Gastrointestinal bleeding

• Gastrointestinal (GI) bleeding is bleeding from anywhere in the gut, from mouth to anus. It is best split at the ligament of Treitz: bleeding proximal to it is upper GI bleeding, distal to it is lower GI bleeding.
• It declares itself in three classic ways: vomiting blood (haematemesis), black tarry stools (melena), or red blood from the rectum (haematochezia). Occult bleeding is hidden and is found only on testing.
• The commonest cause overall is peptic ulcer disease for upper bleeding and diverticular disease for lower bleeding.
• Most patients need two large intravenous lines, resuscitation, blood tests, and an endoscopy, usually within 24 hours.
• The guiding principles are a restrictive transfusion threshold (haemoglobin under 7 g/dL, under 8 g/dL if there is cardiovascular disease), early endoscopy after stabilisation, and treatment of the cause to prevent recurrence.

By the end of this page you should be able to:

1. Define upper and lower GI bleeding, explain the ligament of Treitz boundary, and describe haematemesis, melena, haematochezia, occult and obscure bleeding.
2. List the common causes of upper and lower bleeding and recognise the one or two features that separate them.
3. Carry out the initial assessment: airway, circulation, resuscitation, blood tests, and risk scoring.
4. Choose the right investigation and its timing for upper, lower and obscure bleeding.
5. Manage non-variceal and variceal upper bleeding, and lower bleeding, including when to escalate.
6. Plan long-term management by cause and restarting antithrombotic drugs.
7. Recognise what to do when endoscopy and blood products are limited.

GI bleeding is one of the commonest emergencies in medicine. It is not a single disease: it is a presentation with a long list of causes, and the clinician's first job is to decide where the bleeding is, how fast it is, and how unwell the patient is, then to stop it and prevent it coming back. ^{[2] [4]}

Acute GI bleeding in the United States accounts for roughly 1.7 million emergency department visits each year, about two-thirds upper and one-third lower. In hospital terms, acute upper bleeding occurs in about 67 per 100 000 people and lower bleeding in about 36 per 100 000. ^{[2] [3]} At least 400 000 hospital admissions a year in the United States follow from GI bleeding. ^[3]

Despite improved care, mortality remains significant: upper bleeding carries a mortality of roughly 2 to 10 percent, lower bleeding roughly 2 to 9 percent, and much of this is not from the bleed itself but from old age and other illnesses. ^{[1] [2]}

The ligament of Treitz is a practical boundary, not just an anatomical one: a standard gastroscope reaches it, and a paediatric colonoscope can be advanced through it, so it marks the limit of what upper endoscopy can see. ^[2]

The clinical picture tells you where to look:

• Haematemesis is vomiting blood. It means upper bleeding. Fresh red blood means brisk bleeding; "coffee ground" vomit means blood that has been in the stomach long enough to be altered by acid.
• Melena is black, tarry, foul-smelling stool. It means digested blood from an upper source and is the classic sign of upper bleeding.
• Haematochezia is bright red or maroon blood per rectum. It usually means lower bleeding, but a massive or very rapid upper bleed can also present this way because the blood does not stay in the gut long enough to turn black.
• Occult bleeding causes no visible blood. It is found only because iron-deficiency anaemia or a positive faecal occult blood test prompts investigation.
• Obscure bleeding is bleeding whose source is not found at the first upper endoscopy and colonoscopy. It is most often small bowel bleeding.

A patient can have more than one of these at once, so the pattern is a clue, not a diagnosis. An early fall in blood pressure with a normal or high haemoglobin can be misleading, because in acute bleeding haemoglobin lags behind volume loss.

GI bleeding is common at every age, but its causes change. In Western populations upper bleeding is commoner than lower, and both rise steeply with age because vascular disease, diverticulosis and cancer rise with age. Bleeding is more common in men than women, partly because diverticular and vascular disease are more common in men. ^{[3] [4]}

Lower GI bleeding occurs in roughly 33 to 87 per 100 000 people a year in Western countries and is rising as populations age. ^[4] It accounts for about 20 to 33 percent of all GI haemorrhage episodes. ^[4]

Obscure bleeding, that is bleeding from the small bowel, accounts for roughly 5 percent of all GI bleeding worldwide and is the most common site of obscure bleeding. ^{[2] [4]}

The table compares the common causes. Percentages are approximate and vary between studies and countries.

Other less common causes are sometimes forgotten and worth considering: drug-induced colopathy from non-steroidal anti-inflammatory drugs or anticoagulants, radiation injury, vascular disorders such as polyarteritis nodosa, and infection. Meckel diverticulum is the most common congenital intestinal abnormality and is the commonest cause of substantial bleeding in children. ^{[3] [4]}

Peptic ulcer disease, from Helicobacter pylori infection or non-steroidal anti-inflammatory drugs, remains the commonest single cause of acute upper bleeding, accounting for up to 67 percent of cases. ^[3] Several causes often coexist in an older patient taking aspirin or anticoagulants.

• Haemodynamic instability, syncope, chest pain or breathlessness.
• Melaena with tachycardia or hypotension.
• Cirrhosis, known varices, alcohol excess: suspect variceal bleeding.
• Recent abdominal aortic surgery: suspect an aortoenteric fistula.
• A palpable abdominal mass, weight loss, change in bowel habit or iron-deficiency anaemia: always consider malignancy.
• Anticoagulant or potent antiplatelet use with heavy bleeding.
• Children with bleeding: consider Meckel diverticulum and bleeding disorders.

The history aims to answer four questions: where, how fast, why, and from what.

• Character of the blood. Haematemesis, coffee-ground vomiting, melaena, haematochezia, or blood only on the paper. ^[3]
• Severity and speed. Haemodynamic symptoms (faint, thirst, breathlessness), amount of blood, duration, and clock time. Massive haemorrhage is continuing red blood per rectum with shock. ^[4]
• Risk factors for upper causes. Dyspepsia, previous ulcer, H. pylori, non-steroidal anti-inflammatory drugs and aspirin, alcohol, cirrhosis and varices, retching and vomiting. ^[3]
• Risk factors for lower causes. Known diverticular disease, colorectal polyps or cancer, inflammatory bowel disease, radiation, aortic graft, drugs.
• Medications. Anticoagulants, antiplatelets, non-steroidal anti-inflammatory drugs, selective serotonin reuptake inhibitors, and any supplement that prolongs bleeding. ^[3]
• Past bleeding. Previous episodes and their causes. A previous lower bleed makes a lower source more likely.
• Systemic clues. Weight loss, fevers, change in bowel habit, and family history of colon cancer or polyposis.

The amount of blood passed is usually overestimated by patients and relatives, so rely on haemodynamics rather than the colour of the toilet bowl.

• Vital signs and postural changes. Resting tachycardia and orthostatic hypotension reflect loss of less than 15 percent of blood volume; supine hypotension reflects loss of about 40 percent. ^[3]
• Shock index (heart rate divided by systolic blood pressure) is a quick bedside screen: a value over 1 suggests significant haemorrhage and a need for urgent action. ^[2]
• Abdomen. Tenderness, guarding, masses, organomegaly, ascites, and liver disease stigmata. Tenderness suggests ischaemia or perforation.
• Rectal examination with inspection and a digital rectal examination. Look for haemorrhoids, fissures, masses, and characterise the stool. Blood from a massive upper bleed can appear on the glove.
• Anorectal inspection and, if indicated, proctoscopy or anoscopy for an anorectal source.
• Signs of chronic disease. Clubbing, weight loss, cachexia, jaundice.
• Skin. Spider naevi, palmar erythema and bruising point to portal hypertension.

Do not let a normal haemoglobin reassure you early in a big bleed. Equally, a raised urea with a normal creatinine can be a clue to an upper source.

• Full blood count, haemoglobin and haematocrit to detect anaemia and its severity.
• Urea and creatinine. A blood urea nitrogen to creatinine ratio greater than about 30 to 1 suggests an upper GI source, because digested blood protein is absorbed and metabolised to urea. ^[2]
• Coagulation screen: prothrombin time, INR and activated partial thromboplastin time, plus platelet count. ^[3]
• Liver function tests and lactate. Lactate rises with tissue hypoperfusion. ^[3]
• Cross-match blood early if the patient is unstable or likely to need transfusion.
• If variceal bleeding is suspected, take blood cultures and consider infection markers, because bacterial infection occurs in 35 to 66 percent of cirrhotic patients with variceal bleeding. ^[5]

• Upper endoscopy (oesophagogastroduodenoscopy, OGD) is the first-line investigation for upper bleeding. It is diagnostic and therapeutic.
• Colonoscopy is the first-line investigation for lower bleeding, after preparation.
• CT angiography is non-invasive and finds arterial bleeding, but active bleeding must usually be present at a rate of about 0.3 to 0.5 mL per minute for CT angiography to detect it, or 0.5 to 1.0 mL per minute for conventional angiography. ^{[2] [3]}
• Tagged red cell scanning (technetium-99m) detects bleeding at rates of about 0.1 to 0.5 mL per minute and is used when other tests are negative or in children. ^[3]
• Push enteroscopy and device-assisted enteroscopy inspect the deep small bowel when OGD and colonoscopy are negative.
• Endoscopic ultrasound is increasingly used for non-variceal upper questions.
• Meckel scan (technetium-99m pertechnetate) looks for ectopic gastric mucosa and is the most accurate test for Meckel diverticulum in children. ^[3]

Risk scores sort out who needs urgent intervention and who can be managed as an outpatient. There is no single perfect score, and scores assist rather than replace clinical judgement. ^[2]

• Glasgow-Blatchford score (GBS) uses only the initial clinical and laboratory findings (urea, haemoglobin, systolic pressure, pulse, melena, syncope, liver disease, heart failure). It is the best studied pre-endoscopy score for predicting the need for hospital-based intervention. A GBS of 0 or 1 identifies very low-risk patients who can be managed as outpatients in many systems, although some debate raising this to 2; a GBS higher than 2 is associated with a higher chance of needing endoscopic haemostasis or transfusion. ^{[3] [2]} Its area under the curve for predicting intervention or death is about 0.86, compared with about 0.66 for the admission (pre-endoscopic) Rockall score and about 0.68 for AIMS65. ^[1] GBS also has high sensitivity (about 0.98) for an adverse event, against about 0.93 for the pre-endoscopic Rockall score and about 0.79 for AIMS65. ^[1]
• AIMS65 (albumin, INR, mental status, systolic blood pressure, age over 65) is simple to calculate at the bedside and predicts in-hospital mortality well, but it is less good than GBS at predicting transfusion need, rebleeding or low-risk outpatient suitability. ^[2]
• Rockall score has a pre-endoscopy and a post-endoscopy version. The pre-endoscopy version predicts mortality before endoscopy; the full version adds endoscopic findings and predicts overall mortality, but not rebleeding well. ^{[2] [3]}
• Oakland score is for lower GI bleeding. It uses age, sex, previous admission with lower GI bleeding, rectal findings, heart rate, blood pressure and haemoglobin. A score of 8 or less identifies a lower-risk group suitable for outpatient management in many systems. ^{[2] [3]}

The right sequence saves lives: resuscitation before endoscopy.

Prophylactic intubation before endoscopy is controversial. Evidence from meta-analyses has not shown a reduction in pneumonia, length of stay or mortality, and in some studies aspiration and pneumonia were more common, probably because of selection bias in the sicker patients who were intubated. ^[1]

The practical message is to intubate for severe haematemesis, agitation, an unprotected airway, or falling oxygen levels or conscious level, and to get anaesthetic help early. ^{[1] [3]} Give supplemental oxygen to achieve target saturations. Use face masks cautiously because of aspiration risk. ^[1]

• Place at least two large-bore peripheral cannulae (at least 18 gauge). Short, wide cannulae give higher flow rates than central lines. ^[3]
• Give crystalloid to maintain tissue perfusion; many units give 500 mL in under 15 minutes to an unstable patient, with frequent reassessment. ^[1]
• Aim for a systolic blood pressure around 90 to 100 mmHg in bleeding; over-resuscitation, especially in variceal bleeding, can worsen portal pressure and bleeding. ^{[1] [5]}
• Intensive early resuscitation in upper bleeding has been shown to reduce mortality and myocardial infarction in a small study. ^[1]
• Patients with continuing hypotension despite fluids need high-dependency or intensive care. ^[1]

Use a restrictive transfusion strategy for non-massive bleeding: transfuse when haemoglobin falls below about 7 g/dL, and below about 8 g/dL in patients with cardiovascular disease or acute coronary syndrome. ^{[1] [3]} A Spanish randomised trial of 921 patients found lower 6-week mortality with a restrictive threshold (under 7 g/dL) compared with a liberal one (under 9 g/dL) (hazard ratio 0.55). A large UK cluster trial found no outcome difference between thresholds of under 8 g/dL and under 10 g/dL. Meta-analyses of restrictive versus liberal transfusion in GI bleeding found lower mortality and less rebleeding with the restrictive approach. ^{[1] [5]}

Exsanguinating patients were excluded from most of these trials, and in acute haemorrhage haemoglobin can be artificially high because of haemoconcentration, so clinical judgement remains essential. ^[1] A rough guide is that one unit of packed red cells raises the haemoglobin by about 1 g/dL in an adult. ^[6]

Platelets and clotting: evidence for platelet thresholds in GI bleeding is limited. A common practical threshold is platelets below 50 000 per microlitre before endoscopic therapy, and below 20 000 is generally considered too low even for diagnostic endoscopy. Fibrinogen below 1.5 to 2 g/L should be corrected, usually with cryoprecipitate. ^[3] Massive transfusion protocols with balanced blood products are used for massive bleeding. ^[3]

Correct coagulopathy with the appropriate reversal agents when bleeding is life threatening: vitamin K 2 to 5 mg (orally or intravenously) for warfarin reversal, with prothrombin complex concentrate preferred over fresh frozen plasma for speed, and specific reversal agents for direct oral anticoagulants only in life-threatening bleeds according to local protocols. ^{[1] [3]}

• Acid suppression. High-dose intravenous proton pump inhibitor (PPI) is standard practice once upper bleeding is suspected, often given 12-hourly until endoscopy, even though routine use before endoscopy has not been shown to improve mortality or rebleeding and guidelines differ. ^{[1] [3]}
• Prokinetic. Intravenous erythromycin 250 mg given 30 to 120 minutes before endoscopy improves gastric visualisation and reduces the need for repeat endoscopy and length of stay. ^{[1] [3]}
• Nasogastric lavage is discussed below.
• Tranexamic acid is not recommended for upper bleeding outside trials, after a large international trial showed no mortality benefit and more venous thromboembolism. ^[1]

Upper bleeding is the more dangerous presentation because it is often brisk.

Endoscopy should be done within 24 hours of presentation, once the patient is resuscitated. ^{[1] [3]} Performing it earlier than 6 to 12 hours in high-risk stable patients does not appear to improve outcomes. ^{[1] [2]}

At endoscopy, stable ulcers are treated by the Forrest classification:

• Forrest Ia (spurting) and Ib (oozing) and Forrest IIa (visible vessel) need endoscopic haemostasis. ^[1]
• Forrest IIb (adherent clot) is controversial: endoscopic or medical management alone. ^[1]
• Forrest IIc (pigmented spot) and III (clean base) are low risk and do not need endoscopic therapy. ^[1]

Endoscopic haemostasis is achieved by injecting dilute epinephrine (1 in 10 000) plus a second method such as mechanical clips or thermal coagulation, because epinephrine alone gives only temporary control. Dual therapy beats epinephrine monotherapy. ^{[1] [3]} Topical haemostatic powders (hemospray) can be used as rescue or adjunct therapy when standard methods fail or the field is poor.

After successful endoscopy for a high-risk lesion, give high-dose proton pump inhibitor: an 80 mg intravenous bolus followed by 8 mg per hour for 72 hours reduces rebleeding, surgery and mortality. ^[1] Intermittent high-dose intravenous or even high-dose oral PPI is non-inferior and may be safer and cheaper. ^{[1] [3]} Then step down to a high-dose oral PPI twice daily for two weeks for high-risk lesions, or standard dose for low-risk lesions. ^[1]

Always test for H. pylori at endoscopy (rapid urease test or histology) in ulcer bleeding. These tests are only moderately sensitive in acute bleeding, so retest within 4 weeks if negative. Eradicate H. pylori when positive, and stop non-steroidal anti-inflammatory drugs if possible. ^[1]

If bleeding recurs, repeat endoscopy is the first step. Should endoscopic control fail, or bleeding be uncontrolled, use interventional radiology (angiographic embolisation) or surgery for non-variceal bleeding. ^[1]

Variceal bleeding carries the highest mortality of all upper GI bleeds (roughly 15 to 30 percent at 6 weeks, highest in severe cirrhosis). ^{[5] [3]}

Before endoscopy:

• Resuscitate gently: aim for haemoglobin around 8 to 10 g/dL, systolic pressure above 90 to 100 mmHg, heart rate under 100, and avoid over-transfusion because raised portal pressure worsens bleeding. ^[5]
• Start a vasoactive drug (octreotide, somatostatin, terlipressin or vasopressin) as soon as variceal bleeding is suspected, and continue for 2 to 5 days. Typical doses used are intravenous terlipressin 1 to 2 mg initially then 1 to 2 mg every 4 to 6 hours, or intravenous octreotide 0.025 to 0.05 mg continuously. ^{[1] [5]}
• Give prophylactic antibiotics: bacterial infection occurs in 35 to 66 percent of cirrhotic patients with variceal bleeding, and prophylaxis reduces mortality and rebleeding. Ceftriaxone 1 g once daily is more effective than oral norfloxacin in decompensated cirrhosis; antibiotics are usually given for 3 to 7 days. ^{[1] [3] [5]}
• Correct coagulopathy cautiously; massive transfusion protocols and fresh frozen plasma or platelets may be needed, but evidence for benefit is weak.

At endoscopy (within 12 hours):

• Oesophageal varices: endoscopic variceal band ligation is the standard first treatment. ^{[1] [5]}
• Gastric varices (GOV2/IGV1): endoscopic obturation with cyanoacrylate glue is the first-line therapy; smaller GOV1 varices may be treated with band ligation. ^[5]

If bleeding is not controlled:

• Balloon tamponade (Sengstaken-Blakemore, Minnesota or Linton-Nachlas tube) controls bleeding in up to about 80 percent of oesophageal variceal cases and is a temporary bridge only (not used beyond 24 hours because of risks of aspiration, ulceration or rupture). ^[5]
• Transjugular intrahepatic portosystemic shunt (TIPS) can achieve haemostasis in up to 95 percent of acute variceal bleeds and is the rescue therapy for refractory bleeding; preemptive (early) TIPS is considered in high-risk patients. ^[5]
• Balloon-occluded retrograde transvenous obliteration is an option for gastric varices with a gastrorenal shunt.
• Surgery or liver transplantation is considered in selected patients. ^[5]

Lower bleeding is more often self-limiting and less often lethal, but in older, frail patients it can be serious.

Resuscitate as for upper bleeding, with the same transfusion thresholds. Lower bleeding is clinically suggested by haematochezia with a stable patient, a normal or only slightly raised urea, and no haematemesis or melaena. ^[2]

Anoscopy must be performed early: an anorectal source (haemorrhoids, fissures, rectal tumour) is common, easy to find and easy to treat. Anoscopy should be part of every assessment of presumed lower bleeding. ^[4]

• Colonoscopy after bowel preparation, usually within 24 hours, is the diagnostic and therapeutic mainstay. Preparation in an active bleed requires care; unprepared colonoscopy risks complications. Early colonoscopy finds more bleeding sources but has not clearly improved mortality compared with a 24 to 120 hour window. ^[2]
• CT angiography for brisk or haemodynamically significant bleeding, looking for active arterial extravasation. ^[2]
• Tagged red cell scanning when bleeding is intermittent or too slow for CT angiography. ^[3]
• Angiographic embolisation if CT angiography is positive. ^{[2] [3]}
• Surgery for refractory or massive bleeding that cannot be controlled by endoscopy or radiology; roughly 1.7 percent of lower bleeds need surgery. ^[2]

• Diverticular bleeding, the commonest cause of massive lower bleeding, usually stops on its own; recurrence is common and further bleeding becomes more likely after each episode. ^[4]
• Angiodysplasia responds to endoscopic coagulation but rebleeds in up to 80 percent if left untreated. ^[4]
• Colitis is managed by treating the underlying cause (inflammatory, infectious, ischaemic, radiation).
• Neoplasia is managed by resection according to cancer pathways.
• Meckel diverticulum in children is diagnosed with a Meckel scan and treated surgically. ^[3]

If upper endoscopy and colonoscopy are negative, the bleeding is small bowel (obscure) bleeding until proven otherwise.

• Capsule endoscopy is the usual first step: it is safe and has good yield. ^[2]
• Device-assisted enteroscopy (double-balloon, single-balloon or spiral) follows, both to confirm and to treat lesions (angiodysplasia, tumours, Crohn disease, Meckel diverticulum). ^[2]
• Timing matters less than for upper bleeding, but earlier investigation may give better diagnostic yield; European guidance suggests investigation within about 48 hours of a bleeding episode where feasible. ^[2]
• CT angiography or a tagged red cell scan is preferred first in an unstable patient or when a tumour is suspected. ^[2]

Nasogastric tube placement was once routine in suspected upper bleeding. It is not recommended now: studies have not shown a benefit in clinical outcomes. ^[3]

It can still help in selected situations: visually confirming blood, reducing the risk of aspiration in a patient who cannot protect their airway (as part of intubation), or clearing the stomach before endoscopy. It should not be used to "exclude" upper bleeding, because a duodenal bleed can be negative, and it can be harmful. If tube placement is needed, consider a prokinetic (erythromycin) instead to empty the stomach for visualisation. ^{[1] [3]}

• Peptic ulcer: eradicate H. pylori; stop non-steroidal anti-inflammatory drugs or, if essential, give prophylactic PPI. High-dose PPI for high-risk lesions, then standard-dose PPI for low-risk lesions. ^[1]
• Varices: non-selective beta-blockers, band ligation for secondary prophylaxis, endoscopic surveillance, and treatment of the underlying liver disease (hepatitis treatment, alcohol cessation). ^[5]
• Diverticular bleeding: iron replacement, review of antiplatelets and anticoagulants, and reassurance, because most episodes stop; consider colectomy for recurrent life-threatening bleeding. ^[4]
• Angiodysplasia: endoscopic argon plasma coagulation or clips; rebleeding is common, so follow up. ^[4]
• Malignancy: refer along oncology pathways.
• Colitis: treat the underlying disease (inflammatory bowel disease, infection, ischaemia, radiation).
• Meckel diverticulum: surgical resection. ^[3]

This is where careful balancing matters. Both continuing and stopping drugs can kill, and the risk changes with the reason for the drug.

• Aspirin for primary prevention (no established cardiovascular disease) should be stopped and its need reassessed before restarting. ^[1]
• Aspirin for secondary prevention should generally be continued or restarted soon, because stopping it increases major cardiac events about threefold in pooled analyses, and almost 90-fold in patients with coronary stents. ^[1]
• When aspirin must be interrupted for a life-threatening bleed, guidelines differ on the interval: resumption from the time of haemostasis up to 5 days. ^[1]
• Dual antiplatelet therapy in patients with stents is high risk in both directions; continue if possible, with urgent cardiology advice, and if bleeding is severe, continue aspirin and hold the P2Y12 inhibitor, restarting it within 5 days. ^[1]
• Warfarin should be withheld in significant bleeding, and reversal given with Vitamin K and prothrombin complex concentrate; once haemostasis is achieved, European guidance suggests restarting within 7 days, taking thrombotic risk into account. Endoscopic therapy is considered acceptable with an INR below about 2.5. ^[1]
• Direct oral anticoagulants have short half-lives; for non-life-threatening bleeding, withholding the drug is usually enough. Reversal agents are reserved for life-threatening bleeding and are expensive with uncertain benefit. ^{[1] [3]}
• Regardless of the drug, the decision and timing should be shared between gastroenterology, haematology and the relevant specialist (cardiology, neurology).

• Pregnancy: upper bleeding is managed as above, with attention to maternal and fetal safety; variceal bleeding in cirrhosis needs specialist care.
• Children: think of Meckel diverticulum, bleeding disorders, and inflammatory bowel disease; Meckel scan and targeted surgery are key. ^[3]
• Older adults: more comorbidity, more drugs, higher mortality; avoid over-transfusion and manage drugs carefully.
• Cirrhosis: variceal precautions, antibiotic prophylaxis, gentle resuscitation. ^[5]

• Blood supply limits. Use the restrictive threshold of under 7 g/dL (under 8 g/dL with cardiovascular disease) and transfuse one unit at a time, reassessing. ^{[1] [3] [6]}
• Endoscopy. If OGD is unavailable, a nasogastric tube showing blood plus melaena makes upper bleeding likely, but cannot exclude a duodenal source. ^[3]
• Variceal bleeding. Octreotide, somatostatin or terlipressin, plus oral or intravenous antibiotics, can be started in any emergency department before transfer. Where band ligation is not available, balloon tamponade can temporise, or variceal injection if trained staff are present. ^[5]
• Arterial lower bleeding. CT angiography and embolisation require interventional radiology; if unavailable, unstable patients may need transfer or surgery. ^{[2] [3]}
• Anaemia after bleeding. Oral iron replacement and dietary support matter when follow-up endoscopy is unavailable.

• Upper bleeding is proximal to the ligament of Treitz; lower bleeding is distal; obscure bleeding is usually small bowel.
• Haematemesis and melaena mean upper bleeding; haematochezia usually means lower; occult bleeding is found only on testing.
• Peptic ulcer disease causes most upper bleeds; diverticular disease causes most lower bleeds.
• Resuscitate before investigating: two large peripheral lines, fluids, blood tests, cross-match.
• Transfuse restrictively: under 7 g/dL, or under 8 g/dL with cardiovascular disease; one unit raises haemoglobin about 1 g/dL. ^{[1] [3] [6]}
• Use risk scores to triage: Glasgow-Blatchford for upper, Oakland for lower; do not discharge on a high score.
• OGD within 24 hours for upper bleeding; colonoscopy after preparation for lower; CT angiography for brisk arterial bleeding. ^[1][2]
• Do not use nasogastric lavage routinely; it is not supported by evidence. ^[3]
• Variceal bleeding needs vasoactive drugs (2 to 5 days), antibiotics (ceftriaxone), gentle transfusion and urgent band ligation or glue injection.
• Rebleeding after endoscopy: repeat endoscopy first, then interventional radiology or surgery; TIPS for variceal bleeding.
• Long-term prevention is cause-specific, especially H. pylori eradication and PPI protection for ulcer disease.
• Restarting antithrombotic drugs is a balancing decision; aspirin for secondary prevention should not be stopped lightly.
• Low-resource care rests on early recognition, fluids, restrictive transfusion and timely transfer.

Major supportive topics (gastro-oesophageal reflux disease, gastritis and Helicobacter pylori, peptic ulcer disease, cirrhosis and varices, inflammatory bowel disease, colorectal cancer and polyps, coagulation, blood transfusion and shock) are best read alongside this page.