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Author

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Acknowledgements

Faisal Aziz, MD Assistant Professor of Surgery, Divsion of Vascular and Endovascular Surgery, Department of Surgery, Pennsylvania State University College of Medicine

Faisal Aziz, MD is a member of the following medical societies: American College of Surgeons and American Medical Association

Disclosure: Nothing to disclose.

Simmy Bank, MD Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.

Jeffrey Glenn Bowman, MD, MS Consulting Staff, Highfield MRI

Disclosure: Nothing to disclose.

Carmen Cuffari, MD Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine

Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Brian James Daley, MD, MBA, FACS, FCCP, CNSC Professor and Program Director, Department of Surgery, Chief, Division of Trauma and Critical Care, University of Tennessee Health Science Center College of Medicine

Brian James Daley, MD, MBA, FACS, FCCP, CNSC is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Chest Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Association for Surgical Education, Eastern Association for the Surgery of Trauma, Shock Society, Society of Critical Care Medicine, Southeastern Surgical Congress, and Tennessee Medical Association

Disclosure: Nothing to disclose.

Shane M Devlin, MD, FRCP(C) Clinical Assistant Professor, Department of Internal Medicine, Peter Lougheed Center, University of Calgary, Canada

Shane M Devlin, MD, FRCP(C) is a member of the following medical societies: American Gastroenterological Association, Canadian Association of Gastroenterology, Canadian Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Steven C Dronen, MD, FAAEM Chair, Department of Emergency Medicine, LeConte Medical Center

Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

George T Fantry, MD Associate Professor of Medicine, Department of Internal Medicine, Division of Gastroenterology, University of Maryland School of Medicine

George T Fantry, MD is a member of the following medical societies: American College of Gastroenterology and American Gastroenterological Association

Disclosure: Nothing to disclose.

John Geibel, MD, DSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital

John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract

Disclosure: AMGEN Royalty Consulting; Ardelyx Ownership interest Board membership

David Greenwald, MD Associate Professor of Clinical Medicine, Fellowship Program Director, Department of Medicine, Division of Gastroenterology, Montefiore Medical Center, Albert Einstein College of Medicine

David Greenwald, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, and New York Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Harsh Grewal, MD, FACS, FAAP Clinical Professor of Surgery, Temple University School of Medicine; Chief, Division of Pediatric Surgery, Cooper University Hospital

Harsh Grewal, MD, FACS, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Surgeons, American Pediatric Surgical Association, Association for Surgical Education, Children's Oncology Group, Eastern Association for the Surgery of Trauma, International Pediatric Endosurgery Group, Society of American Gastrointestinal and Endoscopic Surgeons, Society of Laparoendoscopic Surgeons, and SouthwesternSurgical Congress

Disclosure: Nothing to disclose.

Eugene Hardin, MD, FAAEM, FACEP Former Chair and Associate Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King Jr/Drew Medical Center

Disclosure: Nothing to disclose.

Andre Hebra, MD Chief, Division of Pediatric Surgery, Professor of Surgery and Pediatrics, Medical University of South Carolina College of Medicine; Surgeon-in-Chief, Medical University of South Carolina Children's Hospital

Andre Hebra, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, Children's Oncology Group, Florida Medical Association, International Pediatric Endosurgery Group, Society of American Gastrointestinal and Endoscopic Surgeons, Society of Laparoendoscopic Surgeons,South Carolina Medical Association, Southeastern Surgical Congress, and Southern Medical Association

Disclosure: Nothing to disclose.

Juda Zvi Jona MD, FAAP(s), FACS, EUPSA, Clinical Professor of Surgery, Michigan State University College of Human Medicine; Clinical Professor of Surgery, Northwestern University, The Feinberg School of Medicine; Attending Senior Surgeon, Director of Pediatric Surgery Service, Surgical Executive Committee, Sparrow Hospital

Juda Zvi Jona is a member of the following medical societies: Alpha Omega Alpha, American Bronchoesophagological Association, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, Association for Academic Surgery, British Association of Paediatric Surgeons, Central Surgical Association, Children's Oncology Group, and International Pediatric Endosurgery Group

Disclosure: Nothing to disclose.

Daryl Lau, MD, MPH, MSc, FRCP(C) Director of Translational Liver Research, Liver Center, Division of Gastroenterology, Department of Medicine, Beth Israel Deaconess Medical Center; Associate Professor of Medicine, Harvard Medical School

Daryl Lau, MD, MPH, MSc, FRCP(C) is a member of the following medical societies: American Association for the Study of Liver Diseases and American Gastroenterological Association

Disclosure: Nothing to disclose.

Tri H Le, MD Assistant Professor of Medicine, Division of Gastroenterology and Hepatology, Penn State Milton S Hershey Medical Center

Tri H Le, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society of Gastrointestinal Endoscopy, and Crohns and Colitis Foundation of America

Disclosure: Nothing to disclose.

Terence David Lewis, MBBS, FRACP, FRCPC, FACP Program Director, Internal Medicine Residency, & Assistant Chairman, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, Loma Linda University Medical Center

Terence David Lewis, MBBS, FRACP, FRCPC, FACP is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, California Medical Association, Royal College of Physicians and Surgeons of Canada, and Sigma Xi

Disclosure: Nothing to disclose.

B UK Li, MD Professor of Pediatrics, Division of Gastroenterology, Hepatology and Nutrition, Director, Pediatric Fellowships and Gastroenterology Fellowship, Medical Director, Functional Gastrointestinal Disorders and Cyclic Vomiting Program, Medical College of Wisconsin; Attending Gastroenterologist, Children's Hospital of Wisconsin

B UK Li, MD is a member of the following medical societies: Alpha Omega Alpha, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Chris A Liacouras MD, Director of Pediatric Endoscopy, Division of Gastroenterology and Nutrition, Children's Hospital of Philadelphia; Associate Professor of Pediatrics, University of Pennsylvania School of Medicine

Chris A Liacouras is a member of the following medical societies: American Gastroenterological Association

Disclosure: Nothing to disclose.

Wendi S Miller, MD Resident Physician, Department of Emergency Medicine, Emory University School of Medicine

Wendi S Miller, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Southern Medical Association

Disclosure: Nothing to disclose.

Robert K Minkes, MD, PhD Professor of Surgery, University of Texas Southwestern Medical Center at Dallas, Southwestern Medical School; Medical Director and Chief of Surgical Services, Children's Medical Center of Dallas-Legacy Campus

Robert K Minkes, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Waqar A Qureshi, MD Associate Professor of Medicine, Chief of Endoscopy, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine and Veterans Affairs Medical Center

Waqar A Qureshi, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Erick F Rivas, MD, PT Resident Physician, Department of Surgery, Michigan State University College of Human Medicine

Erick F Rivas, MD, PT is a member of the following medical societies: American College of Surgeons

Disclosure: Nothing to disclose.

Ameesh Shah, MD Assistant Professor of Pediatrics, Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Children's Memorial Hospital

Ameesh Shah, MD is a member of the following medical societies: North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Philip Shayne MD, Associate Professor, Program Director and Vice Chair for Education, Department of Emergency Medicine, Emory University School of Medicine

Philip Shayne is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Sanjeeb Shrestha, MD Consulting Staff, Division of Gastroenterology, Gastroenterology Care Consultants

Sanjeeb Shrestha, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, and American Society of Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Mutaz I Sultan, MBChB Makassed Hospital, Israel

Mutaz I Sultan, MBChB is a member of the following medical societies: American Gastroenterological Association and North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Alan BR Thomson, MD Professor of Medicine, Division of Gastroenterology, University of Alberta, Canada

Alan BR Thomson, MD is a member of the following medical societies: Alberta Medical Association, American College of Gastroenterology, American Gastroenterological Association, Canadian Association of Gastroenterology, Canadian Medical Association, College of Physicians and Surgeons of Alberta, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Noel Williams, MD Professor Emeritus, Department of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; Professor, Department of Internal Medicine, Division of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada

Noel Williams, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Jay A Yelon, DO, FACS Associate Professor of Surgery and Anesthesiology, Program Director, Surgical Critical Care Fellowship, New York Medical College; Chief, Division of Trauma and Surgical Critical Care, Westchester Medical Center

Jay A Yelon, DO, FACS is a member of the following medical societies: American Association for the Surgery of Trauma, American Burn Association, American College of Surgeons, American Trauma Society, Association for Academic Surgery, Eastern Association for the Surgery of Trauma, Pan American Trauma Society, Shock Society, Society of Critical Care Medicine, Southeastern Surgical Congress, and Surgical Infection Society

Disclosure: Nothing to disclose.

KALYANAKRISHNAN RAMAKRISHNAN, MD, FRCSE, and ROBERT C. SALINAS, MD, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma

Am Fam Physician. 2007 Oct 1;76(7):1005-1012.

Patient information: See related handout on peptic ulcers, written by the authors of this article.

Peptic ulcer disease usually occurs in the stomach and proximal duodenum. The predominant causes in the United States are infection with Helicobacter pylori and use of nonsteroidal anti-inflammatory drugs. Symptoms of peptic ulcer disease include epigastric discomfort (specifically, pain relieved by food intake or antacids and pain that causes awakening at night or that occurs between meals), loss of appetite, and weight loss. Older patients and patients with alarm symptoms indicating a complication or malignancy should have prompt endoscopy. Patients taking nonsteroidal anti-inflammatory drugs should discontinue their use. For younger patients with no alarm symptoms, a test-and-treat strategy based on the results of H. pylori testing is recommended. If H. pylori infection is diagnosed, the infection should be eradicated and antisecretory therapy (preferably with a proton pump inhibitor) given for four weeks. Patients with persistent symptoms should be referred for endoscopy. Surgery is indicated if complications develop or if the ulcer is unresponsive to medications. Bleeding is the most common indication for surgery. Administration of proton pump inhibitors and endoscopic therapy control most bleeds. Perforation and gastric outlet obstruction are rare but serious complications. Peritonitis is a surgical emergency requiring patient resuscitation; laparotomy and peritoneal toilet; omental patch placement; and, in selected patients, surgery for ulcer control.

Peptic ulcer disease is a problem of the gastrointestinal tract characterized by mucosal damage secondary to pepsin and gastric acid secretion. It usually occurs in the stomach and proximal duodenum; less commonly, it occurs in the lower esophagus, the distal duodenum, or the jejunum, as in unopposed hyperse-cretory states such as Zollinger-Ellison syndrome, in hiatal hernias (Cameron ulcers), or in ectopic gastric mucosa (e.g., in Meckel's diverticulum).

Approximately 500,000 persons develop peptic ulcer disease in the United States each year.1 In 70 percent of patients it occurs between the ages of 25 and 64 years.2 The annual direct and indirect health care costs of the disease are estimated at about $10 billion.1 However, the incidence of peptic ulcers is declining, possibly as a result of the increasing use of proton pump inhibitors and decreasing rates of Helicobacter pylori infection.3

Causes of Peptic Ulcer Disease

H. pylori infection and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) are the predominant causes of peptic ulcer disease in the United States, accounting for 48 and 24 percent of cases, respectively (Table 1).4 A variety of other infections and comor-bidities are associated with a greater risk of peptic ulcer disease (e.g., cytomegalovirus, tuberculosis, Crohn's disease, hepatic cirrhosis, chronic renal failure, sarcoidosis, myeloproliferative disorder). Critical illness, surgery, or hypovolemia leading to splanchnic hypoperfusion may result in gastroduo-denal erosions or ulcers (stress ulcers); these may be silent or manifest with bleeding or perforation.5 Smoking increases the risk of ulcer recurrence and slows healing.

H. PYLORI

Although H. pylori is present in the gastroduodenal mucosa in most patients with duodenal ulcers, only a minority (10 to 15 percent) of patients with H. pylori infection develop peptic ulcer disease.6 H. pylori bacteria adhere to the gastric mucosa; the presence of an outer inflammatory protein and a functional cytotoxin-associated gene island in the bacterial chromosome increases virulence and probably ulcerogenic potential.7 Patients with H. pylori infection have increased resting and meal-stimulated gastrin levels and decreased gastric mucus production and duodenal mucosal bicarbonate secretion, all of which favor ulcer formation. Eradication of H. pylori greatly reduces the incidence of ulcer recurrence—from 67 to 6 percent in patients with duodenal ulcers and from 59 to 4 percent in patients with gastric ulcers.8

NSAIDS

NSAIDs are the most common cause of peptic ulcer disease in patients without H. pylori infection.9 Topical effects of NSAIDs cause submucosal erosions. In addition, by inhibiting cyclooxygenase, NSAIDs inhibit the formation of prostaglandins and their protective cyclooxygenase-2–mediated effects (i.e., enhancing gastric mucosal protection by stimulating mucus and bicarbonate secretion and epithelial cell proliferation and increasing mucosal blood flow). Coexisting H. pylori infection increases the likelihood and intensity of NSAID-induced damage.10

The annual risk of a life-threatening ulcer-related complication is 1 to 4 percent in patients who use NSAIDs long-term, with older patients at the highest risk.11 NSAID use is responsible for approximately one half of perforated ulcers, which occur most commonly in older patients who are taking aspirin or other NSAIDs for cardiovascular disease or arthropathy.12,13  Other risk factors for NSAID-related ulcers are listed in Table 1.4 Proton pump inhibitors and misoprostol (Cytotec) minimize the ulcerogenic potential of NSAIDs and reduce NSAID-related ulcer recurrence.

View/Print Table

Table 1.

Causes of Gastroduodenal Ulcers

CauseComments

Common

Helicobacter pylori infection

Gram-negative, motile spiral rod found in 48 percent of patients with peptic ulcer disease4

NSAIDs

5 to 20 percent of patients who use NSAIDs over long periods develop peptic ulcer disease

NSAID-induced ulcers and complications are more common in older patients, patients with a history of ulcer or gastrointestinal bleeding, those who use steroids or anticoagulants, and those with major organ impairment

Other medications

Steroids, bisphosphonates, potassium chloride, chemotherapeutic agents (e.g., intravenous fluorouracil)

Rare

Acid-hypersecretory states (e.g., Zollinger- Ellison syndrome)

Multiple gastroduodenal, jejunal, or esophageal ulcers

Malignancy

Gastric cancer, lymphomas, lung cancers

Stress

After acute illness, multiorgan failure, ventilator support, extensive burns (Curling's ulcer), or head injury (Cushing's ulcer)

Table 1.

Causes of Gastroduodenal Ulcers

CauseComments

Common

Helicobacter pylori infection

Gram-negative, motile spiral rod found in 48 percent of patients with peptic ulcer disease4

NSAIDs

5 to 20 percent of patients who use NSAIDs over long periods develop peptic ulcer disease

NSAID-induced ulcers and complications are more common in older patients, patients with a history of ulcer or gastrointestinal bleeding, those who use steroids or anticoagulants, and those with major organ impairment

Other medications

Steroids, bisphosphonates, potassium chloride, chemotherapeutic agents (e.g., intravenous fluorouracil)

Rare

Acid-hypersecretory states (e.g., Zollinger- Ellison syndrome)

Multiple gastroduodenal, jejunal, or esophageal ulcers

Malignancy

Gastric cancer, lymphomas, lung cancers

Stress

After acute illness, multiorgan failure, ventilator support, extensive burns (Curling's ulcer), or head injury (Cushing's ulcer)

Diagnosis of Peptic Ulcer Disease

The diagnosis of peptic ulcer disease is usually based on clinical features and specific testing, although it is important to be aware that individual signs and symptoms are relatively unreliable.

CLINICAL FEATURES

Typical symptoms of peptic ulcer disease include episodic gnawing or burning epigastric pain; pain occurring two to five hours after meals or on an empty stomach; and nocturnal pain relieved by food intake, antacids, or antisecretory agents. A history of episodic or epigastric pain, relief of pain after food intake, and nighttime awakening because of pain with relief following food intake are the most specific findings for peptic ulcer and help rule in the diagnosis.14 Less common features include indigestion, vomiting, loss of appetite, intolerance of fatty foods, heartburn, and a positive family history.14 The physical examination is unreliable—in one study, tenderness to deep palpation reduced the likelihood of ulcer.14

The natural history and clinical presentation of peptic ulcer disease differ in individual populations (Table 26,15–18).15 Abdominal pain is absent in at least 30 percent of older patients with peptic ulcers.16 Postprandial epigastric pain is more likely to be relieved by food or antacids in patients with duodenal ulcers than in those with gastric ulcers. Weight loss precipitated by fear of food intake is characteristic of gastric ulcers.

EVALUATION

If the initial clinical presentation suggests the diagnosis of peptic ulcer disease, the patient should be evaluated for alarm symptoms. Anemia, hematemesis, melena, or heme-positive stool suggests bleeding; vomiting suggests obstruction; anorexia or weight loss suggests cancer; persisting upper abdominal pain radiating to the back suggests penetration; and severe, spreading upper abdominal pain suggests perforation. Patients older than 55 years and those with alarm symptoms should be referred for prompt upper endoscopy. Esophagogastroduodenoscopy (EGD) is more sensitive and specific for peptic ulcer disease than upper gastrointestinal barium studies and allows biopsy of gastric lesions.19

Patients younger than 55 years with no alarm symptoms should be tested for H. pylori infection and advised to discontinue the use of NSAIDs, smoking, alcohol, and illicit drug use. Presence of H. pylori can be confirmed with a serum enzyme-linked immunosorbent assay (ELISA), urea breath test, stool antigen test, or endoscopic biopsy (Table 31,19,20). Serum ELISA is the least accurate test and is useful only for diagnosing the initial infection. The stool antigen test is less convenient but is highly accurate and can also be used to confirm H. pylori eradication, as can the urea breath test.19

If test results are positive for H. pylori, the infection should be eradicated and antisecretory therapy, preferably with a proton pump inhibitor, administered for four weeks1,19 (Figure 1). Further management is based on the endoscopic or radiologic diagnosis. Patients with persistent symptoms should be referred for endoscopy to rule out refractory ulcer and malignancy.

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Table 2.

Peptic Ulcer Disease in Different Populations

PopulationFeatures

Children

Incidence: Rare; most ulcers occur between eight and 17 years of age; duodenal ulcer up to 30 times more common than gastric ulcer

Cause: Helicobacter pylori infection contributory

Presentation: Patients may present with poorly localized abdominal pain

Testing: EGD should be performed if ulcer suspected; test- and-treat strategy not recommended; H. pylori testing and treatment recommended only if ulcer is documented by EGD or contrast studies

Treatment: Antisecretory agents

Complications: 25 percent of bleeding duodenal ulcers may be silent; perforation and penetration rare

Older patients

Presentation: More likely to have painless ulcers; 50 percent present acutely (e.g., with perforation); may present with nonspecific complaints (e.g., confusion, restlessness, abdominal distention, fall)

Complications: Perforations associated with mortality three times higher than in younger patients; hemorrhagic complications more likely (20 percent from silent ulcers); more likely to have continued bleeding and to need transfusions and surgery

Patients with stress ulcers

Cause: Breakdown of mucosal protectants as a result of stress leads to splanchnic hypoperfusion and ulcer; risk factors include mechanical ventilation longer than 48 hours, burns, coagulopathy, moderate to severe trauma, head or spinal cord injury, liver failure, and organ transplantation

Presentation: Patients may be asymptomatic or may develop bleeding or perforation

Treatment: Early institution of PPI prophylaxis with oral or intravenous pantoprazole (Protonix) minimizes ulcer risk; histamine H2 blockers and sucralfate (Carafate) are other options for prophylaxis

Pregnant women

Presentation: Ulcer symptoms milder and may improve during pregnancy; vomiting is nocturnal or postprandial and worse in third trimester

Testing: Ultrasonography and EGD are safe diagnostic tests

Treatment: Early, aggressive treatment with PPI recommended; misoprostol (Cytotec) contraindicated; H. pylori infection treated as usual; avoid tetracyclines throughout pregnancyand metronidazole (Flagyl) during first trimester

Complications: Infrequent; hypotension treated vigorously to minimize placental hypoperfusion; risk of miscarriage, abruption, and preterm labor if complications ensue

Table 2.

Peptic Ulcer Disease in Different Populations

PopulationFeatures

Children

Incidence: Rare; most ulcers occur between eight and 17 years of age; duodenal ulcer up to 30 times more common than gastric ulcer

Cause: Helicobacter pylori infection contributory

Presentation: Patients may present with poorly localized abdominal pain

Testing: EGD should be performed if ulcer suspected; test- and-treat strategy not recommended; H. pylori testing and treatment recommended only if ulcer is documented by EGD or contrast studies

Treatment: Antisecretory agents

Complications: 25 percent of bleeding duodenal ulcers may be silent; perforation and penetration rare

Older patients

Presentation: More likely to have painless ulcers; 50 percent present acutely (e.g., with perforation); may present with nonspecific complaints (e.g., confusion, restlessness, abdominal distention, fall)

Complications: Perforations associated with mortality three times higher than in younger patients; hemorrhagic complications more likely (20 percent from silent ulcers); more likely to have continued bleeding and to need transfusions and surgery

Patients with stress ulcers

Cause: Breakdown of mucosal protectants as a result of stress leads to splanchnic hypoperfusion and ulcer; risk factors include mechanical ventilation longer than 48 hours, burns, coagulopathy, moderate to severe trauma, head or spinal cord injury, liver failure, and organ transplantation

Presentation: Patients may be asymptomatic or may develop bleeding or perforation

Treatment: Early institution of PPI prophylaxis with oral or intravenous pantoprazole (Protonix) minimizes ulcer risk; histamine H2 blockers and sucralfate (Carafate) are other options for prophylaxis

Pregnant women

Presentation: Ulcer symptoms milder and may improve during pregnancy; vomiting is nocturnal or postprandial and worse in third trimester

Testing: Ultrasonography and EGD are safe diagnostic tests

Treatment: Early, aggressive treatment with PPI recommended; misoprostol (Cytotec) contraindicated; H. pylori infection treated as usual; avoid tetracyclines throughout pregnancyand metronidazole (Flagyl) during first trimester

Complications: Infrequent; hypotension treated vigorously to minimize placental hypoperfusion; risk of miscarriage, abruption, and preterm labor if complications ensue

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Table 3.

Tests Used in the Diagnosis of Peptic Ulcer

TestComments

EGD

Indicated in patients with evidence of bleeding, weight loss, chronicity, or persistent vomiting; those whose symptoms do not respond to medications; and those older than 55 years

More than 90 percent sensitivity and specificity in diagnosing gastric and duodenal ulcers and cancers

Barium or diatrizoate meglumine and diatrizoate sodium (Gastrografin) contrast radiography (double-contrast hypotonic duodenography)

Indicated when endoscopy is unsuitable or not feasible, or if complications such as gastric outlet obstruction suspected

Diagnostic accuracy increases with extent of disease; 80 to 90 percent sensitivity in detecting duodenal ulcers

Helicobacter pylori testing

Serologic ELISA

Useful only for initial testing (sensitivity, 85 percent; specificity, 79 percent); cannot be used to confirm eradication

Urea breath test

More expensive

Sensitivity, 95 to 100 percent; specificity, 91 to 98 percent; can be used to confirm eradication PPI therapy should be stopped for two weeks before test

Stool antigen test

Inconvenient but accurate (sensitivity, 91 to 98 percent; specificity, 94 to 99 percent) Can be used to confirm eradication

Urine-based ELISA and rapid urine test

Sensitivity, 70 to 96 percent; specificity, 77 to 85 percent Cannot be used to confirm eradication

Endoscopic biopsy

Culture (sensitivity, 70 to 80 percent; specificity, 100 percent), histology (sensitivity, > 95 percent; specificity, 100 percent), rapid urease (CLO) test (sensitivity, 93 to 97 percent; specificity, 100 percent)

Table 3.

Tests Used in the Diagnosis of Peptic Ulcer

TestComments

EGD

Indicated in patients with evidence of bleeding, weight loss, chronicity, or persistent vomiting; those whose symptoms do not respond to medications; and those older than 55 years

More than 90 percent sensitivity and specificity in diagnosing gastric and duodenal ulcers and cancers

Barium or diatrizoate meglumine and diatrizoate sodium (Gastrografin) contrast radiography (double-contrast hypotonic duodenography)

Indicated when endoscopy is unsuitable or not feasible, or if complications such as gastric outlet obstruction suspected

Diagnostic accuracy increases with extent of disease; 80 to 90 percent sensitivity in detecting duodenal ulcers

Helicobacter pylori testing

Serologic ELISA

Useful only for initial testing (sensitivity, 85 percent; specificity, 79 percent); cannot be used to confirm eradication

Urea breath test

More expensive

Sensitivity, 95 to 100 percent; specificity, 91 to 98 percent; can be used to confirm eradication PPI therapy should be stopped for two weeks before test

Stool antigen test

Inconvenient but accurate (sensitivity, 91 to 98 percent; specificity, 94 to 99 percent) Can be used to confirm eradication

Urine-based ELISA and rapid urine test

Sensitivity, 70 to 96 percent; specificity, 77 to 85 percent Cannot be used to confirm eradication

Endoscopic biopsy

Culture (sensitivity, 70 to 80 percent; specificity, 100 percent), histology (sensitivity, > 95 percent; specificity, 100 percent), rapid urease (CLO) test (sensitivity, 93 to 97 percent; specificity, 100 percent)

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Treatment of Peptic Ulcer Disease

Figure 1.

Algorithm for the treatment of peptic ulcer disease. (EGD = esophagogastroduodenoscopy; PPI = proton pump inhibitor; NSAID = nonsteroidal anti-inflammatory drug.)

*—Alarm symptoms include evidence of bleeding (e.g., anemia, heme-positive stool, melena), perforation (e.g., severe pain), obstruction (e.g., vomiting), and malignancy (e.g., weight loss, anorexia).

Treatment of Peptic Ulcer Disease


Figure 1.

Algorithm for the treatment of peptic ulcer disease. (EGD = esophagogastroduodenoscopy; PPI = proton pump inhibitor; NSAID = nonsteroidal anti-inflammatory drug.)

*—Alarm symptoms include evidence of bleeding (e.g., anemia, heme-positive stool, melena), perforation (e.g., severe pain), obstruction (e.g., vomiting), and malignancy (e.g., weight loss, anorexia).

Management of Peptic Ulcer Disease

Treatment of peptic ulcer disease should include eradication of H. pylori in patients with this infection (Table 419,21–25). The recommended duration of therapy for eradication is 10 to 14 days; however, shorter treatment courses (regimens of one, five, and seven days) are being assessed.21,22 Potential benefits of shorter regimens include better compliance, fewer adverse effects, and lower costs.

Administration of an H2 blocker or proton pump inhibitor for four weeks (Table 419,21–25) induces healing in most duodenal ulcers. Proton pump inhibitors provide superior acid suppression, healing rates, and symptom relief and are recommended as initial therapy for most patients. One meta-analysis of randomized controlled trials comparing proton pump inhibitors withH2 blockers showed earlier pain control and better healing rates at four weeks for proton pump inhibitors (85 versus 75 percent).23 A recent systematic review of randomized controlled trials showed that proton pump inhibitors healed duodenal ulcers in more than 95 percent of patients at four weeks and gastric ulcers in 80 to 90 percent of patients at eight weeks.24 Therefore, there is little reason to prescribe proton pump inhibitors for longer than four weeks for duodenal ulcers unless the ulcers are large, fibrosed, or unresponsive to initial treatment.

Eradicating H. pylori is often sufficient in patients with small duodenal ulcers. Repeated EGD with biopsy is recommended to confirm healing of gastric ulcers and to rule out malignancy. Maintenance therapy withH2 blockers or proton pump inhibitors prevents recurrence in high-risk patients (e.g., those with a history of complications, frequent recurrences, ulcers testing negative for H. pylori, refractory giant ulcers, or severely fibrosed ulcers), but it is not generally recommended for patients in whom H. pylori has been eradicated and who are not taking NSAIDs long-term.

REFRACTORY ULCERS

Refractory peptic ulcer disease (i.e., disease that fails to heal after eight to 12 weeks of therapy) may be caused by persistent or resistant H. pylori infection, continued NSAID use, giant ulcers requiring longer healing time, cancer, tolerance of or resistance to medications, or hypersecretory states.26 Therapy for refractory peptic ulcer disease involves treatment of the underlying cause and prolonged administration of standard doses of a proton pump inhibitor (Figure 1). Up to 25 percent of patients with gastric ulcers who continue to take NSAIDs may require proton pump inhibitor therapy for longer than eight weeks.27

SURGERY

Surgery is indicated in patients who are intolerant of medications or do not comply with medication regimes, and those at high risk of complications (e.g., transplant recipients, patients dependent on steroids or NSAIDs, those with giant gastric or duodenal ulcer, those with ulcers that fail to heal with adequate treatment). Surgery should also be considered for patients who have a relapse during maintenance treatment or who have had multiple courses of medications.28

Surgical options for duodenal ulcers include truncal vagotomy and drainage (pyloroplasty or gastrojejunostomy), selective vagotomy (preserving the hepatic and celiac branches of the vagus) and drainage, highly selective vagotomy (division of only the gastric branches of the vagus, preserving Latarjet's nerve to the pylorus), or partial gastrectomy. Surgery for gastric ulcers usually involves a partial gastrectomy. Procedures other than highly selective vagotomy may be complicated by post-procedure dumping and diarrhea.

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Table 4.

Treatment of Peptic Ulcers

TreatmentCommentOptions

Eradication of Helicobacter pylori

Treatment duration is 10 to 14 days (although courses lasting one to seven days have been reported to have comparable effectiveness21,22)

Omeprazole (Prilosec) 20 mg two times daily or lansoprazole (Prevacid) 30 mg two times daily

plus amoxicillin 1 g two times daily or metronidazole (Flagyl) 500 mg two times daily (if allergic to penicillin)

plus clarithromycin (Biaxin) 500 mg two times daily

Ranitidine bismuth citrate (Tritec)* 400 mg two times daily

plus clarithromycin 500 mg two times daily or metronidazole 500 mg two times daily

plus tetracycline 500 mg two times daily or amoxicillin 1 g two times daily Levofloxacin (Levaquin) 500 mg daily

Levofloxacin (Levaquin) 500 mg daily

plus amoxicillin 1 g two times daily

plus pantoprazole (Protonix) 40 mg two times daily

Bismuth subsalicylate (Pepto-Bismol) 525 mg (two tablets) four times daily

plus metronidazole 250 mg four times daily

plus tetracycline 500 mg four times daily

plus H2 blocker for 28 days or proton pump inhibitor for 14 days

Eradication rates 80 to 90 percent or higher

Histamine H2 blockers

70 to 80 percent healing in duodenal ulcer after four weeks, 87 to 94 percent after eight weeks

Ranitidine (Zantac) 150 mg two times daily or 300 mg at night

Famotidine (Pepcid) 20 mg two times daily or 40 mg at night

Cimetidine (Tagamet) 400 mg two times daily or 800 mg at night

Proton pump inhibitors

Treatment duration is four weeks for duodenal ulcer and eight weeks for gastric ulcer 80 to 100 percent healing

Omeprazole 20 mg daily

Lansoprazole 15 mg daily

Rabeprazole (Aciphex) 20 mg daily

Pantoprazole 40 mg daily

Sucralfate (Carafate)

Treatment duration is four weeks blockers Effectiveness similar to H2

1 g four times daily

Surgery

Rarely needed

Duodenal ulcer: truncal vagotomy, selective vagotomy, highly selective vagotomy, partial gastrectomy

Gastric ulcer: partial gastrectomy with gastroduodenal or gastrojejunal anastomosis

Table 4.

Treatment of Peptic Ulcers

TreatmentCommentOptions

Eradication of Helicobacter pylori

Treatment duration is 10 to 14 days (although courses lasting one to seven days have been reported to have comparable effectiveness21,22)

Omeprazole (Prilosec) 20 mg two times daily or lansoprazole (Prevacid) 30 mg two times daily

plus amoxicillin 1 g two times daily or metronidazole (Flagyl) 500 mg two times daily (if allergic to penicillin)

plus clarithromycin (Biaxin) 500 mg two times daily

Ranitidine bismuth citrate (Tritec)* 400 mg two times daily

plus clarithromycin 500 mg two times daily or metronidazole 500 mg two times daily

plus tetracycline 500 mg two times daily or amoxicillin 1 g two times daily Levofloxacin (Levaquin) 500 mg daily

Levofloxacin (Levaquin) 500 mg daily

plus amoxicillin 1 g two times daily

plus pantoprazole (Protonix) 40 mg two times daily

Bismuth subsalicylate (Pepto-Bismol) 525 mg (two tablets) four times daily

plus metronidazole 250 mg four times daily

plus tetracycline 500 mg four times daily

plus H2 blocker for 28 days or proton pump inhibitor for 14 days

Eradication rates 80 to 90 percent or higher

Histamine H2 blockers

70 to 80 percent healing in duodenal ulcer after four weeks, 87 to 94 percent after eight weeks

Ranitidine (Zantac) 150 mg two times daily or 300 mg at night

Famotidine (Pepcid) 20 mg two times daily or 40 mg at night

Cimetidine (Tagamet) 400 mg two times daily or 800 mg at night

Proton pump inhibitors

Treatment duration is four weeks for duodenal ulcer and eight weeks for gastric ulcer 80 to 100 percent healing

Omeprazole 20 mg daily

Lansoprazole 15 mg daily

Rabeprazole (Aciphex) 20 mg daily

Pantoprazole 40 mg daily

Sucralfate (Carafate)

Treatment duration is four weeks blockers Effectiveness similar to H2

1 g four times daily

Surgery

Rarely needed

Duodenal ulcer: truncal vagotomy, selective vagotomy, highly selective vagotomy, partial gastrectomy

Gastric ulcer: partial gastrectomy with gastroduodenal or gastrojejunal anastomosis

Associated Complications

About 25 percent of patients with peptic ulcer disease have a serious complication such as hemorrhage, perforation, or gastric outlet obstruction. Silent ulcers and complications are more common in older patients and in patients taking NSAIDs.16,17 The incidence of serious upper gastrointestinal complications among persons in the general population who do not take NSAIDs is extremely low (less than one per 1,000 person-years).29

BLEEDING

Upper gastrointestinal bleeding occurs in 15 to 20 percent of patients with peptic ulcer disease. It is the most common cause of death and the most common indication for surgery in the disease. In older persons, 20 percent of bleeding episodes result from asymptomatic ulcers.17 Patients may present with hematemesis (bright red or “coffee ground”), melena, fatigue caused by anemia, orthostasis, or syncope.

There are several risk-stratification schemes that can help physicians determine the need for urgent intervention and predict continued or recurrent bleeding after endoscopic therapy. The Rockall risk scoring system is useful in stratifying patients at higher risk of rebleeding and death and has been prospectively validated in different populations (Table 530,31).30

In stable patients with gastrointestinal bleeding, potentially ulcerogenic medications should be discontinued. A proton pump inhibitor should be administered intravenously; this reduces transfusion requirements, need for surgery, and duration of hospitalization, although it does not reduce mortality.32 EGD should be performed to find characteristics that suggest a high rate of bleeding recurrence (e.g., ulcer larger than 1 cm, visible or actively bleeding vessel).30

Patients whose condition is unstable should undergo fluid or packed-cell resuscitation followed by emergent EGD and coagulation of bleeding sites through endoscopic ligation; placement of hemoclips; injection of epinephrine, alcohol, or a sclerosant; or a combination of methods.33

Oral antisecretory therapy should be initiated as soon as patients resume oral intake. Treatment of H. pylori infection is more effective than antisecretory therapy without eradication of H. pylori for preventing recurrent bleeding. Therefore, patients with bleeding peptic ulcers should be tested for H. pylori infection and should be prescribed eradication therapy if results are positive.34 If continued administration of aspirin or NSAIDs is required, concurrent administration of misoprostol or a proton pump inhibitor should be considered.35,36 Patients with nonhealing gastric ulcers should have biopsy to rule out cancer.

Angiographic embolization of bleeding vessels or surgery is indicated if a patient's vital signs or laboratory studies suggest continued or recurrent bleeding.33 Surgical options include gastroduodenotomy and oversewing of the blood vessel with or without vagotomy and drainage in duodenal ulcer; and excision of the ulcer with vagotomy and drainage or partial gastrectomy in bleeding gastric ulcers.

PERFORATION

Perforation occurs in approximately 2 to 10 percent of peptic ulcers.25 It usually involves the anterior wall of the duodenum (60 percent), although it may also occur in antral (20 percent) and lesser-curve (20 percent) gastric ulcers. Perforation of ulcers in children is rare.

Free peritoneal perforation and resulting chemical and bacterial peritonitis is a surgical emergency causing sudden, rapidly spreading, severe upper abdominal pain exacerbated by movement; the pain may radiate to the right lower abdomen or to both shoulders. Fever, hypotension, and oliguria suggest sepsis and circulatory compromise. Generalized abdominal tenderness, rebound tenderness, board-like abdominal wall rigidity, and hypoactive bowel sounds (clinical signs of peritonitis) may be masked in older patients and those taking steroids, immunosuppressants, or narcotic analgesics. Upright or lateral decubitus abdominal radiography or erect chest radiography may demonstrate pneumoperitoneum; however, the absence of this finding does not rule out perforation.17 Sonography, computed tomography, and gastroduodenography are confirmatory.

Initial resuscitation with large-volume crystalloids; nasogastric suction; and administration of intravenous broad-spectrum antibiotics against gram-negative rods, anaerobes, and oral flora are usually followed by laparotomy and placement of an omental patch (Graham patch plication) in patients with perforated duodenal ulcers. In otherwise healthy patients with a history of chronic ulcer and minimal peritoneal contamination, a concurrent, definitive, anti-ulcer procedure (e.g., vagotomy and drainage, highly selective vagotomy) may also be considered. Perforated gastric ulcers are treated with an omental patch, wedge resection of the ulcer, or a partial gastrectomy and reanastomosis. Coexisting H. pylori infection should be eradicated to reduce recurrence and minimize the need for long-term antisecretory therapy and further surgical intervention.25,37 In older patients, mortality rates from perforation and its management may be as high as 30 to 50 percent.1

GASTRIC OUTLET OBSTRUCTION

Peptic ulcer disease is the underlying cause in less than 5 to 8 percent of patients presenting with gastric outlet obstruction. Patients with recurrent duodenal or pyloric channel ulcers may develop pyloric stenosis as a result of acute inflammation, spasm, edema, or scarring and fibrosis.

Symptoms suggesting obstruction include recurrent episodes of emesis with large volumes of vomit containing undigested food; persistent bloating or fullness after eating; and early satiety. Weight loss, dehydration, and a hypo-chloremic, hypokalemic metabolic alkalosis may result; a tympanitic epigastric mass representing the dilated stomach with visible gastric peristalsis also may be observed.

EGD or gastroduodenography (using diatrizoate meglumine and diatrizoate sodium [Gastrografin] or barium) is recommended to determine the site, cause, and degree of obstruction. Malignancy, a more common cause of obstruction (responsible for more than 50 percent of cases), should be ruled out.38 Obstruction resulting from acute inflammation or edema responds well to nasogastric decompression, administration ofH2 blockers or proton pump inhibitors, and eradication of H. pylori. Prokinetic agents should be avoided. Endoscopic pyloric balloon dilatation or surgery (vagotomy and pyloroplasty, antrectomy, or gastroenterostomy) are options to relieve chronic obstruction.25

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Table 5.

Rockall Risk Scoring System for Patients with Peptic Ulcer Disease

FeaturePoints

Age (years)

< 60

0

60 to 79

1

> 79

2

Shock

No shock (SBP ≥ 100, pulse < 100 bpm)

0

Tachycardia (SBP ≥ 100, pulse ≥ 100 bpm)

1

Hypotension (SBP < 100)

2

Comorbid illness

No major comorbid illness

0

CHF, ischemic heart disease, other major comorbidity

2

Liver or renal failure, disseminated cancer

3

Diagnosis

Mallory-Weiss tear, no other lesion identified and no stigmata of recent hemorrhage

0

All other pathology causing bleeding (except cancer)

1

Upper gastrointestinal tract cancer

2

Major stigmata of recent hemorrhage

None or dark spot only

0

Blood in upper gastrointestinal tract, adherent clot, visible or spurting vessel

2

Total:

___

ScoreRisk (%)*
RebleedingMortality

< 3 points

6.2

0.2

3 or 4 points

13

6.8

> 4 points

25

20

Table 5.

Rockall Risk Scoring System for Patients with Peptic Ulcer Disease

FeaturePoints

Age (years)

< 60

0

60 to 79

1

> 79

2

Shock

No shock (SBP ≥ 100, pulse < 100 bpm)

0

Tachycardia (SBP ≥ 100, pulse ≥ 100 bpm)

1

Hypotension (SBP < 100)

2

Comorbid illness

No major comorbid illness

0

CHF, ischemic heart disease, other major comorbidity

2

Liver or renal failure, disseminated cancer

3

Diagnosis

Mallory-Weiss tear, no other lesion identified and no stigmata of recent hemorrhage

0

All other pathology causing bleeding (except cancer)

1

Upper gastrointestinal tract cancer

2

Major stigmata of recent hemorrhage

None or dark spot only

0

Blood in upper gastrointestinal tract, adherent clot, visible or spurting vessel

2

Total:

___

ScoreRisk (%)*
RebleedingMortality

< 3 points

6.2

0.2

3 or 4 points

13

6.8

> 4 points

25

20

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SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendationEvidence ratingReferences

Prompt upper endoscopy is recommended for patients with peptic ulcers who are older than 55 years, those who have alarm symptoms, and those with ulcers that do not respond to treatment.

A

1,19

In patients with peptic ulcer disease, Helicobacter pylori should be eradicated to assist in healing and to reduce the risk of gastric and duodenal ulcer recurrence.

A

1,8

In patients with peptic ulcers, proton pump inhibitors provide acid suppression, healing rates, and symptom relief superior to other antisecretory therapies.

A

23

Patients with bleeding peptic ulcers should be given a proton pump inhibitor to reduce transfusion requirements, need for surgery, and duration of hospitalization. H. pylori testing should be performed and eradication therapy prescribed if results are positive.

A

32,34

In patients with perforated ulcers, coexisting H. pylori infection should be eradicated to minimize the need for long-term antisecretory therapy and further surgical intervention.

C

25,37

SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendationEvidence ratingReferences

Prompt upper endoscopy is recommended for patients with peptic ulcers who are older than 55 years, those who have alarm symptoms, and those with ulcers that do not respond to treatment.

A

1,19

In patients with peptic ulcer disease, Helicobacter pylori should be eradicated to assist in healing and to reduce the risk of gastric and duodenal ulcer recurrence.

A

1,8

In patients with peptic ulcers, proton pump inhibitors provide acid suppression, healing rates, and symptom relief superior to other antisecretory therapies.

A

23

Patients with bleeding peptic ulcers should be given a proton pump inhibitor to reduce transfusion requirements, need for surgery, and duration of hospitalization. H. pylori testing should be performed and eradication therapy prescribed if results are positive.

A

32,34

In patients with perforated ulcers, coexisting H. pylori infection should be eradicated to minimize the need for long-term antisecretory therapy and further surgical intervention.

C

25,37

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