Diseases of the gastrointestinal tract (GIT): how to recognize the enemy in time? Diseases of the digestive system and their prevention Diseases of the digestive system
One of the most dangerous diseases transmitted through the digestive system is botulism. The disease manifests itself several hours after the botulinum bacterium enters the body and begins with vomiting, headaches and abdominal pain, but the temperature usually does not rise. The disease develops quickly and within a day can lead to visual impairment, muscle paralysis and death. The botulinum bacterium lives in the soil and multiplies in an oxygen-free environment (bacterial spores are very resistant to various environmental factors). The botulism bacterium enters the human body with vegetables, mushrooms, and low-quality canned food.
Another dangerous disease is salmonellosis (caused by the bacterium Salmonella). Infection with salmonellosis occurs through products - eggs, milk, meat. With this disease, frequent bowel movements (diarrhea) are observed, the patient quickly weakens and may die. The disease begins with high fever, vomiting, and abdominal pain.
Another very dangerous infectious disease is cholera, caused by the bacterium Vibrio cholerae. Cholera is contracted by drinking or ingesting water, swimming in contaminated water, or washing dishes with contaminated water. Infection can occur by eating food that is contaminated during storage or washing, or through contaminated hands. In addition, Vibrio cholerae can be carried by flies.
Helminthic diseases (helminthiasis)
The causes of helminthic diseases are failure to comply with hygiene rules and consumption of food contaminated with worm eggs.
Ascaris- a roundworm that lives in the human intestine, its length reaches 35 cm. Ascaris larvae develop in the intestine and through the hepatic vein enter the liver, heart, trachea, larynx, pharynx, and then they return to the intestine, where they turn into adults. Roundworms can cause abdominal pain, vomiting and even appendicitis. Ascaris larvae, when they enter the lungs, can cause pneumonia.
The larvae of the flatworm - pork tapeworm (as well as bovine tapeworm) can develop in human muscles, causing serious illness.
Worms have very high fertility (for example, one female roundworm can lay up to 200,000 eggs per day, which, when released into the external environment with feces, can persist in the soil for several years).
Diseases of the stomach and duodenum
Gastritis- inflammation of the gastric mucosa, which, for various reasons (bacteria, mental trauma, improper medication, etc.) cannot cope with the effects of hydrochloric acid and pepsin found in the stomach.
If gastritis is not treated promptly, a stomach ulcer may occur (damage to the mucous membrane, which in the most severe cases can lead to perforation - a through hole in the wall of the stomach). An ulcer of the duodenum (and in the part adjacent to the stomach) is also common.
Liver and gallbladder diseases
The liver often suffers from poor food hygiene. One of the reasons for the death of its cells may be inflammation of the liver - hepatitis (this is the general name for inflammatory liver diseases that arise from various causes and require different treatments). One of the signs of hepatitis is jaundice - yellowing of the patient's skin caused by a violation of the barrier function of the liver. Hepatitis is often viral in nature. The causative agent of the disease is a virus that is stable in environmental conditions and is pathogenic only for humans. If the cause of liver destruction is eliminated in time, the part of the organ that remains undamaged can regenerate.
Under certain conditions, gallstones are formed from the substances that make up bile in the gallbladder. Stones irritate the walls of the gallbladder, leading to their inflammation - acute cholecystitis. If stones block the excretory duct of the pancreas, then inflammation develops in it - pancreatitis. If gallstones cause recurring pain, they are removed (sometimes the entire gallbladder is removed).
Prevention of diseases of the stomach and intestines.
The main and most important prevention of diseases of the digestive system, and not only them, is maintaining a healthy lifestyle. This includes giving up bad habits (smoking, alcohol, etc.), regular physical exercise, avoiding physical inactivity (lead an active lifestyle), adherence to work and rest schedules, adequate sleep, and more. It is very important to have a complete, balanced, regular diet, which ensures that the body receives the necessary substances (proteins, fats, carbohydrates, minerals, trace elements, vitamins), and monitoring of the body mass index.
Preventive measures also include annual medical examinations, even if there is no concern. After 40 years, it is recommended to conduct an annual ultrasound examination of the abdominal organs and esophagogastroduodenoscopy. And in no case should the disease be allowed to progress; if symptoms appear, consult a doctor, and not self-medicate or only traditional medicine.
Compliance with these measures will help to avoid or promptly identify and promptly begin treatment of diseases not only of the digestive system, but also of the body as a whole.
Nutrition for diseases of the stomach and intestines.
Nutrition for diseases of the digestive system must be special. In this regard, in our country, at one time, the Russian Academy of Medical Sciences developed special diets that are suitable not only for diseases of the digestive system, but also of other systems (diets are indicated in articles on the treatment of certain diseases). A specially selected diet is necessary in the treatment of diseases of the digestive system and is the key to successful treatment.
If regular enteral nutrition is not possible, parenteral nutrition is prescribed, that is, when the substances necessary for the body enter directly into the blood, bypassing the digestive system. Indications for the use of this diet are: complete esophageal dysphagia, intestinal obstruction, acute pancreatitis and a number of other diseases. The main ingredients of parenteral nutrition are amino acids (polyamine, aminofusin), fats (lipofundin), carbohydrates (glucose solutions). Electrolytes and vitamins are also introduced taking into account the body's daily needs.
Digestive diseases are a common pathology in childhood. The prevalence of these diseases does not have regional characteristics and currently exceeds 100 cases per 1000 children. In recent years, the possibilities for early diagnosis and treatment of gastrointestinal diseases have significantly expanded. This was facilitated by the development and widespread introduction into practice of endoscopic and new radiation diagnostic methods, which began in the 70-80s. XX century. Role identification Helicobacter pylori in the etiology and pathogenesis of chronic gastritis, gastroduodenitis and peptic ulcer of the stomach and duodenum has made it possible to develop the most rational methods of treating these diseases. In children, the peak incidence of diseases of the digestive system occurs at 5-6 and 9-12 years. At the same time, with age, the frequency of functional disorders of the digestive system decreases and the proportion of organic diseases increases.
DISEASES OF THE STOMACH AND DUODENUM
Acute gastritis
Acute gastritis is an acute inflammation of the gastric mucosa caused by exposure to a strong irritant entering (entered) the stomach cavity.
Etiology
The development of acute gastritis can be caused by exogenous or endogenous factors. The following types of acute gastritis are distinguished.
Acute primary (exogenous) gastritis: - nutritional;
Toxic-infectious.
Acute secondary gastritis, complicating severe infectious and somatic diseases.
Corrosive gastritis, which occurs when concentrated acids, alkalis and other caustic substances enter the stomach.
Acute phlegmonous gastritis (purulent inflammation of the stomach). The causes of acute exogenous and endogenous gastritis are presented in Table 16-1.
Table 16-1.Etiological factors causing acute gastritis
Pathogenesis
With exogenous gastritis of nutritional origin, poor quality food has a direct irritating effect on the gastric mucosa, disrupting the digestion processes and the secretion of enzymes that make up the gastric juice. In foodborne illness (FTI), the gastric mucosa is affected by the pathogen itself (for example, salmonella) and its toxins. With endogenous gastritis, the inflammatory process in the gastric mucosa develops due to the penetration of an etiological agent through the hematogenous route.
Clinical picture
The clinical picture of acute gastritis depends on its form and etiology.
The first symptoms of acute exogenous gastritis of nutritional origin appear a few hours after exposure to a pathological agent. The duration of the disease is on average 2-5 days. The main clinical manifestations are as follows. - Child anxiety, general malaise, excessive drooling, nausea, loss of appetite, feeling of “fullness” in the epigastric region.
Possible chills, then low-grade fever.
Subsequently, abdominal pain intensifies, repeated vomiting occurs, and the vomit contains the remains of food eaten 4-6 hours ago.
Objectively, pale skin, a white-yellow coating on the tongue, flatulence are noted, and upon palpation of the abdomen, pain in the epigastric region.
Diarrhea is possible.
Clinical manifestations of toxic-infectious acute exogenous gastritis resemble those of alimentary gastritis. Features of toxic-infectious gastritis include:
Possibility of developing dehydration due to more frequent vomiting;
Localization of pain in the epigastric and paraumbilical areas;
Severe diarrhea;
Moderate neutrophilic leukocytosis in peripheral blood analysis.
Acute phlegmonous gastritis is very difficult, accompanied by purulent melting of the stomach wall and the spread of pus throughout the submucosa. Phlegmonous gastritis can develop due to stomach injuries or as a complication of peptic ulcer disease. It is characterized by high fever, severe abdominal pain, rapid deterioration of the child's condition, repeated vomiting, sometimes mixed with pus. Neutrophilic leukocytosis with a shift of the leukocyte formula to the left is detected in the blood; leukocyturia and albuminuria are detected in urine analysis.
Diagnostics
Diagnosis is usually based on history and clinical manifestations. In doubtful and severe cases, FEGDS is indicated.
Treatment
Bed rest for 2-3 days. Hunger in the first 8-12 hours from the onset of the disease. It is recommended to drink plenty of frequent drinks in small portions (tea, a mixture of 0.9% sodium chloride solution with 5% glucose solution). After 12 hours, fractional dietary meals are prescribed: mucous pureed puree soups, low-fat broths, crackers, jelly, porridge. By the 5-7th day of illness, the child is usually transferred to a regular table. According to indications (in the first hours of the disease), gastric lavage is prescribed through a gastric tube with a warm 0.5-1% sodium bicarbonate solution or 0.9% sodium chloride solution. For toxic-infectious gastritis, anti-inflammatory therapy and enzymes are prescribed
(pancreatin), antispasmodic drugs (papaverine, drotaverine). Phlegmonous gastritis is treated in a surgical hospital.
Prevention
It is necessary to properly organize the child’s nutrition in accordance with his age, avoid overeating, and avoid fatty, fried and spicy foods. When taking certain medications (for example, acetylsalicylic acid, glucocorticoids), it is necessary to monitor the condition of the gastric mucosa and use antacids.
Forecast
The prognosis of acute gastritis in most cases is favorable - complete recovery.
Chronic gastritis
Chronic gastritis is a long-term inflammation of the gastric mucosa of a diffuse or focal nature with the gradual development of its atrophy and secretory insufficiency, leading to indigestion.
Epidemiological studies indicate the extreme prevalence of this disease, increasing with age. It should be noted that in children, chronic gastritis occurs as an isolated disease in only 10-15% of cases. Much more often, chronic gastritis (usually antral) is combined with damage to the duodenum, biliary tract, and pancreas.
Etiology and pathogenesis
Chronic gastritis most often develops as a result of constantly existing violations of rational nutrition (both in quantitative and qualitative terms): non-compliance with food intake, constant consumption of dry, poorly chewed, too hot or cold, fried, spicy food, etc. Chronic gastritis can develop with long-term use of certain medications (for example, glucocorticoids, NSAIDs, antibiotics, sulfonamides). In recent years, importance has also been attached to hereditary predisposition, since chronic gastritis is more often detected in children with a family history of gastrointestinal diseases.
Plays a significant role in the development of chronic gastritis Helicobacter pylori. This microorganism is often detected in other
family members of a sick child. Helicobacter pylori is able to break down urea (using the enzyme urease), the resulting ammonia affects the surface epithelium of the stomach and destroys the protective barrier, allowing gastric juice access to the tissue, which contributes to the development of gastritis and ulcerative defects of the stomach wall.
Classification
The modern classification of chronic gastritis (“Sydney system”) is based on the morphological features and etiology of chronic gastritis (Table 16-2).
Table 16-2.Modern classification of chronic gastritis*
Clinical picture
The main symptom of chronic gastritis is pain in the epigastric region: on an empty stomach, 1.5-2 hours after eating, at night, often associated with errors in diet. Also characteristic are decreased appetite, heartburn, belching of air or sour, nausea, and a tendency to constipation. When examining the patient, pain in the epigastric region and pyloroduodenal zone is determined by palpation. Subsequently, flatulence, rumbling and a feeling of “transfusion” in the stomach appear.
Diagnostics
The diagnosis is made on the basis of a characteristic clinical picture, objective examination data and special research methods. Of the latter, FEGDS is especially informative, allowing to detect several types of changes in the gastric mucosa: hypertrophic, subatrophic, erosive, and sometimes hemorrhagic gastritis. A functional study of gastric juice allows us to evaluate the secretory, acid- and enzyme-forming functions of the stomach. Pentagastrin, a 0.1% histamine solution, is used as an irritant of the glandular apparatus. At the same time, the pH and proteolytic activity of gastric juice and the amount of hydrochloric acid released (flow-hour) are assessed.
Treatment
Treatment of chronic gastritis should be differentiated, complex and individual, depending on the etiology, morphological changes, the course of the process and the age of the child. The main components of treatment for chronic gastritis are listed below.
In case of severe exacerbation, hospital treatment is necessary.
Diet: food should be mechanically and chemically gentle (mucus soups, pureed vegetables and meat, jelly, porridge, pureed cottage cheese). Everything must be consumed warm every 3 hours (with the exception of the night break).
For increased gastric secretion, antisecretory drugs are prescribed - histamine H2 receptor blockers (for example, ranitidine). The H+,K+-ATPase inhibitor omeprazole is prescribed for 4-5 weeks.
Given the frequent presence Helicobacter pylori, so-called three-component therapy is prescribed: bismuth tripotassium dicitrate for 2-3 weeks, amoxicillin for 1 week and metronidazole for 1 week, in age-specific doses.
For hypermotor dyskinesia in the gastroduodenal zone, myotropic antispasmodics (papaverine, drotaverine), as well as metoclopramide and domperidone, are used.
Multienzyme drugs are indicated (for example, pancreatin - “Pancitrate”, “Creon”).
Outside of exacerbation, patients need sanatorium-resort treatment.
Chronic gastroduodenitis
Chronic gastroduodenitis is characterized by nonspecific inflammatory structural changes in the mucous membrane of the stomach and duodenum, as well as secretory and motor-evacuation disorders.
In children, unlike adults, isolated damage to the stomach or duodenum is observed relatively rarely - in 10-15% of cases. Combined lesions of these departments are much more common. The duodenum, being a hormonally active organ, has a regulatory effect on the functional and evacuation activity of the stomach, pancreas and biliary tract.
Etiology and pathogenesis
The leading etiological role belongs to nutritional (irregular and poor nutrition, abuse of spicy foods, dry food) and psychogenic factors. The significance of these factors increases in the presence of a hereditary predisposition to diseases of the gastroduodenal zone. Psychotraumatic situations in the family, school, and social circle are often realized in the form of SVD, which affects secretion, motility, blood supply, regenerative processes and the synthesis of gastrointestinal hormones. Long-term use of medications (glucocorticoids, NSAIDs), food allergies and other factors that reduce local specific and nonspecific protection of the mucous membrane are also important.
One of the main reasons for the development of chronic gastroduodenitis is infection Helicobacter pylori. Duodenitis develops against the background of gastritis caused by Helicobacter pylori, and metaplasia of the duodenal epithelium into the gastric epithelium, which develops as a result of the discharge of acidic gastric contents into the duodenum. Helicobacter pylori settles in areas of metaplastic epithelium and causes the same changes in them as in the stomach. Foci of gastric metaplasia are unstable to the effects of contents
duodenum, which leads to erosions. Therefore, gastroduodenitis associated with Helicobacter pylori, more often it is erosive.
The above etiological factors have a toxic-allergic effect and cause morphological changes in the mucous membrane of the duodenum. Under these conditions, the role of acid-peptic damage to the mucous membrane in the occurrence of evacuation-motor disorders and a decrease in intraduodenal pH increases. Damaging factors first cause irritation of the mucous membrane, and subsequently - dystrophic and atrophic changes in it. At the same time, local immunity changes, autoimmune aggression develops, and the synthesis of hormones that regulate the motor-secretory function of the pancreatobiliary system is disrupted. In the latter, inflammatory changes also occur. This leads to a decrease in the synthesis of secretin and the saturation of pancreatic juice with bicarbonates, which, in turn, reduces the alkalization of the intestinal contents and contributes to the development of atrophic changes.
Classification
There is no generally accepted classification of chronic gastroduodenitis. They are divided as follows:
Depending on the etiological factor - primary and secondary (concomitant) gastroduodenitis;
According to the endoscopic picture - superficial, erosive, atrophic and hyperplastic;
According to histological data - gastroduodenitis with mild, moderate and severe inflammation, atrophy, gastric metaplasia;
Based on clinical manifestations, phases of exacerbation, incomplete and complete remission are distinguished.
Clinical picture
Chronic gastroduodenitis is characterized by a polymorphism of symptoms and is often combined with other diseases of the digestive system, and therefore it is not always possible to distinguish the manifestations caused by gastroduodenitis itself from the symptoms caused by concomitant pathology.
Gastroduodenitis in the acute phase is manifested by aching, cramping pain in the epigastric region, occurring 1-2 hours after eating and often radiating to the hypochondrium (usually the right) and the umbilical region. Taking food or antacids reduces or stops pain. The pain syndrome may be accompanied by a sensation
feeling of heaviness, distension in the epigastric region, nausea, salivation. In the mechanism of development of pain and dyspeptic symptoms, the main role belongs to duodenal dyskinesia. As a result, duodenogastric reflux intensifies, causing bitter belching, sometimes vomiting with bile, and less often heartburn.
When examining patients, attention is drawn to the pallor of the skin, as well as low body weight. The tongue is covered with a white and yellowish-white coating, often with teeth marks on the side surface. When palpating the abdomen, pain is detected in the pyloroduodenal region, less often around the navel, in the epigastric region and hypochondrium. Mendelian symptom is characteristic. Many patients have Ortner's and Kehr's symptoms.
Children with chronic duodenitis often experience autonomic and psychoemotional disorders: recurrent headaches, dizziness, sleep disturbances, fatigue, which is associated with disruption of the endocrine function of the duodenum. Autonomic disorders can manifest themselves as a clinical picture of dumping syndrome: weakness, sweating, drowsiness, increased intestinal motility, occurring 2-3 hours after eating. With a long break between meals, signs of hypoglycemia may occur in the form of muscle weakness, body tremors, and sharply increased appetite.
Chronic gastroduodenitis has a cyclical course: the exacerbation phase is replaced by remission. Exacerbations more often occur in spring and autumn and are associated with poor diet, overload at school, various stressful situations, infectious and somatic diseases. The severity of the exacerbation depends on the severity and duration of the pain syndrome, dyspeptic symptoms and disturbances in the general condition. Spontaneous pain goes away on average after 7-10 days, palpation pain persists for 2-3 weeks. In general, exacerbation of chronic duodenitis lasts 1-2 months. Incomplete remission is characterized by the absence of complaints in the presence of moderate objective, endoscopic and morphological signs of duodenitis. During the remission stage, neither clinical, nor endoscopic, nor morphological manifestations of inflammation in the duodenum are detected.
Diagnostics
The diagnosis of chronic gastroduodenitis is based on data from clinical observation, studying the functional state of the duodenum, endoscopic and histological (biopsy specimens of the mucous membrane) studies.
With functional duodenal intubation, changes characteristic of duodenitis are revealed: dystonia of the sphincter of Oddi, pain and nausea at the time of introduction of the irritant into the intestine, backflow of magnesium sulfate solution through the probe due to spasm of the duodenum. Microscopy of duodenal contents reveals desquamated intestinal epithelium, and vegetative forms of Giardia are also common. To assess the functional state of the duodenum, the activity of the enzymes enterokinase and alkaline phosphatase in the duodenal contents is determined. The activity of these enzymes is increased in the early stages of the disease and decreases as the severity of the pathological process worsens.
The study of gastric secretion is also important. Its indicators in acidopeptic duodenitis (bulbitis) are usually increased, and when duodenitis is combined with atrophic gastritis and enteritis, they are decreased.
The most informative method for diagnosing gastroduodenitis is FEGDS (see section “Chronic gastritis”).
X-ray examination of the duodenum is not of great importance in the diagnosis of chronic duodenitis, but it allows us to identify various motor-evacuation disorders that accompany the disease or are its cause.
Treatment
Treatment for chronic gastroduodenitis is carried out according to the same principles as for chronic gastritis.
In the acute period of the disease, bed rest is indicated for 7-8 days.
Diet is of great importance. In the first days of illness, is a table recommended? 1, subsequently - table? 5. During the period of remission, proper nutrition is indicated.
For eradication Helicobacter pylori carry out three-component therapy: bismuth tripotassium dicitrate in combination with amoxicillin or macrolides and metronidazole for 7-10 days.
For increased stomach acidity, H2-histamine receptor blockers are recommended, as well as omeprazole for 3-4 weeks.
According to indications, drugs that regulate motility (metoclopramide, domperidone, drotaverine) are used.
During the rehabilitation process, physiotherapy, exercise therapy, and sanatorium treatment are prescribed.
Prevention
If you have a disease of the gastroduodenal zone, it is very important to follow the principles of age-related nutrition, protect the child from physical and
emotional overload. Secondary prevention includes adequate and timely therapy, observation and regular consultations with a pediatric gastroenterologist.
Forecast
With irregular and ineffective treatment, chronic gastritis and gastroduodenitis recur and become the main pathology of adults, which reduces the patient’s quality of life and ability to work.
Peptic ulcer of the stomach and duodenum
Peptic ulcer is a chronic recurrent disease accompanied by the formation of an ulcer in the stomach and/or duodenum, caused by an imbalance between the factors of aggression and protection of the gastroduodenal zone.
In recent years, cases of peptic ulcer disease in children have become more frequent; currently the disease is registered with a frequency of 1 case per 600 children (according to A.G. Zakomerny, 1996). They also note a “rejuvenation” of the disease, an increase in the proportion of pathology with a severe course and a decrease in the effectiveness of therapy. In this regard, gastric and duodenal ulcers in children represent a serious problem in clinical medicine.
ETIOLOGY
The disease develops as a result of the influence of several unfavorable factors on the body, including hereditary predisposition and emotional overload in combination with constant nutritional errors (irregular nutrition, abuse of spicy foods, dry food, etc.). The main causes are considered to be a disorder of the nervous and hormonal mechanisms of the stomach and duodenum, an imbalance between aggressive factors (hydrochloric acid, pepsins, pancreatic enzymes, bile acids) and protective factors (mucus, bicarbonates, cellular regeneration, Pg synthesis). Ulceration is associated with prolonged hyperchloridhydria and peptic proteolysis, caused by vagotonia, hypergastrinemia and hyperplasia of the main glands of the stomach, as well as with gastroduodenal dysmotility and prolonged acidification of the antrobulbar zone.
Plays an important role in the development of peptic ulcer Helicobacter pylori, found in 90-100% of patients in the mucous membrane of the antrum of the stomach.
PATHOGENESIS
There are several mechanisms that lead to increased secretion of hydrochloric acid and pepsins, decreased production of mucous substances and impaired motor regulation of the gastroduodenal zone. An important role in this process is played by the central nervous system, which has a dual effect on the secretion and motility of the stomach and duodenum (Fig. 16-1).
Rice. 16-1.The influence of the central nervous system on the secretion and motility of the stomach and duodenum.
Pathological changes in the central and autonomic nervous system play an important role in disrupting the balance between protective and aggressive factors, contributing to the formation of a peptic ulcer.
CLASSIFICATION
The classification of gastric and duodenal ulcers is given in Table. 16-3.
Table 16-3.Classification of peptic ulcer in children*
* From: Baranov A.A. et al. Pediatric gastroenterology. M., 2002.
CLINICAL PICTURE
The clinical picture depends on the localization of the process and the clinical endoscopic stage of the disease.
Stage I (fresh ulcer)
The leading clinical symptom is pain in the epigastric region and to the right of the midline, closer to the navel; pain occurs on an empty stomach or 2-3 hours after eating (late pain). Half of the children report night pain. A clear “Moynigam” rhythm of pain is noted: hunger-pain-eating-relief. Dyspeptic syndrome is pronounced: heartburn (the earliest and most common symptom), belching, nausea, constipation. Superficial palpation of the abdomen is painful, deep and difficult due to the protective tension of the muscles of the anterior abdominal wall.
An endoscopic examination, against the background of pronounced inflammatory changes in the mucous membrane of the gastroduodenal zone, reveals a defect (defects) of a round or oval shape, surrounded by an inflammatory ridge, with a bottom covered with fibrin deposits of gray-yellow or white color.
In the stomach, ulcers are located mainly in the pyloroantral region (found more often in boys).
In the duodenum, ulcers are localized on the anterior wall of the bulb, as well as in the area of the bulboduodenal junction. Motor-
evacuation disorders include duodeno-gastric reflux and spastic deformation of the bulb.
II stage (beginning of epithelization of the ulcerative defect)
In most children, late pain in the epigastric region persists, but it occurs mainly during the day, and persistent relief occurs after eating. The pain becomes more dull and aching. The abdomen is easily accessible to superficial palpation, but with deep palpation, muscle protection is preserved. Dyspeptic symptoms are less pronounced.
During endoscopic examination, hyperemia of the mucous membrane is less pronounced, swelling around the ulcerative defect is reduced and the inflammatory shaft disappears. The bottom of the defect begins to clear of fibrin, convergence of folds towards the ulcer is noted, which reflects the healing process.
III stage (ulcer healing)
Pain at this stage persists only on an empty stomach; at night, its equivalent may be a feeling of hunger. The abdomen becomes accessible to deep palpation, pain is preserved. Dyspeptic disorders are practically not expressed.
During endoscopy, traces of repair are determined at the site of the defect in the form of red scars of various shapes - linear, circular, stellate. Deformation of the wall of the stomach or duodenum is possible. Signs of the inflammatory process of the mucous membrane of the stomach and duodenum, as well as motor-evacuation disorders, remain.
IV stage (remission)
General condition is satisfactory. No complaints. Palpation of the abdomen is painless. Endoscopically, the mucous membrane of the stomach and duodenum is not changed. However, in 70-80% of cases, a persistent increase in the acid-forming function of the stomach is detected.
Complications
Complications of peptic ulcer disease are recorded in 8-9% of children. Complications occur 2 times more often in boys than in girls.
The structure of complications is dominated by bleeding, and with duodenal ulcers they develop much more often than with gastric ulcers.
Perforation of an ulcer in children often occurs with a stomach ulcer. This complication is accompanied by acute “dagger” pain in the epigastric region, and a state of shock often develops.
Characteristic is the disappearance of hepatic dullness upon percussion of the abdomen due to air entering the abdominal cavity.
Penetration (penetration of an ulcer into neighboring organs) occurs rarely, against the background of a long, difficult process and inadequate therapy. Clinically, penetration is characterized by sudden pain radiating to the back and repeated vomiting. The diagnosis is clarified using FEGDS.
DIAGNOSTICS
The diagnosis of peptic ulcer, in addition to its clinical and endoscopic justification outlined above, is confirmed by the following methods:
Fractional intubation of the stomach with determination of the acidity of gastric juice, flow-hour of hydrochloric acid and pepsin. Characterized by an increase in the pH of gastric juice on an empty stomach and with the use of specific irritants, an increase in the content of pepsins.
X-ray examination of the stomach and duodenum with barium contrast. Direct signs of an ulcer are a symptom of a niche and a typical deformation of the duodenal bulb, indirect signs are pyloric spasm, dyskinesia of the duodenal bulb, hypersecretion of the stomach, etc.
By identifying Helicobacter pylori.
Repeated determination of occult blood in the stool (Gregersen reaction).
TREATMENT
Treatment of patients with gastric and duodenal ulcers should be comprehensive; it is carried out in stages, taking into account the clinical and endoscopic phase of the disease.
Stage I - exacerbation phase. Treatment in a hospital.
Stage II is the phase of subsidence of manifestations, the beginning of clinical remission. Clinical observation and seasonal prevention.
Stage III is the phase of complete clinical and endoscopic remission. Sanatorium treatment.
Stage I
Conservative treatment of peptic ulcer begins immediately after diagnosis. In many patients, the ulcer heals within 12-15 weeks.
Bed rest for 2-3 weeks.
Diet: chemically, thermally and mechanically gentle food. Treatment tables according to Pevzner? 1a (1-2 weeks), ? 1b (3-4 weeks), ? 1 (during remission). Meals should be fractional (5-6 times a day).
Reducing the damaging effects of hydrochloric acid and pepsins.
Non-adsorbable antacids: algeldrate + magnesium hydroxide, aluminum phosphate, simaldrate, etc.;
Antisecretory drugs: histamine H2 receptor antagonists (for example, ranitidine) for 2-3 weeks; H+-, K+- ATPase inhibitor omeprazole for 40 days.
Elimination of hypermotor dyskinesia in the gastroduodenal zone (papaverine, drotaverine, domperidone, metoclopramide).
In the presence of Helicobacter pylori- three-component treatment for 1-3 weeks (bismuth tripotassium dicitrate, amoxicillin, metronidazole).
Taking into account the presence of digestive and absorption disorders - multienzyme drugs (pancreatin).
Stage II
Treatment is carried out by a local pediatrician. He examines the child once every 2 months and carries out anti-relapse treatment in the autumn-winter and spring-winter periods (table 1b, antacid therapy, vitamins for 1-2 weeks).
Stage III
Sanatorium treatment is indicated 3-4 months after discharge from the hospital in local gastroenterological sanatoriums and drinking balneological resorts (Zheleznovodsk, Essentuki).
PREVENTION
Exacerbations of peptic ulcer disease are usually seasonal in nature, so secondary prevention requires regular examination by a pediatrician and the prescription of preventive therapy (antacid medications), if necessary, diet, limitation of school load (1-2 fasting days per week in the form of home schooling). Providing a favorable psycho-emotional environment at home and at school is of great importance.
FORECAST
The course of peptic ulcer disease and long-term prognosis depend on the timing of the primary diagnosis, timely and adequate therapy. To a large extent, the success of treatment depends on the position of the parents and their understanding of the seriousness of the situation. Constant monitoring of the patient by a pediatric gastroenterologist, compliance with the rules of seasonal prevention of exacerbations, hospitalization in a specialized department during exacerbation significantly improves the prognosis of the disease.
DISEASES OF THE SMALL AND LARGE INTESTINE
Chronic non-infectious diseases of the small and large intestines develop quite often, especially in preschool children. They represent a serious medical and social problem due to their high prevalence, difficulties in diagnosis and the severity of the consequences that impair the growth and development of the child. Intestinal diseases can be based on both functional and morphological changes, but it is rarely possible to differentiate them in the early period of the disease.
In young children, due to the anatomical and physiological characteristics of the digestive system, the small and large intestines are often simultaneously involved in the pathological process (enterocolitis). School-age children are characterized by more isolated lesions of the intestinal sections.
Chronic enteritis
Chronic enteritis is a chronic recurrent inflammatory-dystrophic disease of the small intestine, accompanied by a violation of its basic functions (digestion, absorption) and, as a result, a violation of all types of metabolism.
In the structure of the pathology of the digestive organs, chronic enteritis as the main disease is registered in 4-5% of cases.
Etiology
Chronic enteritis is a polyetiological disease that can be either primary or secondary.
Great importance is attached to nutritional factors: dry food, overeating, excess carbohydrates and fats in food with a lack of protein, vitamins and microelements, early transfer to artificial feeding, etc.
In recent years, etiological factors such as exposure to poisons, salts of heavy metals (lead, phosphorus, cadmium, etc.), drugs (salicylates, glucocorticoids, NSAIDs, immunosuppressants, cytostatics, some anti-inflammatory drugs) have often been identified.
biotics, especially with long-term use), ionizing radiation (for example, during x-ray therapy).
The occurrence of diseases of the small intestine is facilitated by congenital and acquired enzymopathies, intestinal malformations, immunity disorders (both local and general), food allergies, surgical interventions on the intestines, diseases of other digestive organs (primarily the duodenum, pancreas, biliary tract ) etc. With the development of chronic enteritis in a child, it is usually difficult to single out one etiological factor. Most often, a combination of a number of factors, both exogenous and endogenous, is identified.
Pathogenesis
Under the influence of any of the above factors or their combination, an inflammatory process develops in the mucous membrane of the small intestine, becoming chronic due to a lack of immune and compensatory-adaptive reactions. The enzymatic activity of the intestinal glands is disrupted, the passage of chyme is accelerated or slowed down, conditions are created for the proliferation of microbial flora, and the digestion and absorption of basic nutrients is disrupted.
Clinical picture
The clinical picture of chronic enteritis is polymorphic and depends on the duration and phase of the disease, the degree of change in the functional state of the small intestine, and concomitant pathology. There are two main clinical syndromes - local and general.
Local intestinal (enteral) syndrome is caused by a violation of parietal (membrane) and cavity digestion. Flatulence, rumbling, abdominal pain, and diarrhea are observed. The bowel movements are usually profuse, with pieces of undigested food and mucus. Possible alternation of diarrhea and constipation. When palpating the abdomen, pain is determined mainly in the peri-umbilical region; Obraztsov’s and Porges’ symptoms are positive. In severe cases, the phenomenon of “pseudoascites” is possible. Intestinal symptoms more often occur when taking milk, raw vegetables and fruits, and confectionery products.
General intestinal (enteral) syndrome is associated with water-electrolyte imbalance, malabsorption of macro- and micronutrients and involvement of other organs in the pathological process (malabsorption syndrome). Characteristic: increased fatigue, irritability, headache, weakness, weight loss of varying severity. Note dry skin, changes
nails, glossitis, gingivitis, seizures, hair loss, impaired twilight vision, increased fragility of blood vessels, bleeding. The above symptoms are caused by polyhypovitaminosis and trophic disorders. In young children (up to 3 years old), anemia and metabolic disorders are often detected, manifested by osteoporosis and brittle bones, and seizures. The severity of general and local enteric syndromes determines the severity of the disease.
Diagnosis is based on medical history, clinical manifestations, results of laboratory and instrumental examination methods. Differentiated carbohydrate loads are carried out with mono- and disaccharides, a test with d-xylose. Endoscopy with targeted biopsy and subsequent histological examination of the biopsy is also informative. In the coprogram, creatorrhea, steatorrhea, and amilorrhea are identified.
Differential diagnosis is carried out with the most frequently developing hereditary and acquired diseases occurring with malabsorption syndrome - acute enteritis, intestinal form of cystic fibrosis, gastrointestinal form of food allergy, celiac disease, disaccharidase deficiency, etc.
Treatment
See section "Chronic enterocolitis".
Chronic enterocolitis
Chronic enterocolitis is a polyetiological inflammatory-dystrophic disease that simultaneously affects the small and large intestines.
Etiology
The disease most often occurs after acute intestinal infections (salmonellosis, dysentery, escherichiosis, typhoid fever, viral diarrhea), helminthiases, diseases caused by protozoa, errors in the diet (long-term irregular, insufficient or excessive nutrition), food allergic reactions. The development of the disease is facilitated by congenital and acquired enzymopathies, immune defects, diseases of the stomach, liver, biliary tract and pancreas, abnormalities of intestinal development, dysbacteriosis, vitamin deficiency, neurogenic, hormonal disorders, radiation exposure, irrational use of medicines, in particular antibiotics, etc. .
Pathogenesis
The pathogenesis is not completely clear. It is believed, for example, that infectious agents can cause disruption of the integrity of cells in the tissues of the digestive tract, promoting their destruction or morphological metaplasia. As a result, Ags are formed that are genetically foreign to the body, causing the development of autoimmune reactions. There is an accumulation of clones of cytotoxic lymphocytes and the production of antibodies directed against the Ag structures of autologous tissues of the digestive tract. They attach importance to the deficiency of secretory IgA, which prevents the invasion of bacteria and allergens. Changes in the normal intestinal microflora contribute to the formation of chronic enterocolitis, secondarily increasing the permeability of the intestinal mucosa to microbial allergens. On the other hand, dysbiosis always accompanies this disease. Chronic enterocolitis can also be secondary, with diseases of other digestive organs.
Clinical picture
Chronic enterocolitis is characterized by a wave-like course: exacerbation of the disease is replaced by remission. During the period of exacerbation, the leading clinical symptoms are abdominal pain and bowel movements.
The nature and intensity of pain may vary. Children more often complain of pain in the navel area, in the lower abdomen with right-sided or left-sided localization. Pain occurs at any time of the day, but more often in the afternoon, sometimes 2 hours after eating, and intensifies before defecation, when running, jumping, driving, etc. Dull nagging pain is more characteristic of damage to the small intestine, intense pain - of the large intestine. Pain equivalents: loose stool after eating or, especially in young children, refusal to eat, selectivity of taste.
Another important symptom of chronic enterocolitis is stool disorder in the form of alternating diarrhea (with primary damage to the small intestine) and constipation (with damage to the large intestine). Frequent urges to defecate (5-7 times a day) with small portions of feces of different consistency (liquid with an admixture of undigested food, with mucus; gray, shiny, foamy, fetid - with a predominance of putrefactive processes) predominate. Often “sheep” or ribbon-like feces appear. The passage of hard feces can cause the formation of anal fissures. In this case, a small amount of scarlet blood appears on the surface of the stool.
Constant symptoms of chronic enterocolitis in children also include bloating and a feeling of distension in the abdomen, rumbling and transfusion in the intestines, increased discharge of gases, etc. Sometimes the clinical picture of the disease is dominated by a psychovegetative syndrome: weakness, fatigue, poor sleep, irritability, and headache develop. Complaints about intestinal dysfunction fade into the background. With a long course of the disease, a delay in the increase in body weight, less often - growth, anemia, signs of hypovitaminosis, and metabolic disorders (protein, mineral) are noted.
Diagnosis and differential diagnosis
Chronic enterocolitis is diagnosed on the basis of anamnestic data, clinical picture (long-term intestinal dysfunction, accompanied by the development of dystrophy), laboratory examination results (anemia, hypo- and dysproteinemia, hypoalbuminemia, decreased concentrations of cholesterol, total lipids, β-lipoproteins, calcium, potassium, sodium in blood serum, detection of mucus, leukocytes, steatorrhea, creatorrhoea, amilorrhea in feces), results of instrumental research methods (sigmoidoscopy, colonofibroscopy, X-ray and morphological studies).
Chronic enterocolitis should be differentiated from prolonged dysentery (see the chapter “Acute intestinal infections”), congenital enzymopathies [cystic fibrosis, celiac disease, disaccharidase deficiency, exudative enteropathy syndrome (see section “Congenital enzymopathies and exudative enteropathy”)], etc.
Treatment
Treatment for chronic enteritis and chronic enterocolitis is aimed at restoring impaired intestinal functions and preventing exacerbations of the disease. The basis of the therapeutic measures carried out is therapeutic nutrition (table 4 according to Pevzner is prescribed). Also prescribed are multivitamins, enzyme preparations (Pancreatin), pre- and probiotics [bifidobacteria bifidum + activated carbon ("Probifor"), "Linex", lactobacilli acidophilus + kefir fungi ("Acipol"), "Hilak-Forte"], enterosorbents ( dioctahedral smectite), prokinetics (trimebutine, loperamide, mebeverine, etc.). According to strict indications, antibacterial drugs are prescribed: Intetrix, nitrofurans, nalidixic acid, metronidazole, etc. Herbal medicine, symptomatic drugs, physiotherapy, and exercise therapy are used. Sanatorium-resort treatment is indicated no earlier than 3-6 months after an exacerbation.
Forecast
With timely and adequate treatment at all stages of rehabilitation, the prognosis is favorable.
Irritable bowel syndrome
Irritable bowel syndrome is a functional disorder of the gastrointestinal tract, manifested by a combination of defecation disorders with pain in the absence of organic changes in the intestine.
At an international expert workshop in Rome (1988), a unified definition of irritable bowel syndrome (Rome Criteria) was developed - a complex of functional disorders lasting more than 3 months, including abdominal pain (usually decreasing after defecation) and dyspeptic disorders (flatulence). , rumbling, diarrhea, constipation or their alternation, feeling of incomplete bowel movement, imperative urge to defecate).
In developed countries, irritable bowel syndrome develops in the adult population with a frequency of 14 to 48%. Women suffer from this disease 2 times more often than men. It is believed that 30-33% of children suffer from functional intestinal disorders.
Etiology and pathogenesis
Irritable bowel syndrome is a polyetiological disease. An important place in its development is given to neuropsychic factors. It has been established that with irritable bowel syndrome, the evacuation function of both the small and large intestines is impaired. Changes in intestinal motor function may be due to the fact that these patients have increased sensitivity of the intestinal wall receptors to stretching, as a result of which pain and dyspeptic disorders occur in them at a lower excitability threshold than in healthy people. Nutritional habits, in particular insufficient intake of plant fiber, play a certain role in the formation of irritable bowel syndrome in children. Significant importance is also attached to the loss of the conditioned reflex to the act of defecation and asynergy of the muscular structures of the pelvic diaphragm, leading to disturbances in the evacuation function of the intestine.
Irritable bowel syndrome can develop secondary to other diseases of the digestive system: gastritis, duodenitis, peptic ulcer of the stomach and duodenum, pancreatitis, etc. Past acute intestinal infections, gynecological diseases in girls, and pathology of the urinary system can play a certain role.
Clinical picture
Depending on the clinical manifestations, there are 3 variants of irritable bowel syndrome: mainly with diarrhea, constipation and abdominal pain and flatulence.
In patients with a predominance of diarrhea, the main symptom is loose stools, sometimes mixed with mucus and undigested food residues, usually 4 times a day, often in the morning, after breakfast, especially during emotional stress. Sometimes there is an imperative urge to defecate and flatulence.
In the second variant of irritable bowel syndrome, stool retention is noted (up to 1-2 times a week). In a number of children, defecation is regular, but is accompanied by prolonged straining, a feeling of incomplete bowel movement, changes in the shape and nature of the stool (hard, dry, sheep type, etc.). In some children, prolonged constipation is replaced by diarrhea, followed by resumption of constipation.
In patients with the third variant of irritable bowel syndrome, cramping or dull, pressing, bursting pain in the abdomen, combined with bloating, predominates. Pain occurs or intensifies after eating, during stress, before defecation and disappears after the passage of gas.
In addition to local manifestations, patients experience frequent headaches, a feeling of a lump in the throat when swallowing, vasomotor reactions, nausea, heartburn, belching, heaviness in the epigastric region, etc. A distinctive feature of irritable bowel syndrome is the variety of complaints. Noteworthy is the discrepancy between the duration of the disease, the variety of complaints and the good appearance of sick children who are physically normally developed.
Diagnosis and differential diagnosis
Diagnosis of irritable bowel syndrome is based on the principle of excluding other intestinal diseases, often using functional, instrumental and morphological examination methods.
Differential diagnosis is carried out with endocrine diseases (hypothyroidism, hyperthyroidism - with constipation; with VIPoma, gastrinoma - with diarrhea), impaired intestinal absorption syndrome (lactase deficiency, celiac disease, etc.), gastrointestinal allergies, acute and chronic constipation, etc.
Treatment
Treatment of patients with irritable bowel syndrome is based on normalization of the diet and nature of nutrition, psychotherapy, prescription
medicines. In order to normalize the state of the central and autonomic nervous system, as well as intestinal motility, exercise therapy, massage, physiotherapy and reflexology are prescribed. The drugs of choice are cisapride, loperamide, pinaverium bromide, mebeverine, etc.
In case of irritable bowel syndrome with diarrhea, dioctahedral smectite, which has pronounced adsorption and cytoprotective properties, has a positive effect. Pre- and probiotics are also used to restore normal microflora [Enterol, bifidobacteria bifidum, bifidobacteria bifidum + activated carbon (Probifor), lactobacilli acidophilus + kefir fungi (Acipol), Hilak-forte, Linex and etc.], antibacterial agents (“Intetrix”, nifuroxazide, furazolidone, metronidazole, etc.), herbal preparations [lingonberry leaves + St. John’s wort herb + successions of tripartite grass + rose hips fruits (“Brusniver”), calendula flowers + chamomile flowers + licorice roots + successions of grass + sage leaves + eucalyptus leaf ("Elekasol")], reducing bloating, rumbling in the stomach, the amount of mucus in the stool.
For irritable bowel syndrome, which occurs with constipation, ballast substances (bran, flax seed, lactulose, etc.) are prescribed.
According to indications, the following are prescribed: antispasmodics (drotaverine, papaverine), anticholinergic blockers (hyoscine butyl bromide, prifinium bromide), drugs that normalize the state of the central and autonomic nervous system (the choice of drug depends on the affective disorders identified in the patient); tranquilizers (diazepam, oxazepam), antidepressants (amitriptyline, pipofezin), neuroleptics (thioridazine) in combination with nootropics and B vitamins. Optimal treatment results can be obtained through joint observation of the patient by a pediatrician and a neuropsychiatrist.
Forecast
The prognosis is favorable.
Congenital enzymopathies and exudative enteropathy
The most common congenital enzymopathies of the gastrointestinal tract are celiac disease and disaccharidase deficiency.
PATHOGENESIS AND CLINICAL PICTURE Celiac disease
Celiac enteropathy is a congenital disease caused by a deficiency of enzymes that break down gluten (cereal protein)
to amino acids, and the accumulation in the body of toxic products of its incomplete hydrolysis. The disease manifests itself more often from the moment of introducing complementary foods (semolina and oatmeal) in the form of copious foamy stools. Then anorexia, vomiting, symptoms of dehydration, and a picture of false ascites appear. Severe dystrophy develops.
When X-ray examination of the intestines with the addition of flour to the barium suspension, sharp hypersecretion, accelerated peristalsis, changes in intestinal tone and the relief of the mucous membrane are observed (symptom of “snow blizzard”).
Disaccharidase deficiency
In young children, it is more often primary, caused by a genetic defect (ρ) in the synthesis of enzymes that break down lactose and sucrose. In this case, lactose intolerance manifests itself as diarrhea after the first feedings with breast milk, sucrose intolerance - from the moment sugar is introduced into the child’s diet (sweet water, supplementary feeding). Characterized by flatulence, watery stools with a sour odor, and the gradual development of persistent malnutrition. Stools, as a rule, quickly return to normal after discontinuation of the corresponding disaccharide.
Exudative enteropathy syndrome
Characterized by the loss of large amounts of blood plasma proteins through the intestinal wall. As a result, children experience persistent hypoproteinemia and a tendency to edema. Primary syndrome of exudative enteropathy is associated with a congenital defect of the lymphatic vessels of the intestinal wall with the development of lymphangiectasia, detected during morphological examination. Secondary syndrome of exudative enteropathy is observed in celiac disease, cystic fibrosis, Crohn's disease, ulcerative colitis, liver cirrhosis and a number of other diseases.
DIAGNOSTICS
Diagnosis is based on a set of clinical and laboratory data, the results of endoscopic and morphological studies. In diagnostics, stress tests are used (for example, d-xylose absorption test, etc.), immunological methods (determination of agliadin antibodies, etc.), as well as methods that make it possible to determine the content of protein, carbohydrates, lipids in feces and blood.
DIFFERENTIAL DIAGNOSTICS
When carrying out differential diagnosis, it is important to take into account the age of the patient at which the first symptoms of the disease appeared.
During the neonatal period, congenital lactase deficiency (alactasia) manifests itself; congenital glucose-galactose malabsorption, congenital enterokinase deficiency, intolerance to cow's milk protein, soy, etc.
TREATMENT
The organization of individual therapeutic nutrition is of decisive importance, in particular the prescription of elimination diets depending on the period of the disease, the general condition and age of the patient, and the nature of the enzyme deficiency. For celiac disease, the diet should be gluten-free (exclude foods rich in gluten - rye, wheat, barley, oatmeal) with a limit on milk. In case of disaccharidase deficiency, it is necessary to avoid consuming sugar, starch or fresh milk (if lactose intolerant). For exudative enteropathy, a diet rich in proteins and limited fat is prescribed (medium chain triglycerides are used). According to indications, in severe cases, parenteral nutrition is prescribed. Enzyme preparations, probiotics, vitamins, and symptomatic therapy are indicated.
FORECAST
The prognosis with strict adherence to an elimination diet and careful prevention of relapses in patients with celiac disease and some enteropathies is generally favorable; with exudative enteropathy, only achieving clinical remission is possible.
Prevention of diseases of the small and large intestine
Secondary prevention includes: careful adherence to a nutritious diet; repeated courses of treatment with vitamins, enzymes (under control of stool condition), enterosorbents, prokinetics, medicinal herbs, probiotics, as well as micro-
neral water (if you are prone to diarrhea, prescribe “Essentuki 4”, heated to 40-50? C); therapeutic exercises and abdominal massage; protecting the child from intercurrent diseases and injuries; excluding swimming in open waters.
In case of chronic enteritis and chronic enterocolitis, during the period of stable remission, physical exercise and preventive vaccinations are allowed.
Observation of children and their treatment during the period of remission is carried out by local pediatricians and gastroenterologists of the clinic in the first year of discharge from the hospital on a quarterly basis. Sanatorium-resort treatment is indicated no earlier than 3-6 months after an exacerbation. The sanatorium therapy complex includes: a gentle training regime, dietary nutrition, according to indications - drinking heated low-mineralized waters, mud applications on the stomach and lower back, radon baths, oxygen cocktails, etc. The duration of the sanatorium treatment course is 40-60 days.
Crohn's disease
Crohn's disease is a chronic nonspecific progressive transmural granulomatous inflammation of the gastrointestinal tract.
The terminal part of the small intestine is most often affected, therefore there are such synonyms for this disease as terminal ileitis, granulomatous ileitis, etc. Any part of the digestive tract from the root of the tongue to the anus can be involved in the pathological process. The frequency of intestinal lesions decreases in the following order: terminal ileitis, colitis, ileocolitis, anorectal form, etc. Focal, multifocal and diffuse forms are also distinguished. The course of Crohn's disease is undulating, with exacerbations and remissions.
Crohn's disease is detected in children of all age groups. The peak incidence occurs between 13 and 20 years of age. Among the sick, the ratio of boys to girls is 1:1.1.
Etiology and pathogenesis
The etiology and pathogenesis of the disease are unknown. The role of infection (mycobacteria, viruses), toxins, food, and some medications, considered as a trigger for the development of acute inflammation, is discussed. Immunological, dysbiotic, and genetic factors are of great importance. A connection has been established between the HLA histocompatibility system and Crohn's disease, in which the DR1 and DRw5 loci are often identified.
Clinical picture
The clinical picture of the disease is very diverse. The onset of the disease is usually gradual, with a long-term course with periodic exacerbations. Acute forms are also possible.
The main clinical symptom in children is persistent diarrhea (up to 10 times a day). The volume and frequency of stool depend on the level of damage to the small intestine: the higher it is, the more frequent the stool, and, accordingly, the more severe the disease. Damage to the small intestine is accompanied by malabsorption syndrome. Blood sometimes appears in the stool.
Abdominal pain is a mandatory symptom in all children. The intensity of pain varies from minor (at the beginning of the disease) to intense cramping associated with eating and defecation. When the stomach is affected, they are accompanied by a feeling of heaviness in the epigastric region, nausea, and vomiting. In the later stages, the pain is very intense and is accompanied by bloating.
General symptoms of the disease: general weakness, weight loss, fever. With significant damage to the small intestine, the absorption and metabolism of proteins, carbohydrates, fats, vitamin B 12, folic acid, electrolytes, iron, magnesium, zinc, etc. are impaired. Hypoproteinemia is clinically manifested by edema. Characterized by delayed growth and sexual development.
The most common extraintestinal manifestations of Crohn's disease: arthralgia, monoarthritis, sacroiliitis, erythema nodosum, aphthous stomatitis, iridocyclitis, uveitis, episcleritis, pericholangitis, cholestasis, vascular disorders.
Complicationsin Crohn's disease are most often associated with the formation of fistulas and abscesses of various locations, intestinal perforation, and peritonitis. Intestinal obstruction and acute toxic dilatation of the colon are possible.
A general blood test reveals anemia (decrease in red blood cells, Hb, hematocrit), reticulocytosis, leukocytosis, increased ESR. A biochemical blood test reveals hypoproteinemia, hypoalbuminemia, hypokalemia, a decrease in the content of microelements, an increase in the level of alkaline phosphatase, β-globulin and C-reactive protein. The severity of biochemical changes correlates with the severity of the disease.
The endoscopic picture of Crohn's disease is characterized by great polymorphism and depends on the stage and extent of the inflammatory process. Endoscopically, 3 phases of the disease are distinguished: infiltration, ulcers-fissures, scarring.
In the infiltration phase (the process is localized in the submucosa), the mucous membrane has the appearance of a “quilt” with a matte surface, the vascular pattern is not visible. Subsequently, aphthae-type erosions appear with isolated superficial ulcerations and fibrinous deposits.
In the ulcer-fissure phase, individual or multiple deep longitudinal ulcerative defects are detected, affecting the muscular layer of the intestinal wall. The intersection of cracks gives the mucous membrane a “cobblestone” appearance. Due to significant swelling of the submucosal membrane, as well as damage to the deep layers of the intestinal wall, the intestinal lumen narrows.
In the scarring phase, areas of irreversible intestinal stenosis are detected.
Characteristic radiological signs (the study is usually carried out with double contrast): segmented lesions, wavy and uneven contours of the intestine. In the colon, irregularities and ulcerations are determined along the upper edge of the segment with preservation of haustration along the lower edge. In the stage of ulcers-cracks - the appearance of a “cobblestone pavement”.
Diagnosis and differential diagnosis
The diagnosis is established on the basis of clinical and anamnestic data and the results of laboratory, instrumental, and morphological studies.
Differential diagnosis of Crohn's disease is carried out with acute and protracted intestinal infections of bacterial and viral etiology, diseases caused by protozoa, worms, malabsorption syndrome, tumors, nonspecific ulcerative colitis (Table 16-4), etc.
Table 16-4.Differential diagnosis of inflammatory bowel diseases*
* According to Kanshina O.A., 1999.
Treatment
The regime during the period of exacerbation is bed rest, then gentle. Medical nutrition - table? 4 according to Pevzner. The nature of the diet largely depends on the location and extent of intestinal damage and the phase of the disease.
The most effective medications are aminosalicylic acid preparations (mesalazine) and sulfasalazine. At the same time, it is necessary to take folic acid and multivitamins with microelements in accordance with the age-specific dose. In the acute phase of the disease and in case of severe complications (anemia, cachexia, joint damage, erythema, etc.), glucocorticoids (hydrocortisone, prednisolone, dexamethasone) are prescribed, less often - immunosuppressants (azathioprine, cyclosporine).
In addition, broad-spectrum antibiotics, metronidazole, probiotics, enzymes (pancreatin), enterosorbents (dioctahedral smectite), antidiarrheal drugs (for example, loperamide), and symptomatic agents are used to treat patients with Crohn's disease. In severe cases of the disease, with the development of hypoproteinemia and electrolyte disturbances, intravenous infusions of solutions of amino acids, albumin, plasma, and electrolytes are performed. According to indications, surgical treatment is carried out - removal of the affected parts of the intestine, excision of fistulas, anastomosis to restore patency.
Prevention
Forecast
The prognosis for recovery is unfavorable; the prognosis for life depends on the severity of the disease, the nature of its course, and the presence of complications. It is possible to achieve long-term clinical remission.
Nonspecific ulcerative colitis
Nonspecific ulcerative colitis is a chronic inflammatory-dystrophic disease of the colon with a recurrent or continuous course, local and systemic complications.
Nonspecific ulcerative colitis is common mainly among the population of industrialized countries (common
The rate among adults is 40-117:100,000). It develops relatively rarely in children, accounting for 8-15% of the incidence in adults. In the last two decades, an increase in the number of patients with ulcerative colitis has been observed both among adults and among children of all age groups. The onset of the disease can occur even in infancy. The gender distribution is 1:1, with boys more often affected at an early age, and girls more often in adolescence.
Etiology and pathogenesis
Despite many years of study, the etiology of the disease remains unclear. Among the various theories of the development of nonspecific ulcerative colitis, the most widespread are infectious, psychogenic and immunological. The search for any single cause of the ulcerative process in the colon has so far been unsuccessful. Viruses, bacteria, toxins, and some food ingredients that can, as triggers, cause the onset of a pathological reaction leading to damage to the intestinal mucosa are suggested as etiological factors. Great importance is attached to the state of the neuroendocrine system, local immune protection of the intestinal mucosa, genetic predisposition, unfavorable environmental factors, psychological stress, and iatrogenic drug effects. With nonspecific ulcerative colitis, a cascade of self-sustaining pathological processes occurs: first nonspecific, then autoimmune, damaging target organs.
Classification
The modern classification of ulcerative colitis takes into account the length of the process, the severity of clinical symptoms, the presence of relapses, and endoscopic signs (Table 16-5).
Table 16-5.Working classification of ulcerative colitis*
Extraintestinal manifestations and complications
* Nizhny Novgorod Research Institute of Pediatric Gastroenterology.
Clinical picture
The clinical picture is represented by three leading symptoms: diarrhea, bleeding in the stool, and abdominal pain. In almost half of the cases, the disease begins gradually. With mild colitis, single streaks of blood are noticeable in the stool, with severe colitis - a significant admixture of it. Sometimes the stool takes on the appearance of a foul-smelling liquid bloody mass. Most patients develop diarrhea, the frequency of stool varies from 4-8 to 16-20 times or more per day. In addition to blood, loose stools contain large amounts of mucus and pus. Diarrhea mixed with blood is accompanied, and sometimes preceded, by abdominal pain - often during meals or before defecation. The pain is cramping, localized in the lower abdomen, in the left iliac region or around the navel. Occasionally, a dysentery-like onset of the disease develops. Very typical for severe nonspecific ulcerative colitis is an increase in body temperature (usually no higher than 38? C), decreased appetite, general weakness, weight loss, anemia, and delayed sexual development.
ComplicationsNonspecific ulcerative colitis can be systemic or local.
Systemic complications are varied: arthritis and arthralgia, hepatitis, sclerosing cholangitis, pancreatitis, severe lesions of the skin, mucous membranes (erythema nodosum, pyoderma, trophic ulcers, erysipelas, aphthous stomatitis, pneumonia, sepsis) and eyes (uveitis, episcleritis).
Local complications in children rarely develop. These include: profuse intestinal bleeding, intestinal perforation, acute toxic dilation or stricture of the colon, damage to the anorectal area (cracks, fistulas, abscesses, hemorrhoids, sphincter weakness with fecal and gas incontinence); colon cancer.
Laboratory and instrumental studies
A blood test reveals leukocytosis with neutrophilia and a shift of the leukocyte formula to the left, a decrease in the content of erythrocytes, Hb, serum iron, total protein, dysproteinemia with a decrease in albumin concentration and an increase in γ-globulins; disturbances in the electrolyte composition of the blood are possible. According to the severity and phase of the disease, the ESR and the concentration of C-reactive protein increase.
Endoscopic research methods play a decisive role in the diagnosis of ulcerative colitis. During colonoscopy in the initial period of the disease, the mucous membrane is hyperemic, swollen, and easily vulnerable. Subsequently, a picture of typical
th erosive-ulcerative process. During the period of manifest manifestations, the circular folds of the mucous membrane thicken, and the activity of the sphincters of the colon is disrupted. With a long course of the disease, the folding disappears, the intestinal lumen becomes tube-shaped, its walls become rigid, and the anatomical bends are smoothed out. Hyperemia and swelling of the mucous membrane increase, and its granularity appears. The vascular pattern is not determined, contact bleeding is pronounced, erosions, ulcers, microabscesses, and pseudopolyps are found.
X-rays reveal a violation of the haustral pattern of the intestine: asymmetry, deformation or its complete disappearance. The intestinal lumen has the shape of a hose, with thickened walls, shortened sections, and smoothed anatomical bends.
Diagnosis and differential diagnosis
The diagnosis is established on the basis of clinical and laboratory data, the results of sigmoidoscopy, sigmoid and colonoscopy, irrigography, as well as histological examination of biopsy material.
Differential diagnosis is carried out with Crohn's disease, celiac disease, diverticulitis, tumors and polyps of the colon, intestinal tuberculosis, Whipple's disease, etc.
Treatment
The greatest importance in the treatment of ulcerative colitis in children is given to diet. Do they prescribe a dairy-free table? 4 according to Pevzner, enriched with protein from meat and fish products, eggs.
The basis of basic drug therapy is sulfasalazine and aminosalicylic acid preparations (mesalazine). They can be taken orally and administered as a medicated enema or suppository into the rectum. The dose of drugs and duration of treatment are determined individually. In severe cases of ulcerative colitis, glucocorticoids are additionally prescribed. Immunosuppressants (azathioprine) are used according to strict indications. Symptomatic therapy and local treatment (microenemas) are also carried out.
An alternative to conservative treatment is surgical - subtotal resection of the intestine with ileorectal anastomosis.
Prevention
Prevention is aimed primarily at preventing relapses. After discharge from the hospital, all patients should be advised
recommend courses of supportive and anti-relapse treatment, including basic drug therapy, diet and a protective-restorative regimen. Patients with nonspecific ulcerative colitis are subject to mandatory dispensary observation. Preventive vaccination is carried out only for epidemiological indications, weakened by vaccine preparations. Children are exempt from exams and physical activity (physical education classes, labor camps, etc.). It is advisable to conduct training at home.
Forecast
The prognosis for recovery is unfavorable; for life, it depends on the severity of the disease, the nature of the course, and the presence of complications. Regular monitoring of changes in the mucous membrane of the colon is indicated due to the possibility of dysplasia.
DISEASES OF THE BILIARY SYSTEM
Etiology and pathogenesis
The formation of pathology of the biliary system in children is facilitated by qualitative and quantitative disorders of the diet: increasing the intervals between meals, early introduction of fatty and spicy foods into the diet, overeating, excess sweets, and a sedentary lifestyle. Psychoemotional disorders, previous perinatal encephalopathy, VDS, and stressful situations predispose children to the development of pathology of the biliary system. A significant role is played by concomitant diseases of the stomach and duodenum, helminthic infestations, giardiasis, anomalies in the development of the gallbladder and biliary system, food
allergies, bacterial infections. Among the bacteria that cause inflammatory processes in the gallbladder and bile ducts, the predominant E. coli and various cocci; less commonly, the cause is anaerobic microorganisms. Hereditary predisposition is also of great importance.
Various lesions of the biliary tract are closely related to each other and have much in common at all stages of pathogenesis. The disease usually begins with the development of biliary dyskinesia, i.e. functional disorders of motility of the gallbladder, bile ducts, sphincters of Lutkens, Oddi and Mirizzi. Against this background, a change in the physicochemical properties of bile occurs, leading to the formation of crystals of bilirubin, cholesterol, etc. As a result, the development of organic inflammatory lesions of the gallbladder and bile ducts, as well as the formation of cholelithiasis, is possible.
Biliary dyskinesia
The functional state of the stomach and duodenum plays an important role in the occurrence of biliary dyskinesia. Impaired sphincter activity, duodenostasis, edema and spasm of the major duodenal nipple lead to hypertension in the biliary system and impaired bile secretion. There are different mechanisms leading to disruption of bile passage. Two possible variants of such mechanisms are shown in Fig. 16-2.
CLINICAL PICTURE AND DIAGNOSTICS
There are hypotonic (hypokinetic) and hypertonic (hyperkinetic) types of dyskinesia. A mixed form is also possible.
Dyskinesia of hypotonic type
The main signs of hypotonic dyskinesia are: decreased muscle tone of the gallbladder, weak contraction, increased volume of the gallbladder. Clinically, this option is accompanied by aching pain in the right hypochondrium or around the navel, general weakness, and fatigue. Sometimes it is possible to palpate a large atonic gallbladder. Ultrasound reveals an enlarged, sometimes elongated gallbladder with normal or delayed emptying. When an irritant (egg yolk) is administered, the transverse size of the gallbladder is usually reduced by less than 40% (normally 50%). Fractional duodenal sounding reveals an increase in the volume of portion B with normal or high
Rice. 16-2.Mechanisms of bile passage disturbance.
what speed of outflow of gallbladder bile, if the tone of the bladder is still preserved. The decrease in tone is accompanied by a decrease in the volume of this portion.
Dyskinesia of hypertensive type
The main signs of hypertensive type dyskinesia: reduction in the size of the gallbladder, acceleration of its emptying. Clinically, this option is characterized by short-term, but more intense attacks of pain localized in the right hypochondrium or around the navel, and sometimes dyspepsia. Ultrasound determines a decrease in the transverse size of the gallbladder after a choleretic breakfast by more than 50%. Fractional duodenal intubation reveals a decrease in the volume of portion B with an increase in the rate of bile outflow.
TREATMENT
Treatment can be carried out both in a hospital and at home. When prescribing treatment, the type of dyskinesia should be taken into account.
Medical nutrition:
Table? 5 with a complete content of proteins, fats and carbohydrates;
Fasting days, for example, fruit-sugar and kefir-curd days (for the purpose of detoxification);
Fruit and vegetable juices, vegetable oil, eggs (to naturally enhance the flow of bile).
Choleretic agents. Choleretic therapy must be carried out over a long period of time, in intermittent courses.
Choleretics (stimulating the formation of bile) - bile + garlic + nettle leaves + activated carbon ("Allohol"), bile + powder from pancreas and the mucous membrane of the small intestine ("Cholenzim"), hydroxymethylnicotinamide, osalmide, cyclovalone, rosehip fruit extract ( "Holosas"); plants (mint, nettle, chamomile, St. John's wort, etc.).
Cholekinetics (promoting the secretion of bile) - increasing the tone of the gallbladder (for example, preparations of common barberry, sorbitol, xylitol, egg yolk), reducing the tone of the bile ducts (for example, papaverine, platiphylline, belladonna extract).
To eliminate cholestasis, tubage according to G.S. is recommended. Demyanov with mineral water or sorbitol. In the morning, the patient is given a glass of mineral water (warm, without gases) to drink on an empty stomach, then for 20-40 minutes the patient lies on his right side on a warm heating pad without a pillow. Tubage is carried out 1-2 times a week for 3-6 months. Another option for tubage: after drinking a glass of mineral water, the patient takes 15 deep breaths using the diaphragm (vertical body position). The procedure is carried out daily for a month.
Acute cholecystitis
Acute cholecystitis is an acute inflammation of the gallbladder wall.
Pathogenesis.Enzymes of microorganisms affect the dehydroxylation of bile acids, enhance the desquamation of the epithelium, influence
affect the neuromuscular system and sphincters of the gallbladder and bile ducts.
Clinical picture. Acute catarrhal cholecystitis is usually manifested by pain, dyspeptic disorders and intoxication.
The pain is paroxysmal in nature, localized in the right hypochondrium, epigastric region and around the navel; the duration of the pain varies from several minutes to several hours. Occasionally, pain radiates to the lower angle of the right scapula, the right supraclavicular region, or the right half of the neck. More often, pain occurs after eating fatty, hot or spicy foods, as well as emotional experiences.
Dyspeptic syndrome is manifested by nausea and vomiting, sometimes constipation.
The main manifestations of intoxication syndrome are febrile fever, chills, weakness, sweating, etc.
Palpation of the abdomen reveals tension in the anterior abdominal wall, positive symptoms of Kehr, Murphy, Ortner and de Mussy-Georgievsky (phrenicus symptom). Possible liver enlargement. Less commonly, jaundice may occur due to obstruction of the common bile duct (due to edema or stones).
Diagnostics.The diagnosis is made on the basis of the clinical picture and ultrasound data (thickening and heterogeneity of the walls of the gallbladder, inhomogeneity of the contents of its cavity).
Treatment.Catarrhal acute cholecystitis is usually treated conservatively in a hospital or at home.
Bed rest (duration depends on the patient’s condition).
Diet - table? 5. Fasting days: fruit-sugar, kefir-curd, apple - to relieve intoxication.
A large amount of liquid (1-1.5 l/day) in the form of tea, fruit drinks, rosehip decoction.
Natural choleretic agents (fruit and vegetable juices, vegetable oil, eggs).
Antispasmodic drugs.
Antibiotics to suppress infection (semi-synthetic penicillins, erythromycin for 7-10 days).
Forecast.In most cases, the prognosis is favorable. However, in approximately 1/3 of patients, acute cholecystitis transforms into a chronic form.
Chronic noncalculous cholecystitis
Chronic cholecystitis is a chronic polyetiological inflammatory disease of the gallbladder, accompanied by
changes in the outflow of bile and changes in its physicochemical and biochemical properties.
Etiology.The etiology of chronic cholecystitis is complex and is largely related to the condition of the biliary system, duodenum and stomach. Disruption of the sphincter apparatus, duodenostasis, edema and spasm of the large duodenal nipple lead to hypertension in the biliary system, impaired bile passage and hypomotor dyskinesia of the gallbladder. Just as in the development of acute cholecystitis, an infectious process (usually bacterial) plays a certain role, promoting the formation of cholesterol crystals.
Pathogenesis.Allergic factors play a certain role in the formation of chronic cholecystitis. Bacterial toxins, chemical and drug exposure aggravate dyskinetic disorders. The role of intestinal dysbiosis is noted. The pathogenesis of chronic cholecystitis is presented in a simplified manner in Fig. 16-3.
Clinical picture. The disease manifests itself as recurrent paroxysmal pain in the epigastric region, right hypochondrium and around the navel, often radiating to the right scapula. During the period of exacerbation of chronic cholecystitis, the clinical picture consists of several components, caused not only by the pathology of the gallbladder, but also by a secondary disorder
Rice. 16-3.Pathogenesis of chronic cholecystitis.
functions of other internal organs. Thus, insufficiency or complete cessation (acholia) of the flow of bile into the intestines leads to disruption of digestion and intestinal motility, changes in the evacuation-motor and secretory functions of the stomach and duodenum, a decrease in the secretion of pancreatic enzymes, the occurrence of fermentation and sometimes putrefactive processes in the intestines, the appearance of dyspeptic disorders (nausea, bitterness in the mouth, decreased appetite, flatulence, constipation or loose stools). As a result, signs of chronic intoxication appear: weakness, low-grade body temperature, dizziness, headache. Body weight decreases, children may lag behind in physical development. The skin and sclera may be somewhat icteric due to cholestasis. The tongue is coated, sometimes swollen, with teeth marks along the edges. When palpating the abdomen, pain in the right hypochondrium and epigastric region is determined.
Diagnostics.During the period of exacerbation, moderate leukocytosis with neutrophilia, an increase in ESR, and a possible increase in bilirubin concentration and alkaline phosphatase activity (due to cholestasis) are detected in the peripheral blood. The diagnosis is established on the basis of anamnesis and clinical and instrumental studies. Ultrasound reveals a thickening of the wall of the gallbladder, an increase in its volume; a thick secretion is often detected in the lumen of the bladder; after a test breakfast, the gallbladder does not completely empty. The bubble may take on a spherical shape.
Differential diagnosis. Acute and chronic cholecystitis is differentiated from other diseases of the gastroduodenal zone - chronic gastroduodenitis, biliary dyskinesia, hepatitis, chronic pancreatitis, etc.
TreatmentChronic cholecystitis during an exacerbation is based on the same principles as the treatment of acute cholecystitis: bed rest, diet? 5 and? 5a with a ratio of proteins, fats and carbohydrates 1:1:4, plenty of fruits and vegetables, fractional meals. Table? 5 for 2 years is recommended during the period of remission. After the second year of observation, the diet can be expanded. In case of severe exacerbation of chronic cholecystitis, detoxification therapy is indicated - intravenous administration of glucose and saline solutions. Otherwise, drug therapy is the same as for acute cholecystitis.
Prevention.If there is a threat of developing chronic cholecystitis, prevention consists of strict adherence to the diet, the use of choleretic agents, including choleretic tea, limiting physical activity (including physical education at school), and reducing emotional stress.
Forecast.Relapses of the disease can lead to the development of anatomical and functional disorders (for example, thickening of the gallbladder wall, the appearance of parietal congestion, possible formation of gallstones).
Chronic calculous cholecystitis
Chronic calculous cholecystitis is rarely observed in pediatric practice. But in recent years (apparently thanks to the use of ultrasound), it has been detected in children more often than before, especially in teenage girls with various types of metabolic disorders.
Etiology and pathogenesis. The formation of cholelithiasis is based on parietal stagnation of bile with hypomotor dyskinesia of the gallbladder, an inflammatory process in the biliary tract and changes in the chemical composition of bile due to metabolic disorders. Under the influence of these factors, cholesterol, calcium, and bilirubin precipitate, especially in the parietal layer of bile, followed by the formation of stones. In young children, pigment stones (yellow, consisting of bilirubin, a small amount of cholesterol and calcium salts) are more often formed; in older children, cholesterol stones (darkish, consisting of cholesterol crystals) are usually found.
Clinical picture. There are two possible clinical picture options for calculous cholecystitis in children. More often, the disease occurs without typical attacks of abdominal pain; only aching pain, heaviness in the upper abdomen, bitterness in the mouth and belching are noted. Less commonly observed is a typical course with repeated attacks of acute pain in the area of the right hypochondrium (biliary colic). The pain can recur many times at certain intervals. Colic is often accompanied by nausea, vomiting, and cold sweat. The passage of a stone can cause temporary blockage of the bile duct, the appearance of acute obstructive jaundice and acholic stool. If the stone is small and has passed through the bile ducts, pain and jaundice are relieved.
Diagnostics.The diagnosis is established on the basis of clinical data and special research methods: ultrasound and x-ray (cholecystography). An ultrasound scan of the gallbladder and bile ducts reveals dense formations. During cholecystography, multiple or single defects in the filling of the gallbladder are recorded.
Treatment.Both drug and surgical treatment are possible. There are drugs that soften and dissolve pigment and cholesterol stones of small diameter (0.2-0.3 cm). However,
Taking into account general metabolic disorders and chronic disorders of biliary function, re-formation of stones is possible. A radical method should be considered cholecystectomy - removal of the gallbladder. Currently, a widely used endoscopic method is laparoscopic cholecystectomy.
DISEASES OF THE PANCREAS
Of all pancreatic diseases, pancreatitis is most often diagnosed in children. Pancreatitis is a disease of the pancreas caused by activation of pancreatic enzymes and enzymatic toxemia.
Acute pancreatitis
Acute pancreatitis can be represented by acute swelling of the gland, hemorrhagic lesions, acute fat necrosis and purulent inflammation.
Etiology
The main etiological factors of acute pancreatitis are as follows.
Acute viral diseases (for example, mumps, viral hepatitis).
Bacterial infections (eg, dysentery, sepsis).
Traumatic damage to the pancreas.
Pathology of the stomach and duodenum.
Diseases of the biliary tract.
Severe allergic reaction.
Pathogenesis
A simplified diagram of the pathogenesis of acute pancreatitis is presented in Fig. 16-4.
Entering the blood and lymph, pancreatic enzymes, products of enzymatic breakdown of proteins and lipids activate the kinin and plasmin systems and cause toxemia, which affects the functions of the central nervous system, hemodynamics and the condition of parenchymal organs. In most children, as a result of exposure to inhibitory systems, the process can be interrupted at the stage of pancreatic edema, then pancreatitis undergoes reverse development.
Classification
Clinical and morphological classification of acute pancreatitis includes the edematous form, fatty pancreatic necrosis and hemorrhagic
Rice. 16-4.The mechanism of development of acute pancreatitis.
pancreatic necrosis. Depending on the clinical picture, acute edematous (interstitial), hemorrhagic and purulent pancreatitis are distinguished.
Clinical picture
Symptoms of the disease largely depend on its clinical form and the age of the child (Table 16-6).
Table 16-6.Clinical picture and treatment of acute pancreatitis*
* From: Baranov A.A. et al. Pediatric gastroenterology. M., 2002.
Diagnostics
The diagnosis is made on the basis of the clinical picture and data from laboratory and instrumental studies.
A general blood test reveals leukocytosis with a shift in the leukocyte formula to the left, and an increase in hematocrit.
In biochemical analysis, an increased content of amylase is noted. For early diagnosis of the disease, repeated (after 6-12 hours) studies of amylase activity in the blood and urine are used. However, its content does not serve as a criterion for the severity of the process. Thus, moderately severe edematous pancreatitis may be accompanied by a high amylase content, and severe hemorrhagic pancreatitis may be accompanied by minimal levels. With pancreatic necrosis, its concentration in the blood decreases.
Ultrasound reveals an increase in the size of the pancreas, its compaction and swelling.
Differential diagnosis
Differential diagnosis of acute pancreatitis is carried out with peptic ulcer of the stomach and duodenum, acute cholecystitis (see relevant sections), choledocholithiasis, acute appendicitis, etc.
Treatment
Treatment, as well as the clinical picture, depends on the form of the disease and the age of the child (see Table 16-6).
Chronic pancreatitis
Chronic pancreatitis is a polyetiological disease of the pancreas with a progressive course, degenerative and destructive changes in the glandular tissue of a focal or diffuse nature, and a decrease in the exocrine and endocrine functions of the organ.
Etiology
In most children, chronic pancreatitis is secondary and associated with diseases of other digestive organs (gastroduodenitis, pathology of the biliary system). As a primary disease, chronic pancreatitis develops in children only in 14% of cases, most often due to fermentopathy or acute abdominal trauma. The toxic effect of drugs cannot be excluded.
Pathogenesis
The mechanism of development of the disease may be due to two factors: difficulty in the outflow of pancreatic enzymes and causes acting directly on glandular cells. Just as with acute pancreatitis, the pathological process in the ducts and parenchyma of the pancreas leads to edema, necrosis, and, over a long period of time, to sclerosis and fibrosis of the organ tissue. Powerful inhibitory systems and protective factors of the gland are able to stop the pathological process at the stage of edema, which is what happens in most cases of reactive pancreatitis.
Origin | Primary Secondary |
Course of the disease | Recurrent Monotonous |
Current severity (form) | Light Moderate Heavy |
Period of illness | Exacerbation Abatement of exacerbation Remission |
Functional state of the pancreas | A. Exocrine function: hyposecretory, hypersecretory, obstructive, normal B. Intrasecretory function: hyperfunction or hypofunction of the insular apparatus |
Complications False cyst, pancreolithiasis, diabetes, pleurisy, etc. |
|
Accompanying illnesses | Peptic ulcer, gastroduodenitis, cholecystitis, hepatitis, enterocolitis, colitis, ulcerative colitis |
* From: Baranov A.A. et al. Pediatric gastroenterology. M., 2002.
The main clinical manifestation of chronic pancreatitis is pain. The pain is often paroxysmal, localized in the upper half of the abdomen - in the epigastric region, right and left hypochondrium. Sometimes they become aching and worsen after eating and in the afternoon. Most often, the occurrence of pain is associated with errors in diet (eating fatty, fried, cold, sweet foods). Sometimes an attack can be triggered by significant physical exertion or an infectious disease. The duration of pain varies - from 1-2 hours to several days. The pain often radiates to the back, right or left half of the chest, and weakens in a sitting position, especially when bending the torso forward. The most typical position for a patient with chronic pancreatitis is the knee-elbow position (in which the pancreas is in a “suspended” state).
Of the pathological symptoms during the period of exacerbation of the disease, symptoms of Mayo-Robson, Kutch, de Mussi-Georgievsky, and Grott are often detected. In most children, the firm and tender head of the pancreas can be palpated.
Chronic pancreatitus is characterized by dyspeptic disorders: loss of appetite, nausea, vomiting that occurs at altitude
pain attack, belching, heartburn. More than a third of patients experience constipation, followed by diarrhea during exacerbation of the disease.
General symptoms of chronic pancreatitis: weight loss, asthenovegetative disorders (fatigue, emotional instability, irritability).
The severity of clinical symptoms is related to the severity of the disease. The process is aggravated by accompanying organic changes in the duodenum (duodenostasis, diverticula) and the biliary system (chronic cholecystitis, cholelithiasis).
Diagnostics
The diagnosis is based on clinical, laboratory and instrumental data.
When studying the content of pancreozymin and secretin, pathological types of pancreatic secretion are detected.
Provocative tests with glucose, neostigmine methyl sulfate, pancreozymin reveal changes in the content of amylase and trypsin.
Using ultrasound, the structure of the gland is determined. If necessary, CT and endoscopic retrograde cholangiopancreatography are used.
Treatment
The basis of treatment for chronic pancreatitis is a diet that reduces pancreatic and gastric secretion. The patient's diet should contain a sufficient amount of protein while limiting fats (55-70 g) and carbohydrates (250-300 g). To relieve pain, drotaverine, papaverine, and bencyclane are prescribed.
The negative effects of exposure to hydrochloric acid are neutralized by prescribing antisecretory drugs - histamine H 2 receptor blockers, as well as other drugs of this series (for example, omeprazole). Given the impaired motility of the duodenum and biliary dyskinesia, metoclopramide and domperidone are prescribed.
During the period of exacerbation of chronic pancreatitis, fasting is recommended for the first 3-4 days, unsweetened tea, alkaline mineral waters, and rosehip decoction are allowed. The means of pathogenetic therapy are inhibitors of proteolytic enzymes (for example, aprotinin). The drugs are administered intravenously in 200-300 ml of 0.9% sodium chloride solution. Doses are selected individually.
Recently, somatostatin (octreotide) has been proposed to suppress pancreatic secretion. It has a multifaceted effect on the gastrointestinal tract: reduces abdominal pain, eliminates intestinal paresis, normalizes the activity of amylase, lipase, trypsin in the blood and urine.
Replacement therapy with enzyme preparations (pancreatin, etc.) is also important. Indications for their use are signs of exocrine pancreatic insufficiency. If an exacerbation of chronic pancreatitis is accompanied by an increase in body temperature, an increase in ESR, and a neutrophilic shift in the leukocyte count to the left, broad-spectrum antibiotics are prescribed.
After discharge from the hospital, patients with chronic pancreatitis are subject to dispensary observation, and they are given courses of anti-relapse treatment. Sanatorium treatment is recommended in Zheleznovodsk, Essentuki, Borjomi, etc.
CHRONIC HEPATITIS
Chronic hepatitis is a diffuse inflammatory process in the liver that continues without improvement for at least 6 months.
The classification of chronic hepatitis, adopted at the International Congress of Gastroenterologists (Los Angeles, 1994), is presented in Table. 16-8.
Table 16-8.Classification of chronic hepatitis
The prevalence of chronic hepatitis has not been precisely established due to the large number of erased and asymptomatic forms and the lack of population studies. Most often, chronic viral hepatitis is detected, caused by the persistence of hepatitis B and C viruses in the body.
Chronic viral hepatitis
Chronic viral hepatitis is a chronic infectious disease caused by hepatotropic viruses and characterized by
characterized by a clinical and morphological picture of diffuse liver inflammation lasting more than 6 months and a symptom complex of extrahepatic lesions.
CHRONIC HEPATITIS B Etiology and pathogenesis
The causative agent of the disease is a DNA virus (hepatitis B virus). The main route of transmission is parenteral. It is believed that chronic hepatitis B is a primarily chronic disease or occurs after an erased or subclinical form of acute infection. The transition of acute hepatitis B to chronic is noted in 2-10% of cases, mainly in mild or latent forms of the disease. The vast majority of patients with chronic hepatitis have no history of acute hepatitis.
It is believed that the cause of the development of chronic hepatitis B may be a lack of immune response due to genetic reasons or immaturity of the body (infection of a fetus, newborn or young child). Infection of a child in the perinatal period and in the first year of life in 90% of cases ends in the formation of chronic hepatitis B or carriage of the hepatitis B virus. Chronic hepatitis B and carriage of HB s Ag are often registered in diseases associated with dysfunction of the immune system: immunodeficiency states, chronic diseases kidneys, chronic lymphocytic leukemia, etc.
Chronic hepatitis B has several phases: initial (immune tolerance); immune response (replicative), occurring with pronounced clinical and laboratory activity; integrative, carriage of HB s Ag. The process usually remains active for 1-4 years and is replaced by the phase of integration of hepatitis B virus DNA into the hepatocyte genome, which coincides with clinical remission of the disease. The process may result in the development of carrier state or cirrhosis of the liver.
The hepatitis B virus itself does not appear to cause cytolysis. Damage to hepatocytes is associated with immune reactions that occur in response to viral (HB s Ag, HB^g) and liver Ags circulating in the blood. During the phase of viral replication, all three Ags of the hepatitis B virus are expressed, immune aggression is more pronounced, which causes massive necrosis of the liver parenchyma and mutation of the virus. As a result of virus mutation, the composition of serum Ags changes, so virus replication and destruction of hepatocytes occur over a long period of time.
Replication of the virus is also possible outside the liver - in bone marrow cells, mononuclear cells, thyroid and salivary glands, which apparently determines the extrahepatic manifestations of the disease.
Clinical picture
The clinical picture of chronic hepatitis B is associated with the phase of viral replication and is polysyndromic.
Almost all patients have a slight intoxication syndrome with asthenovegetative manifestations (irritability, weakness, fatigue, sleep disturbance, headaches, sweating, low-grade fever).
Jaundice is possible, although more often patients are diagnosed with subicterus or mild icterus of the sclera.
Hemorrhagic syndrome, which correlates with the severity of the process, is recorded in approximately 50% of patients; it is expressed in mild nosebleeds, petechial rash on the face and neck, and hemorrhages on the skin of the extremities.
Vascular manifestations (so-called extrahepatic signs) occur in 70% of patients. They include telangiectasias (“spider veins”) on the face, neck and shoulders, as well as palmar erythema, a symmetrical redness of the palms (“palms”) and soles.
Dyspeptic syndrome (bloating, flatulence, nausea, worse after eating and taking medications, belching, anorexia, intolerance to fatty foods, a feeling of heaviness in the right hypochondrium and epigastric region, unstable stool) is associated with both functional inferiority of the liver and concomitant damage biliary tract, pancreas, gastroduodenal zone.
Hepatomegaly is the main and sometimes the only clinical symptom of chronic hepatitis B. The sizes of both lobes of the liver are increased both by percussion and palpation. Sometimes the liver protrudes 6-8 cm from under the edge of the costal arch, has a dense elastic consistency, a rounded or pointed edge, and a smooth surface. Palpation is painful. Signs of liver damage are more pronounced when the process is active. Patients often complain of constant aching pain in the right hypochondrium, which intensifies with physical activity. With a decrease in activity, the size of the liver decreases, palpation becomes less painful, and pain in the liver area bothers the child less.
A pronounced enlargement of the spleen is detected with high hepatitis activity.
Possible endocrine disorders - menstrual irregularities in girls, stretch marks on the thighs, acne, hirsutism, etc.
Extrahepatic systemic manifestations include nervous tics, erythematous spots on the skin, urticaria, erythema nodosum, and transient arthralgia.
A general blood test in the active period and in severe cases of chronic hepatitis B reveals anemia, leukopenia, thrombocytopenia, lymphopenia and an increase in ESR. In the blood serum, an increase in aminotransferase activity by 2-5 times or more, hyperbilirubinemia (increased concentration of conjugated bilirubin), hypoalbuminemia, hypoprothrombinemia, an increase in cholesterol, alkaline phosphatase (3 times or more) and γ-globulins are noted. Using ELISA, RIF, DNA hybridization and PCR, markers of hepatitis B virus replication (HB e Ag, anti-HB e Ag-IgM, viral DNA) are detected.
CHRONIC HEPATITIS C
Etiology.The causative agent of the disease is an RNA virus (hepatitis C virus). The routes of transmission are similar to those of chronic hepatitis B.
Pathogenesis.Chronic viral hepatitis C is the outcome of acute hepatitis C (in 50-80% of cases). The hepatitis C virus has a direct cytopathic effect on hepatocytes. As a result, viral replication and persistence in the body are associated with hepatitis activity and progression.
Clinical picture. Clinical manifestations of chronic hepatitis C are usually mild or absent. Patients are concerned about fatigue, weakness, and dyspeptic disorders. On examination, hepatomegaly, telangiectasia, and palmar erythema are detected. The course of the disease is undulating and long-lasting. A biochemical blood test reveals an increase in alanine aminotransferase (ALT) activity. The diagnosis is based on the detection of specific markers of chronic hepatitis C - RNA of the virus and antibodies to it (in the absence of markers of the hepatitis B virus).
CHRONIC HEPATITIS DELTA
Etiology.The causative agent is a small defective RNA virus (hepatitis D virus); it is contagious only when infected with the hepatitis B virus (since, due to its incomplete genome, it uses proteins of the hepatitis B virus for replication). The main route of transmission is parenteral.
Pathogenesis.Chronic viral hepatitis D is always the outcome of its acute form, which occurs as a superinfection or coinfection in patients with acute or chronic hepatitis B. The hepatitis D virus has a cytopathogenic effect on hepatocytes, maintains activity and promotes the progression of the process in the liver.
Clinical picture. Clinically, symptoms of liver failure are detected (severe weakness, drowsiness during the day, insomnia at night, bleeding, dystrophy). Most patients have jaundice and skin itching, extrahepatic systemic manifestations, enlargement and hardening of the liver. Chronic hepatitis D is characterized by a severe course. Markers of chronic hepatitis D are detected in the blood - viral DNA and antibodies to its Ag. Hepatitis B virus replication is suppressed as liver cirrhosis rapidly develops.
DIAGNOSTICS
Diagnosis of chronic viral hepatitis is based on anamnestic, clinical (intoxication, hemorrhagic syndrome, enlargement and hardening of the liver, extrahepatic signs), biochemical (increased ALT, thymol test, dysproteinemia, hyperbilirubinemia, etc.), immunological (signs of immune inflammation, specific markers ) and morphological data.
DIFFERENTIAL DIAGNOSTICS
TREATMENT
Treatment of chronic viral hepatitis includes first of all basic, then symptomatic and (if indicated) detoxification and antiviral therapy.
Basic therapy includes regimen and diet, prescription of vitamins.
The regimen of patients with chronic hepatitis should be as gentle as possible, in the active period of the disease - half-bed. Limit physical and emotional stress.
When prescribing a diet, the individual tastes and habits of the patient, the tolerance of individual foods and concomitant gastrointestinal diseases are taken into account. They use mainly fermented milk and vegetable products, 50% of fats should be of vegetable origin. Avoid fatty, fried, smoked foods, ice cream, coffee, chocolate, and carbonated drinks. Limit meat and fish broths, as well as the amount of raw fruit. Meals should be fractional (4-5 times a day).
To normalize metabolic processes and vitamin balance, vitamin C (up to 1000 mg/day) and multivitamin preparations are prescribed.
Symptomatic therapy includes the prescription of courses of mineral waters, choleretic and antispasmodic agents, enzyme preparations and probiotics for the treatment of concomitant dysfunctions of the biliary system and gastrointestinal tract.
In case of severe intoxication, intravenous drip administration of povidone + sodium chloride + potassium chloride + calcium chloride + magnesium chloride + sodium bicarbonate (Gemodeza), 5% glucose solution is necessary for 2-3 days.
In the active phase of the disease (phase of virus replication), therapy is carried out with interferon preparations (interferon alpha-2b - subcutaneously 3 times a week for 6 months at a dose of 3 million IU/m 2 body surface; interferon alpha-2a; interferon alpha-p1 are also used ) and other antiviral drugs. The effectiveness of treatment is 20-60%. Chronic viral hepatitis D is resistant to interferon therapy. If antiviral therapy is ineffective, a combination of interferon alpha with antiviral drugs (for example, ribavirin) is possible. For chronic hepatitis B, lamivudine therapy is also carried out.
PREVENTION
Primary prevention has not been developed. Secondary prevention consists of early recognition and adequate treatment of patients with acute viral hepatitis. Children who have suffered acute viral hepatitis B, C, D, G must be registered at the dispensary for at least one year. During the period of clinical observation, it is recommended, in addition to examination to determine the size of the liver, to conduct a biochemical study of blood serum (total bilirubin, transaminase activity, sediment samples, specific markers, etc.). Avoidance of medical vaccinations, limitation of physical activity, strict adherence to diet, and sanatorium-resort treatment (beyond exacerbation) are indicated. Widespread introduction of vaccination against hepatitis A and B will solve the problem of not only acute, but also chronic hepatitis.
FORECAST
The likelihood of a full recovery is low. As the process progresses, liver cirrhosis and hepatocellular carcinoma develop.
Autoimmune hepatitis
Autoimmune hepatitis is a progressive hepatocellular inflammation of unknown etiology, characterized by the presence of periportal hepatitis, hypergammaglobulinemia, liver-associated serum autoantibodies and the positive effect of immunosuppressive therapy.
The prevalence of autoimmune hepatitis in European countries is 0.69 cases per 100,000 population. In the structure of chronic liver diseases, the share of autoimmune hepatitis in adult patients is 10-20%, in children - 2%.
Etiology and pathogenesis
The etiology of autoimmune hepatitis is unknown, and the pathogenesis is not well understood. It is assumed that autoimmune hepatitis develops as a result of a primarily caused disorder of the immune response. Viruses (Epstein Barr, measles, hepatitis A and C) and some medications (for example, interferon) are pointed out as possible trigger factors contributing to the onset of the disease.
In the presence of an appropriate genetic predisposition, with or without the influence of trigger factors, a disorder of immune regulation occurs, manifested by a defect in the function of suppressor T cells, linked by the HLA A1-B8-DR3 haplotype in the white population in Europe and North America, or by the HLA DR4 allele, more common in Japan and other countries of Southeast Asia). As a result, uncontrolled synthesis of IgG class antibodies by B cells occurs, which destroy the membranes of normal hepatocytes. In total, the DR3 and/or DR4 alleles are detected in 80-85% of patients with autoimmune hepatitis. Currently, autoimmune hepatitis types I, II and III are distinguished.
Type I is the classic variant, accounting for about 90% of all cases of the disease. The role of the main autoantigen in autoimmune hepatitis type I belongs to the liver-specific protein (liver specific protein, LSP). Antinuclear antibodies are detected in blood serum (antinuclear antibodies, ANA) and/or antismooth muscle (smooth muscle antibody, SMA) AT titer more than 1:80 in adults and more than 1:20 in children. In 65-93% of patients with this type of hepatitis, perinuclear neutrophil cytoplasmic antibodies (pANCA) are also detected.
Autoimmune hepatitis type II accounts for about 3-4% of all cases, most of the patients are children from 2 to 14 years old. The main autoantigen in autoimmune hepatitis type II is liver microsomal Ag.
and type I kidneys (liver kidney microsomes, LKM-1). In autoimmune hepatitis type II, antibodies to microsomes of liver cells and epithelial cells of the glomerular apparatus of the kidneys type I (anti-LKM-!) are detected in the blood serum.
There is also autoimmune hepatitis type III, characterized by the presence of AT to soluble liver Ag (soluble liver antigen) anti-SLA in the absence of ANA or anti-KLM-1 In patients with type III disease, SMA (35%), antimitochondrial antibodies (22%), rheumatoid factor (22%) and antibodies to liver membrane antigens (anti-LMA) are often detected. (26%).
Clinical picture
The clinical picture in children in 50-65% of cases is characterized by the sudden onset of symptoms similar to those of viral hepatitis. In some cases, the disease begins imperceptibly with asthenovegetative disorders, pain in the right hypochondrium, and slight jaundice. The latter often appears in the later stages of the disease, is unstable and intensifies during exacerbations. The appearance of telangiectasia (on the face, neck, arms) and palmar erythema is characteristic. The liver is compacted and protrudes from under the edge of the costal arch by 3-5 cm, the spleen is almost always enlarged. Autoimmune hepatitis is often accompanied by amenorrhea and infertility; boys may develop gynecomastia. It is possible to develop acute recurrent migratory polyarthritis involving large joints without their deformities. One of the options for the onset of the disease is fever in combination with extrahepatic manifestations.
Laboratory research
A blood test reveals hypergammaglobulinemia, an increase in the concentration of IgG, a decrease in the concentration of total protein, and a sharp increase in ESR. Leukopenia and thrombocytopenia are detected in patients with hypersplenism and portal hypertension syndrome. Autoantibodies against liver cells are detected in the blood serum.
Diagnosis and differential diagnosis
There are “definite” and “probable” autoimmune hepatitis.
A “definite” diagnosis of autoimmune hepatitis implies the presence of a number of indicators: periportal hepatitis, hypergammaglobulinemia, autoantibodies in the blood serum, increased activity of serum transaminases with normal concentrations of ceruloplasmin, copper and a 1 -antitrypsin. At the same time, the concentration of serum γ-globulins exceeds the upper limit of normal by more than 1.5 times, and antibody titers (ANA, SMA and anti-LKM-1) do not
less than 1:80 in adults and 1:20 in children. In addition, there are no viral markers in the blood serum, damage to the bile ducts, copper deposition in the liver tissue and other histological changes suggesting a different etiology of the process, and there is no history of blood transfusions or the use of hepatotoxic drugs. A “probable” diagnosis is justified when the existing symptoms suggest autoimmune hepatitis, but are not sufficient to make a “definite” diagnosis.
In the absence of autoantibodies in the blood serum (about 20% of patients), the disease is diagnosed on the basis of an increase in the activity of transaminases in the blood, pronounced hypergammaglobulinemia, a selective increase in the serum IgG content, typical histological signs and a certain immunological background (detection of other autoimmune diseases in a sick child or his relatives) with the mandatory exclusion of other possible causes of liver damage. Some diagnostic signs of various types of autoimmune hepatitis are given in table. 16-9.
Table 16-9.Diagnostic criteria for different types of autoimmune hepatitis
Differential diagnosis is carried out with chronic viral hepatitis, α1-antitrypsin deficiency, and Wilson-Konovalov's disease.
Treatment
The basis of treatment is immunosuppressive therapy. Prednisolone, azathioprine, or a combination of both are prescribed. Combination therapy is recommended to reduce the likelihood of developing adverse reactions from the use of glucocorticoids: in this case, prednisolone is prescribed in a lower dose than with monotherapy. A positive response to such therapy is one of the criteria for the diagnosis of autoimmune hepatitis. However, if there is no effect, this diagnosis cannot be completely excluded, since the patient may violate the drug regimen or insufficient dosage. The goal of treatment is to achieve complete remission. Remission means the absence of biochemical signs of inflammation [aspartate aminotransferase (AST) activity is no more than 2 times higher than normal] and histological data indicating the activity of the process.
Therapy with prednisolone or a combination of prednisolone with azathioprine allows achieving clinical, biochemical and histological remission in 65% of patients within 3 years. The average duration of treatment until remission is achieved is 22 months. Patients with histologically confirmed cirrhosis of the liver respond to therapy as well as patients without signs of cirrhosis: the 10-year survival rate of patients with or without cirrhosis during therapy is practically the same and is 89 and 90%, respectively. Prednisolone is prescribed at a dose of 2 mg/kg (maximum dose 60 mg/day) with its subsequent reduction by 5-10 mg every 2 weeks under weekly monitoring of biochemical parameters. When transaminase levels are normalized, the dose of prednisolone is reduced to the minimum possible maintenance dose (usually 5 mg/day). If liver tests do not normalize during the first 6-8 weeks of therapy, azathioprine is additionally prescribed at an initial dose of 0.5 mg/kg. If there are no signs of toxicity, increase the dose of the drug to 2 mg/day. Although a decrease in transaminase activity by 80% of the original occurs within the first 6 weeks in most patients, complete normalization of enzyme concentrations occurs only after a few months (after 6 months for autoimmune hepatitis type I, after 9 months for type II). Relapses during therapy occur in 40% of cases, and the dose of prednisolone is temporarily increased. After 1 year from the start of remission, it is recommended to try to cancel immunosuppressive therapy, but only after performing a control puncture biopsy of the liver. In this case, a morphological study should indicate the absence or minimal severity of inflammatory changes. However, in most cases it is not possible to completely cancel immunosuppressive therapy. If autoimmune hepatitis relapses after discontinuation of immunosuppressive drugs,
lifelong maintenance therapy with prednisolone (5-10 mg/day) or azathioprine (25-50 mg/day). Long-term immunosuppressive therapy causes adverse reactions in 70% of children. If glucocorticoid therapy is ineffective, cyclosporine and cyclophosphamide are used.
In 5-14% of patients with a confirmed diagnosis of autoimmune hepatitis, primary resistance to treatment is observed. This small group of patients can be clearly identified already 14 days after the start of treatment: their liver test results do not improve, and their subjective well-being remains the same or even worsens. Mortality among patients in this group is high. They are subject to mandatory consultation at liver transplant centers, as are those patients who develop a relapse that is resistant to therapy during or after treatment. Drug treatment of such patients usually turns out to be ineffective; continuing to take glucocorticoids in high doses only leads to the loss of precious time.
Prevention
Primary prevention has not been developed. The secondary consists of regular follow-up of patients, periodic determination of the activity of liver enzymes, the content of γ-globulins and autoantibodies for timely diagnosis of relapse and strengthening of immunosuppressive therapy. Important points: adherence to a daily routine, limitation of physical and emotional stress, diet, exemption from vaccination, minimal intake of medications. Periodic courses of hepatoprotectors and maintenance therapy with glucocorticoids are indicated.
Forecast
Without treatment, the disease continuously progresses and does not have spontaneous remissions. Improvements in well-being are short-term; biochemical parameters do not normalize. As a result of autoimmune hepatitis, liver cirrhosis of the macronodular or micronodular type is formed. The prognosis for children with primary resistance to treatment is poor. If immunosuppressive therapy is ineffective, patients are advised to undergo liver transplantation. After liver transplantation, the 5-year survival rate in patients with autoimmune hepatitis is more than 90%.
22.09.2014 10:11
The intake of the proper amount of nutrients into the body is the most important factor in ensuring normal human life. The process of receiving the vitamins and minerals necessary for the body is ensured by the digestive organs. Diseases of the digestive system disrupt the normal supply of nutrients to the body and, as a result, the functioning of literally all systems and organs is disrupted. This is why diseases affecting the digestive system must be diagnosed and treated promptly.
How are the digestive organs structured?
Diseases of the digestive system can affect different organs, which anatomy divides into several sections. The digestion process begins with the preliminary processing of food, which is produced in the oral cavity. From there, food goes into the pharynx, then into the esophagus, and finally into the main digestive organ, the stomach.
The stomach, consisting of muscles, has in its internal cavity many glands that produce gastric juice and hydrochloric acid. Food, broken down by the above-mentioned liquids, begins to move into the duodenum, which is the initial section of the intestine. Here the digested food is exposed to bile and pancreatic juice.
Of course, a large number of organs contributes to a variety of ailments - diseases of the digestive system are numerous, painful and can significantly reduce the quality of life.
The longest section of the digestive system is the small intestine. In it, food is completely broken down, and nutrients safely penetrate into the blood. The digestion process is completed in the large intestine - undigested food remains enter it, which are eliminated from the body due to the movement of the large intestine.
Diseases of the digestive system can also affect organs such as the liver and pancreas. It is thanks to these two important organs, as well as the salivary and microscopic glands, that the digestion process occurs. The liver is responsible for the production of bile, and the pancreas is responsible for insulin and enzymes necessary for the breakdown of proteins, fats, and carbohydrates. The salivary glands are responsible for softening ingested food.
Only the coordinated and precise functioning of the digestive system allows us to speak about the normal state of the body; the slightest disturbances and failures in this complex biological mechanism provoke certain diseases of the digestive system. We have to admit that today disturbances in the functioning of the gastrointestinal tract are a very common phenomenon. Poor nutrition, stress, unhealthy food, chronic diseases - all these factors increase the risk of joining the ranks of patients suffering from gastrointestinal diseases. The most common diseases of the digestive system are, first of all, gastritis, dysbacteriosis, duodenitis, peptic ulcer of the duodenum and stomach, reflux esophagitis, erosive bulbitis, food poisoning, intestinal obstruction and many other ailments. Each of the above diseases should be treated correctly and in a timely manner. By ignoring diseases of the digestive system, the patient, due to disruption of the supply of nutrients to the blood, endangers the health of the entire body.
Causes of diseases of the digestive system
Diseases of the digestive system depend on many specific factors. Doctors classify all existing causes that provoke the diseases in question into two categories - internal and external. The fundamental role influencing the occurrence of a particular disease of the digestive system is undoubtedly played by external causes:
. consumption of unhealthy and low-quality food;
. consumption of liquids harmful to the body;
. improper use or abuse of medications.
Diseases of the digestive system are often a consequence of an unbalanced diet. It is, in particular, expressed in excess or, conversely, insufficient consumption of proteins, fats, and carbohydrates. Often, diseases of the digestive system are the result of carelessness and a frivolous attitude towards diet and health in general, we are talking, first of all, about the following:
. prolonged neglect of regular nutrition;
. excessive consumption of spicy, salty and very hot foods;
. the presence of preservatives in daily consumed food.
That is why diseases of the digestive system are so dependent on diet, diet and the quality of foods consumed. The amount of harmful foods in the diet should be kept to a minimum, or even better, reduced to zero. At the first symptoms indicating a particular disease of the digestive system, you should immediately review your diet, eliminating from it all foods that are undesirable for the body.
The thoughtless consumption of essentially harmful liquids - alcohol and its surrogates, soda, and other drinks with preservatives and dyes - causes no less harm to the digestive system.
The next factor that increases the risk of developing any disease of the digestive system is smoking. Stress and anxiety are also very common provocateurs of the ailments in question.
Among the internal causes of diseases of the digestive system are:
. intrauterine developmental defects;
. hereditary factors;
. autoimmune processes.
The main symptom accompanying diseases of the digestive system is pain that occurs in the digestive tract. The intensity of pain varies and depends on the specific disease.
1. Cholecystitis. This disease of the digestive system is accompanied by pain spreading along the hypochondrium - right or left.
2. Pancreatitis. It is accompanied by a girdle pain of unknown localization. Often the pain radiates between the shoulder blades or to the heart area.
3. Stomach ulcer. Perforation of a stomach ulcer causes sharp, intense pain.
The pain can be sharp and aching, weak and intense, it can also depend on the food eaten. For example, patients with pancreatitis and cholecystitis experience unpleasant pain after eating fatty foods. And with a stomach ulcer, the pain begins to increase if a person does not eat for a long time. But pain with hyperacid gastritis can be relieved by drinking milk.
At the first suspicion of gastrointestinal diseases, the doctor, after conducting a thorough examination, uses the following diagnostic methods:
. palpation;
. auscultation;
. percussion.
When conducting a diagnosis, the doctor also takes a detailed interest in the patient’s complaints and studies the medical history.
Typically, diseases of the digestive system require various laboratory tests:
. general blood analysis;
. blood chemistry;
. stool analysis;
. Analysis of urine.
The following research methods can also be used for diagnosis:
. radial;
. Ultrasound of the abdominal cavity;
. fluoroscopy with contrast agents;
. radiography;
. MRI and CT. 
In addition, some diseases of the digestive system may require procedures to evaluate the condition of internal organs and at the same time obtain material for a biopsy. We are talking about the following procedures:
. colonoscopy;
. sigmoidoscopy;
. esophagogastroduodenoscopy;
. laparoscopy.
To examine the stomach in detail, functional tests can be used to obtain information about its motor function and acid secretion. In addition, tests can examine the condition of the small intestine and pancreas.
Treatment of diseases of the digestive system
The treatment plan depends on the specific disease diagnosed in the patient. Diseases of the digestive system, like any ailment, require timely and competent treatment in order to prevent, firstly, complications, and, secondly, the transition of the acute stage to the chronic form.
After conducting the necessary research, the doctor, based on the results obtained, draws up a treatment regimen. The most important step in the treatment of the vast majority of gastrointestinal diseases is, undoubtedly, a special diet. In the acute form of the disease, the patient can be prescribed parenteral nutrition for a certain time - it ensures the supply of all useful substances directly into the blood. Then, the recovering person is prescribed a normal diet, but foods that can trigger the return of symptoms of the disease are eliminated from the diet.
Digestive system diseases are often treated in stages. For example, acute gastritis is treated as follows:
. normalize the excretory functions of the gastrointestinal tract;
. treat the patient with antibiotics;
. Prescribe drugs that allow the cells of the gastric mucosa to renew and normalize metabolism.
Gastrointestinal diseases are often cured in a matter of weeks, but sometimes they take years to cure. As a rule, the speed of treatment is influenced by the timeliness of diagnosis. So, in particular, it is extremely important to diagnose diseases of the digestive system in children in a timely manner - this allows minimizing treatment time.
Often, when gastrointestinal diseases are identified, patients are prescribed complex treatment - it, as a rule, brings maximum effect. For example, with a stomach ulcer, the patient is first recommended to eliminate the causes that provoke the development of the disease. Then the doctor prescribes a course of treatment with medications and diet. At the same time, treatment methods such as physiotherapy, magnetic therapy, laser therapy and others can be prescribed.
For treatment to be successful, the patient himself must be aware of the importance of preventing gastrointestinal diseases. He needs, in particular, to change his lifestyle - eat right, get rid of bad habits, and follow a sleep schedule.
Today, diseases are often diagnosed without any manifestation of clinical symptoms. We are talking about chronic ischemic disease of the digestive organs - it is provoked by damage to the visceral arteries of the abdominal aorta. This disease causes obstruction of the above-mentioned arteries. Detailed diagnosis is extremely important here, otherwise treatment will not be effective. Patients with this problem are shown a special diet (ban on foods that cause flatulence; the patient should eat little, but often). Treatment is carried out using antispasmodic drugs, as well as drugs that normalize blood circulation.
The lack of effect of conservative therapy forces doctors to resort to surgical intervention. There are two options for operations - low-traumatic and abdominal.
Prevention of gastrointestinal diseases
Diseases of the digestive system require mandatory preventive measures, which consist, first of all, of organizing proper nutrition and maintaining a healthy lifestyle. To prevent gastrointestinal diseases, it is necessary to engage in physical activity every day, actively rest and get enough sleep.
A separate preventive measure is regular preventive examinations, which are necessary even in the absence of any warning symptoms. It would be useful to know that people who have crossed the forty-year mark should have an abdominal ultrasound performed annually.
The issue of nutrition is very important in the prevention of gastrointestinal diseases. Nutrition plays almost a key role in the development of the diseases in question. That's why it's so important to eat right - regularly, balanced and varied. Food intake should be moderate - overeating is unacceptable. You can’t eat until you feel full. You should get up from the table slightly hungry.
For smooth and smooth functioning of the digestive system, raw vegetables and fruits must be present in the diet every day. Food must be exclusively fresh. You need to eat it slowly and chew it thoroughly. You need to eat 4-5 times a day, following a meal schedule. The diet should not be filled with excessively hot and cold food. Over time, you should stop eating all refined carbohydrates and limit your salt intake.
Digestive diseases- this group of diseases occupies one of the leading places among diseases of internal organs. The fact is that the digestive system is constantly influenced by various environmental factors - the nature of nutrition, working and living conditions.
In addition to structural changes in the organs of the digestive system, functional disorders may also occur. The internal digestive organs include the esophagus, stomach, intestines, liver, and pancreas. The bile ducts are also involved in digestion.
Digestive diseases are widespread. Most often, these are various inflammatory processes associated with the presence of infection or disruption of the endocrine glands. Any of these diseases in the acute stage requires immediate treatment, since when it becomes chronic, surgical intervention may be required.
Digestive diseases
Diseases of the digestive tract are distinguished by the diversity of their clinical and morphological signs.
They include independent primary diseases, which are studied by a science called gastroenterology, as well as other secondary ones, which are a manifestation of a number of diseases of an infectious and non-infectious nature, acquired or hereditary origin.
These diseases may be based on various general pathological processes, such as alteration, inflammation, hyper- and dysplastic processes, autoimmune disorders and, finally, tumors.
Descriptions of diseases of the digestive system
Causes of digestive diseases
The causes of digestive system disorders are:
Diseases of the digestive system can be caused by exogenous, endogenous, and genetic factors.
Exogenous
These primary causes of the disease include:
- eating dry food,
- eating very hot foods,
- abuse of various spices and spices,
- excessive alcohol consumption,
- smoking,
- consumption of poor quality food,
- lack of diet,
- hasty eating,
- defects of the human masticatory apparatus,
- uncontrolled use of medications,
- unfavorable environmental conditions.
Diseases caused by exogenous factors include gastritis and enteritis, colitis, gastric and duodenal ulcers, cholelithiasis, as well as dyskinesia and cirrhosis of the liver.
Endogenous
Secondary (or endogenous) causes of gastrointestinal diseases are diseases such as diabetes and anemia, obesity and hypovitaminosis, various kidney and lung diseases, and stress. Diseases provoked by endogenous factors are hepatitis and cholecystitis, pancreatitis and enterobiasis.
Genetic
This group includes genetic factors, as well as developmental anomalies, including malformations of the esophagus and benign tumors (both esophagus and stomach), diagnosed abnormal development of the pancreas (for example, cystic fibrosis of the pancreas itself), as well as congenital hypoplasia of the pancreas .
It should be noted that most often gastrointestinal diseases arise from a combination of both endogenous and exogenous factors.
Symptoms of digestive diseases
The symptoms of diseases of the digestive system are varied, but the main signs of the presence of the disease are always present:
- nausea;
- frequent change of stool;
- belching;
- vomit;
- flatulence;
- loss of appetite;
- fast fatiguability;
- weight loss;
- abdominal pain of various locations;
- insomnia.
Other characteristic symptoms are different and depend on the type of disease. In many cases, digestive diseases are accompanied by rashes on the skin.
Diagnosis of diseases of the digestive system
Initially, if the development of diseases of the digestive system is suspected, the doctor must conduct a thorough examination of the patient. During the examination, palpation, percussion, and auscultation are practiced. It is necessary to ask in detail about the complaints and study the anamnesis.
As a rule, for diseases of this type, the patient is prescribed laboratory tests:
- general and biochemical blood tests,
- conducting a general urine test,
- stool analysis.
Radiation research methods are also widely used in the diagnostic process. An informative method is ultrasound examination of the abdominal organs, radiography, fluoroscopy with the use of contrast agents, CT, MRI.
Depending on the disease, procedures may also be prescribed to assess the condition of the internal organs of the digestive system and at the same time obtain material for a biopsy:
- colonoscopy,
- esophagogastroduodenoscopy,
- sigmoidoscopy,
- laparoscopy.
To examine the stomach, it is practiced to use functional tests that provide detailed information about the acid secretion of the stomach, its motor function, as well as the condition of the pancreas and small intestine.
Treatment of diseases of the digestive system
The treatment method is determined after diagnosis. For infectious and inflammatory pathologies, antibacterial therapy is required. The following medications are used: Ciprofloxacin, Cefazolin, Metranidazole.
To treat enzyme deficiency, the drugs “Mezim” and “Pancreatin” are used. Anti-inflammatory and antisecretory agents are also used. Surgical treatment consists of eliminating intestinal obstruction, removing stones, tumor formations, suturing an ulcer, etc.
Nutrition for diseases of the digestive system
Nutrition for diseases of the digestive system must be special. In this regard, in our country, at one time, the Russian Academy of Medical Sciences developed special diets that are suitable not only for diseases of the digestive system, but also of other systems (diets are indicated in articles on the treatment of certain diseases). A specially selected diet is necessary in the treatment of diseases of the digestive system and is the key to successful treatment.
If regular enteral nutrition is not possible, parenteral nutrition is prescribed, that is, when the substances necessary for the body enter directly into the blood, bypassing the digestive system. Indications for the use of this diet are: complete esophageal dysphagia, intestinal obstruction, acute pancreatitis and a number of other diseases.
The main ingredients of parenteral nutrition are amino acids (polyamine, aminofusin), fats (lipofundin), carbohydrates (glucose solutions). Electrolytes and vitamins are also introduced taking into account the body's daily needs.
Prevention of digestive diseases
The main and most important prevention of diseases of the digestive system, and not only them, is maintaining a healthy lifestyle.
This includes giving up bad habits (smoking, alcohol, etc.), regular physical exercise, avoiding physical inactivity (lead an active lifestyle), adherence to work and rest schedules, adequate sleep, and more.
It is very important to have a complete, balanced, regular diet, which ensures that the body receives the necessary substances (proteins, fats, carbohydrates, minerals, trace elements, vitamins), and monitoring of the body mass index.
Preventive measures also include annual medical examinations, even if there is no concern. After 40 years, it is recommended to conduct an annual ultrasound examination of the abdominal organs and esophagogastroduodenoscopy.
And in no case should the disease be allowed to progress; if symptoms appear, consult a doctor, and not self-medicate or only traditional medicine.
Questions and answers on the topic "Diseases of the digestive system"
Question:I eat, go to bed and a bitterness appears in my throat and mouth.
Answer: Bitterness in the mouth and throat is considered a manifestation of many diseases of various types: from otolaryngological and dental pathologies to disorders of the digestive tract. The most likely cause of the feeling of bitterness in the throat is a disruption in the functioning of the biliary tract. You need a face-to-face consultation with a doctor for examination.
Question:Hello! I am 52 years old. Somewhere in 2000, I was examined by a doctor, diagnosed with gastritis and hiatal hernia, pancreatitis, cholecystitis, in general, a whole bunch of diseases. There were stones in the gall bladder. She took various medications, herbal decoctions, and then stopped her treatment. But for many years I have been tormented by heartburn, there are pains in the stomach and liver. I take various medications for heartburn, and for a year, after every meal, I feel heaviness in my stomach and after a while I constantly feel sleepy and have frequent heartburn again. I almost always save myself only with antacids. Please tell me why I start to feel sleepy after eating and whether frequent use of Rennie and Almagel A is harmful?
Answer: First of all, you need to decide on gallstones. If they are present, all your problems will only get worse. An examination by a gastroenterologist is necessary.
Infectious diseases of the human digestive system, or gastrointestinal infections, are a huge group of diseases that differ in the degree of danger, incubation period, severity, etc. In many ways, they are similar in symptoms and routes of infection. Since they affect the intestines and stomach, they are classified as intestinal infections, or infectious diseases of the digestive system.
Kinds
There are many types of infection. The classification is based on the type of pathogens that cause infectious diseases of the digestive system. There are 3 general groups:
- Bacterial.
- Viral.
- Food.
They are also distinguished according to their course - acute inflammatory process and asymptomatic carriage. Food intoxication is not an infection, since it does not involve a pathogen.
Types of intestinal infections
Intestinal infections are localized in the gastrointestinal tract, occur acutely, cause inflammation in the mucous membranes, disrupt digestive processes, and are accompanied by a sharp deterioration in general condition.
About 90% of cases go away on their own, without medications, but provided that the water and electrolyte balance in the body is fully restored. Without this, even a mild form can lead to severe complications. And only 10% of cases require drug therapy. This 10% can be fatal without treatment.
What are the infectious diseases in humans? The causative agents are viruses and bacteria, protozoans. Next, we will look at the most common intestinal infections.
Viral
Viruses that cause major infectious diseases of the digestive system:
- Enterovirus.
- Norovirus.
- Rotavirus or intestinal flu, etc.
Infection occurs through nutritional, household contact (from a patient or a carrier), aerogenously, through unwashed hands, and by drinking unboiled water.
Viruses infect the walls of the stomach and small intestine, and the respiratory tract. The disease occurs more often in the autumn-winter period. With the right approach, cure occurs on the 7th day, but for another month the person remains an infectious carrier.
Treatment of viral infections is symptomatic, the basis is diet, drinking plenty of fluids to restore water and electrolyte balance, and medications for symptoms. Quarantine recommended.
Bacterial
Intestinal bacterial infectious diseases of the digestive system include:
- Staphylococcal infection.
- Escherichia coli.
- Salmonella.
- Shigella - It has several strains.
- Causative agents of acute infections such as typhoid fever, paratyphoid fever, botulism, cholera.
- (Proteus, Pseudomonas aeruginosa) of the body can also affect the intestines when immunity is reduced. Causes purulent processes.
Diseases of the bacterial group often lead to complications and are therefore considered more dangerous.
The routes of infection are contact-household and fecal-oral. Bacteria affect the stomach, intestines, and urinary tract. The complexity of this group of infections is that microorganisms release toxins even after their death, and in such quantities that they can cause toxic shock. Therefore, the goal of treatment is not only to destroy the pathogen, but also to remove toxins from the body. The main role belongs to antibiotics, but only if taken correctly and for a full course. Bacteria very easily become insensitive to them otherwise.
Common symptoms of digestive system infection
Symptoms of infections depend on the pathogen, but there are also common symptoms. The first manifestations do not appear immediately after infection; it can take up to 50 hours. This is the incubation period necessary for the pathogen to penetrate the intestinal wall, begin to reproduce and release toxins. The duration of such a latent period varies among pathogens: for example, with salmonellosis - from 6 hours to 3 days, and in the case of cholera - 1-5 days, but more often symptoms are noted after 12 hours.
Minor discomfort quickly gives way to abdominal pain. Vomiting and diarrhea appear. The temperature rises, chills and signs of varying degrees of intoxication appear.
Vomiting and diarrhea quickly dehydrate the body, and if treatment is not started, irreversible changes occur - disturbances in cardiovascular activity and kidney function, even death.
The temperature can rise to 38-39 degrees, but, for example, with cholera it remains normal, and with staphylococcus it quickly returns to normal.
When vomiting, food debris comes out first, then gastric juice, bile and drunk liquid. The urge to vomit is frequent.
Abdominal pain is acute or aching, cramping, the localization is different. It may be accompanied by flatulence, rumbling, seething, and colic.
Dysentery is characterized by tenesmus - a false urge to stool.
Diarrhea manifests itself differently depending on the pathogen.
With cholera, stool resembles rice water. Salmonellosis is characterized by liquid, green, foul-smelling stool with mucus. With dysentery, mucus and blood come out with the feces. The frequency of stool varies.
General weakness and malaise are the result of intoxication and dehydration. For the same reason, the pulse and breathing quicken, blood pressure decreases, and the skin turns pale. Weakness and a sharp deterioration in appetite also occur.
In 70% of cases, severe thirst appears, indicating dehydration. This leads to seizures and arrhythmias. There may be loss of consciousness, hypovolemic shock.
You definitely need to see a doctor. Even an infectious disease specialist cannot determine the nosology based on complaints alone, but he can make a presumptive diagnosis.
Clinic of diseases of viral origin
Viral infection of the gastrointestinal tract has 3 main forms:
- Easy. Malaise, low-grade or normal temperature are observed. Rotavirus infection is called intestinal flu. In this case, catarrhal symptoms of ARVI are present: runny nose, sore throat, cough. Then rumbling, seething in the stomach, and flatulence are added. In adults, the clinic is often erased, so such patients serve as a source of infection while continuing to work actively. The frequency of stools (mushy) is up to 5 times a day. No special treatment is required.
- Medium severity. Rising temperature to febrile levels. Repeated vomiting, with dehydration. The abdomen is swollen, diarrhea up to 15 times a day, with a strong unpleasant odor and foam. Urine dark, cloudy, intense thirst.
- Severe form. Bowel movements up to 50 times a day, abdominal pain of varying severity, exicosis. Hypovolemic shock develops - a drop in pressure, diuresis of no more than 300 ml per day. The skin is flabby, earthy-grayish, the face is pointed. Severe forms are observed in the weakened and elderly. As a percentage, it does not exceed 25%.
Clinical picture of bacterial infections
Dysentery is an infectious disease that occurs everywhere, more often in the summer. Caused by Shigella bacteria. The source is the patient, as well as consumption of unwashed vegetables or fruits, contaminated water, or while swimming in lakes. This is also related to mentality - people often relieve themselves while swimming.
Salmonellosis, perhaps the most common infection, is active throughout the year. The causative agents of salmonellosis love to nest in perishable products, while in appearance and smell these products are perceived as fresh. Salmonella especially loves eggs, dairy and meat products, and sausages. The bacteria are found inside the eggs, not on the shell. Therefore, washing eggs does not prevent infection.
Salmonella are very tenacious; at 70 degrees they die only after 10 minutes. With low boiling, salting, and smoking, they survive well inside thick pieces. Activity persists for several months.
Classification of forms of salmonellosis:
- localized;
- generalized;
- isolation of bacteria.
The localized form is the most common and develops with all symptoms on the first day. Dangerous with complications. The infection is severe in children.
Staphylococcus is conditionally pathogenic; if the intestinal microflora is normal, it will not develop. Activation occurs when immunity decreases.
Staphylococcal intestinal infection develops quite slowly, and its first manifestations are a runny nose and sore throat, and not a very high temperature.
The clinic then resembles a typical food poisoning. Symptoms:
- abdominal pain;
- vomit;
- diarrhea mixed with blood and mucus;
- general weakness.
Contaminated products often include cakes, salads, creams, dairy products, and eggs. Staphylococcus is difficult to treat due to its mutation and resistance to antibiotics.
Klebsiella and Escherichia coli behave actively when the immune system is weakened - in young children and the elderly, people after surgery, patients with diabetes mellitus, hematological pathologies, alcoholics. It is acute. Treated with probiotics and bacteriophages.
Coccobacilli cause an intestinal infection called yersiniosis. It usually occurs in infants and young men. Its carriers are animals - rodents, livestock. Antibiotics are ineffective, treatment is symptomatic. Within no more than 5 days when taking action.
Intestinal coli infection, escherichiosis, is caused by bacteria of the same name - Escherichia. The infection can affect the intestines, biliary and urinary tracts. It most often affects premature babies and young children.
First aid
Help with the development of intestinal disease of the digestive system (infection) should begin at the first symptoms. You can suspect a problem by a rapid increase in body temperature, diarrhea and vomiting. The general condition is rapidly deteriorating. You need to call an ambulance immediately. Before the doctors arrive, it is necessary to take some measures - rinse the stomach, give a cleansing enema, take a sorbent.
Gastric lavage
It is necessary to remove at least some of the toxins from the body. To lavage the stomach, use water at room temperature, drink 2-3 glasses in one gulp to induce vomiting. According to modern protocols, the use of potassium permanganate solution for rinsing in case of diseases of the digestive system is not recommended. In terms of effectiveness, it is no better than ordinary water, but it can cause a burn to the mucous membrane.
Cleansing enema and sorbent intake
For infectious diseases of the digestive system, it also helps remove bacterial toxins. Use simple boiled water, but only at room temperature. Cold water will cause spasms, and hot water will enhance the absorption of toxins.
Sorbents. Any sorbents will do (Lactofiltrum, activated carbon, Smecta, Phosphalugel, Sorbex). They can be taken until the ambulance arrives. They remove toxins by absorption and reduce the level of intoxication syndrome. Do not exceed the recommended dosage.
Fluid during intestinal infections is necessary for the body first of all. You can drink boiled water, mineral water without gas, green tea. The intake should be in small portions, but often - 5 sips every 10 minutes.
The rest of the assistance will already be provided in the hospital. Basic medications against an infectious disease of the digestive system will be prescribed after diagnosis.
Establishing diagnosis
In addition to examining the patient and collecting a detailed history, blood biochemistry is performed to identify electrolyte failures and disorders of internal organs, and a blood test is taken. necessary to determine the pathogen and prescribe etiological treatment.
Preventive actions
The development of infectious diseases of the digestive system can be prevented, first of all, by observing the rules of personal hygiene, and it is necessary to:
- Wash your hands after visiting the toilet or returning from outside.
- Separate the patient's dishes and household items.
- Buy products in stores where there is a certificate and permission to sell.
- Wash vegetables and fruits thoroughly, even peeled ones; throw away the spoiled ones, without acting on the principle “better in us than in the basin.”
- Drink only filtered or boiled water. You cannot drink from wells and reservoirs.
- Make your own salads without buying ready-made ones in supermarkets. Observe the shelf life of products - meat, milk, eggs, etc.
Prevention of infectious diseases of the digestive system consists not only in clean hands, but also in not trying unwashed fruits at the market, and not purchasing cut melons.
Timely treatment and diagnosis is important. To do this, if a child or an adult shows signs of an infectious disease of the digestive system, you must consult a doctor immediately.
