Gastrointestinal Bleeding

Gastrointestinal (GI) bleeding is one of the most common medical emergencies you will meet on the wards, in the emergency department, and in exams. A patient who vomits bright red blood or passes black tarry stool can look deceptively stable one moment and be in profound shock the next. The skill that separates a safe clinician from an unsafe one is not knowing every rare cause — it is the disciplined sequence of resuscitate first, localise the bleed, stop it, and prevent recurrence. Get that order right and most patients do well. Get it wrong and a treatable ulcer becomes a preventable death.

This page teaches you to think about GI bleeding the way a gastroenterologist does: divide it into upper and lower, recognise the pattern from the history, stabilise the circulation before you reach for the endoscope, and understand why flexible endoscopy transformed a once-blind, often-fatal problem into something we can see and treat directly.

Learning Objectives

• Distinguish upper GI bleeding (UGIB) from lower GI bleeding (LGIB) by presentation and anatomy.
• List the major causes of each and recognise which are life-threatening.
• Apply a structured resuscitation approach (ABC, fluids, transfusion thresholds, reversal of anticoagulation).
• Use risk scores (Glasgow-Blatchford, Rockall, AIMS65) to triage patients.
• Explain the role and timing of endoscopy, and the main endoscopic haemostatic techniques.
• Understand how the invention of flexible endoscopy changed the diagnosis and management of GI bleeding.

Quick Answer

GI bleeding is classified by its source relative to the ligament of Treitz (the duodenojejunal junction): bleeding above it is upper GI bleeding, below it is lower. Upper GI bleeding typically presents with haematemesis (vomiting blood) or melaena (black, tarry, foul stool) and is most often caused by peptic ulcers or oesophageal varices; lower GI bleeding usually presents with haematochezia (fresh red blood per rectum) from diverticulosis, angiodysplasia, haemorrhoids, or colitis. Management always begins with resuscitation — two large-bore IV cannulae, fluids, blood if needed, and correction of coagulopathy — before diagnostic manoeuvres. Endoscopy (upper endoscopy or colonoscopy) is both the key diagnostic and the main therapeutic tool. Risk scores guide who needs urgent intervention and who can be managed as an outpatient. Restrictive transfusion (target haemoglobin around 70 g/L in most patients) improves outcomes.

Where It Came From

For most of medical history, bleeding inside the gut was a black box. A physician could feel a rigid abdomen, watch a patient turn pale, and count a thready pulse — but could not see the source. Autopsy was the only way to learn where the blood had come from, and by then it was too late. The great nineteenth-century need was simple and desperate: to look inside a living person without cutting them open.

The first attempts were crude and often dangerous. In 1868 Adolf Kussmaul famously passed a rigid metal tube down the throat of a sword-swallower to inspect the stomach — a rigid gastroscope that could only be used on the unusually cooperative and could see very little. Rigid instruments dominated for decades: they were painful, offered a poor field of view, and risked perforating the very organ they were meant to examine.

The revolution came from fibre optics. In the 1950s, physicist Harold Hopkins and, crucially, Basil Hirschowitz at the University of Michigan realised that a bundle of thin glass fibres could carry a coherent image around bends. In 1957 Hirschowitz swallowed his own prototype fibre-optic endoscope — the first flexible gastroscope — proving it could be passed safely and steered through the curves of the oesophagus and stomach. This was the birth of modern endoscopy. Suddenly clinicians could directly visualise an ulcer or varix in a living, bleeding patient.

Two further leaps mattered for bleeding specifically. First, the addition of working channels allowed instruments — clips, injection needles, thermal probes — to be passed down the scope, so the endoscopist could not only see the bleeding point but treat it. Second, the charge-coupled device (CCD) video endoscope in the 1980s put the image on a screen, enabling teamwork, teaching, and recording. Together these turned endoscopy from a diagnostic curiosity into the therapeutic backbone of GI bleeding care — the reason mortality from bleeding ulcers fell dramatically over the late twentieth century.

Upper GI Bleeding: Pattern, Causes, and Danger Signs

Upper GI bleeding originates proximal to the ligament of Treitz — oesophagus, stomach, or duodenum. It is roughly four times more common than lower GI bleeding and carries higher mortality, especially when caused by varices.

How it presents. The classic signs are haematemesis and melaena. Fresh red haematemesis suggests brisk, active bleeding; "coffee-ground" vomit is blood altered by gastric acid, implying slower or stopped bleeding. Melaena — black, sticky, offensively smelling stool — results from bacterial and acid degradation of haemoglobin during gut transit and usually indicates an upper source (as little as 50 mL of blood can produce it). Beware: a very brisk upper bleed can transit fast enough to appear as red blood per rectum, and such a patient is often shocked.

Major causes:

• Peptic ulcer disease — the single commonest cause (roughly half of cases). Driven by Helicobacter pylori and NSAIDs. A posterior duodenal ulcer can erode the gastroduodenal artery and bleed torrentially.
• Oesophageal and gastric varices — dilated portosystemic collaterals from portal hypertension, almost always due to cirrhosis. These bleed massively and carry the worst prognosis; suspect them in any known alcoholic or cirrhotic patient.
• Mallory-Weiss tear — a mucosal laceration at the gastro-oesophageal junction after forceful retching or vomiting; often self-limiting.
• Erosive gastritis / oesophagitis, malignancy, and Dieulafoy lesion (an abnormally large submucosal artery that erodes through otherwise normal mucosa — a classic "brisk bleed with no obvious cause" answer in exams).

Worked example. A 58-year-old man on daily ibuprofen for back pain presents with two episodes of coffee-ground vomiting and black stools for a day. Pulse 108, BP 104/68, urea disproportionately raised relative to creatinine (blood is a protein meal digested and absorbed in the small bowel, raising urea). This picture — melaena, NSAID use, raised urea-to-creatinine ratio — points strongly to a bleeding peptic ulcer. He needs risk scoring, a proton-pump inhibitor, and upper endoscopy within 24 hours.

Lower GI Bleeding: Pattern and Causes

Lower GI bleeding arises distal to the ligament of Treitz — small bowel, colon, rectum, anus.

How it presents. The hallmark is haematochezia — fresh or maroon blood passed rectally. Bright red blood coating the stool or on the paper suggests a distal source (haemorrhoids, anal fissure); blood mixed through the stool suggests a more proximal colonic source.

Major causes:

• Diverticulosis — the commonest cause of significant LGIB, especially in older adults. Bleeding is typically painless, brisk, and often stops spontaneously.
• Angiodysplasia — fragile ectatic vessels, common in the elderly and associated with aortic stenosis and renal disease.
• Colorectal cancer and polyps — usually slower, chronic blood loss presenting with iron-deficiency anaemia; never dismiss rectal bleeding in an older patient without excluding malignancy.
• Colitis — infective, ischaemic, or inflammatory bowel disease (ulcerative colitis, Crohn's); bloody diarrhoea with pain and systemic upset.
• Haemorrhoids and anal fissures — common, usually minor, but a diagnosis of exclusion in significant bleeding.

Much LGIB is self-limiting, but a small proportion is massive and demands the same resuscitation-first discipline as UGIB.

Resuscitation: The First and Most Important Step

The exam and the bedside share one rule: treat the patient, not the endoscopy request. Regardless of source, the sequence is:

1. Assess and support Airway, Breathing, Circulation. A patient actively vomiting blood is at risk of aspiration — consider airway protection.
2. Two large-bore (14–16 G) IV cannulae and send bloods: full blood count, urea and electrolytes, liver function, coagulation, and group and crossmatch.
3. Fluid resuscitation with crystalloid to restore circulating volume while blood is prepared.
4. Transfuse red cells using a restrictive threshold — target haemoglobin around 70 g/L (or ~80 g/L in patients with cardiovascular disease). A landmark trial (Villanueva, 2013) showed restrictive transfusion reduced mortality compared with liberal transfusion, partly because over-transfusion in variceal bleeding raises portal pressure and worsens bleeding.
5. Correct coagulopathy. Reverse warfarin (vitamin K plus prothrombin complex concentrate for major bleeding), address direct oral anticoagulants with specific reversal agents where available, and give platelets or fresh frozen plasma per protocol in massive haemorrhage.
6. Specific drugs. For suspected variceal bleeding, start a vasoactive drug (terlipressin or octreotide) and prophylactic antibiotics before endoscopy — both reduce mortality. For suspected ulcer bleeding, a proton-pump inhibitor is commonly given, though its main proven benefit is after endoscopic therapy.

Only once the patient is stabilised do you proceed to definitive localisation and treatment.

Risk Stratification: Deciding Who Needs What, When

Scoring systems turn clinical gestalt into defensible decisions.

• Glasgow-Blatchford Score (GBS): uses pre-endoscopy data (urea, haemoglobin, BP, pulse, melaena, syncope, hepatic/cardiac disease). A score of 0–1 identifies very-low-risk patients who may safely avoid admission and have outpatient endoscopy. It is the best tool for deciding who can go home.
• Rockall Score: predicts rebleeding and mortality; the full version needs endoscopic findings.
• AIMS65: a quick mortality predictor (Albumin, INR, Mental status, Systolic BP, age over 65).

Endoscopy: Seeing and Stopping the Bleed

Endoscopy is the definitive tool. In UGIB, upper GI endoscopy (oesophagogastroduodenoscopy) within 24 hours of presentation is standard for stable patients after resuscitation; unstable patients need it sooner. In LGIB, colonoscopy (usually after bowel preparation) is the mainstay once the patient is stable.

Endoscopic haemostasis combines techniques for durability:

• Injection of dilute adrenaline (epinephrine) — causes vasoconstriction and tamponade; effective but must be combined with a second method, not used alone.
• Thermal — heater probe or bipolar coagulation to coagulate the vessel.
• Mechanical — through-the-scope clips that physically close the vessel; over-the-scope clips for larger lesions.
• Variceal band ligation — rubber bands strangle oesophageal varices; first-line for variceal bleeding.
• Sclerotherapy and tissue adhesives (cyanoacrylate glue) for gastric varices.

When endoscopy fails or bleeding recurs, escalate to interventional radiology (angiographic embolisation), transjugular intrahepatic portosystemic shunt (TIPS) for refractory variceal bleeding, or surgery as a last resort. A balloon tamponade tube (Sengstaken-Blakemore) is a temporising bridge in exsanguinating variceal haemorrhage.

Real-World Applications

• Emergency medicine: rapid ABC assessment and the "resuscitate before you investigate" reflex are drilled precisely because GI bleeds decompensate fast.
• General practice: recognising that painless rectal bleeding in an older adult warrants urgent colonoscopy to exclude cancer, not reassurance about "just piles."
• Chronic disease management: counselling patients on NSAID and anticoagulant risks, eradicating H. pylori, and using PPI co-prescription in high-risk patients prevents ulcer bleeds before they happen.
• Everyday relevance: anyone should know that black tarry stool is a red flag needing urgent assessment, not a dietary curiosity.

Common Mistakes

1. Rushing to endoscopy before resuscitation. Why wrong: an under-resuscitated, hypotensive patient can arrest during sedation and the procedure. Correction: stabilise the circulation first; endoscopy is safer and more successful on a resuscitated patient.
2. Over-transfusing. Why wrong: liberal transfusion increases mortality and, in variceal bleeding, raises portal pressure and provokes further bleeding. Correction: use a restrictive threshold (~70 g/L) unless the patient is actively exsanguinating or has significant cardiac disease.
3. Assuming all rectal blood is a lower GI source. Why wrong: a brisk upper GI bleed can present as haematochezia, and these patients are often shocked. Correction: in an unstable patient with red rectal bleeding, actively consider and exclude an upper source (e.g. nasogastric aspirate or upper endoscopy first).
4. Using adrenaline injection alone for an ulcer. Why wrong: it achieves temporary tamponade but has a high rebleed rate. Correction: always combine injection with a second modality (thermal or clip).

Comparison and Connections

Feature	Upper GI Bleeding	Lower GI Bleeding
Source	Proximal to ligament of Treitz	Distal to ligament of Treitz
Typical presentation	Haematemesis, melaena	Haematochezia
Commonest cause	Peptic ulcer disease	Diverticulosis
Urea-to-creatinine ratio	Often raised	Usually normal
First-line endoscopy	Upper GI endoscopy	Colonoscopy
Overall frequency/mortality	More common, higher mortality	Less common, often self-limiting

Note that melaena signals an upper (or occasionally small-bowel/right-colon) source, whereas haematochezia usually signals a lower source — but a fast upper bleed blurs this line. Variceal bleeding is a distinct entity within UGIB requiring vasoactive drugs, antibiotics, and band ligation rather than the ulcer pathway.

Practice Questions

Recall

Q: What anatomical landmark separates upper from lower GI bleeding? A: The ligament of Treitz (the duodenojejunal junction). Bleeding proximal to it is upper GI; distal is lower GI.

Understanding

Q: Why is the blood urea often disproportionately raised in upper GI bleeding? A: Blood in the gut lumen is a protein meal; it is digested and absorbed in the small intestine, and the nitrogen load is metabolised to urea, raising the urea level relative to creatinine (which is unaffected).

Application

Q: A cirrhotic patient presents with large-volume haematemesis and is tachycardic and hypotensive. After starting resuscitation, which two drug classes should you give before endoscopy, and why? A: A vasoactive agent (terlipressin or octreotide) to lower portal pressure and reduce variceal bleeding, and prophylactic antibiotics — both are proven to reduce mortality in variceal haemorrhage.

Analysis

Q: A stable patient with melaena has a Glasgow-Blatchford Score of 0. What does the evidence support, and what is the reasoning? A: Very-low-risk patients (GBS 0–1) can be safely managed with outpatient endoscopy rather than admission, because their risk of needing intervention or dying is minimal. This spares hospital resources without compromising safety — provided reliable follow-up exists and no other concern (e.g. comorbidity, social factors) mandates admission.

FAQ

Is black stool always GI bleeding? No. Iron tablets and bismuth (e.g. Pepto-Bismol) turn stool black, and beetroot or blueberries can darken it. True melaena is tarry, sticky, and has a distinctive foul smell. When in doubt, it should be assessed.

How much blood loss is dangerous? As little as 50 mL can produce melaena. Significant haemodynamic change (tachycardia, then hypotension) usually appears after losing 15% or more of blood volume — but young, fit patients compensate well and can crash suddenly, so normal early vital signs are reassuring but not conclusive.

Why give a proton-pump inhibitor? A stable clot forms better in a less acidic environment. The clearest proven benefit of high-dose PPI is after endoscopic treatment of a bleeding ulcer, where it reduces rebleeding. Pre-endoscopy PPI is common practice but its independent benefit is smaller.

Does everyone with a GI bleed need endoscopy? Most significant bleeds do, both to diagnose and to treat. Very-low-risk patients (e.g. GBS 0) may have it done as an outpatient. Minor, obviously anal bleeding (small haemorrhoids) in a young patient may need only clinical assessment.

What if endoscopy can't find or stop the bleed? Escalate: repeat endoscopy, angiographic embolisation by interventional radiology, TIPS for refractory variceal bleeding, or surgery as a last resort. Obscure small-bowel bleeding may need capsule endoscopy or CT angiography.

Quick Revision

• Upper vs lower GI bleeding is divided by the ligament of Treitz.
• UGIB: haematemesis/melaena; commonest cause peptic ulcer; worst prognosis with varices.
• LGIB: haematochezia; commonest cause diverticulosis.
• Resuscitate before you investigate: ABC, two large-bore lines, crossmatch, fluids.
• Restrictive transfusion — aim Hb ~70 g/L; over-transfusion worsens outcomes.
• Variceal bleed: add terlipressin/octreotide + antibiotics before scope; treat with band ligation.
• Glasgow-Blatchford 0–1 = safe for outpatient management.
• Endoscopy diagnoses and treats: injection + thermal/clip for ulcers; bands for varices.
• Flexible fibre-optic endoscopy (Hirschowitz, 1957) made direct visualisation and treatment possible.

Related Topics

Prerequisites

• Gastroenterology overview
• Anatomy of the gastrointestinal tract — see Anatomy

Related Topics

• Portal hypertension and cirrhosis — see Gastroenterology
• Peptic ulcer disease and H. pylori
• Shock and fluid resuscitation — see Emergency Medicine
• Transfusion and coagulopathy — see Hematology

Next Topics

• Inflammatory bowel disease
• Colorectal cancer screening — see Oncology