Approach

Endoscopy has become a keystone of both diagnosis and therapy. Nevertheless, the importance of a thorough history and physical examination cannot be emphasised enough, as they allow rapid triage of patients who need care on the medical ward or intensive care unit and will also prioritise patients for urgent versus emergency endoscopy.

History

Blood in the gastrointestinal (GI) tract is both a cathartic and a pro-emetic agent. Taking a thorough history can often identify the likely cause of the bleed before endoscopic confirmation. Specific attention should be directed at the following signs and symptoms.

Nausea and vomiting

  • The absence of nausea and vomiting in the setting of melaena or haematochezia thought to be of upper GI origin suggests a bleeding source distal to the pylorus.

  • Lingering of blood in the lumen of the alimentary canal allows for oxidation of the iron component of haemoglobin (Hb) and has the effect of darkening blood. Coffee-ground emesis is suggestive of a slower, possibly intermittent bleed, and melaena (see below) is overwhelmingly associated with UGIB rather than with lower GI bleeding (LGIB), which is distal to the duodenojejunal junction at the ligament of Treitz.[28] Thus, coffee-ground emesis argues more for peptic ulcer disease (PUD) and makes a variceal bleed less likely.

  • Conversely, brisk haematemesis is suggestive of an actively bleeding lesion, most often a variceal bleed (especially in patients with signs of liver disease or portal hypertension), an actively bleeding gastroduodenal ulcer, or a duodenal Dieulafoy's lesion.

  • UGIB starting after vomiting or retching is suggestive of a Mallory-Weiss tear, although many patients with a Mallory-Weiss tear have no history of vomiting. A spontaneous tear of the oesophagus from retching (Boerhaave's syndrome) can be associated with significant haematemesis.

Melaena

  • Melaena is overwhelmingly associated with UGIB.

  • The duration of melaena can be helpful in determining whether the UGIB is acute or chronic, as many conditions (small bowel arteriovenous malformations, etc.) can lead to chronic melaena. Melaena of less than 24-hour duration is difficult to interpret, but persistent melaena hints at a longer duration of UGIB.

  • Melaena by itself is not reason enough to obtain an emergency endoscopy, but quantifying the amount of melaena can still be helpful for triaging patients.

  • It is important to note that a patient reporting melaena is not the same as the patient actively passing melaenic stools. Bismuth-containing products (e.g., Pepto-Bismol) and iron supplements can make the appearance of stools dark or black. A digital rectal examination, including a faecal occult blood test, must be conducted.

Haematochezia

  • Haematochezia is more often seen in LGIB than in UGIB. However, bright red blood per rectum can be seen in a brisk UGIB where the rapidity of the transit time precludes any digestion. Consequently, assessing the quantity of bleeding is imperative for two main reasons:

    • A large amount of haematochezia with other historical factors suggesting an upper GI source requires rapid diagnosis and treatment by upper GI endoscopy.

    • A smaller amount of haematochezia associated only with bowel movements, or in the absence of other signs suggesting an upper source, points to LGIB. Hence, colonoscopy, not upper GI endoscopy, is indicated.

  • Noting the nature of bleeding is salient: persistent or intermittent haematochezia renders an upper source less likely. Conducting a digital rectal examination with a thorough visual inspection of the anus is necessary to rule out external haemorrhoids as the cause of the haematochezia. Anoscopes should be available in most emergency departments.

  • Gastric varices are strongly associated with massive bleeding and rapid haemodynamic compromise. Dieulafoy's lesions often present with rapid blood loss, although bleeding can be intermittent. Aortoenteric fistulae often present with a 'herald bleed' (an episode of self-limiting bleeding before a massive bleed that can result in exsanguination), in the form of either haematochezia or haematemesis.

Diet

  • Not infrequently, patients who have consumed disproportionately large amounts of red gelatine or red-coloured beverages can interpret red-coloured vomitus as haematemesis.

Constitutional symptoms

  • Upper GI tumours can be associated with involuntary weight loss or night sweats.

Medications

  • PUD is often caused by the use of non-steroidal anti-inflammatory drugs (NSAIDs), alone or in combination with corticosteroids and/or antiplatelet or anticoagulant agents. Corticosteroids used in combination with NSAIDs are very ulcerogenic. Patients experiencing acute cardiovascular events are often treated simultaneously with multiple anticoagulant and antiplatelet agents and frequently develop UGIB. A review of the patient's medications to identify potentially causative agents is mandatory. Patients may be unaware that they are ingesting NSAIDs, as these can be included in antacid preparations or combination over-the-counter pain medications.

  • Patients taking aspirin and/or rivaroxaban who experience GI bleeding have a 20-fold higher risk of new GI cancer diagnosis compared with those with no GI bleeding.[29]

  • Use of ≥4 medications is associated with idiopathic PUD.[30]

History of alcoholism or chronic liver disease

  • Conditions causing portal hypertension predispose patients to developing varices. Any history of chronic and excessive alcohol use, intravenous drug use (or other behaviour that places people at risk of contracting hepatitis), or underlying liver disease strongly suggests a variceal bleed and proper precautions (i.e., intravenous octreotide) are warranted. Of note, compromised liver function leads to coagulopathy; this can be severe and can complicate endoscopic therapy.

Other pertinent medical history

  • Oesophagitis is often seen in the context of long-standing heartburn. Patients may mention a globus sensation; hoarseness can also be present. Many patients who present with melaena and who are suspected of PUD will actually be found to have oesophagitis on endoscopy.

  • Any prior history of PUD makes a recurrence more likely.[30]

  • The presence of a hiatal hernia should raise suspicion for Mallory-Weiss tear.

  • Arteriovenous malformations are associated with cirrhosis, end-stage renal disease, advanced age, and von Willebrand's disease.

  • Dieulafoy's lesions are regarded as congenital vascular aneurysms, yet they are most often symptomatic in men with alcohol histories, cardiovascular disease including hypertension, diabetes, or chronic kidney disease.

  • A history of a vascular graft or aortic aneurysm should markedly heighten clinical suspicion for aortoenteric fistulae.

  • Coagulopathy should be considered with history of genetic abnormalities of clotting (e.g., haemophilia, von Willebrand's disease).

Social history

  • Aside from NSAID use, PUD can also frequently be caused by underlying Helicobacter pylori infection. It is important to assess the risk of H pylori infection, as people who grew up in or have recently travelled to developing countries where infection is endemic are at increased risk.

  • Schistosomiasis is an exceedingly rare cause of portal hypertension. This infection should be considered in select cases of birth, work, or an extensive stay in Asia, South America, Africa, or the Caribbean.

Physical examination

In general, the physical examination should be directed at answering two primary questions:

  • What is the degree of anaemia/hypovolaemia?

  • Are there signs of chronic liver disease that might suggest bleeding varices?

Vital signs can be used to estimate the patient's volume status. Blood pressure may remain normal initially, so increased heart rate is a more sensitive measure of circulatory status.[31] If the patient's other comorbidities are not contraindications, tachycardia with hypotension should trigger aggressive volume resuscitation. If the patient is stable, orthostatic blood pressures should be obtained. Capillary refill, moisture in the mucous membranes, and absence of pallor can also assist in assessing the degree of anaemia/hypovolaemia.

Chronic liver disease causing portal hypertension can present in one or more of the following ways:

  • Encephalopathy with or without asterixis

  • Scleral icterus

  • Spider telangiectasias, also known as spider angioma, on the face, chest, or abdomen

  • Gynaecomastia

  • Hepatomegaly or splenomegaly

  • Ascites

  • Caput medusae with or without Cruveilhier-Baumgarten's bruit

  • Hypogonadism

  • Terry's nails (white nails)[32]

  • Palmar erythema.

Visualising the nares and the oropharynx can sometimes identify a source of bleeding that does not require endoscopic management, as epistaxis or gingival bleeding can sometimes mimic UGIB.

A digital rectal examination is mandatory. Visual inspection of the perineum can rule out the presence of external haemorrhoids. Faecal occult blood testing should be conducted.

The degree, location, and character of pain and discomfort can be helpful. In PUD, ingestion of food often transiently improves abdominal pain; mid-epigastric tenderness to palpation is common. Bleeding is sometimes accompanied by mid-epigastric pain or retrosternal pain in patients with a Mallory-Weiss tear. Aortoenteric fistulae can present with significant abdominal or back pain, and fever.

Oesophagitis is sometimes associated with hoarseness. Cachexia should heighten concern for a GI tumour or other type of tumour. In addition, patients with upper GI tumours sometimes have a palpable abdominal mass and/or enlarged liver.

Laboratory tests and imaging

Key tests to obtain in patients with UGIB include a full blood count and coagulation indices. Because patients with UGIB can experience rapid clinical deterioration, blood should be sent for typing and cross-matching in the event that blood products become necessary. Blood transfusion may be initiated when haemoglobin level reaches 7 g/dL, with a target of approximately 8 g/dL.[12][26]

At most facilities, coagulopathies with an international normalised ratio (INR) >1.4 warrant correction with either vitamin K or fresh frozen plasma, or both. Elevated urea can often be seen in UGIB; as blood passes through the small bowel and is partially digested, it can result in an elevated urea and urea/creatinine ratio.

Gastric lavage by saline infused and aspirated through a nasogastric tube can be considered, although this test can at times be difficult to interpret and often does not alter clinical management.[33][34] The European Society of Gastrointestinal Endoscopy does not recommend the routine use of nasogastric or orogastric aspiration/lavage in patients presenting with acute UGIB.[14]

In cases where the source of the bleed is not evident from the history and physical examination, an abdominal computed tomography scan with oral and intravenous contrast should be obtained.

Endoscopy

Endoscopy is highly effective in diagnosing and treating most causes of UGIB.[2] It is also associated with a reduction in blood transfusion requirements, length of stay in the intensive care unit, and total hospital stay.[35]

Early endoscopy (within 24 hours of hospital admission) has a greater impact than later endoscopy on length of hospital stay and requirements for blood transfusion.[36] In appropriate settings, endoscopy can be used to assess the need for inpatient admission. When evaluated in emergency department settings, up to 46% of haemodynamically stable patients who are evaluated for UGIB with upper endoscopy, and subsequently are found to have low-risk stigmata for recurrent bleeding, can be safely discharged and followed as outpatients.[37][38] Not all hospitals are able to accommodate endoscopic procedures in the emergency setting, but if this is possible it can facilitate triage and rapid commencement of treatment for patients with UGIB.

Endoscopy provides clinicians with many options for the treatment of UGIB causes. Thermal methods to induce cautery (heater probes, bipolar probes, argon plasma coagulation) are widely used. Injection of saline or diluted adrenaline (epinephrine) to induce tamponade was once widespread, but it is no longer used as monotherapy (only in combination with other agents). Mechanical clips (either small through-the-scope clips or over-the-scope clips) are widely available. Haemostatic powders, applied as sprays, are available in the US and in some other parts of the world.[39][40][41][42] They can be used as a primary therapy to control acute bleeding, followed by an adjunctive therapeutic modality (e.g., thermal or mechanical therapy) to provide durable haemostasis.[43][44]


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