eMedicine Specialties > Pediatrics: Surgery > General Surgery

Peptic Ulcer: Surgical Perspective

Author: Carlos A Angel, MD, Associate Professor of Pediatrics, Division of Pediatric Surgery, University of Tennessee School of Medicine; Consulting Staff, East Tennessee Children's Hospital, East Tennessee Pediatric Surgery Group
Contributor Information and Disclosures

Updated: Jul 19, 2006

Introduction

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.

Presentation

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

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

See Intraoperative Details .

Contraindications

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.

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