AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Helicobacter pylori is the most prevalent gastric microbial pathogen in humans. Currently, approximately one half of the global population is thought to be infected with this bacterium, although the prevalence varies in different regions. Unless specific therapy is administered, the infection lasts for a lifetime. Childhood is a critical time for the acquisition of the infection.

Although the route of transmission is poorly understood, the infection is believed to spread through person-to-person transmission through oral-gastric, fecal-oral, and oral-oral routes or through the ingestion of contaminated water. Intrafamilial transmission, particularly mother-to-child and child-to-child transmission, is important. H pylori is firmly established as the most important causative factor in chronic gastritis and gastric and duodenal ulcers in children, and successful eradication of this pathogen greatly reduces the rate of recurrence of duodenal ulcers in affected individuals.

Only a few cases of the mucosa-associated lymphoid tissue (MALT) gastric lymphoma in the presence of H pylori infection have been reported in children, and no reports exist of gastric adenocarcinomas in pediatric patients who are chronically infected with this organism, a known association in the adult population.

Extradigestive disorders associated with H pylori infection in children and adolescents include refractory iron-deficiency anemia, chronic autoimmune thrombocytopenic purpura, and urticaria. The first 2 conditions show improvement with eradication of the organism. Growth retardation seen in children infected with H pylori could result from the effect of inflammation on the release of the gastric hormones leptin and ghrelin, which control appetite.

Advances in the diagnosis and medical therapy of peptic ulcer disease in infants, children, and adolescents have limited the role of the pediatric surgeon in the treatment of peptic ulcer disease to the treatment of resultant complications such as uncontrolled bleeding from the stomach or duodenum, gastric outlet obstruction from recurrent peptic ulceration, and gastric or duodenal perforation.

History of the Procedure

Surgical treatment of peptic ulcer disease in children is derived from the experience of treating adults with the disease. Lester Dragstedt, MD, championed modern treatment of peptic ulcer surgery by introducing the vagotomy, which was based on a better understanding of the vagal drive for acid secretion in the stomach. In the 1940s and 1950s, the most common operations performed for peptic ulcers were truncal vagotomies with pyloroplasties and antrectomies. In the 1960s, recognition of complications such as postvagotomy diarrhea led to development of the proximal gastric vagotomy, which could obviate these problems and the need for a gastric-emptying procedure. Today, these operations can be performed using open or minimally invasive techniques.

Problem

Gastric and duodenal ulcers are infrequent among the pediatric population. These lesions are typically divided into primary and secondary peptic ulcers.

Peptic ulcers are labeled primary when they occur without any predisposing factors, such as acute medical illness, stress, trauma, systemic illness, use of ulcerogenic medications (eg, salicylates, nonsteroidal anti-inflammatory agents [NSAIDs], steroids), smoking, or dietary intake of secretagogues (eg, caffeine, nicotine, alcohol). Primary ulcers occur most commonly in the duodenum or pyloric channel and manifest most often in older children and adolescents. The family history is usually positive for ulcer disease. Primary peptic ulcers may occur in the stomach, but these occurrences are uncommon.

Secondary peptic ulcers are usually associated with stress, neonatal hypoxia, systemic infection, head trauma, burns, chronic illness, and ulcerogenic medications. Secondary peptic ulcers are not associated with hyperacidity. These ulcers usually occur in the stomach. Several conditions linked to increased prevalence of peptic ulcer disease in children include cystic fibrosis, type 1 diabetes mellitus, sickle cell disease, pseudo–Zollinger-Ellison syndrome, systemic mastocytosis, and Crohn disease involving the stomach or duodenum.

Three distinct entities, namely gastric necrosis in neonates, Dieulafoy disease, and Zollinger-Ellison syndrome, are discussed in further detail below.

Frequency

The prevalence of peptic ulcer disease in infants, children, and adolescents is approximately 5 per 10,000 population. H pylori colonization in the stomach has been recognized as an important risk factor in the development of peptic ulcers in children. In developing countries, approximately half of children have colonization of H pylori by age 10 years, whereas colonization in childhood is rare in developed countries. However, in children with a low socioeconomic status, colonization rates in developed countries are similar to those in developing countries.

Etiology

H pylori, described by Warren and Marshall in 1982, is a spiral gram-negative organism with a smooth surface and multiple unipolar flagella. Since its discovery, this bacterium has gained worldwide recognition as an important factor in the pathogenesis of gastritis and peptic ulcer disease. H pylori has the ability to grow in an acidic environment because of its urease-mediated ammonia production, which neutralizes gastric acid. Most organisms settle in the mucus of the gastric antrum without invading the mucosa. Flagella enable H pylori to resist gastric peristalsis, and the bacterium's adhesion properties allow this organism to attach to the gastric epithelium. Mucosal reaction consists of acute and chronic inflammation with neutrophil and lymphocyte infiltration and, in children, lymphonodular hyperplasia.

Numerous studies link H pylori colonization with chronic gastritis in children. Furthermore, H pylori gastritis seems to correlate strongly with duodenal ulcers in this group, in which a 90-100% prevalence of H pylori gastritis has been reported. However, a link between H pylori antral colonization and gastritis is less likely as the etiologic factor of pediatric gastric ulcers. Whether the organism causes the ulcers or plays an important role in maintaining them is unclear; however, eradicating H pylori in affected adults and children heals and cures their recurrent peptic ulcers.

Pathophysiology

Mediators of mucosal inflammation, such as lymphokines and oxygen-free radicals, are involved in the development of gastritis or ulcer disease. Infection with H pylori induces a T-cell response in the lamina propria of the gastric mucosa, which is interferon-gamma predominant. In some instances, chronic imbalance between epithelial cell proliferation and apoptosis may result in mucosal atrophy of the stomach, a predisposing factor in the development of gastric cancer later in life.

Mucosal defenses include intestinal and pancreatobiliary sources of bicarbonate, surface-active phospholipids, mucosal blood flow, and rapid cell exchange rates influenced by substances such as epidermal growth factor. Prostaglandins protect the gastric mucosa by directly inhibiting parietal cell function and acid secretion, increasing mucus production, and promoting mucosal blood flow. Although the presence of hydrochloric acid is necessary for the development of ulcers, gastric acidity tends to be normal or decreased in gastric ulcers (particularly secondary ulcers) and increased in pyloric and duodenal ulcers. Therefore, factors associated with mucosal resistance are more prominent in the etiology of gastric ulcers, and factors affecting acidity predominate in the etiology of pyloric and duodenal ulcers.

The effects of H pylori colonization of the gastric mucosa may take years to become evident. This organism possesses large amounts of urease, allowing it to convert urea to ammonia and carbon dioxide and, thus, gain a survival advantage in an acidic environment. Production of oxygen dismutase and catalase enables H pylori to resist damage from phagocyte-released oxygen free radicals. The microaerophilic metabolism of this bacterium permits its proliferation in the semipermeable layer of mucus that lines the stomach.

After ingestion of the organism, a period of florid proliferation occurs, with resulting gastric inflammation. Usually, the mounted immune response, which may take weeks to months to develop, is ineffectual in eliminating the infection, and chronic superficial gastritis ensues.

Long-term H pylori infection results in chronic inflammatory changes in virtually all individuals. The severity and distribution of these inflammatory changes vary form one person to another. This is a result of the interaction of virulence of the organism and the host's defenses, resulting in antral-predominant gastritis with hyperacidity in some individuals and corpus-predominant atrophic gastritis with hypoacidity, which can predispose to development of adenocarcinoma later in life, in others.

In children with H pylori infection, pentagastrin-stimulated acid secretion is higher for those who develop duodenal ulcers when compared with children in whom only gastritis is evident. Epidemiological studies have shown that strains of H pylori that carry the cagA gene are more virulent. The cagA gene encodes the cagA protein, which, once injected in the cytosol, is then phosphorylated on tyrosine residues and results in alterations in the morphology of epithelial cells. In Japan, where gastric cancer is highly prevalent, 90% of H pylori strains carry the cagA gene. Early infection with H pylori appears to be a risk factor for gastric cancer, but the long time required to develop neoplastic changes explains the lack of H pylori–associated cancers reported in children and adolescents.

Gastric perforations comprise 7% of all neonatal gastrointestinal perforations. These lesions are associated with selective ischemia during episodes of neonatal asphyxia and often involve infants with very low birth weight. Vigorous attempts at resuscitation result in gastric dilatation with overdistention of the greater curvature and angulation of the duodenum. Stress or infection may complicate this condition further by creating a low-flow state. The sequence of events involves venous congestion, venous thrombosis, mucosal damage, ulceration due to corrosion of the tissues by gastric acid, muscular disruption, and perforation. This entity is also known as idiopathic gastric necrosis, or necrotizing gastritis.

Dieulafoy lesions, first described by the French surgeon Georges Dieulafoy in 1897, result in brisk bleeding from a large superficial gastric artery. The mucosal defect is usually small (2-5 mm). In 80% of people with the lesion, it is situated within 6 cm of the gastroesophageal junction. These lesions have also been found in the duodenum, jejunum, and colon. The pathogenesis of Dieulafoy lesions is unclear, but the frequency of lesion occurrence in this location may be related to the vascular architecture of the gastric blood supply because the arterial bed of the lesser curvature arises directly from the arterial chain along the lesser curvature outside the stomach. Although most cases of Dieulafoy lesions occur in adults, case reports of toddlers and children can be found in the literature.

The rare Zollinger-Ellison syndrome results from marked stimulation of serum gastrin and other intestinal hormones by islet cell hypertrophy or tumor. Higher gastrin levels generate increased gastric output and acidity. This syndrome is associated with diarrhea and multiple recurrent duodenal and jejunal ulcers. However, hypergastrinemia can also be observed in conditions such as short bowel syndrome, pyloric stenosis, pheochromocytoma, hyperparathyroidism, and multiple endocrine neoplasia.

Clinical

The presentation of peptic ulcer disease in the pediatric population varies with age.

• Primary peptic ulcers manifest in the first month of life with bleeding and perforation. Most of these ulcers are located in the stomach.
• In school-aged children, postprandial periumbilical pain, vomiting, and bleeding are common.
• In children older than 6 years, the clinical presentation is similar to that of adults, with epigastric pain and acute or chronic blood loss, often leading to iron-deficiency anemia. Associated pain may be nocturnal and is dull rather than burning in nature, with frequent exacerbations and remissions lasting from weeks to months. Pain is relieved with antacids in one third of the children in this age group, and approximately half relate a temporal relationship of pain with meals.
• In children older than 10 years, a male predominance of the disease exists, with a male-to-female ratio of 4:1. A positive family history is also frequent in this age group.

Recurrent ulcers may manifest with gastric outlet obstruction. Acute perforation, bleeding, or penetration into the pancreas may present with acute abdomen, peritonitis, shock, or signs of pancreatitis.

Secondary (stress) peptic ulcers in infants are usually associated with infection, hypoxia, cardiac insufficiency, surgical trauma, or dehydration.

Other predisposing factors include the following:

• Ulcers manifesting in people with burns on more than 25% of their body are known as Curling ulcers and are associated with normal gastric secretions.
• Cushing ulcers are found in people with head trauma or surgery and are associated with gastric hypersecretion.
• Stress ulcers may not always cause symptoms, are often multiple, and may be terminal events. Perforation and (often) massive hemorrhage may be the initial presentation.
• Secondary peptic ulcers may also be associated with use of NSAIDs, steroids, smoking, and alcohol.

For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center and Procedures Center. Also, see eMedicine's patient education articles Peptic Ulcers, Anatomy of the Digestive System, Gastritis, and Barium Swallow.

INDICATIONS

Section 3 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Operative intervention is indicated for massive intractable bleeding or perforation. Rarely, recurrent pyloric channel ulcers or prepyloric ulcers may result in gastric outlet obstruction, which requires an acid-reducing operation combined with a gastric-emptying procedure. Although most upper gastrointestinal bleeding in children responds to medical or endoscopic interventions within 24-48 hours, surgical exploration is indicated if transfusion requirements are excessive (ie, more than 50% of the blood volume in 8 hours or more than 1 blood volume in 24 hours). Perforation of the stomach or duodenum is a life-threatening condition that can lead to peritonitis, hemodynamic collapse, and multiple organ failure if left untreated. Emergent surgical intervention is indicated for suspected or proven perforation.

RELEVANT ANATOMY

Section 4 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

See Intraoperative Details.

CONTRAINDICATIONS

Section 5 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Operations to correct perforation or massive bleeding of the stomach or duodenum can be life-saving and should be performed after optimizing the patient's clinical condition in preparation for surgery. No medical contraindications to surgical therapy exist; however, ethical considerations regarding the family's wishes, chronic or terminal illness and overall quality of life, and the patient's best interest should be part of the decision-making process.

WORKUP

Section 6 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Lab Studies

• In preparation for surgery, patients should have a complete blood count to test for leukocytosis and assess the degree of anemia.
• Patients should also have a complete chemistry panel, including serum glucose, blood urea nitrogen, creatinine, and electrolytes (eg, ionized calcium).
• Blood cultures should be drawn if systemic infection is suspected.
• Because many of these patients (particularly infants) may be septic, coagulation studies are needed to evaluate for coagulation abnormalities, which should ideally be corrected before laparotomy.
• Arterial blood gas measurements are helpful to assess and correct the acid-base balance and to adjust oxygenation and ventilation in patients who are receiving mechanical ventilation.
• The patient's blood should be typed and crossmatched before exploration.

Imaging Studies

• Plain radiographs are useful to diagnose perforations of gastric or duodenal ulcers.
• Although single contrast studies with barium and double contrast studies with air and barium are widely available, these tests are grossly inadequate (except for the rare case of gastric outlet obstruction) for use in confirming the diagnosis of peptic ulcer disease in children because of the low sensitivity and specificity of the tests' findings.
• For cases of massive bleeding that use of an endoscopy cannot control, an angiography can help reveal the bleeding site, thus allowing embolization or injection of vasoconstrictors.

Diagnostic Procedures

• Endoscopy is the diagnostic procedure of choice in the investigation of peptic ulcer disease, gastrointestinal bleeding, and gastritis in pediatric patients. Often, microscopic gastritis may be present in mucosa that appears normal via endoscopy. Nodularity of the antrum is a frequent finding in children with H pylori gastritis.
• Routine antral and duodenal biopsies should be performed. Culture of H pylori in mucosal biopsies is cumbersome and may take up to one week. Rapid tests are available that use the high urease content of H pylori. The biopsy sample is placed in media containing urea and a pH-sensitive indicator to detect ammonia. Reactions that are positive for H pylori are observable in as little as one hour. This rapid urease test has more than 95% sensitivity and specificity in adults; sensitivity and specificity are slightly lower in children because of a lower bacterial burden. Silver or Giemsa preparations may demonstrate spiral organisms on the antral mucosa just below the mucus layer.
• H pylori testing should be reserved for children whose symptoms are severe enough to justify the potential risks of eradication and when peptic ulcer is either proven or a high index of suspicion is present.
• Biopsy-based tests continue to be the criterion standard, but are invasive and expensive. 13C-urea breath testing (13C-UBT) has both a high sensitivity and specificity for diagnosing H pylori infection in children and is noninvasive. Although 13C-UBT is reliable for children younger than 6 years, it may be difficult to perform in younger children. 13C-UBT with a cutoff value of 3.5% stable isotope enrichment over baseline has sensitivity of 97% and specificity of 98%, compared with standard biopsy results, which are used as the standard.
• Recently, a stool antigen enzyme-linked H pylori immunosorbent assay has been developed. This noninvasive test detects H pylori antigens excreted in stool using commercial kits with either monoclonal or polyclonal antibodies and has a reported sensitivity and specificity greater than 93%.

Histologic Findings

Gastritis lymphonodular hyperplasia is a characteristic finding of endoscopic biopsies in children infected with H pylori. Lymphonodular hyperplasia alone has been shown to be highly predictive of H pylori infection and seems to resolve with eradication of the infection. Antral nodularity, however, depends more on inflammation than on the presence of lymphoid follicles. Histologically, the antral mucosa may demonstrate a severe chronic inflammatory infiltrate. The combination of chronic antral inflammation and lymphonodular hyperplasia provides further evidence of H pylori infection.

TREATMENT

Section 7 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Medical therapy

All current recommendations support eradication therapy in all children with peptic ulcers and proven H pylori infection. Eradication therapy has also been suggested for children with MALT lymphoma, atrophic gastritis, and H pylori with a family history of gastric adenocarcinoma. The benefits of eradication therapy in children without ulcers who have gastritis alone are uncertain. Eradication therapy could be considered as an option in children with H pylori infection who also have refractory iron-deficiency anemia or autoimmune thrombocytopenic purpura because complete or partial responses are seen in approximately one half of cases.

The object of therapy is to hasten resolution of the ulcers, ameliorate symptoms, and prevent complications and recurrence. One of the most important goals of treatment is the eradication of H pylori because primary peptic ulcers are likely to recur unless H pylori infection is controlled. Several combinations of therapeutic agents have been recommended. The best success rates are achieved with triple therapy, combining omeprazole with 2 antibiotics (clarithromycin and amoxicillin or metronidazole) for 1-2 weeks.

13C-UBT is a reliable test to confirm successful eradication of H pylori infection and should be performed at least 4 weeks after completion of therapy. Acquired resistance to clarithromycin (up to 45% of H pylori isolates in children) and, to a lesser extent, resistance to metronidazole is cause for concern. If therapy fails, an alternative triple-therapy regimen should be used, substituting one or both of the antibiotics. Bismuth-containing compounds such as bismuth subsalicylate or ranitidine bismuth citrate are optional, but the use of bismuth-containing compounds in children remains controversial.

Secondary ulcers are treated with acid-suppressing medications, such as H2 blockers, proton pump inhibitors, and mucosal protectants (eg, sucralfate). Offending substances (eg, aspirin, NSAIDs, corticosteroids, nicotine, alcohol) should be stopped.

Surgical therapy

Surgical treatment is indicated for intractable pain, gastric outlet obstruction (rare in children), bleeding, or perforation. Even with significant bleeding, the initial treatment should be medical because most upper GI bleeding in children stops in 24-48 hours. Operation is indicated when blood loss approaches half the blood volume in 8 hours or 1 blood volume in 24 hours. If the rate of bleeding allows the stomach to be lavaged for endoscopy, endoscopic cautery or injection of sclerosants or vasoconstrictors may control the bleeding and prevent further bleeding episodes. Hemorrhagic shock and anemia need to be treated with fluid resuscitation and blood transfusions; monitoring for signs of continuous bleeding or hypovolemia is essential.

Knowledge of surgical treatment for peptic ulcer disease in children is derived from the experience of treating adults. Subtotal and, occasionally, total gastrectomies often become necessary for cases of acute neonatal gastric necrosis. For hemorrhagic ulcers in the stomach, simple oversewing of the ulcer followed by medical therapy is sufficient treatment; resection is seldom required.

In older children, the ulcers may be located in the duodenum, and best outcomes are achieved with ligation of the bleeding ulcer and an acid-reducing procedure, such as a vagotomy with a pyloroplasty or a proximal gastric vagotomy. The treatment of perforated gastric or duodenal ulcers includes simple closure of the perforation with an omental patch followed by medical therapy. Acid-reducing procedures are optional. Gastric outlet obstruction is treated with (1) vagotomy and gastrojejunostomy or with (2) antrectomy, selective or truncal vagotomy, and gastroduodenostomy or gastrojejunostomy. For Dieulafoy lesions, when an endoscopy cannot control bleeding, operative treatment should be as conservative as possible, with simple ligation of the bleeding point. Cases of Zollinger-Ellison syndrome can be cured if the gastrinoma is identified and removed. Even if removal is incomplete, the use of proton pump inhibitors can control the disease.

Preoperative details

Fluid resuscitation, preoperative blood transfusions, correction of coagulopathy, and intravenous antibiotics may be necessary to prepare for laparotomy for bleeding or perforated ulcers in children.

Intraoperative details

Operations can be performed with laparoscopic or open approaches. Midline supraumbilical laparotomies are often used. The vagal trunks should be divided adjacent to the intraabdominal portion of the esophagus above the celiac and hepatic branches. When truncal vagotomies are performed, a gastric-emptying procedure, such as a pyloroplasty or gastrojejunostomy, is indicated.

The Heineke-Mikulicz pyloroplasty is the most commonly used method of drainage. Proximal or highly selective vagotomies are accomplished by dividing the Latarjet nerves from the stomach's lesser curvature, beginning 7 cm proximal to the pylorus and ending at least 5 cm proximal to the gastroesophageal junction. Perforations are treated with simple closure reinforced with omentum (Graham patch), with or without vagotomy and pyloroplasty, or with a highly selective vagotomy. To approach a bleeding duodenal ulcer, a longitudinal incision across the pylorus and duodenum usually exposes the bleeding branch of the gastroduodenal artery.

Suture ligation at 4 quadrants is sometimes needed when oversewing the ulcer. Occasionally, when suture ligation fails to stop the bleeding, ligation of the gastroduodenal artery cephalad and inferior to the duodenum, followed by an acid-reducing operation, yields the best results.

Postoperative details

Intravenous fluids, nasogastric decompression, intravenous antibiotics, analgesics, and careful monitoring and support of hemodynamics are mandatory in the immediate postoperative period. The nasogastric tube is removed upon return of gastrointestinal transit, and feeding is slowly begun. Proton pump inhibitors are used throughout the perioperative period, and treatment of H pylori should be instituted immediately after the operative procedure and continued for 2-4 weeks when infection with this organism is suspected or documented. Results of treatment are confirmed later (6-8 wk) with upper GI endoscopy.

COMPLICATIONS

Section 8 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Early complications include wound infections, anastomotic leaks, or recurrence of bleeding. However, morbidity and mortality rates in children are quite low, although they seem to be higher in premature infants with acute gastric necrosis when gastric involvement is extensive. Late complications, such as dumping syndrome, postvagotomy diarrhea, and alkaline reflux, have been reported mostly in adults but can occur in children.

OUTCOME AND PROGNOSIS

Section 9 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

With the advent of H2 blocker and proton pump inhibitor therapy, the frequency of postoperative complications, such as recurrent bleeding episodes or persistent pain, has diminished. Eradication of H pylori achieves cure rates of peptic ulcer disease in as many as 90% of children. Most secondary ulcers heal after the offending agent (eg, NSAIDs, steroids) is discontinued and treatments with acid-reducing agents (eg, H2 blockers, proton pump inhibitors) and mucosal protective agents (eg, sucralfate) are instituted.

FUTURE AND CONTROVERSIES

Section 10 of 11  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

With advances in medical treatment and endoscopic technology, operative treatment for peptic ulcer disease in infants and children will become rare. Furthermore, the operative trend should be toward more conservative procedures because the option of completely suppressing gastric acid production exists and effective treatments to eradicate H pylori are available.

Whether a patient is better off with (1) a vagotomy and pyloroplasty and the potential for dumping syndrome or chronic diarrhea or with (2) a lesser procedure followed by H pylori therapy and long-term use of proton pump inhibitors is unknown. At this time, no solid data exist to resolve this question. Although a highly selective vagotomy would address the problem of gastric emptying, this is a technically demanding and time-consuming procedure, which may not be the best choice in an emergency.

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Contraindications
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

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Article Last Updated: Jul 19, 2006