Upper GI Bleeding

Acute upper gastrointestinal bleeding (UGIB) is a gastroenterological emergency with a mortality of 6%-13%. Despite changes in management, mortality has not significantly improved over a period of 50 years.  Bleeding from the upper gastrointestinal tract (GIT) is about four times as common as bleeding from the lower GIT. It is important to identify patients with a low probability of re-bleeding from patients with a high probability of re-bleeding. The size of the bleeding vessel is important in prognosis. Visible vessels are usually between 0.3 mm and 1.8 mm. Large bleeding vessels cause faster blood loss. Generally, larger vessels are found deeper in the submucosa and serosa and more specifically high in the lesser curve of the stomach and postero-inferiorly in the duodenal bulb.

Endoscopy does not reveal a cause in approximately 20% of patients presenting with apparent acute UGIB. The most common causes are peptic ulcer and oesophago-gastric varices.

  • Peptic ulcer
  • Oesophagitis
  • Gastritis/erosions
  • Erosive duodenitis
  • Varices
  • Portal hypertensive gastropathy
  • Malignancy
  • Mallory-Weiss tear
  • Vascular malformation

Rare causes include:

  • Dieulafoy’s lesion (a vascular malformation of the proximal stomach).
  • Angiodysplasia.
  • Haemobilia (bleeding from the gallbladder or biliary tree).
  • Pancreatic pseudocyst and pseudo-aneurysm.
  • Aortoenteric fistula.
  • Bleeding diathesis.
  • Ehlers-Danlos syndrome.
  • Pseudoxanthoma elasticum.
  • Gastric antral vascular ectasia.
  • Osler-Weber-Rendu syndrome.

The incidence of acute UGIB in the UK ranges between 84-172 per 100,000 per year, causing 50-70,000 hospital admissions per year.

Risk factors for UGIB

An ageing population with associated conditions and a worse prognosis has helped maintain constant mortality figures despite advances in treatment. Mortality is about 7% in patients admitted because of bleeding but some three times higher amongst those developing UGIB whilst in hospital. Peptic ulcer disease is the most common cause of UGIB. Risk factors for peptic ulcer disease are:

  • Alcohol abuse.
  • Chronic renal failure.
  • Non-steroidal anti-inflammatory drug (NSAID) use.
  • Age.
  • Low socio-economic class.

Although duodenal ulcers are more common than gastric ulcers, both contribute nearly equally to the incidence of UGIB. After an initial bleed the risk factors for re-bleeding, with associated higher mortality, are:

  • Age over 60.
  • Presence of signs of shock at admission.
  • Coagulopathy.
  • Pulsatile haemorrhage.
  • Cardiovascular disease.

Bleeding severity can be assessed by:

  • The extent of blood loss.
  • The degree of shock.

Initial assessment may provide an indication of the cause of UGIB:

  • Abdominal pain, eg epigastric pain, diffuse abdominal pain.
  • Bleeding:
    • Haematemesis: bright red haematemesis usually implies active haemorrhage. Patients presenting with haematemesis have a higher mortality than those presenting with melaena alone.
    • Coffee-ground vomit refers to the vomiting of black material which is assumed to be blood; it implies that bleeding has ceased or has been relatively modest.
    • Melaena: black tarry stools, usually due to acute UGIB but occasionally bleeding from the small bowel or right side of the colon.
    • Haematochezia: passage of fresh or altered blood per rectum, usually due to colonic bleeding but occasionally due to profuse upper gastrointestinal or small bowel bleeding.
  • Loss of blood: shock, syncope, presyncope.
  • Features of underlying cause, eg dyspepsia, weight loss, jaundice.
  • Risk factors:
    • Alcohol intake.
    • Drug history is important. Drugs such as NSAIDs, aspirin and corticosteroids are an important cause of bleeding. Iron and bismuth may mimic melaena.
  • Past history of bleeding (haematemesis or melaena) or of anaemia.
  • Retching may precede bleeding with a Mallory-Weiss tear.


The main aim of examination is to assess blood loss and look for signs of shock. A secondary aim is to look for signs of underlying disease and significant comorbid conditions – for example:

  • Pallor and signs of anaemia should be sought.
  • Pulse and blood pressure.
  • Postural hypotension may be detected and usually indicates a blood loss of 20% or more.
  • Other signs of shock:
    • Cool extremities
    • Chest pain
    • Confusion
    • Delirium
  • Evidence of dehydration (dry mucosa, sunken eyes, skin turgor reduced).
  • Stigmata of liver disease may be present (jaundice, gynaecomastia, ascites, spider naevi, flap, etc.).
  • Signs of a tumour may be present (nodular liver, abdominal mass, lymphadenopathy).
  • Subcutaneous emphysema and vomiting suggests Boerhaave’s syndrome (oesophageal perforation).
  • Urine output should be monitored (oliguria is a sign of shock).

Endoscopy is the primary diagnostic investigation in patients with acute UGIB:

  • Endoscopy should be undertaken immediately after resuscitation for unstable patients with severe acute UGIB.
  • Endoscopy should be undertaken within 24 hours of admission for all other patients with UGIB.

Laboratory tests

  • FBC: haemoglobin is measured serially (4-6 hourly in the first day) to help assess trend. The requirement for transfusion is based on initial haemoglobin and a clinical assessment of shock.
  • Crossmatch blood (usually between 2 and 6 units according to rate of active bleeding).
  • Coagulation profile: prothrombin time with activated partial thromboplastin time and an international normalised ratio (INR), fibrinogen level:
    • A consumptive coagulopathy may occur with UGIB. This may be associated with thrombocytopenia. A platelet count of less than 50 with active bleeding requires platelet transfusion and fresh frozen plasma to try to make up for depleted clotting factors.
    • Coagulopathy may be a marker also for advanced liver disease. Low fibrinogen and abnormal LFTs may also indicate liver disease.
  • LFTs to detect underlying liver disease
  • Renal function tests and electrolytes; BUN-to-creatinine ratio (greater than 36 in renal insufficiency suggests UGIB).
  • Calcium level should be assessed to detect hyperparathyroid patients and to monitor the effect of citrated blood transfusions.
  • Gastrin levels can identify the rare gastrinomas causing UGIB.


  • CXR: may identify aspiration pneumonia; pleural effusion, perforated oesophagus.
  • Erect and supine abdominal X ray to exclude perforated viscus and ileus.
  • CT scan and ultrasound can identify:
    • Liver disease.
    • Cholecystitis with haemorrhage.
    • Pancreatitis with haemorrhage and pseudocyst.
    • Aortoenteric fistulae.
  • Nuclear medicine scans have been used to identify areas of active haemorrhage.
  • Angiography may be useful if endoscopy fails to identify site of bleeding.

Consider for admission and early endoscopy if:

  • aged ≥60 years (all patients who are aged >70 years should be admitted); or
  • witnessed haematemesis or haematochezia (suspected continued bleeding); or
  • haemodynamic disturbance (systolic blood pressure <100 mm Hg, pulse ≥100 beats per minute); or
  • liver disease or known varices.

Other significant comorbidity (especially cardiac disease, malignancy) should also lower the threshold for admission.

Resuscitation and initial management

Shocked patients should receive prompt volume replacement. It has been demonstrated that early and aggressive resuscitation reduces mortality in UGIB.

  • Correct fluid losses (place two wide-bore cannulae and also send bloods at the same time). Either colloid or crystalloid solutions may be used to achieve volume restoration prior to administering blood products; red cell transfusion should be considered after loss of 30% of the circulating volume.
  • Transfuse patients with massive bleeding with blood, platelets and clotting factors in line with local protocols for managing massive bleeding. Major haemorrhage protocols should be in place.
  • Decisions on blood transfusion should be based on the full clinical picture; over-transfusion may be as damaging as under-transfusion.
  • Platelet transfusions should not be offered to patients who are not actively bleeding and are haemodynamically stable.
  • Platelet transfusions should be offered to patients who are actively bleeding and have a platelet count of less than 50 x 109/litre.
  • Fresh frozen plasma should be used for patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time (INR) or activated partial thromboplastin time greater than 1.5 times normal.
  • Prothrombin complex concentrate should be used for patients who are taking warfarin and actively bleeding.
  • Recombinant factor Vlla should not be used except when all other methods have failed.

Proton pump inhibitors (PPIs) should not be used prior to diagnosis by endoscopy in patients presenting with acute UGIB.

Source: http://patient.info

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