Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Stabilise lower gastrointestinal bleeding, distinguish minor self-limited bleeding from major or unstable haemorrhage, and sequence CT angiography, colonoscopy, embolisation and follow-up without assuming every fresh bleed is anorectal.
Lower gastrointestinal bleeding usually arises distal to the ileocaecal valve but clinical presentation overlaps upper and small-bowel sources. Haematochezia is fresh or maroon blood passed per rectum; severe upper bleeding can transit rapidly, while slow right-colon bleeding can produce dark stool. Ask about quantity and recurrence, abdominal or anal pain, diarrhoea, change in bowel habit, weight, previous diverticular disease, IBD, radiotherapy, endoscopy and vascular disease. Medicine history must specify warfarin, direct oral anticoagulant, antiplatelets, NSAIDs and exact last dose. Examine perfusion, abdomen, groins and anus, and perform a consented rectal examination when it will assess blood, mass or anorectal source.
Risk stratification controls the route. The BSG defines instability using shock index above one as a practical marker and recommends CT angiography when an unstable patient is suspected of active bleeding. Positive arterial extravasation leads urgently to catheter angiography and embolisation where available; surgery is reserved for uncontrolled haemorrhage after localisation and multidisciplinary discussion. If CTA is negative and haemodynamics remain concerning, an upper source needs investigation. In stable disease, the Oakland score helps separate a minor self-terminating bleed from a major bleed, but comorbidity, social reliability, anticoagulation and clinician concern modify disposition.
Diverticular arterial rupture and colonic angioectasia commonly cause painless overt bleeding, particularly in older adults taking antithrombotic medicines.
Haemorrhoids and fissures produce bright-red blood, but visible anorectal disease should not automatically explain anaemia or persistent change.
Colitis, colorectal cancer, post-polypectomy injury and other lesions bleed through mucosal inflammation, ulceration or tumour friability.
Arterial rupture, inflammatory ulceration or tumour erosion releases blood into the colon or rectum before distal passage.
Rapid passage preserves a bright or maroon appearance, while site and transit determine whether blood coats, mixes with or precedes stool.
Ongoing loss reduces circulating volume and oxygen delivery, with initial haemoglobin sometimes remaining deceptively normal before redistribution.
Ongoing large-volume blood with shock index above one, syncope, hypotension, cool peripheries, oliguria or raised lactate indicates major active bleeding and supports immediate resuscitation and CT angiography.
Sudden painless substantial haematochezia in an older adult with diverticulosis supports a diverticular arterial source. Bleeding often stops spontaneously but can recur, and other causes still need exclusion.
Abrupt cramping abdominal pain followed by bloody diarrhoea, often left sided and after hypotension or with vascular disease, raises colonic ischaemia. Peritonism, acidosis or right-sided disease increases concern for transmural injury.
Blood mixed with diarrhoea, urgency, fever and abdominal pain supports colitis. Travel, antibiotic, immunosuppression and chronicity distinguish infection, C difficile and IBD and determine sampling before immunosuppression.
Persistent or intermittent blood with altered bowel habit, weight loss, iron-deficiency anaemia or a mass requires the current FIT-supported suspected-cancer pathway even if bleeding seems minor.
Bright blood on paper or coating stool with anal pain, prolapse or itching suggests fissure or haemorrhoid. Anaemia, weight loss, blood mixed through stool or a bowel-pattern change prevents premature closure.
Instability, melaena, haematemesis, cirrhosis or no lower source after angiography should prompt urgent upper-GI assessment and endoscopy.
Blood on paper or dripping after stool with clear fissure or haemorrhoids supports a distal source, but alarm features require further investigation.
Bloody diarrhoea with chronic inflammatory features suggests IBD, whereas abrupt cramping after hypotension or vascular stress favours ischaemic colitis.
Large-volume bleeding causes syncope, hypotension and organ hypoperfusion, requiring localisation by CT angiography when ongoing and unstable.
Chronic or recurrent loss causes iron deficiency, fatigue and myocardial supply-demand imbalance, especially in older people with cardiovascular disease.
Assuming diverticula or haemorrhoids are causal can delay cancer or inflammatory diagnosis, while untreated vascular lesions often bleed again.
A high-rate upper gastrointestinal bleed can cross the bowel before blood is digested, producing maroon or fresh stool. Shock with haematochezia should always keep an upper source alive.
Angiographic techniques detect bleeding occurring during acquisition. Intermittent haemorrhage can yield a negative study, so physiological recurrence should trigger renewed localisation rather than false certainty.
A low score identifies patients more likely to be safe for outpatient care, but comorbidity, continued bleeding, anticoagulation and reliable access to urgent investigation remain decisive.
Distal bleeding disease is common and visible, which makes it an attractive stopping point. It can coexist with proximal cancer, IBD or angioectasia and does not explain unexplained anaemia automatically.
Colonic watershed areas are vulnerable after a low-flow episode. Pain followed by blood after hypotension may represent ischaemic colitis even without a large arterial occlusion.
Assuming fresh rectal blood proves a lower source in a shocked patient without considering brisk upper bleeding.
Sending an unstable active bleed for routine colonoscopy preparation instead of urgent CT angiography.
Using a low Oakland score as an automatic discharge order despite ongoing bleeding or unsafe follow-up.
Attributing anaemia and bowel-pattern change to haemorrhoids because they are visible on examination.
Reversing or withholding antithrombotic therapy without recording the indication, thrombosis risk and restart owner.
Proceeding to surgery for unlocalised bleeding without endoscopic and radiological multidisciplinary planning when feasible.
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A patient has ongoing large-volume haematochezia, pulse 120 and systolic blood pressure 95 despite initial resuscitation. Which investigation best localises active bleeding rapidly under the BSG pathway?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Causes have characteristic but overlapping patterns. Diverticular haemorrhage is often painless; angioectasia is recurrent and may be occult; cancer causes change, iron deficiency or intermittent blood; IBD and infection cause diarrhoea and urgency; ischaemic colitis causes acute pain followed by blood, often after hypotension or with vascular risk. Colonoscopy diagnoses mucosa and provides some haemostasis but requires preparation and may miss intermittent small-bowel bleeding. Follow-up must address histology, cancer exclusion, iron deficiency and medicine restart even when bleeding stops spontaneously. A visible haemorrhoid is not a universal causal diagnosis.
Reversal increases thrombosis risk and is not identical for each drug. Confirm last dose and renal function, involve haematology, and create a documented restart decision after bleeding control.
The first haemoglobin may be misleading. Avoid both under-resuscitation and unnecessary over-transfusion, monitor calcium and temperature during major transfusion, and individualise coronary and heart-failure risk.