Gastric ulcer in children: diagnosis and treatment

Peptic ulcer disease in children is a deep defect in the gastric mucosa extending beyond the muscularis mucosae, causing inflammation, pain, and the risk of bleeding. True ulcers are less common in children than in adults, but often go unrecognized due to nonspecific symptoms and subtle manifestations. Key causes include persistent Helicobacter pylori infection and drug-induced mucosal injury. [1]

Over the past decades, the prevalence of Helicobacter pylori infection has been declining globally, gradually changing the structure of causes of childhood ulcers: the relative share of drug-induced and stress-induced ulcers is increasing. Nevertheless, when a child has an ulcer, Helicobacter pylori remains a priority target for diagnosis and treatment, and eradication strategies are regularly updated by international societies of pediatric gastroenterologists. [2]

Current treatment relies on endoscopic confirmation of the ulcer, verification of Helicobacter pylori using two different types of tests, and subsequent treatment with monitoring for cure. The "test and treat immediately without endoscopy" approach is not recommended for children, as it leads to excessive antibacterial therapy and misses other causes of pain. [3]

Early diagnosis and prompt treatment prevent complications such as bleeding, perforation, and pyloric stenosis, and, in the long term, reduce the risk of atrophic changes in the mucosa. It is important for families to understand the warning signs, indications for urgent medical attention, and the stages of examination. [4]

Code according to ICD-10 and ICD-11

In ICD-10, gastric ulcer is coded under category K25 "Gastric Ulcer," with specification of the phase and complications. For children, the same diagnostic codes are used as for adults: acute and chronic forms, with bleeding, with perforation, without complications, as well as "specified" and "unspecified" variants. The choice of code depends on the clinical presentation and endoscopy data. [5]

In ICD-11, these conditions are classified under the section "Diseases of the Esophagus, Stomach, and Duodenum," with detailed entries for gastric ulcers based on activity and complications. If necessary, underlying factors are additionally coded, such as long-term use of nonsteroidal anti-inflammatory drugs, a personal history of peptic ulcer disease, and a separate entry for confirmed Helicobacter pylori infection. [6]

Table 1. Examples of codes for gastric ulcer

Classifier	Code	Description
ICD-10	K25.3	Acute gastric ulcer without bleeding and perforation
ICD-10	K25.7	Chronic gastric ulcer without bleeding and perforation
ICD-10	K25.0, K25.1, K25.2	Acute ulcer with bleeding, with perforation, with both complications
ICD-10	Z87.11	Personal history of peptic ulcer disease
ICD-11	relevant headings for gastric ulcers indicating activity and complications	Clarification on complications and the phase of the process
[7]

Epidemiology

Childhood peptic ulcer disease is significantly less common than adult peptic ulcer disease, but its incidence varies by region depending on the Helicobacter pylori burden and availability of endoscopy. According to meta-analyses, the prevalence of Helicobacter pylori in children worldwide is estimated at approximately 32%, with variations across countries and diagnostic methods. This is a predisposing factor for peptic ulcer disease, particularly in middle- and low-income regions. [8]

In high-income countries, the prevalence of Helicobacter pylori in children is approximately 20% or less, while in middle- and low-income countries it can reach 40% or more. Moreover, the proportion of ulcers among children with chronic abdominal pain is low, emphasizing the need for careful selection for endoscopy. [9]

Some regional observations indicate that, despite the overall downward trend, Helicobacter pylori remains the leading cause of ulcer formation in children, particularly in the duodenum. However, the proportion of drug-induced lesions and stress ulcers remains significant in hospitals. [10]

Updated pediatric guidelines confirm that if an ulcer is detected in a child, the likelihood of a connection with Helicobacter pylori is high and requires active investigation and treatment, followed by eradication monitoring. This impacts both individual and population-based prevention of complications. [11]

Reasons

The primary cause is persistent Helicobacter pylori infection, which disrupts mucosal defenses, alters acid regulation, and provokes chronic inflammation leading to defect formation. In children, this mechanism largely mimics that of adults, but may have less pronounced acid aggression and a greater role for congenital factors. [12]

The second important cause is drug-induced damage to the gastric mucosa due to the use of nonsteroidal anti-inflammatory drugs, glucocorticoids, and some anticoagulants. The risk increases with dehydration, intercurrent infection, fasting, and a combination of several drugs. [13]

Stress ulcers in children occur in severe systemic conditions: sepsis, burns, traumatic brain injury, major surgery, respiratory failure, and intensive care. Mucosal ischemia and impaired microcirculation, coupled with a systemic response, play a leading role. [14]

Less frequently, ulcers are associated with hypersecretory conditions and hereditary syndromes, as well as with liver and kidney diseases, gastroduodenal ulcers in close relatives and an unfavorable ecological and social environment. [15]

Risk factors

Risk factors include confirmed Helicobacter pylori infection, a family history of peptic ulcer disease, prolonged or repeated use of nonsteroidal anti-inflammatory drugs, and burns and traumatic conditions. The combined effect of these factors increases the likelihood of ulcer formation and complications. [16]

Additional risks: smoking in adolescents, alcohol in adolescents, poor nutrition with infrequent meals, severe stress, obesity, iron and vitamin B12 deficiency in chronic gastritis, as well as concomitant use of anticoagulants and antiplatelet agents. [17]

The risk of bleeding increases with previous episodes, with the combination of nonsteroidal anti-inflammatory drugs and glucocorticoids, and in children with coagulopathy. In patients with severe somatic pathology, ulcers may develop more quickly and be more severe. [18]

Control of risk factors and their documentation are important for the choice of tactics: the decision to perform endoscopy, the selection of an eradication regimen, the need for gastroprotection and the intensity of follow-up. [19]

Table 2. Key risk factors

Group	Factor	Comment
Infectious	Helicobacter pylori	The main cause of true ulcers in children
Medicinal	Nonsteroidal anti-inflammatory drugs, glucocorticoids, anticoagulants	The risk is summarized, especially in weakened patients
Stressful	Burns, multiple organ failure, trauma, sepsis	Risk of stress ulcers and bleeding
Behavioral	Smoking, alcohol in teenagers, irregular meals	Increased aggression of the acid factor
Related	Family history of chronic liver and kidney disease	May impair mucosal regeneration
[20]

Pathogenesis

Helicobacter pylori colonizes the gastric mucosa, produces urease, increases local ammonia levels, and disrupts the protective properties of mucus. The inflammatory response alters gastrin and somatostatin production, leading to an imbalance in acid secretion, epithelial damage, and the formation of ulcers. [21]

When administered medicinally, prostaglandin synthesis is blocked, blood flow to the mucosa is reduced, and mucus and bicarbonate synthesis is reduced, making the mucosa vulnerable to acidic conditions. These processes are especially pronounced during dehydration and starvation, when mucosal nutrition deteriorates. [22]

Stress-induced injury is associated with mucosal ischemia and systemic inflammatory mediators. Microcirculatory impairment and hypoxia suppress regeneration, and bile acid reflux enhances chemical damage to the epithelium. [23]

In childhood, genetic and immune factors play a significant role in determining the severity of the inflammatory response to Helicobacter pylori and the rate of healing. This explains the variability in the course of the disease and the different susceptibility to relapse. [24]

Symptoms

The most common symptom is pain in the upper abdomen. The pain is often associated with eating, may intensify at night, and be accompanied by nausea, a feeling of heaviness, and heartburn. In young children, symptoms may be minimal and include refusal to eat, tearfulness, and weight loss. [25]

Warning signs include vomiting blood or "coffee ground" vomit, black stools, severe weakness, and dizziness, all associated with anemia. These symptoms require urgent evaluation and, typically, emergency endoscopy. [26]

Some children experience atypical symptoms: belching, an unpleasant taste in the mouth, early satiety, and persistent nausea. If the condition persists, signs of iron deficiency anemia and vitamin B12 deficiency are possible. [27]

The absence of complaints does not exclude ulcers in severely ill patients in intensive care units, where damage can progress rapidly and lead to occult bleeding. [28]

Classification, forms and stages

The clinical and endoscopic classification includes acute and chronic ulcers, single and multiple, with and without complications. Based on location, ulcers are classified into those of the body of the stomach, the antrum, and the pyloric canal, which influences treatment strategy and prognosis. [29]

Depending on the stage of the process, a distinction is made between an active ulcer with a fibrinous base, a granulation stage, and a scarring stage. The endoscopist evaluates the size, depth, edges, the presence of clots or "vascular scab," and signs of healing. [30]

In children, ulcers are classified by etiology as Helicobacter pylori-associated, drug-induced, and stress-induced. Mixed mechanisms are also possible, such as simultaneous infection and drug-induced injury. [31]

For patient management, stratification of the risk of bleeding and recurrence is important: clinical signs, hemodynamics, laboratory parameters and endoscopic picture are taken into account. [32]

Table 3. Simplified clinical and endoscopic classification

Criterion	Options	Significance for tactics
Phase	Active, granulation, scarring	Determines the duration of therapy
Etiology	Helicobacter pylori, drug-induced, stress-induced	Determines the need for eradication and gastroprotection
Localization	Body, antrum, pyloric canal	Association with the risk of complications
Complications	Bleeding, perforation, stenosis	Indications for emergency care
[33]

Complications and consequences

Acute bleeding manifests as hematemesis or melena and can lead to hypovolemia and anemia. The risk is higher in active ulcers, nonsteroidal anti-inflammatory drug therapy, and in critically ill patients. Urgent endoscopy not only confirms the diagnosis but also ensures hemostasis. [34]

Perforation is less common but requires emergency surgical intervention. Suspicion arises with sudden, stabbing pain, abdominal muscle tension, and signs of peritonitis. Treatment depends on age, severity, and associated medical conditions. [35]

Chronic consequences include scarring and deformation of the pyloric junction, which can lead to impaired gastric emptying, recurrent pain, and weight loss. Long-term persistence of Helicobacter pylori is associated with chronic gastritis and the risk of mucosal atrophy. [36]

Psychosocial consequences include school absences, anxiety, and decreased quality of life for families. Parent and adolescent education increases treatment adherence and reduces the risk of relapse. [37]

Table 4. Main complications

Complication	Clinical signs	Priority actions
Bleeding	Vomiting blood, melena, weakness	Urgent assessment, endoscopic hemostasis
Perforation	Sudden sharp pain, peritonitis	Emergency surgery
Pyloric stenosis	Vomiting, weight loss, delayed evacuation	Endoscopy, correction of tactics
Anemia	Paleness, fatigue	Search for the source of blood loss, treatment
[38]

When to see a doctor

Immediately - if vomiting blood, passing black stools, experiencing severe weakness, fainting, or increasing abdominal pain with muscle tension. These signs indicate a complication and require emergency care. [39]

Routinely - in cases of persistent epigastric pain lasting more than 2 weeks, night pain, weight loss, loss of appetite, and anemia of unknown origin. These symptoms are a reason to discuss endoscopic examination. [40]

Treatment is also indicated after a long course of non-steroidal anti-inflammatory drugs, in adolescent athletes against the background of injuries and repeated administration of analgesics, as well as with a family history of peptic ulcer disease. [41]

It is important for parents to record pain triggers, dietary patterns, medication intake, and the results of previous tests - this will speed up the diagnosis and choice of therapy. [42]

Diagnostics

The diagnostic process for a child with a suspected ulcer begins with a clinical assessment and laboratory tests: a complete blood count to detect anemia, iron levels, and a basic biochemistry panel. If signs of blood loss are present, the blood type and red blood cell reserve are determined. [43]

The "gold standard" is esophagogastroduodenoscopy with ulcer visualization, assessment of bleeding signs, and biopsy sampling. It is recommended to simultaneously perform tests for Helicobacter pylori of various types: rapid urease and histology or culture, as well as molecular methods as indicated. [44]

Noninvasive tests—carbon-13 breath testing and Helicobacter pylori monoclonal antigen in stool—are used to confirm cure after therapy and in certain situations when endoscopy is not possible. Serology is not recommended for primary diagnosis in children due to its low accuracy. [45]

In emergency situations involving bleeding, endoscopy is performed for diagnosis and hemostasis. Ultrasound and radiography are used as indicated if perforation or stenosis is suspected, but do not replace endoscopy. [46]

Table 5. Step-by-step diagnostic algorithm

Stage	Action	Target
1	Clinical evaluation, laboratory	Identify anemia and signs of severity
2	Endoscopy with biopsies	Confirm ulcer, assess risk, take samples
3	Tests for two types of Helicobacter pylori	Verify infection
4	Beginning of therapy	Eradication and healing
5	Monitoring cure with a non-invasive test	Confirm the success of treatment
[47]

Differential diagnosis

It is important to distinguish peptic ulcer disease from functional dyspepsia, gastroesophageal reflux disease, eosinophilic gastritis, biliary tract disease, pancreatitis, and inflammatory bowel disease. Endoscopic confirmation of the ulcer defect and targeted biopsy remain key. [48]

In chronic pain without warning signs and normal test results, functional dyspepsia is more common. In these cases, noninvasive "test and treat" for Helicobacter pylori in children is not recommended. The decision to perform endoscopy is made on an individual basis. [49]

Hematemesis and melena require differentiation between ulcers and gastritis with erosions, mucosal ruptures in the cardiac region, and esophageal varices associated with portal hypertension. Endoscopic assessment of the bleeding source determines the treatment strategy. [50]

In young children, rare causes are considered, such as foreign bodies, caustic lesions, and Zollinger-Ellison syndrome. The clinical history and instrumental data guide the selection of examinations. [51]

Treatment

The basis of therapy is suppression of gastric acid with a proton pump inhibitor at an adequate dose and for a period sufficient to allow the defect to heal. For ulcers caused by Helicobacter pylori, an antibacterial regimen based on the local resistance profile is added, with mandatory monitoring of cure. [52]

The choice of eradication regimen in children is currently shifting toward quadruple therapy with bismuth or optimized regimens that take into account resistance to clarithromycin and metronidazole. Prescribing empirical triple therapy without taking resistance into account is increasingly recognized as ineffective. [53]

In the presence of evidence of high-grade clarithromycin resistance, bismuth-containing regimens with a proton pump inhibitor, amoxicillin, and metronidazole are recommended. Some centers use sequential or concomitant therapy, but it should be in accordance with local guidelines. [54]

Cure monitoring is performed 4-8 weeks after stopping antibiotics and 2 weeks after discontinuing the proton pump inhibitor, using a carbon-13 breath test or a Helicobacter pylori monoclonal antigen in feces. Negative serologic tests do not confirm cure in children. [55]

For drug-induced ulcers, nonsteroidal anti-inflammatory drugs are discontinued first, a course of proton pump inhibitor is initiated, and bismuth or sucralfate is prescribed as indicated. If pain relief is necessary, alternative medications and the shortest possible courses are discussed. [56]

For stress ulcers in intensive care units, prophylactic antisecretory therapy is indicated in high-risk children, along with hemodynamic correction, early nutrition, and treatment of the underlying disease. The choice of agent and dosage are determined by department protocol. [57]

In cases of ulcerative bleeding, endoscopic hemostasis is performed with adrenaline injections, thermocoagulation, or mechanical clips, followed by high-dose antisecretory therapy and observation. The decision to repeat endoscopy is made based on clinical dynamics. [58]

Supportive measures include a diet with regular mealtimes, adequate hydration, limiting irritating foods, and correcting iron and vitamin B12 deficiencies if confirmed. Family education increases adherence and reduces the risk of relapse. [59]

Promising approaches include the use of potassium-competing acid secretion blockers in adolescents, personalized eradication based on molecular resistance data, and digital adherence monitoring tools. Their implementation in children is currently being phased in at centers with relevant experience. [60]

Table 6. Principles for choosing an eradication regimen in children (summarized)

Situation	Preferred approach	Control
High resistance to clarithromycin	Bismuth-containing quaternary scheme	Carbon-13 breath test or stool antigen test
Low resistance and no contraindications	Optimized triple scheme based on local data	Same
Previous unsuccessful course	Alternative regimen taking resistance into account	Same
The impossibility of antibiotics now	Postponement, gastroprotection, re-evaluation	Individually
[61]

Prevention

Primary prevention includes sanitation and hygiene measures, safe water and food, and reducing household transmission of Helicobacter pylori. Family education on hygiene and regular eating habits helps reduce the risk of exacerbations and drug-induced injuries. [62]

Rational pain relief in children is a crucial element in the prevention of drug-induced ulcers: use minimally effective doses, the shortest courses, and avoid the simultaneous administration of multiple agents that are aggressive to the mucosa. If risks are expected, gastroprotection is considered. [63]

After successful eradication of Helicobacter pylori, the risk of ulcer recurrence decreases. Monitoring the healing process and correcting risk factors—family diet, smoking in adolescents, and study and rest routines—consolidate the treatment results. [64]

At the health system level, availability of endoscopy, high-quality laboratory tests and local monitoring of antibiotic resistance are important for informed choice of treatment regimens. [65]

Forecast

In most children, with timely diagnosis and proper treatment, ulcers heal completely, and quality of life is restored. Eradication of Helicobacter pylori significantly reduces the risk of relapse and complications. [66]

An unfavorable prognosis is associated with severe complications - massive bleeding, perforation, pyloric stenosis, as well as repeated episodes of ulceration against the background of continued use of non-steroidal anti-inflammatory drugs. [67]

In intensive care units, outcome is determined by the underlying disease and the quality of stress ulcer prophylaxis. Early nutritional support and hemodynamic monitoring reduce the risk. [68]

Long-term follow-up after recovery is required in cases of unfavorable risk factors and in children with a severe initial course in order to promptly adjust lifestyle and medication support. [69]

FAQ

1. Can a child have an ulcer without a Helicobacter pylori infection?
Yes. Drug-induced and stress-induced ulcers are common in children, especially in hospitals and when taking nonsteroidal anti-inflammatory drugs. However, if an ulcer is confirmed, Helicobacter pylori should always be tested. [70]

2. Do all children with abdominal pain need endoscopy?
No. Most cases of abdominal pain in children are not associated with ulcers. Endoscopy is indicated in cases of alarming signs or a high probability of ulcers based on clinical and laboratory findings. [71]

3. Why can't "test and treat immediately" be done without endoscopy?
In children, this approach leads to overprescribing antibiotics and missing other causes of pain. It is recommended to confirm the ulcer with endoscopy and verify Helicobacter pylori with two tests. [72]

4. What tests should be used to confirm cure?
Carbon-13 breath test or faecal monoclonal antigen test 4-8 weeks after antibiotics and 2 weeks after stopping the proton pump inhibitor. [73]

5. What should you do if your child must take nonsteroidal anti-inflammatory drugs?
Discuss the need, dosage, and duration with your doctor. Consider gastroprotective measures and alternative pain relievers, and monitor symptoms and diet. [74]

6. Is a diet necessary for ulcers?
Regular small meals, adequate hydration, and avoiding specific triggers are recommended. Strict "starvation" diets are not recommended. [75]

7. How to reduce the risk of relapse after treatment?
Confirm cure, eliminate risk factors, follow a diet, avoid uncontrolled nonsteroidal anti-inflammatory drugs, and attend follow-up examinations. [76]

8. Can an ulcer "go silent" without pain?
Yes, especially in critically ill hospitalized patients with stress ulcers, where the first manifestation is anemia or bleeding. [77]

9. Is an ulcer dangerous for the unborn child in adulthood?
With Helicobacter pylori treatment and risk factor correction, the long-term prognosis is favorable, and the risk of recurrence is low. [78]

10. When should I return to sports after an ulcer?
After pain has subsided and clinical evidence of healing has been confirmed, usually after completing a course of therapy. The attending physician determines the timeframe, taking into account the initial severity. [79]