Upper gastrointestinal bleeding is described as blood loss from a gastrointestinal source above the ligament of Treitz. Gastrointestinal bleeding may occur from any part of the gut and remains a significant health problem. Ulcers are the most common cause of hospitalization for upper gastrointestinal (GI) bleeding. Thus, the vast majority of clinical trials of therapy for upper gastrointestinal bleeding focus on ulcer disease.
Acute upper gastrointestinal bleeding (UGIB) continues to be the most common gastrointestinal (GI) emergency. It has an annual UK incidence of 103-172 per 100,000 adults and accounts for over 9,000 deaths a year in the UK. Recent UK data have reported a stable incidence over time and a rise in the proportion of patients with variceal bleeding, but lower overall mortality and need for surgery. Studied mortality trends in England amongst admissions with non-variceal upper gastrointestinal bleeding between 1999 and 2005 and found mortality had declined in younger age groups but not in those aged 80 years or more. Age and sex adjusted mortality rates were shown to have declined by 3.1 % per year from 1999 to 2007 in a similar analysis from Wales. This decline in mortality, despite an increase in variceal bleeding, suggests improvements in overall management. A UK wide audit of upper gastrointestinal bleeding confirmed that most patients are elderly, with a median age of 68 years; 63% of all patients were >60 years of age while 28 % were ≥80 years old.
The percentage of older patients suffering from upper gastrointestinal bleeding has increased rapidly over recent years in the Western world, mostly because of increased life expectancy and widespread use of drugs such as NSAIDS and anticoagulants. Advanced age has been consistently identified as a risk factor for mortality among patients with upper gastrointestinal bleeding, presumably because of a higher prevalence of comorbid illnesses, including cardiovascular and pulmonary disease, in the elderly.
Upper gastrointestinal bleeding is a common medical emergency worldwide and refers to bleeding from the esophagus, stomach, or duodenum. Patients present with hematemesis (bloody or coffee ground emesis) or melena, although hematochezia can occur in the context of a major bleed and is typically associated with hemodynamic instability. Patients with melena present with lower hemoglobin values than patients with hematemesis, probably because presentation is more likely to be delayed. Therefore, patients with melena more often require transfusion, although mortality is lower in patients with melena than in those with hematemesis in some series. Numerous improvements in the management of upper gastrointestinal bleeding have been incorporated into clinical practice in recent years. However, many patients now have risk factors for a poorer outcome, including increasing age and major medical comorbidities.
Melena may be seen in varying stages of blood loss, with as little as 50 ml of blood. Hematemesis (vomiting of bright red blood) is suggestive of moderate to severe bleeding; whereas coffee ground emesis (oxidation of the heme molecule of red blood cells due to gastric acid) suggests more limited bleeding. The yearly incidence of hospitalization for acute upper gastrointestinal bleeding is about 100 per 100,000 people. The upper gastrointestinal bleeding rate of admission to the hospital is six times higher as compared to lower GI bleeding.
Although the cause of a bleeding episode is uncertain until endoscopy is undertaken, guidelines often separate upper gastrointestinal bleeding into variceal and non-variceal bleeding because management and outcomes differ.
The source of bleeding cannot be recognized in 10%-15% of patients with upper gastrointestinal bleeding; either the lesion is hard to identify (such as a Dieulafoy's lesion), obscured by a retained blood clot at endoscopy, or the lesion has already healed by the time endoscopy was performed. The four major risk factors for bleeding peptic ulcers are: Helicobacter pylori (H. pylori) infection, use of non-steroidal anti-inflammatory drugs (NSAIDs), physiologic stress, and excess gastric acid.
Endoscopy allows visualization of source of bleeding and therapeutic intervention or biopsy. Endoscopy should be performed in a non-emergent setting. Patients should be hemodynamically stabilized and should undergo an endoscopy within 24 hours of admission. If the patient is hemodynamically stable on admission and does not have serious comorbidities, an endoscopy should be performed as soon as possible. Patients with endoscopic findings of high-risk stigmata (active bleeding, visible vessel, clots) should be hospitalized for three days assuming no further episode of bleeding occurs. They can be fed with clear liquids soon after endoscopy. Clear liquids provide the advantage that if the patient starts to bleed again, sedation and anesthesia can be given within two hours after the last ingestion. Patients with clean-based ulcers can be discharged home if they have a residence and someone can observe them.
Severe bleeding despite conservative medical treatment or endoscopic intervention occurs in 5%-10% of patients and requires surgery or transcatheter arterial embolization. Surgery is associated with a mortality rate as high as 20%-40% Indeed, patients who developed failed endoscopic hemostasis are likely to be poor surgical candidates with multiple co-morbidities. In the past decade, it has been considered in many institutions as the first-line intervention for massive bleeding from gastroduodenal ulcer after failed endoscopic treatment.
Radiologic embolisation is highly useful for patients with recurrent bleeding despite medical or surgical intervention, but local protocols and expertise vary greatly. The advantages include the avoidance of surgery, the use in high-risk patients unfit for surgery, advanced malignant gastric ulcer, and an occult bleeding not visualized at oesopagogastroduodenoscopy. The bleeding artery is embolized by hemostatic substances such as metal coils, oxidized cellulose, gel foam, or polyvinyl alcohol. Bleeding can also be controlled by selective infusion of vasopressin into the local circulation via the left gastric artery as an adjunct for non-operative management of upper GI bleeding.
The prevention of recurrent bleeding is based on the etiology of the bleeding ulcer. H. pylori is eradicated with triple therapy including a PPI and 2 antimicrobial agents (amoxycillin 1 g or clarithromycin 500 mg or metronidazole 500 mg), all given twice a day for 7-14 days, and, after cure is documented anti-ulcer therapy is generally not given. Cure of H. pylori should be confirmed 4 weeks after treatment with C13 urea breath test for duodenal ulcer or repeat endoscopy for gastric ulcer and if there is suspicion of malignancy. NSAIDs are stopped but if they must be resumed low-dose COX-2-selective NSAID plus PPI is used. Patients with established cardiovascular disease who require aspirin should start PPI and generally reinstitute aspirin soon after bleeding ceases. Patients with idiopathic ulcers receive long-term antiulcer therapy. Because of the side effect of platelet dysfunction with the selective serotonin reuptake inhibitor (SSRI) antidepressant, it should be used with caution, or, ideally a selective serotonin reuptake inhibitor may be an appropriate choice in patients who have increased risk of GI bleeding especially in patients taking NSAID or aspirin.
