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The Digestive system 

                                       

 L2

                                                                                              

 

Stomach and Intestines

 

 

Peptic Ulcer Disease in Children

 

Ulcers

   

are deep lesions that breech the integrity of the epithelium and penetrate 

through the muscularis mucosae, whereas erosions are superficial and stop short of 
the muscularis propria. Both lesions often occur in the presence of gastric 
inflammation or gastritis. Gastric ulcers are generally located on the lesser curvature 
of the stomach, and 90% of duodenal ulcers are found in the duodenal bulb.

 

In children can be classified as:

 

1. primary peptic ulcers: are chronic and more often duodenal, most often 
associated with Helicobacter pylori infection. Idiopathic primary peptic ulcers 
account for up to 20% of duodenal ulcers in children.

 

H. pylori is a gram-negative spiral organism that lives primarily in the mucus layer 
covering gastric epithelial cells. To survive in the harsh environment of the acidic 
stomach, H. pylori produces urease, an enzyme that catalyzes the conversion of urea 
in the gastric juice to ammonia and bicarbonate. These products buffer the gastric 
acid and create a friendly microenvironment for H. pylori.

 

The route of transmission may involve fecal-oral, gastric-oral (in vomitus), or oral-
oral routes. Crowding and poor sanitary conditions are risk factors for acquisition of 
H. pylori. In children, H. pylori infection can present with abdominal pain or vomiting, 
and less often, refractory iron deficiency anemia or growth retardation

.

 

2. Secondary peptic ulcers: are usually more acute in onset and are more often 
gastric. It can result from stress due to sepsis, shock, or an intracranial lesion 
(Cushing ulcer) or in response to a severe burn injury (Curling ulcer). Also occur 
because of aspirin or nonsteroidal anti-inflammatory drug (NSAID) use, 
hypersecretory states like Zollinger-Ellison syndrome.

 


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Clinical Manifestations

 

The presenting symptoms of peptic ulcer disease varies with the age of patient.

 

The classic symptom of peptic ulceration, epigastric pain alleviated by the ingestion 
of food, is present only in a minority of children.

 

In the 1st mo of life, the two main manifestations are gastrointestinal hemorrhage 
and perforation.

 

Between the neonatal period and 2 yr of age, recurrent vomiting, slow growth, and 
gastrointestinal hemorrhage are the major symptoms.

 

 In preschool-aged children, periumbilical postprandial pain. Vomiting and 
hemorrhage.

 

 After 6 yr of age, the clinical features of ulcer disease are like those in adults and 
commonly include epigastric abdominal pain, acute or chronic gastrointestinal 
blood loss (hematemesis, hematochezia, or melena) often leading to iron-
deficiency anemia. 

 

 The pain is often described as dull or aching rather than sharp or burning. It may 
last from minutes to hours, and patients have frequent exacerbations and 
remissions lasting from weeks to months.

 

Nocturnal pain is common.

 

 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. 

 

Diagnosis

 

*Esophagogastroduodenoscopy is the method of choice to diagnose peptic ulcer in 
children. It allows for the direct visualization of esophagus, stomach, and 
duodenum and to take biopsy samples for histologic assessment as well as to 
screen for the presence of H. pylori infection.

 

 

*For detection of H. pylori infection 

 

- Noninvasive tests 

 

1. serologic assays include:

 

A. detection of H. pylori antibody (IgG) in serum, whole blood, urine, or saliva. This 
tests do not distinguish between past and present infection.

 


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B. detection of H. pylori antigens in stool.

 
 

C) is 

13

led with an isotope of carbon (

:  in which urea labe

test (UBT)

 

. Urea breath

2
ingested by the patient. Samples of exhaled air are then collected to detect the 
presence of labeled carbon dioxide released from the breakdown of urea in the 
stomach.

 
 

 - Invasive tests

 

 1. histologically by demonstrating the organism in the biopsy specimens

 

 

2. Rapid urease tests:  In this test, biopsy specimens are placed in a well containing 
agar with a pH-sensitive dye. Presence of urease-producing organisms in the 
sample is signaled by a color change.

 

 
 

Treatment

 

Goals of Ulcer therapy: 

 

1. ulcer healing 

 

2. elimination of the primary cause. 

 

3. relief of symptoms and prevention of complications.

 
 

Treatment of Primary peptic ulcer

 

 

1. H. pylori–related peptic ulcer 

 

 Recommended Eradication Therapies include 2 options:

 
 

First-Line Options

 

*Amoxicillin 50 mg/kg/day up to 1 g bid  

 

Clarithromycin15 mg/kg/day up to 500 mg bid

 

Proton pump inhibitor: omeprazole 1 mg/kg/day up to 20 mg bid

 
 

*Amoxicillin  

 

Metronidazole 20 mg/kg/day up to 500 mg bid

 

Omeprazole

 
 

*Clarithromycin  

 

Metronidazole

 

Omeprazole

 
 


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 Second-Line Options

 

Bismuth subsalicylate1 tablet (262 mg) qid or 15 mL  

 

Metronidazole 20 mg/kg/day up to 500 mg bid 
Omeprazole 
Amoxicillin or Clarithromycin 
 
*These Antibiotics given for 2 weeks, and Omeprazole for 1 month. 

 

2. Idiopathic ulcers: 
Acid suppression alone is the preferred effective treatment. Either proton pump 
inhibitors or H

2

 receptor antagonists (Cimetidine, Ranitidine) may be used. 

 

Surgical therapy 

indications: 
*uncontrolled bleeding 
*perforation 
* obstruction 
 

Secondary peptic ulcer

 

 1. Stress ulceration

 

Usually occurs within 24 hr of onset of a critical illness in which physiologic stress is 
present.  In infants, are usually caused by sepsis, respiratory or cardiac 
insufficiency, trauma, or dehydration. In older children, they are related to trauma 
or other life-threatening conditions (burns, head trauma).

 
 

2. Drug-Related Peptic Disease.

 

Nonsteroidal anti-inflammatory drugs, including aspirin, are common causes of 
gastritis and erosions.  Corticosteroid, iron, calcium salts, potassium chloride, and 
antibiotics, including chloramphenicol, penicillin, tetracyclines, and cephalosporins, 
rarely cause gastritis.

 
 

 

Treatment of secondary peptic ulcer 

 

1. The inciting cause should be removed if possible.

 

2. Control of gastric acidity (should continue for 6 wk if the patient has active 
disease) 

 

*Antacids (1 mL/kg/dose)

 

)

ranitidine

 ,

Cimetidine

(

receptor antagonists 

 

2

H

*

 


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*proton pump inhibitors (omeprazole)

 

 

3. Endoscopy can be used therapeutically to control bleeding not responding to 
medical therapy.  
 

 

 

 

 
  
 
 
 
 

 

   

 

 
 
 

 

  

 
 

 

 

 
 

 

 

 

 

 

 

 

 




رفعت المحاضرة من قبل: Mubark Wilkins
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