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Diagnosis and Management of Benign Gastric and Duodenal Disease

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Diagnosis and Management of Benign Gastric and Duodenal Disease gastrointestinal tract and abdomen DIAGNOSIS AND MANAGEMENT OF BENIGN GASTRIC AND DUODENAL DISEASE Gentian Kristo, MD, and Thomas E. Clancy, MD* The treatment of benign gastric and duodenal disease has expressed in the dictum “no acid, no ulcer.” A contempo- changed in recent decades, refl ecting improved medical rary viewpoint suggests that PUD results from an imbalance management of peptic ulcer disease (PUD) and a decreased between factors damaging the gastroduodenal mucosa and need for surgical intervention. Although surgical therapy those protecting the mucosa [see Table 1].4 was the only effective option for PUD in the past, elective The majority of gastric and duodenal ulcers are caused surgery is increasingly rare in recent decades. Operative by three factors: H. pylori infection, nonsteroidal antiinfl am- therapy for PUD is largely reserved for urgent management matory drug (NSAID) use, and acid hypersecretory states of complications such as hemorrhage, bleeding, or perfora- (e.g., Zollinger-Ellison syndrome [ZES]). Most patients with tion or the management of obstruction from intractable gastroduodenal ulcers will be colonized with H. pylori, disease. The shift away from acid-reducing operations to and recurrence of ulcers is common without treating the damage control procedures refl ects the remarkable success H. pylori infection. H. pylori, a gram-negative spiral organ- of medical management. ism, is present in about half the world population, particu- In this chapter, we focus primarily on the management of larly in developing countries, where up to 20% of healthy benign gastroduodenal disease, with a focus on the workup volunteers will demonstrate infection. Infection of gastric and management of PUD and consideration of relevant epithelium is followed by gastric infl ammation, and the surgical techniques. The management of duodenal diverticu- relationship between H. pylori and ulcer formation has been lar disease is briefl y addressed. Additional gastroduodenal widely demonstrated.5 The presence of ulcers in just a small disease and procedures are considered elsewhere in the fraction of individuals with infection suggests the action of publication, including bariatric surgery, transduodenal other etiologic factors causing ulceration. approaches to the bile duct, cystgastrostomy for intractable NSAIDs cause injury via suppression of prostaglandin pancreatic pseudocysts, and duodenal diverticularization synthesis, which leads to impaired mucosal defense. NSAID for trauma. use can result in a range of lesions, from superfi cial erosions to deeper ulcerations. Mucosal injury caused by NSAIDs is more common in the stomach than the duodenum. Cigarette Peptic Ulcer Disease smoking may impair ulcer healing and may increase the risk epidemiology of H. pylori–related ulceration.6 PUD has an overall point prevalence in the US population presentation/clinical manifestations of 1.8%, with a lifetime incidence of 10%.1 The presence of Most patients with PUD present with mild pain, burning Helicobacter pylori increases the incidence of ulcer to about discomfort, tenderness in the epigastrium, or nausea. Clas- 1% per year, a rate that is six- to 10-fold higher than for sically, the pain from a duodenal ulcer occurs 2 to 3 hours noninfected subjects.2 after a meal, is relieved temporarily with food or antacids, Advances in the medical management of PUD, including and at times awakens patients at night between about 11 pm the use of effective acid-suppressing medications (e.g., and 2 am, when the circadian stimulation of acid secretion histamine receptor antagonists and proton pump inhibitors [PPIs]) and the treatment of H. pylori, have led to a decrease in the incidence of PUD, the rates of hospitalization, and mortality. Despite these trends, PUD remains a signifi cant Table 1 Factors Damaging and Protecting the cause of morbidity and health care costs, with estimates of Gastroduodenal Mucosa4 annual expenditures (excluding medication costs) of $5.65 Damaging factors billion in the United States. Although the need for elective Gastric acid surgical management of uncomplicated duodenal and Pepsin gastric ulcers has steadily decreased in recent decades, the Bile salts rate of emergent surgery for complicated PUD has remained Helicobacter pylori infection 3 Nonsteroidal antiinflammatory drugs (NSAIDs) unchanged, at 7% of hospitalized patients. Smoking Alcohol pathophysiology Stress The relationship between gastroduodenal ulcers and Protective factors gastric acid secretion has been recognized for decades and is Mucus Bicarbonate Endogenous prostaglandins * The authors and editors gratefully acknowledge the contribu- Growth factors tions of the previous author, Stanley W. Ashley, MD, FACS, Cell regeneration to the development and writing of this chapter. Mucosal blood flow Scientifi c American Surgery © 2014 Decker Intellectual Properties Inc DOI 10.2310/7800.2003 06/14 gastro diagnosis and management of benign gastric and duodenal disease — 2 is maximal. Gastric ulcer pain is often aggravated by meals. However, the classic symptoms described are neither sensi- tive nor specifi c and are present in only a small number of patients. Furthermore, the nature of presenting symptoms alone does not differentiate between benign ulcerations and gastric malignancy. diagnosis Given the low predictive value of the signs and symptoms of PUD, the diagnosis of uncomplicated peptic ulcers is diffi cult to make solely on a clinical basis. The diagnosis of PUD is typically made by endoscopy and upper gastrointestinal (UGI) radiography. Endoscopy is the most accurate method of establishing the diagnosis of peptic ulcers, with a reported sensitivity of 92% and specifi city of 100%.7 In addition to identifying the ulcer and its features, location, and size, endoscopy provides an opportunity for biopsies to test for H. pylori and exclude malignancy and for therapeutic interventions for bleeding ulcers. Duodenal ulcers are most often benign and do not require routine biopsy. Multiple biopsies are indicated for all gastric ulcers as even lesions with a benign appearance harbor malignancy in 5 to 11% of cases.8,9 Given the advances in the use of endoscopy in recent Figure 1 Upper gastrointestinal series in which double contrast decades, the role of radiographic UGI series in the diagnosis (barium and air) is used, showing rounded collection of barium in of PUD has decreased, leading to a parallel decline in techni- an ulcer in the duodenal bulb of a patient presenting with dyspepsia cal expertise. However, it can be useful when endoscopy is (uncomplicated duodenal ulcer). unavailable or in patients not eligible to undergo endoscopy. Diagnosis of peptic ulcer on UGI series requires demonstra- sensitivity of 90 to 95% and a specifi city of 95 to 100%. tion of barium within an ulcer niche, which is generally Histologic examination of tissue samples remains the gold round or oval and may be surrounded by a smooth mound standard for determining the presence of H. pylori and can of edema.10,11 Secondary changes include folds radiating to also provide additional information regarding the presence the crater and regional deformities secondary to spasm, of gastritis, intestinal metaplasia, or mucosa-associated edema, and scarring [see Figure 1]. The accuracy of the UGI lymphoid tissue. radiography varies with the technique being used; single- Routine culture of the gastric biopsy specimens for contrast techniques (using liquid barium only) may miss as H. pylori is not recommended as it is relatively expensive, many as 50% of duodenal ulcers, whereas double-contrast and diagnosis requires more time (3 to 5 days). However, studies (using air and liquid barium) create a more detailed the incidence of antimicrobial resistance is high in patients view of the stomach lining and can detect 80 to 90% of with refractory peptic ulcers, and they may benefi t from ulcers.10,11 When radiographic features suggestive of cancer culture and antibiotic sensitivity testing. are present, endoscopy with biopsies is warranted. Routine laboratory tests are of limited value in evaluating treatment patients with uncomplicated PUD. When ZES is suspected, The medical management of PUD includes treatment with a fasting serum gastrin level may be useful. drugs that reduce the production of gastric acid (antacids, However, laboratory tests do play an important role in the histamine receptor antagonists, and most notably PPIs), diagnosis of H. pylori infection. The serologic determination create a protective coating over the ulcer craters to prevent of anti–H. pylori IgG antibodies in peripheral blood has high further peptic damage (sucralfate), increase mucosal blood sensitivity (90 to 100%) but variable specifi city (76 to 96%). fl ow and the secretion of bicarbonate and mucus (prosta- Serology is preferred for initial diagnosis when endos copy glandin analogues such as misoprostol used in NSAID- is not required. Urea breath testing has a sensitivity of 88 induced ulcers), and treat H. pylori infection. In addition to 95% and a specifi city of 95 to 100% for establishing the to drug therapy, general measures such as cessation of presence of H. pylori infection12 and is the test of choice smoking and alcohol and discontinuation of NSAID use for confi rming successful eradication of the organism 4 to are recommended. 6 weeks after the cessation of antibiotic treatment. In patients infected with H. pylori, the current pharmaco- Although endoscopy is not indicated solely for the pur- logic therapy consists
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