Most benign gastric disorders are either inflammatory or neoplastic. A variety of vascular, mechanical, congenital, and traumatic disorders also affect the stomach. Some of these are covered in other chapters of this book. Surgical management of benign gastric disorders has evolved significantly over the last 40 years. Elective peptic ulcer surgery for intractability has largely been replaced by medical management, though urgent operation for perforation is not uncommon, and occasional elective ulcer operation is still necessary for obstruction or nonhealing. Most elective (and even urgent) gastric procedures can now be performed with laparoscopy (and in some cases with robotic assistance) if local expertise is available. Intraoperative endoscopic guidance with or without ultrasound allows accurate lesion localization and can help the surgeon perform a more targeted resection when wide margins are not necessary.

Helicobacter pylori−induced chronic gastritis is the most important risk factor for peptic ulcer and gastric adenocarcinoma, a major cause of cancer death worldwide. Successful H pylori treatment largely eliminates recurrent peptic ulcer in infected patients, and eradication of H pylori worldwide would eliminate most cases of gastric adenocarcinoma. H pylori infection is also associated with mucosa-associated lymphoid tissue (MALT) lymphoma, dyspepsia, hyperplastic gastric polyps, and even idiopathic thrombocytopenic purpura (ITP). When Marshall and Warren elucidated the relationship between H pylori and peptic ulcer disease, a discovery for which they were later awarded the Nobel Prize in medicine, they rekindled the hypothesis that this common clinical malady was an infectious disease. It is now clear that most gastric adenocarcinoma is also related to chronic Helicobacter gastritis.

H pylori is a gram-negative spiral flagellated organism that currently infects more than half of the people in the world. The prevalence of H pylori infection varies among populations and is strongly correlated with socioeconomic conditions. In a number of developing countries, H pylori infection affects more than 80% of middle-aged adults, and reinfection risk after curative treatment is high. Infection rates are lower in industrialized countries. Epidemiological data indicate that the prevalence of infection in the United States has been declining since the second half of the 19th century, with the decreases corresponding to improvements in hygiene and sanitation. Nonetheless, H pylori infection is predicted to remain endemic in the United States for the next century. Human beings are the only reservoir for H pylori. Infection is presumed to occur by oral ingestion of the bacterium. Family members of infected individuals are at increased risk of infection. In developing countries, most people become infected during childhood. A number of occupations also show increased rates of H pylori infestation, notably healthcare workers. Infection with H pylori is a chronic disease and does not resolve spontaneously without specific treatment. Worldwide, H pylori–induced gastritis accounts for 80% to 90% of all gastritis.

H pylori has evidently adapted to the hostile gastric environment and displays a number of features that permit its entry into the surface mucus layer, attachment to gastric epithelial cells, evasion of host immune responses, and persistent colonization of the surface epithelium and gastric pits despite luminal acidity. Up to 15% of the protein in a Helicobacter organism is composed of cytoplasmic urease that converts periplasmic urea into CO₂ and ammonia, the latter buffering the surrounding acid. H pylori infection is not invasive of the gastric mucosa, and the host immune response is triggered by the attachment of bacteria to gastric epithelial cells. The initial inflammatory response is characterized by recruitment of neutrophils, followed sequentially by T and B lymphocytes, plasma cells, and macrophages. The resultant chronic gastric inflammation in affected individuals is characterized by enhanced mucosal expression of multiple cytokines and the presence of reactive oxygen and nitrogen species, and long-term infection is associated with mucosal cell DNA damage and chromosomal instability.

The relationship between H pylori infection and peptic ulceration is overwhelmingly strong and multiple observations establish H pylori as a factor in the pathogenesis of peptic ulceration.Unfortunately, an effective vaccine has not yet been developed. H pylori infection is invariably followed by the development of chronic gastritis, and the organism is the primary cause of chronic active gastritis worldwide. The infectious response to H pylori is characterized by non-erosive inflammation of the gastric mucosa. Antral gastritis is present histologically in patients with peptic ulcer, and H pylori can be isolated from inflamed gastric mucosa of ulcer patients. Postprandial hypergastrinemia and elevated basal acid secretion are common. Gastric metaplasia of the duodenal bulb develops after infestation of the antral mucosa. Metaplastic gastric epithelium in the duodenum is colonized by H pylori from gastric sources, and this gastric metaplasia is extremely common in duodenal epithelium surrounding areas of peptic ulceration. Eradication of H pylori with antibiotics that have no effect on acid secretion leads to ulcer healing, and treatment of peptic ulceration with bismuth compounds, which inhibit H pylori, is associated with reduced rates of ulcer relapse relative to acid suppression therapy. Relapse of duodenal ulcer after eradication of H pylori may be preceded by reinfection of the gastric mucosa by the organism.

However, it is clear that infection by H pylori alone does not cause peptic ulceration in most individuals, suggesting the existence of other pathogenetic factors. Up to half of patients evaluated for dyspepsia have histologic evidence of Helicobacter infection but no ulcer. In developed countries, one-fifth of healthy volunteers harbor the bacteria, and the incidence of bacterial infestation increases with age in the healthy, asymptomatic population. The occurrence of peptic ulcers in only a fraction of individuals who harbor the organism suggests that other factors must also act to induce ulceration. Even in the presence of active H pylori infection, strong acid suppression usually heals peptic ulcer, an observation consistent with the old dictum “no acid, no ulcer.” However long-term proton pump inhibitor (PPI) use in patients with active Helicobacter infection is associated with corpus predominant gastritis, which leads to atrophic gastritis and increases the risk of gastric cancer.

Testing for H pylori infection should be performed in patients with peptic ulcer, gastritis, significant dyspepsia, MALT lymphoma, and early gastric cancer. Noninvasive methods for diagnosis of H pylori infection include the urea breath test, serology, and detection of stool antigen. The urea breath test is based on production of urease by H pylori in the gastric mucosa, and a positive test indicates active infection. C 14-labeled urea is ingested and C 14-labeled CO₂ is produced and excreted in the breath. This test has a sensitivity and specificity of greater than 90%. The urea breath test is useful for initial diagnosis of infection and for follow-up after eradication therapy, since unlike serology, it is positive only in the presence of active infection. The stool antigen test is another noninvasive test to detect active H pylori infection. Both polyclonal and monoclonal kits have been developed. Different kits are available for both outpatient and inpatient settings. These tests may perform differently in different geographic locations according to the antigenic composition of the circulating strains, so it is recommended that only locally validated tests be used. Because H pylori induces a strong immunologic response, serological testing is useful but may not be as accurate as the urea breath test or the stool antigen test, and a positive serology persists after eradication of H pylori infection. Consideration should be given to confirming a positive H pylori serology with another more accurate test. H pylori infection can also be diagnosed by histologic evaluation of gastric biopsies and/or the rapid urease test on fresh biopsies. Culture of H pylori is not routine and is usually reserved for recurrent infection and for antibiotic sensitivity testing when second-line therapy has failed. All of these tests for H pylori have a false negative rate.

Patients with a positive test should be treated, and in the appropriate clinical scenario, some patients with a negative test should probably be treated as well (unexplained gastritis; recurrent or intractable peptic ulcer). Documented eradication of H pylori infection is the goal of treatment in each patient. An enormous worldwide experience has developed relating to H pylori eradication. More than 2000 articles report the results of antibiotic trials, and a large number of summary articles and meta-analyses are available. It is important to note that none of the therapeutic regimens reported to date cure H pylori infection in 100% of patients. To be effective, antimicrobial drugs must be combined with gastric acid secretion inhibitors or bismuth salts (Table 29-1). In the absence of treatment, eradication of H pylori infection is very rare. The Maastricht V/Florence Consensus Report provides current recommendations for diagnosis and treatment of H pylori infection in various clinical scenarios, including recommendations for areas with high metronidazole and clarithromycin resistance (Fig. 29-1). The United States currently demonstrates high clarithromycin resistance but low to intermediate metronidazole resistance, similar to the patterns for most of central and southern European countries. Ideally, a treatment regimen is chosen with 90% effectiveness, and repeat noninvasive testing to confirm eradication is performed. Treatment failure requires an alternative course of therapy. Failure to eradicate infection after two tries should prompt Helicobacter culture and sensitivity testing, and referral to a specialist. With assiduous treatment, Helicobacter eradication can be achieved in nearly every patient. Patients with atrophic gastritis require endoscopic surveillance.

Dyspepsia is a very common symptom complex characterized by pain and discomfort centered in the upper abdomen. Up to 50% of patients who present with dyspepsia may have Helicobacter infection, depending on the regional prevalence of the latter. Patients with dyspepsia and alarm symptoms require esophagogastroduodenoscopy (EGD). Testing and treatment for Helicobacter should be considered. Functional dyspepsia is diagnosed when there are no endoscopic or histologic findings, or when chronic symptoms persist after Helicobacter eradication has been documented, but it is important to note that Helicobacter-associated dyspeptic symptoms may persist for a while after eradication. When a dyspeptic patient has no diagnostic workup, the condition is classified as “non-investigated dyspepsia.” For surgeons, the importance of non-ulcerative dyspepsia relates to its place in the differential diagnosis of epigastric pain. There is no role for surgery in the treatment of this disorder.

Atrophic gastritis is characterized by shrinkage or disappearance of gastric glands along with loss of parietal and chief cells. By far the most common cause is chronic H pylori infection, particularly the corporal distribution (as opposed to the antral distribution, which is more typically associated with peptic ulcer disease). Autoimmune destruction of cells (pernicious anemia) and chemical irritation (eg, bile reflux) can also result in atrophic gastritis. Some patients with atrophic gastritis develop intestinal metaplasia in the gastric mucosa, which may progress to dysplasia and then to gastric cancer. Numerous cofactors have been implicated including diet, altered gastric microbiome, genetics, and hypergastrinemia. Patients with atrophic gastritis are at risk for gastric cancer and some warrant endoscopic surveillance. Patients with metaplastic atrophic gastritis are at higher risk for gastric cancer, and those with dysplastic metaplasia even higher. Patients with high-grade dysplasia may benefit from gastrectomy. The cancer risk is related to the extent of the atrophic gastritis and intestinal metaplasia, and grading systems have been developed to stratify cancer risk based on endoscopic findings. Two such systems are the operative link on gastritis assessment (OLGA) and the operative link on gastric intestinal metaplasia (OLGIM) assessment. These systems define the severity (stage) of atrophic gastritis based on the histologic grading of at least five gastric biopsies (lesser and greater curve antrum; lesser and greater curve corpus; angularis incisura) (Table 29-2). Since pathologists are more likely to agree on the histological diagnosis of intestinal metaplasia than they are on atrophic gastritis, the latter tool (OLGIM) may be more useful in stratifying gastric cancer risk. Patients stratified as Stage 3 or 4 gastritis and those with pernicious anemia may benefit from surveillance endoscopy every 3 years. Serum markers are also useful in helping to identify patients with atrophic gastritis, who usually have increased serum gastrin and iron deficiency due to parietal cell loss and hypochlorhydria or achlorhydria, decreased pepsinogen I levels due to chief cell loss, and B₁₂ deficiency due to parietal cell loss and concomitant loss of intrinsic factor.

Epidemiology

Peptic ulcer disease (includes duodenal, gastric, and marginal ulcers) is a major public health problem in the United States and a source of substantial health care expenditure (Table 29-3). Overall, peptic ulcer mortality and hospitalization rates have declined from over 200,000 admissions in 1993 down to about 150,000 in 2006. Hemorrhage continues to be the most frequent presentation at hospital admission, followed by perforation and obstruction, but perforation is by far the most common indication for operation nowadays. Currently bleeding peptic ulcer is typically treated successfully with endoscopic techniques, occasionally with help from interventional radiology, and emergency operation for bleeding is unusual. Although overall mortality rates in patients hospitalized for peptic ulcer decreased slightly (2.7%, down from 3.8%), no change was seen in the determinants of mortality. Perforation is still associated with the highest mortality, followed by obstruction and then bleeding. The mortality from surgical intervention decreased over the time period but remains high compared to endoscopy and embolization. In parallel with the discovery of H pylori and the subsequent development of improved therapies for its eradication, surgical treatment of peptic ulcer has changed dramatically, with the virtual elimination of elective operations for intractable peptic ulcer disease. Operative therapy is now used mostly for urgent or semi-elective treatment of complications from the disease; ie, perforation, obstruction, bleeding, and rarely nonhealing.

Pathophysiology

The pathogenesis of peptic ulceration is multifactorial but increasingly understood to be a consequence of H pylori infection and nonsteroidal anti-inflammatory drug (NSAID) use. Before recognition of the role of H pylori, ulcer disease was conceived as an imbalance between acid and pepsin secretion and mucosal defense, with the balance shifted toward peptic injury and disease. In groups of patients, increases in acid secretion are well documented, and although gastric acid is crucial in the development of ulcers, an acquired defect in mucosal defense exists to tip the balance away from health. Mucosal infestation of the antrum with H pylori is the factor that contributes to ulceration in most patients both by weakening local defenses and increasing acid secretion. Aspirin and NSAID use is the second most important factor in ulcer pathogenesis, largely via weakened mucosal defenses. Other factors such as exogenous steroids and acute stress undoubtedly play a role in ulcer formation (Table 29-4). Substantial evidence implicates cigarette smoking as a significant risk factor in the development of chronic peptic ulcers. Smokers appear to have an increased risk of developing H pylori infection relative to nonsmokers. Cigarette smoking impairs ulcer healing and increases the risk of recurrent and/or marginal ulceration. Continued smoking blunts the effectiveness of active ulcer therapy. Cigarette smoking increases both the probability that surgery will be required and the risks of operative therapy. When H pylori is eradicated in smokers, they appear to have no greater risk of peptic ulceration than nonsmokers. This observation suggests that smoking is probably not an independent risk factor for ulcer disease but acts by increasing the harmful effects of bacterial infection. Cessation of smoking is a key goal of anti-ulcer therapy.

Abnormalities of gastric acid secretion in patients with peptic ulceration have been recognized for more than 50 years. The formation of peptic ulcers clearly depends on gastric secretion of acid and pepsin. This association is emphasized by the dictum “no acid—no ulcer,” and H pylori infection is known to secondarily induce alterations in gastric acid secretion. Abnormalities of mucosal function have been invoked as contributing factors to peptic injury. In support of this concept, several agents that are used to treat peptic ulceration are cytoprotective. The ability of such agents to heal ulcers suggests that abnormalities in mucosal defense, in addition to abnormalities in acid secretion, cause ulceration. Most cytoprotective agents act via mucosally secreted bicarbonate or on mucosal prostaglandin production.

NSAIDs are a major risk factor for the development of acute ulceration and for hemorrhagic complications of ulceration. NSAIDs produce a variety of lesions, ranging from superficial mucosal erosions to deeper ulcerations. While the mucosal injury caused by NSAIDs is more common in the stomach than in the duodenum, ulcer complications occur with equal frequency in these two sites. H pylori and NSAID use independently increase the risk of peptic ulcer and ulcer bleeding. These agents also act synergistically. In the duodenum, it appears likely that invasive H pylori–associated ulcers are compounded by the direct injurious effects of NSAIDs. The injurious actions of NSAIDs are secondary to suppression of prostaglandin production. Numerous experimental models have demonstrated that NSAIDs injure the gastroduodenal mucosa. Ulcers resembling those occurring in humans can be produced by administration of NSAIDs to animals, and NSAID-associated gastric ulcers can be prevented by the coadministration of prostaglandin analogues. Ulcers associated with NSAIDs heal rapidly when the drug is withdrawn, corresponding temporally to reversal of antiprostaglandin effects. Clinically significant ulceration of the stomach and duodenum is estimated to occur at a rate of 2% to 4% per patient-year in NSAID users. The risks of long-term NSAID use are increased by H pylori infection and cigarette smoking. The incidence of NSAID-related ulcer complications is highest in older patients, as is attendant mortality rate. Peptic ulcer disease is rare in individuals who are H pylori–negative and who do not receive NSAID medications.

Diagnosis

Peptic ulceration is typically characterized by nonradiating epigastric pain described as burning, stabbing, or gnawing. Referral of pain to the back may indicate posterior penetration of the ulcer. The pain is usually related to eating, with duodenal ulcer pain relieved by eating, which sometimes makes gastric or marginal ulcer pain worse. Ingestion of antacids or initiation of antisecretory agents (H2 antagonists or PPIs) usually provides prompt relief. In uncomplicated cases, physical examination is usually normal. The differential diagnosis includes a variety of diseases originating in the epigastrium and upper GI tract. Common disorders to be distinguished include non-ulcer dyspepsia, gastritis, gastric neoplasia, cholelithiasis and related diseases of the biliary system, neoplastic lesions of the liver, and both inflammatory and neoplastic disorders of the pancreas. In dyspeptic patients, especially those older than 50 years of age, the most important differential diagnoses are peptic ulceration and gastric cancer.

The evaluation of patients with suspected peptic ulceration usually involves endoscopic examination of the esophagus, stomach, and duodenum. In controlled trials, endoscopy was both more sensitive (92% vs 54%) and more specific (100% vs 91%) than radiographic examination, but the latter should be considered if perforation is suspected. The most frequent site for duodenal peptic ulceration is the first portion of the duodenum, with the second portion less frequently involved. Peptic ulceration of the third or fourth portions of the duodenum is distinctly unusual and raises the possibility of gastrinoma or nonpeptic causes of ulceration such as cancer or ischemia. Peptic ulcers in the pyloric channel or the prepyloric area are similar in appearance to duodenal ulcers and should be treated as such (type 3 gastric ulcers). Endoscopic demonstration of a duodenal ulcer does not require duodenal biopsy but should prompt mucosal biopsy of the gastric antrum to demonstrate the presence of H pylori and guide subsequent therapy.

Peptic Ulcer Location

The three typical locations for peptic ulcer are duodenal, gastric, and marginal or anastomotic, and the pathophysiology and treatment vary by location. In the United States, benign gastric ulcers are found in approximately 90,000 new patients a year, about one-fifth that of duodenal ulceration. The opposite is found in Japan, where gastric ulcers are 5 to 10 times more common. Gastric ulcer is more common in men than women and occurs in a patient cohort approximately 10 years older than that of duodenal ulceration. In symptomatic patients, upper GI endoscopy is the preferred method for diagnosing peptic ulcers, though radiologic studies are often complementary. About 10% of gastric ulcers are malignant or associated with malignancy, so aggressive biopsy and brushings, as well as careful follow-up to demonstrate healing, are mandatory. All gastric ulcers should undergo multiple biopsies, obtained from the perimeter of the lesion. The addition of endoscopic brushings to multiple biopsies increases diagnostic accuracy to approximately 95%. Although benign gastric ulcers may occur in any location in the stomach, more than half are located along the lesser curvature proximal to the incisura angularis. Fewer than 10% of benign ulcers are located on the greater curvature. Most benign gastric ulcers lay within 2 cm of the histologic transition between fundic and antral mucosa. Gastric ulcers are classically categorized as type 1 (lesser curvature near angularis incisura), type 2 (gastric ulcer associated with active or inactive duodenal ulcer), type 3 (prepyloric ulcer), type 4 (juxtacardia ulcer), and type 5 (greater curvature ulcer). Similar to duodenal ulceration, H pylori infection plays an important role in the pathogenesis of benign gastric ulcers. Antibiotic Helicobacter treatment regimens useful for duodenal ulcer have also been used for benign gastric ulceration. The response of gastric ulcers to Helicobacter treatment is equivalent to that of duodenal ulcers. Recurrence or persistence of gastric ulcers after H pylori eradication may indicate persistent or recurrent infection, but more likely represents persistence of other risk factors such as smoking and/or NSAID use. In addition to H pylori infection, alterations in gastric motility have been demonstrated in some patients with benign gastric ulcers. Motility defects include delayed gastric emptying, abnormal pyloric sphincter function, prolonged high-amplitude gastric contractions, duodenogastric reflux, and alterations in the gastric migrating motor complex. These alterations have not been definitively demonstrated to be pathogenic, and their relevance to gastric ulceration is unsettled.

Marginal ulcers are peptic ulcers which characteristically occur on the jejunal side of the gastrojejunostomy following distal gastrectomy, gastric bypass, or simple gastrojejunostomy. The risk of marginal ulceration is related to the acid/peptic load delivered into the jejunum (a site unaccustomed to any acid), and luminal jejunal buffering (largely absent in Roux gastrojejunostomy). So risk factors for marginal ulceration include Roux gastrojejunostomy, large gastric pouch after distal gastrectomy or Roux-en-Y gastric bypass (RYGBP), gastrogastric fistula after RYGBP, retained or excluded antrum, and incomplete or inadequate vagotomy. Other factors to consider are ischemia and permanent suture material. Marginal ulcers are prone to the same complications that bedevil duodenal or gastric ulcer including perforation, obstruction, bleeding, and nonhealing. Cancer is usually not a concern with marginal ulcer unless the anastomosis was performed many years ago, and then stump cancer becomes a consideration.

Operative Treatment of Peptic Ulcer Disease

It is well recognized that elective operation for intractable peptic ulcer disease has largely disappeared. Operative intervention is now performed primarily for the treatment of ulcer complications which are (in decreasing order of operative frequency): perforation, obstruction, bleeding, and nonhealing (Table 29-5). The role of the traditionally “definitive” ulcer operations (parietal cell vagotomy, vagotomy and drainage, vagotomy and antrectomy) is less clear. Both surgeon questionnaire and evaluation of administrative database suggest that vagotomy for ulcer nowadays is unusual, as is definitive ulcer operation in the setting of perforation or bleeding. Cancer remains an important part of the differential diagnosis in gastric ulcer, obstructing peptic ulcer disease, and marginal ulcer if (it occurs many years after gastrojejunostomy). Ultimately, recurrent peptic ulcer is almost inevitable if one or more of the following persist: Helicobacter infection, NSAID use, smoking, inadequate acid suppression. Lifelong acid suppression should be considered in all patients hospitalized for peptic ulcer. The operative mortality for emergency ulcer operation is 10% to 20%. This speaks to the frailty and degree of chronic illness seen in many patients requiring peptic ulcer surgery today.

Perforated Peptic Ulcer

Patients with perforated peptic ulcer have a hospital mortality risk of 10% to 20%. Most patients with perforated peptic ulcer are adequately treated by peritoneal washout and omental patch, with subsequent elimination of risk factors (ie, treat Helicobacter; stop smoking; stop NSAIDs; take acid suppression). The postoperative elimination of risk factors is very important. In the absence of peritonitis and systemic inflammatory response, nonoperative management may be considered if careful radiologic evaluation confirms that the ulcer has sealed. However, the large majority of patients with perforated ulcer need urgent operation, which can be done laparoscopically or open. Biopsy to rule out cancer should be done in patients with perforated gastric ulcer, and perforated marginal ulcer if the gastrojejunostomy was done many years ago. Wedge resection may be preferable to omental patch for some perforated gastric ulcers. In the setting of shock, perforation >48 hours, or dangerous medical comorbidity (eg, recent MI, pulmonary hypertension, multisystem organ failure [MSOF], cirrhosis), definitive ulcer operation should be eschewed. In the stable patient, definitive operation may be considered for chronic ulcer which has failed medical management and if postoperative elimination of risk factors is unlikely.

Though simple omental patch with postoperative Helicobacter treatment has been shown to eliminate recurrent or persistent ulcer symptoms in most patients with perforated duodenal ulcer, some patients will fail H pylori eradication or have other significant risk factors such as smoking and NSAID use. Furthermore, extrapolation from duodenal ulcer to gastric or marginal ulcer may be inappropriate. Thus it is reasonable to consider definitive operation on a case-by-case basis in the stable patient with peptic ulcer perforation. For perforated duodenal ulcer, definitive procedures include parietal cell vagotomy, truncal vagotomy and drainage (pyloroplasty incorporating the perforation or gastrojejunostomy), and truncal vagotomy and antrectomy (perhaps most appropriate for giant duodenal perforations). For perforated gastric ulcer, definitive operations include distal gastrectomy to include the ulcer, and wedge resection with vagotomy and drainage. For marginal ulcer, definitive operation includes resection of the gastrojejunostomy with the perforation, along with additional stomach if deemed appropriate.

Obstructing Peptic Ulcer

By far the most common cause of gastric outlet obstruction is cancer (pancreas, duodenum, stomach), and it is worthwhile keeping this in mind when treating patients for peptic ulcer obstruction. All three peptic ulcer varieties (duodenal, gastric, marginal) can cause chronic scarring resulting in intractable gastric outlet obstruction manifested by chronic nausea, vomiting, epigastric pain, weight loss, food intolerance, and even sitophobia. Patients with suspected obstructing peptic ulcer should have upper endoscopy with biopsy and CT scan. Traditional barium fluoroscopic studies may also be revealing. Endoscopic balloon dilation can be transiently helpful in up to half of these patients, but multiple dilations are usually necessary and most patients eventually require operation. The gold standard procedure for obstructing duodenal or prepyloric gastric ulcer is distal gastrectomy with Billroth 2 gastrojejunostomy, and truncal vagotomy. An acceptable alternative operation is laparoscopic gastrojejunostomy and selective vagotomy, which can be done minimally invasively. If the obstructing ulcer disease is primarily prepyloric, attempt should be made to obtain lumenal biopsies at the site of obstruction. Subsequently, if indicated, the gastrojejunostomy can be reversed (eg, for severe dumping if the pyloric channel is patent) or converted to distal gastrectomy with Billroth 2 or Roux gastrojejunostomy (eg, for persistent symptoms or concern about malignancy). However, this “lesser operation” may miss or delay the diagnosis of an unexpected obstructing cancer. The hospital mortality for patients with obstructing peptic ulcer is 2% to 3%.

Bleeding Peptic Ulcer

Although bleeding remains the most common reason for hospitalization in peptic ulcer patients, with a hospital mortality around 3%, it is no longer a common indication for surgery due to the efficacy of endoscopic treatment and occasionally radiologic embolization. Aggressive treatment with IV acid suppression is important too. Bleeding peptic ulcer is the most common cause of clinically significant upper GI bleeding. Most patients (75%) have low-risk bleeds, but 25% of patients have high-risk bleeds, and essentially all the deaths from bleeding ulcer occur in this latter group. Clinical and endoscopic parameters can identify this high-risk group (Table 29-6), which should be managed by a multidisciplinary team in a special unit or intensive care unit. After initial resuscitation, early endoscopy should be performed and bleeding sites treated with epinephrine injection and an energy source. Endotracheal intubation for airway protection is considered on a case-by-case basis. Rebleeding should prompt repeat endoscopic treatment or angiography. Surgery should be considered for refractory bleeding requiring multiple transfusions, especially if associated with episodes of hemodynamic instability, and for high-risk lesions, such as deep penetrating ulcer with a subjacent named artery. Bleeding from erosion of the ulcer into the gastroduodenal, left gastric, or splenic artery is very likely to persist or recur after endoscopic therapy alone.

Bleeding marginal ulcers are best treated with resection. Occasionally the ulcer has eroded into named vessels such as the splenic artery or middle colic artery, so the surgeon should be prepared for these contingencies. Bleeding gastric ulcer can be treated with oversewing, wedge resection, or definitive gastrectomy to include the ulcer. Traditionally, vagotomy for gastric ulcer has been deemed unnecessary. Though hemigastrectomy and damage control remains an option, it is best to avoid definitive ulcer operation in the setting of shock or profound coagulopathy. Surgical options for the management of bleeding duodenal ulcer include oversewing, either alone or with definitive ulcer operation, usually vagotomy and drainage. Classically the pyloroduodenotomy, which is made to access the bleeding ulcer, is incorporated into a pyloroplasty. Alternatively, the pyloric incision is closed and gastrojejunostomy performed. Then truncal vagotomy is done. Antrectomy with truncal vagotomy can be considered in stable patients, especially those with giant bleeding duodenal ulcer. However, management of the duodenal stump can be challenging since the ulcer must be securely oversewn or resected.

Regardless of operation performed, certain and secure ulcer hemostasis by suture ligation should be the most important goal of any operation for bleeding peptic ulcer. Much has been written about the proverbial and useful “U-stitch” to secure hemostasis in a deep duodenal ulcer with a hole in the gastroduodenal artery near a large pancreatic side branch. Deep “over-and-over” sutures may accomplish the same thing. Extralumenal ligation of the gastroduodenal or left gastric artery may occasionally also be helpful. Compared to simple oversewing and vagotomy and drainage, rebleeding may be less common after distal gastrectomy for bleeding peptic ulcer, but the operative mortality is higher. Overall, current hospital mortality in patients requiring operation for bleeding peptic ulcer is 10% to 20%.

Intractable or Nonhealing Peptic Ulcer

Operation for nonhealing peptic ulcer should be performed only after careful deliberation and diagnostic evaluation. Nonhealing or intractability should indeed be a rare indication for ulcer operation today, and the patient referred for surgical evaluation of intractable peptic ulcer disease should raise red flags for the surgeon. Since acid secretion can be totally blocked and H pylori eradicated with modern medication, it is important to ask why the patient has a persistent ulcer diathesis. All causes of nonhealing peptic ulcer should be considered prior to operative treatment (Table 29-7).

Surgical treatment may be considered in patients with nonhealing or intractable peptic ulcer disease who have multiple recurrences, large ulcers (>2 cm), complications (obstruction, perforation, or hemorrhage), or suspected gastric cancer. Though nonhealing ulcers may represent an undiagnosed malignancy, this is unusual nowadays. Typically patients with intractable or nonhealing peptic ulcer experience suboptimal outcomes after ulcer operation, which may result in chronic weight loss of up to 10% to 20%. Before embarking on an ulcer operation in a patient for intractability or nonhealing, it is prudent for the surgeon to envision this degree of weight loss, since this is what the patient might look like after an ill-conceived ulcer operation. The obvious corollary is that operation for intractability or nonhealing ulcer should be avoided in asthenic patients. Sadly, the thin patient can be an easy target for a big ulcer operation in the hands of the inexperienced ulcer surgeon.