cherry red spots" [8]
- Angiography: "mother-in-law phenomenon" (early filling, delayed emptying of contrast — it comes early and stays late!) [8]
Most common cause of PR bleeding in age < 50 [2][4]. Very common — 4.4% prevalence in general population [3].
Pathophysiology:
- Degeneration of supporting fibroelastic tissues and smooth muscles with age and chronic straining → anal cushions displaced caudally → dilatation and engorgement of the arteriovenous plexuses → prolapse [7][8].
- This is NOT primarily a "varicose vein" phenomenon — it is a sliding anal cushion problem with loss of tissue support.
- May acutely thrombose: the plexus thromboses within the cushion → painful, large, swollen, irreducible mass with marked sphincter spasm [7][8].
Risk Factors: Aging, prolonged sitting on toilet, increased intra-abdominal pressure (constipation, chronic cough, ascites, pregnancy), genetic predisposition, low-fibre diet, obesity [2][4][7].
Classification of Internal Haemorrhoids [4]:
| Grade | Description |
|---|---|
| 1st degree | Bleeding only, no prolapse |
| 2nd degree | Prolapse on defecation, reduces spontaneously |
| 3rd degree | Prolapse, requires manual reduction |
| 4th degree | Permanently prolapsed, cannot be reduced |
Key Features:
- Internal haemorrhoids: painless bright-red outlet-type bleeding (blood coating stool, dripping into toilet bowl, or on toilet paper after defecation) — painless because above the dentate line (autonomic innervation) [3][4][7].
- External haemorrhoids: pain after defecation → severe perianal pain if thrombosed (somatic innervation below dentate line) [7].
- May have: prolapse, anal itching (mucus secretion irritating perianal skin), mucous discharge [3][4][7].
Critical Clinical Point
Definition: A tear in the anoderm distal to the dentate line [4].
Pathophysiology:
- Passage of hard stool or other local trauma → stretching of anal mucosa beyond its capacity → tear in the anoderm [4].
- The tear exposes the internal anal sphincter beneath → reflex spasm of the internal sphincter → this pulls the edges of the fissure apart and impairs healing [4].
- Additionally, the posterior midline of the anal canal has the poorest blood supply (the inferior rectal artery branches supply this area last) → ischaemia further impairs healing [4].
- This creates a vicious cycle: fissure → spasm → ischaemia → impaired healing → chronic fissure [4].
90% occur in the posterior midline — because that's where the blood supply is worst. If you see a fissure that is lateral, off-midline, multiple, or painless, think of secondary causes: Crohn's disease, TB, syphilis, HIV, anal cancer [4].
Key Features:
- Tearing pain with passage of bowel movements — the hallmark. Patients describe it as "passing broken glass." The pain may persist for hours after defecation (due to sustained sphincter spasm) [4].
- Bright rectal bleeding — limited to a small amount on toilet paper or surface of stool [4].
- Perianal pruritus or skin irritation [4].
- Acute fissures typically heal within 6 weeks; chronic fissures develop a sentinel skin tag (externally) and hypertrophied anal papilla (internally) — the classic triad of chronic anal fissure [4].
~10% of PR bleeding in patients > 50 years [3]. In Hong Kong, CRC is the most common cancer by incidence [5].
Pathophysiology:
- Bleeding occurs due to overlying erosion or ulceration of the tumour surface [2][3].
- The tumour outgrows its blood supply → surface necrosis → chronic, low-grade oozing → often presents as iron deficiency anaemia or FOBT-positive rather than overt haematochezia [3].
- Right-sided tumours (caecum, ascending colon): more likely to present with occult bleeding and anaemia (blood is degraded during transit → may not be visibly red).
- Left-sided tumours (descending, sigmoid): more likely to present with visible PR bleeding, change in bowel habit, and obstructive symptoms (the lumen is narrower on the left).
- Rectal tumours: tenesmus (sensation of incomplete evacuation due to the mass occupying the rectal vault), PR bleeding mixed with mucus, and 80% are within fingertip range on digital rectal examination [1].
Key Features (the "red flag" constellation) [1][3][5]:
- Change in bowel habits: alternating diarrhoea and constipation
- Change in stool calibre (pencil-thin stools) — from luminal narrowing
- Tenesmus — mass in rectum mimics sensation of residual stool
- Constitutional symptoms: weight loss, loss of appetite, malaise
- Passage of mucus — especially with villous adenomas (can cause secretory diarrhoea and even hypokalaemia)
- Metastatic symptoms: jaundice (liver), bone pain, SOB (lungs), ascites (peritoneal)
Risk Factors [5]:
- Age > 50, male, family history, personal history of polyps or CRC
- IBD (UC > CD) — risk increases after 8–10 years of pancolitis
- Polyposis syndromes: FAP, HNPCC (Lynch syndrome)
- Diet: red/processed meat, high fat, low fibre
- Lifestyle: obesity, DM, smoking, alcohol, physical inactivity
- Drugs: NSAIDs and aspirin are protective; androgen deprivation therapy increases risk
Ulcerative Colitis (UC):
- Bloody diarrhoea (mucoid loose stools) is the hallmark — because the inflammation is mucosal and continuous, starting from the rectum and extending proximally → friable, bleeding mucosa [4][9].
- Bleeding more commonly associated with UC than Crohn's disease [3].
- Extra-intestinal manifestations: arthritis, episcleritis/uveitis, erythema nodosum, pyoderma gangrenosum, primary sclerosing cholangitis [3].
- Protective factors for UC: prior appendicectomy, smoking (paradoxically) [9].
Crohn's Disease (CD):
- Transmural, skip-lesion pattern → deep ulcers, fistulae, abscesses.
- PR bleeding can occur but is less prominent than in UC.
- Right ileal/ileocaecal disease is most common → may present with RLQ pain and occult bleeding.
Most common form (> 50%) of ischaemic GI injury [6]. 90% occur in patients > 60 years [6].
Pathophysiology:
- Non-occlusive (95%): transient systemic low-flow states (hypotension, cardiac failure, post-cardiac surgery, vasopressors) → preferentially affects watershed areas [6].
- Occlusive (5%): arterial embolism (AF, valvular disease) or thrombosis (atherosclerosis) or rarely venous thrombosis [4][6].
- The colon receives less blood flow than the rest of the GIT and is therefore most vulnerable to ischaemia [6].
- Damage is largely mediated by reperfusion injury (transmural necrosis only in 15% when ischaemia is prolonged) [6].
Key Features:
- Sudden onset cramping abdominal pain (milder and more lateral than mesenteric ischaemia) [6]
- Mild-to-moderate rectal bleeding develops ≤ 24 hours after onset of abdominal pain — fresh or dark, more common with left colonic ischaemia [6]
- Urgency to defecate [6]
- Clinical triad: abdominal pain + bloody diarrhoea + cardiovascular risk factors [6]
- Labs: ↑↑WCC, metabolic acidosis, ↑lactate, ↑LDH, ↑CPK [6]
Risk Factors [6]: AF, heart failure, atherosclerosis, recent MI, aortic surgery, vasopressors, cocaine, hypercoagulable states, dialysis.
Infectious causes include Campylobacter, Salmonella [1], C. difficile (especially post-antibiotic), CMV (in immunosuppressed), amoebic dysentery, and TB [2][3].
Key Features:
- Fever, diarrhoea (bloody or watery), abdominal pain, nausea/vomiting
- Travel history, food history, contact history, immunosuppression status are key
- C. difficile: recent antibiotic use → toxin-mediated mucosal injury → pseudomembranous colitis
- CMV colitis: in immunosuppressed (HIV, transplant) → deep colonic ulcers, can cause massive bleeding
Pathophysiology:
- Radiation therapy for pelvic malignancies (cervical, prostate, bladder) → epithelial atrophy and fibrosis with obliterative endarteritis → chronic mucosal ischaemia → fragile telangiectatic vessels that bleed [3][4].
- Acute: < 6 weeks after therapy; Chronic/delayed: > 9 months but can be > 10 years [3].
Key Features: Diarrhoea, rectal urgency/tenesmus, PR bleeding [3].
Anal Fistula:
- Cryptoglandular hypothesis (90%): obstruction of anal gland ducts → infection → abscess → discharge along path of least resistance → fistula tract [7].
- Presents with intermittent perianal discharge + pain; palpable cord-like tract [7].
Rectal Prolapse:
- Protrusion of rectal wall through the anus (complete = full thickness; partial = mucosa only) [4].
- Bleeding from mucosal trauma and congestion.
- Affects mainly elderly women; associated with chronic straining, multiparity, pelvic floor dysfunction [4].
Solitary Rectal Ulcer:
- Associated with straining and rectal prolapse (internal intussusception).
- A rarity but a known pitfall [1].
Anal Carcinoma:
A rarity [1] but important in young patients with unexplained LGIB.
- Rule of 2s: 2% of population, 2 feet from ileocaecal valve, 2 inches long, 2 types of ectopic tissue (gastric and pancreatic), symptomatic before age 2.
- Contains ectopic gastric mucosa → acid secretion → ulceration of adjacent ileal mucosa → painless massive PR bleeding (often dark/maroon as it originates from the small bowel).
- True diverticulum (all layers of bowel wall) unlike colonic diverticula.
- Diagnosis: Technetium-99m pertechnetate scan (Meckel's scan) — the radiotracer is taken up by ectopic gastric mucosa.
6. Classification of Rectal Bleeding
Rectal bleeding can be classified in several clinically useful ways:
| Category | Definition | Common Causes |
|---|---|---|
| Acute overt | Visible blood, recent onset ± haemodynamic compromise | Diverticular disease, angiodysplasia, massive UGIB |
| Chronic overt | Visible blood over days to weeks | Haemorrhoids, CRC, IBD, fissure |
| Occult | FOBT-positive or iron deficiency anaemia without visible blood | CRC, angiodysplasia, small bowel lesions |
| Character | Likely Source | Pathophysiological Basis |
|---|---|---|
| Bright red blood on toilet paper / coating stool | Anorectal (haemorrhoids, fissure) | Outlet-type: blood is fresh because it originates distal to the rectum and has no time for degradation |
| Bright red blood mixed with stool | Left colon (sigmoid, descending) | Short transit time from left colon → minimal degradation |
| Dark or maroon blood mixed with stool | Right colon | Longer transit time → partial degradation of haemoglobin |
| Blood by itself (torrential) | Diverticular disease, angiodysplasia, rectal varices | Brisk arterial/venous bleeding overwhelming normal stool formation |
| Melaena (black, tarry) | Upper GI (above ligament of Treitz) | Haemoglobin degraded by gastric acid and intestinal bacteria → haematin (black) |
| Blood + mucus | Rectal tumour, IBD (proctitis), villous adenoma | Mucus secretion from inflamed or neoplastic mucosa |
| Cyclic PR bleeding | GI endometriosis | Ectopic endometrial tissue bleeds with menstrual cycle |
| Severity | Features |
|---|---|
| Minor | Small volume, no haemodynamic compromise, likely anorectal source |
| Major | > 150 mL blood loss, haemodynamic instability, requires resuscitation |
| Massive | Ongoing transfusion requirement, haemodynamic instability despite resuscitation |
7. Clinical Features
7.1 Symptoms — with Pathophysiological Basis
| Symptom | Pathophysiological Basis |
|---|---|
| Bright red blood on toilet paper or dripping after defecation | Outlet-type bleeding from haemorrhoids or fissures — blood is deposited on the surface of stool or drips after passage because the source is at or very near the anal verge [3][7] |
| Blood coating the surface of stool | Source in the anus or rectum — stool is formed before it reaches the bleeding point, so blood is applied externally [3] |
| Blood mixed with faeces | Source above the sigmoid colon — blood has time to mix with stool during transit [3][8] |
| Dark/maroon coloured blood | Right-sided colonic source — longer transit allows bacterial degradation of haemoglobin → darker colour [2][3] |
| Profuse, painless haematochezia (blood by itself) | Torrential bleeding from diverticular disease or angiodysplasia — rate of bleeding overwhelms stool, blood passes on its own [3] |
| Bloody diarrhoea (blood + mucus + frequent loose stools) | Colitis (IBD, infective, ischaemic) — mucosal inflammation → increased secretion, impaired absorption, and mucosal friability causing bleeding [3] |
| Passage of mucus with blood | Suggests rectal tumour or proctitis [1] — villous adenomas secrete large volumes of mucus; rectal cancers may have overlying mucus from goblet cell activity |
| Melaena | Upper GI source (or rarely right colon) — haemoglobin converted to acid haematin by gastric acid (black) + bacterial degradation → tarry, foul-smelling stool |
| Symptom | Pathophysiological Basis | Suggests |
|---|---|---|
| Pain on defecation (tearing/sharp) | Fissure → tear in somatic-innervated anoderm below dentate line → sharp pain; internal sphincter spasm sustains it [4] | Anal fissure |
| Painless bleeding | Internal haemorrhoids (autonomic innervation above dentate line) or diverticular bleeding (no peritoneal inflammation) [2][4] | Haemorrhoids, diverticular disease, angiodysplasia |
| Severe perianal pain (unrelated to defecation) | Thrombosed external haemorrhoid → acute distension of somatic-innervated tissue, or perianal abscess → infection in perianal space [7] | Thrombosed haemorrhoid, perianal abscess |
| Cramping abdominal pain → then PR bleeding within 24h | Ischaemic colitis — mucosal ischaemia → pain, then reperfusion → mucosal sloughing and bleeding [6] | Ischaemic colitis |
| Alternating diarrhoea and constipation | Partial colonic obstruction by tumour → stool backs up (constipation) → bacterial liquefaction → overflow diarrhoea [5] | CRC |
| Tenesmus | Rectal mass stimulates stretch receptors → constant sensation of needing to defecate despite empty rectum [5][8] | Rectal cancer, proctitis |
| Pencil-thin stools | Tumour narrowing the rectal/sigmoid lumen → stool is compressed as it passes [5] | CRC |
| Weight loss, anorexia, malaise | Tumour metabolic demand + chronic bleeding → cancer cachexia and iron deficiency [5] | CRC, lymphoma |
| Urgency to defecate | Rectal inflammation (proctitis, UC, radiation) → reduced rectal compliance → smaller volumes trigger the urge to defecate [3][6] | IBD, radiation proctitis, ischaemic colitis |
| Fever, rigors, night sweats | Systemic inflammatory response to infection [3] | Infective colitis |
| Jaundice, bone pain, dyspnoea | Metastatic spread: liver → jaundice, bone → pain, lung → dyspnoea [3][5] | Advanced CRC |
| Dizziness, syncope, palpitations, SOB on exertion | Anaemic symptoms — chronic blood loss → iron deficiency → reduced oxygen-carrying capacity → compensatory tachycardia [3] | Any chronic bleeding source |
| Cause | Classic Symptom Pattern |
|---|---|
| Haemorrhoids | Painless bright red outlet-type bleeding, prolapsing mass, pruritus |
| Anal fissure | Tearing pain on defecation, small amount of bright blood on paper, constipation history |
| Diverticular bleeding | Painless, usually profuse haematochezia (not chronic), few abdominal symptoms |
| Angiodysplasia | Painless, less severe than diverticular, intermittent, elderly |
| CRC | Change in bowel habit, constitutional symptoms, low-grade intermittent bleeding, iron deficiency |
| UC | Bloody diarrhoea with mucus, urgency, tenesmus, extra-intestinal manifestations |
| Ischaemic colitis | Sudden crampy abdominal pain → PR bleeding within 24h, CVS risk factors |
| Infective colitis | Fever, diarrhoea ± blood, TOCC, recent antibiotics (C. diff) |
| Radiation proctitis | History of pelvic radiotherapy, tenesmus, PR bleeding (may be delayed years) |
7.2 Signs — with Pathophysiological Basis
| Sign | Pathophysiological Basis | Significance |
|---|---|---|
| Pallor (conjunctival, palmar) | Chronic blood loss → iron deficiency anaemia → reduced haemoglobin → pallor [1][3] | Suggests chronic/occult bleeding |
| Tachycardia, hypotension | Acute volume depletion → baroreceptor-mediated sympathetic activation → ↑HR; insufficient preload → ↓BP | Haemodynamic compromise — acute significant bleed |
| Postural hypotension | ≥ 20 mmHg systolic drop on standing → indicates ≥ 15% blood volume loss | Early sign of hypovolaemia |
| Koilonychia (spoon nails) | Chronic iron deficiency → impaired nail bed keratinisation | Chronic occult blood loss (CRC, angiodysplasia) |
| Angular cheilitis, glossitis | Iron deficiency → impaired epithelial cell turnover | Chronic bleeding |
| Cachexia, temporal wasting | Malignancy → increased catabolic cytokines (TNF-α, IL-6) → muscle wasting | Advanced CRC |
| Lymphadenopathy (left supraclavicular = Virchow's node, or inguinal) | Lymphatic spread of tumour: Virchow's node ← thoracic duct ← abdominal malignancy; inguinal ← anal cancer below dentate line | Metastatic CRC or anal cancer [7] |
| Jaundice, hepatomegaly | Liver metastases from CRC → biliary obstruction or replacement of hepatocytes | Metastatic CRC |
| Spider naevi, caput medusae, gynaecomastia | Signs of chronic liver disease → portal hypertension → rectal varices | Portal hypertensive bleeding |
| Skin lesions | Erythema nodosum, pyoderma gangrenosum (IBD); hereditary haemorrhagic telangiectasia on lips/fingertips (Osler-Weber-Rendu) | IBD, HHT |
| Sign | Pathophysiological Basis | Significance |
|---|---|---|
| Palpable abdominal mass | Tumour large enough to be palpable through the abdominal wall; right-sided colon tumours often grow larger before causing symptoms (wider lumen) | CRC (especially caecal/ascending) |
| Tenderness over the left iliac fossa | Inflammation of sigmoid diverticula → localised peritoneal irritation | Diverticulitis (though diverticular bleeding is usually painless) |
| Tenderness over the splenic flexure or left colon | Ischaemia of watershed area → mucosal/transmural inflammation | Ischaemic colitis |
| Distension | Bowel obstruction from tumour or stricture | CRC, diverticular stricture |
| Ascites | Peritoneal carcinomatosis (CRC) or portal hypertension (liver disease) | Advanced CRC, chronic liver disease |
| Hepatomegaly (hard, nodular, non-tender) | Liver metastases | Metastatic CRC |
| Splenomegaly | Portal hypertension → splenic congestion | Cirrhosis with portal hypertension |
This is the single most important examination in the assessment of rectal bleeding. 80% of rectal tumours are within fingertip range [1].
Inspection:
- Perianal skin: excoriation (pruritus, mucus from haemorrhoids/fistula), skin tags (chronic fissure, Crohn's), condylomata (HPV), scars (prior surgery), sinuses (fistula, pilonidal)
- Anal fissure: usually seen at the posterior midline (6 o'clock in lithotomy position); sentinel skin tag externally [4]
- Prolapsed haemorrhoids: engorged, purple/blue swellings at 3, 7, 11 o'clock
- Thrombosed external haemorrhoid: tense, blue, extremely tender perianal lump [7]
- Rectal prolapse: circumferential concentric mucosal folds (cf. haemorrhoidal prolapse = radial folds) [4]
- Fistula external opening: may discharge pus; palpable cord-like tract towards anal canal [7]
Palpation (DRE):
- Pain: anal fissure (may be too painful to examine — do NOT force), perianal abscess, thrombosed haemorrhoid
- Induration: fibrosis, chronic fissure, tumour
- Mass: rectal cancer — hard, irregular, may be fixed. Assess distance from anal verge, size, mobility, circumferential extent [4][7]
- Anal tone (resting = internal anal sphincter; squeeze = external anal sphincter): reduced tone in rectal prolapse, neurological conditions [4][7]
- Blood on gloved finger: confirms PR bleeding; colour gives clue to source
- Prostate (in males) / rectovaginal septum (in females) — assess for extraluminal masses [7]
Proctoscopy:
- Essential for visualising internal haemorrhoids — 1st/2nd degree haemorrhoids may not be palpable on DRE [7]
- Allows direct visualisation of the distal anal canal and lower rectum
Murtagh's Key History [1]:
Nature of the bleed: fresh versus altered blood, mixed with faeces and/or mucus, in toilet bowl or on underwear. Quantity of bleeding: slight, moderate or torrential. Associated symptoms (e.g. weight loss, constipation, diarrhoea, pain, weakness, presence of lumps, urgency, unsatisfied defecation, recent change of bowel habit).
A systematic approach from the senior notes [3][8]:
-
The bleeding itself:
- Presentation: acute vs chronic, occult vs overt
- Colour: bright red, dark/maroon, melaenic
- Relationship to stool: mixed with (proximal), on surface (distal), on paper only (anorectal), by itself (torrential)
- Timing: with defecation (outlet), independent of defecation (colonic)
- Quantity: spot on paper vs bowl full of blood
- Previous episodes
-
Bowel habit:
-
Anorectal symptoms:
- Pain, pruritus, prolapsing mass → anorectal pathology
-
Upper GI symptoms:
- Haematemesis, coffee ground vomitus, melaena → upper GI bleed
-
Red flag / malignancy symptoms:
- Age > 50, constitutional symptoms, family history, prior polyps/IBD
- Metastatic symptoms: jaundice, bone pain, SOB, ascites
-
Complications:
- Shock: extreme thirst, confusion, pallor, oliguria
- Symptomatic anaemia: SOB on exertion, postural dizziness, syncope, chest pain, palpitation [3]
-
Important history:
- Comorbidities: cardiopulmonary disease, HF/RF, liver disease, bleeding disorders
- Drug history: NSAIDs (small bowel ulcers, diverticular bleeding), antiplatelets, anticoagulants [3]
- Travel/food/contact history (infective causes)
- History of abdominal irradiation (radiation proctocolitis) [3]
- Surgical history (prior polypectomy → post-polypectomy bleeding)
General inspection (evidence of anaemia) and vital signs
Abnormal examination, anal inspection, digital rectal examination, proctosigmoidoscopy
FBE and ESR
Stool M&C
Faecal occult blood
Colonoscopy
Consider abdominal X-ray, CT colonography, angiography, small bowel enema (depending on clinical findings)
1. Black, tarry (melaena) stool indicates bleeding from upper GIT: rare distal to lower ileum.
2. Frequent passage of blood and mucus indicates a rectal tumour or proctitis.
3. If substantial haemorrhage, consider diverticular disease, angiodysplasia or more proximal lesions (e.g. Meckel diverticulum, duodenal ulcers).
4. New bleeding age > 55 years demands colonic investigation.
5. 80% of rectal tumours are within fingertip range.
6. In young adults, diagnosis is likely to be haemorrhoids or a fissure.
High Yield Summary
Definition: Rectal bleeding = passage of blood per rectum. LGIB = bleeding distal to the ligament of Treitz. 10–15% of haematochezia may be from an upper GI source.
Most Common Causes by Age:
- < 50 years: Haemorrhoids, anal fissure
-
65 years: Diverticular disease (most common overall cause of LGIB), angiodysplasia
Murtagh's Framework:
- Probability: Haemorrhoids, fissure, polyp, diverticular disease
- Serious: Ischaemic colitis, angiodysplasia, CRC, IBD, intussusception
- Pitfalls: Rectal prolapse, anal trauma, villous adenoma
- Rarities: Meckel's diverticulum, solitary rectal ulcer
Character of Blood:
- On surface/paper = anorectal
- Mixed with stool = above sigmoid
- By itself (torrential) = diverticular disease, angiodysplasia
- Blood + mucus = rectal tumour or proctitis
- Melaena = upper GI
Key Anatomy:
- Dentate line: above = painless (autonomic), below = painful (somatic)
- Haemorrhoid positions: 3, 7, 11 o'clock
- Watershed areas: Griffiths' point (splenic flexure), Sudeck's point (rectosigmoid)
- Asian diverticula are predominantly right-sided
Red Flags for CRC: Age > 50, change in bowel habit, pencil-thin stools, tenesmus, constitutional symptoms, family history, iron deficiency anaemia.
DRE is mandatory — 80% of rectal tumours are within fingertip range. Always exclude other causes even when haemorrhoids are found.
Active Recall — Rectal Bleeding (Definition to Clinical Features)
[1] Lecture slides: murtagh merge.pdf (p78–79, "Rectal bleeding") [2] Senior notes: felixlai.md (Lower GI bleeding, sections 510–511) [3] Senior notes: Ryan Ho Fundamentals.pdf (p281–283, "Lower GI Bleeding") [4] Senior notes: felixlai.md (Anal canal anatomy, haemorrhoids, anal fissures, rectal prolapse, sections 1092–1116) [5] Senior notes: Ryan Ho GI.pdf (p163, "Colorectal Cancer"; p106–109, "Lower GI Bleeding"; p160, "Diverticular Bleeding") [6] Senior notes: Ryan Ho GI.pdf (p146, "Ischaemic Colitis"); felixlai.md (Ischaemic colitis, section 1053) [7] Senior notes: maxim.md (Haemorrhoids, Anal fistula, Anal carcinoma, sections 228–239) [8] Senior notes: maxim.md (Diverticular disease, Angiodysplasia, LGIB approach, sections 158–197) [9] Senior notes: felixlai.md (Ulcerative colitis, section 974)
Differential Diagnosis of Rectal Bleeding
The differential diagnosis of rectal bleeding is one of the most commonly examined topics in clinical medicine. The key challenge is that the symptom — blood per rectum — is shared by conditions ranging from the trivially benign (a small haemorrhoidal bleed) to the immediately life-threatening (massive diverticular haemorrhage) to the insidiously fatal (colorectal carcinoma). Your job is to risk-stratify and pattern-recognise using the character of bleeding, associated symptoms, patient demographics, and examination findings.
This is the framework you should have at your fingertips. It forces you to think beyond the "probable" and actively consider what you must not miss.
| Category | Conditions |
|---|---|
| Probability diagnosis | Haemorrhoids / perianal haematoma, anal fissure, colorectal polyp, diverticulitis (note: diverticular bleeding is the more relevant entity for PR bleed), excoriated skin (anal pruritus) [1] |
| Serious disorders not to be missed | Vascular: ischaemic colitis, angiodysplasia (vascular ectasia), anticoagulant therapy · Infection: enteritis (e.g. Campylobacter, Salmonella) · Cancer/Tumours: colorectal, caecum, lymphoma, villous adenoma · Other: inflammatory bowel disease (colitis/proctitis), intussusception [1] |
| Pitfalls (often missed) | Rectal prolapse, anal trauma (accidental / non-accidental), villous adenoma [1] |
| Rarities | Meckel diverticulum, solitary ulcer of rectum [1] |
Why Murtagh's Framework Matters
This four-tier system ensures you don't anchor on a benign diagnosis. Haemorrhoids are extremely common and will be present coincidentally in many patients — but calling everything "haemorrhoids" is how colorectal cancers get missed. The framework forces you to actively exclude the serious conditions before settling on the probable.
Thinking anatomically helps you localise the bleed and choose the right investigation. LGIB is defined as bleeding distal to the ligament of Treitz [2][3], but remember that 10–15% of haematochezia originates from an upper GI source — never forget to consider this, especially in massive bleeds [3][5].
| Anatomical Source | Cause | Approximate % of LGIB | Key Pathophysiology |
|---|---|---|---|
| Massive Upper GI | Peptic ulcer, variceal bleed [3] | < 10% | Brisk bleeding overwhelms GI transit → blood not degraded → presents as haematochezia rather than melaena |
| Large Bowel | Diverticular disease (17–40%) | — | Rupture of vasa recta draped over diverticulum dome (arterial bleeding) [2][3][5] |
| Angiodysplasia (2–30%) | — | Degenerative submucosal AVMs; venous bleeding, less massive but recurrent [2][3] | |
| Colitis (9–11%): infective (C. difficile, CMV, amoebic, TB), inflammatory (UC, CD), ischaemic, radiation [3] | — | Mucosal inflammation/ischaemia → friable mucosa → bleeding | |
| Neoplasm (7–33%): carcinoma, large polyps, post-polypectomy [3] | — | Overlying erosion/ulceration of tumour surface [3][5] | |
| Small Bowel (~5%) | Meckel's diverticulum, jejunoileal diverticula, angiodysplasia, small bowel tumours, NSAID-induced ulcers, Crohn's/TB enteritis, aortoenteric fistula [3] | ~5% | Meckel's: ectopic gastric mucosa → acid secretion → ileal ulceration; aortoenteric fistula: graft erosion into duodenum (herald bleed → massive exsanguination) |
| Anorectal (~10%) | Haemorrhoids, fissure-in-ano, anal/rectal ulcers, rectal varices [3] | ~10% | Haemorrhoids: engorgement of anal cushion AV plexus; fissure: mucosal tear below dentate line; rectal varices: portosystemic collateral dilatation |
The exam often asks you to differentiate between causes. Here is a systematic comparison table that maps each differential to its characteristic bleeding pattern, associated features, and key distinguishing points.
3.1 Causes Differentiated by History
| Aetiology | Bleeding Pattern | Key Distinguishing Features |
|---|---|---|
| UGI bleed | Melaena, haematemesis, coffee ground vomitus. Should be considered especially in severe haematochezia (10–15% from UGI) [3][5] | History of peptic ulcer disease, NSAID use, liver disease. Haemodynamic instability disproportionate to volume of PR blood |
| Diverticular disease | Painless, usually profuse haematochezia (not chronic) [3][5] | Acute onset, self-limiting (80–85%), few abdominal symptoms. Diverticulitis and diverticular bleeding rarely coexist [2][5]. In Asia: right-sided predominance [2] |
| Angiodysplasia | Painless, less severe than diverticular but tends to be intermittent [3][5] | Usually in elderly, may be associated with vascular malformations (e.g. HHT) and aortic stenosis [3][5]. Recurrent episodes. May present as occult bleeding with iron deficiency anaemia |
| Colorectal carcinoma | Low-grade, intermittent bleeding; often FOBT+ or IDA [3][5] | > 50y, male, smoker, FHx, Hx of IBD, polyps and colorectal CA. Alternating diarrhoea and constipation, pencil-thin stools, tenesmus. Loss of appetite, loss of weight, malaise. Intractable pain, jaundice/RUQ discomfort, dyspnoea, bone pain [3][5][8] |
| Colitis — Inflammatory (IBD) | Usually bloody diarrhoea. Extra-intestinal manifestations: arthritis, episcleritis/uveitis, erythema nodosum [3][5] | UC: continuous mucosal inflammation from rectum → bloody mucoid diarrhoea, urgency, tenesmus. CD: skip lesions, perianal disease, fistulae. Bleeding more commonly associated with UC than Crohn's [3] |
| Colitis — Ischaemic | Mild-to-moderate PR bleeding within 24h of abdominal pain onset [3][5][6] | CVS risk factors, acute MI, stroke [3][5]. Sudden cramping abdominal pain → bloody diarrhoea. Watershed area distribution |
| Colitis — Infective | Bloody diarrhoea with systemic symptoms [3][5] | Fever, chills, rigors, night sweats, nausea/vomiting, diarrhoea, pain. TOCC, immunosuppression (CMV colitis). Previous TB exposure/infection, BCG vaccination status [3][5] |
| Radiation proctocolitis | Chronic PR bleeding, may be delayed years | Hx of abdominal irradiation [3][5]. Diarrhoea, rectal urgency/tenesmus. Obliterative endarteritis → chronic mucosal ischaemia [3] |
| Haemorrhoids | Blood coating stools or bleeding following defecation [5] | May note perianal prolapsing mass, pruritus (mucus secretion) ± pain (if thrombosed) [5]. Outlet-type: fresh red blood on paper/surface of stool. Risk factors: constipation, pregnancy [8] |
| Anal fissure | Small amount of bright blood on paper/surface of stool [4][5] | Hx of constipation. Severe sharp pain upon defecation [5]. Posterior midline tear. If off-midline or atypical → think Crohn's, TB, HIV, cancer [4] |
| Rectal prolapse | Blood with mucus discharge | Prolapsing mass, faecal incontinence, incomplete evacuation. Often missed (a Murtagh pitfall) [1]. Mainly elderly women [4] |
The Bleeding Pattern is Your Best Differentiator
- Outlet-type (on paper, after defecation): haemorrhoids, fissure
- Mixed with stool: proximal colonic source (CRC, IBD, right-sided diverticular)
- Blood by itself (torrential): diverticular disease, angiodysplasia, rectal varices
- Blood + mucus: rectal tumour, proctitis, villous adenoma [1][8]
- Frequent passage of blood and mucus indicates a rectal tumour or proctitis [1]
One of the highest-yield clinical shortcuts is to consider the most likely diagnosis by age group:
| Age Group | Most Likely Cause | Why |
|---|---|---|
| Children | Intussusception [1], Meckel's diverticulum, polyps, infectious colitis | Intussusception: ileocolic telescoping → "redcurrant jelly" stool. Meckel's: ectopic gastric mucosa → ileal ulceration |
| Young adults | Haemorrhoids or a fissure [1] | Low-fibre diet, constipation, straining. IBD also peaks in this age group (20–40y) |
| Adults 40–55 | Haemorrhoids, IBD, polyps, early CRC | Need to start considering malignancy, especially with red flags |
| Adults > 55 | New bleeding demands colonic investigation [1] | CRC incidence rises steeply. Diverticular disease, angiodysplasia also become prevalent |
| Elderly (> 65) | Diverticular disease, angiodysplasia, CRC, ischaemic colitis | Degenerative vascular changes, high prevalence of diverticulosis, cardiovascular comorbidities predisposing to ischaemic colitis |
Understanding the mechanism of bleeding is essential for exam answers and for choosing the right treatment.
| Cause | Mechanism of Bleeding | Type | Severity |
|---|---|---|---|
| Diverticular disease | Vasa recta rupture (arterial) into diverticulum | Arterial | Can be severe/massive [3] |
| Angiodysplasia | Thin-walled submucosal AVM rupture (venous) | Venous | Usually moderate, but recurrent [2][3] |
| CRC | Surface erosion/ulceration of tumour | Capillary ooze | Low-grade, chronic, intermittent [3] |
| IBD (UC) | Diffuse mucosal inflammation → friability | Mucosal | Variable — usually moderate, rarely life-threatening [3] |
| Ischaemic colitis | Mucosal ischaemia → sloughing → reperfusion injury | Mixed | Usually mild-to-moderate [6] |
| Haemorrhoids | Engorgement of arteriovenous cushion plexus | Arterial (from superior rectal artery branches) | Usually mild; rarely massive |
| Anal fissure | Tear through anoderm exposing submucosal vessels | Capillary/small vessel | Minimal — drops on paper |
| Rectal varices | Portosystemic collateral dilatation (portal HTN) | Venous (portal) | Can be severe [3] |
| Meckel's diverticulum | Ectopic gastric mucosa → acid → adjacent ulceration | Arterial | Can be massive [3] |
6. Special Differentials Often Tested
This is a favourite exam question because all three present with "something coming out of the anus."
| Feature | Prolapsed Haemorrhoids | Complete Rectal Prolapse | Prolapsed Polyp |
|---|---|---|---|
| Mucosal folds | Radial (spoke-like grooves between cushions) | Concentric (circular rings — full thickness wall) | Smooth, pedunculated mass |
| Positions | 3, 7, 11 o'clock | Circumferential | Variable, usually single |
| Palpation | Soft, compressible | Full-thickness wall feel (like "doughnut") | Firm, polypoid |
| Associated features | Pruritus, mucus, outlet bleeding | Faecal incontinence (75%), mucus discharge | Often incidental; may bleed |
| Demographics | Any age; risk: straining, pregnancy | Elderly women [4] | Any age; ↑ with age |
Both are common causes of painless LGIB in the elderly and a frequent comparison in exams:
| Feature | Diverticular Bleeding | Angiodysplasia |
|---|---|---|
| Mechanism | Arterial (vasa recta rupture) | Venous (thin-walled AVM) |
| Severity | Can be massive/profuse | Less massive, more intermittent |
| Self-limiting | 80–85% [3] | 85–90% [3] |
| Rebleeding | 14–38% [3] | 25–85% [3] — higher recurrence |
| Site | Right > left (especially in Asia) | Right colon / caecum |
| Associations | Age, obesity, NSAIDs, aspirin | Aortic stenosis (Heyde syndrome), HHT, ESRD |
| Endoscopy | Active bleeding / visible vessel / clot in diverticulum | Cherry-red spots [8] |
| Angiography | Contrast extravasation | "Mother-in-law phenomenon" (early filling, delayed emptying) [8] |
Always consider an upper GI source, especially in severe haematochezia [1][3][5].
| Feature | Upper GI Bleed | Lower GI Bleed |
|---|---|---|
| Typical presentation | Haematemesis, coffee ground vomitus, melaena | Haematochezia (bright/dark red PR blood) |
| NG aspirate | Bloody or coffee-ground | Clear (may have bile if pylorus patent) |
| BUN:Creatinine ratio | > 30:1 (blood in upper GI is "digested" → urea absorbed) | Normal |
| Haemodynamic status | More commonly unstable for a given degree of haematochezia | Variable |
| Key pitfall | 10–15% of haematochezia is from UGI source — must do OGD if massive bleeding source unclear [3][5] |
Cirrhotic patients deserve special mention because bleeding may come from multiple concurrent sources [10][11]:
- Variceal bleeding (50–90%): oesophageal or gastric varices [11]
- Portal hypertensive gastropathy: friable "snake-skin" mucosa → diffuse oozing [10]
- Rectal varices: portosystemic shunt between superior and inferior rectal veins [3]
- Peptic ulcer disease: still common in cirrhotics
- Generalised bleeding tendency: pancytopenia (hypersplenism), ↓ coagulation factor production [10]
- Mallory-Weiss syndrome: especially in alcoholic cirrhosis [10][11]
Exam Pitfall — Bleeding in Cirrhotics
Do NOT assume all GI bleeding in a cirrhotic patient is variceal. Variceal bleeding is NOT the only cause of GI bleeding in a cirrhotic patient [11]. You must do an OGD to identify the actual source — it may be a peptic ulcer, portal hypertensive gastropathy, or even a Mallory-Weiss tear.
Sometimes the exam gives you a clinical vignette rather than asking you to list causes. Here is how to approach common presentations:
| Presentation | Top Differentials | Key Discriminators |
|---|---|---|
| Painless massive PR bleed in elderly | Diverticular disease, angiodysplasia | Diverticular = profuse single episode; angiodysplasia = less massive but more recurrent |
| Painful PR bleeding with defecation | Anal fissure | Tearing pain, posterior midline, small amount on paper |
| Painless outlet-type fresh blood + prolapsing mass | Haemorrhoids (internal) | 3, 7, 11 o'clock; reducible (grade 2–3) or irreducible (grade 4) |
| Bloody diarrhoea + abdominal pain + fever | Infective colitis, IBD flare | TOCC, antibiotics (C. diff), extra-intestinal features (IBD) |
| Bloody diarrhoea + sudden abdominal pain in elderly | Ischaemic colitis | CVS risk factors, watershed area tenderness, ↑WCC/lactate |
| Change in bowel habit + PR blood + weight loss | Colorectal carcinoma | Age > 50, family history, tenesmus, pencil-thin stools |
| PR bleeding + history of pelvic radiotherapy | Radiation proctocolitis | Can present acutely (< 6 weeks) or delayed (> 9 months, even > 10 years) [3] |
| PR bleeding + known liver disease | Rectal varices, variceal bleed, PHG, PUD | Look for stigmata of chronic liver disease; OGD essential |
| PR bleeding in a child | Intussusception, Meckel's diverticulum, polyp | Intussusception: colicky pain, "redcurrant jelly" stool, sausage-shaped mass; Meckel's: painless massive bleed |
The following Mermaid diagram illustrates a clinical reasoning pathway for rectal bleeding:
9. Don't-Miss Differentials — Expanded Reasoning
Why you must not miss it: CRC is the most common cancer by incidence in Hong Kong [5]. Early detection dramatically improves survival (5-year survival stage I ~90% vs stage IV ~10%). Every patient with PR bleeding, especially new bleeding age > 55 years, must have colonic investigation [1].
Discriminating features in history [3][5][8]:
- Constitutional symptoms: weight loss, anorexia, malaise
- Change in bowel habits: alternating diarrhoea and constipation
- Change in stool calibre — pencil-thin stools from luminal narrowing [8]
- Tenesmus — mass in rectum mimicking residual stool [8]
- IO symptoms (in advanced cases): abdominal distension, colicky pain, vomiting [8]
- Metastatic symptoms: jaundice (liver), bone pain, SOB (lungs), ascites (peritoneum) [5]
- Family history of CRC or polyposis syndromes [5][8]
- Previous colonoscopy/FOBT results, personal history of polyps or IBD [8]
Clinical pearl — "Right side bleeds, left side blocks" [8]:
- Right colon: wider lumen, liquid stool → tumour grows large before causing symptoms → presents with occult bleeding and iron deficiency anaemia rather than overt haematochezia
- Left colon: narrower lumen, solid stool → obstructive symptoms (alternating bowel habit, colicky pain) + visible PR bleeding
- Rectosigmoid: haematochezia is the earliest and most common symptom; tenesmus, bloody mucoid discharge, pencil-thin stools [8]
Listed under "serious disorders not to be missed" in Murtagh's [1]. In adults, intussusception is uncommon but when it occurs, a pathological lead point (polyp, lymphoma, Meckel's diverticulum) is often present [4]. In children, most cases are ileocolic and idiopathic (hypertrophied Peyer's patches acting as lead points after viral infection) [4].
Classic triad in children: colicky abdominal pain (episodic, with drawing-up of legs) + vomiting + "redcurrant jelly" stools (blood + mucus from mucosal venous congestion and ischaemia of the intussuscepted segment).
Listed both as a "serious disorder" and a "pitfall" in Murtagh's — often missed [1]. Large villous adenomas (particularly rectal) can secrete copious mucus → present with mucoid PR discharge, sometimes with enough fluid and electrolyte loss to cause hypokalaemia and dehydration (secretory villous adenoma). They also have the highest malignant potential among colorectal polyps.
Listed under "vascular" serious disorders [1]. Patients on warfarin, DOACs, or heparin are at increased risk of GI bleeding from any pre-existing lesion. The anticoagulant doesn't create the lesion — it unmasks it by preventing haemostasis at a site that would otherwise clot off. An important clinical pearl: PR bleeding in an anticoagulated patient still warrants investigation for the underlying lesion (especially CRC) — don't just blame the anticoagulant.
| Category | Cause | Key Feature | Mechanism |
|---|---|---|---|
| Anatomical | Diverticular disease | Painless profuse haematochezia | Vasa recta arterial rupture |
| Vascular | Angiodysplasia | Painless intermittent, elderly, right-sided | Degenerative submucosal AVM |
| Ischaemic colitis | Pain → bleeding < 24h, CVS RFs | Watershed mucosal ischaemia | |
| Rectal varices | Severe bleeding + liver disease | Portal HTN portosystemic shunt | |
| Neoplastic | CRC | Change bowel habit, constitutional Sx | Surface erosion/ulceration |
| Villous adenoma | Mucoid discharge ± hypokalaemia | Secretory mucus + dysplasia | |
| Lymphoma | Constitutional Sx, mass | Mucosal infiltration | |
| Inflammatory | UC | Bloody mucoid diarrhoea, extra-intestinal | Continuous mucosal inflammation |
| Crohn's disease | Perianal disease, skip lesions | Transmural inflammation | |
| Radiation proctitis | Hx pelvic RT, delayed onset | Obliterative endarteritis | |
| Infective | Campylobacter, Salmonella, C. diff, CMV, TB, amoeba | Fever, diarrhoea, TOCC | Mucosal invasion/toxin |
| Anorectal | Haemorrhoids | Painless outlet-type, prolapse | Cushion degeneration |
| Anal fissure | Tearing pain, posterior midline | Mucosal tear + sphincter spasm | |
| Rectal prolapse | Prolapsing mass, incontinence | Pelvic floor weakness | |
| Anal fistula | Intermittent discharge + pain | Cryptoglandular infection | |
| Anal carcinoma | Painful bleeding + mass, HPV | SCC below dentate line | |
| Small bowel | Meckel's diverticulum | Painless massive bleed in child/young adult | Ectopic gastric mucosa → ulcer |
| Aortoenteric fistula | "Herald bleed" then massive | Graft erosion | |
| Iatrogenic | Post-polypectomy | Bleeding after recent colonoscopy | Vessel disruption at polypectomy site |
| Anticoagulant therapy | Any pre-existing lesion unmasked | Impaired haemostasis |
High Yield Summary — Differential Diagnosis of Rectal Bleeding
Murtagh's framework: Probability (haemorrhoids, fissure, polyp, diverticular disease) → Serious (ischaemic colitis, angiodysplasia, anticoagulants, infections, CRC, lymphoma, villous adenoma, IBD, intussusception) → Pitfalls (rectal prolapse, anal trauma, villous adenoma) → Rarities (Meckel's, solitary rectal ulcer).
By age: Young → haemorrhoids/fissure. > 55 → must investigate colon. Elderly → diverticular disease, angiodysplasia, CRC, ischaemic colitis.
By bleeding pattern: Outlet-type → anorectal. Mixed with stool → proximal colon. Torrential by itself → diverticular/angiodysplasia. Blood + mucus → rectal tumour/proctitis. Melaena → upper GI.
Don't-miss rules: (1) 10–15% of haematochezia is from UGIB. (2) CRC must be excluded in patients > 55 with new bleeding. (3) 80% rectal tumours are within fingertip reach. (4) Haemorrhoids don't explain away bleeding — always exclude other sources. (5) In cirrhotics, not all bleeding is variceal — do OGD. (6) Right side bleeds, left side blocks (CRC). (7) Anticoagulant-related bleeding still needs investigation for the underlying lesion.
Active Recall — Differential Diagnosis of Rectal Bleeding
References
[1] Lecture slides: murtagh merge.pdf (p78–79, "Rectal bleeding") [2] Senior notes: felixlai.md (Lower GI bleeding, sections 510–511) [3] Senior notes: Ryan Ho Fundamentals.pdf (p281–283, "Lower GI Bleeding") [4] Senior notes: felixlai.md (Anal fissures section 1099–1100; Rectal prolapse section 1116; Intussusception section 1549) [5] Senior notes: Ryan Ho GI.pdf (p107–109, "Lower GI Bleeding"; p160, "Diverticular Bleeding"; p163–165, "Colorectal Cancer") [6] Senior notes: Ryan Ho GI.pdf (p146, "Ischaemic Colitis") [8] Senior notes: maxim.md (Diverticular disease section 193; LGIB DDx table section 158; Angiodysplasia section 197) [10] Senior notes: felixlai.md (Portal hypertensive gastropathy and variceal haemorrhage, sections 652) [11] Senior notes: Ryan Ho GI.pdf (p324, "Variceal Haemorrhage")
Diagnostic Criteria, Algorithm and Investigations for Rectal Bleeding
Rectal bleeding does not have a single "diagnostic criterion" the way a metabolic or autoimmune disease does. Instead, the diagnosis is a stepwise process governed by three sequential priorities [3][5]:
- Save the patient — resuscitation and haemodynamic stabilisation
- Find the bleeding — localisation of the bleeding site
- Stop the bleeding — endoscopic, angiographic or surgical haemostasis
Think of it this way: you cannot investigate a dead patient, and you cannot treat what you haven't found. The order is always resuscitate → localise → treat.
The choice of investigation depends on:
- Haemodynamic stability — an unstable patient cannot sit through a bowel-prepped colonoscopy
- Severity and acuity — occult bleeding is investigated differently from massive overt bleeding
- Suspected source — outlet-type bleeding → proctoscopy first; concern for UGIB → OGD first
Why OGD Before Colonoscopy in Severe Haematochezia?
10–15% of patients with severe haematochezia have an upper GI source [2][3][5]. A brisk duodenal ulcer bleed or variceal haemorrhage can transit the entire bowel without being degraded to melaena. If there is any concern for a UGI source (haematemesis, melaena, coffee-ground vomitus, haemodynamic instability disproportionate to visible PR blood, elevated BUN:Cr ratio), perform OGD before colonoscopy [3][5]. An alternative rapid screen is NG tube aspiration — bile-stained but non-bloody aspirate makes an upper GI source very unlikely [3][5].
3. Bedside Assessment — Before Any Investigation
The history and physical examination are themselves diagnostic instruments. Key points were covered in prior sections, but for the investigation framework, note:
Key history [1]:
Nature of the bleed, including fresh versus altered blood, mixed with faeces and/or mucus, in toilet bowl or on underwear. Quantity of bleeding: slight, moderate or torrential. Associated symptoms (e.g. weight loss, constipation, diarrhoea, pain, weakness, presence of lumps, urgency, unsatisfied defecation, recent change of bowel habit).
Key examination [1]:
General inspection (evidence of anaemia) and vital signs Abnormal examination, anal inspection, digital rectal examination, proctosigmoidoscopy
This is the first and most critical step — it determines the urgency and sequence of investigation.
| Parameter | Interpretation |
|---|---|
| Heart rate | Tachycardia (> 100 bpm) suggests ≥ 15–30% blood volume loss |
| Blood pressure | Hypotension (SBP < 90) suggests ≥ 30–40% loss |
| Postural BP | ≥ 20 mmHg systolic drop on standing = orthostatic hypotension → ≥ 15% loss |
| Urine output | < 0.5 mL/kg/h suggests inadequate renal perfusion |
| Mental status | Confusion/agitation suggests severe hypovolaemia |
| Temperature | ↓ body temperature can cause ↓ efficiency of clotting factors — prevent hypothermia [3][5] |
Physical examination checklist [3][5]:
- Vitals: BP/P, RR, postural BP, fever
- General: pallor (anaemia), dehydration (CRT, dry tongue), extra-abdominal manifestations of IBD
- Abdomen: mass, tenderness, signs of chronic liver disease, hepatosplenomegaly, ascites
- Digital rectal examination + proctoscopy: confirm haematochezia, assess stool colour, look for anorectal pathologies (haemorrhoids, fissure, masses) [3][5]
Key investigations [1]: FBE and ESR, Stool M&C, Faecal occult blood
| Investigation | What to Look For | Why / Interpretation |
|---|---|---|
| CBC with differentials [2][5] | Hb, Hct, MCV, WCC, platelets | Hb may be normal initially in acute bleeding — the patient is losing whole blood (cells + plasma proportionally), so the Hb concentration doesn't drop until fluid resuscitation dilutes the remaining blood [2]. Microcytic anaemia (↓ MCV) → chronic occult blood loss (e.g. CRC, angiodysplasia). ↑ WCC → infection or ischaemic colitis |
| Type and cross-match [2][5] | Blood group, antibody screen | Required for all haemodynamically unstable patients or those likely to need transfusion. Don't wait — send this early |
| Clotting profile (PT/INR, aPTT) [2][5] | Coagulopathy | Liver disease (↓ clotting factor production), anticoagulant therapy (warfarin → ↑ INR; heparin → ↑ aPTT). Must correct before invasive procedures |
| LFT [2] | Albumin, transaminases, bilirubin, ALP | Chronic liver disease → portal hypertension → rectal varices. Low albumin → poor nutritional status / chronic disease. Raised ALP/bilirubin → liver metastases (CRC) |
| RFT [2] | Urea (BUN), creatinine | BUN-to-creatinine ratio is a key discriminator: Normal BUN:Cr (< 20:1 or urea:Cr < 100:1) in LGIB vs elevated (> 30:1) in UGIB — because blood in the upper GI tract is "digested" and the protein is absorbed as urea [2]. Also assesses hydration and pre-renal failure. Chronic renal disease → baseline low Hb (deficient erythropoietin), so interpret CBC with caution [2] |
| Iron profile [12] | Serum iron, ferritin, TIBC, transferrin saturation | Iron deficiency anaemia (↓ ferritin, ↓ iron, ↑ TIBC) → chronic occult blood loss → investigate for CRC or angiodysplasia |
| Lactate, ABG [8] | Serum lactate, pH, base excess | ↑ Lactate and metabolic acidosis suggest tissue hypoperfusion — seen in massive bleeding or ischaemic colitis |
| ESR / CRP [1] | Inflammatory markers | ↑ in IBD, infective colitis, ischaemic colitis, malignancy |
| Stool M&C [1][2] | Microscopy, culture, sensitivity | Look for Campylobacter, Salmonella, Shigella, E. coli O157:H7, Entamoeba histolytica (amoebic dysentery) [2]. Also send C. difficile toxin (especially post-antibiotic patients) [2] |
| Faecal occult blood (FOBT) [1] | Guaiac or immunochemical test | Detects occult bleeding not visible to the naked eye. Positive FOBT in a patient with iron deficiency anaemia → must investigate with colonoscopy. Also used as a screening tool for CRC in asymptomatic populations |
| CEA (carcinoembryonic antigen) [12][13] | Serum level | NOT recommended as a screening or diagnostic test for CRC — low sensitivity (~50% of CRC only elevated) and low specificity (false positives in smoking, TB, IBD, pregnancy) [12]. Its role is in pre-operative baseline for surgical planning and post-operative surveillance for detecting recurrence [12][13] |
Why Is Hb Normal in Acute Bleeding?
A common student mistake is expecting the Hb to drop immediately in acute haemorrhage. In acute blood loss, you lose both red cells AND plasma in equal proportion — so the concentration of Hb (which is what the blood test measures) stays the same initially. The Hb only drops once the body starts auto-transfusing interstitial fluid into the vascular space, or once you give IV fluids for resuscitation, diluting the remaining red cells. Serial Hb monitoring is therefore essential — a falling Hb trend is more informative than a single value [2].
5. Endoscopic Investigations
Endoscopy is the cornerstone of diagnosis in rectal bleeding because it allows direct visualisation, tissue biopsy, and therapeutic intervention in one sitting.
| Feature | Proctoscopy | Rigid Sigmoidoscopy |
|---|---|---|
| Reach | Anal canal + distal rectum (~10 cm) | Up to sigmoid colon (~25 cm) [14] |
| Sedation | Not required | Not required |
| Bowel prep | Fleet enema × 1–2 | Fleet enema × 2 |
| Key indication | Exclusion of bleeding from anorectal disorders [2][3] — especially internal haemorrhoids (grade 1–2 may not be palpable on DRE [7]) | Anorectal pathology, low rectal tumours (assess true height, biopsy within reach), conservative Mx of sigmoid volvulus [14] |
| Limitations | Cannot visualise above rectum | Cannot see beyond sigmoid; no sedation → limited tolerance |
Clinical pearl: Proctoscopy should be the first investigation in outlet-type bleeding (blood on paper, dripping after defecation) in a young patient without red flags [8]. If a clear anorectal source is found AND there are no red flags (age < 45, no FHx, no change in bowel habit), you may not need a full colonoscopy. But if the patient is > 45 or has ANY red flags for CRC, proceed to colonoscopy regardless [7].
- Reaches up to the descending colon (~60 cm) [14]
- Requires low-residue diet for 3 days + Fleet enema × 2 [14]
- No sedation required (office procedure)
- Indication: fresh PR bleed without alarming symptoms in a patient < 40–45 years [14]
- Limitation: cannot visualise the right colon — since ~30% of CRC is right-sided and right-sided tumours are increasing, flexible sigmoidoscopy alone is considered inadequate for a complete work-up if CRC is suspected [5]
- Proceed to colonoscopy if: PR bleed in age > 45, change in bowel habit/tenesmus, FHx of CRC [7]
Colonoscopy: diagnostic yield = 75–90%, low complication rate [3][5]
| Aspect | Details |
|---|---|
| Reach | Entire colon from rectum to caecum; usually also intubate the ileocaecal valve to exclude distal small bowel bleeding [3][5] |
| Bowel preparation | Polyethylene glycol (PEG) solution — ↑ diagnostic yield but does not ↑ morbidity. NOT feasible in unstable patients [3][5] |
| Timing | Should be performed early (ideally within 24h of presentation for acute LGIB) — to obtain a diagnosis before bleeding stops and to allow therapeutic intervention [3][5] |
| Diagnostic capability | Direct visualisation + biopsy + genetic/molecular analysis of tissue. Missed CRC only in 2–6% [5] |
| Therapeutic capability | Especially effective in angiodysplasia and diverticular disease [3][5]: sclerosant/vasoconstrictor injections, heat probe, electrocoagulation, laser, haemoclips, argon plasma coagulation (APC), band ligation |
Key Endoscopic Findings by Cause:
| Cause | Endoscopic Appearance |
|---|---|
| Diverticular bleeding | Active bleeding, non-bleeding visible vessel, or adherent clot located in a diverticulum — but these definite sources are only identified in 21% [5]. Multiple diverticula are usually present → the challenge is identifying which one bled |
| Angiodysplasia | "Cherry red spots" — flat or slightly raised, bright red mucosal lesions 2–10 mm, usually in caecum/ascending colon [8] |
| CRC | Majority are endoluminal masses (exophytic or polypoid), may be friable, necrotic, or ulcerated with bleeding. May be circumferential → obstruct distal scoping. Important to scope entire colon — synchronous tumour in 3–5%, synchronous polyps in 30–50% [5] |
| UC | Extensive ulceration of the mucosa; surface is irregular, friable, erythematous, with loss of normal vascular markings [2]. Continuous from rectum extending proximally. Pseudopolyps in chronic disease |
| Crohn's disease | Skip lesions, deep serpentine ulcers ("cobblestone" pattern), aphthous ulcers, strictures, fistula openings |
| Ischaemic colitis | Oedematous folds, submucosal haemorrhage ("thumbprinting" on AXR corresponds to oedematous mucosa), ischaemic ulcers, necrosis of colonic wall in severe cases [2] |
| Radiation proctitis | Vascular telangiectasia on scope — fragile, dilated mucosal vessels in the irradiated segment [3] |
| Haemorrhoids | Engorged vascular cushions at 3, 7, 11 o'clock positions; seen best on proctoscopy (not colonoscopy, as insufflation can decompress them) [3][5] |
Important — Colonoscopy Low Diagnostic Yield in Massive Bleeding
Colonoscopy has a low diagnostic yield in massive bleeding because poor visualisation from blood in an unprepared colon makes it difficult to identify the source [8]. In these cases, CT angiography or mesenteric angiography is preferred. Colonoscopy is best when the patient has been stabilised and bowel-prepped.
Indicated if the bleeding source is not identified on colonoscopy [2], or if there is concern for an upper GI source (haematemesis, melaena, severe haematochezia with haemodynamic instability). Generally prefer OGD before colonoscopy in practice [3][5] — because an upper GI source is potentially more dangerous and faster to investigate.
Alternative quick screen: NG tube aspiration — if the aspirate contains bile (confirming the tube has passed into the duodenum) and no blood, an upper GI source is very unlikely [3][5].
6. Radiological Investigations
| Aspect | Details |
|---|---|
| Principle | IV contrast injection followed by rapid helical CT → detects contrast extravasation into the bowel lumen at the site of active bleeding |
| Sensitivity | Detects bleeding rates ≥ 0.3–0.5 mL/min (better than conventional angiography at ≥ 0.5–1.0 mL/min) |
| Advantages | Widely available, fast, and minimally invasive for localisation of active haemorrhage [2]. Non-operator-dependent. Can identify non-vascular pathology (masses, diverticulitis, abscess) as a bonus |
| Disadvantages | Lacks therapeutic capability (cannot embolise), requires radiation exposure and IV contrast [2] (risk of contrast nephropathy, allergic reaction) |
| Role | First-line imaging in haemodynamically unstable patients where colonoscopy is not feasible, or when colonoscopy fails to identify the source [8]. Guides subsequent mesenteric angiography for therapeutic embolisation |
| Aspect | Details |
|---|---|
| Principle | Selective catheterisation of SMA, subsequently IMA and coeliac vessels by Seldinger technique → look for contrast extravasation [2][3] |
| Sensitivity | Detection requires active bleeding of 0.5–1.0 mL/min [2]. Diagnostic yield 27–67% [3] |
| Advantages | Localisation of bleeding site is very accurate [2]. Allows therapeutic capability: intra-arterial vasopressin injection or transcatheter embolisation (super-selective catheterisation) [2][8]. Can diagnose non-bleeding lesions (e.g. angiodysplasia, SB tumours). Can be done intra-operatively to guide surgery [3] |
| Disadvantages | Not sensitive for slow/intermittent bleeding. Risk of intestinal ischaemia with embolisation. More invasive (arterial puncture, contrast load) [3] |
| Key finding — Angiodysplasia | "Mother-in-law phenomenon" — early filling (arterial phase), persistent opacification (venous phase), delayed emptying → the contrast arrives early and stays late [8]. Also: dilated, tortuous vessels, arteriovenous shunting, vascular tuft |
| Key finding — Active bleeding | Contrast extravasation into bowel lumen |
There are two main types:
| Type | Technetium-99m (⁹⁹ᵐTc) Pertechnetate-Labelled RBC | Technetium-99m Sulphur Colloid |
|---|---|---|
| Technique | RBCs drawn, labelled in vitro with ⁹⁹ᵐTc → re-injected IV → serial abdominal images over up to 24h [2][12a] | IV injection of ⁹⁹ᵐTc-labelled colloid → rapid imaging |
| Minimum bleeding rate | 0.1–0.4 mL/min → more sensitive than angiography [2][12a] | 0.1 mL/min |
| Delayed imaging | Yes — can image up to 24h → can detect intermittent bleeding [2][12a] | No — colloid rapidly cleared by reticuloendothelial system (liver/spleen) → short imaging window |
| Localisation | Poor localisation of bleeding site [2] — blood moves within bowel lumen (anterograde and retrograde peristalsis) | Poor — limited by liver/spleen uptake obscuring adjacent sites |
| Therapeutic value | None [2] | None |
| Role | Screening tool to confirm bleeding prior to angiography in non-life-threatening cases [2]. Best for intermittent bleeding where angiography would be negative. If positive → proceed to angiography for precise localisation and therapy | Largely superseded by tagged RBC scan |
Diagnostic criteria for positive RBC scan [12a]:
- 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 as a first step? Because it is more sensitive (detects slower bleeding), can detect intermittent bleeding via delayed imaging, and is less invasive [12a]. However, its poor spatial resolution means it cannot precisely pinpoint the bleeding vessel — so a positive RBC scan is usually followed by angiography for precise localisation and embolisation.
| Aspect | Details |
|---|---|
| Principle | ⁹⁹ᵐTc-pertechnetate is actively accumulated by gastric mucosa (pertechnetate behaves like chloride ions → actively secreted by gastric parietal cells). Ectopic gastric mucosa in a Meckel's diverticulum will take up the tracer [13a] |
| Pre-medication | H2-receptor blockers (e.g. ranitidine/famotidine) — inhibit excretion of the isotope into the bowel lumen after uptake, increasing sensitivity [13a] |
| Indication | Young patients with unexplained GI bleeding (especially painless massive PR bleed in children) [3][13a] |
| False positives | Intestinal duplications (also contain ectopic gastric mucosa) |
| False negatives | No or inadequate heterotopic gastric mucosa; rapid bleeding causing dilution of radiotracer [13a] |
- Not a primary diagnostic tool for rectal bleeding, but can show supportive findings:
- Thumbprinting: thickened oedematous bowel wall folds in ischaemic colitis
- Dilated bowel: bowel obstruction (from CRC or diverticular stricture)
- Pneumatosis intestinalis: gas in the bowel wall → advanced ischaemia/necrosis
- Free gas under diaphragm (on erect CXR): perforation (perforated diverticulitis, perforated CRC)
- Consider abdominal X-ray [1] as part of the initial work-up, especially if there is abdominal pain or distension
Beyond CTA for active bleeding, standard CT is invaluable for:
- Diverticulitis: bowel wall thickening, pericolic fat stranding, abscess, free air [8a]
- CRC staging: CT TAP (chest, abdomen, pelvis) for local extent and distant metastases [12]
- Ischaemic colitis: bowel wall thickening, mesenteric stranding, pneumatosis
- Abscess/fistula assessment in complicated diverticular disease or Crohn's
| Aspect | Details |
|---|---|
| Technique | Spiral CT with IV contrast + air insufflation per rectum → computer-generated "fly-through" simulating colonoscopy [12][13] |
| Indication | When colonoscopy is incomplete (due to obstructing tumour or patient intolerance) [12] |
| Performance | Similar diagnostic accuracy to colonoscopy for tumours > 1 cm; can provide extraluminal information (staging) [13] |
| Limitations | High radiation dose, not therapeutic (still need colonoscopy for biopsy), requires bowel prep (stools can simulate polyps) [13] |
- Largely superseded by CT colonography due to risk of barium peritonitis and lower diagnostic accuracy [12][13]
- Double-contrast barium enema (DCBE): barium + air → classic "apple-core" lesion (near-circumferential involvement) in CRC [12]
- Only considered when colonoscopy and CT colonography are not available or feasible
7. Advanced / Second-Line Investigations
These are employed when standard "top-and-tail" endoscopy (OGD + colonoscopy) fails to identify the source — the so-called GI bleeding of obscure origin [14a].
- Patient swallows a capsule containing a camera → transmits images wirelessly as it transits the small bowel
- Best for: occult/intermittent small bowel bleeding (angiodysplasia, Crohn's, small bowel tumours)
- Contraindication: intestinal obstruction (capsule may impact) → do CT/MR enterography beforehand to exclude strictures [8]
- Not therapeutic
- Scope with two inflatable balloons → allows sequential advancement deep into the small bowel from either the oral or anal route [8]
- Diagnostic AND therapeutic (biopsy, cauterisation, polypectomy)
- Used for intermittent small bowel bleeding (angiodysplasia, Dieulafoy lesion) when capsule endoscopy has identified a target [8]
- Cross-sectional imaging with oral contrast optimised for small bowel visualisation
- Useful for detecting Crohn's disease extent, small bowel tumours, Meckel's diverticulum complications
- MR enterography preferred in young patients (no radiation)
| Scenario | First-Line | Second-Line | Rationale |
|---|---|---|---|
| Outlet-type bleeding, young, no red flags | DRE + Proctoscopy ± Flexible sigmoidoscopy | Colonoscopy if no source or red flags emerge | Most likely haemorrhoids/fissure; avoid over-investigation |
| New bleeding age > 55 | Colonoscopy | CT colonography if incomplete | "New bleeding age > 55 demands colonic investigation" [1] — to exclude CRC |
| Acute massive PR bleed, haemodynamically unstable | Resuscitate → OGD (to exclude UGIB) → CTA or mesenteric angiography | Emergency surgery if above fails | Cannot bowel-prep for colonoscopy; need rapid localisation |
| Acute moderate PR bleed, stable after resuscitation | Urgent colonoscopy (within 24h with bowel prep) | CTA → angiography if colonoscopy non-diagnostic | Colonoscopy is both diagnostic and therapeutic |
| Bloody diarrhoea with fever | Stool MCS + C. diff toxin + Colonoscopy with biopsy | CT abdomen if complications suspected | Need to differentiate infective vs IBD vs ischaemic colitis |
| Occult bleeding / iron deficiency anaemia | Colonoscopy + OGD ("top and tail") | Capsule endoscopy → DBE for small bowel | Most occult GI bleeding is from the colon or upper GI; if both negative, investigate the small bowel |
| Suspected Meckel's diverticulum (young patient) | Meckel's scan (⁹⁹ᵐTc pertechnetate) | Diagnostic laparoscopy if scan negative but clinical suspicion high | Ectopic gastric mucosa takes up pertechnetate |
| Known cirrhosis with PR bleed | OGD (to exclude oesophageal/gastric varices) + Proctoscopy (rectal varices) | Colonoscopy if non-variceal source | Multiple potential sources in cirrhotics — must investigate all |
FBE and ESR
Stool M&C
Faecal occult blood
Colonoscopy
Consider abdominal X-ray, CT colonography, angiography, small bowel enema (depending on clinical findings)
1. Black, tarry (melaena) stool indicates bleeding from upper GIT: rare distal to lower ileum.
2. Frequent passage of blood and mucus indicates a rectal tumour or proctitis.
3. If substantial haemorrhage, consider diverticular disease, angiodysplasia or more proximal lesions (e.g. Meckel diverticulum, duodenal ulcers).
4. New bleeding age > 55 years demands colonic investigation.
5. 80% of rectal tumours are within fingertip range.
6. In young adults, diagnosis is likely to be haemorrhoids or a fissure.
| Modality | Min. Bleed Rate | Localisation | Therapeutic | Key Advantage | Key Limitation |
|---|---|---|---|---|---|
| Colonoscopy | Any (if visible) | Excellent | Yes | Gold standard; diagnostic yield 75–90%; biopsy + therapy | Needs bowel prep; poor in massive bleed |
| CTA | ≥ 0.3 mL/min | Good | No | Fast, widely available, non-operator-dependent | No therapy; radiation + contrast |
| Mesenteric angiography | ≥ 0.5–1.0 mL/min | Excellent | Yes (embolisation) | Precise; therapeutic | Invasive; misses slow/intermittent bleed |
| Tagged RBC scan | ≥ 0.1–0.4 mL/min | Poor | No | Most sensitive; detects intermittent bleed | Poor localisation; no therapy |
| Meckel's scan | N/A | Good | No | Specific for ectopic gastric mucosa | False negatives if no gastric mucosa |
| Capsule endoscopy | Occult/slow | Good (SB) | No | Non-invasive SB visualisation | Cannot be used in obstruction; no therapy |
| DBE | Occult/slow | Good (SB) | Yes | Therapeutic capability in SB | Operator-dependent; time-consuming |
| CT colonography | N/A | Good | No | Non-invasive; extraluminal info | Still needs CLN for biopsy |
High Yield Summary — Diagnosis of Rectal Bleeding
Three priorities: Resuscitate → Localise → Stop bleeding.
First step in all patients: History + DRE + Proctoscopy. These alone can diagnose haemorrhoids, fissure, and low rectal masses.
Colonoscopy is the gold standard (diagnostic yield 75–90%) but needs bowel prep and a stable patient. Perform within 24h for acute LGIB.
Always exclude UGIB in massive haematochezia — OGD before CLN, or NG aspirate to screen.
Unstable + massive bleed → CTA or mesenteric angiography (can also embolise).
Occult/intermittent bleed → Tagged RBC scan (most sensitive at 0.1–0.4 mL/min) → if positive, angiography for localisation.
BUN:Cr ratio: > 30:1 suggests upper GI source (digested blood → urea absorbed). Normal in LGIB.
Hb may be normal initially in acute bleeding — serial monitoring essential.
CEA is NOT for screening CRC — use for pre-op baseline and post-op surveillance.
Murtagh's key investigations: FBE, ESR, stool M&C, FOBT, colonoscopy. Consider AXR, CT colonography, angiography, small bowel enema.
Active Recall — Diagnosis and Investigations of Rectal Bleeding
References
[1] Lecture slides: murtagh merge.pdf (p78–79, "Rectal bleeding") [2] Senior notes: felixlai.md (Lower GI bleeding diagnosis, sections 511–514) [3] Senior notes: Ryan Ho Fundamentals.pdf (p281–285, "Lower GI Bleeding — Approach, Investigations and Management") [5] Senior notes: Ryan Ho GI.pdf (p107–111, "Lower GI Bleeding — Approach, Investigations and Management"; p160, "Diverticular Bleeding"; p162, "Meckel's Diverticulum"; p166, "CRC Diagnostic Investigations") [7] Senior notes: maxim.md (Haemorrhoids examination and investigation, section 229) [8] Senior notes: maxim.md (Acute management of LGIB, sections 158–161; Angiodysplasia investigations, section 197; Diverticular disease investigations, section 194) [12] Senior notes: felixlai.md (CRC biochemical tests and radiology, section 1011) [12a] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p62, "Red Blood Cell Scan") [13] Senior notes: maxim.md (CRC investigations, section 217) [13a] Senior notes: maxim.md (Meckel's scan, section 712) [14] Senior notes: maxim.md (Flexible sigmoidoscopy and rigid sigmoidoscopy, section 73)
Management of Rectal Bleeding
The management of rectal bleeding is governed by three sequential priorities — the same framework used for diagnosis, because in GI bleeding, investigation and treatment often happen simultaneously [3][5]:
Save the patient → Find the bleeding → Stop the bleeding [3][5]
A few critical facts set the context:
- 75% of lower GI bleeding stops spontaneously [3][5] — so many patients will not need any intervention beyond resuscitation and observation. However, you must still investigate to find the cause, because something like CRC won't bleed forever but will still kill the patient.
- 15–20% of patients with acute LGIB require surgery [3][5].
- The specific definitive management depends entirely on the underlying cause — you manage the bleeding acutely, then treat the disease.
3. Phase 1: Initial Assessment and Resuscitation
This is the life-saving phase — it applies to ALL patients with significant rectal bleeding, regardless of the suspected cause.
| Step | Action | Rationale |
|---|---|---|
| NPO | Nil by mouth | Patient may need urgent endoscopy or surgery — a full stomach increases aspiration risk [5] |
| IV access | 2 large-bore IV cannulae (14–16G) at antecubital veins [8][15] | Large-bore access allows rapid volume resuscitation. Two lines because one may fail or be needed for blood products while the other runs crystalloid |
| Stop anticoagulants | Withhold warfarin, DOACs, heparin, antiplatelets [8] | These drugs impair haemostasis. Reverse if actively bleeding and haemodynamically compromised (vitamin K for warfarin, idarucizumab for dabigatran, andexanet alfa for factor Xa inhibitors) |
| Monitor vitals | Shock chart hourly: BP/P, RR, body temperature [3][5] | Track haemodynamic response to resuscitation. ↓ body temperature can cause ↓ efficiency of clotting factors — prevent hypothermia [3][5] |
| Foley's catheter | Urine output ≥ 0.5 mL/kg/h [3][5] | Urine output is the best bedside indicator of end-organ perfusion. Oliguria (< 0.5 mL/kg/h) = inadequate resuscitation |
| Cardiac monitor + pulse oximetry | Continuous | Detect arrhythmias from hypovolaemia, monitor oxygenation [3][5] |
| ± CVP line | Central venous pressure monitoring | Consider in patients with heart failure or renal failure (risk of fluid overload) to guide resuscitation [3][5] |
A — Airway: Intubate if the patient is decompensated (confused, GCS ↓) or has massive haematemesis with aspiration risk [3][5].
B — Breathing: O₂ via nasal cannula to ↑ O₂-carrying capacity of remaining blood [3][5]. Even though Hb may be dropping, maximising the oxygen saturation of what Hb remains is crucial.
C — Circulation: Large-bore IV cannula with colloid/crystalloid infusion ± blood transfusion [3][5].
- Start with rapid crystalloid bolus (500–1000 mL of normal saline or Hartmann's solution over 5–10 minutes) [15]
- Reassess BP/P after each bolus — repeat if not responding [15]
- If still unstable after 2 L crystalloid → likely needs blood transfusion [3][5]
Indications for blood transfusion [3][5]:
- Profuse bleeding
- Persistent haemodynamic instability despite crystalloid resuscitation
- Symptomatic anaemia
- Acute MI/unstable angina with low Hb
Transfusion targets:
- General: Hb 7–8 g/dL (restrictive strategy — over-transfusion can ↑ portal pressure in variceal bleeding and is associated with ↑ mortality) [11]
- Ischaemic heart disease: consider higher target (Hb 8–9 g/dL)
- Correct coagulopathy: FFP if PT prolonged, platelets if < 50 × 10⁹/L and actively bleeding
Bloods to send simultaneously [3][5]:
- CBC, RFT, LFT, clotting profile, type and screen/cross-match, lactate, ABG
The 'Lethal Triad' of Massive Haemorrhage
In massive bleeding, be vigilant for the lethal triad: hypothermia + acidosis + coagulopathy. Each worsens the others in a vicious cycle. Hypothermia impairs clotting enzyme function. Acidosis inhibits clotting factor activity. Coagulopathy causes more bleeding → more volume loss → more hypothermia and acidosis. Prevent hypothermia (warm fluids, blankets), correct acidosis (restore perfusion), and correct coagulopathy (blood products) simultaneously.
4. Phase 2: Localisation and Haemostasis — Cause-Specific Treatment
Once the patient is resuscitated (or concurrently in life-threatening situations), you move to finding the bleed and stopping it. The treatment modality depends on the underlying cause.
This is the first-line therapeutic modality for most causes of GI bleeding, because it can be performed during the diagnostic colonoscopy.
Indications for endoscopic haemostasis [8]:
Stigmata of recent haemorrhage: active bleeding, non-bleeding visible vessel, adherent clot
| Modality | Mechanism | Best Suited For | Key Points |
|---|---|---|---|
| Adrenaline injection (1:10,000) | Volume effect (tamponade) + local vasoconstriction + platelet aggregation | Initial haemostasis in most causes | Not used alone — stops bleeding in 90–95% initially but often rebleeds after absorption (~1h). Must combine with a second modality [8][3a][5a] |
| Thermal — Argon plasma coagulation (APC) | Ionised argon gas delivers non-contact coagulation → superficial tissue desiccation | Angiodysplasia (thin-walled lesions), radiation proctitis | ↓ energy depth than heat probe → ↓ risk of perforation → ideal for thin-walled structures and diffuse superficial oozing [3a][5a][8] |
| Thermal — Heat probe / Bipolar diathermy | Contact coagulation → coaptive sealing of vessel | Visible vessel in diverticular bleeding, peptic ulcers | Risk of perforation (direct thermal injury to wall) [3a][5a] |
| Mechanical — Haemoclips / Endoscopic clips | Physically compress the bleeding vessel closed | Diverticular bleeding (clip the vasa recta), large visible vessels, Mallory-Weiss tears | Durable haemostasis; no thermal injury [3a][5a][8] |
| Endoscopic band ligation | Rubber band strangulates the bleeding point → ischaemic necrosis | Diverticular bleeding, rectal varices, oesophageal varices | Similar to RBL for haemorrhoids — the band cuts off blood supply [8] |
| Haemospray | Nanopowder applied to bleeding surface → large surface area induces haemostasis | Salvage when other modalities fail; diffuse oozing | Usually temporary bridge; limited availability [5a] |
| Injection sclerotherapy | Sclerosant (e.g. sodium tetradecyl sulphate, ethanolamine oleate) injected into/around vessel → thrombosis and fibrosis | Rectal varices (local injection), oesophageal varices | Largely replaced by band ligation for oesophageal varices; still used for rectal varices [3] |
Standard Dual Therapy for Active GI Bleeding
The standard approach for endoscopic haemostasis in active bleeding is dual therapy: adrenaline injection + a second modality (thermal, mechanical, or band ligation) [3a][5a][8]. Adrenaline alone has an unacceptably high rebleeding rate. The second modality provides definitive haemostasis — think of adrenaline as "buying time" by tamponade while you apply the definitive clip or coagulation.
Contraindication to endoscopy: Perforation — gas insufflation during endoscopy can cause pneumoperitoneum → abdominal compartment syndrome → ↓ venous return and death + diaphragmatic splinting compromising ventilation [5a].
| Aspect | Details |
|---|---|
| Technique | Selective catheterisation of SMA/IMA/coeliac axis → identify extravasation → super-selective catheterisation of the bleeding vessel → embolisation with coils, gel foam, or particles [2][8] |
| Indications | Failed endoscopic haemostasis; patient too unstable for colonoscopy; ongoing active bleeding with identifiable source on CTA/angiography [8] |
| Advantages | Does not require bowel prep; can be done in haemodynamically unstable patients; equally effective as surgery in patients who failed endoscopy and associated with fewer complications [2a]; reduces need for surgery without increasing mortality [2a] |
| Disadvantages | Risk of intestinal ischaemia (especially if non-super-selective); requires active bleeding at time of procedure (≥ 0.5–1.0 mL/min); contrast nephropathy; arterial puncture complications [3] |
| Specific uses | Diverticular bleeding, post-polypectomy bleeding, angiodysplasia (when endoscopy fails), rectal varices (if combined with TIPS) |
TAE should be considered in patients who are high risk for surgery [2a]. Think of it as a less invasive alternative to the operating theatre, though it carries its own risks (ischaemia) and requires interventional radiology expertise.
Surgery is required in approximately 15–20% of patients with acute lower GI bleed [3][5].
- Haemodynamic instability despite adequate resuscitation
- Massive blood transfusion ( > 6 units)
- Frequent re-bleeding
- On anticoagulant or antiplatelets (higher bleeding risk, lower threshold for definitive haemostasis)
| Scenario | Procedure | Outcome |
|---|---|---|
| With pre-operative localisation | Segmental resection (resect only the segment containing the bleeding source) | Rebleeding 0–15%, mortality 0–13% [3] |
| Without localisation — colonic source | Subtotal/total colectomy (remove entire colon) | Mortality 0–40% [3] — higher because these are the sickest patients |
| Without localisation — unknown source | Intra-operative colonoscopy or enteroscopy for localisation → then directed resection | Preferred over blind segmental resection |
| Blind segmental resection | Resect a segment based on clinical suspicion (no confirmed localisation) | Rebleeding up to 75% [3] — avoid whenever possible |
Why Pre-Operative Localisation Matters Enormously
Blind segmental resection has a rebleeding rate of up to 75% [3] because you may be removing the wrong segment. Pre-operative localisation (by colonoscopy, CTA, or angiography) is essential to guide the surgeon to the correct segment. If localisation is impossible and the patient is exsanguinating, subtotal colectomy (removing the entire colon) is safer than guessing — but carries significant morbidity and mortality.
5. Cause-Specific Management
| Phase | Management |
|---|---|
| Acute | Resuscitation → Colonoscopy (first-line) for localisation and endoscopic haemostasis: adrenaline injection, endoscopic clips/band ligation, bipolar diathermy [3][5][8] |
| If colonoscopy fails | CTA → Mesenteric angiography with embolisation [5][8] |
| Localisation pathway | Colonoscopy → angiography → on-table lavage and colonoscopy → subtotal colectomy and ileostomy if the bleeding source still cannot be identified [8a] |
| Indications for surgery | Haemodynamically unstable despite adequate resuscitation; excessive blood transfusion > 6 units; frequent rebleeding or persistent bleeding [2a] |
| Elective/semi-elective | Semi-elective segmental resection after 2nd bleeding episode — because natural history is commonly recurrent (14–38% rebleed) [3][5] |
| Long-term prevention | Lifestyle modification: high-fibre diet, bulk laxative (e.g. methylcellulose), weight reduction. Avoid stimulant laxatives and NSAIDs [8a] |
50% of diverticular bleeding stops spontaneously [8a]. But the recurrence rate is high enough that after a second episode, most surgeons would recommend elective resection.
| Phase | Management |
|---|---|
| Conservative | Bed rest, tranexamic acid [8] — tranexamic acid is an anti-fibrinolytic that stabilises clots (inhibits plasminogen → plasmin conversion) |
| Endoscopic | Argon plasma coagulation (APC) is the modality of choice (↓ perforation risk, ideal for thin-walled lesions) or monopolar electrocautery [8] |
| Interventional radiology | Mesenteric angiogram for super-selective catheterisation and embolisation — if endoscopy fails or is not feasible [8] |
| Surgical | Only in selected patients because of high mortality [8]. Indications: failed endoscopic AND angiographic treatment; severe acute life-threatening GIB; multiple angiodysplastic lesions that cannot be managed otherwise. Approach: resection (right hemicolectomy) with anastomosis [8] |
| Medical (for recurrent) | Consider octreotide (↓ splanchnic blood flow), thalidomide (anti-angiogenic), oestrogen (controversial — limited evidence). Address underlying conditions: replace aortic valve in Heyde syndrome (resolves the acquired vWD) |
This is one of the most commonly tested management topics.
Principle: conservative treatment for ALL patients — lifestyle modification and symptom control first [4].
Grading and Management Ladder [4][7]:
| Grade | Description | Management Options |
|---|---|---|
| I | Bleeding only, no prolapse | Dietary modification, rubber band ligation (RBL), injection sclerotherapy, infrared coagulation [4] |
| II | Prolapse at defecation, spontaneous reduction | Lifestyle, medical, RBL [7] |
| III | Prolapse requiring manual reduction | Lifestyle, medical, RBL + surgery [7] |
| IV | Chronic prolapse that is irreducible ± strangulated | Surgery [7] |
Conservative Management [4][7]:
- Diet: high-fibre diet, increase fluid intake (to soften stools and reduce straining), avoid spicy food
- Toileting habits: avoid prolonged sitting on toilet, avoid prolonged straining
- Exercise, weight loss
- Medical: stool softeners, bulking agents (e.g. Metamucil/psyllium), topical antiseptic (KMnO₄ sitz bath), topical haemostatic (e.g. Faktu), topical astringent (e.g. Anusol), topical analgesics
Office-Based Procedures [7]:
| Procedure | Technique | Key Details |
|---|---|---|
| Rubber band ligation (RBL) | Apply rubber bands to strangulate the haemorrhoidal cushion via Barron's bander → ischaemic necrosis → slough off within 10 days | Efficacy: 70% resolve, 30% recur. Up to 3 bandings at ≥ 1 cm above dentate line (to avoid somatic pain). Indication: symptomatic Grade II/III internal haemorrhoids. Complications: pain, bleeding (7–10 days post-banding due to sloughing). Contraindication: anticoagulant use, immunocompromised [7] |
| Injection sclerotherapy | 5% phenol in almond oil injected submucosally → fibrosis → obliterate vascular channels and fix position | Largely abandoned now: risk of allergy to nuts and intraprostatic injection [7] |
| Infrared coagulation | Infrared light → thermal coagulation → fibrosis | Suitable for Grade I; less effective than RBL for larger haemorrhoids |
| HALO (haemorrhoidal artery ligation operation) | Doppler-guided ligation of feeding arteries | Mainly for bleeding symptoms, indicated for Grade II/III haemorrhoids. Lowest post-op complications but highest recurrence rate [7] |
Surgical Excision — Haemorrhoidectomy [7]:
Indications:
- Grade III/IV internal haemorrhoids
- Symptomatic internal/external haemorrhoids refractory to other treatments
- Fibrosed haemorrhoids
- Haemorrhoidal bleeding leading to anaemia [4]
| Technique | Details |
|---|---|
| Conventional haemorrhoidectomy | For internal ≥ Grade III or external haemorrhoids. 3-leaf clover excision: excise the three cushions at 3, 7, 11 o'clock but leave mucosal bridges between them — avoid circumferential excision → prone to anal stenosis [7] |
| Closed (Ferguson) | Close wound by continuous suture; more commonly used [7] |
| Open (Milligan-Morgan) | Leave wound open, heal by secondary intention; preferred for acute gangrenous haemorrhoids (prevents further tissue oedema and necrosis) [7] |
| Stapled haemorrhoidopexy (PPH) | For internal only; less painful but higher recurrence rate; less favoured now due to poorer long-term outcomes [7] |
Efficacy of haemorrhoidectomy: 95% resolve [7].
Complications of haemorrhoidectomy [7]:
- Pain (~100%) — due to internal anal sphincter spasm
- Urinary retention — caused by pain/anal spasm, fluid overload, rectal packing, drugs (narcotics, anticholinergics), pre-existing outflow tract obstruction. Mx: leave urinary catheter for 24h [7]
- Faecal incontinence (injury to sphincter), anal fissure, anal stenosis [7]
| Phase | Management |
|---|---|
| Conservative (acute, < 6 weeks) | Increased dietary fibre and water intake; stool softener/laxatives; warm sitz bath (relaxes anal sphincter and improves blood flow to anal mucosa); topical analgesics (lidocaine jelly) [4] |
| Topical vasodilators | Topical nifedipine ointment or topical nitroglycerin (GTN) ointment — mechanism: relaxes the internal anal sphincter (smooth muscle) → breaks the cycle of spasm → allows healing by restoring blood flow to the posterior midline [4] |
| If fails 8 weeks of medical Rx | Botulinum toxin type A injection — chemical denervation of the internal anal sphincter → relaxation → healing [4]. OR Lateral internal sphincterotomy — surgical division of part of the internal anal sphincter → permanent reduction in resting anal pressure → definitive treatment but carries risk of faecal incontinence [4] |
Why do sphincter-relaxing treatments work? The pathogenesis of chronic anal fissure is a vicious cycle: tear → spasm of internal anal sphincter → pulls edges apart + reduces blood flow to posterior midline → impaired healing → chronic fissure. Breaking the spasm (with GTN, nifedipine, botulinum toxin, or sphincterotomy) interrupts this cycle and allows healing [4].
Management of CRC-related bleeding is treatment of the underlying cancer. Endoscopic haemostasis has a limited role — you cannot clip a cancer into submission [3]. The definitive treatment is surgical resection ± adjuvant chemotherapy/radiotherapy, which is a large topic covered separately. Key points relevant to the bleeding context:
- Endoscopic Tx has limited role for CRC bleeding [3]
- Urgent colonoscopy to biopsy, tattoo location, and plan surgery
- Emergency surgery if presenting with obstruction, perforation, or uncontrollable bleeding
- Usually managed medically — 5-ASA (mesalazine), corticosteroids, immunomodulators (azathioprine), biologics (anti-TNF, vedolizumab) [3]
- May require emergency colectomy if life-threatening bleeding — this is rare but well-recognised in fulminant UC [3]
- Bloody diarrhoea in IBD is a marker of disease activity → treat the flare, not just the bleeding
- Most cases are transient — supportive care: IV fluids, bowel rest (NPO), broad-spectrum antibiotics (for bacterial translocation), close monitoring [6]
- Surgery (colectomy) if: transmural necrosis, perforation, peritonitis, clinical deterioration despite medical therapy
- Address underlying cardiovascular risk factors
| Modality | Details |
|---|---|
| Topical | Sucralfate enema or glucocorticoid enema — mucosal protection and anti-inflammatory |
| Endoscopic | Argon plasma coagulation (APC), infrared coagulation, laser, 4% formalin injection — all aim to cauterise/obliterate the telangiectatic vessels |
| Surgery | Proximal stoma (faecal diversion to rest the rectum), proctectomy (rarely done — only for refractory cases) [3] |
| Modality | Details |
|---|---|
| Local | Injection sclerotherapy [3] |
| Systemic | Address portal hypertension: non-selective beta-blockers (propranolol/nadolol) to ↓ portal pressure |
| If uncontrolled | TIPS (transjugular intrahepatic portosystemic shunt) — creates a low-resistance channel between the portal and hepatic veins → decompresses the portal system → reduces variceal pressure [3] |
| Scenario | Management |
|---|---|
| Symptomatic | Resect. Narrow base → simple diverticulectomy (excision at base and suture). Broad base / ulceration at margin / mesenteric border → segmental bowel resection + primary anastomosis [8] |
| Asymptomatic, detected on imaging | Do NOT resect [8] |
| Asymptomatic, detected during surgery | Depends on age: Child → resect. Adult < 50y → resect if palpable, length > 2 cm, broad base > 2 cm. Adult > 50y → do not resect [8] |
Cirrhotic patients deserve a dedicated approach because they bleed from multiple potential sources and have impaired coagulation:
- Haemodynamic stabilisation: maintain SBP 90–100 mmHg (excessive volume can ↑ portal pressure → early rebleeding) [11]
- Volume resuscitation: keep UO > 0.5 mL/kg/h [11]
- Packed cells ± FFP/platelets: keep Hb 7–8 g/dL, Hct 21–24% [11]
- Correct coagulopathy: Vitamin K₁ (if cholestatic element), FFP, platelets [11]
- Routine prophylactic antibiotics for 7 days — to prevent spontaneous bacterial peritonitis and bacteraemia which worsen bleeding outcomes [11]
- Emergency OGD for diagnosis and haemostasis [11]
- Intubation considered if massive bleeding (↓ risk of aspiration) [11]
For variceal bleeding specifically [11]:
- Vasoactive agents to ↓ portal venous pressure: Terlipressin (1st line) — synthetic ADH analogue → mesenteric arteriolar constriction → ↓ portal inflow. Octreotide if IHD (ADH analogues may precipitate MI) [11]
- Endoscopic treatment: band ligation (oesophageal varices), tissue adhesives (gastric varices), sclerotherapy (rectal varices) [11]
- Sengstaken-Blakemore tube: temporising measure only — balloon tamponade if endoscopy not available or failed [11]
- TIPS: if endoscopic + medical therapy fails — creates portosystemic shunt, decompresses varices [11]
- Emergency surgery: portocaval shunts, splenorenal shunt, or non-shunt surgery (oesophageal transection, Sugiura devascularisation) — associated with 50% mortality, reserved for those failing other treatment with good liver function [11]
| Indication | Rationale |
|---|---|
| Haemodynamic instability despite adequate resuscitation | Patient is exsanguinating — needs definitive source control |
| Massive blood transfusion ( > 6 units) | Indicates ongoing significant haemorrhage not controlled by other means |
| Frequent re-bleeding | Endoscopic/IR haemostasis has failed to provide durable control |
| On anticoagulant or antiplatelets | Lower threshold for surgery because pharmacological haemostasis is impaired |
| Failed endoscopic and angiographic therapy | Exhausted less invasive options |
| Procedure | Rebleeding Rate | Mortality |
|---|---|---|
| Segmental resection with localisation | 0–15% | 0–13% |
| Blind segmental resection | Up to 75% | Higher |
| Subtotal colectomy | Low | 0–40% |
After the acute bleed is controlled, the focus shifts to treating the underlying cause and preventing recurrence:
| Cause | Secondary Prevention |
|---|---|
| Diverticular disease | High-fibre diet, weight reduction, avoid NSAIDs and stimulant laxatives. Elective segmental resection after 2nd bleeding episode [3][8a] |
| Angiodysplasia | Treat associated conditions (aortic valve replacement in Heyde syndrome). Consider octreotide for recurrent bleeding. Iron supplementation for chronic anaemia |
| Haemorrhoids | Lifestyle modification (diet, toileting habits, exercise). Escalate to RBL or surgery if recurrent [4][7] |
| Anal fissure | Maintain soft stools (fibre, water, stool softeners). Topical vasodilators. Sphincterotomy if chronic [4] |
| CRC | Oncological follow-up: CEA surveillance, colonoscopy (1 year post-op, then 3y, 5y, then every 5y), CT TAP yearly [13] |
| IBD | Disease-modifying therapy (5-ASA, immunomodulators, biologics). CRC surveillance colonoscopy after 8–10 years of disease [5] |
| Radiation proctitis | Endoscopic APC sessions for recurrent telangiectasia; sucralfate/glucocorticoid enemas [3] |
| Anticoagulant-related | Investigate and treat underlying lesion. Discuss risk-benefit of restarting anticoagulation with haematology/cardiology |
High Yield Summary — Management of Rectal Bleeding
Three priorities: Resuscitate → Localise → Stop bleeding.
Resuscitation: NPO, 2 large-bore IV, crystalloid then blood if needed. Stop anticoagulants. Monitor: shock chart hourly, Foley catheter (UO ≥ 0.5 mL/kg/h), prevent hypothermia. Transfuse if profuse bleeding, persistent instability, symptomatic anaemia, or ACS with low Hb.
Endoscopic haemostasis is first-line: dual therapy (adrenaline + clip/thermal/band). APC is ideal for angiodysplasia and radiation proctitis. Clips/band for diverticular bleeding. Never use adrenaline alone.
TAE if endoscopy fails or patient too unstable for colonoscopy. Equally effective as surgery with fewer complications.
Surgery in 15–20%: indications = haemodynamic instability despite resuscitation, > 6 units transfused, frequent rebleeding, failed endoscopic/IR therapy. Always try to localise pre-operatively — blind segmental resection has 75% rebleeding rate.
Haemorrhoids: Conservative for all → RBL for Grade II/III → Haemorrhoidectomy for Grade III/IV or refractory. 3-leaf clover excision, avoid circumferential excision (stenosis).
Anal fissure: Fibre + sitz bath + topical GTN/nifedipine → Botox or lateral internal sphincterotomy if fails 8 weeks.
Cirrhotic bleeding: Conservative Hb target (7–8 g/dL), terlipressin 1st line, prophylactic antibiotics 7 days, emergency OGD. TIPS if endoscopy fails.
Active Recall — Management of Rectal Bleeding
References
[2a] Senior notes: felixlai.md (Management of diverticular bleeding and PUD haemorrhage, sections 577, 948) [3] Senior notes: Ryan Ho Fundamentals.pdf (p281–286, "Lower GI Bleeding — Approach, Investigations and Management") [3a] Senior notes: Ryan Ho Fundamentals.pdf (p255, "Endoscopic Tx Modalities") [4] Senior notes: felixlai.md (Haemorrhoids treatment section 1093; Anal fissure treatment section 1100) [5] Senior notes: Ryan Ho GI.pdf (p106–111, "Lower GI Bleeding — Approach, Investigations and Management") [5a] Senior notes: Ryan Ho GI.pdf (p45, "Endoscopic Tx Modalities") [6] Senior notes: Ryan Ho GI.pdf (p146, "Ischaemic Colitis") [7] Senior notes: maxim.md (Haemorrhoids management, sections 230–231) [8] Senior notes: maxim.md (Acute management of LGIB, sections 160–161; Angiodysplasia management, section 197; Meckel's management, section 197) [8a] Senior notes: maxim.md (Diverticular disease management, section 194) [11] Senior notes: Ryan Ho GI.pdf (p324–325, "Variceal Haemorrhage Management") [13] Senior notes: maxim.md (CRC follow-up, section 227) [13a] Senior notes: maxim.md (Meckel's management, section 712) [15] Senior notes: Ryan Ho Critical Care.pdf (p21, "Management of Hypovolemic Shock")
Complications of Rectal Bleeding
Complications of rectal bleeding arise from two broad categories: (A) complications of the bleeding itself (i.e. what happens when you lose blood) and (B) complications of the underlying cause (i.e. what the disease that caused the bleeding goes on to do if left untreated) and (C) complications of treatment (i.e. iatrogenic harm from the investigations and interventions we use to manage the bleeding). A systematic understanding of all three is essential.
1. Complications of the Bleeding Itself
These are the direct physiological consequences of blood loss and apply regardless of the underlying aetiology.
Shock: extreme thirst, confusion, pallor, oliguria [3]
Pathophysiology from first principles:
- Acute blood loss → ↓ circulating volume → ↓ venous return → ↓ cardiac preload → ↓ stroke volume → ↓ cardiac output → ↓ tissue perfusion → end-organ ischaemia
- The body compensates initially via sympathetic activation: tachycardia, peripheral vasoconstriction (cold clammy extremities, pallor, delayed capillary refill), ↑ renin-angiotensin-aldosterone system (Na⁺/H₂O retention to restore volume), ADH release (water retention, oliguria)
- When compensation is overwhelmed (typically > 30–40% blood volume loss) → decompensated shock → hypotension, confusion, obtundation, anuria
Clinical grading of haemorrhagic shock:
| Class | Blood Loss | Heart Rate | BP | Mental Status | Urine Output |
|---|---|---|---|---|---|
| I | < 15% ( < 750 mL) | Normal or slight ↑ | Normal | Normal | Normal |
| II | 15–30% (750–1500 mL) | > 100 | Normal (↓ pulse pressure) | Anxious | 20–30 mL/h |
| III | 30–40% (1500–2000 mL) | > 120 | ↓ | Confused | 5–15 mL/h |
| IV | > 40% ( > 2000 mL) | > 140 | ↓↓ | Obtunded | Negligible |
Why does the body get confused? The brain requires ~15% of cardiac output. When CO drops sufficiently, cerebral perfusion falls below the autoregulatory threshold → neuronal dysfunction → confusion, agitation, eventually obtundation. This is a late and ominous sign.
Complications of shock itself:
- Multi-organ dysfunction syndrome (MODS): prolonged hypoperfusion damages kidneys (acute tubular necrosis → acute kidney injury), liver (ischaemic hepatitis), gut (bacterial translocation → sepsis), lungs (ARDS)
- Disseminated intravascular coagulation (DIC): massive tissue injury and hypoperfusion activate the coagulation cascade diffusely → consumption of clotting factors and platelets → paradoxical simultaneous clotting AND bleeding
- The lethal triad: hypothermia + metabolic acidosis + coagulopathy — each worsens the others in a self-perpetuating cycle (discussed in the Management section)
Symptomatic anaemia: SOB on exertion, postural dizziness, syncope, chest pain, palpitation, lethargy or fatigue [3]
Acute anaemia (from acute blood loss):
- Rapid drop in oxygen-carrying capacity → compensatory tachycardia, ↑ respiratory rate, ↑ 2,3-DPG (shifts oxygen-haemoglobin dissociation curve rightward → more O₂ unloaded to tissues)
- If severe → myocardial ischaemia (chest pain, ST changes on ECG), syncope, acute heart failure (especially in elderly patients with pre-existing cardiac disease)
Chronic anaemia (from occult bleeding — e.g. CRC, angiodysplasia):
- Iron deficiency anaemia — chronic blood loss depletes iron stores → impaired haemoglobin synthesis → microcytic, hypochromic anaemia
- Gradual onset allows better compensation, so patients may tolerate remarkably low Hb levels (e.g. Hb 5–6 g/dL) before becoming symptomatic
- Symptoms: fatigue, exertional dyspnoea, pallor, koilonychia (spoon nails), angular cheilitis, glossitis, pica (craving non-food substances like ice or clay)
- The anaemia itself is not the complication per se — it is the clue that leads you to the diagnosis. An unexplained iron deficiency anaemia in any adult mandates investigation of the GI tract (OGD + colonoscopy) to exclude malignancy
Acute-on-Chronic Anaemia
A patient with chronic occult bleeding (e.g. right-sided CRC) may have adapted to a low Hb. An acute bleeding episode on top of this → sudden further drop in an already depleted oxygen-carrying capacity → disproportionate haemodynamic compromise. This is why comorbidities (especially cardiopulmonary disease) make patients more susceptible to hypoxaemia [3].
When patients receive large volumes of blood products (typically defined as ≥ 10 units pRBC in 24h or replacement of entire blood volume), they are at risk of:
| Complication | Mechanism |
|---|---|
| Hyperkalaemia | Stored blood leaks intracellular K⁺ over time; rapid transfusion delivers a potassium bolus → cardiac arrhythmias |
| Hypocalcaemia | Citrate anticoagulant in stored blood chelates calcium → ↓ ionised Ca²⁺ → myocardial depression, coagulopathy, tetany |
| Hypothermia | Stored blood is refrigerated at 4°C; rapid infusion drops core temperature → ↓ clotting factor efficiency, cardiac arrhythmias |
| Dilutional coagulopathy | Packed RBCs contain no clotting factors or platelets; replacing blood volume with pRBC alone "dilutes" the remaining clotting factors → bleeding worsens |
| Transfusion-related acute lung injury (TRALI) | Donor antibodies against recipient WBC antigens → non-cardiogenic pulmonary oedema → acute hypoxia within 6h of transfusion |
| Volume overload (TACO) | Especially in patients with HF or RF → pulmonary oedema |
| Transfusion reactions | Febrile, allergic, haemolytic (ABO incompatibility) |
2. Complications of the Underlying Causes
These are the complications that arise from the diseases responsible for the bleeding, either from the natural history of the disease or if treatment is delayed.
| Complication | Pathophysiology | Key Features |
|---|---|---|
| Recurrent bleeding | 14–38% rebleeding rate after first episode [3]; the structural abnormality (vasa recta draped over diverticulum) persists | Often indication for semi-elective segmental resection after 2nd episode [3] |
| Diverticulitis | Obstruction of diverticulum by faecolith → stasis → bacterial overgrowth → inflammation (note: diverticulitis and diverticular bleeding rarely coexist [3]) | Triad of lower abdominal pain + fever + leucocytosis |
| Pericolic/pelvic abscess | Microperforation of inflamed diverticulum contained by pericolic fat and mesentery → abscess formation | Persistent fever despite antibiotics; tender mass on PR; managed by IV antibiotics ± percutaneous drainage depending on Hinchey classification [8a] |
| Perforation with peritonitis | Free perforation of diverticulum → faecal contamination of peritoneal cavity → generalised peritonitis and sepsis | Hinchey III (purulent peritonitis) or IV (faecal peritonitis) → emergency Hartmann's operation. Mortality up to 20% if perforated with diffuse peritonitis [5] |
| Fistula formation | Inflammation erodes into adjacent organ → abnormal communication. Most common: colovesical fistula → recurrent dysuria, pneumaturia, faecaluria [8a] | Also: colovaginal (feculent vaginal discharge), coloenteric, colocutaneous |
| Stricture and obstruction | Repeated inflammation → fibrosis and scarring → luminal narrowing → LBO (large bowel obstruction). SBO from adhesions to inflamed bowel [8a] | Chronic abdominal pain, constipation, progressive obstructive symptoms |
| Complication | Pathophysiology |
|---|---|
| Strangulation and thrombosis | Prolapsed internal haemorrhoids (Grade IV) become trapped by anal sphincter spasm → venous congestion → swelling → cannot reduce → if blood supply cut off → strangulation → thrombosis → intense pain [4] |
| Gangrene | Sustained strangulation → complete ischaemia → necrosis of haemorrhoidal tissue [4] |
| Ulceration | Chronically prolapsed haemorrhoids exposed to friction and pressure → mucosal ulceration → secondary infection [4] |
| Fibrosis | Chronic inflammation → replacement of vascular cushion with fibrous tissue → hard, non-reducible mass [4] |
| Portal pyaemia | Extremely rare but life-threatening — thrombosed haemorrhoidal veins (draining into portal system above dentate line) → septic thrombophlebitis → portal venous bacteraemia → liver abscesses [4] |
| Iron deficiency anaemia | Chronic low-grade bleeding from haemorrhoids → iron depletion over months/years |
| Complication | Pathophysiology |
|---|---|
| Chronicity | Failure of the acute fissure to heal (> 6 weeks) → development of the chronic fissure triad: sentinel skin tag (external), hypertrophied anal papilla (internal), and exposed internal sphincter fibres at the base of the fissure [4] |
| Abscess and fistula | Deep chronic fissure can become a portal of entry for infection → perianal abscess → fistula-in-ano (especially if secondary cause like Crohn's) |
| Faecal avoidance and constipation | Pain on defecation → patient avoids opening bowels → harder stools → worsens the fissure on next attempt → vicious cycle |
| Complication | Pathophysiology | Clinical Presentation |
|---|---|---|
| Bowel obstruction | Tumour growth narrows the lumen → partial then complete obstruction. More common with left-sided tumours (narrower lumen, solid stool). Circumferential "napkin-ring" lesions are the classic culprits | Colicky abdominal pain, distension, vomiting, absolute constipation. If competent ileocaecal valve → closed-loop obstruction → risk of caecal perforation |
| Perforation | Tumour erodes through the bowel wall, or ischaemic necrosis of the tumour itself, or perforation proximal to an obstructing lesion (caecal blow-out from closed-loop obstruction) | Acute abdomen, peritonitis, septic shock. Rigidity, guarding, rebound tenderness [16] |
| Fistula formation | Tumour invades adjacent organs → rectovesical fistula (faecaluria, pneumaturia, recurrent UTI), rectovaginal fistula (feculent vaginal discharge) [5][16] | |
| Local invasion | Direct extension into: sacral nerves → intractable pelvic pain; bladder trigone → LUTS; ureter → hydroureter/hydronephrosis [5] | |
| Metastatic disease | Liver (most common — via portal venous drainage) → jaundice, RUQ pain, hepatomegaly. Lung → SOB, cough. Peritoneum → ascites. Bone → pain. Brain → neurological deficits [5] | |
| Iron deficiency anaemia | Chronic occult blood loss from tumour surface erosion → progressive iron depletion | May be the presenting feature of right-sided CRC |
| Complication | Pathophysiology |
|---|---|
| Toxic megacolon | Severe colitis → inflammation extends beyond mucosa into muscle layer → loss of muscular tone → massive non-obstructive colonic dilatation (≥ 6 cm transverse colon or > 9 cm caecum) + systemic toxicity (fever > 38°C, HR > 120, anaemia, hypoalbuminaemia). More common in UC but can occur in Crohn's colitis [17]. AXR shows grossly dilated colon (3-6-9 rule) with thumbprinting. Risk of perforation. Mx: bowel rest, IV steroids, broad-spectrum Abx; 50% require urgent colectomy [17] |
| Fulminant colitis | Severe acute flare: > 10 bloody stools/day, continuous bleeding, abdominal pain and distension, fever, anorexia. High risk of progressing to toxic megacolon [16a] |
| Perforation | Most commonly as a consequence of toxic megacolon. Associated with high mortality [16a] |
| Stricture | Repeated inflammation → fibrosis → luminal narrowing → obstruction. Should be considered malignant until proven otherwise by endoscopy with biopsy [16a] |
| Colorectal cancer | Chronic mucosal inflammation → dysplasia → carcinoma sequence. Risk increases with ↑ extent and ↑ duration of colitis (pancolitis > left-sided). Time frame: ~8–10 years after onset in extensive disease [17]. Requires surveillance colonoscopy |
| Malnutrition | Poor intake + protein-losing enteropathy + malabsorption → weight loss, vitamin deficiencies (B12, folate, iron), coagulopathy, osteomalacia [17] |
| Perianal disease (Crohn's) | Anal fissures (20%), perianal fistulae (20–30%), anorectal abscesses (~50%) [17] |
| Severe haemorrhage | Up to 10% of Crohn's patients; may require urgent colectomy [17] |
| Complication | Pathophysiology |
|---|---|
| Transmural necrosis | Prolonged ischaemia → full-thickness bowel wall infarction (occurs in ~15% — the majority have only mucosal/submucosal injury with reperfusion recovery) [6] |
| Perforation and peritonitis | Necrotic bowel loses structural integrity → perforation → faecal peritonitis → septic shock |
| Stricture | Ischaemic injury heals with fibrosis → luminal narrowing → chronic obstruction |
| Sepsis and MODS | Bacterial translocation across damaged mucosa → systemic sepsis → organ failure |
3. Complications of Treatment (Iatrogenic)
| Phase | Complication | Mechanism |
|---|---|---|
| Pre-operative | Sedation-related: hypoxaemia, respiratory depression, aspiration pneumonia, hypotension, cardiac arrhythmia, AMI [16b] | Most frequent complication class; due to benzodiazepines/opioids used for sedation |
| Bowel preparation: fluid and electrolyte disturbances, nausea/vomiting [16b] | Large-volume PEG solutions cause fluid shifts | |
| Intra-operative | Bleeding: from biopsy site or polypectomy site | Disruption of submucosal vessels; usually self-limited |
| Perforation: most feared complication | Mechanical (scope tip), barotrauma (air insufflation), or thermal (electrocautery during polypectomy). Gas insufflation through a perforation → pneumoperitoneum → abdominal compartment syndrome [16b] | |
| Post-operative | Delayed bleeding (typically day 5–7) | Sloughing of the coagulation eschar that was covering a blood vessel after polypectomy [16b] |
| Post-polypectomy syndrome | Electrocoagulation injury → transmural burn → focal peritonitis without frank perforation. Presents with fever, focal tenderness, leucocytosis 1–5 days post-polypectomy [16b]. Usually managed conservatively (NPO, IV antibiotics) |
| Modality | Complication |
|---|---|
| Adrenaline injection | Rebleeding after absorption (~1h); rarely systemic effects (tachycardia, hypertension) if large volume absorbed |
| Thermal (heat probe, APC) | Perforation — thermal injury penetrates too deep, especially in thin-walled structures (caecum, right colon). APC is safer (↓ energy depth) but not risk-free [3a][5a] |
| Haemoclips | Clip displacement → rebleeding; rarely perforation from mechanical pressure |
| Band ligation (RBL) | Pain, bleeding 7–10 days post-banding due to sloughing of ligated tissue. Contraindicated in patients on anticoagulants or immunocompromised [7]. Post-banding sepsis (rare but life-threatening) |
| Complication | Mechanism |
|---|---|
| Intestinal ischaemia/infarction | Embolisation material occludes not only the target vessel but also collateral supply → downstream bowel ischaemia. Risk is higher with non-super-selective embolisation [3] |
| Arterial dissection or perforation | Catheter manipulation in diseased (atherosclerotic) vessels |
| Contrast nephropathy | Iodinated contrast → direct tubular toxicity + renal vasoconstriction → AKI. Risk factors: pre-existing CKD, diabetes, dehydration |
| Groin haematoma / pseudoaneurysm | Arterial puncture site complications |
| Rebleeding | Target vessel recanalises or collateral pathways open → bleeding recurs |
These apply to segmental colectomy, subtotal colectomy, low anterior resection, APR, and Hartmann's procedure — the operations performed for bleeding-related conditions (diverticular disease, CRC, IBD, etc.).
Immediate / Intra-operative:
- General anaesthetic risks
- Bleeding: injury to spleen (splenic flexure mobilisation in TME), presacral venous plexus, major vessels [13]
- Injury to neighbouring structures: left ureter and gonadal vessels, iliac artery, duodenum, bladder, seminal vesicles, autonomic nerve injury (especially in rectal surgery) [13]
- Sympathetic nerve injury → urinary incontinence, impaired ejaculation
- Parasympathetic nerve injury → urinary retention, erectile dysfunction [13]
Early ( < 30 days):
- Surgical site infection (5–15%) [16]
- Post-operative ileus — temporary impairment of bowel motility after abdominal surgery; resolves spontaneously in most cases [16]
- Anastomotic leakage — classically on day 4–7 [5]. Incidence: 1–5% overall but up to 10% in low anterior resection (ileoileal < ileocolic < colocolic < ileoanal) [5]. Risk factors: liver/renal impairment, steroid use, suboptimal bowel condition, emergency surgery, surgeon experience. Presents as diffuse feculent peritonitis + septic shock (free leak) or abscess/enterocutaneous fistula (contained leak) [5][16]
- DVT/PE (immobilisation-related)
- Early stoma complications: stomal bleeding, stomal necrosis, stomal retraction, mucocutaneous separation, skin irritation and dermatitis (most common in ileostomy due to high-output alkaline enzymatic effluent) [16]
Late ( > 30 days):
- Anastomotic stricture — may require finger dilatation (low anastomosis) or endoscopic balloon dilatation (high anastomosis) [16]
- Fistula: enterocutaneous (most close spontaneously), rectovaginal/rectourinary (require proximal faecal diversion) [16]
- Late stoma complications: parastomal hernia, stomal prolapse, stomal stenosis [16]
- Low anterior resection (LAR) syndrome: change in bowel movement (frequency, urgency, faecal incontinence) persisting ≥ 1 month after surgery due to colonic dysmotility, neorectal reservoir dysfunction, and anal sphincter dysfunction [13]. Prevention: post-op pelvic floor muscle exercise [13]. Management: antidiarrhoeal, transanal irrigation, pelvic floor rehab, sacral nerve stimulation [13]
- Anterior resection syndrome — encompasses fecal frequency, urgency, clustering, and incontinence after rectal resection [16]
| Timing | Complication | Mechanism/Details |
|---|---|---|
| Early | Pain (~100%) | Due to internal anal sphincter (IAS) spasm [7] |
| Urinary retention | Multifactorial: pain → reflex sphincter spasm, fluid overload, rectal packing, drugs (narcotics, anticholinergics), pre-existing outflow tract obstruction. Mx: urinary catheter for 24h [7] | |
| Reactionary haemorrhage | Bleeding within 24h, usually from slipped ligature | |
| Late | Secondary haemorrhage | Bleeding at 7–14 days due to infection and sloughing of tissue |
| Faecal incontinence | Injury to internal or external anal sphincter during excision [7] | |
| Anal stenosis | Excessive tissue excision, especially if circumferential. This is why the 3-leaf clover technique preserves mucosal bridges [7] | |
| Anal fissure | Post-operative scarring narrows the anal canal → hard stools tear the anoderm |
| Category | Key Complications |
|---|---|
| Bleeding itself | Hypovolaemic shock (Classes I–IV), symptomatic anaemia (acute and chronic/iron deficiency), massive transfusion complications (hyperkalaemia, hypocalcaemia, hypothermia, dilutional coagulopathy, TRALI, TACO) |
| Diverticular disease | Recurrent bleeding, diverticulitis, abscess, perforation/peritonitis, fistula (colovesical MC), stricture/obstruction |
| Haemorrhoids | Strangulation/thrombosis, gangrene, ulceration, fibrosis, portal pyaemia, iron deficiency anaemia |
| Anal fissure | Chronicity, abscess/fistula, faecal avoidance/constipation cycle |
| CRC | Obstruction, perforation, fistula, local invasion, metastases (liver, lung, peritoneum, bone), iron deficiency anaemia |
| IBD | Toxic megacolon, fulminant colitis, perforation, stricture, CRC (long-term), malnutrition, perianal disease, severe haemorrhage |
| Ischaemic colitis | Transmural necrosis, perforation, stricture, sepsis/MODS |
| Colonoscopy | Sedation-related, bowel prep side effects, perforation, bleeding, post-polypectomy syndrome |
| Endoscopic Rx | Rebleeding (adrenaline), perforation (thermal), post-RBL bleeding/sepsis |
| TAE | Intestinal ischaemia, contrast nephropathy, arterial complications, rebleeding |
| Colorectal surgery | Anastomotic leak (day 4–7), infection, ileus, stoma complications, autonomic nerve injury, LAR syndrome |
| Haemorrhoidectomy | Pain, urinary retention, faecal incontinence, anal stenosis, secondary haemorrhage |
High Yield Summary — Complications of Rectal Bleeding
From the bleeding: Hypovolaemic shock (tachycardia → hypotension → confusion → oliguria → death). Symptomatic anaemia (acute: syncope, chest pain; chronic: iron deficiency with koilonychia, glossitis). Massive transfusion complications (lethal triad of hypothermia + acidosis + coagulopathy; hyperkalaemia, hypocalcaemia, TRALI).
From the underlying cause: Always think about what happens if you DON'T treat the disease. CRC → obstruction, perforation, metastases. Diverticular disease → recurrent bleeding (14–38%), diverticulitis, abscess, perforation, fistula. IBD → toxic megacolon (3-6-9 rule on AXR), fulminant colitis, long-term CRC risk. Haemorrhoids → strangulation, thrombosis, gangrene.
From treatment: Colonoscopy perforation is the most feared complication. Anastomotic leak classically presents day 4–7 with sepsis. Haemorrhoidectomy → pain (100%), urinary retention, faecal incontinence, anal stenosis. Post-RBL bleeding at 7–10 days. TAE → intestinal ischaemia. Blind segmental resection → 75% rebleeding rate.
Key exam numbers: Anastomotic leak 1–5% (up to 10% in LAR). Haemorrhoidectomy efficacy 95%. RBL: 70% resolve, 30% recur. Diverticular rebleeding 14–38%. Toxic megacolon: 50% respond to medical Rx, 50% need urgent colectomy.
Active Recall — Complications of Rectal Bleeding
References
[3] Senior notes: Ryan Ho Fundamentals.pdf (p281–286, "Lower GI Bleeding") [3a] Senior notes: Ryan Ho Fundamentals.pdf (p255, "Endoscopic Tx Modalities") [4] Senior notes: felixlai.md (Haemorrhoid complications section 1097; Anal fissure section 1100) [5] Senior notes: Ryan Ho GI.pdf (p160, "Diverticular Bleeding Prognosis"; p175, "Complications of Colorectal Resection") [5a] Senior notes: Ryan Ho GI.pdf (p45, "Endoscopic Tx Modalities") [6] Senior notes: Ryan Ho GI.pdf (p146, "Ischaemic Colitis") [7] Senior notes: maxim.md (Haemorrhoidectomy complications, sections 230–231) [8a] Senior notes: maxim.md (Diverticular disease complications, section 194; Hartmann's operation, section 198) [13] Senior notes: maxim.md (Post-operative complications of CRC surgery, LAR syndrome, section 226–227) [16] Senior notes: felixlai.md (Colorectal surgery complications, sections 1022, 1035) [16a] Senior notes: felixlai.md (UC complications, sections 986–987) [16b] Senior notes: felixlai.md (Colonoscopy complications, sections 133–134; Post-polypectomy complications, section 1047) [17] Senior notes: Ryan Ho GI.pdf (p122, "Complications of IBD — Crohn's and UC")
High Yield Summary
Definition: Rectal bleeding = passage of blood per rectum. LGIB = bleeding distal to the ligament of Treitz. 10–15% of haematochezia may be from an upper GI source.
Most Common Causes by Age:
- < 50 years: Haemorrhoids, anal fissure
-
65 years: Diverticular disease (most common overall cause of LGIB), angiodysplasia
Murtagh's Framework:
- Probability: Haemorrhoids, fissure, polyp, diverticular disease
- Serious: Ischaemic colitis, angiodysplasia, CRC, IBD, intussusception
- Pitfalls: Rectal prolapse, anal trauma, villous adenoma
- Rarities: Meckel's diverticulum, solitary rectal ulcer
Character of Blood:
- On surface/paper = anorectal
- Mixed with stool = above sigmoid
- By itself (torrential) = diverticular disease, angiodysplasia
- Blood + mucus = rectal tumour or proctitis
- Melaena = upper GI
Key Anatomy:
- Dentate line: above = painless (autonomic), below = painful (somatic)
- Haemorrhoid positions: 3, 7, 11 o'clock
- Watershed areas: Griffiths' point (splenic flexure), Sudeck's point (rectosigmoid)
- Asian diverticula are predominantly right-sided
Red Flags for CRC: Age > 50, change in bowel habit, pencil-thin stools, tenesmus, constitutional symptoms, family history, iron deficiency anaemia.
DRE is mandatory — 80% of rectal tumours are within fingertip range. Always exclude other causes even when haemorrhoids are found.
High Yield Summary — Differential Diagnosis of Rectal Bleeding
Murtagh's framework: Probability (haemorrhoids, fissure, polyp, diverticular disease) → Serious (ischaemic colitis, angiodysplasia, anticoagulants, infections, CRC, lymphoma, villous adenoma, IBD, intussusception) → Pitfalls (rectal prolapse, anal trauma, villous adenoma) → Rarities (Meckel's, solitary rectal ulcer).
By age: Young → haemorrhoids/fissure. > 55 → must investigate colon. Elderly → diverticular disease, angiodysplasia, CRC, ischaemic colitis.
By bleeding pattern: Outlet-type → anorectal. Mixed with stool → proximal colon. Torrential by itself → diverticular/angiodysplasia. Blood + mucus → rectal tumour/proctitis. Melaena → upper GI.
Don't-miss rules: (1) 10–15% of haematochezia is from UGIB. (2) CRC must be excluded in patients > 55 with new bleeding. (3) 80% rectal tumours are within fingertip reach. (4) Haemorrhoids don't explain away bleeding — always exclude other sources. (5) In cirrhotics, not all bleeding is variceal — do OGD. (6) Right side bleeds, left side blocks (CRC). (7) Anticoagulant-related bleeding still needs investigation for the underlying lesion.
High Yield Summary — Diagnosis of Rectal Bleeding
Three priorities: Resuscitate → Localise → Stop bleeding.
First step in all patients: History + DRE + Proctoscopy. These alone can diagnose haemorrhoids, fissure, and low rectal masses.
Colonoscopy is the gold standard (diagnostic yield 75–90%) but needs bowel prep and a stable patient. Perform within 24h for acute LGIB.
Always exclude UGIB in massive haematochezia — OGD before CLN, or NG aspirate to screen.
Unstable + massive bleed → CTA or mesenteric angiography (can also embolise).
Occult/intermittent bleed → Tagged RBC scan (most sensitive at 0.1–0.4 mL/min) → if positive, angiography for localisation.
BUN:Cr ratio: > 30:1 suggests upper GI source (digested blood → urea absorbed). Normal in LGIB.
Hb may be normal initially in acute bleeding — serial monitoring essential.
CEA is NOT for screening CRC — use for pre-op baseline and post-op surveillance.
Murtagh's key investigations: FBE, ESR, stool M&C, FOBT, colonoscopy. Consider AXR, CT colonography, angiography, small bowel enema.
High Yield Summary — Management of Rectal Bleeding
Three priorities: Resuscitate → Localise → Stop bleeding.
Resuscitation: NPO, 2 large-bore IV, crystalloid then blood if needed. Stop anticoagulants. Monitor: shock chart hourly, Foley catheter (UO ≥ 0.5 mL/kg/h), prevent hypothermia. Transfuse if profuse bleeding, persistent instability, symptomatic anaemia, or ACS with low Hb.
Endoscopic haemostasis is first-line: dual therapy (adrenaline + clip/thermal/band). APC is ideal for angiodysplasia and radiation proctitis. Clips/band for diverticular bleeding. Never use adrenaline alone.
TAE if endoscopy fails or patient too unstable for colonoscopy. Equally effective as surgery with fewer complications.
Surgery in 15–20%: indications = haemodynamic instability despite resuscitation, > 6 units transfused, frequent rebleeding, failed endoscopic/IR therapy. Always try to localise pre-operatively — blind segmental resection has 75% rebleeding rate.
Haemorrhoids: Conservative for all → RBL for Grade II/III → Haemorrhoidectomy for Grade III/IV or refractory. 3-leaf clover excision, avoid circumferential excision (stenosis).
Anal fissure: Fibre + sitz bath + topical GTN/nifedipine → Botox or lateral internal sphincterotomy if fails 8 weeks.
Cirrhotic bleeding: Conservative Hb target (7–8 g/dL), terlipressin 1st line, prophylactic antibiotics 7 days, emergency OGD. TIPS if endoscopy fails.
High Yield Summary — Complications of Rectal Bleeding
From the bleeding: Hypovolaemic shock (tachycardia → hypotension → confusion → oliguria → death). Symptomatic anaemia (acute: syncope, chest pain; chronic: iron deficiency with koilonychia, glossitis). Massive transfusion complications (lethal triad of hypothermia + acidosis + coagulopathy; hyperkalaemia, hypocalcaemia, TRALI).
From the underlying cause: Always think about what happens if you DON'T treat the disease. CRC → obstruction, perforation, metastases. Diverticular disease → recurrent bleeding (14–38%), diverticulitis, abscess, perforation, fistula. IBD → toxic megacolon (3-6-9 rule on AXR), fulminant colitis, long-term CRC risk. Haemorrhoids → strangulation, thrombosis, gangrene.
From treatment: Colonoscopy perforation is the most feared complication. Anastomotic leak classically presents day 4–7 with sepsis. Haemorrhoidectomy → pain (100%), urinary retention, faecal incontinence, anal stenosis. Post-RBL bleeding at 7–10 days. TAE → intestinal ischaemia. Blind segmental resection → 75% rebleeding rate.
Key exam numbers: Anastomotic leak 1–5% (up to 10% in LAR). Haemorrhoidectomy efficacy 95%. RBL: 70% resolve, 30% recur. Diverticular rebleeding 14–38%. Toxic megacolon: 50% respond to medical Rx, 50% need urgent colectomy.
Palpitations
Palpitations are the subjective awareness of one's own heartbeat, often perceived as rapid, irregular, or forceful cardiac contractions.
Shortness Of Breath
Shortness of breath, or dyspnea, is the subjective sensation of difficulty or discomfort in breathing, arising from cardiovascular, pulmonary, neuromuscular, or psychogenic causes that increase ventilatory demand or impair gas exchange.