Severe gastrointestinal bleeding

Severe gastrointestinal bleeding is bleeding from the gut that causes haemodynamic instability, a rapid fall in haemoglobin, or a need for transfusion or urgent endoscopic, radiological or surgical haemostasis.

Site. Upper bleeding arises proximal to the ligament of Treitz and causes haematemesis, coffee ground vomit or melaena. Lower bleeding arises distal to it and usually causes haematochezia. Small bowel bleeding is uncommon and is diagnosed after upper and lower sources are excluded.

Variceal and non-variceal. Variceal bleeding in portal hypertension carries a higher mortality and needs vasoactive drugs, antibiotics and band ligation. Non-variceal bleeding is mostly peptic ulcer disease.

Severity. Signs of severity are systolic pressure under 90 mmHg, heart rate over 100 beats/min, shock index (heart rate divided by systolic pressure) over 1.0, syncope, ongoing haematemesis or fresh rectal blood, and haemoglobin under 70 g/L. The Glasgow-Blatchford score (0 to 23) identifies patients needing intervention, and a score of 0 to 1 defines a low risk group suitable for outpatient care. The Rockall score and AIMS65 predict re-bleeding and death.

Key distinctions. Brisk upper bleeding can present as maroon stool or haematochezia with shock. Haemoglobin may be normal in the first hours. A raised urea with a normal creatinine suggests an upper source.

History.

• Haematemesis, melaena, rectal blood, volume and duration, syncope, chest pain, dyspnoea.
• Preceding retching (Mallory-Weiss tear), dyspepsia, weight loss, dysphagia.
• Alcohol, liver disease, hepatitis B or C, schistosomiasis, previous varices or banding.
• Drugs: aspirin, clopidogrel, NSAIDs, corticosteroids, SSRIs, warfarin, direct oral anticoagulants, iron and bismuth (black stool without blood).
• Previous aortic graft or aneurysm repair, previous gastrointestinal surgery, inflammatory bowel disease, diverticular disease, radiotherapy, bleeding tendency.

Examination.

• Pulse, blood pressure, postural change when safe, capillary refill, mottling, urine output, mental state.
• Stigmata of chronic liver disease (jaundice, spider naevi, ascites, splenomegaly, caput medusae), hereditary haemorrhagic telangiectasia lesions, abdominal mass or tenderness, scars.
• Rectal examination for melaena or blood.

Red flags.

• Shock, haematemesis with ongoing bleeding, syncope.
• Known cirrhosis or varices, aortic graft, anticoagulation, or age over 60 with comorbidity.
• Peritonism (perforation), chest pain, or encephalopathy.

Special groups. Pregnancy: the same approach with left lateral tilt after 20 weeks and shielded imaging where possible. Children: weight based fluids and blood. Region specific: schistosomal and hepatitis B related portal hypertension, typhoid intestinal haemorrhage, hookworm and amoebic colitis.

Upper gastrointestinal.

• Peptic ulcer disease (duodenal and gastric), erosive gastritis, erosive oesophagitis.
• Oesophageal varices, gastric varices, portal hypertensive gastropathy.
• Mallory-Weiss tear, Dieulafoy lesion, gastric antral vascular ectasia, Cameron lesion.
• Gastric cancer, oesophageal cancer, gastrointestinal stromal tumour.
• Aortoenteric fistula (any gastrointestinal bleeding after aortic graft surgery until proven otherwise).
• Haemobilia, haemosuccus pancreaticus.

Lower gastrointestinal.

• Diverticular bleeding, angiodysplasia, haemorrhoids, colorectal cancer, post polypectomy bleeding.
• Ischaemic colitis, infective colitis (including amoebic colitis), inflammatory bowel disease, radiation proctitis.
• Meckel diverticulum (young patients), small bowel tumour, hereditary haemorrhagic telangiectasia, typhoid intestinal haemorrhage.

Coagulopathy. Anticoagulant effect, antiplatelet effect, liver failure, disseminated intravascular coagulation, thrombocytopenia, uraemia.

Mimics. Swallowed blood from epistaxis or haemoptysis, iron, bismuth, beetroot, food dyes, vaginal bleeding.

Immediate. Capillary glucose, blood gas with lactate, full blood count, urea, creatinine, electrolytes, liver tests, coagulation with fibrinogen, group and crossmatch, ECG and troponin in older patients or those with cardiac disease. A urea to creatinine ratio (both in mmol/L) over 100 favours an upper source. Calculate the Glasgow-Blatchford score.

Upper bleeding.

• Endoscopy after resuscitation: within 24 hours for most patients, and within 12 hours of presentation when variceal bleeding is suspected. Unstable patients have endoscopy as soon as they are resuscitated, with airway protection.
• Forrest classification directs therapy: active spurting (Ia), oozing (Ib), non-bleeding visible vessel (IIa) and adherent clot (IIb) need endoscopic treatment. Clean base (III) and flat pigmented spot (IIc) need none.
• If endoscopy cannot find the source, CT angiography, or repeat endoscopy with a side viewing scope.

Lower bleeding.

• Unstable: resuscitate, exclude an upper source with endoscopy if there is any suspicion, then CT angiography (detects bleeding at about 0.3 to 0.5 mL/min), followed by catheter angiography and embolisation.
• Stable: colonoscopy within 24 hours after bowel preparation. Proctoscopy and sigmoidoscopy for suspected anorectal causes.
• Capsule endoscopy or enteroscopy for obscure bleeding once the patient is stable. Technetium labelled red cell scan has limited accuracy.

Limitations. Haemoglobin lags behind blood loss. Nasogastric aspiration is not reliable to exclude an upper source. CT angiography needs active bleeding at the time of the scan and contrast, which needs care in kidney impairment.

Resuscitation.

• Airway protection (intubate for ongoing haematemesis with reduced consciousness or before endoscopy when the airway is at risk), oxygen to saturation 94 to 98%, two large bore cannulae (14 to 16 G), monitoring and urinary catheter.
• Restrictive transfusion: red cells at haemoglobin under 70 g/L, aiming for 70 to 90 g/L (threshold 80 g/L and target 100 g/L with cardiovascular disease). In variceal bleeding aim for 70 to 80 g/L, since over transfusion raises portal pressure and re-bleeding. Isotonic crystalloid 500 mL boluses for hypotension with reassessment after each.
• Major haemorrhage: activate massive transfusion with red cells, plasma and platelets in near equal proportions, calcium chloride 10% 10 mL IV after every 4 units of red cells, fibrinogen under 1.5 g/L treated with concentrate 2 to 4 g IV or cryoprecipitate, and platelets to over 50 x 10^9/L during active bleeding.
• Reversal: warfarin with 4 factor prothrombin complex concentrate 25 to 50 units/kg IV plus vitamin K 5 to 10 mg IV slowly over 10 minutes; dabigatran with idarucizumab 5 g IV; factor Xa inhibitors with prothrombin complex concentrate 50 units/kg IV or the specific antidote from the product label. Do not reverse a mild INR rise in cirrhosis, where INR does not reflect bleeding risk.
• Stop NSAIDs and anticoagulants. Tranexamic acid is not advised for gastrointestinal bleeding because it increases venous thromboembolism without reducing mortality.

Before endoscopy.

• Omeprazole 80 mg IV as a single bolus (evidence for benefit before endoscopy is limited); monitor for allergy and hypomagnesaemia with prolonged use.
• Erythromycin 250 mg IV over 30 minutes, 30 to 120 minutes before endoscopy, as a single dose to clear the stomach; avoid with prolonged QTc and interacting drugs (clarithromycin, azole antifungals, amiodarone).

Non-variceal upper bleeding.

• Endoscopic therapy for Forrest Ia to IIb lesions: adrenaline injection (1 in 10,000) combined with a second method (clips or thermal coagulation). Adrenaline alone is not enough.
• After successful therapy: omeprazole 80 mg IV bolus then 8 mg/hour infusion for 72 hours (or 40 mg IV every 12 hours), then 40 mg orally twice daily to day 14, then 20 to 40 mg once daily for 4 to 8 weeks; maximum 8 mg/hour infusion; monitor magnesium, sodium and Clostridioides difficile infection with long courses. This is a deliberate high dose course and differs from usual daily acid suppression.
• Test for Helicobacter pylori and eradicate (14 days of combination therapy chosen from local resistance), then confirm eradication at 4 or more weeks after treatment and 2 weeks off proton pump inhibitors.
• Re-bleeding: repeat endoscopy once, then interventional radiology (transcatheter arterial embolisation) or surgery.
• Antiplatelets: continue aspirin for secondary prevention if possible, or restart within 3 to 5 days of haemostasis. Anticoagulants are restarted when haemostasis is secure, usually within 7 days, with the timing agreed by the stroke or cardiology team for high thrombotic risk.

Variceal bleeding.

• Terlipressin 2 mg IV every 4 hours until bleeding is controlled (usually 24 to 48 hours), then 1 mg every 4 hours, for up to 5 days; maximum 12 mg daily; monitor ECG, sodium, peripheral and mesenteric ischaemia, bronchospasm and fluid overload; avoid with ischaemic heart disease, peripheral vascular disease, pregnancy and hypoxia; reduce or stop with kidney impairment or worsening perfusion. Alternative: octreotide 50 micrograms IV bolus then 50 micrograms/hour for 2 to 5 days; monitor glucose and heart rate.
• Antibiotics from presentation: ceftriaxone 1 g IV once daily for up to 7 days (stop earlier when bleeding is controlled and the patient is eating); maximum 2 g daily in this use; monitor for diarrhoea and kidney function. Alternative in penicillin or cephalosporin allergy is directed by local resistance data.
• Band ligation within 12 hours of presentation (tissue glue injection for gastric varices).
• Early transjugular intrahepatic portosystemic shunt within 72 hours (preferably 24 hours) for Child-Pugh class C (score 10 to 13) or class B with active bleeding at endoscopy.
• Balloon tamponade (Sengstaken-Blakemore or similar) as a temporary bridge for no more than 24 hours, after intubation, for uncontrolled bleeding; monitor for oesophageal injury.
• Encephalopathy prevention: lactulose 25 mL orally every 12 hours, titrated to 2 to 3 soft stools daily (evidence is limited for primary prevention). Correct hypokalaemia, avoid sedatives and constipation.
• Secondary prophylaxis: banding every 2 to 4 weeks until eradication plus propranolol 20 to 40 mg orally twice daily, titrated to a resting heart rate of 55 to 60 beats/min, maximum 160 mg daily with ascites (320 mg daily without); or carvedilol 6.25 mg orally once daily, increased after 3 days to 6.25 mg twice daily, maximum 12.5 mg daily; stop if systolic pressure under 90 mmHg, sodium under 130 mmol/L or acute kidney injury; avoid in asthma (propranolol) and severe bradycardia.

Lower bleeding. Resuscitate and correct coagulopathy. Most diverticular and angiodysplasia bleeds stop spontaneously. Colonoscopic clips, adrenaline injection or coagulation for an identified lesion, catheter embolisation for ongoing bleeding, and surgery (segmental resection directed by localisation) as a last resort. Stop NSAIDs and review anticoagulants.

Monitoring. Observations every 15 minutes while unstable, then hourly. Hourly urine output, haemoglobin every 4 to 6 hours initially, lactate, coagulation, electrolytes, glucose, and daily creatinine.

Referral and escalation. Gastroenterology or endoscopy for all, critical care for shock or airway risk, interventional radiology for re-bleeding, surgery for failed endoscopic and radiological control or perforation, and hepatology for variceal bleeding.

Admission criteria. All patients with a Glasgow-Blatchford score over 1, any shock, active bleeding, anticoagulation, cirrhosis or comorbidity. Patients with a score of 0 to 1 and a safe home setting may be managed as outpatients with early follow up.

Discharge and safety netting. Discharge after endoscopy shows a low risk lesion and haemoglobin is stable for 24 hours or more (72 hours of observation after high risk stigmata treatment). Patients are told to return for black stool, vomiting blood, dizziness, fainting or chest pain, to avoid NSAIDs and alcohol, and to complete acid suppression and eradication therapy.