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Peptic Ulcer Disease in Children
Peptic ulcer disease, resulting from inflammation caused by an imbalance between cytoprotective and cytotoxic factors in the stomach and duodenum, manifests with varying degrees of gastritis or frank ulceration. The pathogenesis of peptic ulcer disease is multifactorial, but the final common pathway for the development of ulcers is the action of acid and pepsin-laden contents of the stomach on the gastric and duodenal mucosa and the inability of mucosal defense mechanisms to allay those effects. Abnormalities in the gastric and duodenal mucosa can be visualized on endoscopy, with or without histologic changes. Deep mucosal lesions that disrupt the muscularis mucosa of the gastric or duodenal wall define peptic ulcers. Gastric ulcers are generally located on the lesser curvature of the stomach, and 90% of duodenal ulcers are found in the duodenal bulb. While there are no large population-based pediatric studies, rates of peptic ulcer disease in childhood appear to be low. Large pediatric centers anecdotally report an incidence of 5-7 children with gastric or duodenal ulcers per 2,500 hospital admissions each year.
Ulcers in children can be classified as primary peptic ulcers, which are chronic and more often duodenal, or secondary, which are usually more acute in onset and are more often gastric ( Table 361.1 ). Primary ulcers are most often associated with Helicobacter pylori infection; idiopathic primary peptic ulcers account for up to 20% of duodenal ulcers in children. Secondary peptic ulcers can result from stress caused by sepsis, shock, or an intracranial lesion (Cushing ulcer), or in response to a severe burn injury (Curling ulcer). Secondary ulcers are often the result of using aspirin or nonsteroidal antiinflammatory drugs (NSAIDs); hypersecretory states like Zollinger-Ellison syndrome (see Chapter 361.1 ), short bowel syndrome, and systemic mastocytosis are rare causes of peptic ulceration.
Table 361.1
Etiologic Classification of Peptic Ulcers
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* Requires search for other specific causes. NSAID, nonsteroidal antiinflammatory drug. (From Vakil N, Megraud F: Eradication therapy for Helicobacter pylori, Gastroenterology 133:985–1001, 2007.)
Pathogenesis
Acid Secretion
By 3-4 yr of age, gastric acid secretion approximates adult values. Acid initially secreted by the oxyntic cells of the stomach has a pH of approximately 0.8, whereas the pH of the stomach contents is 1-2. Excessive acid secretion is associated with a large parietal cell mass, hypersecretion by antral G cells, and increased vagal tone, resulting in increased or sustained acid secretion in response to meals and increased secretion during the night. The secretagogues that promote gastric acid production include acetylcholine released by the vagus nerve, histamine secreted by enterochromaffin cells, and gastrin released by the G cells of the antrum. Mediators that decrease gastric acid secretion and enhance protective mucin production include prostaglandins.
Mucosal Defense
A continuous layer of mucous gel that serves as a diffusion barrier to hydrogen ions and other chemicals covers the gastrointestinal (GI) mucosa. Mucus production and secretion are stimulated by prostaglandin E 2 . Underlying the mucous coat, the epithelium forms a second-line barrier, the characteristics of which are determined by the biology of the epithelial cells and their tight junctions. Another important function of epithelial cells is to secrete chemokines when threatened by microbial attack. Secretion of bicarbonate into the mucous coat, which is regulated by prostaglandins, is important for neutralization of hydrogen ions. If mucosal injury occurs, active proliferation and migration of mucosal cells occurs rapidly, driven by epithelial growth factor, transforming growth factor-α, insulin-like growth factor, gastrin, and bombesin, and covers the area of epithelial damage.
Clinical Manifestations
The presenting symptoms of peptic ulcer disease vary with the age of the patient. Hematemesis or melena is reported in up to half of the patients with peptic ulcer disease. School-age children and adolescents more commonly present with epigastric pain and nausea, similar to the presentation generally seen in adults. Dyspepsia, epigastric abdominal pain, and fullness are also seen in older children. Infants and younger children usually present with feeding difficulty, vomiting, crying episodes, hematemesis, or melena. In the neonatal period, gastric perforation can be the initial presentation.
The classic symptom of peptic ulceration, epigastric pain alleviated by the ingestion of food, is present only in a minority of children. Many pediatric patients present with poorly localized abdominal pain, which may be periumbilical. The vast majority of patients with periumbilical or epigastric pain or discomfort do not have a peptic ulcer, but rather a functional GI disorder, such as irritable bowel syndrome or nonulcer (functional) dyspepsia. Patients with peptic ulceration rarely present with acute abdominal pain from perforation or symptoms and signs of pancreatitis from a posterior penetrating ulcer. Occasionally, bright red blood per rectum may be seen if the rate of bleeding is brisk and the intestinal transit time is short. Vomiting can be a sign of gastric outlet obstruction.
The pain is often described as dull or aching, rather than sharp or burning, as in adults. It can last from minutes to hours; patients have frequent exacerbations and remissions lasting from weeks to months. Nocturnal pain waking the child is common in older children. A history of typical ulcer pain with prompt relief after taking antacids is found in <33% of children. Rarely, in patients with acute or chronic blood loss, penetration of the ulcer into the abdominal cavity or adjacent organs produces shock, anemia, peritonitis, or pancreatitis. If inflammation and edema are extensive, acute or chronic gastric outlet obstruction can occur. In a child with a normal diet for age, iron deficiency anemia may suggest peptic ulceration. Other gastric causes of iron deficiency anemia include autoimmune gastritis, gastric hyperplasia, and possible Jervell and Lange-Nielson syndrome ( KCNQ1 mutations).
Diagnosis
Esophagogastroduodenoscopy is the method of choice to establish the diagnosis of peptic ulcer disease. It can be safely performed in all ages by experienced pediatric gastroenterologists. Endoscopy allows the direct visualization of esophagus, stomach, and duodenum, identifying the specific lesions. Biopsy specimens must be obtained from the esophagus, stomach, and duodenum for histologic assessment as well as to screen for the presence of H. pylori infection. Endoscopy also provides the opportunity for hemostatic therapy including clipping, injection, and the use of thermal coagulation.
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