Background Gastric and duodenal ulcers usually cannot be differentiated based on history alone, although some findings may

be suggestive (see Diagnosis). Epigastric pain is the most common symptom of both gastric and duodenal ulcers. It is characterized by a gnawing or burning sensation and occurs after meals classically, shortly after meals with gastric ulcer and !"# hours afterward with duodenal ulcer. In uncomplicated peptic ulcer disease ($%D), the clinical findings are few and nonspecific. &'larm features( that warrant prompt gastroenterology referral)*+ include bleeding, anemia, early satiety, une,plained weight loss, progressive dysphagia or odynophagia, recurrent vomiting, and family history of GI cancer. $atients with perforated $%D usually present with a sudden onset of severe, sharp abdominal pain. (-ee .linical $resentation.) In most patients with uncomplicated $%D, routine laboratory tests usually are not helpful/ instead, documentation of $%D depends on radiographic and endoscopic confirmation. 0esting for H pylori infection is essential in all patients with peptic ulcers. 1apid urease tests are considered the endoscopic diagnostic test of choice. 2f noninvasive tests, fecal antigen testing is more accurate than antibody testing and is less e,pensive than urea breath tests. ' fasting serum gastrin level should be obtained in certain cases to screen for 3ollinger"Ellison syndrome. (-ee 4or5up.) %pper GI endoscopy is the preferred diagnostic test in the evaluation of patients with suspected $%D. Endoscopy provides an opportunity to visualize the ulcer, to determine the presence and degree of active bleeding, and to attempt hemostasis by direct measures, if re6uired. $erform endoscopy early in patients older than 78"89 years and in patients with associated so"called alarm features. :ost patients with $%D are treated successfully with cure of H pylori infection and;or avoidance of nonsteroidal anti" inflammatory drugs (<-'IDs), along with the appropriate use of antisecretory therapy. In the %nited -tates, the recommended primary therapy for H pylori infection is proton pump inhibitor ($$I)=based triple therapy. )*+ 0hese regimens result in a cure of infection and ulcer healing in appro,imately >8"?9@ of cases. )!+ %lcers can recur in the absence of successful H pylori eradication. (-ee 0reatment and :anagement.) In patients with <-'ID"associated peptic ulcers, discontinuation of <-'IDs is paramount, if it is clinically feasible. Aor patients who must continue with their <-'IDs, proton pump inhibitor ($$I) maintenance is recommended to prevent recurrences even after eradication of H pylori.)#, 7+ $rophylactic regimens that have been shown to dramatically reduce the ris5 of <-'ID"induced gastric and duodenal ulcers include the use of a prostaglandin analog or a $$I. :aintenance therapy with antisecretory medications (eg, B! bloc5ers, $$Is) for * year is indicated in high"ris5 patients. (-ee :edication.) 0he indications for urgent surgery include failure to achieve hemostasis endoscopically, recurrent bleeding despite endoscopic attempts at achieving hemostasis (many advocate surgery after ! failed endoscopic attempts), and perforation. $atients with gastric ulcers are also at ris5 of developing gastric malignancy. Anatomy Cecause many surgical procedures for peptic ulcer disease ($%D) entail some type of vagotomy, a discussion concerning the vagal innervation of the abdominal viscera is appropriate (see image below). 0he left (anterior) and the right (posterior) branches of the vagus nerve descend along either side of the distal esophagus. 's they enter the lower thoracic cavity, they can communicate with each other through several cross"branches that comprise the esophageal ple,us. Bowever, below this ple,us, the ! vagal trun5s again become separate and distinct before the anterior trun5 branches to form the hepatic, pyloric, and anterior gastric (also termed the anterior nerve of DatarEet) branches. 0he posterior trun5 branches to form the posterior gastric branch (also termed the posterior nerve of DatarEet) and the celiac branch. 0he parietal cell mass of the stomach is segmentally innervated by the terminal branches from each of the anterior and posterior gastric branches. 0hese terminal branches are divided during a highly selective vagotomy. 0he gallbladder is innervated from efferent branches of the hepatic division of the anterior trun5. .onse6uently, transection of the anterior vagus trun5 (performed during truncal vagotomy) can result in a dilated gallbladder with inhibited contractility and subse6uent cholelithiasis. 0he celiac branch of the posterior vagus innervates the entire midgut (with the e,ception of the gallbladder). 0hus, division of the posterior trun5 during truncal vagotomy may contribute to postoperative ileus.

Fagal innervation of stomach. Pathphysiology $eptic ulcers are defects in the gastric or duodenal mucosa that e,tend through the muscularis mucosa. 0he epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining and as a result of cholinergic stimulation. 0he superficial portion of the gastric and duodenal mucosa e,ists in the form of a gel layer, which is impermeable to acid and pepsin. 2ther gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that lies near the mucosa. $rostaglandins of the E type ($GE) have an important protective role, because $GE increases the production of both bicarbonate and the mucous layer. In the event of acid and pepsin entering the epithelial cells, additional mechanisms are in place to reduce inEury. 4ithin the epithelial cells, ion pumps in the basolateral cell membrane help to regulate intracellular pB by removing e,cess hydrogen ions. 0hrough the process of restitution, healthy cells migrate to the site of inEury. :ucosal blood flow removes acid that diffuses through the inEured mucosa and provides bicarbonate to the surface epithelial cells. %nder normal conditions, a physiologic balance e,ists between gastric acid secretion and gastroduodenal mucosal defense. :ucosal inEury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. 'ggressive factors, such as <-'IDs, H pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing bac5 diffusion of hydrogen ions and subse6uent epithelial cell inEury. 0he defensive mechanisms include tight intercellular Eunctions, mucus, mucosal blood flow, cellular restitution, and epithelial renewal. 0he gram"negative spirochete H pylori was first lin5ed to gastritis in *?>#. -ince then, further study of H pylori has revealed that it is a maEor part of the triad, which includes acid and pepsin, that contributes to primary peptic ulcer disease. 0he uni6ue microbiologic characteristics of this organism, such as urease production, allows it to al5alinize its microenvironment and survive for years in the hostile acidic environment of the stomach, where it causes mucosal inflammation and, in some individuals, worsens the severity of peptic ulcer disease. 4hen H pylori colonizes the gastric mucosa, inflammation usually results. 0he causal association between H pylori gastritis and duodenal ulceration is now well established in the adult and pediatric literature. In patients infected with H pylori, high levels of gastrin and pepsinogen and reduced levels of somatostatin have been measured. In infected patients, e,posure of the duodenum to acid is increased. Firulence factors produced by H pylori, including urease, catalase, vacuolating cytoto,in, and lipopolysaccharide, are well described. :ost patients with duodenal ulcers have impaired duodenal bicarbonate secretion, which has also proven to be caused by H pylori because its eradication reverses the defect )8+ . 0he combination of increased gastric acid secretion and reduced duodenal bicarbonate secretion lowers the pB in the duodenum, which promotes the development of gastric metaplasia (ie, the presence of gastric epithelium in the first portion of the duodenum). H pylori infection in areas of gastric metaplasia induces duodenitis and enhances the susceptibility to acid inEury, thereby predisposing to duodenal ulcers. Duodenal colonization by H pylori was found to be a highly significant predictor of subse6uent development of duodenal ulcers in one study that followed *>* patients with endoscopy"negative, nonulcer dyspepsia )G+ . Etiology $eptic ulcer disease ($%D) may be due to any of the followingH

H pylori infection Drugs Difestyle factors -evere physiologic stress Bypersecretory states (uncommon) Genetic factors

H pylori infection H pylori infection and <-'ID use account for most cases of $%D. 0he rate of H pylori infection for duodenal ulcers in the %nited -tates is less than I8@ for patients who do not use <-'IDs. E,cluding patients who used <-'IDs, G*@ of duodenal ulcers and G#@ of gastric ulcers were positive for H pylori in one study. 0hese rates were lower in whites than in nonwhites. $revalence of H pylori infection in complicated ulcers (ie, bleeding, perforation) is significantly lower than that found in uncomplicated ulcer disease. Drugs <-'ID use is a common cause of $%D. 0hese drugs disrupt the mucosal permeability barrier, rendering the mucosa vulnerable to inEury. 's many as #9@ of adults ta5ing <-'IDs have GI adverse effects. Aactors associated with an increased ris5 of duodenal ulcers in the setting of <-'ID use include history of previous peptic ulcer disease, advanced age, female se,, high doses or combinations of <-'IDs, long"term <-'ID use, concomitant use of anticoagulants, and severe comorbid illnesses. ' long"term prospective study found that patients with arthritis who were older than G8 years who regularly too5 low"dose aspirin were at an increased ris5 for dyspepsia severe enough to necessitate the discontinuation of <-'IDs. )I+ 0his suggests that better management of <-'ID use should be discussed with older patients in order to reduce <-'ID"associated upper GI events. 'lthough the idea was initially controversial, most evidence now supports the assertion that H pylori and <-'IDs are synergistic with respect to the development of peptic ulcer disease. ' meta"analysis found that H pylori eradication in <-'ID" naive users before the initiation of <-'IDs was associated with a decrease in peptic ulcers )>+ . 'lthough the prevalence of <-'ID gastropathy in children is un5nown, it seems to be increasing, especially in children with chronic arthritis treated with <-'IDs. .ase reports have demonstrated gastric ulceration from low"dose ibuprofen in children, even after Eust * or ! doses)?+ . .orticosteroids alone do not increase the ris5 for $%D/ however, they can potentiate ulcer ris5 in patients who use <-'IDs concurrently. 0he ris5 of upper GI tract bleeding may be increased in users of the diuretic spironolactone )*9+ or serotonin reupta5e inhibitors with moderate to high affinity for serotonin transporter )**+ . Lifestyle factors Evidence that tobacco use is a ris5 factor for duodenal ulcers is not conclusive. -upport for a pathogenic role for smo5ing comes from the finding that smo5ing may accelerate gastric emptying and decrease pancreatic bicarbonate production. Bowever, studies have produced contradictory findings. In one prospective study of more than 7I,999 men with duodenal ulcers, smo5ing did not emerge as a ris5 factor. )*!+ Bowever, smo5ing in the setting of H pylori infection may increase the ris5 of relapse of $%D.)*#+ -mo5ing is harmful to the gastroduodenal mucosa, and H pylori infiltration is denser in the gastric antrum of smo5ers.)*7+ Ethanol is 5nown to cause gastric mucosal irritation and nonspecific gastritis. Evidence that consumption of alcohol is a ris5 factor for duodenal ulcer is inconclusive. ' prospective study of more than 7I,999 men with duodenal ulcer did not find an association between alcohol inta5e and duodenal ulcer. )*!+ Dittle evidence suggests that caffeine inta5e is associated with an increased ris5 of duodenal ulcers. Severe physiologic stress -tressful conditions that may cause $%D include burns, .<- trauma, surgery, and severe medical illness. -erious systemic illness, sepsis, hypotension, respiratory failure, and multiple traumatic inEuries increase the ris5 for secondary (stress) ulceration. .urling ulcers are associated with a brain tumor or inEury and typically are single, deep ulcers that are prone to perforation. 0hey are associated with high gastric acid output and are located in the duodenum or stomach. E,tensive burns are also associated with .urling ulcers. -tress ulceration and upper"GI hemorrhage are complications that are increasingly encountered in critically ill children in the intensive care setting. -evere illness and a decreased gastric pB are related to an increased ris5 of gastric ulceration and hemorrhage.

Hypersecretory states (uncommon) 0he following are among hypersecretory states that may, uncommonly, cause $%DH

Gastrinoma (3ollinger"Ellison syndrome) or multiple endocrine neoplasia type I (:E<"I) 'ntral G cell hyperplasia -ystemic mastocytosis Casophilic leu5emias .ystic fibrosis -hort bowel syndrome Byperparathyroidism

Physiologic factors In up to one third of patients with duodenal ulcers, basal acid output (C'2) and ma,imal acid output (:'2) are increased. In one study, increased C'2 was associated with an odds ratio )21+ of up to #.8, and increased :'2 was associated with an 21 of up to I for the development of duodenal ulcers. Individuals at especially high ris5 are those with a C'2 greater than *8 mE6;h. 0he increased C'2 may reflect the fact that in a significant proportion of patients with duodenal ulcers, the parietal cell mass is increased to nearly twice that of the reference range. )*8+ In addition to the increased gastric and duodenal acidity observed in some patients with duodenal ulcers, accelerated gastric emptying is often present. 0his acceleration leads to a high acid load delivered to the first part of the duodenum, where ?8@ of all duodenal ulcers are located. 'cidification of the duodenum leads to gastric metaplasia, which indicates replacement of duodenal villous cells with cells that share morphologic and secretory characteristics of gastric epithelium. Gastric metaplasia may create an environment that is well suited to colonization by H pylori. enetics :ore than !9@ of patients have a family history of duodenal ulcers, compared with only 8"*9@ in the control groups. In addition, wea5 associations have been observed between duodenal ulcers and blood type 2. Aurthermore, patients who do not secrete 'C2 antigens in their saliva and gastric Euices are 5nown to be at higher ris5. 0he reason for these apparent genetic associations is unclear. ' rare genetic association e,ists between familial hyperpepsinogenemia type I (a genetic phenotype leading to enhanced secretion of pepsin) and duodenal ulcers. Bowever, H pylori can increase pepsin secretion, and a retrospective analysis of the sera of one family studied before the discovery of H pylori revealed that their high pepsin levels were more li5ely related to H pylori infection. Additional etiologic factors 'ny of the following may be associated with $%DH

Bepatic cirrhosis .hronic obstructive pulmonary disease 'llergic gastritis and eosinophilic gastritis .ytomegalovirus infection Graft versus host disease %remic gastropathy Benoch"-chJnlein gastritis .orrosive gastropathy .eliac disease Cile gastropathy 'utoimmune disease .rohn disease 2ther granulomatous gastritides (eg, sarcoidosis, histiocytosis K, tuberculosis) $hlegmonous gastritis and emphysematous gastritis 2ther infections, including Epstein"Carr virus, BIF, Helicobacter heilmannii, herpes simple,, influenza, syphilis, Candida albicans,histoplasmosis, mucormycosis, and anisa5iasis .hemotherapeutic agents, such as 8"fluorouracil (8"A%), methotre,ate (:0K), and cyclophosphamide Docal radiation resulting in mucosal damage, which may lead to the development of duodenal ulcers

%se of crac5 cocaine, which causes localized vasoconstriction, resulting in reduced blood flow and possibly leading to mucosal damage

Epidemiology !nited States statistics In the %nited -tates, $%D affects appro,imately 7.8 million people annually. 'ppro,imately *9@ of the %- population has evidence of a duodenal ulcer at some time. 2f those infected with H pylori, the lifetime prevalence is appro,imately !9@. 2nly about *9@ of young persons have H pylori infection/ the proportion of people with the infection increases steadily with age. 2verall, the incidence of duodenal ulcers has been decreasing over the past #"7 decades. 'lthough the rate of simple gastric ulcer is in decline, the incidence of complicated gastric ulcer and hospitalization has remained stable, partly due to the concomitant use of aspirin in an aging population. 0he hospitalization rate for $%D is appro,imately #9 patients per *99,999 cases. 0he prevalence of $%D has shifted from predominance in males to similar occurrences in males and females. Difetime prevalence is appro,imately **"*7@ in men and >"**@ in women. 'ge trends for ulcer occurrence reveal declining rates in younger men, particularly for duodenal ulcer, and increasing rates in older women. 0rends reflect comple, changes in ris5 factors for $%D, including age"cohort phenomena with the prevalence of H pylori infection and the use of <-'IDs in older populations. "nternational statistics 0he fre6uency of $%D in other countries is variable and is determined primarily by association with the maEor causes of $%DH H pylori and <-'IDs.)*G+ Prognosis 4hen the underlying cause is addressed, the prognosis is e,cellent. :ost patients are treated successfully with eradication of H pylori infection, avoidance of <-'IDs, and the appropriate use of antisecretory therapy. Eradication of H pylori infection changes the natural history of the disease, with a decrease in the ulcer recurrence rate from G9"?9@ to appro,imately *9"!9@. Bowever, this is a higher recurrence rate than previously reported, suggesting an increased number of ulcers not caused by H pylori infection. 4ith regard to <-'ID"related ulcers, the incidence of perforation is appro,imately 9.#@ per patient year, and the incidence of obstruction is appro,imately 9.*@ per patient year. .ombining both duodenal ulcers and gastric ulcers, the rate of any complication in all age groups combined is appro,imately *"!@ per ulcer per year. 0he mortality rate for $%D, which has decreased modestly in the last few decades, is appro,imately * death per *99,999 cases. If one considers all patients with duodenal ulcers, the mortality rate due to ulcer hemorrhage is appro,imately 8@. 2ver the last !9 years, the mortality rate in the setting of ulcer hemorrhage has not changed appreciably despite the advent of histamine"! receptor antagonists (B!1's) and proton pump inhibitors ($$Is). Bowever, evidence from meta"analyses and other studies has shown a decreased mortality rate from bleeding peptic ulcers when intravenous $$Is are used after successful endoscopic therapy.)*I, *>, *?, !9+ Emergency operations for peptic ulcer perforation carry a mortality ris5 of G"#9@. )!*+ Aactors associated with higher mortality in this setting include the followingH

-hoc5 at the time of admission 1enal insufficiency Delaying the initiation of surgery for more than *! hours after presentation .oncurrent medical illness (eg, cardiovascular disease, diabetes mellitus 'ge older than I9 years .irrhosis Immunocompromised state Docation of ulcer (mortality associated with perforated gastric ulcer is twice that associated with perforated duodenal ulcer.)

Patient Education

$atients should be warned of 5nown or potentially inEurious drugs and agents. -ome e,amples are as followsH

<-'IDs 'spirin 'lcohol 0obacco .affeine (eg, coffee, tea, colas)

2besity has been shown to have an association with peptic ulcer disease ($%D), and patients should be counseled regarding benefits of weight loss. -tress reduction counseling might be helpful in individual cases but is not needed routinely. History 2btaining a medical history, especially for peptic ulcer disease, H pylori infection, ingestion of <-'IDs, or smo5ing, is essential in ma5ing the correct diagnosis. Gastric and duodenal ulcers usually cannot be differentiated based on history alone, although some findings may be suggestive. Epigastric pain is the most common symptom of both gastric and duodenal ulcers. It is characterized by a gnawing or burning sensation and occurs after meals classically, shortly after meals with gastric ulcer and !"# hours afterward with duodenal ulcer. Aood or antacids relieve the pain of duodenal ulcers but provide minimal relief of gastric ulcer pain. Duodenal ulcer pain often awa5ens the patient at night. 'bout 89">9@ of patients with duodenal ulcers e,perience nightly pain, as opposed to only #9"79@ of patients with gastric ulcers and !9"79@ of patients with nonulcer dyspepsia (<%D). $ain typically follows a daily pattern specific to the patient. $ain with radiation to the bac5 is suggestive of a posterior penetrating gastric ulcer complicated by pancreatitis. $atients who develop gastric outlet obstruction as a result of a chronic, untreated duodenal ulcer usually report a history of fullness and bloating associated with nausea and emesis that occurs several hours after food inta5e. ' common misconception is that adults with gastric outlet obstruction present with nausea and emesis immediately after a meal. 2ther possible manifestations include the followingH

Dyspepsia, including belching, bloating, distention, and fatty food intolerance Beartburn .hest discomfort Bematemesis or melena resulting from gastrointestinal bleeding. :elena may be intermittent over several days or multiple episodes in a single day. 1arely, a bris5ly bleeding ulcer can present as hematochezia. -ymptoms consistent with anemia (eg, fatigue, dyspnea) may be present -udden onset of symptoms may indicate perforation. <-'ID"induced gastritis or ulcers may be silent, especially in elderly patients. 2nly !9"!8@ of patients with symptoms suggestive of peptic ulceration are found on investigation to have a peptic ulcer.

'larm features that warrant prompt gastroenterology referral )*+ include the followingH

Cleeding or anemia Early satiety %ne,plained weight loss $rogressive dysphagia or odynophagia 1ecurrent vomiting Aamily history of GI cancer

Physical E#amination In uncomplicated $%D, the clinical findings are few and nonspecific and include the followingH

Epigastric tenderness (usually mild) 1ight upper 6uadrant tenderness may suggest a biliary etiology or, less fre6uently, $%D. Guaiac"positive stool resulting from occult blood loss :elena resulting from acute or subacute gastrointestinal bleeding

-uccussion splash resulting from partial or complete gastric outlet obstruction

$atients with perforated $%D usually present with a sudden onset of severe, sharp abdominal pain. :ost patients describe generalized pain/ a few present with severe epigastric pain. 's even slight movement can tremendously worsen their pain, these patients assume a fetal position. 'bdominal e,amination usually discloses generalized tenderness, rebound tenderness, guarding, and rigidity. Bowever, the degree of peritoneal findings is strongly influenced by a number of factors, including the size of perforation, amount of bacterial and gastric contents contaminating the abdominal cavity, time between perforation and presentation, and spontaneous sealing of perforation. 0hese patients may also demonstrate signs and symptoms of septic shoc5, such as tachycardia, hypotension, and anuria. <ot surprisingly, these indicators of shoc5 may be absent in elderly or immunocompromised patients or in those with diabetes. $atients should be as5ed if retching and vomiting occurred before the onset of pain. Approach $onsiderations 0esting for H pylori infection is essential in all patients with peptic ulcers. In most patients with uncomplicated peptic ulcer disease ($%D), routine laboratory tests usually are not helpful. Documentation of $%D depends on radiographic and endoscopic confirmation. If the diagnosis of $%D is suspected, obtaining .C. count, liver function tests (DA0s), amylase, and lipase may be useful. .C. count and iron studies can help detect anemia, which is an alarm signal that mandates early endoscopy to rule out other sources of chronic GI blood loss. H pylori %esting 0esting for H pylori infection is essential in all patients with peptic ulcers. Endoscopic or invasive tests for H pylori include a rapid urease test, histopathology, and culture. 1apid urease tests are considered the endoscopic diagnostic test of choice. 0he presence of H pylori in gastric mucosal biopsy specimens is detected by testing for the bacterial product urease. Aecal antigen testing identifies active H pylori infection by detecting the presence of H pylori antigens in stools. 0his test is more accurate than antibody testing and is less e,pensive than urea breath tests. 0hree 5its (ie, .D2test, Bp"fast, $ylorite5) are commercially available for H pylori testing, and each contains a combination of a urea substrate and a pB sensitive indicator. 2ne or more gastric biopsy specimens are placed in the rapid urease test 5it. If H pylori is present, bacterial urease converts urea to ammonia, which changes the pB, resulting in a color change. %rea breath tests detect active H pylori infection by testing for the enzymatic activity of bacterial urease. In the presence of urease produced by H pylori, labeled carbon dio,ide (heavy isotope, carbon"*#, or radioactive isotope, carbon"*7) is produced in the stomach, absorbed into the bloodstream, diffused into the lungs, and e,haled. 2btain histopathology, often considered the criterion standard to establish a diagnosis of H pylori infection , if the rapid urease test result is negative and a high suspicion for H pylori persists (presence of a duodenal ulcer). 'ntibodies (immunoglobulin G )IgG+) to H pylori can be measured in serum, plasma, or whole blood. 1esults with whole blood tests obtained from finger stic5s are less reliable. Endoscopy %pper GI endoscopy is the preferred diagnostic test in the evaluation of patients with suspected $%D. It is highly sensitive for the diagnosis of gastric and duodenal ulcers, allows for biopsies and cytologic brushings in the setting of a gastric ulcer to differentiate a benign ulcer from a malignant lesion, and allows for the detection of H pylori infection with antral biopsies for a rapid urease test and;or histopathology in patients with $%D. (-ee the images below.) 't endoscopy, gastric ulcers appear as discrete mucosal lesions with a punched"out smooth ulcer base, which often is filled with whitish fibrinoid e,udate. %lcers tend to be solitary and well circumscribed and usually are 9.8"!.8 cm in diameter. :ost gastric ulcers tend to occur at the Eunction of the fundus and antrum, along the lesser curvature. Cenign ulcers tend to have a smooth, regular, rounded edge with a flat smooth base and surrounding mucosa that shows radiating folds. :alignant ulcers usually have irregular heaped"up or overhanging margins. 0he ulcerated mass often protrudes into the lumen, and the folds surrounding the ulcer crater are often nodular and irregular.

Gastric ulcer with punched"out ulcer base with whitish fibrinoid e,udates.

Gastric ulcer (lesser curvature) with punched"out ulcer base with whitish e,udate.

Gastric cancer. <ote the irregular heaped up overhanging margins.

Gastric cancer with ulcerated mass. :ore than ?8@ of duodenal ulcers are found in the first part of the duodenum/ most are less than * cm in diameter. )!!+ Duodenal ulcers are characterized by the presence of a well"demarcated brea5 in the mucosa that may e,tend into the muscularis propria of the duodenum (see the images below).

Gastric cancer with ulcerated mass.

Duodenal ulcer in a #8"year"old

woman who presented with tarry stools and a hemoglobin level of I8 g;D. Duodenal ulcer in a G8"year"old man with osteoarthritis who presented with hematemesis and melena stools. 0he patient too5 napro,en on a daily basis. ' meta"analysis has shown that for individuals who undergo endoscopy for dyspepsia, the most common finding is erosive esophagitis (though prevalence was lower when the 1ome criteria were used to define dyspepsia) followed by peptic ulcer. )!#+ &adiography In patients presenting acutely, a chest radiograph may be useful to detect free abdominal air when perforation is suspected. 2n upper GI contrast study with water"soluble contrast, the e,travasation of contrast indicates gastric perforation. Double"contrast radiography performed by an e,perienced radiologist may approach the diagnostic accuracy of upper GI endoscopy. Bowever, it has been replaced largely by diagnostic endoscopy, when available. 'n upper GI series is not as sensitive as endoscopy for establishing a diagnosis of small ulcers (L 9.8 cm). It also does not allow for obtaining a biopsy to rule out malignancy in the setting of a gastric ulcer or to assess for H pylori infection in the setting of a gastroduodenal ulcer. Angiography 'ngiography may be necessary in patients with a massive GI bleed in whom endoscopy cannot be performed. 'n ongoing bleeding rate of 9.8 mD;min or more is needed for the angiography to be able to accurately identify the bleeding source. 'ngiography can depict the source of the bleeding and can help provide needed therapy in the form of a direct inEection of vasoconstrictive agents. Serum astrin Level

' fasting serum gastrin level should be obtained in certain cases to screen for 3ollinger"Ellison syndrome. -uch cases include the followingH

$atients with multiple ulcers %lcers occurring distal to the duodenal bulb -trong family history of $%D $eptic ulcer associated with diarrhea, steatorrhea, or weight loss $eptic ulcer not associated with H pylori infection or <-'ID use $eptic ulcer associated with hypercalcemia or renal stones %lcer refractory to medical therapy %lcer recurring after surgery

Secretin Stimulation %est

' secretin stimulation test may be re6uired if the diagnosis of 3ollinger"Ellison syndrome cannot be made on the basis of the serum gastrin level alone. 0his test can distinguish 3ollinger"Ellison syndrome from other conditions with a high serum gastrin level, such as use of antisecretory therapy with a proton pump inhibitor, renal failure, or gastric outlet obstruction. Biopsy ' single biopsy offers I9@ accuracy in diagnosing gastric cancer, but I biopsy samples obtained from the base and ulcer margins increase the sensitivity to ??@. Crush cytology has been shown to increase the biopsy yield, and this method may be useful particularly when bleeding is a concern in a patient with coagulopathy. Histologic 'indings 0he histology of gastric ulcer depends on its chronicity. 0he surface is covered with slough and inflammatory debris. Ceneath this neutrophilic infiltration, active granulation with mononuclear leu5ocytic infiltration and fibrinoid necrosis may be seen. In chronic superficial gastritis, lymphocytes, monocytes, and plasma cells often infiltrate the mucosa and submucosa. Emergency Department (orkup 0he ED wor5up will vary depending on presentation and includes the followingH

.omplete blood count is used to evaluate acute or chronic blood loss. Electrolytes, C%<, and creatinine levels are useful tests for critical"appearing patients who re6uire fluid resuscitation. 0ype and screen and crossmatched blood for transfusion is indicated in unstable or potentially critical patients. a$00, $0, and I<1 are indicated in patients with active bleeding and those on anticoagulants. 'mylase, lipase, and liver transaminase levels can be helpful to rule out other common causes of epigastric pain. $atients younger than 88 years with no alarm features should be referred for noninvasive testing for H pylori infection in the outpatient setting.)*+

Emergency Department $are $resentations of peptic ulcer disease and gastritis usually are indistinguishable in the ED, and thus, the management is generally the same. 0reatment goals in the acute setting are the relief of discomfort and protection of the gastric mucosal barrier to promote healing. 'dminister supportive therapy as needed. :ost patients with gastritis or peptic ulcer disease do not re6uire acute interventions. Bigh"ris5 patients include those with the following characteristicsH

Cleeding with hemodynamic instability 1epeated hematemesis or any hematochezia Aailure to clear with gastric lavage .oagulopathy .omorbid disease (especially cardiac, pulmonary, or renal) 'dvanced age

Drug treatments 'ntacids or a GI coc5tail (typically an antacid with an anesthetic such as viscous lidocaine and;or an antispasmodic) may be used as symptomatic therapy/ however, relief of symptoms with a GI coc5tail is not a diagnostic indicator. Empiric treatment of H pylori is not recommended. 0herapy is indicated only after confirmation of infection. 0hese tests are not performed in the ED. Empiric trial of acid suppression in patients younger than 88 years without alarm features may be initiated with $$I for 7"> wee5s. 'ppropriate follow"up is re6uired to assess response in !"7 wee5s. )7G+ 'nticholinergic agents are contraindicated. Bleeding :assive gastric bleeds are the most difficult complication to treat. :ainstays of resuscitation include the followingH

Establishment of ade6uate IF access and volume replacement, initially with crystalloid/ in the face of continued hypotension after ! D, consider blood transfusion.

' central venous catheter to monitor such resuscitation may be considered. 'irway protection with intubation should be considered in the case of massive bleeding. <G suction helps to 5eep the stomach empty and contracted. IF $$I has been shown to reduce mortality in upper GI bleeds and reduces the incidence of rebleeding and the need for surgical intervention)7I+ / emergent surgical or endoscopic intervention may be re6uired

$atients with significant or potentially significant hemorrhage re6uire admission, usually to the intensive care unit. Surgical $are for Perforated Peptic !lcer 4ith the success of medical therapy, surgery has a very limited role in the management of $%D. Elective peptic ulcer surgery has been virtually abandoned. In the *?>9s, the number of elective operations for peptic ulcer disease dropped more than I9@, and emergent operations accounted for more than >9@. )7>+ In general, 8@ of bleeding ulcers eventually re6uire operative management. 0he indications for urgent surgery include the followingH

Aailure to achieve hemostasis endoscopically 1ecurrent bleeding despite endoscopic attempts at achieving hemostasis (many advocate surgery after ! failed endoscopic attempts) $erforation

0he appropriate surgical procedure depends on the location and nature of the ulcer. :any authorities recommend simple oversewing of the ulcer with treatment of the underlying H pylori infection or cessation of <-'IDs for bleeding $%D. 'dditional surgical options for refractory or complicated $%D include vagotomy and pyloroplasty, vagotomy and antrectomy with gastroduodenal reconstruction (Cillroth I) or gastroEeEunal reconstruction (Cillroth II), or a highly selective vagotomy. 2nly one prospective randomized trial has compared laparoscopic surgery with open surgery for perforated ulcer. 0he study found that the only difference between the ! groups was reduced need for analgesia and an increased operative time in the laparoscopic group. .ontraindications for laparoscopic repair for perforated peptic ulcer include large perforations, a posterior location of the perforation, and a poor general state of health. )#7+ -urgical complications include pneumonia (#9@), wound infection, abdominal abscess (*8@), cardiac problems (especially in those MI9 y), diarrhea (#9@ after vagotomy), and dumping syndromes (*9@ after vagotomy and drainage procedures). 0o see complete information on -urgical 0reatment of $erforated $eptic %lcer, please go to the main article by clic5ing here. Diet ' special diet is not indicated for patients with duodenal ulcers. It is a common"sense approach to avoid any food or beverages that may aggravate symptoms. 'lthough the lin5 between duodenal ulcers and alcohol is inconclusive, moderation of alcohol inta5e may be recommended for other health reasons. Approach $onsiderations 0reatment of peptic ulcers varies depending on the etiology and clinical presentation. 0he initial management of a stable patient with dyspepsia differs from the management of an unstable patient with upper GI hemorrhage. In the latter scenario, failure of medical management not uncommonly leads to surgical intervention. 0reatment options include empiric antisecretory therapy, empiric triple therapy for H pylori infection, endoscopy followed by appropriate therapy based on findings, and H pylori serology followed by triple therapy for patients who are infected. Creath testing for active H pylori infection may be used. Endoscopy is re6uired to document healing of gastric ulcers and to rule out gastric cancer. 0his usually is performed G"> wee5s after the initial diagnosis of $%D. Documentation of H pylori cure with a noninvasive test, such as the urea breath test or fecal antigen test, is appropriate in patients with complicated ulcers. Given the current understanding of the pathogenesis of $%D, most patients with $%D are treated successfully with cure of H pylori infection and;or avoidance of <-'IDs, along with the appropriate use of antisecretory therapy. .omputer models have suggested that obtaining H pylori serology followed by triple therapy for patients who are infected is the most cost"effective approach/ however, no direct evidence from clinical trials provides confirmation.

$erform endoscopy early in patients older than 78"89 years and in patients with associated so"called alarm symptoms, such as dysphagia, recurrent vomiting, weight loss, or bleeding. 'ge is an independent ris5 factor for the incidence and mortality from bleeding peptic ulcer, with the ris5 increasing in persons older than G8 years and increasing further in those older than age I8 years.)!7+ In one study, at least ! ris5 factors (previous duodenal ulcer, H pylori infection, use of '-';<-'ID, and smo5ing) were present in two thirds of persons with acute gastroduodenal bleeding. )!8+ 0he indications for urgent surgery include failure to achieve hemostasis endoscopically, recurrent bleeding despite endoscopic attempts at achieving hemostasis (many advocate surgery after ! failed endoscopic attempts), and perforation. :any authorities recommend simple oversewing of the ulcer with treatment of the underlying H pylori infection or cessation of <-'IDs for bleeding $%D. 'dditional surgical options for refractory or complicated $%D include vagotomy and pyloroplasty, vagotomy and antrectomy with gastroduodenal reconstruction (Cillroth I) or gastroEeEunal reconstruction (Cillroth II), or a highly selective vagotomy. Bleeding Peptic !lcers 0he principles of management of bleeding peptic ulcers outlined below are e6ually applicable to both gastric and duodenal ulcers. Endoscopic therapy %pper GI bleeding secondary to a bleeding peptic ulcer is a common medical condition. Endoscopic evaluation of the bleeding ulcer can decrease the duration of the hospital stay by identifying patients at low ris5 for rebleeding. :oreover, endoscopic therapy reduces the li5elihood of recurrent bleeding and decreases the need for surgery. $atients can be stratified as having high or low ris5 for rebleeding depending on the presence or absence of stigmata seen on the initial endoscopic e,amination. Bigh"ris5 stigmata are the followingH

'ctive hemorrhage (?9@ ris5 of rebleeding) ' visible vessel (89@ ris5 of rebleeding) ' fresh overlying clot (#9@ ris5 of rebleeding)

%lcers with such stigmata re6uire endotherapy, while ulcers with a clean base need not be treated endoscopically. In the absence of these stigmata, patients can be discharged home on medical therapy within 7> hours. -everal modalities of endoscopic therapy are available, such as inEection therapy, coagulation therapy, hemostatic clips, argon plasma coagulator, and combination therapy. )!G+ InEection therapy is performed with epinephrine in a *H*9,999 dilution or with absolute alcohol. 0hermal endoscopic therapy is performed with a heater probe, bipolar circumactive probe, or gold probe. $ressure is applied to cause coagulation of the underlying artery (coaptive coagulation). .ombination therapy with epinephrine inEection followed by thermal coagulation appears to be more effective than monotherapy for ulcers with a visible vessel, active hemorrhage, or adherent clot. Bemoclips have been used successfully to treat an acutely bleeding ulcer by appro,imating ! folds and clipping them together. -everal clips may need to be deployed to appro,imate the gastric ulcer folds. In treating high"ris5 bleeding ulcers, combined therapy with epinephrine and hemoclips seems to be more efficacious than inEection alone. Bowever, it is not clear whether hemoclip use or thermal coagulation is more effective in treating an acutely bleeding ulcer/ both modalities are used depending on physician e,perience and e6uipment availability. %rgent esophagogastroduodenoscopy (EGD) is the treatment of choice in the setting of a bleeding peptic ulcer for diagnostic and therapeutic reasons. Endoscopy provides an opportunity to visualize the ulcer, to determine the degree of active bleeding, and to attempt hemostasis by direct measures. $rimary endoscopic hemostatic therapy (EB0) is successful in about ?9@ of patients/ when this fails, transcatheter embolization may be useful. )!I+ :edical management usually serves as an adEunct to direct endoscopic therapy. 1is5 factors that predict rebleeding following EB0 for nonvariceal upper GI bleeding include the followingH

Aailure to use a $$I after the endoscopic procedure Endoscopically demonstrated bleeding, especially peptic ulcer bleeding EB0 monotherapy $ost"EB0 use of heparin

Cleeding in a patient with moderate"to"severe liver disease )!>+ $re"endoscopic hemodynamic instability .omorbid illness Darge ulcer size $osterior wall duodenal ulcer)!?+

0hese high"ris5 persons may be considered for initial care in the I.% and follow"up (second"loo5) endoscopy, especially because many of these factors (advanced age, comorbidities, in"hospital bleeding, rebleeding, hypovolemic shoc5, need for surgery) are associated with hospital mortality. )#9+ Acid suppression 'cid suppression is the general pharmacologic principle of medical management of acute bleeding from a peptic ulcer. 1educing gastric acidity is believed to improve hemostasis primarily through the decreased activity of pepsin in the presence of a more al5aline environment. $epsin is believed to antagonize the hemostatic process by degrading fibrin clots. Cy suppressing acid production and maintaining a pB above G, pepsin becomes mar5edly less active. .oncomitant H pylori infection in the setting of bleeding peptic ulcers should be eradicated, as this lowers the rate of rebleeding. )#*, #!+ 0wo classes of acid"suppressing medications currently in use are histamine"! receptor antagonists (B!1's) and proton pump inhibitors ($$Is).)##+ Coth classes are available in intravenous and oral preparations. E,amples of B!1's include ranitidine, cimetidine, famotidine, and nizatidine. E,amples of $$Is include omeprazole, pantoprazole, lansoprazole, and rabeprazole. B!1's are an older class of medications, and in the setting of an actively bleeding duodenal ulcer, their use has been largely superseded by the use of $$Is. :any gastroenterologists assert that intravenous $$I therapy maintains hemostasis more effectively than intravenous B!1'. 0hus, intravenous B!1' no longer has a role in the management of bleeding peptic ulcers.
)#7+

$$Is have a very good safety profile, although attention must continue to be focused on adverse effects, especially with long" term and;or high"dose therapy, such as Clostridium difficile infection, community"ac6uired pneumonia, hip fracture, and vitamin C*! deficiency. )#8+ Dong"term use of $$Is is also associated with decreased absorption of some medications. $$Is impair gastric secretion of acid/ thus, absorption of any medication that depends on gastric acidity, such as 5etoconazole and iron salt, is impaired with long"term $$I therapy. In addition, achlorhydria (absence of intragastric acidity) may be associated with iron deficiency anemia, because the ferric form of iron must be converted to the ferrous form by gastric acid. :ost iron absorbed is in the ferrous form. $arenteral $$I administration is indicated after successful endoscopic therapy for ulcers with high"ris5 signs, such as active bleeding, visible vessels, and adherent clots. $arenteral $$I use before endoscopy is a common practice. Cased on intragastric pB data, nonvomiting patients with bleeding ulcers may be treated with oral lansoprazole (*!9"mg bolus, followed by #9 mg every # h).)#G+ 4hen indicated, intravenous pantoprazole or omeprazole is administered as an >9"mg bolus followed by a continuous >"mg;h infusion for I! hours. ' study by .han et al determined that intravenous, standard"dose omeprazole was inferior to high"dose omeprazole in preventing rebleeding after endoscopic therapy for peptic ulcer bleeding. )#I+ 0his treatment is changed to oral $$I therapy after I! hours if no rebleeding occurs. In a study by 'ndriulli et al, standard"dose $$I infusion was found to be as effective as a high"dose regimen in reducing the ris5 of recurrent bleeding following endoscopic hemostasis of bleeding ulcers, according to a study by 'ndriulli et al. 0he primary end point was the in"hospital rebleeding rate (determined on repeat endoscopy). $atients with actively bleeding ulcers and those with a nonbleeding visible vessel or an adherent clot were treated with (*) epinephrine inEection and;or thermal coagulation, then randomized to receive an intensive regimen of >9"mg $$I bolus, followed by > mg;h as continuous infusion for I! hours, or (!) a standard regimen of a 79"mg $$I bolus daily, followed by saline infusion for I! hours. 'fter the infusion, all patients were given !9 mg $$I twice daily orally. )#>+ In the intensive $$I regimen group, rebleeding recurred in **.>@, whereas in the standard regimen group, rebleeding recurred in >.*@. :ost of the rebleeding episodes occurred during the initial I!"hour infusion. 0he duration of hospital stay was less than 8 days for #I.9@ in the intensive regimen group and 7I.9@ in the standard group. 0here were fewer surgical interventions in the standard group. Aive patients in each treatment group died. )#>+ ' .anadian database (1%GCE) indicated some benefit for parenteral $$I in decreasing rebleed rates. )#7+ <o randomized, controlled trial has provided evidence to support the use of parenteral $$I in this setting, but giving oral $$I both before and after EB0 for persons with peptic ulcers with signs of recent hemorrhage can be Eustified on the grounds of cost"effectiveness.
)*I+

4hether acid suppression improves therapeutic outcomes of peptic ulcers compared with placebo may be more important than the issues raised above. :any researchers have compared parenteral $$I therapy with placebo, and overall, the results have demonstrated a shorter period of bleeding and a decreased incidence of rebleeding with $$I therapy. -ome studies have demonstrated a decreased need for emergency surgery and blood transfusion/ however, evidence that parenteral $$I reduces mortality from ulcer bleeding is relatively recent. )*>+ H pylori "nfection In the %nited -tates, the recommended primary therapy for H pylori infection is proton pump inhibitor ($$I)=based triple therapy.)*+ 0hese regimens result in a cure of infection and ulcer healing in appro,imately >8"?9@ of cases. )!+ %lcers can recur in the absence of successful H pylori eradication. Dual therapies, which are alternative regimens for treating H pylori infection, are usually not recommended as first"line therapy, because of a variable cure rate that is significantly less than the cure rate achieved with triple therapy. -pouses and H pylori =positive family members of H pylori =positive persons should be considered for testing and treatment of H pylori infection,)#?+ since mother"to"child transmission may be a maEor route of H pylori infection.)79+ %riple)therapy regimens $$I"based triple therapy regimens for H pylori consist of a $$I, amo,icillin, and clarithromycin for I"*7 days. ' longer duration of treatment (*7 d vs I d) appears to be more effective and is currently the recommended treatment. 'mo,icillin should be replaced with metronidazole in penicillin"allergic patients only, because of the high rate of metronidazole resistance. )7*+ In patients with complicated ulcers caused by H pylori, treatment with a $$I beyond the *7"day course of antibiotics and until the confirmation of the eradication of H pylori is recommended. $$I"based triple therapies are a *7"day regimen as shown belowH 2meprazole ($rilosec)H !9 mg $2 bid or Dansoprazole ($revacid)H #9 mg $2 bid or 1abeprazole ('ciphe,)H !9 mg $2 bid or Esomeprazole (<e,ium)H 79 mg $2 6d Plus .larithromycin (Cia,in)H 899 mg $2 bid and 'mo,icillin ('mo,il)H * g $2 bid Alternative triple)therapy regimens 0he alternative triple therapies, also administered for *7 days, are as followsH 2meprazole ($rilosec)H !9 mg $2 bid or Dansoprazole ($revacid)H #9 mg $2 bid or

1abeprazole ('ciphe,)H !9 mg $2 bid or Esomeprazole (<e,ium)H 79 mg $2 6d Plus .larithromycin (Cia,in)H 899 mg $2 bid and :etronidazole (Alagyl)H 899 mg $2 bid *uadruple therapy Nuadruple therapies for H pylori infection are generally reserved for patients in whom the standard course of treatment has failed. Nuadruple treatment includes the following drugs, administered for *7 daysH

$$I, standard dose, or ranitidine *89 mg, $2 bid Cismuth 8!8 mg $2 6id :etronidazole 899 mg $2 6id 0etracycline 899 mg $2 6id

.onsider maintenance therapy with half of the standard doses of B!"receptor antagonists at bedtime in patients with recurrent, refractory, or complicated ulcers, particularly if cure of H pylori has not been documented or if an H pylori =negative ulcer is present. +edical +anagement of ,SA"D !lcers 0reat H pylori infection if it is present. Discontinuation of <-'IDs is paramount, if it is clinically feasible. Aor patients who must continue with their <-'IDs, $$I maintenance is recommended to prevent recurrences even after eradication of H pylori.)#, 7+ If <-'IDs must be continued, changing to a .2K"! selective inhibitor is an option. Bowever, use of a traditional <-'ID and once"daily $$I is comparable to a selective .2K"! inhibitor with respect to ulcer bleeding in patients with a history of peptic ulcer disease)7!+ . In general, G"> wee5s of therapy with a $$I is re6uired for complete healing of a duodenal ulcer. 'ctive ulcers associated with <-'ID use are treated with an appropriate course of $$I therapy and the cessation of <-'IDs. Aor patients with a 5nown history of ulcer and in whom <-'ID use is unavoidable, the lowest possible dose and duration of the <-'ID and co"therapy with a $$I or misoprostol are recommended. Deterrence and prevention $rimary prevention of <-'ID"induced ulcers includes the followingH

'void unnecessary use of <-'IDs %se acetaminophen or nonacetylated salicylates when possible %se the lowest effective dose of an <-'ID and switch to less to,ic <-'IDs, such as the newer <-'IDs or cycloo,ygenase"! (.2K"!) inhibitors, in high"ris5 patients without cardiovascular disease

.onsider prophylactic or preventive therapy for the following patientsH

$atients with <-'ID"induced ulcers who re6uire chronic, daily <-'ID therapy $atients older than G9 years $atients with a history of $%D or a complication such as gastrointestinal bleeding $atients ta5ing concomitant steroids or anticoagulants or patients with significant comorbid medical illnesses

$rophylactic regimens that have been shown to dramatically reduce the ris5 of <-'ID"induced gastric and duodenal ulcers include the use of a prostaglandin analog or a $$I according to the following regimensH

:isoprostol *99"!99 mcg $2 7 times per day 2meprazole !9"79 mg $2 every day Dansoprazole *8"#9 mg $2 every day

' !998 study showed that in patients with aspirin"induced ulcer, contrary to popular belief, aspirin plus esomeprazole (<e,ium) was superior to clopidogrel ($lavi,) in preventing recurrent gastric ulcer bleeding. )7#+ 0his was further confirmed in a double"blind randomized study in !99G by Dai and colleagues. )77+ In a study by Bsu et al, combining esomeprazole and clopidogrel reduced the recurrence of peptic ulcers in patients with atherosclerosis and a history of peptic ulcers more than the use of clopidogrel alone. )78+ 0his combination did not influence the action of clopidogrel on platelet aggregation. $omplications of Peptic !lcer Disease 1efractory, symptomatic peptic ulcers, though rare after eradication of H pylori infection and the appropriate use of antisecretory therapy, are a potential complication of $%D. 2bstruction is particularly li5ely to complicate $%D in cases refractory to aggressive antisecretory therapy, H pylori eradication, or avoidance of <-'IDs. 2bstruction may persist or recur despite endoscopic balloon dilation. $erforation is also a possibility. $enetration, particularly if not walled off or if a gastrocolic fistula develops, is a potential complication. In addition, ulcer bleeding, particularly in patients with a history of massive hemorrhage and hemodynamic instability, recurrent bleeding on medical therapy, and failure of therapeutic endoscopy to control bleeding is a serious complication. $atients with gastric ulcers are also at ris5 of developing gastric malignancy. 0he ris5 is appro,imately !@ in the initial # years. 2ne of the important ris5 factors is related to H pylori infection. H pylori is associated with atrophic gastritis, which, in turn, predisposes to gastric cancer. H pylori infection is associated with gastric lymphoma or mucosa"associated lymphoid tissue (:'D0) lymphoma. <ormal gastric mucosa is devoid of organized lymphoid tissue. H pylori infection promotes ac6uisition of lymphocytic infiltration and often the formation of lymphocytic aggregates and follicles from which :'D0 lymphoma develops. Eradication of H pylori is very important in this group of patients because eradication of H pylori has been shown to cause a remission of :'D0 lymphoma. :alignancy should be strongly considered in the case of a persistent nonhealing gastric ulcer. Endoscopic ultrasound e,amination may be helpful for assessing mucosal invasion or detecting associated adenopathy in such patients. -urgical resection should be considered if evidence of cancerous transformation is present. $onsultations -urgical consultation is recommended for all patients with bleeding ulcers, especially those patients who are at high ris5 of significant bleeding. -uch ulcers include those that have caused hemodynamic instability, those that are actively bleeding, and those that show a visible vessel on endoscopy. Long)%erm +onitoring :aintenance therapy with antisecretory medications (eg, B! bloc5ers, $$Is) for * year is indicated in high"ris5 patients. Bigh" ris5 patients include those with recurrent ulcers and those with complicated or giant ulcers. If H pylori eradication is not achieved despite repeat treatment, maintenance antisecretory therapy should be recommended. .onsider maintenance therapy with half of the standard doses of B!"receptor antagonists at bedtime in patients with recurrent, refractory, or complicated ulcers, particularly if cure of H pylori has not been documented or if an H pylori =negative ulcer is present. $atients with refractory ulcers may continue receiving once"daily $$I therapy indefinitely. In this setting, if H pylori is absent, consider a secondary cause of duodenal ulcer, such as 3ollinger"Ellison syndrome +edication Summary 0he goals of pharmacotherapy are to eradicate H pylori infection, to reduce morbidity, and to prevent complications in patients with peptic ulcers. 'cid suppression is the general pharmacologic principle of medical management of acute bleeding from a peptic ulcer, using histamine"! receptor antagonists (B!1's) and proton pump inhibitors ($$Is). )##+ Coth classes are available in intravenous or oral preparations. Discontinuation of <-'IDs is paramount, if it is clinically feasible. Aor patients who must continue with their <-'IDs, $$I maintenance is recommended to prevent recurrences even after eradication of H pylori.

0he recommended primary therapy for H pylori infection is proton pump inhibitor ($$I)=based triple therapy. 'ntacids or a GI coc5tail (typically an antacid with an anesthetic such as viscous lidocaine and;or an antispasmodic) may be used as symptomatic therapy in the ED. :aintenance treatment with antisecretory medications (eg, B! bloc5ers, $$Is) for * year is indicated in high"ris5 patients. Bigh"ris5 patients include those with recurrent ulcers and those with complicated or giant ulcers. If H pylori eradication is not achieved despite repeat treatment, maintenance antisecretory therapy should be recommended. $atients with refractory ulcers may continue receiving once"daily $$I therapy indefinitely. In this setting, if H pylori is absent, consider a secondary cause of duodenal ulcer, such as 3ollinger"Ellison syndrome $rimary prevention of <-'ID"induced ulcers includes avoiding unnecessary use of <-'IDs, using acetaminophen or nonacetylated salicylates when possible, and using the lowest effective dose of an <-'ID and switching to less to,ic <-'IDs. Proton Pump "nhi-itors $lass Summary $$Is are inhibitors of the gastric BO;PO "'0$ase (proton pump) enzyme system, which catalyzes the e,change of B O and PO. Fiew full drug information .mepra/ole (Prilosec)

2meprazole decreases gastric acid secretion by inhibiting the parietal cell BO;PO '0$ pump. It usually is given with clarithromycin and amo,icillin (or metronidazole if the patient is allergic to penicillin) if giving proton pump inhibitor=based triple therapy. It might decrease the incidence of <-'ID"induced peptic ulcers and can be used to help prevent peptic ulcers in long"term <-'ID users at high ris5. Fiew full drug information Lansopra/ole (Prevacid)

Dansoprazole decreases gastric acid secretion by inhibiting the parietal cell BO;PO '0$ pump. It usually is given with clarithromycin and amo,icillin (or metronidazole if the patient is allergic to penicillin) if giving proton pump inhibitor=based triple therapy. It might decrease the incidence of <-'ID"induced peptic ulcers and can be used to help prevent peptic ulcers in long"term <-'ID users at high ris5. Fiew full drug information &a-epra/ole (Aciphe#)

1abeprazole decreases gastric acid secretion by inhibiting the parietal cell BO;PO '0$ pump. It is used for short"term (7"> w5) treatment and relief of symptomatic erosive or ulcerative gastroesophageal reflu, disease. $atients not healed after > wee5s should consider an additional >"wee5 course. Fiew full drug information Esomepra/ole (,e#ium)

Esomeprazole is an -"isomer of omeprazole. It inhibits gastric acid secretion by inhibiting the BO;PO"'0$ase enzyme system at the secretory surface of gastric parietal cells. It is used in severe cases and in patients who have not responded to B! antagonist therapy. Esomeprazole is used for up to 7 wee5s to treat and relieve symptoms of active duodenal ulcers, and it may be used for up to > wee5s to treat all grades of erosive esophagitis. Fiew full drug information

Pantopra/ole (Protoni#)

$antoprazole suppresses gastric acid secretion by specifically inhibiting the BO;PO"'0$ase enzyme system at the secretory surface of gastric parietal cells. %se of the intravenous preparation has only been studied for short"term use (ie, I"*9 d). H0 &eceptor Blockers $lass Summary B! bloc5er antihistamine agents are used in the short"term treatment of an active duodenal ulcer and as prophyla,is in the long term. Fiew full drug information $imetidine (%agamet)

.imetidine can be used as primary therapy to heal ulcers not associated with B pylori infection. 0he duration of treatment is G" > wee5s. ' longer treatment course might be re6uired for gastric ulcers. Fiew full drug information 'amotidine (Pepcid)

Aamotidine competitively inhibits histamine at B! receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations. Fiew full drug information ,i/atidine (A#id)

<izatidine competitively inhibits histamine at B! receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.
Fiew full drug information &anitidine (1antac)

1anitidine inhibits histamine stimulation of the B! receptor in gastric parietal cells, which, in turn, reduces gastric acid secretion, gastric volume, and hydrogen ion concentrations.
Antimicro-ials $lass Summary 'ntimicrobial agents e,ert an antibacterial effect on H pylori. Fiew full drug information Amo#icillin (Amo#il2 Biomo#2 %rimo#) 0his is a component of drug combination therapy that effectively treats duodenal ulcer or gastric ulcers associated with B pylori infection. It interferes with the synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria. 'dminister with omeprazole or lansoprazole plus clarithromycin in proton pump inhibitor= based triple therapy. Fiew full drug information

$larithromycin (Bia#in) 0his is a semisynthetic macrolide antibiotic that reversibly binds to the $ site of the 89- ribosomal subunit of susceptible organisms and may inhibit 1<'"dependent protein synthesis by stimulating the dissociation of peptidyl t"1<' from ribosomes, causing bacterial growth inhibition. 0his component of drug combination therapy effectively treats duodenal ulcer or gastric ulcers associated with B pylori infection. It interferes with the synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria. 'dminister with omeprazole or lansoprazole plus clarithromycin in proton pump inhibitor=based triple therapy. Fiew full drug information %etracycline (Sumycin) .omponent of drug combination therapy that effectively treats duodenal ulcer or gastric ulcer associated with B pylori infection. %sually used in combination with bismuth subsalicylate and metronidazole. Fiew full drug information +etronida/ole ('lagyl2 'lagyl E&) 0his is a component of drug combination therapy that effectively treats duodenal ulcers or gastric ulcers associated with B pylori infection. It is active against various anaerobic bacteria and protozoa. It appears to be absorbed into cells. 0he intermediate"metabolized compounds formed bind D<' and inhibit protein synthesis, causing cell death. Antidiarrheal Agents $lass Summary 'ntidiarrheal agents may have antisecretory and antimicrobial action. Bismuth (Pepto)Bismol2 Pink Bismuth2 Bismatrol2 Devrom)

0his is a highly insoluble salt of trivalent bismuth and salicylic acid. Greater than >9@ of salicylic acid is absorbed from oral doses of bismuth subsalicylate chewable tablets. It controls diarrhea by reducing fluid secretion into the intestinal lumen, by binding bacterial to,ins, or by acting as an antimicrobial agent.
$ytoprotective Agents $lass Summary .ytoprotective agents stimulate mucus production and enhance blood flow throughout the lining of the gastrointestinal tract. 0hese agents also wor5 by forming a coating that protects the ulcerated tissue. E,amples of cytoprotective agents include misoprostol and sucralfate. Fiew full drug information +isoprostol ($ytotec) :isoprostol is a prostaglandin analog that can be used to decrease the incidence of peptic ulcers and complications in long" term <-'ID users at high ris5. Fiew full drug information Sucralfate ($arafate) -ucralfate binds with positively charged proteins in e,udates and forms a viscous adhesive substance that protects the GI lining against pepsin, peptic acid, and bile salts. It is used for short"term management of ulcers.