Differential diagnosis of the functional and organic diseases of stomach in
children.
Diseases of the gastrointestinal tract in children and adolescents are fairly common diseases.
In recent years, there is an increase in the whole gastrointestinal tract. And for the last 5 years of this disease on the rise of gastric ulcer and 12 duodenal ulcer in both children ( 1.2 times ) and in adolescents ( 1.3 times). Among the factors contributing to the development of peptic ulcer disease, discusses the role of adverse environmental factors, invasion of microorganisms, errors in diet, smoking, etc. is important genetic factor.
Every day, pediatricians are faced with digestive diseases in children. The most common chronic inflammatory disease of the stomach and duodenum – chronic gastritis and chronic gastro. Complexity diagnosis of these diseases in children due to the fact that young children are rarely able to do correctly describe their complaints, and the older children and teenagers sometimes deliberately hide the symptoms. Typically, information about the child’s illness reported by parents and relatives. Therefore crucial for making the correct diagnosis and appropriate treatment are viewing pediatric gastroenterologist and the application of modern methods of research.
Chronic diseases of the stomach and duodenum often begin in preschool and school age. Gradually recurrent disease leading to pronounced anatomical changes in the body and eventually to the loss of ability to work with the disability of the adult population. Observations leading gastroenterologists indicate that in the last 10 years, the children recorded an increase in the frequency of severe gastritis and gastroduodenitis, leading to the development of peptic ulcer disease, multiple erosions and degeneration of the mucous membrane of the stomach ( atrophy subatrophy ).
Chronic gastroduodenitis more common in children with a hereditary predisposition to the disease, with decreased due to the prolonged illness earlier compensatory- adaptive capabilities of the organism. Formation of chronic diseases of the stomach and duodenum 12 are more prone to children born to mothers with pregnancy pathology and pathological labor who were bottle-fed and having a family history of allergies.
FUNCTIONAL DISEASES OF ESOPHAGUS AND STOMACH IN CHILDREN
Gastroesophageal reflux disease is the most common esophageal disorder in children of all ages. Gastroesophageal reflux (GER) signifies the retrograde movement of gastric contents across the lower esophageal sphincter (LES) into the esophagus. Although occasional episodes of reflux are physiologic, exemplified by the regurgitation of normal infants, the phenomenon becomes pathologic (GERD) in children who have episodes that are more frequent or persistent, and thus produce esophagitis or esophageal symptoms, or in those who have respiratory sequelae.
Factors determining the esophageal manifestations of reflux include the duration of esophageal exposure (a product of the frequency and duration of reflux episodes), the causticity of the refluxate, and the susceptibility of the esophagus to damage. The LES, supported by the crura of the diaphragm at the gastroesophageal junction, together with valvelike functions of the esophagogastric junction anatomy, form the antireflux barrier. In the context of even the normal intra-abdominal pressure augmentations that occur during daily life, the frequency of reflux episodes is increased by insufficient LES tone, by abnormal frequency of LES relaxations (see later), and by hiatal herniation that prevents the LES pressure from being proportionately augmented during abdominal straining. Normal intra-abdominal pressure augmentations may be further exacerbated by straining or respiratory efforts. The duration of reflux episodes is increased by lack of swallowing (during sleep) and by defective esophageal peristalsis. Vicious cycles ensue because chronic esophagitis produces esophageal peristaltic dysfunction (low amplitude waves and propagation disturbances), decreased LES tone, and inflammatory esophageal shortening that induces hiatal herniation, all of them worsening reflux.
Transient LES relaxation (TLESR) is the major primary mechanism allowing reflux to occur. TLESRs occur independent of swallowing, reducing LES pressure to 0–2mmHg (above gastric), and last more than 10s; they appear by the 26 wk of gestation. A vagovagal reflex, composed of afferent mechanoreceptors in the proximal stomach, a brain stem pattern generator, and efferents in the LES, regulates TLESRs. Gastric distention (postprandially, or due to abnormal gastric emptying or air swallowing) is thus the main stimulus for TLESRs. Whether GERD is caused by a higher frequency of TLESRs or by a greater incidence of reflux during TLESRs is debated; both are likely in different individuals. Straining during a TLESR makes reflux more likely, as do positions that place the gastroesophageal junction below the air-fluid interface in the stomach. Other factors influencing gastric pressure-volume dynamics, such as increased movement, straining, obesity, large volume or hyperosmolar meals, and increased respiratory effort (e.g., coughing, wheezing) may have the same effect.
Epidemiology and Natural History
Infant reflux becomes symptomatic during the first few months of life, peaking at about 4 mo and resolving in most by 12 mo and nearly all by 24 mo. Symptoms in older children tend to be chronic, waxing and waning, but completely resolving io more than half, resembling adult patterns. A genetic predisposition as an autosomal dominant form is located on chromosome 13q14 and chromosome 9.
Most of the common clinical manifestations of esophageal disease can signify the presence of GERD. Infantile reflux manifests more often with regurgitation (especially postprandially), signs of esophagitis (irritability, arching, choking, gagging, feeding aversion), and resulting failure to thrive; symptoms resolve spontaneously in the majority by 12 to 24 mo. Older children, in contrast, may have regurgitation during the preschool years; complaints of abdominal and chest pain supervene during later childhood and adolescence. Occasional children present with neck contortions designated Sandifer syndrome. The respiratory (extraesophageal) presentations are also age dependent: GERD in infants may manifest as obstructive apnea or as stridor or lower airway disease in which reflux complicates primary airway disease such as laryngomalacia or bronchopulmonary dysplasia. In contrast, airway manifestations in older children are more frequently related to asthma or to otolaryngologic disease such as laryngitis or sinusitis.
For most of the typical GERD presentations, a thorough history and physical examination suffice to reach the diagnosis initially. This initial evaluation aims to identify the pertinent positives in support of GERD and its complications and the negatives that make other diagnoses unlikely. The history may be facilitated and standardized by questionnaires (the Infant Gastroesophageal Reflux Questionnaire, the I-GERD), which also permit quantitative scores to be evaluated for their diagnostic discrimination. Important diagnoses to consider in the evaluation of an infant or a child with chronic vomiting are milk and other food allergies, pyloric stenosis, intestinal obstruction (especially malrotation with intermittent volvulus), nonesophageal inflammatory diseases, infections, inborn errors of metabolism, hydronephrosis, increased intracranial pressure, rumination, and bulimia. Focused diagnostic testing, depending on the presentation and the differential diagnosis, may then supplement the initial examination.
Most of the esophageal tests are of some use in particular patients suspected of GERD. Contrast (usually barium) radiographic study of the esophagus and upper gastrointestinal tract is performed in children with vomiting and dysphagia to evaluate for achalasia, esophageal strictures and stenosis, hiatal hernia, and gastric outlet or intestinal obstruction. Extended esophageal pH monitoring of the distal esophagus, no longer considered the sine qua non of a GERD diagnosis, provides a quantitative and sensitive documentation of acidic reflux episodes, the most important type of reflux episodes for pathologic reflux. The distal esophageal pH probe is placed at a level corresponding to 87% of the nares-LES distance, based on regression equations using the patient’s height, by fluoroscopic visualization, or by manometric identification of the LES. Normal values of distal esophageal acid exposure (i.e., pH < 4) are generally established as less than 5–8% of the total monitored time. The most important indications for esophageal pH monitoring are to assess efficacy of acid suppression during treatment, to evaluate apneic episodes in conjunction with a pneumogram, and to evaluate atypical GERD presentations such as chronic cough, stridor, and asthma. Dual pH probes, adding a proximal esophageal probe to the standard distal one, are used in the diagnosis of extraesophageal GERD, identifying upper esophageal acid exposure times of about 1% of the total time to be threshold values for abnormality. Endoscopy allows diagnosis of erosive esophagitis and complications such as strictures or Barrett esophagus; esophageal biopsies may diagnose histologic reflux esophagitis in the absence of erosions while simultaneously eliminating allergic and infectious causes. Endoscopy is also used therapeutically to dilate reflux-induced strictures. Radionucleotide scintigraphy using technetium may demonstrate aspiration and delayed gastric emptying when these are suspected. The intraluminal impedance testing is a cumbersome test, infrequently used clinically, but can document nonacid reflux. Laryngotracheobronchoscopy evaluates for visible airway signs that are associated with extraesophageal GERD, such as posterior laryngeal inflammation and vocal nodules; it may permit diagnosis of silent aspiration (during swallowing or during reflux) by bronchoalveolar lavage with subsequent quantification of lipid-laden macrophages in airway secretions.
Esophageal manometry permits evaluation for dysmotility, particularly in preparation for antireflux surgery. Empirical antireflux therapy, using a time-limited trial of high-dose proton pump inhibitor (PPI), has been demonstrated in adults to be a cost-effective strategy for diagnosis; although not formally evaluated in older children, it has also been applied to this age group. However, failure to respond to such empirical treatment, or a requirement for the treatment for prolonged periods, mandates formal diagnostic evaluation.
Conservative therapy and lifestyle modification form the foundation of GERD therapy.
Dietary measures for infants include normalization of feeding techniques, volumes, and frequency if abnormal. Thickening of formula with a tablespoon of rice cereal per ounce of formula results in fewer regurgitation episodes, greater caloric density (30kcal/oz), and reduced crying time, although it may not modify the number of nonregurgitant reflux episodes. A short trial of a hypoallergenic diet may be used to exclude milk or soy protein allergy before pharmacotherapy. Older children and adults should be counseled to avoid acidic foods (tomatoes, chocolate, mint) and beverages (juices, carbonated and caffeinated drinks).
Positioning measures are particularly important for infants, who cannot control their positions independently. Seated position worsens infant reflux and should be avoided in infants with GERD. Esophageal pH monitoring has shown significantly more reflux episodes in infants in supine and side positions compared with the prone position, but evidence supporting the supine position to reduce the risk of sudden infant death syndrome has led the
Pharmacotherapy is directed at ameliorating the acidity of the gastric contents or at promoting its aboral movement.
Antacids are the most commonly used antireflux therapy and are readily available over-the-counter. They provide rapid but transient relief of symptoms by acid neutralization. The long-term regular use of antacids cannot be recommended because of side effects of diarrhea (magnesium) and constipation (aluminum) and rare reports of more serious side effects of chronic use.
Histamine-2 receptor antagonists (H2RAs)—cimetidine, famotidine, nizatidine, and ranitidine—are widely used antisecretory agents and act by selective inhibition of histamine receptors on gastric parietal cells. There is a definite benefit of H2RAs in treatment of mild-to-moderate reflux esophagitis. H2RAs are recommended as first-line therapy because of their excellent overall safety profile.
Proton pump inhibitors (PPIs)—omeprazole, lansoprazole, pantoprazole, rabeprazole, and esomeprazole—provide the most potent antireflux effect by blocking the hydrogen-potassium ATPase channels of the final common pathway in gastric acid secretion. PPIs are superior to H2RAs in the treatment of severe and erosive esophagitis. Doses of omeprazole for children have been established (0.7–3.3 mg/kg/day), higher than those used in adults on a dose per weight basis.
Prokinetic agents available in the
Surgery, usually fundoplication, is effective therapy for intractable GERD in children, particularly those with refractory esophagitis or strictures and those at risk for significant morbidity from chronic pulmonary disease. It may be combined with a gastrostomy for feeding or venting. The current availability of potent acid-suppressing medication mandates more rigorous analysis of the relative risks (or costs) and benefits of this relatively irreversible therapy in comparison to long-term pharmacotherapy. Some of the risks of fundoplication include a wrap that is “too tight»(producing dysphagia or gas-bloat) or “too loose»(and thus incompetent). Surgeons may choose to perform a “tight” (360°, Nissen) or “loose” (<360°, Thal, etc.) wrap or to add a gastric drainage procedure (e.g., pyloroplasty) to improve gastric emptying, based on their experience and the patient’s disease. Preoperative accuracy of diagnosis of GERD and the skill of the surgeon are two of the most important predictors of successful outcome.
Esophageal: Esophagitis and Sequelae—Stricture, Barrett Esophagus,
Esophagitis may manifest as irritability, arching, and feeding aversion in infants; chest or epigastric pain in older children; and rarely as hematemesis, anemia, or Sandifer syndrome at any age. Prolonged and severe esophagitis leads to formation of strictures, generally located in the distal esophagus, producing dysphagia, and requiring repeated esophageal dilations and often fundoplication. Long-standing esophagitis predisposes to metaplastic transformation of the normal esophageal squamous epithelium into intestinal columnar epithelium, termed Barrett esophagus, a precursor of esophageal adenocarcinoma.
Barrett esophagus
Esophagitis and regurgitation may be severe enough to induce failure to thrive because of caloric deficits. Enteral (nasogastric or nasojejunal, or percutaneous gastric or jejunal) or parenteral feedings are sometimes required to treat such deficits.
Extraesophageal: Respiratory (“Atypical”) Presentations.
It is important to include GERD in the differential diagnosis of children with unexplained or refractory otolaryngologic and respiratory complaints. GERD may produce respiratory symptoms by direct contact of the refluxed gastric contents with the respiratory tract (aspiration or microaspiration) or by reflexive interactions between the esophagus and respiratory tract (inducing laryngeal closure or bronchospasm). Frequently, GERD and a primary respiratory disorder interact, and a vicious cycle between them worsens both diseases. Many children with these extraesophageal presentations do not have typical GERD symptoms, making the diagnosis difficult. These atypical GERD presentations require a thoughtful approach to the differential diagnosis that considers a multitude of primary otolaryngologic (infections, environmental allergies, postnasal drip, voice overuse) and pulmonary (asthma, cystic fibrosis) disorders. Therapy for the GERD must be more intense (usually incorporating a PPI) and prolonged (usually at least 3 to 6 mo). Subspecialist assistance from the perspective of the airway disease (otolaryngology, pulmonology) and the reflux disease (gastroenterology) is often warranted and useful, both for specialized diagnostic testing and for optimizing intensive management.
The esophageal epithelium is infiltrated by eosinophils, typically in a density exceeding 15 per high-power field.
Presenting symptoms include vomiting, chest or abdominal pain, and dysphagia with occasional food impactions or strictures. Most patients are male. The mean age at diagnosis is 7 yr with the duration of symptoms of 3 yr. Patients often have atopy, associated food allergies, peripheral eosinophilia (50% of patients), and elevated IgE levels. Endoscopically the esophagus presents a granular, furrowed, or ringed appearance; esophageal histology reveals eosinophilia. It is differentiated from GERD by its general lack of erosive esophagitis, by its greater eosinophil density, and by its refractoriness to antireflux therapies.
Treatment involves elimination diets for those with proven allergies, whereas inhaled and systemic corticosteroids have been used successfully for nonresponders and for nonallergic (“primary”) eosinophilic esophagitis. Little is known about its natural history, but it seems that eosinophilic esophagitis left untreated may result in stricture formation.
Uncommon, and most often afflicting immunocompromised children, infective esophagitis is caused by fungal agents, such as Candida and Torulopsis glabrata; viral agents, such as herpes simplex, cytomegalovirus, and varicella zoster; and bacterial infections, including diphtheria and tuberculosis. The typical presenting signs and symptoms are odynophagia, dysphagia, and retrosternal pain; there may also be fever, nausea, and vomiting. Esophageal candidiasis commonly, but not always, presents as concurrent oropharyngeal infection and may affect immunocompetent as well as immunocompromised children. Esophageal viral infections may also present in immunocompetent hosts as an acute febrile illness. Infectious esophagitis, like other forms of esophageal inflammation, may occasionally progress to esophageal stricture. Diagnosis of infectious esophagitis is made by endoscopy and histopathologic examination; adding polymerase chain reaction, tissue-viral culture, and immunocytochemistry enhances the diagnostic sensitivity. Treatment is with appropriate antimicrobial agents, analgesics, and antacids.
These acute injuries are produced by contact with a damaging agent. Medications implicated in “pill»esophagitis include tetracycline, potassium chloride, ferrous sulfate, and nonsteroidal anti-inflammatory medications, with the tablet most often ingested at bedtime with inadequate water. This practice often produces acute discomfort followed by progressive retrosternal pain, odynophagia, and dysphagia; endoscopy shows a focal lesion often localized to one of the anatomic narrowed regions of the esophagus or to an unsuspected pathologic narrowing. Treatment is supportive; lacking much evidence, antacids, topical anesthetics, and bland or liquid diets are often used.
Organic diseases of children stomach
and duodenum diseases
Chronic gastritis, by definition, is a histopathological entity characterized by chronic inflammation of the stomach and duodenum mucosa. Gastritides can be classified based on the underlying etiologic agent (eg, Helicobacter pylori, bile reflux, nonsteroidal anti-inflammatory drugs [NSAIDs], autoimmunity, allergic response) and the histopathological pattern, which may suggest the etiologic agent and clinical course (eg, H pylori–associated multifocal atrophic gastritis). Other classifications are based on the endoscopic appearance of the gastric mucosa (eg, varioliform gastritis). Although minimal inflammation is observed in some gastropathies, such as those associated with NSAID intake, because they are frequently included in the differential diagnosis.Gastritis is associated with a variety of medications, medical and surgical conditions, physical stresses, social habits, chemicals, and infections. Some of the more common causes of gastritis are these.
The causes of chronic diseases of the stomach and duodenum may be divided into exogenous (external), endogenous (internal) and infectious. To exogenous factors include: food poisoning and intestinal infections deferred, long-term violations of the regime and the quality of food (rare or frequent meals, irregular intervals between them), use of products, mechanical and chemical irritants gastroduodenal mucosa, eating cold food, poor chewing food.
Among the endogenous factors of the greatest importance is attached to the neuro-reflex effects on the stomach and duodenum from other affected organs of digestion, gall bladder and liver, pancreas, intestines.
Medications
· Aspirin (more than 300 medications contain some form of aspirin)
· Nonsteroidal anti-inflammatory drugs (NSAIDs, such as ibuprofen)
· Steroids (Prednisone is one example)
· Potassium supplements
· Iron tablets
· Cancer chemotherapy medications
· Swallowing poisons or objects
· Corrosives (acid or lye)
· Swallowed foreign bodies (paper clips or pins)
· Medical and surgical conditions
· Physical stress in the critically ill
· After medical procedures (such as endoscopy, in which a specialist looks into the stomach with a small lighted tube)
· After an operation to remove part of the stomach
· After medical radiation treatment for cancer
· Infections
· Tuberculosis
· Bacterial infections (H pylori infection is the most common. Many other bacteria—even those that usually cause pneumonia or bladder infections—can cause gastritis.)
· Viral infections, fungal (yeast) infections, parasites, and worms
· Autoimmune diseases
· Pernicious anemias.
Chemical or reactive gastritis is caused by injury of the gastric mucosa by reflux of bile and pancreatic secretions into the stomach, but it can also be caused by exogenous substances, including NSAIDs, acetylsalicylic acid, chemotherapeutic agents. These chemicals cause epithelial damage, erosions, and ulcers that are followed by regenerative hyperplasia, histologically detectable as foveolar hyperplasia and damage to capillaries, with mucosal edema, hemorrhage, and proliferation of smooth muscle in the lamina propria. Inflammation in these lesions caused by chemicals is minimal or lacking; therefore, the term gastropathy or chemical gastropathy is more appropriate to describe these lesions than is the term chemical or reactive gastritis as proposed by the updated
Helicobacter pylori is a Gram-negative, microaerophilic bacterium that can inhabit various areas of the stomach, particularly the antrum. It causes a chronic low-level inflammation of the stomach lining and is strongly linked to the development of duodenal and gastric ulcers and stomach cancer. Over 80% of individuals infected with the bacterium are asymptomatic.
The bacterium was initially named Campylobacter pyloridis, then renamed C. pylori to correct a Latin grammar error. When 16S rRNA gene sequencing and other research showed in 1989 that the bacterium did not belong in the genus Campylobacter, it was placed in its own genus, Helicobacter. The genus derived from the ancient Greek «spiral»or»coil“. The specific epithet pylōri means»of the pylorus»or pyloric valve (the circular opening leading from the stomach into the duodenum), from the Ancient Greek word πυλωρός, which means gatekeeper.
More than 50% of the world’s population harbor H. pylori in their upper gastrointestinal tract. Infection is more prevalent in developing countries, and incidence is decreasing in Western countries. H. pylori’s helix shape (from which the generic name is derived) is thought to have evolved to penetrate the mucoid lining of the stomach.
Pathophysiology:
The pathophysiology of gastritis complicating a systemic disease, such as hepatic cirrhosis, uremia, or another infection, is described in the relevant disease articles. The pathogenesis of the most common forms of gastritis is described as follows.
Classification of the chronic gasroduodenitis
Form
Acute
Acute
Chronic
Special:
n Granulomatous
n Eosinophilous
Etiology
n Autoimmune
n H. pylori
n Reflux-gastritis
n Reactive
n Idiopathic
Localization
n Antral
n Fundal
n Pangastritis
n Duodenitis
Endoscopies disorders
n Superficial
n Erosive
n Hemorrhagic
n Atrophic
n Hyperplastic
Histology
n Superficial
n without atrophy of glands
n with atrophy of glands
n Atrophic
n Intestinal methaplasia
Secretion
n
n Increased
n decreased
Period
n Exacerbation
n Non-full clinical remission
n Full clinical remission
n Clinical, endoscopy morphological remission
n Duodenogastric reflux
n Mild
n Moderate
n Severe
Infectious granulomatous gastritis
Granulomatous gastritis is a rare entity. Tuberculosis may affect the stomach and cause caseating granulomas. Fungi can also cause caseating granulomas and necrosis, a finding that is usually observed in patients who are immunosuppressed. Granulomatous gastritis: In multisystemic diseases, specific symptoms related to gastric involvement may be minor. Caseating granulomas secondary to tuberculosis may be found in the absence of lung disease in patients who are malnourished, immunosuppressed, or alcoholic. Patients with Crohn disease and gastric involvement may report gastric pain, nausea, and vomiting. Gastric involvement in Crohn disease is almost invariably associated with intestinal disease, and intestinal manifestations predominate. Sarcoidosis of the stomach is usually associated with granulomatous inflammation in other locations, especially the lungs, hilar nodes, or salivary glands. About 10% of patients with sarcoid involvement in the stomach are asymptomatic. Patients who are symptomatic present with gastric ulcers, hemorrhage pyloric stricture, and gastric outlet obstruction. Idiopathic isolated granulomatous gastritis: This diagnosis is established only when known entities associated with granulomas are excluded.
Gastritis in patients who are immunosuppressed
Cytomegalovirus (CMV) infection of the stomach is observed in patients with underlying immunosuppression. Histologically, typical intranuclear eosinophilic inclusions and, occasionally, smaller intracytoplasmic inclusions are found. A patchy, mild inflammatory infiltrate is observed in the lamina propria. Viral inclusions are present in gastric epithelial cells and in endothelial or mesenchymal cells in the lamina propria. Severe necrosis may result in ulceration. Herpes simplex causes basophilic intranuclear inclusions in epithelial cells. Mycobacterial infections by Mycobacterium avium-intracellulare are characterized by diffuse infiltration of the lamina propria by histiocytes, which rarely form granulomas.
Autoimmune gastritis
This type of gastritis is associated with serum antiparietal and anti-intrinsic factor (IF) antibodies. The gastric corpus undergoes progressive atrophy, IF deficiency occurs, and patients may develop pernicious anemia.
The development of chronic atrophic gastritis limited to corpus-fundus mucosa and marked diffuse atrophy of parietal and chief cells characterize autoimmune atrophic gastritis. Autoimmune gastritis is associated with serum antiparietal and anti-IF antibodies that cause IF deficiency, which, in turn, causes decreased availability of cobalamin and, eventually, pernicious anemia in some patients.
Autoantibodies are directed against at least 3 antigens, including IF, cytoplasmic (microsomal-canalicular), and plasma membrane antigens. Two types of IF antibodies are detected, ie, types I and II. Type I IF antibodies block the IF-cobalamin binding site, thus preventing the uptake of vitamin B-12. Cell-mediated immunity also contributes to the disease. T-cell lymphocytes infiltrate the gastric mucosa and contribute to epithelial cell destruction and resulting gastric atrophy.
Lymphocytic gastritis
This is a type of chronic gastritis with dense infiltration of the surface and foveolar epithelium by T lymphocytes, and associated chronic infiltrates are in the lamina propria. Because of similar histopathology relative to celiac disease, lymphocytic gastritis has been proposed to result from intraluminal antigens. High anti–H pylori antibody titers have been found in patients with lymphocytic gastritis, and, in limited studies, the inflammation disappeared after H pylori eradication. However, many patients with lymphocytic gastritis are serologically negative for H pylori. A number of cases may develop secondary to intolerance to gluten and drugs such as ticlopidine. Lymphocytic gastritis can be observed in children but is usually detected in late adulthood. On average, patients are aged 50 years. Lymphocytic gastritis: This type mostly affects middle-aged or elderly patients. It may be associated with chronic H pylori infection, gluten-sensitive enteropathy, and Ménétrier disease. It may represent a hypersensitivity reaction involving the gastric body. Lymphocytic gastritis has been described complicating MALT lymphoma and gastric carcinoma.
Eosinophilic gastritis
Large numbers of eosinophils may be observed with parasitic infections such as those caused by Eustoma rotundatum and anisakiasis. Eosinophilic gastritis can be part of the spectrum of eosinophilic gastroenteritis. Although the gastric antrum is commonly affected, this condition can affect any segment of the GI tract and can be segmental. Patients frequently have peripheral blood eosinophilia. In some cases, especially in children, eosinophilic gastroenteritis can result from food allergy, usually to milk or soy protein. Eosinophilic gastroenteritis can also be found in some patients with connective tissue disorders, including scleroderma, polymyositis, and dermatomyositis. Eosinophilic gastroenteritis: Some patients have underlying connective tissue disorders. Patients with predominant mucosal involvement may report nausea, vomiting, and abdominal pain related to the ingestion of specific foods. Patients with involvement of the muscularis propria and resulting thickening and rigidity may present with outlet obstruction symptoms. Many patients have a history of allergy, peripheral eosinophilia, asthma, eczema, or food sensitivity. Some patients respond to removal of these items from the diet, and they often respond to steroid treatment.
Radiation gastritis
Small doses of radiation (up to 1500 R) cause reversible mucosal damage, whereas higher radiation doses cause irreversible damage with atrophy and ischemic-related ulceration. Reversible changes consist of degenerative changes in epithelial cells and nonspecific chronic inflammatory infiltrate in the lamina propria. Higher amounts of radiation cause permanent mucosal damage, with atrophy of fundic glands, mucosal erosions, and capillary hemorrhage. Associated submucosal endarteritis results in mucosal ischemia and secondary ulcer development.
Ischemic gastritis
Ischemic gastritis is believed to result from atherosclerotic thrombi arising from the celiac and superior mesenteric arteries.
Clinic of chronic gastritis ( CG)
Clinical manifestations of chronic gastritis and gastroduodenita children are nearly identical and accurately determine the location of the inflammatory process is possible only with the help of endoscopic methods. not separate features of chronic gastritis and gastroduodenitis. The main symptom of both one and the other of the disease are pain in the abdomen. In children with chronic gastritis and gastroduodenitis are intense, often paroxysmal. Localized pain mainly by»spoon»- the so –called»epigastric region.»The pain may move in the right upper quadrant, especially when combined with the defeat of gastro biliary system. Keep in mind that some of the children and the pain can be mild. If a child comes back throw the contents of 12 duodenal ulcer in the stomach ( duodenal reflux ), the sharp pains are paroxysmal iature. Perhaps fever, nausea and vomiting with bile. Sometimes, such an attack is considered»acute»abdomen and differential diagnosis with appendicitis.
In chronic gastritis and gastroduodenite pain usually occur on an empty stomach and decrease after meals. In recent years, increasingly began to be registered»early adopters»of pain that occur within 20-30 minutes after eating. In children, the equivalent of the early pain can be considered early satiety.
With increased acid gastric function in older children revealed a classic rhythm of pain, which is called»moyniganovsky»- on behalf of the doctor B.Moynihan. This is the kind of rhythm : hunger, pain, eating, pain – relief.
Among the factors facilitating the pain is more often called the children receiving small amounts of food or milk. Enhance the use of pain fatty foods, overeating, exercise.
Seasonal exacerbations are identified with a term of more than 3 years of the disease, usually in late September and October due to a change in diet and in March and April due to the influence of meteorological factors.
Required companion of chronic gastritis and gastroduodenitis – dyspeptic disorders. There is loss of appetite, nausea, heartburn, intolerance of fried and fatty foods, belching. Quite often identified violations of the chair, the more often it is a tendency to constipation.
An objective examination of most of the children show signs of chronic intoxication and vitamin deficiencies : pallor, blueness under the eyes, brittle nails, a tendency to hair loss, weight loss and a decrease in the elasticity of the skin. On palpation of the abdomen is determined by pain in the upper abdomen and in the right upper quadrant. It often appears muscular defense in the area of greatest pain. On palpation of the abdomen is often determined by muscle tension and tenderness in the epigastric region.
HCG associated with H. pylori infection may manifest symptoms of dyspepsia with severe pain in the epigastric region,»hungry»and nocturnal pain. These symptoms are due to increased gastric secretion and motor-evacuation disorders that result from infection with Helicobacter.
Among chronic gastritis in children are rare autoimmune, chemical, radiation and other forms of the disease. In the diagnosis of these forms except for specific endoscopic and morphological changes are important symptoms of the underlying disease. The main differential diagnostic criteria of chronic gastritis are presented in
Isolated inflammation of the mucous membrane only 12 duodenal ulcer ( duodenitis ) is not common, usually occurs combined lesion of the stomach and duodenum 12. In this regard, there is no clear diagnostic symptoms isolated duodenitis
Features of chronic gastroduodenitis in children
Wears common character
Mostly acidity
Often accompanied by reflux ( gastritis esophageal, duodenal gastric ), which complicates treatment
Rarely comes a malignancy
Among the common lesions of the esophagus,»gastroesophageal reflux disease»( GERD). Gastro- oesophageal reflux of failure is a consequence of the obturator mechanism cardia ( hypnotics, increase intragastrialnogo pressure, fatty foods, chocolate). GERD causes of reflux esophagitis, peptic ulcers of the esophagus, stenosis. If the biopsy is cylindrical, rather than squamous epithelium that is the»esophagus Bareta»- is treated as a precancer.
Laboratory testing:
Most tests are designed to exclude other causes of the symptoms, leaving gastritis as the only cause of your symptoms. Check of the vital signs (pulse, blood pressure)
· The findings of gastritis are»nonspecific.»This means that upper abdominal tenderness just as likely may be caused by gastritis as by an ulcer or an inflamed gallbladder or liver.
· Laboratory testing: Most tests are designed to exclude other causes of , leaving gastritis as the only cause of your symptoms. No standard panel of laboratory tests can diagnose gastritis. Some doctors will do extensive laboratory testing. Others may do no laboratory testing at all.
· Blood tests (looking mostly for anemia, a low blood count)
· Tests of the liver and kidney functions
· Urinalysis
· Tests of the gallbladder and pancreas
· X-rays
· An ECG (a heart wave tracing)
· Additional testing: The doctor may test your blood for evidence of H pylori infection, thought to be associated with many cases of gastritis.
Specialists: The doctor also may refer you to a gastroenterologist, a specialist in diseases of the stomach, intestines, and colon. The gastroenterologist may in turn recommend an endoscopy.
· Rapid urease test from gastric biopsy tissue; Rapid urease test from gastric biopsy tissue; Bacterial culture of gastric biopsy: This is usually performed in the research setting or to assess antibiotic susceptibility in patients for whom first-line eradication therapy fails.
· Urea breath test with nonradioactive carbon isotope (
When viewed fibrogastroscope normal mucosa of the stomach and duodenum pale pink or red, smooth, shiny, with wrinkles, easily deals with inflating the stomach with air. During peristalsis folds well converge and become star-shaped pattern. The mucous membrane is covered with a thin layer of mucus. Hemorrhage, erosion, and other defects or focal lesions of the mucous missing.
Endoscopic picture in chronic non-atrophic (antral) gastritis is characterized by marked hyperemia and edema of the mucosa of the stomach, the presence of submucosal hemorrhages and erosions, hyperplasia of the folds. Often detected as slower gastric emptying, antral stasis and pyloric spasm
A similar pattern is found with endoscopic chronic duodenitis: inflammatory edema and hyperemia, easy contact bleeding, hemorrhage and erosion. In atrophic duodenitis is thinning of the mucosa, her pallor. In most cases, these changes are of local nature. The most common lesion is detected duodenal bulb, at least – the distal duodenitis. Last accompanied by the development of inflammatory edema of papilla Fatteri ( papillita ) which delays the escape not only the duodenum, but also pancreatic juice and bile, ie, biliary dyskinesia and impaired pancreatic exocrine function.
Treatment.
Treatment of children with chronic gastritis and gastroduodenitis conducted a comprehensive, taking into account the causes of the disease and the presence of changes in other organs and body systems.
Preferably with exacerbation child hospitalized in a specialized children’s gastroenterology department. However, in some situations, when a child is non-contact and expresses categorical protest against hospitalization, treatment is acceptable in the home.
Psychotherapy is very important, especially in older children and adolescents. It is advisable to spend time with her parents.
Of the general measures recommended walks in the fresh air after a meal – at least 30-40 minutes. Do not take a horizontal position for 2-3 hours after a meal. Night sleep should be 8-10 hours.
Contraindicated in children sudden physical exertion, causing an abrupt increase in intra-abdominal pressure : jumping, intense running, lifting weights.
Diet is built taking into account the form of the disease and gastric acidity. Food must be fractional : 4-5 times a day, a small volume portions. The highest break between meals should not exceed 4 hours. The last meal – in 19-20 hours. Excluded from the diet foods that increase bile secretion : vegetable oils and animal fats in its pure form, fried foods, egg yolks, eggs, cream, fat sour cream, cakes and pastries. Preferably use of fermented milk products, but not of whole milk. All children with chronic inflammatory diseases of the stomach and duodenum 12 categorically contraindicated vysokogazirovannye drinks»Coca –Cola»,»Pepsi– Cola»,»Fanta»and others. Detrimental factor is the long-term ( more than 10-15 minutes ) the use of chewing gum.
Be sure to get regular chair. The tendency to constipation should increase the ingestion of vegetables, especially beets. In the diet include prunes, dried apricots, dried fruits in the form of steamed. The tendency to diarrhea vegetables excluded from the diet. Preference is given to semolina and rice porridge, fresh cottage cheese.
Another important factor is tobacco smoking, both with passive and direct- smoking junior and senior high school students.
Drug therapy should be given the state of the secretory function of the stomach. The detection of Hp infection are assigned different antibiotic regimens of combination antibiotic 2-3.
Children with high acidity is prescribed antacids. In pediatric use nonabsorbable antacids containing aluminum and magnesium – almagel, almagel A Fosfalyugel, Maalox, Gustav. Gastrofarm addition to neutralizing acids, stimulates repair processes in the gastroduodenal mucosa.
As a basic therapy is widely used in children’s clinic sucralfate (Venter ), which provides an antacid, anti-inflammatory and antispasmodic.
Bismuth salt forms on the surface of ulcers and erosions protective film that protects it from the aggressive action of gastric juice. This is a well-known drug de-nol, ventrisol, bismofalk etc.
Justified the appointment of a group of patients with drug blockers of histamine H2 -receptor antagonists, which reduce acid production and secreted, especially at night. The first generation of these drugs is cimetidine. The drugs of second and third generation are ranitidine, famotidine, roxatidine.
Effective treatment of erosive gastroduodenitis proton pump inhibitor omeprazole. Use of drugs from the group of peripheral M- acting anticholinergics : gastrotsepin.
When expressed pain syndrome appointed antispasmodics.
To eliminate the regulatory functions of the central nervous system disorders and emotional stress are shown sedatives and tranquilizers.
A fundamentally different approach to the treatment of chronic gastroduodenitis proceeding with secretory insufficiency. This category of patients should be the appointment of substitution therapy – betatsid, atsidin – pepsin with meals. To stimulate regeneration and recovery mucosa shows the assignment of protein hydrolysates. Good results are obtained by administering courses pentoksil, metiluratsila. Mandatory in the complex treatment of patients is the appointment of B vitamins ( B1, B12 ), C, vitamin U in the form of salts of methionine sulfone.
With involvement in the pathological process of biliary tract and pancreas shows the assignment of enzymes.
In order to optimize the acid- peptic factor along with diet commonly used designation of mineral waters ( Slavyanovskaya, Essentuki 17 ARZNI, Mirgorodskaya, etc.). Mineral water is taken 20-30 minutes before meals 3-4 times a day. The course of treatment is 4-6 weeks. Also shown are the extracts of wormwood, sage, plantain, ash, calendula.
Highly effective use of homeopathic remedies. Use classical homeopathic products, and various complexes: Mucosa, Echinacea compositum, etc.
Physiotherapy include electrophoresis, ozocerite or paraffin baths, short-wave therapy, hydrotherapy. Therapeutic exercise is required in the treatment of these patients
Ozokeritotherapy
Choose an individual complex therapy in children with chronic gastritis and gastroduodenitis can only pediatric gastroenterologist because of the need to take into account a very large number of clinical features of the disease and the interaction of different groups of drugs together. Therefore, a timely appeal to specialized counseling centers, a comprehensive examination and appropriate treatment of patients will avoid subsequent transformation gastroduodenita gastritis or peptic ulcer disease and in the development of complicated forms of the disease.
Peptic ulcers
A peptic ulcer is a sore on the lining of the stomach or duodenum, the beginning of the small intestine. Less commonly, a peptic ulcer may develop just above the stomach in the esophagus, the tube that connects the mouth to the stomach.
A peptic ulcer in the stomach is called a gastric ulcer. One that occurs in the duodenum is called a duodenal ulcer. People can have both gastric and duodenal ulcers at the same time. They also can develop peptic ulcers more than once in their lifetime.
Peptic ulcers are common. Each year in the
A bacterium called Helicobacter pylori (H. pylori) is a major cause of peptic ulcers. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen, are another common cause. Rarely, cancerous or noncancerous tumors in the stomach, duodenum, or pancreas cause ulcers.
H. pylori is a type of bacteria—a germ that may cause infection. H. pylori infection is common, particularly in developing countries, and often begins in childhood. Symptoms usually don’t occur until adulthood, although most people never have any symptoms.
H. pylori causes more than half of peptic ulcers worldwide. The bacterium causes peptic ulcers by damaging the mucous coating that protects the stomach and duodenum. Damage to the mucous coating allows powerful stomach acid to get through to the sensitive lining beneath. Together, the stomach acid and H. pylori irritate the lining of the stomach or duodenum and cause an ulcer.
Yet, most people infected with H. pylori never develop ulcers. Why the bacterium causes ulcers in some people and not in others is not known. Most likely, development of ulcers depends on characteristics of the infected person; the type, or strain, of H. pylori present; and factors researchers have yet to discover.
Researchers are not certain how H. pylori is transmitted, although they think it may be spread through contaminated food or water. People may pick up the bacterium from food that has not been washed well or cooked properly or from drinking water that has come from an unclean source.
Other research is exploring how infection spreads from an infected person to an uninfected person. Studies suggest that having contact with the stool or vomit of an infected person can spread H. pylori infection. And H. pylori has been found in the saliva of some infected people, which means infection could be spread through direct contact with saliva.
Frequency:
· In the
Race: H pylori–associated chronic gastritis appears to be more common among Asian and Hispanic people than in people of other races. In the
Sex: Chronic H pylori–associated gastritis affects both sexes with similar frequency. The female-to-male ratio for autoimmune gastritis has been reported to be 3:1. Lymphocytic gastritis affects men and women at similar rates.
Age: Age is the most important variable relating to the prevalence of H pylori infection, with persons born before 1950 having a notably higher rate of infection than people born after 1950. For example, roughly half of people older than 60 years are infected, compared to 20% of people younger than 40 years. This increase in infection prevalence with age largely is apparent rather than real, reflecting a continuing overall decline in the prevalence of H pylori infection. Because the infection is typically acquired in childhood and is lifelong, the high proportion of older individuals (eg,) who are infected is the long-term result of infection that occurred in childhood when standards of living were lower. The prevalence will decrease as people who are currently aged 40 years and have a lower rate of infection grow older (a birth cohort phenomenon).
Clinics of duodenal and gastric ulcers
Abdominal discomfort is the most common symptom of both duodenal and gastric ulcers. Felt anywhere between the navel and the breastbone, this discomfort usually is a dull or burning pain occurs when the stomach is empty—between meals or during the night may be briefly relieved by eating food, in the case of duodenal ulcers, or by taking antacids, in both types of peptic ulcers lasts for minutes to hours
comes and goes for several days or weeks.
Other symptoms include
Ø weight loss
Ø poor appetite
Ø bloating
Ø burping
Ø nausea
Ø vomiting
The abdominal discomfort of peptic ulcers
– feels like a dull or burning pain
– occurs when the stomach is empty—between meals or during the night
– may be briefly relieved by eating food, in the case of duodenal ulcers, or by taking antacids, in both types of peptic ulcers
– lasts for minutes to hours
– comes and goes for several days or weeks
Emergency Symptoms
A person who has any of the following symptoms should call a doctor right away:
· sharp, sudden, persistent, and severe stomach pain
· bloody or black stools
· bloody vomit or vomit that looks like coffee grounds
These “alarm” symptoms could be signs of a serious problem, such as
· Bleeding (when acid or the peptic ulcer breaks a blood vessel)
· Perforation (when the peptic ulcer burrows completely through the stomach or duodenal wall)
· Obstruction (when the peptic ulcer blocks the path of food trying to leave the stomach)
Classification of the peptic ulcer
Localization
· Stomach
· Duodenum
· Clinical and endoscopies stage
· Acute ulcer
· Ulcer epithelization
· Ulcer repairing (healing) with duodenitis (or gastritis)
· Clinical and endoscopies remission
Period
· Exacerbation
· Non-full clinical remission
· Full clinical remission
· Clinical, endoscopy morphological remission
Secretion
·
· Increased
· decreased
Complication
· Bleeding
· Perforation
· Penetration
· Stenosis
· Perivisceritis
Diagnostics
Noninvasive Techniques
If a patient has peptic ulcer symptoms, the doctor first asks about use of over-the-counter and prescription NSAIDs. Patients who are taking an NSAID are asked to stop, reduce the dose, or switch to another medication.
Physical findings
The physical examination is of little contributory value in gastritis and gastroduodenitis. However, some findings are specifically associated with the particular complications of H pylori–associated gastritis and autoimmune gastritis.
· In uncomplicated H pylori–associated gastritis, clinical findings are few and nonspecific.
· Epigastric tenderness may exist.
· If gastric ulcers coexist, guaiac-positive stool may result from occult blood loss.
· Bad breath (ie, halitosis) and abdominal pain or discomfort may occur, with bloating associated with bacterial overgrowth syndrome.
· Physical findings may result from the development of pernicious anemia and neurologic complications in patients with autoimmune atrophic gastritis.
· With severe cobalamin deficiency, the patient is pale and has slightly icteric skin and eyes. The pulse is rapid.
· If gastritis symptoms do occur, pain or discomfort of some kind often is present.
General clinical features:
· The pain is usually in the upper central portion of abdomen (the»pit»
of stomach).
· Patients also can feel gastritis pain in the left upper portion of abdomen and in back. The pain seems to»go right straight through»a person as it travels from your belly to back.
· People often use the terms burning, aching, gnawing, or sore to describe the pain. Usually, feeling a vague sense of discomfort, but the pain may be sharp, stabbing, or cutting.
· Patient often will feel the urge to belch, but belching either doesn’t relieve the pain or relieves it only briefly.
· Nausea and vomiting may occur. The vomit may be clear, green or yellow, blood-streaked, or completely bloody depending on the severity of the stomach and duodenum inflammation.
· Children may become pale and sweaty, and their heart may race. This can happen even if they are not dehydrated or losing a lot of blood internally.
· People with gastritis who are very ill and bleeding from the stomach may faint or feel as if they may faint, but fainting is rare. You also may feel short of breath.
· Sometimes, children may have chest pain or severe stomach pain.
· Someone with gastritis who is critically ill may vomit large amounts of blood. Bloody bowel movements, or dark, sticky, very foul-smelling bowel movements may occur if you are bleeding internally.
· Auscultation of the heart usually reveals a systolic flow murmur.
· A Physical examination
· A check of vital signs (pulse, blood pressure)
· Doctor will be considering all the other things besides gastritis that could cause symptoms. The doctor must check patient skin, listen to heart and lungs, and examine rectum and abdomen in detail. During this exam the doctor is checking bowel movement for blood that is not visible to the naked eye. If blood is found in the bowel movement, other tests may be ordered.
X-ray investigation of the stomach
Atrophic gastritis may be assessed by measuring serum levels of the pepsinogen I–to–pepsinogen II ratio. Pepsinogen I (PGA, PGI) and pepsinogen II (PGC, PGII) are synthesized and secreted by gastric chief cells. After secretion into the gastric lumen, they are converted into proteolytic active pepsins. The level of PGA in the serum decreases as loss of gastric chief cells during gastric atrophy occurs, resulting in a decreased PGI/PGII ratio. Gastric carcinoma occurs, especially the intestinal type, usually in association with severe atrophic gastritis. Measuring the levels of pepsinogen I and II and the pepsinogen I/II ratio in the serum is useful for screening atrophic gastritis and gastric cancer in regions with high incidence of these diseases.
Then the doctor tests to see presence of H. pylori. Testing is important because H. pylori-induced ulcers are treated differently than ulcers caused by NSAIDs.
Doctors use one of three simple, noninvasive tests to detect H. pylori in a patient’s blood, breath, or stool. Because the breath test and stool test more accurately detect H. pylori than the blood test, some doctors prefer to use one of these two tests. Each test described below is easily performed, often in an outpatient setting such as a doctor’s office or lab.
Blood test. A blood sample is taken from the patient’s vein and tested for H. pylori antibodies. Antibodies are substances the body produces to fight invading harmful substances—called antigens—such as the H. pylori bacterium.
Urea breath test. The patient swallows a capsule, liquid, or pudding that contains urea “labeled” with a special carbon atom. After a few minutes, the patient breathes into a container, exhaling carbon dioxide. If the carbon atom is found in the exhaled breath, H. pylori is present, as this bacterium contains large amounts of urease, a chemical that breaks urea down into carbon dioxide and ammonia.
Stool antigen test. The patient provides a stool sample, which is tested for H. pylori antigens.
Invasive Techniques
If a patient has any alarm symptoms, the doctor orders an endoscopy or upper gastrointestinal (GI) series. Often performed as outpatient procedures in a hospital, both procedures are painless and allow the doctor to look inside the patient’s stomach and duodenum.
For an endoscopy, the patient is lightly sedated. The doctor passes an endoscope—a thin, lighted tube with a tiny camera on the end—into the patient’s mouth and down the throat to the stomach and duodenum. With this tool, the doctor can closely examine the lining of the esophagus, stomach, and duodenum.
The doctor can use the endoscope to take photos of ulcers or remove a tiny piece of tissue—no bigger than a match head—to view with a microscope. This procedure is called a biopsy. The biopsied tissue is examined to see if H. pylori is present.
· Performing an upper GI endoscopy is essential to establish a diagnosis of gastritis.
· Endoscopic findings in granulomatous gastritis include mucosal nodularity with cobblestoning, multiple aphthous ulcers, linear or serpiginous ulcerations, thickened antral folds, antral narrowing, hypoperistalsis, and duodenal strictures. Extensive gastric involvement may resemble linitis plastica.
· Lymphocytic gastritis at endoscopy shows enlarged folds and aphthoid erosions, with the appearance of small, heaped-up, volcanolike mounds pocked with a central crater. This endoscopic pattern has also been described as varioliform gastritis.
· The endoscopic findings of reflux and chemical gastropathy are those of a gastric mucosa that is red or has red streaks with areas of apparent hemorrhage.
· Diagnosis of H pylori–associated gastritis: The criterion standard method to assess whether H pylori is the underlying cause of gastritis is histological identification of the organism. Histological examination is also used to evaluate the degree and distribution of gastritis. Obtain at least 2 biopsies from the gastric antrum, 2 from the corpus, and 1 from the incisura.
· Special stains to identify H pylori, such as Warthin-Starry, Giemsa, or Genta stain, may be necessary when the organisms are not observed and chronic gastritis is obvious.
· At late stages of infection with extensive atrophic gastritis, the numbers of H pylori organisms are markedly decreased because intestinal metaplasia creates an unfavorable environment for H pylori. In these cases, other tests, such as the urea breath test, and serological evidence of infection may provide evidence for H pylori infection.
Histologic Findings: H pylori–associated gastritis can display different levels of severity. H pylori organisms are found within the gastric mucous layer and frequently accumulate in groups of bacteria at the apical side of gastric surface cells, occasionally in the lower portions of the gastric foveolae, and rarely within the deeper areas of the mucosa in association with glandular cells.
Patients with typical cases of infection initially develop chronic active gastritis in which H pylori are observed in both the antrum and corpus, but the organisms usually are more numerous in the antrum. Polymorphonuclear leukocytes infiltrate the lamina propria, glands, surface epithelium, and foveolar epithelium, occasionally spilling into the lumen and forming small microabscesses. Lymphoid aggregates and occasional well-developed lymphoid follicles are observed expanding the lamina propria of the mucosa, and occasional lymphocytes permeate the epithelium. In disease of longer duration, significant loss of gastric glands is observed, in a condition known as gastric atrophy.
Esophagogastroduodenoscopy
Normal duodenal mucus membrane
|
Atrophic duodenitis
|
|
Superficial duodenitis
Erosion duodenitis
|
|
Esophagogastroduodenoscopy (EGD) is the procedure of choice for the detection of PUD in the pediatric population.
EGD allows direct visualization of the mucosa, localization of the source of bleeding, and diagnosis of H pylori infection via analysis of biopsy specimens, culturing, or detection of urease activity.
Therapeutic endoscopy for acute bleeding (coagulation of a bleeding ulcer with a heater probe or injection with vasoconstricting agents) is another important indication for EGD.
The gross appearance of an active ulcer seen using EGD is a round or oval punched-out lesion with a smooth white base and surrounding mucosa that is red and edematous.
Consider nasogastric (NG) lavage in a child who is ill and in whom an upper GI tract hemorrhage is suspected, as evidenced by hematemesis or melena.
If an ulcer is bleeding, the doctor can use the endoscope to inject medicines that help the blood clot or to guide a heat probe that burns tissue to stop bleeding—a process called cauterization.
For an upper GI series, the patient drinks a white, chalky liquid called barium. The barium makes the esophagus, stomach, and duodenum and any ulcers show up on an x ray. Sedation is not necessary for this procedure.
Treatment
Peptic ulcers caused by H. pylori are treated with drugs that kill the bacteria, reduce stomach acid, and protect the stomach and duodenal lining.
Antibiotics are used to kill H. pylori. Antibiotic regimens may differ throughout the world because some strains of H. pylori have become resistant to certain antibiotics—meaning that an antibiotic that once destroyed the bacterium is no longer effective. Doctors closely follow research on antibiotic treatments for H. pylori infection to know which treatment strategy will destroy which strain.
Medicines that reduce stomach acid include proton pump inhibitors (PPIs) and histamine receptor blockers (H2 blockers). Both acid-reducing medicines help relieve peptic ulcer pain after a few weeks and promote ulcer healing. PPIs and H2 blockers work in different ways:
ü PPIs suppress acid production by halting the mechanism that pumps acid into the stomach.
ü H2 blockers work by blocking histamine, which stimulates acid secretion.
Bismuth subsalicylate (Pepto-Bismol) coats ulcers, protecting them from stomach acid. Although bismuth subsalicylate may kill H. pylori, it is used with—not in place of—antibiotics in some treatment regimens.
In the
Bismuth quadruple therapy is another treatment strategy used in the
cannot take amoxicillin—a penicillin-like antibiotic—because of a penicillin allergy
has been treated before with a macrolide antibiotic, such as clarithromycin
is still infected with H. pylori because triple therapy failed to kill the bacteria
Triple therapy and bismuth quadruple therapy may cause nausea and other side effects, including
· stomach upset
· diarrhea
· headache
· a metallic taste
· a darkened tongue or stools
· sensitivity to the sun
Although antibiotics can cure 80 to 90 percent of ulcers caused by H. pylori, eliminating the bacteria can be difficult. Patients must take all medicines exactly as prescribed, even when the peptic ulcer pain is gone.
At least 4 weeks after treatment, doctors test patients using a breath or stool test to be sure the H. pylori infection has been cured. Blood tests are not useful after treatment because a patient’s blood can test positive for H. pylori even after the bacteria have been eliminated.
If infection is still present, ulcers could recur or, less commonly, stomach cancer could develop. Thus, some patients need to take more than one round of medicines to kill the H. pylori bacteria. Bismuth quadruple therapy is one of several treatments used after initial treatment has failed—a strategy called “rescue»or “salvage” therapy. In the second round of treatment, the doctor prescribes different antibiotics than those used in the first round. Amoxicillin, however, can be used again to treat H. pylori infection because H. pylori resistance to this antibiotic is rare.
An antacid may make the ulcer pain go away temporarily, but it will not kill H. pylori. People being treated for an H. pylori ulcer should check with their doctor before taking antacids. Some of the antibiotics used to kill H. pylori may not work as well if combined with an antacid.
ULCER COMPLICATIONS ARE:
1. Bleeding
2. Perforation
3. Penetration ulcers
4. Scar stenosis
5. Malignancy ulcers
Perforation
BLEEDING – the most frequent and serious complication, it is found in 15-20% of patients and is responsible for almost half of all deaths in this disease.
Occurs mainly in young men. More frequent minor bleeding, massive rarer. Sometimes a sudden massive bleeding is the first manifestation of the disease. Bleeding occurs as a result of Arroz vessel ulcer, venous stasis or venous thrombosis.
The reason it can be a variety of homeostasis. In this particular role for enteric possessing anticoagulant properties. The higher the acidity of the juice and pepsin activity, the less pronounced coagulation properties of blood.
Symptomatology – depends on the amount of blood loss. Minor bleeding characterized by pale skin, dizziness, weakness. In marked bleeding observed – Milena, single or repeated vomiting color ”coffee grounds».
Image ulcers can lead to exposure of the vessel wall of the affected organ, and its»erosion of»acid. There is bleeding. Symptoms depend on the amount of blood loss.
Signs of bleeding:
• sudden weakness
• fainting
• a drop in blood pressure
• vomiting red blood or “coffee grounds”(clotted blood)
• liquid black tarry stools (known as melena)
ULCER PERFORATION – one of the most difficult and dangerous complications. It occurs in 7 % of cases. Most often there is a perforation of ulcers 12 duodenal ulcer. However, perforation of stomach ulcers accompanied by higher mortality. In the vast majority of cases – is free perforation into the abdominal cavity. In 20% of ulcers of the stomach and the back of the 12 – duodenal ulcer observed»covered»perforation caused the rapid development of fibrinous inflammation and perforated cover
seal small holes, the left lobe of the liver or pancreas gland. Manifests sudden sharp ( dagger ), pain in the upper abdomen. The suddenness and intensity of the pain does not come as expressed in any other states. The patient receives forced position with knees pulled up to her stomach, trying to do not move. On palpation there is a pronounced stress muscles of the anterior abdominal wall. In the first hours after the perforation in patients develop vomiting, which further the development of
peritonitis is repeated, bradycardia replaced Tachycardia, pulse weak filling. Have fever, leukocytosis, increased erythrocyte sedimentation rate.
When X-rays of the abdomen under Iris is determined gas.
PENETRATION – is characterized by the penetration of ulcers. In contact with the stomach or bulb 12 duodenal ulcer organs – the liver, pancreas, small gland.
The clinical picture in acute recalls perforation, but the pain is less intense. soon after joining signs of destruction of the body in which there was penetration
( girdle pain and vomiting with lesions of the pancreas, pain in the right upper quadrant radiating to the right shoulder and in the back at the penetration of the liver, etc.) In some cases, penetration occurs gradually. In setting diagnosis should be considered a permanent pain syndrome, leukocytosis, low-grade fever, etc.
PYLORIC STENOSIS – ulcers Develops gradually. Cicatricial narrowing of the pyloric canal has circular iature, and in the initial portion 12 of the duodenum process extend eccentrically. Symptoms of this complication depends on the degree of narrowing of pylorus and duration gastric emptying. In the phase compensation can be a feeling of heaviness, fullness in the stomach, especially after consumption of abundant food. Sometimes there is regurgitation, vomiting. In phase subcompensation there is a growing pains, increased vomiting in vomit frequently are leftovers, adopted the day before. For the phase of decompensation characterized by severe disturbances in the form of a sharp reduction in body weight, dehydration, hypoproteinemia, hypokalemia, azotemia and etc.
Of MALIGNANCY – observed almost exclusively in the localization stomach ulcers. Malignancy ulcers, 12 duodenal ulcer occurs very rare. When malignant ulcer pain becomes constant, lose relationship with food intake, reduced appetite, increases attrition, experience nausea, vomiting, low-grade fever, anemia, accelerated ESR, steadfastly benzidine positive sample.
Prevention
No one knows for sure how H. pylori is spreading, so prevention is difficult. Researchers are trying to develop a vaccine to prevent—and even cure—H. pylori infection. To help prevent infection, doctors advise people to
wash their hands with soap and water after using the bathroom and before eating
eat food that has been washed well and cooked properly drink water from a clean, safe source.
To help prevent an H. pylori infection, people should
– wash their hands after using the bathroom and before eating
– eat properly prepared food
– drink water from a clean, safe source
Reference:
A – Basic:
1. Pediatrics. Textbook. / O. V. Tiazhka, T. V. Pochinok, A. N. Antoshkina et al. / edited by O. Tiazhka – Vinnytsia : Nova Knyha Publishers, 2011 – 584 pp. : il.
2. ISBN 978-966-382-355-3Nelson Textbook of Pediatrics, 19th Edition Kliegman, Behrman. Published by Jenson & Stanton, 2011, 2608. ISBN: 978-080-892-420-3.
3. Illustrated Textbook of Paediatrics, 4th Edition. Published by Lissauer & Clayden, 2012, 552 p. ISBN: 978-072-343-566-2.
4. Denial Bernstein. Pediatrics for medical Students. – Second edition, 2012. – 650 p.
