Author: Janet Skinner / Editor: Alasdair Gray, Tadgh Moriarty / Reviewer: Chris Gray / Code: ACCS LO 2, GC1, GC2, GC8, GP6, HP3, RP7, SLO1, SLO3, SuP5 / Published: 28/06/2021


Upper gastrointestinal (GI) haemorrhage is a common presentation to the emergency department, and accounts for approximately 50-70,000 admissions per year [NICE].

The overall incidence of acute upper GI bleeding in the UK ranges from 84-172 per 100,000 of the population per year [NICE]. Incidence is highest in the elderly, and lower socioeconomic groups.

Despite changes in medical management, mortality has remained at around 10% for the last fifty years [NICE].


An upper GI haemorrhage can be defined as any bleeding which occurs from a source proximal to the “ligament of Treitz” [2]. This is the suspensory ligament of the duodenum that marks the duodenojejunal junction.

Common causes of upper GI bleeding in the UK are shown in the chart above.

Peptic ulcer disease is the most common cause of upper GI bleeding, accounting for just over half of its hospital admissions.[17,18]

In peptic ulcer disease, haemorrhage occurs from erosion to a blood vessel at the ulcer base.

In patients with liver disease, increased portal venous pressure results in greater blood flow through collateral vessels (particularly in the distal oesophagus). These vessels can become dilated and tortuous, making them prone to bleeding.

The anatomical locations of the causes of upper GI bleeds are shown in the image below

There are a number of signs and symptoms which may identify a patient having a GI bleed. Identifying the presence of upper GI bleed can range from relatively easy to more challenging. In some instances where haematemesis (present in 50%) or melaena (present in 70%) exists – the diagnosis is easier. It can be more difficult to identify in those patients which present with syncope (or parasyncope), dizziness, haematochezia, hypotension or tachycardia. A high index of suspicion is required for these symptoms. Hypotension (Systolic BP < 90mmHg)– is associated with a increased risk of mortality (odds ratio 9.8).[19]

Patients with haematemesis tend to have more severe bleeds than those with only melaena. [5]

Points to look for in the history

  • Known or suspected liver disease
  • Profuse recent vomiting (suggests Mallory-Weiss tear)
  • Previous peptic ulcer disease or gastritis
  • Known or previous Helicobacter pylori infection
  • Alcohol (not a direct pointer to variceal bleeding – peptic ulcer disease bleeding is still more common within this cohort)

Medication, particularly NSAIDs which increase the risk of UGIB four-fold

Learning Bite

Do a PR early as it may confirm fresh melaena.

Blood transfusion decision should be based on the full clinical picture. It should be noted that over-transfusion has complications, and that studies have shown a reduction in mortality when transfusion is restricted to patients with a haemoglobin less than 7g/dL (less than 9g/dL in unstable coronary artery disease).

Platelet transfusion should only be offered to patients with a platelet count less than 50 x 109/litre who are actively bleeding.

Fresh frozen plasma (FFP) should be used in actively bleeding patients with a prothrombin time (PT), INR, or activated partial thromboplastin time (aPTT) greater than 1.5 times the normal upper limit. Cryoprecipitate can be used in patients with a fibrinogen that remains less than 1.5g/L despite using FFP.

For patients taking warfarin who are actively bleeding, offer prothrombin complex concentrate (PCC). If bleeding has stopped, follow local warfarin protocols.

Thromboelastography can also be used if readily available to guide transfusion of clotting products.

Learning Bite:

Patients with melena tend to present with lower haemoglobin values than those with haematemesis (most likely due to presentation being slightly later with melena)

If there is evidence of haemodynamic instability; tachycardia (but remember elderly or those on beta blockers may not mount a tachycardia), widened pulse pressure, tachypnoea, or hypotension (which may be a late sign particularly in younger patients) – involve senior EM staff early and begin resuscitation following the ABC approach.

  • High concentration oxygen via non-rebreather mask with reservoir bag
  • Two large bore peripheral intravenous cannulae (if access is difficult consider US guided or IO access)
  • Bloods (see investigations)
  • Transfuse according to local protocols and consider activating major haemorrhage protocols early
  • Urinary catheter to measure urine output
  • Urgent referral to GI service or surgery (depending on access to endoscopy and in-hours/out-of-hours – check your local policy!)
  • Involve critical care team

Variceal Bleed

Variceal bleeds are uncommon, even in patients with a known alcohol related liver disease. Mortality is high and up to 30% of patients with known varices are likely to re-bleed [VREEBURG].

A variceal bleed is suggested by evidence of decompensated liver disease, such as jaundice, ascites or encephalopathy.

Known or suspected variceal bleeds should always be considered high risk as, in hospital, mortality is approximately 50% [JALAN].

All patients should be referred for urgent endoscopy and should undergo a critical care review to determine need for admission to a high dependency area.

Glasgow-Blatchford Score

The Glasgow-Blatchford score is the risk assessment tool of choice in the emergency department [BLATCHFORD] (table 1). It is calculated using 4 components – medical history (hepatic disease, heart failure), symptoms (melaena, syncope), signs (tachycardia, blood pressure), and blood tests (haemoglobin, urea).

An online score calculator is ideal to use as individual components can have values between 0 and 6. The maximum score is 29. NICE recommends that patients with a Blatchford score of 0 can be considered for early discharge with outpatient endoscopy follow up [NICE].

Blatchford score

Risk marker


Urea6.5 – 7.5
8.0 – 9.9
10.0 – 24.9
Haemoglobin (g/dL) for men12 – 12.9
10.0 – 11.9
Haemoglobin (g/dL ) for women10.0 – 11.9
Systolic blood pressure (mmHg)100-109
Other markersPulse >100
Hepatic disease
Cardiac failure


Rockall Score

Another risk assessment tool is the Rockall score. Rockall et al (1996)[ROCKALL] identified risk factors in 4185 patients with an upper GI haemorrhage. The score was validated on a further population of 625 patients and found to predict mortality but not the rate of re-bleeding (see Table 1).

The score consists of three clinical parameters (age, presence of shock, and comorbidity) and two parameters that rely on endoscopic findings (blood and diagnosis). The maximum pre-endoscopy Rockall score is 7 and post-endoscopy is 11. A Rockall score of 3 before endoscopy approximates with a 10% mortality rate and a score of 6, a 50% mortality rate.

The main disadvantage of the Rockall score is that it requires findings at endoscopy to calculate all the components of the score. However, the pre-endoscopy score can be used to help to identify those with high mortality that may benefit from critical care admission.

Learning Bite

Both the Glasgow-Blatchford and Rockall scores are useful tools to aid the clinician in identifying high-risk upper GI bleeds. The Blatchford Score can be used in conjunction with clinical assessment to identify low-risk patients who may be suitable for ED discharge.

Rockall score













BP>100 P<100


BP>100 P>100







Cardiac failure or IHD

Renal failure, liver failure or disseminated malignancy


No blood or dark spot only


Blood in upper GI tract, adherent clot or spurting vessel



Mallory-Weiss tear

All other diagnoses

GI tract malignancy

Score Mortality %
0 0.2
1 2.4
2 5.6
3 11
4 24.6
5 39.6
6 48.9
7 50

Summary of Risk Assessment

Risk is categorized the following way:

  • Low risk: Glasgow-Blatchford Score 0 – consider discharge with outpatient endoscopy
  • Moderate risk: admit to appropriate inpatient specialty for urgent endoscopy
  • High risk: Rockall Score (pre-endoscopy) 3, haemodynamic instability, known varices – resuscitate, admit to critical care area for emergency endoscopy

Clinical diagnosis is largely based on the patient’s history, however investigations are useful to risk assess and guide management.


  • Venous Blood gas can help to assess haemoglobin level quickly but do not rely solely on this – there is a lag period between blood loss and Hb drop!
  • Urea and electrolytes (urea will be raised after a significant volume bleed)
  • Full blood count
  • Coagulation screen (derangement of clotting in liver diseases)
  • Liver function tests (identifying liver disease)
  • Cross match (type specific or full cross match depending on urgency)
  • Chest x-ray, 12-lead ECG
  • Little role for abdominal x-ray- CT abdomen may be of more benefit if concern about diverticular bleed, or small bowel obstruction

Non-variceal Bleeds


PPIs, such as omeprazole or pantoprazole, are widely used. Theoretically, they reduce bleeding by increasing the pH of the normally acidic gastric environment, leading to clot stability. They have been shown post-endoscopy to reduce the re-bleeding rate and need for surgery, but have no effect on overall mortality [sreehdaran].

Evidence for their use before endoscopy is conflicting. A Cochrane review in 2010 found that pre-endoscopy PPIs reduced findings of recent serious bleeding and the need for treatment during endoscopy [SREEDHARAN]. However, current guidance from NICE is that PPI therapy should not be commenced pre-endoscopy, as there is no evidence that it improves clinically significant outcomes, such as mortality, re-bleeding rate or need for surgery [NICE].

Learning Bite

Whilst PPIs are commonly used in the management of upper GI bleeds, there is little evidence to support their use in the ED.



Octreotide is not recommended for routine use in patients with acute non-variceal bleeds, but can be used as an adjunct to therapy where there is a delay in endoscopy. [SALTZMANN]

Antifibrinolytic therapy

The Halt It trial published its results in 2020 and included over 12,000 patients randomised to receive either tranexamic acid (TXA) or placebo. This showed no significant difference in death due to bleeding. Secondary outcomes revealed a slightly higher rate of venous thromboembolic events in the TXA group. This would suggest that TXA does not reduce death from GI bleeding and should not be routinely used as part of the treatment of GI bleeding.[21]

Variceal Bleeds

Somatostatins and vasopressins

Two classes of drugs are widely used in the management of variceal haemorrhage. These include somatostatins (Octreotide) and vasopressins (Terlipressin).

Somatostatins cause a relaxation of vascular smooth muscle and reduce portal venous pressure. Vasopressins cause arterial vasoconstriction, reducing portal venous pressure but at the risk of end-organ ischaemia. A systematic review has shown no reduction in the number of deaths with somatostatins.

However, Terlipressin was noted to be safe and effective. Terlipressin has been shown to reduce blood loss from actively bleeding varices and confers a 34% relative risk reduction in risk of mortality. Terlipressin is also more convenient as it can be given as a bolus.

Learning Bite

Terlipressin should be given in ED to any patient with suspected variceal bleeding.

Vitamin K

A Cochrane review concludes that there is no evidence of efficacy for the administration of Vitamin K in patients with liver disease who have an upper GI haemorrhage.


20% of cirrhotic patients with acute variceal bleeding will develop a bacterial infection within 48 hours [LEE].

All patients with acute upper gastrointestinal bleeding where the source is suspected or confirmed varices should be given prophylactic therapy with antibiotics such as ciprofloxacin or ceftriaxone.

Learning Bite

Broad Spectrum antibiotics (usually Ceftriaxone) should be given early in ED to any patient with suspected variceal bleeding.


Endoscopy is the gold standard for diagnosing and treating an upper GI haemorrhage. The timing of endoscopy is important, and should take place only after the patient is adequately resuscitated. Common therapies include injection or thermal therapy for a bleeding peptic ulcer, or banding of oesophageal varices.

Endoscopy controls bleeding initially in around 90% of patients with bleeding peptic ulcers [PALMER]. Mallory-Weiss tears normally stop without endoscopic intervention.

Patients should be assessed clinically and risk stratified using scoring systems to help determine how urgently endoscopy should be performed and to what level of care facility they should be admitted.

Learning Bite

High-risk bleeds need urgent endoscopy, both for diagnosis and therapy.

Balloon Tamponade

Balloon tamponade, via the insertion of a Sengstaken-Blakemore tube (3 lumen) or Minnesota tube (4 lumen due to inclusion of an oesophageal aspiration port), should be undertaken in patients with a variceal haemorrhage that has continued to bleed despite medical therapy when endoscopy is not immediately available.

Tamponade provides good control of bleeding in 90%, although most will re-bleed within 24 hours [JALAN]. The main role of these tubes is to buy time to endoscopy.

Balloon Tamponade Procedure

  1. RSI should be undertaken to secure the airway
  2. Test the balloons on the tube to the maximally recommended volume, then fully deflate them
  3. Lubricate the tube, then pass orally to a depth of 50-60cm
  4. Insert air into the gastric aspiration port and listen with a stethoscope over the stomach and lungs. Inflate gastric balloon with 50ml air
  5. Confirm placement with chest x-ray (gastric balloon in stomach)
  6. Inflate the gastric balloon with air in 50-100ml increments up to the maximally recommended volume (250-300ml for SVT or 450-500 for Minnesota). Stop if resistance is encountered. Clamp the port
  7. Further x-ray to confirm position
  8. Pull balloon back against gastric fundus. Mark at the lips. Traction with 500ml bag of fluid and rope-and-pulley system
  9. The oesophageal balloon should only be inflated if bleeding continues (inflate to 40mmHg)
  10. The EMCrit blog has some further tips, as well as a video to help to explain the above steps more easily.

Balloon Tamponade Complications

  • Oesophageal necrosis and perforation from inflation of the oesophageal balloon, or the gastric balloon in an incorrect position
  • Aspiration if the airway is not secured first
  • Mucosal ulceration from pressure (do not leave in situ for more than 24-36 hours, and periodically deflate and reinflate)
  • Proximal migration of the tube causing airway obstruction
  • Ongoing haemorrhage from incorrect insertion or position

Further treatment options if endoscopy fails include surgery, angiography and embolisation, or TIPSS. Transjugular Intrahepatic Porto-Systemic Shunt is a radiological intervention in which a connection is made between the portal and hepatic venous systems to reduce portal venous pressure. This procedure may be performed in patients with varices who continue to bleed despite other therapies.

Learning Bite

Balloon tamponade is an effective method of controlling a variceal haemorrhage until definitive intervention.

In assessing the patient with an upper GI bleed there are several pitfalls. The most important of these is failing to recognise those patients that require prompt resuscitation, urgent endoscopy and admission to a critical care area (haemodynamic abnormalities or a Rockall score of three or more).

It is vital, in a shocked patient with no apparent cause, to perform a rectal exam early to avoid missing melaena. Be aware of the patient with an unexplained postural hypotension or syncope and assess for an unrecognised GI haemorrhage.

In terms of variceal bleeds: consider antibiotics and terlipressin early. If considering a Sengstaken tube, remember to secure the airway prior to it’s insertion.

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