Presentation on theme: "Management of Acute Bleeding from a Peptic Ulcer N Engl J Med 2008;359:928-37."— Presentation transcript:
Management of Acute Bleeding from a Peptic Ulcer N Engl J Med 2008;359:928-37
Epidemiology The vast majority of acute episodes of UGI bleeding (80 to 90%) have nonvariceal causes, with peptic ulcer accounting for the majority of lesions. The annual incidence of bleeding from a peptic ulcer may be decreasing worldwide ( the incidence is 60 per 100,000 population) – –an increasing proportion of episodes related to the use of aspirin and NSAID Peptic ulcer bleeding is seen predominantly among the elderly – –68% > 60Y/O and 27% >80Y/O Mortality associated with peptic ulcer bleeding remains high at 5 to 10%
Management of Acute Bleeding from a Peptic Ulcer, According to Clinical Status and Endoscopic Findings
The first priority in treatment is correcting fluid losses and restoring hemodynamic stability.
Initial Management Assess hemodynamic status – –Tachycardia (pulse, ≥100 beats per minute) – –Hypotension (systolic blood pressure, <100 mm Hg), – –postural changes (an increase in the pulse of ≥20 beats per minute or a drop in systolic blood pressure of ≥20 mm Hg on standing) – –Mucous membranes, neck veins, urine output Obtain CBC, electrolytes, BUN/Cr, PT INR/ APTT, blood type, and cross- match
Initial Management Initiate resuscitation with crystalloid intravenous fluids with the use of large-bore IV-access catheters – –two peripheral catheters of 16 to 18 gauge – –a central catheter if peripheral access is not available PRBC – –If tachycardia or hypotension is present – –If the hemoglobin level is less than 10 g per deciliter. Oxygen correction of coagulopathy
The insertion of a NG tube The presence of red blood in the NG aspirate is an adverse prognostic sign 15% of patients without bloody or coffee- ground material in NG aspirates are found to have high-risk lesions on endoscopy The use of a large-bore OG tube with gastric lavage – –improve visualization of the gastric fundus on endoscopy – –not improve the outcome. No role for occult-blood testing of aspirate
Initial Management Consider giving a single 250-mg IV dose of erythromycin 30 to 60 minutes before endoscopy – –promote gastric motility and substantially improve visualization of the gastric mucosa on initial endoscopy. – –not improve the diagnostic yield of endoscopy substantially or to improve the outcome Consider initiating treatment with an IV PPI (80-mg bolus dose plus continuous infusion at 8 mg/hr) while awaiting early endoscopy – –down-staging of endoscopic lesions – –not have an effect on outcomes – –The cost- effectiveness remains controversial No role for H2 blocker
Risk-Stratification Tools for Upper Gastrointestinal Hemorrhage Blatchford scores from 0 to 23, with higher scores indicating higher risk The Rockall score : -Used clinical and endoscopic criteria -The scale ranges from 0 to 11 points, with higher scores indicating higher risk.
Early endoscopy The cornerstone of treatment performed within 24 hours Improve certain outcomes – –the number of units of blood transfused – –the length of the hospital stay Determine the cause of bleeding, ascertain prognosis, and administer endoscopic therapy. Treatment recommendations have focused on the first 72 hours after presentation and endoscopic evaluation and therapy, since this is the period when the risk of rebleeding is greatest (90 %)
High-risk — Forrest grade IA, IB, or IIA Perform endoscopic hemostasis – –contact thermal therapy – –mechanical therapy ( hemoclips ) – –epinephrine injection, followed by contact thermal therapy or by injection of a second injectable agent. Epinephrine injection as definitive hemostasis therapy is not recommended The endoscopist should use the most familiar hemostasis technique
High-risk — Forrest grade IA, IB, or IIA Admit the patient to a monitored bed or ICU setting(for the first 24 hours of what is usually at least a 3-day hospital stay) Treat with an IV PPI (80-mg bolus dose plus continuous infusion at 8 mg per hour) for 72 hours after endoscopic hemostasis No role for H2 blocker, somatostatin, or octreotide. Initiate oral intake of clear liquids 6 hours after endoscopy in patients with hemodynamic stability Transition to oral PPI after completion of IV therapy. Perform testing for Helicobacter pylori; initiate treatment if the result is positive.
Effect of Proton-Pump Inhibition in Peptic-Ulcer Bleeding
Gastric acid impairs clot formation, promotes platelet disaggregation, and favors fibrinolysis Inhibiting gastric acid and raising the intragastric pH to 6 or more and maintaining it at that level may promote clot stability, thus decreasing the likelihood of rebleeding. Although data from clinical trials support the use of a bolus followed by a continuous infusion of proton-pump inhibitors, recent studies from North America show that even a high-dose, continuous infusion of proton- pump inhibitors may not sustain an intragastric pH of 6 or more. The reduction in mortality appears to occur only among patients with high- risk stigmata who have first undergone endoscopic therapy, a finding that supports the use of medical therapy as an adjunct to but not a replacement for endoscopic hemostasis.. Intravenous bolus loading followed by continuous infusion of proton-pump inhibitors is more effective than bolus dosing alone in decreasing the rates of rebleeding and the need for surgery
High-dose oral PPI The use of high-dose oral PPI in peptic- ulcer bleeding has been shown in Asian populations reductions – –the risk of rebleeding – –the need for surgery – –the risk of death These results may not be completely generalizable to North American or European populations
Second-look endoscopy Planned, second-look endoscopy that is performed within 24 hours after initial endoscopic therapy has not been recommended. It provided only a limited reduction in the rate of rebleeding. (Two meta-analyses) It may not be cost-effective when medical therapy leading to profound acid suppression is used. Repeat endoscopy may be considered on a case-by- case – –if there are clinical signs of recurrent bleeding – –if there is uncertainty regarding the effectiveness of hemostasis during the initial treatment.
Forrest grade IIB Forrest classification
High-risk — Forrest grade IIB Consider endoscopic removal of adherent clot, followed by endoscopic hemostasis if underlying active bleeding or nonbleeding visible vessel is present. Admit the patient to a monitored bed or ICU setting. Treat with IV PPI (80-mg bolus dose plus continuous infusion at 8 mg per hour) for 72 hours after endoscopy, regardless of whether endoscopic hemostasis was performed No role for H2 blocker, somatostatin, or octreotide Initiate oral intake of clear liquids 6 hours after endoscopy in patients with hemodynamic stability Transition to an oral PPI after completion of IV therapy. Perform testing for H. pylori; initiate treatment if the result is positive.
Forrest grade IICForrest grade III Forrest classification
Low-risk — Forrest grade IIC or III Do not perform endoscopic hemostasis. Consider early hospital discharge after endoscopy if the patient has an otherwise low clinical risk and safe home environment. Treat with an oral PPI. Initiate oral intake with a regular diet 6 hours after endoscopy in patients with hemodynamic stability. Perform testing for H. pylori; initiate treatment if the result is positive.
Predictors of failure of endoscopic treatment History of peptic ulcer disease Previous ulcer bleeding The presence of shock at presentation Active bleeding during endoscopy Large ulcers (>2 cm in diameter) Large bleeding vessel (≥2 mm in diameter) Ulcers located on the lesser curve of the stomach or on the posterior or superior duodenal bulb
After endoscopy If there is clinical evidence of ulcer rebleeding, repeat endoscopy with an attempt at endoscopic hemostasis,obtain surgical or interventional radiologic consultation for selected patients. For selected patients, discuss the need for ongoing use of NSAIDs, antiplatelet agents, and concomitant therapy with a gastroprotective agent.