Acute nonvariceal upper gastrointestinal bleeding (NVUGIB) is a gastrointestinal emergency that has considerable morbidity and mortality. Peptic ulcer bleeding is the most common cause of upper gastrointestinal bleeding (UGIB), and it is responsible for about 31% to 67% of all cases, followed by erosive disease and variceal bleeding. Mallory-Weiss tears, Dieulafoy's lesions, vascular ectasia, and neoplasm comprise the remainder of the possible causes.1 The mortality rate has remained unchanged at 3.5% to 7.4% over the past several decades.2,3,4 Higher mortality is likely associated with one of the following features: hemoglobin <7.0 g/dL, American Society of Anesthesiologists class 4, age >80, renal failure, rebleeding, and failure of endoscopic treatment.5,6 Seventy percent of UGIB is recovered spontaneously without recurrence; however, 10% of patients continue to bleed and 20% experience continued or recurrent bleeding in the first 24 to 72 hours.7 Most high-risk stigmata lesions require around 72 hours to regress into a low-risk appearance after endoscopic therapy, and most rebleeding (about 80%) in high-risk patients occurs within the first 72 hours.8 Therefore, it is suggested that patients with high-risk lesions be admitted to hospital for the 72 hours of high-dose intravenous proton pump inhibitors (IV PPI) therapy after endoscopic hemostasis.8 Furthermore, IV PPI has been found to be cost-effective because it lowers the ration of patients with active bleeding lesions on endoscopic view, thus it reduced the need for further intervention.9,10,11

Before endoscopy, several preventive management strategies can be used to reduce hemostasis-related adverse effects, including volume replacement, restoration of hemodynamic stability, and amendment of coagulopathy. On presentation with UGIB, immediate evaluation and appropriate resuscitation should be carried out. The nasogastric tube insertion in selected patients should be considered because the findings may have prognostic value. Patients should be stratified into low-risk and high-risk groups by using prognostic scales, laboratory data, and endoscopic criteria, as well as by applying a clinical assessment. Very low-risk patients may be discharged, but all other patients should be hospitalized and categorized as low-risk or high-risk to determine treatment options.12,13

Blood transfusions should be considered for a patient with a hemoglobin level of 7.0 g/dL or less. Oral PPI therapy can be administered for low-risk patients, but high-risk patients should be treated with endoscopic and IV high-dose PPI. IV PPI therapy prior to endoscopy may be considered to downstage the endoscopic lesion and decrease the need for endoscopic intervention but it should not delay endoscopy. All patients should be considered for secondary prophylaxis, including a Helicobacter pylori test and treatment, the use of cyclooxygenase-2 antagonists as an alternative to nonsteroidal anti-inflammatory drugs (NSAIDs), and PPI for those taking low-dose aspirin.12,13 The Glasgow-Blatchford scoring system may be used at first assessment, but after endoscopy the full Rockall scoring system should be followed.14,15,16 The scores are calculated using the tables below (Tables 1, 2).

Endoscopy is important for the primary diagnosis and management of acute NVUGIB. Early endoscopy (within 24 hours of presentation) is recommended for most patients with acute UGIB.13 Early endoscopy is related to significant reductions in length of hospital stay, as compared to delayed endoscopy and a decreased need for surgery in elderly patients. Rapid endoscopy within 6 hours did not demonstrate advantages in the outcomes of mortality, need for surgery and transfusion requirements compared with endoscopy within 24 hours.17,18

High-risk lesions for rebleeding include actively spurting lesions (Forrest class IA), oozing blood (class IB), a nonbleeding visible vessel (class IIA), and an adherent clot (class IIB). Low-risk lesions include flat pigmented spots (Forrest class IIC) and clean-based ulcers (class III).19 An endoscopic hemostatic procedure is not required for patients with low-risk stigmata (a clean-based ulcer [III] or a flat pigmented spots [IIc]). A clot in an ulcer bed (IIB) needs to be removed with targeted irrigation, and appropriate treatment should be performed for the underlying lesion. The necessity of endoscopic therapy for ulcers with adherent clots is still debating. Endoscopic hemostatic therapy is required for patients with high-risk stigmata (active bleeding [IA, IB] or a visible vessel in an ulcer bed [IIA]).19 Epinephrine injection is not sufficient for complete hemostasis and should be used in combination with other hemostatic modality.12,13 Clips or thermocoagulation should be used in patients with high-risk lesions, either alone or in combination with other hemostatic modalities. A second-look endoscopy is generally recommended in cases when rebleeding is suspected.13,20,21 Relevant conscious sedation and appropriate use of sedative drugs such as midazolam and propofol during endoscopic hemostasis enhances the success rates and patient's satisfaction.11,22

Many hemostatic methods are available for effective endoscopic hemostasis. These can be categorized based upon their mechanism of action, as follows: 1) injection therapy, 2) mechanical therapy, 3) thermal coagulation, or 4) a combination of these. Several new endoscopic treatments were introduced and applied to control NVUGIB.

Complications during endoscopic hemostatic procedure, including aspiration pneumonia and perforation, have been minimal. A pooled analysis for all modalities has shown a complication rate of 0.5% (95% confidence interval, 0.4 to 0.8).38 Clips and epinephrine injection had the lowest rates of perforation, while the heater probe group had the highest rate.39 Other factors, such as the quality of the endoscopist's skill, unstable patient, poor sedation, poor visual field due to blood, and difficult area of reach, can affect the complications.39

Despite studious attempts with different modalities, endoscopic hemostasis therapy is sometimes unsuccessful. Factors that could predict the failure of endoscopic hemostasis include: large ulcers (2 cm in size), located at the bulbar duodenum or the lesser curvature of the stomach, active bleeding, hemodynamic instability, and the presence of comorbid illnesses.40,41,42 Angiographic embolization may be used as a rescue therapy when there is refractory bleeding to any endoscopic hemostasis. Perforation, uncontrolled bleeding, or unstable vital signs despite repeated hemostasis would be indications of emergent surgery.43

Early endoscopic approachment is important in the identification and management of NVUGIB, especially for patients with high-risk lesions such as active bleeding and visible vessels. Endoscopic hemostatic therapy has been considered as the pivotal treatment for NVUGIB as it has been shown to reduce rebleeding, the need for surgery, mobidity, and mortality. Many safe and effective devices are available for endoscopic hemostasis. Although epinephrine injection provides more beneficial effects than pharmacological methods, the use of clips, thermocoagulation, or a therapeutic option that combines more than one treatment approach is more effective than injection treatment alone. Promising results have recently been reported for the application of hemostasis using Hemospray powder or OTSCs. Selection of the optimal hemostatic device depends upon the characteristics of the lesion, the physician's ability, the availability of the equipment, the patient's clinical conditions, and cost. In addition, adequate H. pylori eradication, PPI therapy, and the withdrawal of NSAIDs can further reduce the rebleeding and mortality rates.1,44