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CHAPTER 60

Peptic Ulcer Disease in Children

Oludayo Adedapo Sowande
Jennifer H. Aldrink

Introduction Helicobacter pylori and Peptic Ulcer Disease
Peptic ulcer disease (PUD) results from a disruption in the mucosal H. pylori, a gram-negative microaerophilic spirochete, has been impli-
lining of the stomach or duodenum, allowing penetration through the cated in the development of gastritis and peptic ulcer disease in both
muscularis mucosa. Over the years, the causative role of Helicobacter adults and children in the presence of acid and pepsin. H. pylori infec-
pylori in the etiology of primary PUD has been proven. Despite increas- tion is mainly acquired during childhood. In India, almost 80% of the
ing attention to PUD as a cause of abdominal pain in children, many population has been infected by the age of 10 years, compared to less
cases of PUD in children are not recognized until they are compli- than 10% of the population in developed countries. H. pylori infec-
cated by haemorrhage, perforation, or gastric outlet obstruction. This tion is thought to be transmitted mainly through the faecal-oral route
is invariably associated with an increase in morbidity and mortality. in developing countries. Most infected individuals are asymptomatic;
Demographics approximately 15% develop peptic ulcer disease and 1% develop gas-
tric cancer. The organism has a unique ability to survive in the harsh
PUD is an uncommon disease of childhood, with an estimated fre-
acidic environment of the stomach by producing the enzyme urease,
quency of 1 case in 2,500 hospital admissions in the United States. Data
which allows it to alkalinize its microenvironment and survive for long
for developing countries, especially from Africa, are scarce, but peptic
periods of time. The organism also produces myriad other virulence
ulceration is being increasingly recognized in children in the develop-
factors such as catalase, vacuolating cytotoxin, and lipopolysaccharide.
ing world. A prevalence rate of 2% has been found among children pre-
The organism has been classified as a class A carcinogen by the World
senting with abdominal pain. The majority of cases are duodenal ulcers.
Health Organization (WHO) because it has been causally associated
The male-to-female ratio for all childhood PUD is 1.5:1. However,
with gastric carcinoma and lymphoproliferative disorders.
no sex difference in the incidence of primary PUD has been noted in
infants or young children. Clinical Presentation
Aetiology History
Peptic ulcer diseases in children and adolescents can be classified into A detailed history and physical examination are the mainstays of diag-
two aetiologies, primary and secondary. nosis, supplemented by diagnostic investigations where available. The
Primary PUD is commonly associated with H. pylori infection. most common symptom in PUD is abdominal pain. A high index of
Primary ulcers are more likely to be chronic, more common in blood suspicion is necessary in children because abdominal pain is a com-
group O and may be familial in 30–40% of PUD cases. It may be mon complaint; distinguishing the pain of PUD from other causes of
associated with elevated serum gastrin level, but this finding is abdominal pain is a major challenge. The child’s inability to describe
inconsistent in children. the symptoms very well may hinder the diagnosis. Not uncommonly,
Secondary PUD occurs as a result of accompanying stressful medical the diagnosis is not considered at all in children because PUD is thought
or surgical conditions. It may follow severe burns (Curling’s ulcer), largely to be a disease of adults.
severe head injury (Cushing’s ulcer), and ingestion of nonsteroidal The pain of PUD in toddlers and preschool age children is usually
anti-inflammatory drugs (NSAIDs). Mucosal ischaemia, in association dull and vague, quite unlike what is described in adults, and may or may
with increased gastric acid and pepsin production, and with decreased not be aggravated by food intake. The older child and adolescent may,
prostaglandins and mucus production, has been implicated in the however, present in the typical adult fashion with sharp and burning
development of secondary PUD. pain localized to the periumbilical or epigastric regions. The pain may
In general, PUD results from an interaction between protective exhibit periodicity with frequent exacerbations and remissions over
forces that prevent a breach in the integrity of the gastric and duodenal weeks to months. There may be recurrent vomiting, leading to poor
mucosa and those that contribute to mucosal inflammation and weight gain. Vomiting of food ingested over a few days should raise the
ulceration (Table 60.1). suspicion of gastric outlet obstruction. A possibility of a family history
of peptic ulceration should be sought as well as a history of ingestion
Table 60.1: Protective and disruptive mechanisms for PUD.
of NSAIDs.
Protective Mechanisms Disruptive Mechanisms As in adults, PUD may be complicated by perforation, gastrointestinal
1. Secretion of water-insoluble 1. Gastric hyperacidity tract (GIT) bleeding (hematemesis with melena), and gastric outlet
gastric mucus and bicarbonate 2. Acid-dependent pepsin obstruction. These complications may occur even in the absence of
2. Protective phospholipids 3. Mucosal ischemia pain. Presentation in infants, particularly in neonates, is usually acute
3. Rapid turnover of gastric 4. Helicobacter pylori infection
mucosal cells 5. Sepsis and may manifest as acute perforation or haemorrhage, even in the
4. Normal mucosal blood flow 6. Traumatic injuries and burns absence of recognizable stress.
5. Inhibited acid secretion 7. Drugs (steroids) The natural history of peptic ulcers in children has been well
8. Alcohol correlated with age. In early life (2–6 years), there is a tendency
9. Cigarette smoking towards bleeding and perforation. In the age group of 7–11 years,
10. Stress