Haematemesis and melaena

Introduction

Upper gastrointestinal bleeding (UGIB) is a common medical emergency with substantial morbidity and mortality. Over the last two decades, there have been advances in drug therapy for peptic ulcer disease and varices, improvements in endoscopic techniques, interventional radiology and surgical management, in addition to advances in resuscitation and supportive care. Mortality for patients presenting with UGIB remains around 6% to 10%, although there is some evidence that mortality has declined in the United Kingdom and the United States. Fewer patients (approximately 2%) now require emergency surgery. Patients with UGIB are increasingly elderly and have more co-morbidity than in the past, which may explain the slow improvement in mortality despite the many technical advances in management, particularly endoscopy. Patients now rarely die of exsanguination but more commonly of multiple organ failure secondary to pre-existing co-morbidities.

Definitions, epidemiology and pathogenesis

UGIB is defined as any bleeding within the GI tract proximal to the ligament of Treitz. Any bleeding arising distal to that point is a lower GI bleed. Haematemesis is the vomiting of bright red blood. ‘Coffee-ground vomiting’ is the vomiting of digested blood clot, whereas melaena is the passage of black, tarry stools as a result of the bacterial degradation of haemoglobin within the gut. Melaena usually represents a source of UGIB, but it can rarely occur due to a lower GI source of bleeding. Haematochezia is the passage of bright red blood per rectum and, in the context of UGIB, represents a briskly bleeding source of haemorrhage. Melaena of itself is not associated with poorer outcomes in UGIB, but haematochezia due to an upper GI source is associated with double the risk of death.

Peptic ulceration remains the most common cause of UGIB despite the recognition and treatment of Helicobacter pylori infection as a primary cause of peptic ulcer disease (accounting for 36% of cases in a recent UK audit). The pathogenesis of peptic ulcer disease is complex but is closely related to a variety of risk factors, including H. pylori infection, use of non-steroidal anti-inflammatory drugs (NSAIDs) including aspirin, smoking and alcohol use.

Gastroduodenal erosions and oesophagitis make up a further 15% of cases. Oesophago-gastric varices, resulting from portal hypertension, are the source of 11% of episodes of UGIB and up to 20% in patients less than 60 years old. Mallory-Weiss tears, the result of repeated vomiting, reportedly account for less than 5% of cases (although patients with a typical history often do not undergo endoscopy) and usually do not require specific treatment. The remaining causes (all <2%) include vascular lesions, such as angiodysplasia, a Dieulafoy lesion and aortoenteric fistula.

Prevention

The development of peptic ulcer disease is closely related to management of the risk factors. The effective identification and eradication of H. pylori has led to a significant reduction in the incidence of peptic ulcer disease as the cause of UGIB.

There is little doubt that restricting the prescription of NSAIDs in the elderly (the highest-risk group for the development of UGIB from NSAIDs and the age group with the highest risk of mortality from UGIB) could prevent a significant number of episodes of UGIB. This is particularly relevant to emergency medicine practice, where NSAIDs are often prescribed as analgesia for musculoskeletal conditions. Care should be taken to prescribe the safest drugs (ibuprofen is the most common NSAID with a low risk profile) for the shortest possible time at the lowest effective dose. Cyclo-oxygenase (COX)-2 selective NSAIDs have been found to cause reduced GI injury, but their use is limited by their increased cardiovascular risks. If patients are assessed as at high risk for possible UGIB, NSAIDs should be avoided or, if unavoidable, a proton pump inhibitor (PPI) should be prescribed with the NSAID to maximize gastric mucosal protection.

Clinical features

It is usually necessary to determine whether the blood loss is from a GI source. Blood from the nose or oropharynx can be swallowed, resulting in haematemesis and/or melaena. If bleeding is thought to be from the upper GI tract, then a number of diagnoses must be considered (see later).

The following historical clues and caveats must be considered:

• A history of epigastric pain or dyspepsia suggests peptic ulcer disease. However, peptic ulcer disease may be painless, particularly in the elderly and in those taking NSAIDs and corticosteroids.

• A positive history of gastric or duodenal ulcer disease or reflux oesophagitis is associated with an approximately 50% chance of finding the same diagnosis at endoscopy.

• The risk of UGIB in patients taking NSAIDs is double that of patients not taking NSAIDs and is still higher than baseline in patients taking PPIs as gastric protection.

• The classic history of nausea and repeated vomiting prior to bleeding occurs in approximately one-third of cases of Mallory-Weiss tear.

• UGIB with a history of alcohol abuse and the stigmata of portal hypertension is suggestive of varices. However, up to 40% of patients with cirrhosis who present with GI bleeding are bleeding from causes other than varices (commonly from gastric erosions).

• Conditions associated with stress ulcers include burns, major trauma, head injury, sepsis and hypotension.

• Patients with chronic renal failure have a high incidence of angiodysplasia, peptic ulcer disease and oesophagitis.

• A history of aortic surgery and GI bleeding raises the possibility of an aortoenteric fistula, even if the initial bleeding episode is not significant (the first bleed is often the ‘herald bleed’).

• Clinical evidence of a coagulopathy should be sought, as this will influence subsequent investigation, treatment and prognosis.

• Current drug treatment should be identified, particularly the use of anticoagulants (traditional or novel), antiplatelet drugs, and NSAIDs.

• Stool examination, by rectal examination if required, is essential. As previously described, stool colour has prognostic significance. Testing for occult blood further increases the sensitivity of this examination as commercial kits are able to detect as little as 6 mg of haemoglobin per gram of stool. A positive test is dependent on the time of onset of bleeding in relation to GI transit time. False positives may be produced by certain bacterial and vegetable peroxidases, such as bananas and horseradish. False negatives may result from ferrous salts.

Clues to the speed or acuity of blood loss include the following:

• The most likely diagnosis. Varices produce large amounts of dark (venous) blood; aortoenteric fistulae produce massive bright red haematemesis and haematochezia, with profound circulatory collapse.

• Signs of haemodynamic instability and response to initial resuscitation. If there is a poor response, there is likely to be significant haemorrhage.

• The character of the vomitus. Ongoing haematemesis is associated with large blood loss; ‘coffee-ground’ altered vomiting or clear fluid is often associated with a slower rate of bleeding.

• The colour of the stool (see earlier).

• The nasogastric aspirate if a tube is already in the stomach (commonly ‘old age home’ residents receiving enteral nutrition). Note that the practice of inserting a nasogastric tube in the emergency department (ED) to assess the aspirate is no longer recommended, as the absence of blood does not exclude significant bleeding.

The key message is that if there is haemodynamic instability or other evidence of significant ongoing UGIB, fluid resuscitation should continue but arrangements should be made to expedite emergency upper GI endoscopy. The accuracy of diagnosis is not important at this stage but the identification of major ongoing bleeding is.

Clinical investigations