eMedicine Specialties > Pediatrics: General Medicine > Gastroenterology

Peptic Ulcer Disease

Author: Ameesh Shah, MD, Assistant Professor of Pediatrics, Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Children's Memorial Hospital
Coauthor(s): Meta Carroll, MD, Department of Pediatrics, Division of Emergency Medicine, Assistant Professor of Pediatrics, Children's Memorial Hospital; B UK Li, MD, Director, Children's Memorial Hospital of Chicago; Professor, Division of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Northwestern University
Contributor Information and Disclosures

Updated: Sep 10, 2007

Introduction

Background

The lesion of peptic ulcer disease (PUD) is a disruption in the mucosal layer of the stomach or duodenum. An ulcer is distinguished from an erosion by its penetration through the muscularis mucosa or the muscular coating of the gastric or duodenal wall. PUD results from the imbalance between defensive factors that protect the mucosa and offensive factors that disrupt this important barrier. Some mucosal protective factors include the water-insoluble mucous gel layer, local production of bicarbonate, regulation of gastric acid secretion, and adequate mucosal blood flow. Aggressive factors include the acid-pepsin environment, infection with Helicobacter pylori, and mucosal ischemia.

Primary peptic ulcers are still relatively uncommon in children and account for roughly 1 in 2500 pediatric hospital admissions. Primary ulcers are seen more often in adolescents than in children and tend to recur after initial healing. Although affected children are thought to have high acid secretion, this has not been proven. Many of the primary ulcers seen in teenagers are now thought to be associated with H pylori infection. Secondary ulcers are seen in head trauma, severe burns, and in use of corticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs).

Pathophysiology

The 2 most important concepts in understanding the pathophysiology of PUD in children are the host factors that serve to protect the GI mucosa from ulceration and the inflammatory mediators and aggressive factors that contribute to mucosal inflammation and ulceration.

An overlying physiochemical barrier provides cytoprotection of the gastric mucosa. This barrier comprises water-insoluble gastric mucus, gastrically produced bicarbonate, an unstirred water layer, phospholipids, rapid shedding of cells resulting from epidermal growth factor, normal mucosal blood flow, prostaglandin-stimulated bicarbonate, mucus production, and inhibited acid secretion.

Contributors to mucosal inflammation and ulceration include endogenous factors, such as gastric acidity, acid-dependent pepsin, and mucosal ischemia, as well as exogenous factors, such as drugs (eg, NSAIDs, aspirin, corticosteroids), alcohol, cigarette smoking, corrosive chemicals (eg, lye), and emotional stress. In patients with traumatic injuries, burns, sepsis, respiratory failure, or other critical systemic illnesses, many factors can contribute to erosions and ulcers, including mucosal ischemia, increased gastric acid and pepsin production, higher levels of endogenous catecholamines and steroids, and decreased prostaglandins and mucus production. Important mediators of mucosal inflammation and resultant ulceration include oxygen free radicals, lymphokines, and monokines.

The gram-negative spirochete, H pylori, was first linked to gastritis in 1983. Since then, further study of H pylori has revealed that it is a major part of the triad, which includes acid and pepsin, that contributes to primary PUD. The unique microbiologic characteristics of this organism, such as urease production, allows it alkalinize 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 PUD.

When H pylori colonizes the gastric mucosa, inflammation usually results. The casual 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, exposure of the duodenum to acid is increased. Virulence factors produced by H pylori, including urease, catalase, vacuolating cytotoxin, and lipopolysaccharide, are well described. However, the specific roles of these factors and the secretory disturbances associated with H pylori infection in subsequent duodenal ulceration remains unclear.

Frequency

United States

PUD is an uncommon disease of childhood, with an estimated frequency of 1 case in 2500 hospital admissions. The estimated prevalence of childhood PUD in large general pediatric practices is 1.7%. In large pediatric medical centers with busy gastroenterology practices, only 5 primary ulcers may be diagnosed per year. The annual incidence of primary duodenal ulcers is estimated to be 5 cases per 100,000 children.

The prevalence of H pylori infection is substantially higher than this, an estimated 10% in industrialized countries. H pylori infection can be diagnosed on endoscopic biopsy and urea breath testing. However, serology alone is not recommended because it is overly sensitive and does not help in distinguishing bacterial colonization from peptic injury.

The true incidence of secondary ulcers is unknown and depends on the frequency of systemic illness, traumatic injury, and use of injurious agents. Studies of risk factors for stress ulceration are being conducted in critically ill children, especially those in intensive care units.

International

The prevalence of H pylori infection in developing countries is as high as 50-100%. The prevalence of PUD is increasing in developing countries.

Mortality/Morbidity

The highest mortality rates are found in young infants with secondary stress ulcers, who may present acutely with life-threatening GI hemorrhage or intestinal perforation. In contrast, children with primary gastritis or duodenal ulcer disease have low mortality rates.

• GI bleeding is one of the most common presentations of ulcer disease in neonates. GI hemorrhage occurs in both primary and secondary PUD. GI blood loss may be acute and catastrophic, particularly in neonates or in children with a critical medical illness or traumatic injuries, or it may have a slow and chronic course, without posing a serious threat to life.
• Perforation of an ulcer is the second main manifestation of PUD in neonates. However, any child who is critically ill or injured is at risk for stress ulceration and perforation. Perforation is often preceded by or associated with GI hemorrhage.
• Obstruction of the gastric outflow tract because of edema or scarring most often occurs in the setting of duodenal or pyloric channel ulcers.

Race

In the United States, the prevalence of H pylori infection is higher in blacks and Hispanics than in whites not of Hispanic origin.

Sex

The male-to-female ratio for all childhood PUD is 1.5:1. The incidence of primary PUD is 2- to 3-fold higher in boys than in girls; however, no sex difference in the incidence of primary PUD has been noted in infants or young children.

Age

• Primary PUD is uncommon in infants and in children younger than 10 years. The prevalence of primary PUD increases during adolescence.
• Secondary PUD can affect patients of all ages, but its prevalence is increased in patients younger than 6 years.

Clinical

History

• In children in whom peptic ulcer disease (PUD) is suspected, include the following in the history:
  • Review of past illnesses and chronic medical conditions
  • Family history of ulcer disease, including known H pylori infection, or conditions affecting the GI tract (eg, Crohn disease)
  • Character, location, frequency, duration, severity, and exacerbating (especially meals in children) and alleviating factors of abdominal pain
  • Vomiting and description of gastric material
  • Bowel habits and description of stool (eg, profuse diarrhea seen in Zollinger-Ellison syndrome [ZES])
  • Prescribed and over-the-counter (OTC) medications, especially NSAIDs and corticosteroids
  • Prior diagnostic testing and specific GI therapies
  • Appetite, diet, and weight changes
  • Family and social stressors
  • Alcohol ingestion and smoking habits
• Abdominal pain is the most common symptom of childhood PUD.
  • The pain is usually dull and vague. The pain is most likely to be dull and aching rather than sharp and burning, as adults describe. Food intake often causes the pain to worsen; this is the opposite of the adult pattern.
  • The pain may be poorly localized or localized to the periumbilical or epigastric areas.
  • In preschool-aged children, the pain is typically periumbilical and worsens after eating.
  • After the age of 6 years, the child's description of pain may be similar to the description by adults. The classic pain of PUD (ie, pain that awakens the child, worsens with food, and is relieved by fasting) is described infrequently, but it helps in distinguishing GI pathology from psychogenic pathology when present.
  • Frequent exacerbations and remissions of pain extend over weeks to months.
• Vomiting in infants and toddlers may be associated with slow growth. Recurrent vomiting is also noted in preschool- and school-aged children.
• GI tract bleeding (eg, melena, hematochezia, hematemesis) may be another presentation in children.
  • In infants and particularly neonates, serious underlying illness and stress ulceration most commonly manifest as acute perforation or hemorrhage.
  • GI bleeding may lead to iron-deficiency anemia (IDA), and patients may present with vague complaints of fatigue, headache, dyspnea, or malaise.
• For children with ulcer perforation, the symptoms are consistent with peritonitis and abrupt in onset.

Physical

• Include the following in the physical examination:
  • Observation of the general appearance of the child
  • Evaluation of vital signs
  • Assessment of perfusion with attention to mental status, heart rate, pulses, and capillary refill
  • Assessment of hydration status with attention to moisture of the mucous membranes and skin turgor
  • Observation of any pallor of the skin and conjunctivae
  • Thorough chest examination
  • Careful inspection, auscultation, and palpation of the abdomen, with notation of any liver or spleen enlargement
  • Rectal examination and stool guaiac testing
  • Pelvic examination in sexually active female patients with pain
  • Examination of the testicles and inguinal area in male patients
• Hemorrhage accompanies PUD in 15-20% of patients.
• Acute abdomen resulting from perforation of the GI tract occurs in 5% of children with PUD.

Causes

• Primary PUD
  • Genetic factors may be important, as indicated by the observation that as many as 50% of children with PUD have a first- or second-degree relative with PUD. In addition, a concordance rate that is 3 times higher in monozygotic than in dizygotic twins has been described, and children with blood group O have an increased incidence of PUD.
  • Emotional stress has been described as a factor predisposing children to PUD.
  • Alcohol has been documented to produce inflammation, erosions, and hemorrhage in the gastric mucosa in animal and adult human studies. Caffeine intake also predisposes children to PUD.
  • Clinical and laboratory data provide strong evidence that H pylori infection causes chronic gastritis and primary duodenal ulcer disease. H pylori gastritis has not been strongly associated with gastric ulceration in children.
  • Compared with people who do not smoke cigarettes, those who do are twice as likely to develop PUD. Smoking may lead to ulceration, slow healing, and an increased risk of recurrent disease.
• Secondary PUD
  • Corticosteroids, NSAIDs, and aspirin use predispose children to stress ulceration. These drugs disrupt the mucosal permeability barrier, rendering the mucosa vulnerable to injury. As many as 30% of adults taking NSAIDS have GI adverse effects. Although the prevalence of NSAID gastropathy in children is unknown, it seems to be increasing, especially in children with chronic arthritis treated with NSAIDS. Recent case reports have demonstrated gastric ulceration from low-dose ibuprofen in children, even after 1 or 2 doses.¹
  • Serious systemic illness, sepsis, hypotension, respiratory failure, and multiple traumatic injuries increase the risk for secondary (stress) ulceration.
    • The ulcer associated with a brain tumor or injury, or Curling ulcer, is characterized as single, deep, and prone to perforation. It is associated with high gastric acid output, and it is located in the duodenum or stomach.
    • Extensive burns are also associated with ulcers, namely Curling ulcers.
    • Stress ulceration and upper-I hemorrhage are complications being encountered more often than before in critically ill children in the intensive care setting. Severe illness and a decreased gastric pH, are related to an increased risk of gastric ulceration and hemorrhage. Neutralization of gastric acid inactivates proteolytic pepsin, which is responsible for gastric mucosal injury. Therefore, gastric pH of critically ill children should be maintained at more than 6 to prevent injury.
  • ZES is a rare disorder that can cause gastric or duodenal ulcers, usually multiple, from excessive acid secretion. ZES should be suspected if the patient has severe peptic ulceration, kidney stones, watery diarrhea or malabsorption. ZES can also be associated with multiple endocrine neoplasias type I, which occurs at an age earlier than does isolated ZES. Patients with ZES usually have fasting serum gastrin levels of more than 200 pg/ml and basal gastric acid hypersecretion at more than 15 mEq/h. Protein pump inhibitor (PPI) therapy should be discontinued at least 2 weeks before the gastrin level is measured.

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