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 esophagealsymptoms, 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 theesophagogastric 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 esophagealperistalsis. 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. Avagovagal 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 InfantGastroesophageal 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 apneumogram, 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 upperesophageal 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 usedtherapeutically 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 withextraesophageal 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. Empiricalantireflux 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 becounseled 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 American Academy of Pediatrics and the North American Society ofPediatric Gastroenterology and Nutrition to recommend nonprone positioning during sleep. During awakes periods when the infant is observed, prone position and upright carried position may be used to minimize reflux. The efficacy of positioning for older children is unclear, but some evidence suggests a benefit to left side position and head elevation during sleep. Head elevation should utilize elevation of the head of the bed, rather than excess pillows, to avoid abdominal flexion and compression that might worsen reflux.
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 ofdiarrhea (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 antisecretoryagents 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 United States include metoclopramide (dopamine-2 and 5HT-3 antagonist), bethanechol(cholinergic agonist), and erythromycin (motilin receptor agonist). Most of these increase LES pressure; some improve gastric emptying or esophageal clearance. None affects the frequency of TLESRs. The available controlled trials have not demonstrated much efficacy for GERD.
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.
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 refractoryotolaryngologic 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.
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 termgastropathy or chemical gastropathy is more appropriate to describe these lesions than is the term chemical or reactive gastritis as proposed by the updated Sydney classification of gastritis. Importantly, mixed forms of gastropathy and other types of gastritis, especially H pylori gastritis, may coexist. No single classification of gastritis provides an entirely satisfactory description of all types of gastritis.
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 pylōrimeans»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:
Granulomatous
Eosinophilous
Etiology
Autoimmune
H. pylori
Reflux-gastritis
Reactive
Idiopathic
Localization
Antral
Fundal
Pangastritis
Duodenitis
Endoscopies disorders
Superficial
Erosive
Hemorrhagic
Atrophic
Hyperplastic
Histology
Superficial
without atrophy of glands
with atrophy of glands
Atrophic
Intestinal methaplasia
Secretion
Normal
Increased
decreased
Period
Exacerbation
Non-full clinical remission
Full clinical remission
Clinical, endoscopy morphological remission
Duodenogastric reflux
Mild
Moderate
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 Crohndisease 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 intranuclearinclusions 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 andanisakiasis. 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.»Thepain 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»andnocturnal 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
Ø Wears common character
Ø Mostly acidity
Ø Often accompanied by reflux ( gastritis esophageal, duodenal gastric ), which complicates treatment
Ø 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 nolaboratory 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 (13C) or with radioactive carbon isotope (14C); Diagnosis of autoimmune gastritis; Antiparietal and anti-IF antibodies in the serum; Achlorhydria, both basal and stimulated, and hypergastrinemia; Low serumcobalamin (vitamin B-12) levels (<100 pg/mL); Possible abnormal result on Schilling test (can be corrected by IF).
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»andothers. 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 thegastroduodenal 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, Echinaceacompositum, etc.
Physiotherapy include electrophoresis, ozocerite or paraffin baths, short-wave therapy, hydrotherapy. Therapeutic exercise is required in the treatment of these patients
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 United States, about half a million people develop a peptic ulcer.
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 US: Approximately 35% of adults are infected with H pylori, but the prevalence of infection in minority groups and immigrants from developing countries is much higher. Children aged 2-8 years in developing nations acquire the infection at a rate of about 10% per year; whereas, in the United States, children become infected at a rate of less than 1% per year. This major difference in the rate of acquisition in childhood is responsible for the differences in epidemiology between developed countries and developing countries. Socioeconomic differences are the most important predictor of the prevalence of the infection in any group. Higher standards of living are associated with higher levels of education and better sanitation, so the prevalence of infection is lower.
Race: H pylori–associated chronic gastritis appears to be more common among Asian and Hispanic people than in people of other races. In the United States, H pylori infection is more common among black, Native American, and Hispanic people than among white people, a difference that has been attributed to socioeconomic factors. Autoimmune gastritis is more frequent in individuals of northern European descent and in African American people, and it is less frequent in southern European and Asian people.
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
– weight loss
– poor appetite
– bloating
– burping
– nausea
– 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
– Normal
– 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 straightthrough»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 patientskin, 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.
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 antrumand 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 (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 viaanalysis 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 withvasoconstricting 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 andsurrounding 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 evidencedby 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:
PPIs suppress acid production by halting the mechanism that pumps acid into the stomach.
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 United States, clarithromycin-based triple therapy—triple therapy, for short—is the standard treatment for an ulcer caused by H. pylori. The doctor prescribes the antibiotic clarithromycin, a PPI, and the antibiotics amoxicillin or metronidazole for 10 to 14 days. Because research shows higher cure rates with 14 days of treatment, some doctors now prescribe triple therapy for this longer period.
Bismuth quadruple therapy is another treatment strategy used in the United States. The patient takes a PPI, bismuth subsalicylate, and the antibiotics tetracycline and metronidazole for 10 to 14 days. Bismuth quadruple therapy is used to treat patients in one of several situations, including if the patient
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
The liver is the largest digestive gland. It is involved in metabolic processes, the accumulation of various substances, the development of bile, promotes digestion of fats.
This organ plays a major role in metabolism and has a number of functions
in the body, including glycogen storage, decomposition of red blood cells, plasma protein synthesis, hormone production, and detoxification. It lies below the diaphragm in the thoracic region of the abdomen. It produces bile, an alkaline compound which aids in digestion, via the emulsification of lipids. It also performs and regulates a wide variety of high-volume biochemical reactions requiring highly specialized tissues, including the synthesis and breakdown of small and complex molecules, many of which are necessary for normal vital functions.
Synthesis
Ø Proteins are produced and secreted by the liver
Ø A large part of amino acid synthesis
Ø The liver performs several roles in carbohydrate metabolism:
Ø Gluconeogenesis (the synthesis of glucose from certain amino acids, lactate or glycerol). Note that humans and some other mammals cannot synthesize glucose from glycerol.
Ø Glycogenolysis (the breakdown of glycogen into glucose)
Ø Glycogenesis (the formation of glycogen from glucose)(muscle tissues can also do this)
Ø The liver is responsible for the mainstay of protein metabolism, synthesis as well as degradation.
Ø The liver also performs several roles in lipid metabolism:
Ø Cholesterol synthesis
Ø Lipogenesis, the production of triglycerides (fats).
Ø The liver produces coagulation factors I (fibrinogen), II (prothrombin), V, VII, IX, X and XI, as well as protein C, protein S andantithrombin.
Ø In the first trimester fetus, the liver is the main site of red blood cell production. By the 32nd week of gestation, the bone marrow has almost completely taken over that task.
Ø The liver produces and excretes bile (a yellowish liquid) required for emulsifying fats. Some of the bile drains directly into the duodenum, and some is stored in the gallbladder.
Ø The liver also produces insulin-like growth factor 1 (IGF-1), a polypeptide protein hormone that plays an important role in childhood growth and continues to have anabolic effects in adults.
Ø The liver is a major site of thrombopoietin production. Thrombopoietin is a glycoprotein hormone that regulates the production of platelets by the bone marrow.
Biliary Dyskinesia
Gallbladder disease that occurs without gallstones is called biliary dyskinesia or acalculous gallbladder disease. It can be acute (arising suddenly, often as a one-time occurrence) or chronic (persistent, recurrent). Acute acalculous gallbladder disease usually occurs in patients who are very ill from other disorders. Chronic acalculous gallbladder disease may be caused by dysfunctional muscle or valve defects that impair the gallbladder’s ability to contract and release bile.
The term biliary dyskinesia refers to abnormal gallbladder function characterized by right upper quadrant abdominal pain (sometimes radiating to the upper back or shoulder blades) after eating fatty or fried foods, heavy meals with nausea/vomiting or bloating, followed by loosening of stools. The excess build up of pressure in the bile ducts is thought to be responsible for these typical gallbladder symptoms. Like gallstone disease, billiary dyskinesia is much more common in girls.
Etiology
Factors leading to biliary dyskinesia (BDK):
– Neurocirculatory dysfunction of various origins
– Deferred acute viral hepatitis
– Constitutional characteristics of the child with vegetative dystonia and
– Neurosis
– Food allergy, atopic diathesis
– Any chronic pathology of the gastrointestinal tract (especially inflammatory)
– Parasitosis of gastrointestinal tract
– Genetic predisposition
– Chronic foci of infection in the body
– Poisoning, ecopathology, prolonged abuse of industrial food products
– Endocrine diseases (obesity, hyperthyroidism, diabetes mellitus)
Predisposing factors
The main predisposing factors in the development of BD are: inadequate regulatory mechanisms, and innervation of the nervous system, which is characteristic of childhood, caused by hereditary high excitability and lability of the nervous system, characterized by its violation of the tone of the autonomic component and muscular weakness.
Leading role in the pathogenesis of BD has vegetoneurosis, leading to reductions discoordination gall bladder and sphincter apparatus. The second mechanism of BD is hormonal. In the regulation of bile intestinal hormones play an important role, among which there are both stimulating (cholecystokinin etc.) and inhibitory (glucagon, etc.), the contractile function of the gallbladder. Adverse factors affecting the autonomic nervous system and hormonal regulation, lead to impaired motor function and changes in physico-chemical and bacteriostatic properties of bile.
Depending on the origin of BD two types – primary and secondary are distinguished. Primary dyskinetic violation occurs due to the development of neurohumoral regulation of the biliary system. In this regard, the primary BD often occur in children with a variety of somatoform disorders, or more familiar to our doctors, neurosis, vegetative-vascular dysfunction, diencephalicsyndrome, psychosomatic syndrome in children with neuro-arthritic constitution anomaly. Important role in the development of primary BD is a violation of diet: long intervals between meals, overeating, force-feeding, abuses of oily or spicy food. Risk factors are also transferred acute infection (viral hepatitis, dysentery, salmonellosis), allergic diseases (allergic rhinitis, obstructive bronchitis, atopic dermatitis).
The development of secondary BD is the type of viscero-visceral reflexes in pathological states of digestive organs. As a rule, secondary dyskinetic is caused by chronic cholangitis, chronic duodenitis, chronic enterocolitis, helminthic infestation. Of particular importance is giardiasis (zhiardiaz) of the small intestine. Giardia in the mucosa of the duodenum attach to the microvilli, causing pronounced dystrophic changes in the epithelium.
Pathogenesis
The idea that dyskinesias of the gallbladder are a purely functional disorders is currently under review. Not onlyhypomotoric, but even hypermotoric forms of dyskinesias occur at the level of organic changes of hepatocytes, which is a kind of primary factor contributing to the disruption of not only internal but also extrahepatic biliary tract, including the gallbladder. This pathology is a certain type of cholestasis. However, it does not exclude the role of vascular (neuro) dystonia in the development ofdyskinesias of biliary system. So, two main factors lead to motility disorders:
1. Violation of the functional state of hepatocytes and disholiya (changing composition of bile)
2. Violation of neurogenic regulation of the muscular wall of GB as the central (neurocirculatory dysfunction, neurosis) and peripheral (in the pathology of the gastrointestinal tract-type viscero-visceral reflexes) genesis.
At the same time it is estimated that the BD may be caused by the violation of enteral secretion of hormones (cholecystokinin, motilin, and others) at chronic pathology of duodenal and small intestine. Changes of the rhythm of bile proceed in the intestine reduces the bactericidal properties of the upper gastrointestinal tract, leading to dysbiosis, intestinal dyskinesia. Long-lasting dyskinesia, causing congestion and infection of bile, throw intestinal contents in gall bladder (reflux) leads to cholecystitis. With the predominance of sympatic tone of the nervous system of patients hypotonic dyskinesia is characterized (80% ofdyskinesias), with parasympatic – hypertensive.
Different variants of sphincter of Oddi structure
Classification
hypertonic-hyperkinetic dyskinesia
hypotonic-hypokinetic dyskinesia
Clinical manifestation of hypertonic-hyperkinetic dyskinesia
Duration of the disease up to 1 yr.
Pain syndrome
Dyspeptic syndrome
Manifestations of vegetative dysfunction, neurotic symptoms
Clinical manifestation of hypotonic-hypokinetic dyskinesia
Pain syndrome
Dyspeptic syndrome
Hepatomegaly
Gallbladder symptoms are positive
The clinic is determined by the type of dyskinesias. Most patients have symptoms of neurosis: fatigue, irritability, tearfulness, temper, headaches, palpitations, sweating. In addition, children complained of pain in the right hypochondrium, epigastrium.
In hypertensive form of BD children complain of paroxysmal, stabbing pain in the right hypochondrium or in the right side. Young children show umbilical area. Very rarely pain irradiates in right shoulder and shoulder blade.
The typical symptom of this state is a sharp pain in the right side during fast running or walking fast, due to additional stretching of the capsule and without an enlarged liver with increased inflow of venous blood. Particularly obvious symptom of this is manifested in physical education classes or training, while mobile games, dancing, after the errors in the diet, emotional stress.
The pain is of short duration, easily relieved by antispasmolitics. During the attack the patient may be exited, he suffers nausea, rarely vomiting, palpitations, headache, polyuria. On palpation the abdomen during the attack and after the pain is the most pronounced at the point of the projection of the gall bladder (a symptom of Kera). Outside of acute attack palpation is not painful or there is little pain sensitivity in the right hypochondrium. The liver is not enlarged. The phenomena of intoxication if they are expressed are due to major illness. In the interictal period, children feel good, but occasionally complain of pain briefly spastic character in the epigastrium, right hypochondrium and often in the umbilical region after irritating foods, carbonated drinks and cold food. The pain disappeared spontaneously or after taking antispasmolitics.
Hypotonical form of BD is characterized by almost constant, dull aching pain in his right side. Emotional stress, errors in the diet may increase the pain.
Hypokinetic-hypotonic type of BD occurs more often in children with a predominance of sympathetic tone of the autonomic nervous system. Clinically hypomotor dyskinesia is characterized by dull, often permanent, non-intensive pain in the righthypochondrium, sometimes – the feeling of heaviness, tension in the same area. Under the influence of adverse factors the pain syndrome may be intensified, but seizures that resemble the intensity of hyperkinetic-hypertonic dyskinesia, occur rarely. In children may be signs of dyspepsia: nausea, bitter taste in the mouth, decreased appetite. Palpation of the abdomen reveals the pain in the projection of the gallbladder. In some patients there may be positive Ortner symptom (pain in the heel of hand effleurage on the right costal arch), rarely – Musso (pain in the gallbladder that occurs after pressure on the phrenic nerve between the legs sternocleidomastoid muscle).
Cholestasis is the reason of increasing of the liver, which is soft-elastic, mobile and painless. After duodenal tubing or application of holekinetics its size reduces or normalizes. It should be emphasized that in BD, except for changes in motility of biliary tract, there is a disturbance of homeostatic balance. In the body of the child may develop functional changes in the respiratory, cardiovascular, nervous and other systems. The concentration of bile lipoprotein complex reduces, which is very important in the digestion. These disorders promote dysbiosis, reducing the synthesis of vitamins.
An indispensable companion of the disease is dyspepsia. In children there are decreased appetite and nausea. Often, young patients caot tolerate fatty and sugary foods: after its use they have nausea and vomiting. Sometimes older children complain of a bitter taste in the mouth. Unstable stool appears.
Plan of examination
Fool blood count
Biochemical test of blood:
Serum aminotransferase
Serum bilirubin (predominantly the direct reacting fraction)
Serum alkaline phosphatase
Albumin and globulin level
Stool test
US of the abdominal cavity + cholekynetics for functional investigations
USD of liver
S-form of gall bladder on USD
It is desirable to make the child fractional duodenal intubation.
Phases of bile flow may be characterized briefly as follows.
The first phase is choledochic. In response to the stimulation of duodenal wall transparent light-yellow bile appears. The time of selecting the first portion of bile, the rate of expiration portion A and the total amount of this portion are taken into account.
The second phase – a time of closed sphincter of Oddi. At this stage, the bile is not allocated. It is refractory period: if it is shortened, it means lower the tone of the sphincter of Oddi, unless extended – about hypertension sphincter.
The third phase is a time of the opening of the sphincter of Oddi (in response to the action choletcystokinetic solution) prior to the appearance of gall bile (portion B). Extension of this phase indicates obstructed bile through the cystic duct.
The fourth phase – a period of emptying of the gall bladder (it depends on the tone of his muscles and sphincter Lyutkens). Trouble (interrupted) allocation of portions after the introduction of the stimulus is a sign of stagnation of bile in the gall bladder, hypotension of its muscles and permeability of the cystic duct.
The fifth phase – the selection of hepatic bile (portion C). If, during this phase to re-enter through the probe stimulus, in some patients may be received an additional amount of gall bile (portion B), which indicates incomplete emptying of the gall bladder and hypotension of its muscles.
Biochemical methods are used to determine in portions B and C concentration of bile acids, cholesterol and bilirubin. In children with hyperkinetic disorders of biliary tract cholesterol and lipid complex in the portion B are lower. Inhypokinesia they are increased.
The change of parameters in the various portions of bile depends on the type of dyskinesia. In most cases, bile microscopy reveals a violation of the colloidal equilibrium of bile (an increase in the number of cholesterol crystals, calciumbilirubinate). Very often in children parasites are present in bile – vegetative forms of Giardia, opistarchos eggs, larvaeStroingyloides stercoralis and others.
During duodenal intubation in patients with hyperkinetic and hypertonic form of dyskinesia cystic reflex is labile and sometimes it turns out to magnesium sulphate, and sometimes – after 2-3 hours or not at all apparent. Quantity of B portion is more frequently increased, it flows slowly and is concentrated (spastic cholestasis). In patients with hypokinetic form of dyskinesia cystic reflex is variable, often weak and is observed only in the application of strong stimuli. With the weakening of the sphincter Oddi bile immediately after the introduction of the probe follows, a differentiation portions A, B, C is difficult. Portion B is taken out (more than 60 ml) and long period (time of bile in more than 25 min) due to atopic cholestasis, but the closed sphincter of Oddi is small (less than 3 minutes). The results of ultrasound and contrast cholecystography help to differentiate type of dyskinesia.
Cholangiography
Cholangiography is an examination that uses X-rays and contrast medium (dye) to view your bile ducts. It is often used to see if the bile ducts are blocked, such as in obstructive jaundice, where the bile is blocked from flowing into the duodenum and spills into the blood. Obstructive jaundice can be caused by gallstones blocking the bile ducts.
In the procedure, the contrast medium is injected into the body and a series of X-rays taken to reveal any gallstones, other obstructions or narrowing in the bile ducts.
Several techniques can be used to introduce the dye into the body.
–Percutaneous transhepatic cholangiography (PTC) .The dye is injected through the skin into the bile ducts within the liver (intrahepatic biliary ducts). This is done using ultrasound to guide where the needle goes.
–Intraoperative cholangiography. The dye is injected directly into the bile duct during a gallbladder operation.
–Endoscopic retrograde cholangiopancreatography (ERCP). The dye is injected into the common bile duct and the pancreatic duct through a catheter that’s passed down an endoscope. The endoscope is a thin, flexible lighted tube that is gently passed down your throat and through your stomach, until it reaches the duodenum. Irrespective of how it is introduced, once the dye is in the bile ducts, it can spread into the whole biliary drainage system. Then X-rays can be taken to show up any narrowing or blockages in the drainage system. The resulting radiographic record is called a cholangiogram.
–Magnetic resonance cholangiopancreatography (MRCP)
Magnetic resonance cholangiopancreatography (MRCP) is a relatively new technique for viewing the bile ducts, the pancreatic duct and the gallbladder. No contrast medium has to be administered for MRCP, unlike the other techniques mentioned here. MRCP uses magnetic resonance imaging (MRI) to produce detailed pictures.
Magnetic resonance imaging uses radiofrequency waves directed at the body (you do not feel anything) to excite hydrogen atoms in the molecules of water in your body. This is done in a strong magnetic field, which causes the nuclei of your hydrogen atoms to align. These nuclei emit radio signals when they return to their natural alignment. The signals are used to build up a computerised image that shows differences in body tissues based on the amount of water in them. This enables extremely clear and detailed pictures to be obtained of the bile ducts and pancreatic ducts.
MRCP is an outpatient procedure that involves lying very still in an MRI scanner for several minutes at a time. The entire experience should be over in less than 20 minutes. There is no exposure to radiation, but MRCP is not suitable for people with some types of metal objects in their body — ask the centre performing the test for more details.
MRCP is very safe and effective, with images comparable to ERCP. However, ERCP has the added advantage that therapeutic procedures can be performed at the same time. All these things will be taken into account when deciding which test to order.
The basis of treatment of sick children with BD is an integrated approach. It means that the activities must be carried out in several directions:
Sanitation foci of chronic infection
Antiparasite therapy
Normalization of the immune defense due to normal nutrition and regime
Hypoallergization
Elimination of hypovitaminosis and intestinal dysbiosis.
Nutrition
Nutrition should be chemically, mechanically and thermally gentle (diet 5). Eating is recommended 5-6 times a day to ensure an uninterrupted separation of bile. This takes into account the morning and evening reception dairy products: yogurt, sour milk, etc. Eating should be sought on equal distribution of food during the day. Dinner should be given to children for 2-3 hours before bedtime, and without heavy meat dishes. At BD overeating is unacceptable!
In acute phase extractives are excluded from the diet: pepper, mustard, horseradish, onion, garlic, sorrel, radish, smoked meat, mushrooms, pickled products, meat, fish, spicy sauce. You should not use high-melting fats: lamb, pork, beef or goose fat. Digestion of fats in BD is difficult due to the irregular income of bile in the intestine and reduce the enzyme activity of the pancreas – lipase. There is preferred vegetable oils (sunflower, olive), because their processing does not require a significant amount of bile and enzymes. There are excluded power pastry cream, paste, chocolate, cocoa, and organic coffee, chocolates, oily fish, cold meats with fat.
Treatment of hypertonic-hyperkinetic dyskinesia
1. Diet N 5
2. Spasmolitics:
platyphyllini hydrotartratis (amp. 0.2 % 1 ml)
papaverini hydrochloridum (tab. 0.01, amp. 2 % 2 ml)
no-spa (tab. 0.04 or amp. 2 % 2 ml)
3. Choleretic:
cholagon
allocholum
cholenzynum
galstena
hepabene
Treatment of hypotonic-hypokinetic dyskinesia
1. Diet N 5
2. Prokinetic: motilium, domperidone (tabl. 0.01 g) 1 mg/kg/day
3. Choleretic and cholekinetic drugs:
– cholagon
– allocholum
– cholenzynum
– galstena
– hepabene
– chophytol
A good therapeutic effect has physiotherapy: diadinamothermia, electrophoresis with magnesium sulfate on the liver,ozokerite applications. After the treatment the patient should be within 2-3 months to comply with a light diet. Twice a year, it is expedient to hold a course choleretic therapy, using the collection of medicinal plants, chosen in view of this type of dyskinesia.
Cholecystitis
Cholecystitis is inflammation of the gall bladder.
Causes and pathology
Cholecystitis is often caused by cholelithiasis (the presence of choleliths, or gallstones, in the gallbladder), withcholeliths most commonly blocking the cystic duct directly. This leads to inspissation (thickening) of bile, bile stasis, and secondary infection by gut organisms, predominantly E. coli and Bacteroides species.
The gallbladder’s wall becomes inflamed. Extreme cases may result iecrosis and rupture. Inflammation often spreads to its outer covering, thus irritating surrounding structures such as the diaphragm and bowel.
Less commonly, in debilitated and trauma patients, the gallbladder may become inflamed and infected in the absence ofcholelithiasis, and is known as acute acalculous cholecystitis.
Clinics
Upper right-side abdominal pain
Biliary colic – spasmodic upper abdominal pain
Biliary colic after a fatty meal
Abdominal discomfort
Pain under right shoulder blade
Risk factors in Children
Gallstone disease is relatively rare in children. When gallstones occur in this age group they are more likely to be pigment stones. Girls do not seem to be more at risk than boys are. The following conditions may put children at higher risk:
– Spinal injury
– History of abdominal surgery
– Sickle-cell anemia
– Impaired immune system
– Intravenous nutrition
– Ethnicity
Because gallstones are related to diet, particularly fat intake, the incidence of gallstones varies widely among nations and regions. For example, Hispanics and Northern Europeans have a higher risk for gallstones than people of Asian and African descent do. People of Asian descent who develop gallstones are most likely to have the brown pigment type.
Genetics
Having a family member or close relative with gallstones may increase the risk of gallstones. Up to one-third of cases of painful gallstones may be related to genetic factors.
Defects in transport proteins involved in biliary lipid secretion appear to predispose certain people to gallstone disease, but this alone many not be sufficient to create gallstones. Studies indicate that the disease is complex and may result from the interaction between genetics and environment. Some studies suggest immune and inflammatory mediators may play key roles.
Obesity
Obesity. Being overweight is a significant risk factor for gallstones. In such cases, the liver over-produces cholesterol, which is delivered into the bile and causes it to become supersaturated. Some evidence suggests that specific dietary factors (saturated fats and refined sugars) are the primary culprit in these cases, although studies are conflicting. Animal studies, however, suggest that obesity itself, not any particular foods, triggers the process leading to cholesterol supersaturation and the formation of stones.
Two Types of Cholecystitis:
1. Acute cholecystitis – this type is characterized by a sudden inflammation of the gallbladder that causes abdominal pain. Usually an attack of acute cholecystitis is hastened when a gallstone lodges in the small duct (cystic duct) leading from the gall bladder to the common bile duct.
Symptoms:
Severe pain in the upper right part of the abdomen, just below the breastbone. Often there is also pain in the back or left shoulder blade. Pain usually starts after eating.
Some patients also suffer nausea and vomiting these too are provoked by eating fried and fatty foods.
Jaundice or yellowing of the eyes or skin. Sometimes when a patient has gallstones, a stone may pass out of the gall bladder and lodge in the common bile duct, obstructing the outflow of bile which causes jaundice.
Fever
2. Chronic cholecystitis – is characterized by an inflammation of the gallbladder that lasts a long time. It may be caused by repeat attacks of acute cholecystitis.
Symptoms:
– Nausea
– Abdominal pain
– Indigestion and diarrhea, but some people don’t usually experience any symptoms. The symptoms usually come and go.
Cholecystitis is usually diagnosed by a history of the above symptoms, as well as examination findings. Laboratory and imaging tests (Ultrasound, Cholescintigraphy, CT Scan) are used to confirm the diagnosis and exclude other possible causes.
Distended hydropic and hyperemic gallbladder in acute cholecystitis due to stone obstruction in the gallbladder neck or cystic duct.
LEFT: US of a normal gallbladder after an overnight fast shows the wall as a pencil-thin echogenic line (arrow).
RIGHT: US in the postprandial state shows pseudothickening of the gallbladder.
A
B
A.The normal gallbladder wall is usually perceptible at CT as a thin rim of soft-tissue density that enhances after contrast injection.
B. LEFT: US in patient with acute cholecystitis shows the layered appearance of a thickened gallbladder wall, with a hypoechoicregion between echogenic lines
RIGHT: At contrast-enhanced CT the thick-walled gallbladder contains a hypodense outer layer (arrow) due to subserosaloedema.
Thickening of the gallbladder wall is a relatively frequent finding at diagnostic imaging studies.
A thickened gallbladder wall measures more than 3 mm, typically has a layered appearance at sonography and at CT frequently contains a hypodense layer of subserosal oedema that mimics pericholecystic fluid.
This is a CT scan of the upper abdomen showing cholecystitis (gall stones).
Your diet after cholecystitis treatment is as important and crucial as the surgery itself because of your body’s weakened system.
It is important to implement a cholecystitis diet to your lifestyle if you have recently had surgery or are experiencing symptoms ofchelecystitis.
Acute cholecystitis symptoms can be troublesome, but do not be alarmed. Symptoms can be treated through tweaking a few things in your diet.
Below is a list of some of the best foods to add to your kitchen when implementing a cholecystitis diet.
Diet
1. Olive Oil
Natural olive oil that is raw and unrefined has been proven effective in the natural remedies of acute cholecystitis. Approximately 30 ml of olive oil should be taken upon waking in the morning. You may choose to immediately follow the olive oil with about 100 ml of lemon juice or grapefruit juice. This morning cocktail should be taken every morning for weeks if necessary to eliminate waste and provide successful cholecystitis treatment. The oil can also lessen the likelihood of symptoms of cholecystitis.
2. Raw Beetroot Juice
Raw beet root juice cleanses the system and is great when a patient has experienced symptoms of cholecystitis. Drinking approximately 100 ml of beet juice twice daily will help to eliminate the possibilities of developing acute cholecystitis. Beet juice provides an effective and natural cholecystitis treatment. Beet juice can be used as a preventive measure as well.
3. Black Seed Oil
Black seed oil is a highly effective natural remedy for cholecystitis treatment. If you experience acute cholecystitis it is recommended that your cholecystitis diet include fibrous material that keeps your digestive tract moving. Black seed oil may cause highly loose stools but if taken in moderation can provide the desired effect and cleansing needed.
4. Hemp
By adding approximately two teaspoons or dessert spoonfuls to your cholecystitis diet you caaturally provide yourself with a highly effective cholecystitis treatment from the comforts of your own home. If you have been diagnosed with or experienced symptoms accompanied with cholecystitis, hemp can be beneficial to add to your diet and reduces the risk of acquiring other problems like acute cholecystitis.
5. Lemon Juice
Lemon juice is a great supplemental food to add to water or squirt on top of fish as part of your cholecystitis diet. The acid in the lemon juice breaks down fatty acids in the bile that is digesting the food.
6. Vinegar
Vinegar is an excellent supplemental food to add to dishes when cooking as a part of your cholecystitis diet. Similar to lemon juice, the acid in the vinegar breaks down fatty acids. Symptoms of cholecystitis can be greatly alleviated by incorporating vinegar and lemon juice.
7. Avocados
Avocados are a great food to add to your cholecystitis diet. They contain essential oils that are natural and are rich in vitamins your body needs.
8. Blackberries
Blackberries are rich in fiber and essential nutrients and vitamins that promote a healthy digestive system. Consuming berries every day will eliminate constipation and keep things moving at a steady rate. Your cholecystitis diet after treatment is important and at least two servings of berries each day can provide your body with important nutrients it requires to function properly.
9. Lecethin Granuals
By adding approximately two teaspoons or dessert spoonfuls of lecithin granules to your cholecystitis diet you caaturally provide yourself with a highly effective cholecystitis treatment from the comforts of your own home.
10. Dandelion
Drinking approximately 125 ml of dandelion juice daily can prevent acute cholecystitis symptoms from occurring. This is a great herb to add to your cholecystitis diet.
Treatment:
Patient will need to stay in the hospital, and are given antibiotics (intravenously) to treat infections and other medications are also given to control abdominal pain and vomiting.
CC is most often treated by the surgical removal of the gall bladder to prevent symptoms from coming back. In some chronic cases if the risk of surgery is high or if the symptoms are not severe the doctor may simply recommend a diet that is low in fat.
Chronic pancreatitis
Chronic pancreatitis is inflammation of the pancreas that does not heal or improve—it gets worse over time and leads to permanent damage. Chronic pancreatitis, like acute pancreatitis, occurs when digestive enzymes attack the pancreas and nearby tissues, causing episodes of pain.
The chronic form of pancreatitis can be triggered by one acute attack that damages the pancreatic duct. The damaged duct causes the pancreas to become inflamed. Scar tissue develops and the pancreas is slowly destroyed.
Other causes of chronic pancreatitis are
– hereditary disorders of the pancreas
– cystic fibrosis—the most common inherited disorder leading to chronic pancreatitis
– hypercalcemia—high levels of calcium in the blood
– hyperlipidemia or hypertriglyceridemia—high levels of blood fats
– some medicines
– certain autoimmune conditions
– unknown causes
Episodes of abdominal pain and diarrhea lasting several days come and go over time and can progress to chronic pancreatitis. A diagnosis of hereditary pancreatitis is likely if the person has two or more family members with pancreatitis in more than one generation.
Clinics
Most patients with chronic pancreatitis experience upper abdominal pain, although some have no pain at all. The pain may spread to the back, feel worse when eating or drinking, and become constant and disabling. In some cases, abdominal pain goes away as the condition worsens, most likely because the pancreas is no longer making digestive enzymes.
Other symptoms include
nausea
vomiting
weight loss
diarrhea
oily stools
Patients with chronic pancreatitis often lose weight, even when their appetite and eating habits are normal. The weight loss occurs because the body does not secrete enough pancreatic enzymes to digest food, so nutrients are not absorbed normally. Poor digestion leads to malnutrition due to excretion of fat in the stool.
Diagnosis
Chronic pancreatitis is often confused with acute pancreatitis because the symptoms are similar. As with acute pancreatitis, the doctor will conduct a thorough medical history and physical examination. Blood tests may help the doctor know if the pancreas is still making enough digestive enzymes, but sometimes these enzymes appear normal even though the person has chronic pancreatitis.
In more advanced stages of pancreatitis, when malabsorption and diabetes can occur, the doctor may order blood, urine, and stool tests to help diagnose chronic pancreatitis and monitor its progression.
After ordering x rays of the abdomen, the doctor will conduct one or more of the tests used to diagnose acute pancreatitis—abdominal ultrasound, CT scan, EUS, and MRCP.
Treatment
Treatment for chronic pancreatitis may require hospitalization for pain management, IV hydration, and nutritional support. Nasogastric feedings may be necessary for several weeks if the person continues to lose weight.
When a normal diet is resumed, the doctor may prescribe synthetic pancreatic enzymes if the pancreas does not secrete enough of its own. The enzymes should be taken with every meal to help the person digest food and regain some weight. The next step is to plan a nutritious diet that is low in fat and includes small, frequent meals. A dietitian can assist in developing a meal plan. Drinking plenty of fluids and limiting caffeinated beverages is also important.
Complications
As with acute pancreatitis, ERCP is used to identify and treat complications associated with chronic pancreatitis such as gallstones, pseudocysts, and narrowing or obstruction of the ducts. Chronic pancreatitis also can lead to calcification of the pancreas, which means the pancreatic tissue hardens from deposits of insoluble calcium salts. Surgery may be necessary to remove part of the pancreas.
In cases involving persistent pain, surgery or other procedures are sometimes recommended to block the nerves in the abdominal area that cause pain.
When pancreatic tissue is destroyed in chronic pancreatitis and the insulin-producing cells of the pancreas, called beta cells, have been damaged, diabetes may develop. Patients with a family history of diabetes are more likely to develop the disease. If diabetes occurs, insulin or other medicines are needed to keep blood glucose at normal levels. A health care provider works with the patient to develop a regimen of medication, diet, and frequent blood glucose monitoring.
Chronic hepatitis
Chronic hepatitis is inflammation of the liver that lasts at least 6 months.
Common causes are hepatitis B and C viruses and drugs.
Many patients have no symptoms until the liver has become severely scarred.
Chronic hepatitis can result in cirrhosis, with an enlarged spleen, fluid accumulation in the abdominal cavity, and deterioration of brain function. A biopsy is done to confirm the diagnosis.
Drugs, such as antiviral drugs or corticosteroids, may be used, and for advanced disease, liver transplantation may be needed.
Chronic hepatitis, although much less common than acute hepatitis, can persist for years, even decades. In most people, it is quite mild and does not cause significant liver damage. However, in some people, continued inflammation slowly damages the liver, eventually resulting in cirrhosis (severe scarring of the liver), liver failure, and sometimes liver cancer.
Cirrhosis
CLASSIFICATION
– Viral
Hepatitis B
Hepatitis C
Hepatitis D
– Autoimmune
– Drug induced
– Metabolic
Causes
Chronic hepatitis is usually caused by one of the hepatitis viruses. Hepatitis C virus causes about 60 to 70% of cases, and at least 75% of acute hepatitis C cases become chronic. About 5 to 7% of hepatitis B cases, sometimes with hepatitis D co-infection, become chronic. Hepatitis A and E viruses do not cause chronic hepatitis.
Certain drugs can cause chronic hepatitis, particularly when they are taken for a long time. They include isoniazid, methyldopa, nitrofurantoin and, rarely, acetaminophen.
Drug Related
– Dose related: 6 MP, methotrexate and acetaminophen
– Idiosyncratic: phenytoin, phenobarbital and carbamezipine
|
Acetaminophen |
Erythromicin |
|
Halothane |
Estrogen |
|
Valporic Acid |
Anabolic steroids |
|
Isoniazide |
Ceftriaxone |
|
Sulfonamides |
Cyclophosphamide |
|
Phenytoin |
OCP |
|
Methotrexate |
Chlorpromazine |
|
Metabolic Wilson Disease |
|
|
Alpha 1 anti-trypsin deficiency |
|
|
Tyrosiniemia |
|
|
Niemann-Pick disease type 2 |
|
|
Glycogen storage Disease IV |
|
|
Cystic Fibrosis |
|
|
Galactosemia |
|
|
Bile Acid Synthetic Abnormalities |
|
Wilson’s disease, a rare hereditary disorder involving abnormal retention of copper in the liver, may cause chronic hepatitis in children. Other causes include alcoholic hepatitis, fatty liver not due to alcohol use (nonalcoholic steatohepatitis), and alpha1-antitrypsin deficiency (a hereditary disorder).
No one knows exactly why a particular virus or drug causes chronic hepatitis in some people but not in others or why the degree of severity varies. In many people with chronic hepatitis, no obvious cause can be found. In some of these people, the chronic inflammation resembles inflammation caused by the body attacking its own tissues (an autoimmune reaction, but this connection has not been proven. This type of inflammation called autoimmune hepatitis, is more common among women than men.
Clinics
In about two thirds of people, chronic hepatitis develops gradually without causing any obvious symptoms until cirrhosis occurs. In the remaining one third, it develops after a bout of acute viral hepatitis that persists or returns (often several weeks later).
Symptoms often include a vague feeling of illness (malaise), poor appetite, and fatigue. Sometimes affected patients also have a low-grade fever and some upper abdominal discomfort. Jaundice is rare.
Complications of chronic liver disease and cirrhosis may eventually develop. They can include an enlarged spleen, spiderlike blood vessels in the skin, redness of the palms, and accumulation of fluid in the abdominal cavity. Liver malfunction may lead to deterioration of brain function (hepatic encephalopathy), particularly in people with cirrhosis due to hepatitis C.
Spiderlike blood vessels in the skin
Redness of the palms
Skin hemorrhagies Pigmentation of skin
Nose hemorrhagies
Autoimmune hepatitis may cause other symptoms that can involve virtually any body system, especially in girls. Such symptoms include acne, cessation of menstrual periods, joint pain, lung scarring, inflammation of the thyroid gland and kidneys, and anemia. Often there are scratches of the skin.
Scratches and formed as a result of these cracks on the skin are a gateway for infection.
In many people, chronic hepatitis does not progress for years. In others, it gradually worsens. The outlook depends partly on which virus is the cause:
Chronic hepatitis C leads to cirrhosis, which develops over a period of years, in about 15 to 25% of people. The risk of liver cancer is increased but only if cirrhosis is present.
There are many signs of cirrhosis that provider may find. It may have red palms or small spider-like veins on the face or body.
Cirrhosis: Another problem caused by high pressure in the veins of the liver is ascites. Fluid leaks out into the belly and it begins to fill it up. This can make the abdomen enlarge like a balloon filled with water. The legs can get swollen too.
Chronic hepatitis B tends to worsen, sometimes rapidly, and increases the risk of liver cancer.
Chronic co-infection with hepatitis B and D causes cirrhosis in up to 70%.
Autoimmune hepatitis can be effectively treated in most people, but some develop cirrhosis, with or without liver failure.
Chronic hepatitis caused by a drug may completely resolve once the drug is stopped.
Diagnosis
Discrimination between hepatitis A and B is becoming easier as the serologic and clinical characteristics of each type become better known. Hepatitis A is generally a benign pediatric illness with few sequelae. In contrast, hepatitis B is more often associated with complications and may progress to chronic liver disease in as many as 10% of cases. Chronic persistent hepatitis appears to be a benign disorder not requiring therapy. Occasionally related etiologically to virus B, chronic active hepatitis is often associated with severe clinical illness. However, it generally responds to steroid therapy, at least initially, and may be arrested or cured.
Diagnostic criteria related to CH include the following
Chronic hepatitis B: HBsAg positive for more than six months, serum HBV DNA greater than 20,000 IU per mL (lower values of 2,000 to 20,000 IU per mL often occur with HBeAg-negative chronic hepatitis B), persistent or intermittent elevation in alanine transaminase (ALT) or aspartate transaminase (AST) levels, and liver biopsy showing chronic hepatitis with moderate or severe necroinflammation.
Inactive HBsAg carrier state: HBsAg positive for more than six months, HBeAg negative and anti-HBeAg positive, serum HBV DNA less than 2,000 IU per mL, persistently normal ALT and AST levels, liver biopsy confirming absence of significant hepatitis.
Resolved hepatitis B: known history of acute or chronic hepatitis B or the presence of anti-hepatitis B core antigen (anti-HBcAg) with or without anti-HBsAg, HBsAg negative, undetectable serum HBV DNA (very low levels may be detectable with sensitive prostate-specific antigen assays), and normal ALT levels. Hepatitis B S Ag > 6 months
– Variable biochemical tests
– Congenital ( 85% rate) or acquired
– Other Markers: DNA PCR, HBe Ag, Anti-HB c , Anti- HB e
– 1-5% of acute attacks become chronic
– 70 % cirrhosis
– HCC carcinoma ( monitor alpha fetoprotein)
Doctors may suspect hepatitis C when patients have typical symptoms, when blood tests to evaluate liver function are abnormal, or when they have had hepatitis C before. Blood tests are done and may help establish the diagnosis, identify the cause, and determine the severity of liver damage. However, a liver biopsy is essential for a definite diagnosis. The liver biopsy also enables a doctor to determine how severe the inflammation is and whether any scarring or cirrhosis has developed. The biopsy may help identify the cause of hepatitis. Occasionally, a biopsy needs to be done more than once.
If people have chronic hepatitis B, ultrasonography and blood tests to measure alpha–fetoprotein levels are done annually to screen for liver cancer. Levels of alpha–fetoprotein (a proteiormally produced by immature liver cells in fetuses) usually increase when liver cancer is present. People with chronic hepatitis C are screened similarly, but only if they have cirrhosis.
Contrast Harmonic Imaging
Contrast harmonic imaging (CHI) is a new Doppler technology using the non-linear properties of ultrasound contrast agents. CHI is promising to further improve the differential diagnosis of liver lesions and the detection of metastases.
Magnetic Resonance Imaging (MRI)
A new technique uses a modified form of Magnetic Resonance Imaging (MRI) to accurately measure the elasticity of the liver. By applying vibrations to the liver, MRE obtains pictures of the mechanical waves passing through the organ. The wave pictures are then processed to generate a quantitative image of tissue stiffness.
Noninvasive Approaches Offer Substantial Market Potential in Liver Disease
Diagnostics
Novel noninvasive liver diagnostics tests have a good potential to revolutionize the diagnosis in hepatology. Up to now liver biopsy is widely considered the diagnostic gold standard for the diagnosis of liver fibrosis and liver cirrhosis. However, biopsy as an invasive procedure is not appropriate for all patients with liver disease. There fore noninvasive liver diagnostics tests might play a significant role in the management of patients with liver disease.
Abdominal ultrasound shows hyperechoic fibrotic tissue around the portal vein (p) and the hepatic hilus. (a: aorta, v: vena cava; p: portal vein; gb: gallbladder).
Encephalopathy
A liver that is working poorly may not be able to get rid of toxic substances like ammonia (which comes from the intestines), and it may allow these substances to go into the brain and cause confusion.
Besides confusion, toxins in the brain cause changes in sleep, mood, concentration, and memory. If it gets really bad, it can even cause a coma.
These are all symptoms of hepatic encephalopathy. If there is encephalopathy, may be problems driving, writing, calculating, and performing other activities of daily living. Signs of encephalopathy are trembling and hand “flapping.”
Encephalopathy may occur when there is an infection or internal bleeding, and it may also occur if patients are constipated or take too many water pills or take tranquilizers or sleeping pills.
Algorithm for the management of chronic HBV infection. (ALT = alanine transaminase; HBeAg = hepatitis B e antigen;HBsAg = hepatitis B surface antigen; HBV = hepatitis B virus.)
If a drug is the cause, the drug is stopped. If another disorder is the cause, it is treated.
Hepatitis B and C: People with progressive chronic hepatitis B or C are usually given antiviral drugs. For hepatitis B,entecavir, adefovir or lamivudine is usually used. These drugs are taken by mouth, as is telbivudine , a new drug for which little information is available. Interferon-alpha or pegylated interferon-alpha, given by injection under the skin, may be used instead of an oral drug. Hepatitis B tends to recur once drug treatment is stopped and may be even more severe. Thus, an antiviral drug may need to be taken indefinitely.
For hepatitis C, pegylated interferon-alpha plus ribavirin is most effective. This combination may stop the inflammation. After taking these drugs for 6 months to 1 year, 45 to 75% of patients improve and have no further problems.
Antiviral drugs used to treat chronic hepatitis commonly cause side effects. Lamivudine may have fewer side effects than the others. These drugs should not be taken by patients who have certain conditions:
– Advanced cirrhosis due to hepatitis B
– A transplanted organ
– A reduced number of blood cells (cytopenia), such as red blood cells (anemia)
– Substance abuse.
If family members and close contacts of people with chronic hepatitis B have not been vaccinated, they should be. They are also given hepatitis B immune globulin. Such measures are not necessary for chronic hepatitis C.
Autoimmune Hepatitis: Usually, corticosteroids (such as prednisone) are used, sometimes with azathioprine , a drug used to suppress the immune system. These drugs suppress the inflammation, relieve symptoms, and improve long-term survival. Nevertheless, scarring in the liver may gradually worsen. Stopping these drugs usually leads to recurrence of the inflammation, so most people have to take the drugs indefinitely.
Complications:
Regardless of the cause or type of chronic hepatitis, complications require treatment. For example, treating ascites involves restriction of salt consumption, bed rest, and sometimes drugs. If brain function deteriorates, eliminating protein from the diet can help.
Liver Transplantation
Transplantation may be considered for patients with severe liver failure. However, in patients who have hepatitis B or hepatitis C, the virus tends to infect the transplanted liver. In patients with hepatitis B, the virus tends to severely damage the transplanted liver over months or a few years, but taking lamivudine may improve the outcome. In patients with hepatitis C, the virus virtually always recurs in the transplanted liver, but the infection is usually so mild that people are likely to survive for many years.
This gift of new life brings its own set of potential complications and requires lifelong medications to prevent rejection. Liver transplantation is considered for people in situations such as these:
When other medical or surgical treatments have failed to correct the life-threatening problems caused by cirrhosis
To treat some cancerous tumors of the liver or bile ducts such as hepatocellular carcinoma
To correct abnormalities in metabolism or anatomical function that may limit long-term health and are cured by liver transplant
Children who are born with congenital disorders
In the pediatric experience, survival of both the recipient and the transplanted liver (graft) at 1 year is about 90%. Donor complications have been very few.
Prevention
There have been safe and effective, active and passive immunisation preparations for hepatitis B for more than 30 years. Worldwide, the primary mode of transmission of the virus is from mother to newborn baby. The earlier this infection is acquired the more likely chronic hepatitis will evolve.
Perinatal transmission can be effectively interrupted by passive immunisation of the newborn baby with hepatitis B immune globin, together with a series of three active vaccinations starting at birth and given over the subsequent 6 months of life.
Universal vaccination throughout the world has been underway to varying degrees for many years and ultimately should sharply reduce the prevalence of hepatitis B disease, in particular the risk of HCC. An estimated 400 million people now have active hepatitis B.
Unfortunately, there are neither passive nor active vaccines for hepatitis C virus. Most hepatitis C in the world is a result of parenteral transmission either by transfusion of blood products or, more commonly, re-use of syringes, needles, or both. The introduction of blood-donor screening for hepatitis C virus some 16 years ago, as well as hepatitis B virus 35 years ago in developed countries, has virtually eliminated post-transfusion hepatitis. Unfortunately, in underdeveloped countries, particularly in rural areas, blood products remain infected. Concerted efforts toward implementing sterile technique and the use of disposable needles and syringes, mainly in health-care settings, are much needed. A more difficult challenge is the worldwide prevention of illicit drug use, as well as treating infected drug users.
For those already infected with hepatitis C, most will develop chronic hepatitis. 30% will develop cirrhosis over a 30-year period and will subsequently develop associated complications, in particular HCC. Pegylated interferon with ribavirin can successfully eradicate this viral infection in around 50% of patients. However, this therapy is expensive and the treatment is fraught with side-effects. There are phase II clinical trials underway assessing the safety and efficacy of orally administered antivirals (eg, protease and polymerase inhibitors) that hopefully will eventually lead to even more effective therapy with fewer side-effects. The incidence of HCC secondary to chronic hepatitis C is rising. Some of these patients can be treated with liver transplantation andtumour ablative techniques but, unlike hepatitis B, recurrent infection with hepatitis C virus is almost 100% in recipients of liver transplantation.
Acute liver failure
Acute liver failure (ALF) is a broad term and encompasses both fulminant hepatic failure (FHF) and subfulminant hepaticfailure. It is a rare but potentially fatal disease, especially if complicated by hepatic encephalopathy and impaired protein synthesis.Incidence of acute liver failure is low only about 2000 cases annually occurring in the US.
More than 350 million people worldwide are inflicted by Hepatitis B Virus and about 170 million by Hepatitis C. 20% ofthose patients with chronic viral hepatitis might develop liver cirrhosis which might end in the need of a liver transplantation (LTx).
Today many patients in hepatology who develop acute liver failure recover with supportive treatment but with continueddeterioration or having adverse prognostic factors, orthotopic liver transplantation (OLT) is often required. Approximately 6% ofOLTs performed in the United States are for fulminant hepatic failure (FHF). Prior to orthotopic liver transplantation (OLT) for FHF,the mortality rate was generally greater than 80%. However, with improved intensive care, the prognosis is much better now than inthe past, with some series reporting approximately a survival rate of 60%.
Infectious Acute Liver Failure
In many countries viral hepatitis is a common cause for FHF, especially hepatitis A and hepatitis B, it is extremely uncommonin hepatitis C. Survival rates in HAV patients with FHF are about 50-60%, much more favourable than the outcome for patients withother hepatitis. These patients account for a substantial proportion (10-20%) of the pediatric liver transplants in some countriesdespite the relatively mild infection that is observed in many children infected with HAV. In the developing world, acute HBVinfection dominates as a cause of FHF.
Another cause for an infectious acute liver failure may be a sepsis.
A hepatic coma is observed relatively rarely and is connected with the severe diseases which will destroy liverparenchima(infectious viral hepatitis, cirrhosis of liver, poisoning by mushrooms). It is conditioned by insufficiency of detoxinfunction of liver which promote to penetration of toxins in CNS. At a hepatic coma in most cases the comatose state develops gradually, thus deep disorders of consciousness are rarely.
Other causes for acute liver failure include:
o Acute Fatty Liver (as a result of pregnancy, tetracyclines, alcohol or Reye syndrome)
o Multi Organ/Liver Failure after heart surgery
o The HELLP (hemolysis, elevated liver enzymes and low platelets) syndrome occurs in 0.1-0.6% of pregnancies and usually is associated with preeclampsia.
o Wilson’s Disease (hereditary copper accumulation) may infrequently present with acute liver failure. Without OLT, this is almost uniformly fatal.
o Ischemic Liver Failure after surgical procedures and occlusion of hepatic artery.
o Cryptogenic Acute Liver Failure (for nearly 15% of patients in the US, the cause of the acute liver failure remains indeterminate)
Differential Diagnoses
Alpha-1-antitrypsin deficiency
All causes of Neonatal Jaundice
A clinic is characterized by psychical excitation with the signs of hallucinations, dellirium, conditioned reflexes are low-spirited with saving of unconditioned reflexes. Muscular tone and tendon reflexes are promoted, quite often there are the meningeal signs. An icterus is a permanent sign. As a result of change of formation of prothrombini and oppression of thromocytopoesis there are bleeding from a skin and mucus membranes. Breathing is deep, toxic, from a mouth sweetish smell of fresh liver is hearihg.Tachycardia, increased tones of heart, arterial blood pressure is low. A liver at first is enlarged. In the period of development of coma quickly becomes soft and decrteased (yellow dystrophy of liver). In a blood: hyperbilirubinemia due to direct faction,hypernitrogenemia, hyperproteinemia. In urine: aminiaciduria, proteinuria, cylinduria, billiar pigments.
|
Signs |
Hypochloremic |
Hepatic |
Acetonemic(nondiabetic) |
|
|
Previous or basic disease |
Diseases which are accompanied by vomit |
Disease of liver: infectious hepatitis,hepatocholengitis, innate and acquired cirrhosis of liver |
Having a fever diseases, cyclicacetonemic vomit |
|
|
Beginning |
Slow |
Gradual |
Gradual |
|
|
Consciousness |
Gradual loss of consciousness |
Gradual development of the comatose state, which passes through all stages, but rarely reaches to the deep coma, hallucinations and delirium |
Oblivion, somnolence, passes through all stages, sopor, coma |
|
|
Motive activity |
Adynamia, tetania,hyperreflection, catalepsy, fibric convultions |
Spastics, that reaches tocontructure, increased reflexes, meningealsymptims |
Blood pressure is low, and reflexes are reduced |
|
|
Convultions |
– |
– |
Rarely |
|
|
Breathing |
Encreased, superficial, unpleasant smell from a mouth |
Deep, toxic (Kussmaul), smell of raw liver (meat) |
Deep, toxic, strong smell of acetone from a mouth |
|
|
Cardio-vascular changes |
Deaf tones, low АP speed-up soft pulse, arrhythmia |
Tachycardia, palpitation, blood pressure is low, soft incomplete filling pulse |
Deaf cardiac tones, soft pulse low АP |
|
|
Changes of digestion |
Absence of appetite, diarrhea and vomit |
Vomit, pneumatic stomach, increase of spleen |
Absolute absence of appetite, massive vomit |
|
|
Liver |
Depending on the basic disease |
Decreased |
Increased, sickly |
|
|
Eyes |
Pupils wide |
Pupils are extended |
Without the changes |
|
|
Skin |
Turgor is diminished and elasticity |
Dry icteric or subicteric, slightly swollen, point hemorrhage |
Dry, pale, cheeks are red |
|
|
Edemata |
Absent |
Small |
Absent |
|
|
Blood |
Leucocytosishypochloremia,alcalosis |
Direct billirubin (+++), increase of products of disintegration |
Hypochloremia,acidoketonemiaabsence ofhyperglucemia |
|
Urine |
Oliguria, anuria, albumen (+), a little amount of form elements |
Billirubin (++), at acute yellow atrophy decreases,aminoacidiria (leycini,tirosini), insignificant albuminuria |
Acetone,acetovinegar acid,glucosuria (-) |
Help on a prehospital stage at a hepatic coma
1. Oxygentherapy by an oxygen pillow.
2. At convultions – 20 % solution of Oxybutiratis sodium 50-100 mg/kg of mass intravenously streamly slowly on 10-15 ml 10 % Glucose or 0,5 % solution of Seduxeni 0,1 ml/kg of of mass intravenously streamly or intramuscular.
3. After help and at diminishment of clinical sings hospitalization. During transporting intravenous in drops introduction of isotonicisolution of sodium chloride.
Help on a hospital stage
1. Infusion therapy. Common amount of liquid for introduction – 60-70 % age-old necessity: 2/3 day’s volume the liquid – Glucose 5-10 % solution, other (1/3 liquids) are expanders, salt solutions (Reopoliglucini, isotonic solution of sodium chloride, the Ringer solution).
2. Cocarboxylazae 5 mg/kg of mass, 5 % solution of ascorbinati sodium 150-500 mg intravenously streamly.
3. Glucocorticoids ( Prednisoloni a 5-10 mg/kg of mass on day) by even doses in 3-4 hours without the nightly interruption intravenously streamly.
4. Intravenously in drops ingibitors of proteolysis: Trasiloli, Gordox to 100 000-250000 U daily, Contricali to 50000 U daily (in 3-4 introductions).
5. At hypokaliemia intravenously in drops 4 % or 7,5 % solution of potassium chloride in a dose 2 mmol/kg daily (1 ml 7,5 % to solution contains 1 mmol/l of potassium).
6. Syngrom therapy:
– at convultions: 20 % solution of Oxybutiratis sodium 50-100 mg/kg of mass or 0,5 % solution of Seduxeni 0,1 ml/kg of ofmass intravenously streamly slowly on 10 ml 5-10 % Glucose;
– at edema syndrome: 1 % of Lasix solution 1-3 mg/kg of mass daily intramuscular or intravenously streamly; Mannitoli 1-3 g/kg of the mass on one introduction (as 30 % solution) intravenously in drops;
– at cardiac insufficiency: 0,06 % Corgliconi solution or Strophantini 0,05% 0,01-0,015 ml/kg intravenously streamly on 10 mlisotonici solution of sodium chloride;
– at a hemorrhagic syndrome: 5 % solution -aminocaproni acids 0,1 ml/kg of the mass for one occasion dose intravenously indrops; 1 % solution of Vicasoli 0,5-1,0 ml intramuscular 1-2 times per day ; 10 % solution of calcium gluconati a 1 ml/yr of life intravenously streamly; Fibrinogeni intravenously in drops 1,5-2 mg/kg of the mass daily.
7. Antibiotics (Pennicillini, Cephalosporins).
8. In absence of effect from base treatment — replaceable blood transfusion, hemosorbtion, amino acid dialysis with nextPlasmophoresis, transplantation of liver.
Reye Syndrome (acute hepatic encephalopathy) is a malignant syndrome at the infectious diseases. Conditioned superfluously by acute hepatic insufficiency with the metabolic disturbance, that arises up at the acute viral diseases treated by the high doses of salicylics. Inherent to the children, thus than junior child, the more frequent it meets.
Definition
Reye syndrome is sudden (acute) brain damage (encephalopathy) and liver function problems of unknown cause.
The syndrome has occurred with the use of aspirin to treat chickenpox or the flu in children. However, it has become very uncommon since aspirin is no longer recommended for routine use in children.
Саrdiac arrhythmias (Greek arrhythmia is the lack rhythm) are
various functional disorders of automatism, excitability and conductivity of the myocardium, often resulting in failure of normal sequence, or heart rate.
Etiology
Cardiac arrhythmias may be caused by:
Ø – functional disorders (psychogenic, reflex)
Ø – organic disorders (heart disease, cardiomyopathy,
myocardiodystrophy, carditis, etc.)
Ø – toxic disorders (eg, an overdose of drugs digitalis)
Ø-hormonal disorders (eg, imbalance of hormones thyroid)
Ø – electrolyte disturbances (eg, changes in the level of potassium in the blood)
Ø – mechanical disorders (surgery, trauma)
Ø – congenital disorders (eg, WPW syndrome).
Types of Arrhythmia in Children
There are many different kinds of abnormal heart rhythms. If an abnormal rhythm occurs, it’s important to find out what kind it is. Treatment recommendations depend on its type. Arrhythmias can cause the heart rate to be irregular, fast or slow. Fast rhythms are called tachycardia. Slow ones are called bradycardia.
Causes:
Causes of fast heart rate (Tachycardia):
– Supraventricular Tachycardia
– Atrioventricular nodal reentrant tachycardia
– Atrioventricular reentrant tachycardia including WPW syndrome
– Others
– Ectopic atrial tachycardia
– Atrial flutter
– Atrial fibrillation
– Ventricular tachycardia
– Ventricular fibrillation
Causes of slow heart rate (Bradycardia):
– Sick sinus syndrome
– Various degree of heart block
Premature atrial contraction (PAC) and premature ventricular
contraction (PVC)
– Tachycardia
– Supraventricular tachycardia (SVT)
– Wolff-Parkinson-White syndrome
– Ventricular tachycardia (VT)
– Bradycardia
– Sick sinus syndrome
– Complete heart block
ECG diagnostics
Premature beats or extra beats most often cause irregular heart rhythms. Those that start in the upper chambers (atria) are called premature atrial contractions or PACs. Premature ventricular contractions or PVCs start in the ventricles. If you’ve ever had the feeling that your heart “skipped a beat,” it was probably from this type of arrhythmia. The heart really doesn’t skip a beat. Instead, an extra beat comes sooner thaormal. Then there’s usually a pause that causes the next beat to be more forceful. You felt this more-forceful beat.
Often the cause of VPBs is not known. They can happen even though you may have a normal, healthy heart.
Sometimes, something happens to make a part of the heart’s ventricle muscle electrically unstable, causing the extra heartbeat. The electrical instability can be caused by:
a scar in the heart muscle
too little oxygen getting to the muscle because of heart disease
medicines such as pseudoephedrine
a blow to the chest
imbalance of electrolytes (body minerals) in the body.
An electrocardiogram (ECG) is the only test that can confirm a diagnosis of VPBs. The ECG records the electrical activity of your heart. A 24-hour tape recording of the ECG shows when you have VPBs. It also shows how many occurred. These recordings can help your healthcare provider decide on treatment.
Tachycardia
A fast heart rate is called tachycardia. The definition of “too fast” usually depends on the person’s age and physical activity. A newborn has tachycardia if the resting rate is more than 160 beats per minute. A teenager is considered to have tachycardia if the resting heart rate is more than 90 beats per minute. An exercising teenager may have a normal heart rate of up to 200 beats per minute.
Paroxismal tachycardia
Paroxismal tachycardia is the attacks of acute tachycardia (more than 150-180 per 1 minute), which arises up suddenly and lasts from a few seconds to a few hours. The reasons of paroxismal tachycardia are various: congenital pathology of the explorer system of heart (the WPW syndrome), organic heart diseases, neurovegetative disturbances of organism, acute infectious diseases etc. There is the ektopic nidus of excitation in some area of myocardium or explorer system, which sends the impulse of high- frequency and becomes the driver of cardiac rhythm. Acute increasing of cardiac contractions diminishes efficiency of separate paroxismal tachycardia, causes diminishment of percussion volume of heart and violation of blood circulation . Blood supply of organs, tissues and heart are diminished. It predetermines violation of exchange processes in myocardium. As a result of attack of paroxismal tachycardia there is coronal insufficiency and insufficiency of circulation of blood. Depending on localization of pathological nidus the supraventricular and abdominal forms of paroxismal tachycardia are distinguished.
Clinic. The attack of tachycardia begins suddenly. Children complain on the unpleasant feelings in the region of heart, squeezing pain in a breast, pain in a epigastrial area. Quite often the attack is accompanied by dizziness, vomit. Children often feel fear. Skin is pale, cyanosys appears sometimes, swelling and pulsation of neck veins are present. The signs of cardiac insufficiency occur with the long duration attack: cyanosys increases, the shortness of breath appears, enlargement of liver, oliguria, the edema. Pulse of the weak filling, frequency cardiac contractions arrives at 150-300 per 1 minute. Cardiac tones are increased, embriocardia. Arterial pressure is reduced.
Diagnostics of paroxismal tachycardia at the children of breast-feeding age is difficulte. The common state of child is severe, that is related to the signs of cardiac insufficiency. Quite often the attack is accompanied by pneumonia, myocarditis, fibroelastosis of heart and other pathology. The diagnosis and determination of form of paroxismal tachycardia is conducted by electrocardiography. The general electrocardiography criteria of paroxismal tachycardia are: outbreak and sudden end, absence of compensating pause, frequency of cardiac contractions more than 150 per 1 minute, presence of 3 and anymore group of extrasystols. In addition, for supraventricular paroxismal tachycardia characteristically are: presence of the unusual indent Р (at atria form) and its absence at a аrtrioventricular form, well-kept form of the QRS complex, duration of the QRS complex not more than 0,12 seconds. At abdominal paroxismal tachycardia always indent Р is absent, the QRS complex is deformed and extended (more than 0,12seconds),it is marked presence of аrtrioventricular dissociation.
This exercise electrocardiogram shows wide QRS tachycardia during exercise. The recovery ECG arly shows atrial flutter with variable conduction. The rest ECG probably represents atrial flutter with 2:1 conduction rather than sinus rhythm. Exercise testing helped establish this atrial arrhythmia.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p 210.)
Severe sinus arrhythmia in a 15-year-old boy was detected by a Holter monitor during sleeping and waking (this tracing) hours. The patient also had severe sinus bradycardia with dizziness and syncope.
A permanent pacemaker was implanted, and the patient had no further symptoms.
Paper speed was 25 mm/s, and calibration was 1 mV/10 mm.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p 255.)
An example of complete AV block. Note the lack of conduction to the ventricle of P waves occurring after the T wave.(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, р. 307.)
Standard 12-lead electrocardiogram showing atrial flutter with classic “sawtooth” flutter waves in leads II, III, aVF, V<SB:0.039>1</SS>, V<SB:0.039>2</SS>, and V<SB:0.039>3</SS>.
There is 4:1 atrioventricular conduction. (From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p 334.)
Standard 12-lead electrocardiogram showing atrial flutter with undulating P waves in all leads.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p 335.)
Atrial flutter with 1:1 atrioventricular conduction. <IT+>Top panel:<IT-> Surface electrocardiogram (ECG).
<IT+>Bottom panel:<IT-> Atrial electrogram (AEG). Small arrows show the atrial activity at approximately 300 bpm; the atrial polarity changes midway through the tracing; initially the atrial deflections are positive, and later they are negative. Large arrows point to ventricular activation.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p 346.)
IT+>A,<IT-> Sinus tachycardia, rate 200–230/min. P waves are clearly visible, with normal P wave axis. <IT+>B,<IT-> Supraventricular tachyarrhythmia, rate 230/min. P waves are clearly visible with an abnormal P wave axis. (From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p393.)
Atrial flutter with varying second-degree AV block.
Ventricular tachycardia alternating with sinus rhythm.
Arrows mark fusion complexes.
(From Gillette PC, Carson A Jr (eds): Pediatric Arrhythmias. Philadelphia, WB Saunders, 1990, p 393.)
Sinus tachycardia is a normal increase in the heart rate. It occurs with fever, excitement and exercise. No treatment is needed. Rarely, disease, such as anemia (low blood counts) or increased thyroid activity can cause this fast heart rate. In these cases, when the disease is treated, the tachycardia goes away.
Supraventricular tachycardia (SVT)
The most common abnormal tachycardia in children is supraventricular tachycardia (SVT). It’s also called paroxysmal atrial tachycardia (PAT) or paroxysmal supraventricular tachycardia (PSVT). The fast heart rate involves both the heart’s upper and lower chambers. This isn’t a life-threatening problem for most children and adolescents. Treatment is only considered if episodes are prolonged or frequent. For many infants, SVT is a time-limited problem. Treatment with medications often stops after six to 12 months.
SVT may occur in very young infants with otherwise-normal hearts. The heart rate is usually more than 220 beats a minute. Infants with an SVT episode may breathe faster thaormal and seem fussy or sleepier than usual. This situation must be diagnosed and treated to return the heart rate to normal. Once the rhythm is normal, medication usually can prevent future episodes.
Sometimes SVT can be detected while a baby is still in the womb. Then the mother may take medications to slow her baby’s heart rate. If an older infant or child has SVT, the child may be aware of the rapid heart rate. This may be associated with palpitations, dizziness, lightheadedness, chest discomfort, upset stomach or weakness. Some children can learn ways to slow down their heart rate. Straining — such as closing the nose and mouth and trying to breathe out — may be successful. This is called a Valsalva maneuver.
Older children are more likely to have more episodes of tachycardia. They’re more likely to need prolonged treatment. They also may need more diagnostic tests. It’s unusual for episodes of SVT to keep a child from enjoying normal activities. Most children who have episodes of tachycardia stay well even though they may need to keep taking medicine.
Treatment
Treating SVT usually has two parts. The first is stopping a current episode; the second is preventing recurrences. The approach to preventing recurrences depends on the child’s age. In some cases — especially those of infants — the child may need to enter the hospital for treatment and special studies.
Vagal Maneuvers
Gagging
Quickly drinking ice-cold water
Straining by sealing the nose and closing your mouth while trying to breath out hard
Using tension by pushing hard against a wall and holding your breath
Headstand
Diving reflex (immersion of face into ice cold water)
Placing an ice cold cloth on the face
Sometimes simple procedures can stop a fast heart rhythm. Gagging or putting ice on the face are examples. Child’s doctor can explain this in more detail. At other times intravenous medications may be needed to control or stop the tachycardia. Another way to stop SVT is to place a small catheter (a thin, flexible tube) through the nostril into the esophagus. A small amount of electricity is sent through this catheter to stop the SVT. On rare occasions doctors stop SVT by giving a small electrical shock to the chest wall. This is called electrical counter shock or cardioversion. A sedative or anesthetic is given before this procedure.
Wolff-Parkinson-White syndrome
Wolff-Parkinson-White (WPW) syndrome is a condition where the heart ventricles become pre-excited. In the normal heart beat, first the sinoatrial (SA) node signals the atria of the the heart to contract, This is then followed by the atrioventricular (AV) node signalling the heart ventricles to contract. The electrical signal for this contraction travels from the SA node to the AV node via the electrical pathway of the bundle of its.
In Wolff-Parkinson-White (WPW) syndrome another additional electrical pathway called the bundle of Kentallows for electrical signals to travel from the SA to the AV node. This will result in ventricular pre-excitation (the ventricles may become over stimulated) and paroxyomal reentrant tachycardia (raised heart rate).
If an abnormal conduction pathway runs between the atria and ventricles, the electrical signal may arrive at the ventricles sooner thaormal. This condition is called Wolff-Parkinson-White syndrome (WPW syndrome). It’s named after the three people who first described it. WPW syndrome is recognized by certain changes on the ECG. Many people with WPW syndrome don’t have symptoms but are at risk of sudden cardiac arrest.
Help on prehospital stage
1. To give the promoted, halfsitting position to the child.
2. To release a patient from squeezing clothes.
3. To provide access of fresh air.
4. Reflex irritation of vagus nerve: vomit reflex, tension (the Valsalvi method), delay of breathing, squat, drink of cold water, cold rub of skin, sharp transition from sitting position in horizontal one, the Ashner reflex (pressure on the upper inside of eyeballs), caroic reflex (massage and stamping in the area of carotic sinus), bending of feet to the abdomen and their unbending. These meatures are effective at supraventricular paroxismal tachycardia and do not influence on the abdominal form of tachycardia.
5. Sedative therapy: infuse of valleriani 10-20 drops, Corvaloli – 1 drop per theyear of life.
6. Potassium orotatis 10-20 mg/kg of mass per day or other medicines of potassium orally.
7. Hospitalization.
Help on hospital stage
At the supraventricular form of tachycardia:
1. Oxygentherapy by the 40 % moistened oxygen.
2. 0,25 % Isoptini solution 0,1-0,15 mg/kg of mass of intravenously streamly slowly on 20 ml 10 % of glucose solution (except for the syndrome of preterm excitation of ventricles).
3. In default of effect – 10 % Novocainamidi solution 3-6 mg/kg of mass on a 10-15 мл isotonic solution of chloride sodium together with 1 % Mesatoni (0,1-0,3 ml) intravenously streamly slowly.
4. In 1,5-2 hours – 0,05 % Strophantini solution 0,01-0,015 mg/kg of mass (0,1-0,3 ml depending on age) with 10 ml 10 % of glucose solution intravenously streamly slowly (it is not used for the syndrome of preterm excitation of ventricles).
5. At presence of syndrome of preterm excitation of ventricles – Cordaroni (Amiodaron) 0,5 % solution per 5 mg/kg of mass on 20 ml of 10 % glucose solution intravenously streamly, then intravenously in drops in the same dose on 100,0 ml of 10 % glucose solution.
6. 0,5 % Seduxeni solution 0,3-0,5 mg/kg of the masses intravenously streamly slowly.
7. In default of effect electro-impulsive therapy is used.
At the ventricular form of tachycardia:
1. Oxygentherapy through the mask by 40 % the moistened oxygen 5 litre in a minute.
2. Lidocaini 1 or 2 % solution in dose 1-3 mg/kg of the masses on a 10-15 ml or 5 % glucose solution intravenously streamly, farther slow infusion in supporting dose 1-2 mg/kg/hr on a 50-100 ml of іsotonic solution of sodium chloride or 5 % glucose solution.
3. In default of effect in 20-30 minutes – 10 % solution of Novocainamidi 3-6 mg/kg of mass on a 10-15 ml of іsotonic solution of sodium chloride together with 1 % Mesatoni solution (0,1-0,3 ml) intravenously streamly slowly.
4. After 2-4 hours – 2,5 % Aymalini solution 1 mg/kg of mass on a 10 ml of іsotonic solution of sodium chloride of intravenously streamly slowly (during 7-10 minutes).
5. Cordaroni (Amyodran) 0,5 % solution in the dose of a 5 mg/kg of mass on 20 ml of 10 % glucose solution , then intravenously in drops in that dose on 100 ml of 10 % glucose solution.
6. In default of effect electro-impulsive therapy is used.
ACUTE VASCULAR INSUFFICIENCY
Acute vascular insufficiency is the damage of extacardiac blood circulation , that develops acutely and is characterized by disparity of vascular volume to circulatory blood volume. The reasons of acute vascular insufficiency are various: from psychical and reflex influence on regulation of blood circulation to the severe infectious diseases.
Two forms of acute vascular insufficiency are distinguished: syncope and collapse.
Syncope
A syncope is the sudden, more frequent brief loss of consciousness, conditioned by acute low hemorrhagic circulation of cerebrum, that occur as a result of psychogenes or reflex influence on regulation of blood circulation. It is the most frequent, mild form of acute vascular insufficiency. It occurs at children with the liability of the vascular system. The reason very often may be: a fright, strong emotions, tension, promoted sensitiveness to the pain irritants or unpleasant procedures (injections, blood analysis, blood view). The overstrain, insufficiency of oxygen in the apartment, long durations of orthostatic loadings, infectious diseases, anaemias, vegeto-vascular distonias of pubertal age can lead to the loss of consciousness.
Clinic.
There are: weakness, dizziness, nausea, appeals on vomit. It is accompanied by darkening in eyes, by noise in ears with a next brief loss of consciousness. Consciousness is gradually lost, a patient falls or slowly goes down on the floor. Skin covers pale, pupils are extended, react on light. Extremities are cold by touch. Breathing is superficial, rare, bradycardia, pulse of the weak filling and tension, threadlike. Tones of heart are muffled. Arterial pressure is reduced.
Help on prehospital stage
1. To put a patient on the back with high position of feet.
2. To free a child from squeezing clothes, loosen a collar.
3. To provide access of fresh air.
4. To splash or to wipe a person by cold water.
5. To slap a patient on cheeks.
6. To give to breathe the exhalations of liquid ammonia, vinegar or other irritating substants.
7. To put a warm hot-water bottle to the feet and pound a body and extremities of patient.
Help on hospital stage
1. Oxygentherapy by the 40 % moistened oxygen through a mask.
2. Subcutaneously to enter Cordiamini in dose 0,015 mlл/kg of the masses.
3. it is possible to do subcutaneous or intramuscular introduction of 10 % Coffeine sodium bensoatis 0,1 ml/yr of life.
4. Prednisoloni 3 % solution intravenously streamly in one dose 1-2 mg/kg of the masses of body.
Collapse
A collapse is the acute falling of vascular tone, as a result of defeat of vascular-regulative center, which is characterized by the increase of circulatory volume blood due to its depositing in tissues. Decreasing of volume of circulatory blood results in the insufficient returning of blood to the heart, decreases the minute volume and development of hypoxia of brain, all organs and tissues. The reason of collapse is severe forms of acute infectious, purulent-septic diseases, different genesis toxemia, expressed pain syndrome, supraadrenal insufficiency.
Three forms of collapse are distinguished: symphatotonic, paralytic, vagotonic.
Symphatotonic collapse is the initial start of some severe toxemia and hypercatecholamines. As a result of irritation of alpha-receptors the spasm of arteriolles and commulation of blood in the vein system through arteriovenousis anasthomosis occur. The less of blood comes back to the heart, microcirculation is violated, hypoxia of organs and tissues is the result of the process.
Clinic: A pallor skin, cold extremities, the increase of body temperature and systolic arterial pressure. Tones of heart are loud, tense, diuresis are diminished. The patient is excited, reflexes are promoted, convultions may occur.
Help on prehospital stage
1. To lay a child on the back with high position of feet.
2. To release a patient from squeezing clothes, loosen a collar.
3. To provide access of fresh air.
4. To give plenty of warm drink.
5. To put a warm hot-water bottle to the feet, rub a body and extremities by 40 % ethyl alcohol solution.
6. Hospitalization.
Help on hospital stage
1. Oxygentherapy through the mask by 40 % of the moistened oxygen 5liter per minute.
2. Reopolyglucini (Polyglucini or plasma) 10 ml/kg of the masses intravenously in drops.
3. 5 % solution of ascorbinati sodium 0,2 ml/kg of mass for one dose on 5,0 ml of 10 % glucose solution intravenously streamly.
4. Cocarboxylazaea 5 mg/kg of mass for one dose on 5,0 ml of 10 % glucose solution intravenously streamly.
5. To renew the vascular tone:
– 0,25 % solution of Droperidoli in dose 0,2-0,3 mg/kg of the masses intravenously streamly slowly;
– 2,4 % solution of Euphyllini in dose of 3-6 mg/kg of mass on a 50-100 ml of isotonic solution of sodium chloride intravenously in drops;
– when the effect is low – 2,5 % solution of Aminasini in a dose 3 mg/kg or 0,1 ml/kg of the masses on 50 ml of 5 % glucose solution intravenously in drops .
Paralytic collapse – is the second more severe phase of the same pathological state. As a result of damage of microcirculation and hypoxia histamins, kinings, prostoglandins etc. are accumulated. Action of these products on alpha-receptors results in the loss of their sensitiveness. Paresis of vessels, increase of penetration of their walls occurs. The blood yet in a greater amount is deposited in tissues. Considerably flow of the blood to the heart goes down, arterial pressure falls.
Clinic. The child is undynamic, consciousness is darkened, the lines of face are sharp. The marble skin is covered with cold, sticky sweat, veins are empty. The first tone is slamming, a pulse is threadlike, arterial pressure is reduced, diuresis is considerably diminished.
Help on prehospital stage
1. To lay a child on the back with high position of feet.
2. To release a patient from squeezing clothes, loosen a collar.
3. To provide access of fresh air.
4. To give plenty of warm drink.
5. To put a warm hot-water bottle to the feet, rub a body and extremities by 40 % solution of ethyl spiritus.
6. Cordiamini in dose 0,015-0,02 ml/kg of the masses subcutaneously.
7. 3 % solution of Prednisoloni in a dose 1-2 mg/kg of the masses intramuscular.
8. Hospitalization.
Help on a hospital stage
1. To lay a child on the back with high position of feet.
2. Oxygentherapy through the mask by 40 % of the moistened oxygen 5liter per a minute.
3. Cordiamini in a dose 0,015-0,02 ml/kg of the masses subcutaneously.
4.3 % solution of Prednisoloni in a dose 1-2 mg/kg of the masses of intravenously streamly.
5. Reopolyglucini (Polyglucini or plasma) 10 ml/kg of the masses intravenously in drops.
6. 5 % solution of ascorbinati sodium 0,2 ml/kg of the masses on 5,0 ml of 10 % glucose solution intravenously streamly.
7. Cocarboxylazaea 5 mg/kg of mass on 5,0 ml 10 % of glucose solution intravenously streamly.
8. To renew the vascular tone:
– 1 % solution of Mesatoni in dose 0,01-0,03 ml/kg of the masses (or
0,2 % solution of Noradrenalini in dose 0,05-0,1 ml/hr of life) intravenously in drops in 200 ml of 5 % glucose solution (40-60 drops per 1 minute till achievement of the subnormal sizes of arterial pressure, then the speed of infusion is regulated so that arterial pressure must be supported at attained level).
Vagotonic collapse is conditioned by the increase of tone of vagus nerve, that results in expansion of аrteriovenousis anasthomosisthe. This type of collapse is marked at traumas and operations on the organs of abdominal region. A blood is deposited in the vein system, microcirculation is violated, returning of blood to the heart diminishes, hypoxia of organs and tissues develops.
Clinic. A hiccup, vomit, proof red dermographism are present, salivation, bradycardia, multiplied difference between maximal and minimum arterial pressure.
Help on prehospital stage
1. To lay a child on the back with high position of feet.
2. To release a patient from squeezing clothes, loosen a collar.
3. To provide access of fresh air.
4. To give plenty of warm drink.
5. To put a warm hot-water bottle to the feet, rub a body and extremities by 40 % solution of ethyl alcohol.
6. Cordiamini in a dose of 0,015-0,020 ml/kg of the masses subcutaneously.
7. 3 % solution of Prednisoloni in dose 1-2 mg/kg of the masses intramuscular.
8. Hospitalization.
Help on a hospital stage
1. To lay a child on the back with high position of feet.
2. Oxygentherapy through the mask by 40 % of the moistened oxygen 5 litres per minute.
3. Cordiamini in dose 0,015-0,020 ml/kg of the masses subcutaneouly.
4. 3 % solution of Prednisolony in dose 1-2 mg/kg of the masses of intravevously streamly.
5. Reopolyglucini (Polyglucini or plasma) 10 ml/kg of the masses intravevously in drops.
6. 5 % solution of sodium ascorbinati 0,2 ml/kg of the masses on 5,0 ml of 10 % glucose solution intravevously streamly.
7. Cocarboxylazae 5 mg/kg of mass on 5,0 ml of 10 % glucose solution intravevously streamly.
8. To renew of vascular tone:
– 1 % solution of Mesatoni in a dose 0,01-0,03 ml/kg of the masses (or 0,2 % solution of Noradrenalini in a dose 0,05-0,1 ml/hr of life) of intravevously in drops in 200 ml of 5 % glucose solution (40-60 drops per 1 minute till the subnormal sizes of arterial pressure, then speed of infusion is regulated so that arterial pressure must be supported at attained level).
