List of used literature. Topic: Acute cholecystitis Acute cholecystitis literature

Therapeutic nutrition for cholecystitis and pancreatitis Alexander Gennadievich Eliseev

List of used literature

Introduction

The founder of medicine, the ancient Greek scientist Hippocrates (lived around 460–377 BC) said: “Let your food be your medicine, and food be your medicine.” The famous eastern scientist and doctor Avicenna (Abu Ali Ibn Sina, years of life 980–1037 BC) in his main work “The Canon of Medical Science” emphasized the importance of “medicinal food”. Academician A. A. Pokrovsky, a leading Russian nutritionist, author of the concept of a balanced diet, believes that the effect of food components on the body is comparable to the effect of pharmacological drugs.

Food is one of the environmental factors that have a powerful effect on the body, and this effect can be both positive and negative. Everything that a person eats is first broken down, then absorbed in the form of microscopic particles and carried through the bloodstream throughout the body. The growth processes, the very development of the body and the preservation of health are directly determined by a rational, balanced diet. When the disease occurs, the metabolism in the body changes, so changing the nature of nutrition can improve metabolism and actively influence the course of the disease.

Briefly, the concept of a balanced diet can be formulated as follows: for the normal functioning of the body, it is not enough to provide it only with the necessary amount of energy and proteins (building materials), one must also introduce essential nutritional factors into the diet and maintain the necessary balance of all substances supplied with food. Essential nutritional factors include essential amino acids (components of proteins), vitamins that the body itself cannot create, some fatty acids, minerals and trace elements. There are quite strict relationships between the essential nutritional factors, the violation of which first entails changes in the physiological state of the body, metabolic disorders, and then diseases. Based on the concept of a balanced diet, the necessary proportions of individual substances in food rations have been developed.

We present the main nutritional deficiencies that are characteristic of modern man and can lead to disease:

– excess high-calorie nutrition that does not correspond to lifestyle (most often in combination with low physical activity);

– eating too fatty foods;

– increased content of table salt in the diet (especially with canned food, marinades, smoked meats and other preparations);

– excessive consumption of sugar, sweets and sugary drinks;

– insufficient consumption of vegetables, fruits, fruits and berries;

– deficiency of fermented milk products;

– monotonous food;

– violation of the diet (irregularity), as well as fast, hasty eating;

– nutrition that is not appropriate for age (elderly people, with low energy needs, consume excessive amounts of high-calorie foods).

According to the Institute of Nutrition of the Russian Academy of Medical Sciences (Russian Academy of Medical Sciences), the daily diet of many, if not most Russians, is incorrectly balanced in its main components; it is dominated by energy-intensive foods: bread, potatoes, flour (including sweet confectionery) products, animal fats. At the same time, the diet lacks foods containing essential amino acids, polyunsaturated fatty acids, dietary fiber, vitamins and minerals. It is noted that the daily diet has become richer in taste, but less balanced in composition; it is excessively high in calories, but does not provide the body with the required amount of necessary components.

The importance of therapeutic nutrition in the treatment of various diseases not only does not decrease over time, but, on the contrary, increases. This phenomenon is explained by several circumstances: food and its components can have a direct damaging effect on the digestive organs; long-term use of medications for chronic diseases with frequent exacerbations often leads to deterioration in the functioning of the stomach, pancreas, and gallbladder, causing various digestive disorders; Long-term drug therapy naturally reduces the therapeutic effect of medications, and in some cases leads to the emergence of new pathological conditions, most often to disorders of the gastrointestinal tract and allergic diseases. The role of therapeutic nutrition is also significantly increased by environmental problems and frequent stress (a characteristic feature of modern times).

Modern dietetics makes it possible to ensure that therapeutic diets correspond to the disorders in the body that develop during a particular disease. This approach helps eliminate metabolic disorders caused by the disease, normalizes the course of chemical reactions and restores the altered functions of the organ caused by the disease. Therapeutic nutrition can influence the biochemical processes of the body in a similar way to a medicine.

Based on knowledge about the body’s normal need for energy and the necessary components of food for a healthy person, adjustments are made to the patient’s diet in accordance with the diagnosis of the disease, the characteristics of metabolic disorders, the course of the disease, and its stage. Adjustments are made by changing the quantity and proportions of food components required for a given disease. The simplest example is that limiting table salt in the diet of patients with hypertension leads to a decrease in blood pressure. The importance of dietary nutrition is especially great in the treatment and prevention of diseases of the digestive system. And for some diseases (for example, in patients with hereditary intolerance to fructose and galactose), diet therapy is the only reasonable method of treatment.

Cholecystitis

Cholecystitis (cholecystitis; from the Greek chole – “bile” + kystis – “bladder” + itis) – inflammation of the gallbladder.

There are acute and chronic cholecystitis. In the acute form of the disease, inflammation of the mucous membrane of the gallbladder occurs, severe abdominal pain appears, and symptoms of intoxication develop (from the Greek toxikon - “poison, poisoning”). Chronic cholecystitis, in addition to symptoms, is distinguished by a recurrent course (from relapse - repetition), atrophy and sclerosis of the walls of the gallbladder, a disorder of its motor function, changes in the physical and chemical properties of bile.

Anatomy and physiology of the gallbladder

Gallbladder (vesica fellea) It is a fairly thin-walled hollow muscular organ of the digestive system, in which bile accumulates, its concentration increases, and from which bile periodically (during meals) enters the common bile duct and the duodenum. In addition, the gallbladder, as part of the biliary system, regulates and maintains the pressure of bile in the biliary tract at the required level.

The gallbladder is located on the lower surface of the liver in the corresponding fossa (gallbladder fossa). Usually it has a pear-shaped, less often conical shape. In people of tall, fragile build with thin bones (asthenics), the shape of the gallbladder is often oblong, elongated or spindle-shaped; in people of short stature, strong build with broad bones (in picnics), it is bag-shaped, round. The length of the gallbladder ranges from 5–14 cm, averaging 6–10 cm, its width reaches 2.5–4 cm, and its capacity is 30–70 ml. However, the wall of the gallbladder is easily stretchable; it can hold up to 200 ml of fluid.

The gallbladder has the following anatomical parts: the fundus is the widest part, the body and neck are the narrowed part. The gallbladder has two walls: the upper one is adjacent to the lower surface of the liver, the lower wall is freer, it can come into contact with the stomach and duodenum.

After eating, the gallbladder in the fundus and body begins to contract, and its neck expands at this time. Then the entire gallbladder contracts, the pressure in it increases and a portion of bile is released into the common bile duct.

The duration of gallbladder contraction depends on the amount of fat in the food - the more fat the food contains, the longer the gallbladder will remain in a contracted state. Among everyday foods, egg yolks, animal fats and vegetable oils most contribute to the secretion of bile. The gallbladder in men empties faster than in women; It also empties faster in people over 50 years of age than in younger people. The period of bile release is replaced by a period of filling its bladder. The release of bile during the day is associated with food intake. At night, the bladder fills with bile. Normally, during digestion, the gallbladder makes energetic rhythmic and tonic contractions, but with pathology, dyskinesia develops (from the Latin dis - “not”, and from the Greek kinema - “movement”) - uncoordinated, untimely, insufficient or excessive contraction of the gallbladder. Dyskinesia can occur in two variants (types): hyperkinetic (from the Greek hyper - “above, above”) and hypokinetic (from the Greek hypo - “under, below, below”), i.e. movements can be excessive (hyper ) or insufficient (hypo).

Bile is produced continuously by liver cells. Outside of digestion, liver bile enters the gallbladder and is concentrated (condensed) there. During a meal, the gallbladder empties and remains in a contracted state for 30–45 minutes. During this period, water and electrolytes enter its lumen, the gallbladder is thus washed, as it were, freed from excess particles accumulated in it.

Bile is a secretion produced by liver cells with a yellowish-brown liquid consistency. Under normal conditions, the amount of bile produced by the liver per day can reach 1.5 thousand - 2 thousand ml. Bile has a rather complex composition, it contains bile acids, phospholipids (lipids - fats), bilirubin, cholesterol and other components and plays an important role in the physical and chemical processing of food and, above all, in the digestion and absorption of fat.

The formation and secretion of bile performs two important functions in the body:

– digestive – bile components (primarily bile acids) are vital for the digestion and absorption of dietary fat;

– removal from the body of toxic substances that cannot be neutralized by processing and are not excreted by the kidneys.

Bile can remove various harmful compounds from the body, including medicinal ones.

General information about the disease

Medical statistics show that up to 10% of the adult population of most countries of the world suffers from inflammation of the gallbladder. Women suffer from cholecystitis 3–4 times more often than men. In addition to gender, the prevalence of the disease is directly related to age and body weight: cholecystitis is more often detected in obese and elderly people, and by the age of 60, approximately 30% of women have gallstones.

Reasons for the development of cholecystitis

Stones (concrements) inside the gallbladder and their movement lead to mechanical damage to the mucous membrane, help maintain the inflammatory process and disrupt the evacuation of bile from the bladder into the ducts. By injuring the inner wall of the gallbladder, large stones cause the formation of erosions and ulcerations of the mucous membrane, followed by the formation of adhesions and deformations of the gallbladder. All these processes contribute to infection and long-term preservation of microbes in the bladder cavity.

The most important factor contributing to the development of chronic cholecystitis is bile stagnation. The cause of bile stagnation can be several: dyskinesia of the biliary tract, congenital anomaly (deformation) of the outlet of the gallbladder, inflammation, stone formation, pregnancy, sedentary lifestyle, concomitant diseases. In this case, the physical and chemical properties of bile change, in particular, its bactericidal (antimicrobial) ability decreases, while conditions are created for the further development of the inflammatory process. Stagnation of bile leads to increased pressure in the gallbladder, its stretching, increased swelling of the wall, compression of blood vessels and disruption of blood circulation in the wall, which ultimately increases the intensity of the inflammatory process. Increasing the viscosity of bile also contributes to the formation of gallstones.

Due to disorders of the motor functions of the biliary tract and changes in the properties of bile, the development of cholecystitis is facilitated by diseases of the digestive system - hepatitis (inflammation of the liver), duodenitis (inflammation of the duodenum).

More rarely, cholecystitis develops as a result of abdominal trauma in the right hypochondrium, sepsis, or burns.

In the development of gallbladder pathology, the role of hereditary predisposition has been established. So, the predisposing factors for gallbladder pathology are: being female, overweight, age (over 60 years), poor nutrition (excessive caloric content of food, consumption of increased amounts of fatty meats and fish, animal fats, flour dishes with a simultaneous deficiency in food intake). vegetable diet), alcohol abuse, irregular diet, low physical activity, unfavorable heredity, long-term use of certain medications (clofibrate - an anti-sclerotic drug, contraceptives and some other drugs), diabetes, pancreas and intestinal diseases.

Classification of cholecystitis

There are acute and chronic cholecystitis. If acute cholecystitis is limited to superficial inflammation of the gallbladder wall and very acute but passing symptoms, then chronic cholecystitis occurs with pronounced changes in the gallbladder wall, impaired circulation of bile, changes in its composition and properties, and lasts more than six months.

Often cholecystitis is caused by infection. Depending on the routes of penetration of microorganisms, they are distinguished:

– ascending cholecystitis, when microbes rise from the duodenum;

– descending – in case of penetration of microbes into the bladder from above from the liver;

– hematogenous (from the Greek haima = haimatus - “blood”), when microorganisms use blood vessels to move;

– lymphogenous develops when microbes use lymphatic vessels.

Due to the fact that inflammation of the gallbladder can occur both with and without stones in it, and these two forms have significant differences, it is customary to distinguish calculous (stone-like) and non-calculous (stoneless) cholecystitis.

During chronic cholecystitis, the following are distinguished:

– exacerbation phase;

– phase of fading exacerbation, when some of the symptoms of the disease have disappeared, and the other part is mild compared to the period of exacerbation;

– the remission phase, in which there are no symptoms of the disease and the patient often feels practically healthy.

Cholecystitis Clinic

The main clinical manifestations of inflammation of the gallbladder are: pain in the upper abdomen and heaviness in the right hypochondrium, dyspeptic symptoms (nausea, vomiting, bitterness in the mouth, heartburn, etc.), increased body temperature, a tendency to constipation, itchy skin. All of these symptoms are characteristic of acute cholecystitis or exacerbation of chronic cholecystitis.

For acalculous cholecystitis, dull aching pain in the right hypochondrium after eating fatty, fried foods is more typical, radiating (radiating) to the right scapula or collarbone, less often to the angle of the lower jaw on the right. Calculous cholecystitis typically manifests itself as biliary (hepatic) colic. Biliary colic is an intense paroxysmal pain in the right hypochondrium that occurs after an error in diet (eating fatty, fried foods) or after a bumpy ride.

The manifestations of cholecystitis are also influenced by the functional state of the gallbladder. Dyskinesia of the gallbladder means a violation of its motor activity - uncoordinated, untimely, insufficient or excessive contraction of the gallbladder. Dyskinesia can occur in a hypertonic or hypotonic type. Cholecystitis occurring with dyskinesia of the hypertonic type is more often manifested by attacks of typical biliary colic (severe paroxysmal pain in the right hypochondrium), while with dyskinesia of the hypotonic type, the clinical manifestations are more modest - pain in the right hypochondrium is dull aching in nature, associated with the intake of fatty, fried food, alcohol, are accompanied by nausea, bitterness in the mouth and other dyspeptic symptoms, rumbling in the stomach and bowel dysfunction (usually constipation).

Symptoms of acute cholecystitis . The disease begins acutely with an attack of pain in the right hypochondrium (as well as an exacerbation of chronic cholecystitis), often suddenly against the background of apparent well-being. In other cases, an attack of pain for several days may be preceded by heaviness in the epigastric region, bitterness in the mouth, and nausea. An attack of the disease is usually provoked by errors in diet, physical or emotional stress. The main manifestation of acute cholecystitis is pain. The pain in a typical case is of the nature of biliary colic - the attack begins suddenly, often at night, and is manifested by sharp cramping pain in the right hypochondrium, which extends under the right shoulder blade, into the right shoulder, into the right collarbone, lower back, right half of the neck and face. If the pancreas is involved in the process, the pain may be in the left hypochondrium and be of a girdling nature. Rarely, pain can radiate to the left half of the chest and be accompanied by cardiac arrhythmia. The pain can be so severe that patients sometimes lose consciousness. The duration of a painful attack ranges from several days to 1–2 weeks. Over time, the intensity of the pain decreases, it becomes constant, dull, and periodically intensifies. Pain in acute cholecystitis is mainly caused by impaired outflow of bile, inflammatory edema and stretching of the gallbladder.

The pain syndrome is accompanied by nausea and vomiting, which, as a rule, do not bring relief. Often, patients with acute cholecystitis experience increased body temperature, flatulence and constipation. As the disease progresses, the temperature may rise to 38–40 °C, at the same time chills appear, the general condition worsens significantly, weakness, headache appear, and intoxication develops. Acute cholecystitis may be accompanied by jaundice. The duration of acute cholecystitis, which occurs without complications, ranges from 2–3 weeks to 2–3 months.

Complications of acute cholecystitis. The most serious complications of acute cholecystitis include: empyema of the gallbladder, perforation (perforation) with subsequent development of biliary peritonitis, pancreatitis (inflammation of the pancreas), cholagnitis (inflammation of the biliary tract).

Symptoms of chronic cholecystitis . Chronic inflammation of the gallbladder can occur independently or be the outcome of acute cholecystitis. Clinical manifestations depend on the period of the disease (exacerbation or remission), the presence or absence of stones and complications, and the type of concomitant biliary dyskinesia.

The leading symptom of exacerbation of chronic cholecystitis is pain. Pain appears, as a rule, in connection with the consumption of fatty, fried foods or alcohol; less often, an attack develops due to emotional overstrain, active shaking, accompanied by shaking of the body, as well as in connection with cooling or smoking.

The intensity of pain ranges from mild to severe (typical biliary colic). Previously, severe pain in chronic (mainly calculous) cholecystitis was called morphine, since sometimes only narcotic painkillers (morphine) alleviated the condition of patients. Attacks of biliary colic can end quite quickly, but sometimes last for several days with short breaks.

Pain with calculous cholecystitis is not always stronger than with acalculous cholecystitis. Sometimes, especially with concomitant hypertensive biliary dyskinesia, pain in patients with acalculous cholecystitis can be very intense, while with calculous cholecystitis in elderly patients the pain syndrome is not always pronounced.

In some cases, non-calculous cholecystitis is asymptomatic or its manifestations are masked by manifestations of diseases of the gastrointestinal tract (gastritis, colitis, chronic appendicitis). In general, the pain syndrome with acalculous cholecystitis is less pronounced in comparison with calculous cholecystitis and is less often accompanied by a visible deterioration in the general condition. Often the symptoms of acalculous cholecystitis are quite varied and atypical, which makes its diagnosis difficult.

At the same time, pain with acalculous cholecystitis can be persistent; They are localized in the right hypochondrium and occur 40–90 minutes after a meal, especially a large and fatty one, as well as after a bumpy ride and when carrying heavy objects for a long time. In most patients, pain is localized in the right hypochondrium; less often, patients complain of pain in the epigastric region or pain that does not have a clear localization. Approximately a third of patients associate the appearance of painful sensations with nervous shock and anxiety. Pain often occurs or worsens while sitting. Most often, the pain is characterized as aching or pulling. As a rule (85%), in the absence of stones in the gallbladder, the pain is monotonous, and only in 10–15% of patients the pain is of the nature of biliary colic. A combination of dull, constant and acute paroxysmal pain is observed in 12% of patients. Often the pain is combined with nausea, belching (air or food).

With concomitant dyskinesia of the hypertonic type, the pain is sharp, paroxysmal, and with dyskinesia of the hypotonic type, the pain is insignificant, monotonous, and fairly constant.

The localization of pain during an attack can vary, the pain can be diffuse, but most often pain with cholecystitis is observed in the right hypochondrium. In addition to the typical location in the right hypochondrium, the pain can also be localized around the navel, at the lower part of the sternum or in the lower abdomen on the right. Uncharacteristic localization of pain is observed, as a rule, with prolapse of the liver or an atypical location of the gallbladder.

During exacerbation of cholecystitis, pain radiates (gives) more often to the right side: to the lumbar region to the right of the spine, less often to the right arm, groin area, lower jaw. The pain can also radiate to the left arm and to the heart area. Localization of pain to the left of the navel indicates involvement of the pancreas in the pathological process. When the inflammatory process spreads to the tissues surrounding the gallbladder (pericholecystitis, from the Greek peri - “near, near”) the pain is constant and is associated with changes in body position.

Although pain due to inflammation of the gallbladder is noted by almost all patients, sometimes pain due to cholecystitis may be completely absent; in these cases, the patient feels a feeling of heaviness, pressure or burning in the right hypochondrium.

After pain, most often patients with chronic cholecystitis complain of dyspeptic disorders: changes in appetite, nausea, belching, bitterness in the mouth, etc. About half of patients with chronic cholecystitis experience vomiting, which can either reduce (usually with concomitant hypoknesia of the biliary tract) or and increase (in case of hypertonic condition of the biliary tract) pain. An admixture of bile is often found in the vomit, then the vomit is colored green or yellow-green, although vomiting without bile is occasionally possible. With frequently repeated vomiting during the urge, only almost pure bile with an admixture of gastric juice is released, while there is no food mass. The presence of blood in vomit is characteristic of ulcerative damage to the mucous membrane or due to injury to the gallbladder wall by a stone. In chronic cholecystitis, without exacerbation, vomiting usually occurs when the diet is violated - after eating fatty, fried foods, smoked foods, spicy seasonings, alcohol, sometimes after strong psycho-emotional disturbances, smoking.

Vomiting is usually accompanied by other dyspeptic symptoms: decreased or increased appetite, change in taste, a feeling of bitterness in the mouth, a metallic taste, heartburn, nausea, belching, heaviness in the pit of the stomach and in the right hypochondrium, a feeling of fullness in the upper abdomen, rumbling and bloating, disturbance chair.

Persistent heartburn is often combined with a dull pain in the chest. After a heavy meal, there may be a feeling of a “stake” behind the sternum, and occasionally there are slight difficulties in the passage of food through the esophagus. When the intestines are involved in the process, bloating is periodically observed, accompanied by mild pain spread throughout the abdomen. In patients with chronic cholecystitis, there is a tendency to constipation, diarrhea is rare, and alternation of constipation and diarrhea is possible.

Bitterness in the mouth, moderate pain or a feeling of heaviness in the right hypochondrium may persist for quite a long time after an attack of cholecystitis. Inflammation of the gallbladder is characterized by bitter belching or a constant bitter taste in the mouth. Body temperature during an attack may increase slightly (37.2–37.5 °C) or reach high numbers (39–40 °C).

Itching of the skin and icteric discoloration of the skin are inconsistent manifestations of chronic cholecystitis and are associated with cholestasis (impaired outflow of bile), which most often occurs when the bile ducts are blocked by a stone. With intense itching, there may be scratching on the skin.

In children and young people, acalculous cholecystitis is more often observed, which occurs with vivid symptoms, increased body temperature, and symptoms of intoxication.

In elderly and senile people, calculous cholecystitis predominates, often occurring atypically: the pain syndrome is mild or absent, dyspeptic disorders predominate (bitterness in the mouth, nausea, poor appetite, flatulence, constipation), fever is observed infrequently and rarely reaches high numbers.

Patients with chronic cholecystitis also experience other symptoms - lethargy, increased irritability, excitability, sleep disturbance, etc., however, these phenomena may accompany other diseases and have no diagnostic value.

During chronic cholecystitis, there are periods of remission (no symptoms) and periods of exacerbation, when the symptoms of the disease are clearly expressed. Exacerbation of the inflammatory process is often caused by errors in diet, excessive physical activity, as well as acute inflammatory diseases of other organs. Chronic cholecystitis most often has a benign course.

According to the severity of the course, chronic cholecystitis is divided into three degrees: with a mild form of the disease, exacerbations are recorded no more than once a year, a moderate form is characterized by three or more exacerbations during the year, with a severe form, exacerbations occur 1-2 times a month or even more often .

The mild form is characterized by mild pain and rare exacerbations. With this form, pain in the right hypochondrium intensifies only against the background of a diet violation and with significant physical exertion. Nausea, vomiting, bitterness in the mouth and other dyspeptic symptoms are observed infrequently and are not pronounced. Appetite usually does not suffer. The duration of an exacerbation in mild forms of the disease usually does not exceed 1–2 weeks. An exacerbation is most often caused by a violation of the diet (fatty, fried foods) and/or diet, fatigue, acute infection (flu, sore throat, etc.). With moderate severity of the disease, severe pain predominates in the symptoms; in the interictal period, pain is persistent, associated with eating fatty foods, intensifies after physical stress and errors in diet, sometimes pain occurs after significant neuro-emotional stress or overwork, in some cases the cause of the exacerbation cannot be determined. Dyspeptic symptoms with moderate severity of the disease are pronounced, vomiting is often observed. Attacks of typical biliary colic can be repeated several times in a row, accompanied by radiation to the lower back on the right, under the right shoulder blade, and to the right arm. Vomiting occurs first with food, then with bile, and there is often an increase in body temperature. To eliminate pain, you have to resort to medications (administration of painkillers and antispasmodics). Already by the end of the first day after the onset of the attack, icteric staining of the skin and mucous membranes may appear; in some cases, liver dysfunction is observed. Moderate course of chronic cholecystitis can be complicated by cholangitis (inflammation of the bile ducts).

The severe form of chronic cholecystitis is characterized by severe pain (classic biliary colic) and distinct dyspeptic disorders. Often, simultaneous dysfunction of the liver and pancreas occurs.

Complications of chronic cholecystitis. The most common and dangerous complications of chronic cholecystitis are:

– destruction (from the Latin destructio – “destruction, disruption of the normal structure”) of the gallbladder – empyema, perforation, leading to the leakage of bile into the abdominal cavity and the development of peritonitis and the formation of biliary fistulas. Violation of the integrity of the gallbladder may be caused by the pressure of the stone against the background of the inflammatory process in the wall of the organ;

– cholangitis (inflammation of the intrahepatic bile ducts);

– biliary pancreatitis is an inflammation of the pancreas caused by chronic cholecystitis;

– Jaundice develops when the common bile duct is blocked by a stone. Bile, having no outlet into the duodenum, enters the blood and poisons the body. This type of jaundice is called mechanical;

– reactive hepatitis (damage to the liver as a directly adjacent organ) develops with prolonged inflammation of the gallbladder;

– gallbladder cholesterosis develops when its wall becomes saturated with calcium salts as a result of the disease. The result of this process is the so-called “disabled” gallbladder, which is only partially working.

Diagnosis of cholecystitis

The diagnosis of cholecystitis is established on the basis of a comprehensive examination of the patient, including the study of the symptoms of the disease, the implementation and interpretation (from the Latin interpretatio - “interpretation, explanation”) of the results of instrumental and laboratory research methods. The clinical manifestation of the disease is described in the section “symptoms of chronic cholecystitis”.

Basic instrumental research methods.

Ultrasound examination (ultrasound). Among other methods for diagnosing pathology of the biliary tract, ultrasound currently occupies a leading place. The advantages of the method include its safety, ease of burden for the patient, quick receipt of research results, etc. Ultrasound makes it possible to detect an increase or decrease in the size of the gallbladder, thickening and compaction of its walls, deformation (constriction, bends), the presence of stones in the cavity of the bladder, increased viscosity of bile , impaired contractile function of the gallbladder (dyskinesia), development of complications.

Ultrasound is performed in the morning on an empty stomach no earlier than 12 hours after the last meal. On the eve of the study, it is necessary to empty the intestines (do an enema); in case of increased gas formation, take digestive enzymes (festal, pancreatin, etc.) for 3 days before the test, 1 tablet 3 times with meals, and also exclude dark varieties of bread, legumes, and cabbage from the diet.

X-ray examination gallbladder (cholecystography) allows you to identify deformations and abnormalities in the development of the gallbladder and other signs of cholecystitis.

Esophagogastroduodenoscopy, FGDS, abbreviated as FGDS, means examination of the esophagus, stomach and duodenum using fiber optics (people sometimes call it “light bulb”). Explanation of the term: esophago - esophagus, gastro - stomach, duodeno - duodenum, copy - look.

Laparoscopy(from the Greek lapara - “belly” and skopeo - “look, observe”) means examination of the gallbladder and the surrounding space using fiber optics introduced through a small incision in the abdominal wall, allows you to assess the position, size, condition of the surface and color of the gallbladder , surrounding organs.

Method of retrograde (from the Latin retro - “back”) pancreatocholangiography– a combination of X-ray and endoscopic examination methods allows to identify pathology of the bile ducts and pancreatic duct.

Basic laboratory tests.

General blood test allows you to confirm the presence and determine the severity of the inflammatory process.

Biochemical blood test(determining the level of bilirubin, enzymes, etc.) reveals dysfunction of the liver and pancreas accompanying cholecystitis.

Duodenal sounding(insertion of a probe into the lumen of the duodenum) makes it possible to examine bile and thereby not only clarify the pathology of the biliary system, but also assess the predisposition to cholelithiasis. The procedure involves inserting a probe into the lumen of the duodenum - an elastic rubber tube (its outer diameter is 4.5–5 mm, wall thickness is 1 mm, length 1.4 thousand–1.5 thousand mm).

Duodenal intubation is performed on an empty stomach and does not require special preparation. During probing, three portions of bile are obtained:

– portion A – duodenal bile, it has a golden yellow color;

– portion B – bladder bile, its color is dark brown;

– portion C is liver, it is lighter.

Contraindications to duodenal intubation are severe diseases of the upper respiratory tract, cardiovascular and pulmonary insufficiency, cirrhosis of the liver, acute surgical diseases of the abdominal cavity, severe exacerbation of cholecystitis and pancreatitis, exacerbation of peptic ulcer disease.

Treatment of cholecystitis depends on the stage of the disease (exacerbation or remission), the severity of the process (mild, moderate or severe), the presence of complications (empyema, cholangitis, pancreatitis, jaundice) and stones. Treatment can take place in a hospital setting or at home (outpatient). During periods of severe exacerbation, patients are hospitalized in the gastroenterological or therapeutic department. In case of severe pain, especially in patients with newly developed disease, or in case of complications with obstructive jaundice and with the threat of developing destructive cholecystitis, the patient is subject to emergency hospitalization in the surgical department. Outpatient treatment is prescribed for mild and uncomplicated disease. In the case of an acute form of the disease or an exacerbation of a chronic disease, bed rest is prescribed, and fasting for 1–2 days is also possible.

Therapeutic nutrition for cholecystitis

Diet plays a fundamentally important role in the treatment of the disease, since it is impossible to replace the gallbladder. It is almost impossible to count on a positive result without building proper nutrition in the treatment of cholecystitis. It is necessary to strictly follow dietary principles not only during exacerbation of the disease; It is necessary to adhere to dietary recommendations even without exacerbation of the process. As is known, errors in nutrition are the main factor causing exacerbation of cholecystitis. Diet is necessary at all stages of treatment, starting from the first hours of hospital stay, and further, at the outpatient stage, in a sanatorium, at home. With the help of a diet, you can create rest for the inflamed gallbladder or, conversely, enhance its activity (in particular, its contractility and motor ability), influence the processes of bile secretion - ensure the rhythmic outflow of bile, eliminate its stagnation.

The balanced diet of patients with cholecystitis should be complete and balanced; the diet includes regular meals in small portions 5–6 times a day, preferably at certain hours. Dishes are prepared mainly steamed or boiled; vegetables can be baked in the oven.

Patients suffering from cholecystitis need to monitor their body weight, since excess weight is a factor contributing to the development of the disease.

Therapeutic nutrition for acute cholecystitis

The diet during the acute period of the disease provides for maximum sparing of the entire digestive system. For this purpose, in the first days of the disease, it is recommended to administer only liquids: warm drinks are prescribed in small portions (still mineral water mixed with boiled water, weak tea, sweet fruit and berry juices diluted with water, rosehip decoction).

After 1 or 2 days, which is determined individually by the degree of activity of symptoms (primarily pain) and the severity of inflammation, pureed food is prescribed in limited quantities: mucous and pureed soups (rice, semolina, oatmeal), pureed porridge (rice, oatmeal, semolina), jelly, jellies, mousses from sweet fruits and berries. Further, the diet includes low-fat cottage cheese, pureed and steamed lean meat, and lean fish. White bread crackers are also allowed. The patient receives food in small portions 5–6 times a day, preferably at certain hours.

After another 5–10 days from the onset of the disease, diet No. 5a is prescribed.

General characteristics of the diet: a complete diet, but with some restriction of fat (70–80 g). If dyspeptic syndrome (nausea, heartburn, taste, bitterness in the mouth, bloating, etc.) is pronounced, then the daily amount of fat is limited to 50 g. Proteins and carbohydrates are administered in accordance with the physiological norm (80–90 g of proteins, 300–350 g carbohydrates).

Culinary processing of food: the main method of cooking is boiling or steaming. Fried foods are excluded. Mostly food is prepared pureed.

Diet: small meals - at least 5 times a day.

First courses: vegetarian soups (1/2 serving) with pureed vegetables or cereals, milk soup are allowed.

Meat and fish: lean meats in the form of soufflés, quenelles, and steamed cutlets are allowed. Chicken can be given in pieces, but in boiled form. Fresh, low-fat boiled fish is allowed.

Dairy dishes: non-sour cottage cheese (preferably homemade), protein omelettes, milk, mild cheeses.

Fats: butter, vegetable oil.

Vegetables (in addition to boiled ones) and fruits can be prescribed to a limited extent in raw pureed form.

Only dried white bread is allowed.

Prohibited foods and dishes.

Any fried foods, legumes (peas, lentils, beans), vegetables and herbs rich in essential oils (garlic, onions, radishes, radishes), any fats (pork, lamb, etc.), except butter and vegetable oil, are excluded. fresh bread, baked goods, alcohol, spices, hot seasonings.

Too hot and cold dishes are also excluded (food is served warm).

Below we present an approximate one-day menu for diet No. 5a of pureed dishes.

The energy value of the menu is 2430 kcal, protein content - 92.06 g, fat - 76.36 g, carbohydrates - 337.8 g.

After the name of the dish (product), its yield is indicated in grams. Anatoly Ivanovich Babushkin

From the book A powerful force in the fight against disease. Homeopathy. Treatment regimens for common diseases. Elimination of the consequences of treatment with antibiotics and hormones author Yuri Anatolyevich Savin

From the book Great Guide to Massage author Vladimir Ivanovich Vasichkin

From the book Massage. Lessons from a great master author Vladimir Ivanovich Vasichkin

From the book Me and My Heart. An original method of rehabilitation after a heart attack author Anatoly Ivanovich Babushkin

From the book Vibration Therapy. Vibrations replace all pills! author Vyacheslav Biryukov

From the book 365 golden breathing exercises author Natalya Olshevskaya

From the book Let's regain lost health. Naturopathy. Recipes, techniques and advice of traditional medicine author Irina Ivanovna Chudaeva

From the book “The Wise Organism” System. 5 ways to teach your body to be healthy at any age author Vladimir Alekseevich Sholokhov

From the book Delicacies for Diabetics. Emergency culinary assistance author Tatiana Rumyantseva

From the book Cholesterol: Another Great Deception. Not everything is so bad: new data author Efremov O. V.

From the book Cleansing and restoring the body with folk remedies for liver diseases author Alevtina Korzunova

From the book Dangerous Medicine. Crisis of traditional methods of treatment author Arusyak Arutyunovna Nalyan

Federal Agency for Health and Social Development"

Department of Pediatric Surgical Diseases faculty with a course in endoscopy and endosurgery

FOR TEACHER

TO THE PRACTICAL LESSON

Topic “Acute cholecystitis”

Approved at the department meeting

Protocol No. 10

«__ 19 ___" April 2007

Head Department of Surgical Diseases, Faculty of Pediatrics

with a course of endoscopy and endosurgery software

State Educational Institution of Higher Professional Education KrasSMA Roszdrav

Doctor of Medical Sciences, Prof.________________________________E.V. Kasparov

assistant Boyakova N.V.

Krasnoyarsk

1. Lesson topic: “Acute cholecystitis”

2. Form of organization of the educational process: practical lesson

3. Theme meaning: Acute calculous cholecystitis is one of the severe manifestations of cholelithiasis. Mortality in acute cholecystitis remains quite high, especially in people over 60 years of age. Timely cholecystectomy for gallstone disease avoids the development of acute cholecystitis.

4. Learning Objectives:

4.1. General goal: to prepare a qualified doctor who is well versed in the diagnosis of cholecystitis.

4.2. Learning goal: to be able to diagnose cholecystitis

4.3. Psychological and pedagogical goals: developing the doctor’s responsibility for diagnosing acute cholecystitis, timely cholecystectomy for cholelithiasis will avoid the development of acute cholecystitis.

5. Place of the lesson: The practical lesson is carried out in the training room, supervision of patients in the wards, in the reception and diagnostic department, dressing room, and operating room. Monitoring the level of knowledge and conducting the results of the lesson is carried out in the training room. The duration of the practical lesson is 180 minutes.

6. Lesson equipment: tables, slides, computer training program.

7. Structure of the topic content: Lesson chronomap (lesson plan)

Lesson stages

duration

equipment

Organization of the lesson

Formulation of the topic and purpose

Control of the initial level of knowledge and skills

Tests on the topic, see surgical diseases from 65-81 (test control)

Disclosure of educational-target issues

Independent work of students (supervision of patients is carried out under the supervision of a teacher.) Advisory assistance is provided, typical errors are identified.

Clinical analysis of patients

Conclusion on the lesson (final control) in writing or orally with assessment of knowledge

Solving situational problems. Look:

Surgical diseases, situational tasks,

Homework assignment

8. Abstract

ACUTE CHOLECYSTITIS-nonspecific inflammation of the gallbladder. In 85-95%, inflammation of the gallbladder is combined with stones. In more than 60% of cases of acute cholecystitis, microbial associations are cultured from bile: most often Escherichia coli, streptococci, salmonella, clostridia, etc. In some cases, acute cholecystitis occurs when pancreatic enzymes reflux into the gallbladder (enzymatic cholecystitis).

It is possible for an infection to enter the gallbladder during sepsis. Collagenoses, leading to narrowing and thrombosis of the cystic artery, can cause the development of gangrenous forms of acute cholecystitis. Finally, in approximately 1% of cases, the cause of acute cholecystitis is a tumor lesion, leading to obstruction of the cystic duct.

Thus, in the vast majority of cases, for the occurrence of acute cholecystitis, obstruction of the cystic duct or the gallbladder itself in the area of ​​Hartmann's pouch is necessary. Stagnation of bile with rapid development of infection causes the typical clinical picture of the disease. Violation of the barrier function of the mucous membrane of the gallbladder may be due to necrosis as a result of a significant increase in intraluminal pressure during cystic duct obstruction; in addition, direct pressure of the stone on the mucous membrane leads to ischemia, necrosis and ulceration. Violation of the barrier function of the mucous membrane leads to the rapid spread of inflammation to all layers of the bladder wall and the appearance of somatic pain.

Symptoms, course. It occurs more often in women over 40 years of age. Early symptoms of acute cholecystitis are very diverse. While the inflammation is limited to the mucous membrane, there is only visceral pain without clear localization, often involving the epigastric region and the navel area. The pain is usually dull in nature. Muscle tension and local soreness are not detected. There may be no changes in the blood during this period.

The diagnosis is based primarily on the medical history (the appearance of pain after an error in diet, anxiety, shaking), pain on palpation of the edge of the liver and the area of ​​the gallbladder. However, when complete obstruction of the cystic duct occurs and infection quickly attaches, the pain intensifies significantly, moves to the right hypochondrium, radiates to the supraclavicular region, interscapular space, and lumbar region. Nausea, vomiting, sometimes repeated (especially with cholecystopancreatitis). The skin may be icteric (in 7-15% of cases acute cholecystitis is combined with choledocholithiasis). The temperature is low-grade, but it can rise quickly and reach 39 degrees. WITH.

On examination: patients often have high nutrition, the tongue is coated. The abdomen is tense and lags behind when breathing in the right hypochondrium, where a tense, painful gallbladder or inflammatory infiltrate can be palpated (depending on the duration of the disease). Locally positive symptoms of Ortner - Grekov, Murphy, Shchetkin - Blumberg.

In the blood - leukocytosis with a shift of the formula to the left, increased levels of serum amylase and urine diastase (cholecystopancreatitis), hyperbilirubinemia (choledocholithiasis, edema of the major duodenal papilla, compression of the common bile duct with infiltrate, cholecystopatitis).

Ultrasound examination of the gallbladder and biliary tract provides significant assistance in diagnosis (effectiveness is about 90%). In typical cases of acute cholecystitis, the diagnosis is simple. Differential diagnosis is carried out with a perforated gastric and duodenal ulcer, acute appendicitis, acute pancreatitis, renal colic, myocardial infarction, basal right-sided pneumonia, pleurisy, herpes zoster with damage to the intercostal nerves.

Complications: diffuse peritonitis. Acute cholecystitis is one of the most common causes of diffuse peritonitis. Clinical picture: typical onset of the disease, usually on the 3-4th day there is a significant increase in pain, muscle tension of the entire abdominal wall, diffuse pain and positive symptoms of peritoneal irritation throughout the abdomen. The clinical picture for perforated cholecystitis is somewhat different: at the time of perforation of the gallbladder, there may be a short-term decrease in pain (imaginary well-being), followed by an increase in peritoneal symptoms and increased pain.

A subhepatic abscess occurs as a result of delimitation of the inflammatory process during destructive cholecystitis due to the greater omentum, the hepatic angle of the colon and its mesentery. The duration of the disease is usually more than 5 days. Patients have severe pain in the right half of the abdomen, high temperature, sometimes of a hectic nature. On examination, the tongue is coated, the abdomen lags behind during breathing in the right half, sometimes a formation is detected by eye, which moves in a limited way when breathing. On palpation, muscle tension and a painful, stationary infiltrate of varying sizes are observed. A general X-ray examination of the abdominal and thoracic organs reveals paresis of the colon, limited mobility of the right dome of the diaphragm, and possibly a slight accumulation of fluid in the sinus. Very rarely the fluid level in the abscess cavity is detected. Ultrasound examination of the liver and biliary tract helps in diagnosis.

Empyema of the gallbladder is caused by blockage of the cystic duct with the development of infection in the gallbladder while maintaining the barrier function of the mucous membrane. Under the influence of conservative therapy, the pain characteristic of acute cholecystitis decreases, but does not go away completely, a feeling of heaviness in the right hypochondrium, a slight increase in temperature, and there may be slight leukocytosis in the blood are disturbing. The abdomen is soft, a moderately painful gallbladder can be felt in the right hypochondrium, mobile, with clear contours. During surgery, puncture of the bladder produces pus without bile.

Treatment of acute cholecystitis. Urgent hospitalization in a surgical hospital. If diffuse peritonitis is present, emergency surgery is indicated. Before surgery - premedication with antibiotics. The operation of choice is cholecystectomy with revision of the biliary tract, sanitation and drainage of the abdominal cavity. Mortality during emergency surgical interventions reaches 25-30%, and is especially high in septic shock.

In the absence of symptoms of diffuse peritonitis, conservative therapy is indicated with simultaneous examination of the patient (respiratory organs, cardiovascular system, ultrasound examination to identify stones in the gall bladder). The complex of conservative therapy includes: local cold, intravenous administration of antispasmodics, detoxification therapy, broad-spectrum antibiotics. If the calculous nature of cholecystitis is confirmed (by ultrasound) and there are no contraindications from the respiratory and circulatory system, early (no later than 3 days from the onset of the disease) surgery is advisable: it is technically simpler, prevents the development of complications of acute cholecystitis, and has minimal mortality. In case of severe concomitant pathology, especially in old age, laparoscopic puncture of the bladder with aspiration of the contents and washing of its cavity with antiseptics and antibiotics can be used to adequately prepare the patient for surgery. After 7-10 days, an operation is performed - cholecystectomy with revision of the biliary tract.

Prevention of acute cholecystitis is timely surgical treatment of cholelithiasis.

Chronic cholecystitis- chronic inflammation of the gallbladder. The disease is common, more common in women.

Etiology, pathogenesis. Bacterial flora (Escherichia coli, streptococci, staphylococci, etc.), in rare cases - anaerobes, helminthic infestation (roundworms) and fungal infection (actinomycosis), hepatitis viruses; cholecystitis of toxic and allergic nature occurs. Penetration of microbial flora into the gallbladder occurs by enterogenous, hematogenous or lymphogenous routes. A predisposing factor in the occurrence of cholecystitis is stagnation of bile in the gallbladder, which can be caused by gallstones, compression and kinks of the bile ducts, dyskinesia of the gallbladder and biliary tract, disturbances in the tone and motor function of the biliary tract under the influence of various emotional stress, endocrine and autonomic disorders , reflexes from pathologically altered organs of the digestive system. Stagnation of bile in the gallbladder is also facilitated by prolapse of the viscera, pregnancy, sedentary lifestyle, rare meals, etc.; The reflux of pancreatic juice into the bile ducts during dyskinesia with its proteolytic effect on the mucous membrane of the bile ducts and gallbladder is also important.

The direct impetus for an outbreak of the inflammatory process in the gallbladder is often overeating, especially the intake of very fatty and spicy foods, the intake of alcoholic beverages, an acute inflammatory process in another organ (tonsillitis, pneumonia, adnexitis, etc.).

Chronic cholecystitis can occur after acute cholecystitis, but more often it develops independently and gradually, against the background of cholelithiasis, gastritis with secretory insufficiency, chronic pancreatitis and other diseases of the digestive system, obesity.

Symptoms, course. Characterized by a dull, aching pain in the right hypochondrium that is constant or occurs 1-3 hours after eating a large and especially fatty and fried meal. The pain radiates upward, to the area of ​​the right shoulder and neck, right shoulder blade. Periodically, a sharp pain reminiscent of biliary colic may occur. Dyspeptic symptoms are common: a feeling of bitterness and a metallic taste in the mouth, belching of air, nausea, flatulence, defecation disorders (often alternating constipation and diarrhea), as well as irritability, insomnia. Jaundice is not typical. When palpating the abdomen, as a rule, sensitivity and sometimes severe pain in the projection of the gallbladder onto the anterior abdominal wall and slight muscular resistance of the abdominal wall (resistance) are determined. The symptoms of Mussi - Georgievsky, Ortner, Obraztsov - Murphy are often positive. The liver is somewhat enlarged with a dense and painful edge on palpation due to complications of chronic cholecystitis (chronic hepatitis, cholangitis). In most cases, the gallbladder is not palpable, since it is usually wrinkled due to a chronic scar-sclerosing process. During exacerbations, neutrophilic leukocytosis, increased ESR and temperature reaction are observed. During duodenal intubation, it is often not possible to obtain cystic portion B of bile (due to impaired concentration ability of the gallbladder and impaired bladder reflex) or this portion of bile is only slightly darker in color than A and C, and is often cloudy. Microscopic examination of the duodenal contents reveals a large amount of mucus, desquamated epithelial cells, “leukocytes”, especially in portion B of bile (the detection of “leukocytes” in bile is not given the same importance as before; as a rule, they turn out to be the nuclei of decaying cells of the duodenal epithelium) . Bacteriological examination of bile (especially repeated) makes it possible to determine the causative agent of cholecystitis.

During cholecystography, a change in the shape of the gallbladder is noted, often its image is unclear due to a violation of the concentrating ability of the mucous membrane, sometimes stones are found in it. After taking an irritant - cholecystokinetics (usually two egg yolks) - insufficient contraction of the gallbladder is noted. Signs of chronic cholecystitis are also determined by echography (in the form of thickening of the walls of the bladder, its deformation, etc.).

The course in most cases is long, characterized by alternating periods of remission and exacerbation; the latter often arise as a result of eating disorders, drinking alcohol, heavy physical work, acute intestinal infections, and hypothermia. The prognosis is favorable in most cases. Deterioration of the general condition of patients and temporary loss of their ability to work - only during periods of exacerbation of the disease. Depending on the characteristics of the course, latent (sluggish) forms are distinguished, the most common being recurrent, purulent-ulcerative forms of chronic cholecystitis. Complications: addition of chronic cholangitis, hepatitis, pancreatitis. Often the inflammatory process is the “impetus” for the formation of gallstones.

Chronic cholecystitis is differentiated from cholelithiasis (these two diseases are often combined) and chronic cholangitis. Of primary importance are cholecysto- and cholegraphy data, especially repeated ones to exclude gallstones, as well as echography.

Treatment. During exacerbations of chronic cholecystitis, patients are hospitalized in surgical or therapeutic hospitals and treated as for acute cholecystitis. In mild cases, outpatient treatment is possible. Prescribe bed rest, dietary nutrition (diet No. 5a), with meals 4-6 times a day, antibiotics (oletethrin, erythromycin, chloramphenicol, ampicillin orally or glycocycline, monomycin, etc. parenterally). Sulfonamide drugs (sulfadimezin, sudfa-pyridazine, etc.) are also prescribed. To eliminate biliary dyskinesia, spastic pain, and improve bile outflow, antispasmodic and anticholinergic drugs are prescribed (papaverine hydrochloride, no-spa, atropine sulfate, platiphylline hydrotartrate, etc.), and in case of mild exacerbations and during the period of subsidence of inflammatory phenomena, duodenal intubation (after 1 -2 days, for a course of 8-12 procedures) or so-called blind, or probeless, tubes with magnesium sulfate or warm mineral water (Essentuki No. 17, etc.). For severe inflammatory pain, amidopyrine or analgin IM, perinephric novocaine blockades are used, novocaine is administered - 30-50 ml of a 0.25-0.5% solution intradermally over the area of ​​maximum pain, or electrophoresis with novocaine is prescribed to this area. During the period of subsidence of the inflammatory process, thermal physiotherapeutic procedures can be prescribed to the area of ​​the right hypochondrium (diathermy, UHF, inductothermy, etc.).

To improve the outflow of bile from the gallbladder, both during exacerbations and during remissions, choleretic drugs are widely prescribed: allochol (2 tablets 3 times a day), cholenzyme (1 tablet 3 times a day), decoction (10:250) of flowers sandy immortelle (1/2 cup 2-3 times a day before meals); decoction or infusion of corn silk (10:200, 1-3 tablespoons 3 times a day) or their liquid extract (30-40 drops 3 times a day); choleretic tea (brew one tablespoon with 2 cups of boiling water, take the strained infusion 1/2 cup 3 times a day 30 minutes before meals); cyclone, nicodine, etc., as well as olimetine, rovahol, enatine (0.5-1 g in capsules 3-5 times a day) and holagol (5 drops for sugar 30 minutes before meals 3 times a day). These drugs have antispasmodic, choleretic, nonspecific anti-inflammatory and diuretic effects. For a mild attack of biliary colic, Cholagol is prescribed 20 drops per dose.

Chronic cholecystitis is treated with mineral water (Essentuki No. 4 and No. 17, Slavyanovskaya, Smirnovskaya, Mirgorodskaya, Naftusya, Novo-Izhevskaya, etc.), as well as magnesium sulfate (1 tablespoon of 25% solution 2 times a day) or Karlovy Vary salt (1 teaspoon in a glass of warm water 3 times a day). After the exacerbation of cholecystitis subsides and for the prevention of subsequent exacerbations (preferably annually), sanatorium-resort treatment is indicated (Essentuki, Zheleznovodsk, Truskavets, Morshin and other sanatoriums, including local ones, intended for the treatment of cholecystitis).

If conservative treatment fails and frequent exacerbations occur, surgical treatment of chronic cholecystitis is performed (usually cholecystectomy).

Prevention of chronic cholecystitis consists of following a diet, playing sports, exercising, preventing obesity, and treating focal infections.


acute cholecystitis

Etiology and pathogenesis

Classification

Complication

Prevention

chronic cholecystitis

Classification

Etiology

Pathogenesis

Flow

Complications

Prevention

list of used literature

Cholecystitis is an inflammation of the gallbladder. There are acute and chronic cholecystitis.

ACUTE CHOLECYSTITIS

Acute cholecystitis is one of the most common surgical diseases, and ranks second in frequency after appendicitis.

The problem of acute cholecystitis over the past three decades has been relevant both due to the widespread prevalence of the disease and due to the presence of many controversial issues. Currently, noticeable successes can be noted: mortality during surgical treatment has decreased. There is especially much disagreement regarding the timing of intervention. In many ways, the answer to this question is determined by the attitude formulated by B. A. Petrova: an emergency or urgent operation at the height of an attack is much more dangerous than a planned one, after the acute phenomena have subsided.

Etiology and pathogenesis

The occurrence of acute cholecystitis is associated with the action of more than one, several etiological factors, but the leading role in its occurrence belongs to infection. The infection enters the gallbladder in three ways: hematogenous, enterogenous and lymphogenous.

In the hematogenous route, the infection enters the gallbladder from the general circulation through the common hepatic artery system or from the intestinal tract through the portal vein further into the liver. Only when the phagocytic activity of the liver decreases do microbes pass through cell membranes into the bile capillaries and further into the gallbladder.

The lymphogenous route of infection into the gallbladder is possible due to the extensive connection of the lymphatic system of the liver and gallbladder with the abdominal organs. Enterogenous (ascending) - the route of spread of infection into the gallbladder is possible due to diseases of the terminal section of the common section of the common bile duct, functional disorders of its sphincter apparatus, when infected duodenal contents can be thrown into the bile ducts. This path is the least likely.

Inflammation in the gallbladder does not occur when an infection enters the gallbladder, unless its drainage function is impaired and there is no bile retention. In case of disruption of the drainage function, the necessary conditions are created for the development of the inflammatory process.

Factors affecting the outflow of bile from the bladder: stones, kinks in the elongated or tortuous cystic duct, its narrowing.

Acute cholecystitis arising from cholelithiasis accounts for 85-90%. Chronic changes in the gallbladder in the form of sclerosis and atrophy of the elements of the gallbladder walls are also important.

The bacteriological basis of acute cholecystitis are various microbes and their associations. Among them, the main ones are gram-negative bacteria of the Escherichia coli group and gram-positive bacteria of the genus Staphilococcus and Sterptococcus. Other microorganisms that cause inflammation of the gallbladder are extremely rare.

Due to the anatomical and physiological connection of the biliary tract with the excretory ducts of the pancreas, the development of enzymatic cholecystitis is possible. Their occurrence is associated not with the action of a microbial factor, but with the flow of pancreatic juice into the gallbladder and the damaging effect of pancreatic enzymes on the tissue of the bladder. As a rule, these forms are combined with symptoms of acute pancreatitis. Combined forms of acute pancreatitis and cholecystitis are considered as an independent disease, called “cholecysto-pancreatitis”.

It is well known that vascular changes in the wall of the gallbladder are important in the pathogenesis of acute cholecystitis. The rate of development of the inflammatory process and the severity of the disease depend on the circulatory disorder in the bladder due to thrombosis of the cystic artery. The consequence of vascular disorders are foci of necrosis and perforation of the bladder wall. In elderly patients, vascular disorders associated with age-related changes can cause the development of destructive forms of acute cholecystitis (primary gangrene of the gallbladder).

Classification

The question of the classification of acute cholecystitis, in addition to its theoretical significance, is of great practical importance. A rationally compiled classification gives the surgeon the key to not only correctly classifying this or that form of acute cholecystitis to a certain group, but also choosing the appropriate tactics in the preoperative period and during surgery.

One way or another, the classification of acute cholecystitis, as a rule, is based on a clinical and morphological principle - the dependence of the clinical manifestations of the disease on pathoanatomical changes in the gallbladder, abdominal cavity and on the nature of changes in the extrahepatic bile ducts. This classification distinguishes two groups of acute cholecystitis: complicated and uncomplicated.

Uncomplicated includes all pathological forms of inflammation of the gallbladder that are routinely encountered in clinical practice - catarrhal, phlegmonous and gangrenous cholecystitis. Each of these forms should be considered as a natural development of the inflammatory process, a gradual transition from catarrhal inflammation to gangrene. An exception to this pattern is primary gangrenous cholecystitis, since the mechanism of its development is primary thrombosis of the cystic artery.

Acute inflammation of the gallbladder can occur with or without stones in its lumen. The accepted division of acute cholecystitis into tubeless and calculous is conditional, since regardless of whether there are stones in the bladder or absent, the clinical picture of the disease and treatment tactics will be almost the same for each form of cholecystitis.

The group of complicated cholecystitis consists of complications that are directly related to inflammation of the gallbladder and the spread of infection beyond its boundaries. These complications include peri-vesical infiltration and abscess, perforation of the gallbladder, peritonitis of varying prevalence, biliary fistulas, acute pancreatitis, and the most common complications are obstructive jaundice and cholangitis. Complicated forms occur in 15–20% of cases.

Complications

In some cases, the disease can become chronic; this is more often observed with purulent or phlegmous cholecystitis or with catarrhal disease.

If the course is unfavorable, the acute period of the disease is prolonged, complications may occur: perforation of the gallbladder in the abdominal cavity with the development of peritonitis or the spread of infection to internal organs with the formation of biliary fistulas, ascending cholangitis, liver abscesses, etc.

Prevention

Maintaining a balanced diet, physical exercise, preventing lipid metabolism disorders, eliminating foci of infection.

CHRONIC CHOLECYSTITIS.

Inflammation of the gallbladder wall, caused by prolonged irritation either from a stone, or from repeated acute inflammatory processes, or from bacterial persistence.

Classification

1. Cholecystitis:

a) calculous

b) stoneless

Etiology:

Infection - often conditionally - pathogenic flora: Escherichia coli, streptococcus, staphylococcus, typhoid bacilli, protozoa (giardia).

Bile itself has a bactericidal effect, but when the composition of the bile changes and especially when it stagnates, bacteria can rise through the bile duct into the gallbladder. Under the influence of infection, cholic acid is converted into lithocholic acid. Normally, this process occurs only in the intestines. If bacteria penetrate the gallbladder, then this process begins to take place in it. Lithocholic acid has a damaging effect and inflammation of the bladder wall begins; these changes can be accompanied by infection.

Dyskinesia can be in the form of spastic contraction of the gallbladder and in the form of its atony with stagnation of bile. At first there may be changes of a purely functional nature. Next, there is an inconsistency in the action of the bladder and sphincters, which is associated with a violation of the innervation and humoral regulation of the motor function of the gallbladder and bile ducts.

Normally, regulation is carried out as follows: contraction of the gallbladder and relaxation of the sphincters - the vagus. Spasm of the sphincters, overflow of the gallbladder - sympathetic nerve. Humoral mechanism: in the duodenum, 2 hormones are produced - cholecystokinin and secretin, which act like a vagus and thereby have a regulatory effect on the gallbladder and pathways. Violation of this mechanism occurs with vegetative neurosis, inflammatory diseases of the gastrointestinal tract, disturbances in nutritional rhythm, etc.

Dyscholia is a violation of the physicochemical properties of bile.

The concentration of bile in the bladder is 10 times greater than in the liver. Normal bile is made up of bilirubin, cholesterol (insoluble in water, so to keep it dissolved as a colloid requires the presence of coats), phospholipids, bile acids, pigments, etc. Normally, bile acids and their salts (chalates) relate to cholesterol as 7:1, if the amount of cholesterol increases, for example to 1O:1. then it precipitates, thereby contributing to the formation of stones.

Dycholia is promoted by high levels of cholesterol (with diabetes, obesity, familial hypercholesterolemia), bilirubin (with hemolytic anemia, etc.), fatty and bile acids. However, infection of bile is of great importance. In practice, the above factors are most often combined. The damaging effect of lithocholic acid, when it is formed in the gallbladder instead of the duodenum under the influence of infection, is associated with changes in pH, precipitation of calcium salts, etc.

Pathogenesis.

Chronic cholecystitis (XX) is caused by stagnation of bile and changes in its physicochemical properties. Such altered bile may be accompanied by an infection. The inflammatory process can be provoked by a stone, an abnormal development of the bladder, or dyskinesia of the latter. Inflammation of the gallbladder can contribute to further stone formation. Inflammation causes secondary deformation, wrinkling of the bladder, and the formation of various closed cavities from the folds of the mucous membrane. Inside these folds there is infected bile, the spread of which supports inflammation of the gallbladder wall.

It is possible for infection to penetrate the bile ducts and passages with the development of cholangitis and damage to the liver tissue itself with the development of cholangiohepatitis. Calculous cholecystitis is fraught with obstruction of the bile duct and the development of dropsy, and with suppuration, empyema of the gallbladder. A stone may cause perforation of the gallbladder wall.

The course of chronic cholecystitis:

Recurrent; hidden latent flow; attacks of hepatic colic. The course in most cases is long, characterized by alternating periods of remission and exacerbation; the latter often arise as a result of eating disorders, drinking alcohol, heavy physical work, acute intestinal infections, and hypothermia. The prognosis is favorable in most cases. Deterioration of the general condition of patients and temporary loss of their ability to work - only during periods of exacerbation of the disease. Depending on the characteristics of the course, latent (sluggish) forms are distinguished, the most common being recurrent, purulent-ulcerative forms of chronic cholecystitis. Complications: addition of chronic cholangitis, hepatitis, pancreatitis. Often the inflammatory process is the “impetus” for the formation of gallstones.

Complications

Transition of inflammation to surrounding tissues: pericholecystitis, periduodenitis, etc. Transition of inflammation to surrounding organs: gastritis, pancreatitis. Cholangitis with transition to biliary cirrhosis of the liver. There may be obstructive jaundice. If the stone is stuck in the cystic duct, then dropsy, empyema occurs, and possible perforation followed by peritonitis; sclerosis of the bladder wall, and later cancer may occur.

Indications for surgery:

Obstructive jaundice for more than 8-12 days, frequent attacks of hepatic colic, non-functioning gallbladder - small, wrinkled, does not contrast. Hydrocele and other prognostic adverse complications.

Prevention

Sanitation of foci of chronic infection, timely and rational treatment of cholecystitis, diet, prevention of helminthic infestations, acute intestinal diseases, sports, prevention of obesity.


List of used literature

1. Great medical encyclopedia

2. “Cholecystitis” Auth. Anna Kuchanskaya Ed. "All"

St. Petersburg 2001

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    Abstract on topic: Acute cholecystitis

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    1. Acute cholecystitis: epidemiology, relevance, frequency of infectious complications


    As noted in the literature, acute cholecystitis refers to acute inflammatory diseases of the gallbladder. It usually occurs with a suddenly developing disruption of bile circulation as a result of blockage of the gallbladder. Destructive processes in the bladder wall are often observed. In most patients it is associated with cholelithiasis (hereinafter referred to as cholelithiasis). More often, acute cholecystitis develops against the background of chronic inflammation of the gallbladder. It can be considered an acute complication of chronic gallbladder diseases.

    Acute cholecystitis develops in the mouth due to the combined influence of three factors:

    · Violation of the exchange of bile components - discrinia. The main components of bile - bilirubin and cholesterol - are poorly soluble in water and are in solution due to the emulsifying effect of bile acids. For cholesterol to precipitate, its equilibrium state with bile acids must be disrupted. This occurs either when the concentration of cholesterol increases (for example, in obesity, diabetes, pregnancy), or when the concentration of bile acids decreases (inflammation caused by intestinal bacteria, in which their chenodeoxycholic acid is formed lithocholic acid, which can precipitate). In addition, estrogens inhibit the transport of bile acids, so women of reproductive age are more susceptible to the occurrence of cholelithiasis. Less frequently formed bilirubin stones are usually associated with massive hemolysis in hemolytic anemia.

    · Stagnation of bile due to hypomotor (hypotonic) or hypermotor (hypertonic) dyskinesia of the biliary tract leads to increased absorption of the liquid part and an increase in the concentration of salts in the bile. Pregnancy, constipation, physical inactivity, and foods low in fat contribute to bile stagnation.

    · Inflammation, which results in the formation of exudate, the basis of which is protein and mineral salts (Ca 2+). It is believed that the protein is the core around which the stones are deposited. Ca 2+ also promotes the formation of bilirubin stones.

    The role of infection in the development of cholelithiasis has not yet been proven. The formation of a dense stone leads, on the one hand, to disruption of the outflow of bile, and on the other, to the development of inflammatory processes due to constant mechanical action.

    Epidemiology. According to the General Surgery Clinic of MMA named after. Over the past 12 years, Sechenov has operated on about 1000 patients with acute cholecystitis, of which 32% were caused by complications of obstructive jaundice and purulent cholangitis, all the rest were caused by acute calculous cholecystitis. According to general data, from 350,000 to 500,000 people undergo cholecystectomy annually, with a mortality rate close to 1.5%. Low mortality is mainly achieved by performing more operations early, without severe exacerbation of cholecystitis.

    Relevance of the problem GSD is one of the most common diseases of the digestive system. Over the past decade, an increase in the incidence of cholelithiasis has been observed in Russia and abroad. Acute cholecystitis still remains a pressing problem in modern emergency surgery, especially geriatric surgery, since mainly elderly and senile people are ill and undergo surgery.

    The percentage of patients with acute cholecystitis from general surgical patients is 20-25%. It is a common pathology and is equal to the level of acute appendicitis and sometimes even exceeds it.

    If we take into account mortality rates, then acute cholecystitis is superior to appendicitis, strangulated hernias, perforated gastroduodenal ulcers and is only slightly inferior to acute intestinal obstruction. Overall mortality rates range from 2-12% across different institutions. There is no tendency to decrease and reaches 14-15% during operations at the height of the attack; in older people it reaches 20%. This figure increases sharply as patients age. During emergency operations in patients over 80 years of age, postoperative mortality exceeds 40-50%, which makes these operations extremely risky.

    However, if we take into account the indicators when operations were performed against the background of subsided inflammatory phenomena, after examinations and preparation of patients, then we can observe a decrease in the mortality rate, which is equal to 0.5-1% for individual surgeons.

    Of the types of acute cholecystitis, the most common is acute calculous cholecystitis. In the practice of emergency surgery, acalculous processes account for no more than 2-3% of cases - these are mainly vascular lesions of the gallbladder in people with widespread atherosclerosis, diabetes mellitus, etc.

    Frequency of infectious complications. In the etiology, a certain role is assigned to infection, but microflora in the gallbladder is detected only in 33-35% of cases, and bacteriological examination of the gallbladder wall with cholecystitis (surgical material) reveals the presence of microflora in only 20-30% of patients. This is explained by the fact that with normally functioning liver tissue, microbes entering the liver by hematogenous or lymphogenous routes die (A. M. Nogaller, Ya. S. Zimmerman). Only with a decrease in the bactericidal properties of the liver and the general resistance of the body is it possible for pathogenic microflora to penetrate the gallbladder. However, it is known that the introduction of microorganisms into the intact gallbladder does not cause inflammation in it, since bile has bacteriostatic properties.

    2. Modern classification, etiology of surgical site infection. Risk factors on the part of the patient


    Classification of acute cholecystitis. The following clinical and morphological forms of acute cholecystitis are distinguished: catarrhal, phlegmonous and gangrenous (with or without perforation of the gallbladder).

    Catarrhal cholecystitis characterized by intense constant pain in the right hypochondrium, epigastric region with irradiation to the right shoulder blade, shoulder, right half of the neck. At the onset of the disease, pain can be paroxysmal in nature due to increased contraction of the gallbladder wall, aimed at eliminating occlusion of the bladder neck or cystic duct. Vomiting of gastric and then duodenal contents often occurs, which does not bring relief to the patient. Body temperature rises to subfebrile levels. Moderate tachycardia develops up to 80-90 beats per minute, and sometimes a slight increase in blood pressure is observed. The tongue is moist and may be coated with a whitish coating. The abdomen participates in the act of breathing; there is only a slight lag in the upper parts of the right half of the abdominal wall in the act of breathing.

    With palpation and percussion of the abdomen, sharp pain occurs in the right hypochondrium, especially in the area of ​​​​the projection of the gallbladder. Tension of the abdominal wall muscles is absent or slightly expressed.

    Symptoms of Ortner, Murphy, Georgievsky-Mussi are positive. In 20% of patients, an enlarged, moderately painful gallbladder can be felt. The blood test shows moderate leukocytosis (10-12 109/l).

    Catarrhal cholecystitis, like hepatic colic, in most patients is provoked by errors in diet. Unlike colic, an attack of acute catarrhal cholecystitis can be longer (up to several days) and is accompanied by nonspecific symptoms of the inflammatory process (hyperthermia, leukocytosis, increased ESR).

    Phlegmonous cholecystitis has more pronounced clinical symptoms: the pain is much more intense than with the catarrhal form of inflammation, intensified by breathing, coughing, and changing body position. Nausea and repeated vomiting occur more often, the patient’s general condition worsens, body temperature reaches febrile levels, tachycardia increases to 100 beats per minute or more. The abdomen is somewhat swollen due to intestinal paresis; when breathing, the patient spares the right half of the abdominal wall, bowel sounds are weakened. Upon palpation and percussion of the abdomen, sharp pain occurs in the right hypochondrium, and pronounced muscle protection is also noted here; It is often possible to detect an inflammatory infiltrate or an enlarged, painful gallbladder. The examination reveals a positive Shchetkin-Blumberg symptom in the right upper quadrant of the abdomen, Ortner, Murphy, Georgievsky-Mussi symptoms, leukocytosis up to 12-18 10 9 /l with a shift of the formula to the left, an increase in ESR.

    A distinctive feature of the phlegmonous process is the transition of inflammation to the parietal peritoneum. There is an enlargement of the gallbladder: its wall is thickened, purple-bluish in color. There is a fibrinous coating on the peritoneum covering it, and purulent exudate in the lumen.

    If in the catarrhal form of acute cholecystitis, microscopic examination reveals only initial signs of inflammation (swelling of the bladder wall, hyperemia), then in phlegmonous cholecystitis, pronounced infiltration of the bladder wall with leukocytes is detected, tissue impregnation with purulent exudate, sometimes with the formation of small ulcers in the bladder wall.

    Gangrenous cholecystitis usually is a continuation of the phlegmonous stage of inflammation, when the body's natural defense mechanisms are unable to limit the spread of virulent microflora. Symptoms of severe intoxication with symptoms of local or general purulent peritonitis come to the fore, which is especially pronounced with perforation of the gallbladder wall. The gangrenous form of inflammation is observed more often in elderly and senile people with reduced regenerative abilities of tissues, decreased reactivity of the body and impaired blood supply to the gallbladder wall due to atherosclerotic damage to the abdominal part of the aorta and its branches.

    When the inflammatory process transforms into a gangrenous form, there may be some reduction in pain and an apparent improvement in the general condition of the patient. This is due to the death of sensory nerve endings in the gallbladder. However, quite quickly this period of imaginary well-being is replaced by increasing intoxication and symptoms of widespread peritonitis. The condition of the patients becomes severe, they are lethargic and inhibited. The body temperature is febrile, severe tachycardia develops (up to 120 beats per minute or more), rapid and shallow breathing. The tongue is dry, the abdomen is swollen due to intestinal paresis, its right parts do not participate in the act of breathing, peristalsis is sharply suppressed, and in case of widespread peritonitis, it is absent. The protective tension of the muscles of the anterior abdominal wall becomes more pronounced, and symptoms of peritoneal irritation are revealed. Percussion sometimes detects dullness of sound over the right lateral canal of the abdomen. Blood and urine tests show high leukocytosis with a sharp shift in the leukocyte formula to the left, an increase in ESR, disturbances in the electrolyte composition of the blood and the acid-base state, in the urine - proteinuria, cylindruria (signs of destructive inflammation and severe intoxication).

    Etiology of surgical site infection. The occurrence of acute cholecystitis is promoted by a number of factors, one of which is infection. Infection enters the gallbladder in three ways: hematogenous, enterogenous and lymphogenous. ü hematogenous route - the infection enters the gallbladder from the general circulation through the common hepatic artery system or from the intestinal tract through the portal vein further into the liver. Only when the phagocytic activity of the liver decreases do microorganisms pass through cell membranes into the bile capillaries and further into the gallbladder. ü Lymphogenic route - the infection enters the gallbladder due to the extensive connection of the lymphatic system of the liver and gallbladder with the abdominal organs. ü Enterogenous (ascending) pathway - the spread of infection into the gallbladder occurs when there is a disease of the terminal section of the common section of the common bile duct, a functional disorder of its sphincter apparatus, when infected duodenal contents can be thrown into the bile ducts. This path is the least likely. In this case, inflammation in the gallbladder does not occur unless its drainage function is impaired and there is no bile retention. In case of disruption of the drainage function, the necessary conditions are created for the development of the inflammatory process. Among the microorganisms that develop acute cholecystitis, the main ones are gram-negative bacteria of the Escherichia coli group and gram-positive bacteria of the genus Staphilococcus and Sterptococcus. Other microorganisms that cause inflammation of the gallbladder are extremely rare. Surgical site infections account for up to 40% of overall infectious complications. Of these, 2/3 are associated with the area of ​​the surgical incision, and 1/3 have infection of an organ or cavity. Infections can be classified based on penetration into the abdominal cavity (Fig. 1).

    Causative agents of infection in the surgical area include Staphylococcus aureus, coagulase-negative staphylococci, Enterococcus spp. and Escherichia coli (Table 1).

    Rice. 1. Classification of surgical site infection on a section of the abdominal wall

    Table 1. Most common pathogens causing surgical site infections

    Pathogen

    Infection rate, %

    Staphylococcus aureus

    Coagulase-negative staphylococci

    Enterococcus spp.

    Escherichia coli

    Pseudomonas aeruginosa

    Enterobacter spp.

    Proteus mirabilis

    Klebsiella pneumoniae

    Other streptococci

    Candida albicans

    Group D streptococci (not enterococci)

    Other gram-positive aerobes

    Bacteroides fragilis


    In the past, there has been an increase in the number of studies into the development of surgical site infections caused by methicillin-resistant Staphylococcus aureus and Candida albicans. After surgery, the source of wound infections can be the endogenous flora of the skin, mucous membranes or hollow organs - staphylococci.

    During operations on the gastrointestinal tract, typical pathogens are gram-negative bacilli (E. coli), gram-positive microorganisms (enterococci) and anaerobes (Bacteroides fragilis). When operating on acute cholecystitis, the main source of infection is biliary tract infections (we have already described them earlier) - E. coli and Klebsiella spp., much less often - other gram-negative microorganisms, streptococci or staphylococci. Among anaerobes, the most common are Clostridium spp.

    Exogenous sources of infection include the microflora of medical personnel, the operating room, operating equipment, surgical instruments and materials. Exogenous flora includes aerobes, mainly gram-positive cocci - staphylococci and streptococci. It is also necessary to take into account the patient’s concomitant infection or colonization of another localization, diabetes, smoking, use of hormonal drugs, obesity (>20% of the “ideal” body weight), extremely old or young age, nutritional deficiency, and blood transfusions prior to surgery.

    Risk factors on the part of the patient.

    Factors include:

    · Age over 40 years

    Female gender (twice as often as men)

    Obesity

    · Pregnancy (the more pregnancies there were, the higher the risk)

    · Hyperlipidemia

    Loss of bile salts (eg, small bowel resection or lesion)

    · Diabetes mellitus

    · Prolonged fasting

    Total parenteral nutrition

    Genetic and ethnic factors

    Low fiber, high fat diet

    · Cystic fibrosis

    Taking lipid-lowering drugs (clofibrate)

    Dyskinesia of the gallbladder

    3. Modern approaches to the prevention of infectious complications in the surgical area. Principles of perioperative antibiotic prophylaxis


    Antibiotic prophylaxis refers to the prescription of an antibacterial drug to a patient to treat microbial contamination of a surgical wound or the development of infectious complications of the surgical site (SSI). The main goal of antibiotic prophylaxis is to reduce surgical site infection.

    There are prescriptions of antibiotics for the purposes of therapy and prevention. If there is a therapeutic effect, the drugs are prescribed to treat an already diagnosed infection. In case of prophylaxis, antibiotics are prescribed to avoid infection.

    In the modern understanding, prophylaxis with antibiotics provides that contamination of a surgical wound is almost inevitable, even if all aseptic and antiseptic conditions are observed, and by the end of the operation in 80–90% of cases, the wounds are contaminated with various microflora, mainly staphylococci. However, when performing ABP, you should not strive for complete disinfection of bacteria, since their reduction facilitates the functioning of the immune system and prevents the development of purulent infection.

    There is now sufficient experience that recommends administering an antibiotic no earlier than 1 hour before surgery. If this fact is ignored, the administration of antibiotics after surgery is ineffective in reducing the incidence of postoperative wound infections.

    The criteria for choosing antibiotic prophylaxis are:

    The most likely pathogen after surgery is staphylococci, so the drug must be active against staphylococci. The spectrum of activity should also include anaerobic infections.

    Doses should correspond to therapeutic doses, and the time should be 30-40 minutes before surgery.

    The frequency of administration is based on the half-life of the antibiotic. Repeated doses are prescribed when the duration of the operation exceeds 2 times the half-life of the drug.

    Duration of antibiotic administration. In the absence of direct indications, the administration of an antibiotic is not effective, i.e. does not prevent the development of SSI.

    The main route of administration is intravenous, which ensures optimal concentration in the blood and tissues.

    Nowadays, many effective antibiotics are known. The most effective and safer are cephalosporin antibiotics of the first and second generations. They are well tolerated by the body, have good pharmacokinetic parameters and have an optimal cost. These include cefazolin, which is used in conditionally clean operations (using implants).

    If allergic reactions to penicillins occur, antibiotics active against gram-positive pathogens, such as lincosamides, should be used, and in patients with a high risk of carriage of methicillin-resistant S. aureus (MRSA) or from departments with a high frequency of MRSA, vancomycin is recommended for ALD. In Russia, the prevalence of MRSA strains is very high, amounting to 33.5%, and this necessitates the inclusion of vancomycin in the ABP protocols in the relevant departments. But the use of vancomycin as an ABP does not lead to a decrease in the proportion of MRSA in the structure of SSI.

    However, in surgery there are certain limitations for the widespread use of cephalosporins for the purpose of ALD.

    When operations on the biliary tract, distal parts of the small intestine, large intestine or appendix, it is necessary to use antibiotics active against pathogens of the Enterobacteriaceae family and anaerobes, in particular the Bacteroides fragilis group. Table 2 presents the different antibiotic prophylaxis regimens used in abdominal surgery depending on the anatomical site. It is very important to know about the localization of a particular pathogen, their sensitivity to antibiotics, in order to choose effective antibiotic prophylaxis.

    Type or location of operation

    Preparation

    Dose and route of administration for adults

    Esophagus, stomach, duodenum (including endoscopic interventions), high-risk group 1

    Amoxicillin/clavulanate

    1.2 g, intravenous

    Ampicillin/sulbactam

    1.5 g, intravenously

    Cefuroxime

    1.5 g, intravenously

    Biliary tract, high-risk group 2

    Amoxicillin/clavulanate

    1.2 g, intravenous

    Ampicillin/sulbactam

    1.5 g, intravenously

    Cefuroxime

    1.5 g, intravenously

    Large intestine

    Planned operations

    kanamycin (or gentamicin)

    1 g, parenteral

    Erythromycin 3

    1 g, orally

    Amoxicillin/clavulanate

    1.2 g, intravenous

    Ampicillin/sulbactam

    1.5 g, intravenously

    Emergency operations

    Amoxicillin/clavulanate

    1.2 g, intravenous

    Ampicillin/sulbactam

    1.5 g, intravenously

    Gentamicin 5

    0.08 g, intravenous

    Metronidazole

    0.5 g, intravenously

    Hernioplasty with implantation of artificial materials 4

    Cefazolin

    1–2 g, intravenously

    Cefuroxime

    1.5 g, intravenously

    Appendectomy (appendix without perforation)

    Amoxicillin/clavulanate

    1.2 g, intravenous

    Ampicillin/sulbactam

    1.5 g, intravenously

    Note.
    1 Morbid obesity, esophageal obstruction, reduced gastric acidity or weakened gastrointestinal motility.
    2 Age over 70 years, acute cholecystitis, non-functioning gallbladder, obstructive jaundice, common bile duct stones. Laparoscopic cholecystectomy – in the absence of risk factors, prophylaxis is not indicated.

    3 A short course of decontamination is carried out after an appropriate diet and gastric cleansing: kanamycin (gentamicin) and erythromycin 1 g at 13:00, 14:00 and 23:00 1 day before surgery and at 8:00 on the day of surgery.

    4 Laparoscopic or non-laparoscopic hernioplasty without implantation of artificial materials and in the absence of risk factors - ABP is not indicated.

    5 May cause neuromuscular blockade.


    The most used ABP in abdominal surgery is amoxicillin/clavulanate, because the activity of first generation cephalosporins against gram-negative microorganisms is insufficient and the absence of second generation cephalosporins with antianaerobic activity on the market. The effectiveness of amoxicillin/clavulanate in ALD was demonstrated by comparing the latter with cefamandole in 150 patients undergoing biliary tract surgery. The incidence of postoperative infectious complications and length of hospitalization were similar in both groups.

    Many studies have been conducted on the activity of amoxicillin/clavulanate and in all cases it has been proven to be more effective than other drugs. It is more convenient in dosing and is affordable. Many studies have confirmed that, in terms of cost and effectiveness, the use of amoxicillin/clavulanate is not inferior to other numerous recommended ABP regimens in abdominal surgery. According to unpublished data from a multicenter study of the resistance of pathogens of nosocomial infections in intensive care units (RESORT) of 21 cities and 33 departments in the Russian Federation, in 166 patients with intra-abdominal infections 62% of E. coli strains, 92% of Proteus mirabilis strains and 60% strains of Proteus vulgaris were sensitive to amoxicillin/clavulanate. The data presented determine the priority position of ABP regimens using amoxicillin/clavulanate, recommended by modern national guidelines on ABP, in relation to other antibiotics for abdominal surgical interventions.

    The spectrum of activity of amoxicillin/clavulanate includes gram-positive cocci, including penicillin-resistant strains of S. aureus and S. epidermidis, streptococci and enterococci, most gram-negative rods, including β-lactamase-producing strains, as well as spore-forming and non-spore-forming anaerobes, including B. fragilis.

    The basic principles of antibiotic therapy in abdominal surgery include the following:

    1. This is a mandatory component of complex therapy for abdominal surgical infection.

    2. focus on preventing reinfection that continues after surgery at the source of infection and, thus, on preventing recurrent intra-abdominal infection.

    3. drugs must not only be active against all etiologically significant pathogens, but also have adequate penetrating ability into the site of inflammation or destruction, which is determined by the pharmacokinetic characteristics of the antibiotics.

    4. the need to take into account potential side and toxic effects, to assess the severity of the underlying and concomitant pathology of the surgical patient.

    4. Drugs of choice for the prevention of infectious complications during surgical interventions for acute cholecystitis

    To treat patients with acute cholecystitis, justified active treatment tactics are necessary. This tactic is due to the fact that:

    1) morphological changes occur in the gallbladder during inflammatory processes, which never disappear without a trace and lead to the development of numerous complications;

    2) with infusion-drug therapy, the ongoing improvement in the patient’s condition does not always reflect the “reversibility” of the inflammatory process. In practice, it was observed that during infusion therapy, including antibiotic therapy, and against the background of clinical signs of improvement in the patient’s condition, gangrene of the gallbladder, its perforation or peri-vesical abscess developed.

    Already in the first hours after a patient’s admission to the hospital with a diagnosis of acute cholecystitis, the tactics of antibiotic therapy are decided, after it is fully diagnosed using ultrasound and laparoscopic methods. But the operation is performed at different times from the moment of hospitalization. During the preoperative period of hospital stay, intensive therapy is carried out, the duration of which depends on the category of severity of the patient’s physical condition.

    Table 3. Antibiotics used for acute cholecystitis

    Very good

    Moderately

    Azithromycin

    Aztreons

    Amogxicillin

    Amikacin

    Azlocillin

    Ampicillin

    Carbenicillin

    Vancomycin

    Doxycycline

    Clindamycin

    Colistin

    Gentamicin

    Clarithromycin

    Latamoxef

    Methicillin

    Dicloxacillin

    Mezlocillin

    Pincomycin

    Metronidazole


    Piperacillin

    Ofloxacin

    Cephalothin

    Ketoconazap

    Rifampicin

    Penicillin, Imipenem

    Cefoxitin

    Netilmicin

    Roxithromycin

    Streptomycin

    Ceftazidime

    Oxacillin

    Tetracycline

    Chloramphenicol

    Cefuroxime

    Tobramycin

    Co-trimoxazole

    Cefazolin


    Cephalexin

    Cefotiam

    Cefamandole


    Ceftriaxone

    Cefoperazone



    Erythromycin

    Meropenem



    Antibiotics are not able to limit the destructive process in the gallbladder and therefore, many patients with acute cholecystitis begin using antibiotics during surgery in order to avoid purulent-inflammatory complications. The duration of their administration is the entire period of the operation.

    In a small number of patients at high operational risk, antibiotics are used in the program of conservative treatment of acute cholecystitis to block the dissemination of infection and the development of a systemic inflammatory response.

    Drugs of choice

    Ceftriaxone 1-2 g/day + metronidazole 1.5-2 g/day

    Cefoperazone 2-4 g/day + metronidazole 1.5-2 g/day

    Ampicillin/sulbactam 6 g/day

    Amoxicillin/clavulanate 3.6-4.8 g/day

    Alternate mode

    Gentamicin or tobramycin 3 mg/kg per day + ampicillium 4 g/day + metronidazole 1.5-2 g/day

    Netilmicin 4-6 mg/kg per day + metronidazole 1.5-2 g/day

    Cefepime 4 g/day + metronidazole 1.5-2 g/day

    Fluoroquinolones (ciprofloxacin 400-800 mg intravenously) + Metronidazole 1.5-2 g/day.

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LIST OF ABBREVIATIONS.

INTRODUCTION

CHAPTER 1. PROBLEMS AND PROSPECTS FOR DIAGNOSIS AND SURGICAL TREATMENT OF ACUTE CALCULOUS CHOLECYSTITIS (LITERATURE REVIEW)

CHAPTER 2. CLINICAL MATERIAL. METHODS OF DIAGNOSIS AND TREATMENT.

2.1 Characteristics of clinical material.34;

2.2. Methods of diagnosis and treatment in patients with acute calculous cholecystitis.47"

2.2.1. General laboratory diagnostics.

2.2.2. Microbiological diagnosis of acute calculous cholecystitis.

2.2.3. Methods of instrumental diagnosis and treatment.50"

2.2.4. Methods for studying free radical processes in patients with acute calculous cholecystitis.

2.2.5. Methods of statistical processing of the results of the study.

CHAPTER 3. FREE RADICAL PROCESSES IN THE DEVELOPMENT OF DESTRUCTIVE CHANGES IN THE GALLBLADDER IN PATIENTS WITH ACUTE CALCULOUS

CHOLECYSTITIS.81"

3.1. Data from the analysis of markers of the stages of free radical processes in patients with acute calculous cholecystitis upon admission to the hospital.

3.2. Analysis of the dynamics of free radical processes in patients* with various forms of acute calculous cholecystitis.

3.3. Prognostic value of the components of free radical* processes in patients with acute calculous cholecystitis.

3.4. Pathophysiological rationale for the feasibility of antioxidant therapy in the treatment of patients with acute calculous cholecystitis.

CHAPTER 4. ANALYSIS OF THE RESULTS OF CONSERVATIVE THERAPY AND MINIMALLY INVASIVE INTERVENTIONS IN PATIENTS WITH ACUTE CALCULOUS CHOLECYSTITIS

4.1. General principles of conservative therapy and reasons for refusing surgery in patients with acute calculous cholecystitis.114^

4.2. Catamnesis of patients with acute calculous cholecystitis treated conservatively.

4.3. Features of the clinical picture and treatment tactics during conservative therapy in patients with high anesthetic risk.

4.4. Place of fine-needle punctures and/microcholicystostomies in the treatment of acute calculous cholecystitis.130“

4.5. Clinical and laboratory analysis of the effectiveness of antioxidant therapy in patients with acute calculous cholecystitis treated conservatively and/or undergoing minimally invasive interventions. 132*

CHAPTER 5. TREATMENT OF COMPLICATED FORMS OF ACUTE CALCULOUS CHOLECYSTITIS AND DISEASES COMPLICATING ITS COURSE.

5.1. Treatment of complicated forms of acute calculous cholecystitis.

5.1.1. Treatment of patients with acute calculous cholecystitis complicated by peripysical infiltrate.

5.1.2. Surgical treatment of patients with acute calculous cholecystitis complicated by peritonitis.

5.1.3. Microbial landscape and antibacterial therapy in patients with acute calculous cholecystitis.

5.2. Treatment of patients with diseases complicating the course of acute calculous cholecystitis.

5.2.1. Treatment of patients with acute calculous cholecystitis in combination with cholecystolithiasis.

5.2.2. Treatment of patients with acute calculous cholecystitis in combination with pathology of the double tree.

CHAPTER 6. ANALYSIS OF THE RESULTS OF SURGICAL TREATMENT OF PATIENTS WITH ACUTE CALCULOUS CHOLECYSTITIS.

6.G. Evaluation of the results of surgical interventions performed* in patients with different forms of acute calculous cholecystitis at different periods.

6/2. Analysis of the effectiveness of multi-stage surgical interventions in patients with acute calculous cholecystitis.

6.3. Features of the clinical picture and surgical tactics in patients with acute calculous cholecystitis with a high surgical and anesthetic risk.

6.4. Comparative assessment of the immediate and long-term results of open and videolaparoscopic cholecystectomy in patients with acute calculous cholecystitis.i.;.

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Introduction of the dissertation (part of the abstract) on the topic “Acute calculous cholecystitis (diagnosis and treatment - 25 years of search)”

Relevance of the study

Acute calculous cholecystitis (ACC), occurring in 10-15% of patients hospitalized in hospitals with acute surgical pathology, remains one of the most common diseases in urgent abdominal surgery. A large number of publications by domestic and foreign authors illustrates the continued interest in this problem.

Recent decades have been marked by significant advances in the treatment of ACC, which became possible thanks to the development and implementation of new technologies that allow us to reconsider the existing ones; presentations. about patient management tactics. Over the past years, interventions for: ACC have been carried out in; emergency, urgent and “cold” periods of the disease, and surgical tactics are based on clinical and laboratory symptoms and instrumental diagnostics, which are very important for objectification; availability; the nature and degree of the inflammatory process: gallbladders (GB). At the same time, studies devoted to predicting the course of ACC. based on other objective, including laboratory, criteria; in modern literature are almost never found.

Dissatisfaction with the results of the open; cholecystectomy (LC) forced surgeons* to look for alternative solutions, “and already at the end of the 20th century, laparoscopic cholecystectomy (LCC) and mini-access operations were widely introduced into everyday practice, which made it possible to make a technological leap, reducing the trauma of operations and shortening the postoperative rehabilitation period . As application experience accumulates? new methods of surgical treatment, the indications for various types of surgical interventions were revised. As a result, for example, videoscopic intervention began to be considered by some surgeons as the “gold standard” in the treatment of not only? chronic, but also acute cholecystitis.

However, even today there are a number of unresolved issues, primarily related to a differentiated approach to the management of patients! catarrhal and destructive forms of ACC of different age groups; in the presence of a high degree of surgical and anesthetic risk, the occurrence of various complications and polymorbidity complicating the course of ACC. The indications and place of various options for radical treatment and the timing of its implementation in the named contingent of patients have not been fully determined. They confirm the impossibility of an unambiguous choice of the only one. surgeries, increasing the frequency of conversion (switching from video laparoscopic to open cholecystectomy) in clinics that are carried away. LCE, and a general increase in patients with postcholecystectomy syndrome.

Recommendations for the widespread use of early operations require the development of a mandatory comprehensive examination that would make it possible to predict the course of ACC based on parameters reflecting processes that are integral components of the pathogenesis of this disease, to which modern pathological physiology includes free radical oxidation. The use of such an expanded diagnostic program may be advisable and even necessary for selecting patients for different methods of surgical or conservative treatment. We did not find any works answering these questions in the available medical literature.

Considering the aging of the population and the progressive increase in the number of comorbid patients, questions of choice and treatment tactics arise when they develop ACC. Elderly patients with many concomitant diseases today form an ever-increasing group of patients with high surgical and anesthetic risk. Somatic pathology, complicating the course of cholecystitis in these patients, is one of the causes of death. It was in these patients with ACC that it began to be used; multi-stage treatment, including purely conservative components, minimally invasive and radical surgical interventions. However, this multi-stage approach still requires clarification of the timing, volume and type of surgical interventions. various forms of ACC, complications, including those that occur at different stages of the disease, as well as with concomitant diseases that complicate them; course of ACC and course of the postoperative period.

Due to the accumulation of large clinical material, prerequisites have emerged for the transition of quantitative assessments accepted in practical medicine to a qualitatively different level of our understanding* of clinical problems using the results of fundamental scientific developments in everyday surgical practice, which will allow achieving the goals of this study: improving the results of treatment of complicated and uncomplicated ACC on the basis of improving the diagnostic and treatment algorithm and developing approaches to differentiated management of patients.

Research objectives

Conducting a retrospective and prospective analysis of approaches to the treatment of patients with ACC in a multidisciplinary hospital over 27 years.

Determining the value of various instrumental studies in choosing treatment tactics in patients with ACC.

Conducting a comparative analysis of the levels of various markers of free radical processes (FRP) and their dynamics in patients with ACC with varying severity of the process, at different times and with different outcomes of the disease.

Study of a long-term follow-up of patients with ACC of varying severity and age, causing high degrees of anesthetic risk, who were not radically operated upon first admission to the hospital to clarify the characteristics of the course of their cholelithiasis.

Development of criteria for prognosis of the course of ACC and indications for different types of surgical interventions and/or conservative1 therapy based on quantitative correlation, multifactorial and discriminant analysis of various components of the SRP, features of the clinical picture and standard screening laboratory monitoring.

Development of surgical treatment tactics in patients with different forms of ACC, in the presence of various complications and pathologies that aggravate the course of the disease.

Evaluation of the results of antioxidant pharmacological correction! SRP in patients with ACC.

Determining the effectiveness of non-radical methods of surgical treatment of patients with ACC with high surgical and anesthetic risk.

Evaluation of the effectiveness of various methods of radical surgical treatment of complicated and uncomplicated ACC with clarification of the timing and scope of surgical interventions.

Development of an optimal algorithm for examination and treatment of patients with ACC with determination of indications and differentiated management tactics for patients.

Scientific novelty

Based on the retrospective and prospective analysis, a mathematical model was created that made it possible to develop an optimal algorithm for the examination and treatment* of patients, which determines the indications for the use of various variants of tactics for the differentiated management of patients with ACC.

For the first time, based on large clinical material based on the study of long-term follow-up of patients who underwent ACC, individual approaches to minimally invasive and radical methods of surgical treatment with high operational and anesthetic risks have been developed. ,

For the first time in domestic and world practice, a comparative, quantitative analysis was carried out, which proved the pathogenetic role of SRP. in the formation of destruction of the gallbladder in ACC, which made it possible for the first time to develop criteria for early prognosis of the course of ACC, to objectify the indications for differentiated therapy and demonstrated its effectiveness in cases of decreased parameters in patients with ACC; their own antiperoxide protection: .

Algorithms for differentiated treatment of ACC have been developed, pathogenetically substantiated and tested on large clinical material, including a set of conservative methods; "ig: multi-stage surgical treatment for various forms of the disease; the occurrence of complications; as well as pathology complicating the course of ACC.

Practical significance

The potential dangers of unreasonably widespread use of LCE have been identified.

Are the features developed based on large clinical material? surgical procedures and their sequence, taking into account the timing1 of one or another type of surgical procedure. Developed? algorithms for antioxidant therapy to correct the damaging, local and systemic effects of SRP in patients with ACC of varying severity.

The possibilities and timing of the combined use of various (minimally invasive and radical) surgical methods of treatment - ACC in patients with catarrhal and destructive ACC, in the event of complications, in patients with a high anesthetic risk - have been determined. These rational patient management schemes are easily implemented in everyday clinical practice.

Provisions for defense

1. In patients with ACC, in 73.1% of cases, destructive forms of the disease develop, caused, among other things, by late hospitalization against the background of comorbid conditions, leading to blurred and atypical clinical and laboratory* picture of the disease and increasing the surgical and anesthetic risk, requiring new approaches" to assessing the severity of ACC, its prognosis and treatment.

2. Based on large follow-up material in patients who did not undergo radical surgery during the first hospitalization for ACC, features of the course of cholelithiasis with a high percentage of severe relapses were revealed, which indicates the need for the earliest possible radical treatment, including in patients with a high anesthetic risk , due to polymorbidity and age of patients.

3. In patients with ACC, there is a high correlation between the level of destructive changes in the gallbladder wall and the prognosis of the disease with indicators of PRP*, including* with indicators of the intensity of leukocyte chemiluminescence (basal and stimulated zymosan - PIHLb and PICLs), which allow assessing oxygen stage of oxidative stress, levels of plasma antiperoxide activity (ALA), which characterizes the state of the body’s own antioxidant reserves, and malondialdehyde (MDA), which is a marker of the lipid component of PSA.

4. Assessment of the disorder of energy synthesis leading in patients with ACC to the formation of local and systemic maladaptation-hyperergic reactions that underlie the occurrence of complicated forms of the disease and its severe course, makes it possible to objectify the criteria for early prognosis of the course and outcome of ACC and argue for the need for the use of energy-corrective therapy.

5. Algorithms for examination and treatment have been developed that allow the successful use of optimal individualized options for the management of patients with ACC at the early stages, including the use of alternative and multi-stage methods with a high surgical and anesthetic risk, as well as patients admitted at different times from the onset of the disease and /or the presence of various local and systemic complications and diseases complicating the course of ACC.

The work was performed at the hospital surgery clinic No. 1 of the medical faculty of the State Budgetary Educational Institution of Higher Professional Education, Russian National Research Medical University named after. N.I. Pirogov Ministry of Health and Social Development of Russia on the basis of the City Clinical Hospital No. 15 of Moscow named after O.M. Filatov and the Department of Human Pathology of the Faculty of Professional Education of Doctors of the State Educational Institution of Higher Professional Education of Moscow State Medical University named after. THEM. Sechenov

Implementation into practice

The options for examination and treatment of patients with ACC proposed in the dissertation work have been introduced into the practice of surgical departments* of the City Clinical Hospital No. 15 named after O.M. Filatov, Moscow, in the surgical departments of the Republican Clinical Hospitals of the Kabardino-Balkarian Republic and the Republic of Dagestan.

Certain provisions of the dissertation are included in lectures and work programs for teaching students, as well as* methodological recommendations of the Department of Hospital Surgery No. 1, Faculty of Medicine, State Budgetary Educational Institution of Higher Professional Education, Russian National Research Medical University named after. N.I. Pirogov Ministry of Health and Social Development of Russia, Department of Human Pathology, Faculty of Professional Education of Doctors, State Educational Institution of Higher Professional Education, Moscow Medical University named after I.M. Sechenov.

Approbation of work

The main provisions of the work and the results of the research were presented at the joint scientific and practical conference of the departments of hospital* surgery No. 1 of the medical faculty of the State Budgetary Educational Institution of Higher Professional Education RNRMU named after N.I. Pirogov and, Department of Human Pathology of the First Moscow State Medical University named after. THEM. Sechenov, as well as at the IV All-Russian Congress on Endoscopic Surgery (Moscow, February 21-23, 2001), the 6th Moscow International Congress on Endoscopic Surgery (Moscow, April 24-26, 2002), the International Surgical Congress (Moscow, February 22-25 2003), II Congress of Gerontologists and Geriatricians of Russia (Moscow, October 1-3, 2003), IX International Conference of Surgeons-Hepatologists of Russia and CIS Countries (Omsk, September 15-17, 2004), Scientific and Practical Conference

Republican Clinical Hospital of the KBR (2004), X Anniversary Moscow International Congress on Endoscopic Surgery (Moscow, April 19-21, 2006), XIII International Congress of Hepatological Surgeons of Russia and the CIS Countries (Almaty, September 27-29, 2006), Congress “Man and medicine" (Moscow, 2009, 2010), XI Congress of Surgeons of the Russian Federation (Volgograd, May 25-27, 2011).

Publications

Scope and structure of the dissertation

The dissertation is presented on 292 pages of typewritten text, consists of an introduction, 6 chapters, a conclusion, conclusions, practical recommendations and a list of references. The work is illustrated with tables, photographs, drawings, diagrams and brief extracts from case histories. The bibliographic index includes 493 sources, of which 258 are domestic and 235 are foreign.

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Conclusion of the dissertation on the topic “Surgery”, Khokonov, Mukhamed Amirkhanovich

1. Patients with acute cholecystitis make up 11% of the total? hospitalized in surgical hospitals, 94.1% of them are patients with ACC, while 26.9% have the catarrhal form of the disease, and 73.1% have destructive forms of the disease, including 2.1% gangrenous. Among patients with ACC, women (67.4%) and people under 65 years of age (58%) predominate. 24.1% of patients go to the hospital later than 3 days from the onset of the disease.

2. The reasons for late presentation, which accompanies a large number of destructive forms of ACC, is the blurred clinical and laboratory picture of the disease against the background of comorbid conditions, which are significantly more common in older age groups. In patients with ACC, comorbidity in 52% of cases is due to the presence of ischemic heart disease, in 43% - hypertension, in 23.5% - diseases of the central nervous system, in 15% - kidney pathology, in 10% - diabetes mellitus, in 6% - diseases of the lungs , in 5.6% - metabolic syndrome, and in 42% - a combination of several diseases. The frequency of surgical and anesthetic risk of stage IV AAA, due to high comorbidity, occurs in 2.43% of patients.

3. In patients with ACC, it is mandatory to conduct a comprehensive instrumental examination, including ultrasound, duodenoscopy, X-ray methods for assessing the condition of the biliary tree, which makes it possible to detect inflammatory changes in the gallbladder with an accuracy of up to 97% in the catarrhal form and 92% in the destructive form, in 88 % reveal peripysical infiltrate. Peripysical infiltrate complicates ACC in 13.3% of patients, cholangitis - in 5.1%, acute pancreatitis - in 13.6%, peritonitis - in 1.8%. Pathological processes complicating the course of the underlying disease occur. with ACC: choledocholithiasis in 16.7% of cases, parafateral diverticulum in

13.9%, BDS stenosis - in 2.7%. Taking these complications and pathological processes into account makes it possible to justify the choice of individualized tactics for the management of patients with ACC.

4. In patients with ACC, especially in older age groups and/or with existing comorbidity, standard screening laboratory methods do not timely reflect the severity of the patient’s condition. At the same time, the analysis of SRP in patients with ACC revealed a high correlation of multidirectional changes in the levels of markers of various stages of oxidative stress, such as a change in the ratio of markers of the stage of oxygen initiation PIHLb/PIHLs -CA to the level of 64.19, a decrease in one’s own antiperoxide reserves (APA of secondary plasma< 21,05) и рост маркера этапа липидной-пероксидации (МДА >9.55 µmol/l) with the level of destructive changes in the gallbladder wall and the nature of maladaptive systemic reactions, which allows with an 82% probability (/7=0.013) to diagnose the form of the disease and predict its course already on the first day.

5. Studying the dynamics of the course of PSA in patients with ACC made it possible to optimize the tactics of antioxidant therapy, the implementation of which improves the prognosis, reducing from 12.1 to 8.3% the frequency of transition from catarrhal forms to destructive ones, reducing the need for MCS and the frequency of urgent operations from 26.4 up to 14.9%.

6. The reason for medical refusal of radical treatment of patients with ACC in 14.2% of cases is somatic pathology; in 19.5% - diseases of the organs of the hepatopancreatobiliary zone, in 25.1% - a combination of causes. In case of high surgical and anesthetic risk in patients with destructive forms of ACC, the method of choice is minimally invasive drainage manipulations of the gallbladder followed by transfistula sanitation. Such tactics can reduce mortality from 17.1% after ACE and 11.1% after videolaparoscopic CE to 1.4%, primarily due to the reduction in the number and severity of systemic complications.

7. Refusal to carry out radical treatment of ACC after successful relief of acute symptoms of the disease is not justified and leads to a high percentage of relapse (during the first year in 51.8% of cases, during the first 3 years in 83.1%), mainly in patients over 65 years of age with primarily diagnosed destructive forms of cholecystitis. Recurrence of ACC in 4.7% is complicated by peritonitis, and in persons with a high surgical and anesthetic risk, peritonitis develops in 13.8% of cases. In this group of patients, relapse of the disease occurs in 69.9% of cases during the first year after discharge from the hospital. Drainage left at discharge upon discharge reduces the number of relapses, leading to re-application in 28.3% of cases, and independently falling out of the gallbladder during the first 6* months in 26.1% of patients, increases the likelihood of relapse during the first year.

8. Peritonitis complicates the course of ACC in 1.8% of cases, occurring more often in females (89.3%), elderly and senile people and is local in 75.7% of cases, diffuse in 24.3% and 10.3% - spilled. In case of local and diffuse peritonitis, complicating the course of ACC, the videolaparoscopic technique should be considered justified both for the sanitation of the primary focus and the abdominal cavity, which leads to a reduction in complications from the abdominal wall from 1.8 to 0.1%, intra-abdominal ones - from 7. 5 to 4.1% and systemic - from 2.9 to 0.9% compared to open surgery due to less trauma and early activation of patients. For diffuse peritonitis, there is no alternative to laparotomy.

9. In case of verified catarrhal ACC, videolaparoscopic intervention can be performed at any time, regardless of the duration of the disease. Carrying out LCE in early stages leads to a decrease in the number of complications, compared with open surgery, on the part of the abdominal wall (from 7. 3 to 1%), intra-abdominal - from 11.3 to 4.5% and systemic - from 6.4% to 1.2%, as well as to a reduction in hospital stay Before any type of cholecystectomy, it is necessary to ensure the absence of hyperbilirubinemia, pathology of the duodenum (according to duodenoscopy) and signs of biliary stasis (according to ultrasound). Underestimation of these circumstances may increase the number of patients with postcholecystectomy syndrome to 12.1%.

Yu. The presence of PJI is the main criterion for choosing the timing of surgical treatment and the type of cholecystectomy. In case of destructive ACC, complicated by a formed peripysical infiltrate or empyema, in order to effectively relieve inflammation before cholecystectomy, the use of MCS is most justified. Until the characteristics of the flora and antibiogram are obtained, the best results are achieved by the use of III-1U generation cephalosporins and fluoroquinolones. The introduction of antibiotics into the cavity of the gallbladder does not improve results of treatment, and therefore parenteral administration of antibiotics is preferable. When cultivating 3 (15.2%) and 4 (6.1%) microorganisms from the gastrointestinal tract, a particular severity of the disease was noted (destructive); ) changes in the wall of the gallbladder and local complications of ACC in the form of peripysical abscesses.

P. In case of ACC, in 78.4% of cases, it is necessary to use multi-stage surgical treatment, including using methods of decompression of the gallbladder, when destructive forms of ACC, peripysical infiltrate and / pathology of hepaticocholedochus are identified. In patients over 65 years of age, TSH of the gallbladder is less effective for stopping the inflammatory process in the peripysical tissue than MCS, since it more often ends up open; surgery - in 7.5 and 3.5% of patients, respectively.

12.0optimal deadlines; ChE in these cases is a period not earlier than the 3-4th week based on. laboratory and instrumental data. confirming resorption: peripysical infiltrate. LCE for destructive cholecystitis after. MHS in? early terms (within the first 2 weeks)? after drainage of the gallbladder leads to an increase in the number of conversions: .

13. In the case of uncomplicated ACC, the use of urgent treatment is justified; HE. In this case, preference should be given to the videolaparoscopic technique. The optimal timing for LCE in the early stages (in the first 2 days from hospitalization), in case of destructive forms of ACC and the absence of pathology from the biliary tract, acute pancreatitis, peritonitis, requiring special treatment, is? 3rd day from the moment of illness;, which is confirmed by the least; conversion percentage (1.4%). After decompression of the gallbladder; carried out in the catarrhal form of ACC, LCE can be performed; at any time, regardless of the duration of the disease; the age of the patient and the timing of the start of surgical treatment.

14. Video laparoscopic cholecystectomy has advantages over acute cholecystectomy in patients with catarrhal and mild forms of phlegmonous ACC due to a reduction in the number of complications due to the early activation of patients. The use of LCE in patients with preserved infiltrate increases the number of intra- and postoperative complications, therefore it should be used with great caution and, in case of the slightest concern, end with conversion. The conversion rate for LCE in the delayed period after decompression of the gallbladder is 5.2%, and the rate is significantly higher for destructive ACC (6.3%) compared to catarrhal (1.7%).

1. In order to select differentiated tactics for the management of patients with ACC, it is necessary to conduct an examination, including an assessment of surgical and anesthesiological risk, a set of laboratory tests confirming the presence of biliary stasis and the degree of destruction of the gallbladder wall according to PSA markers, as well as ultrasound to verify the form of the disease and the condition of the perivysical tissue . If pathology of the extrahepatic bile ducts is suspected, the complex of examinations must be supplemented with retrograde cholangiopancreatography. Performing LCE without first conducting the specified diagnostic program increases the risk of developing PCES.

2. When identifying ACC, it is necessary to make a decision on its mandatory radical treatment, one- or multi-stage and the type of which depends on the form and timing of the disease, the presence and severity of complications, as well as the patient’s condition. The feasibility of radicalism in the treatment of ACC is due to the high percentage and unfavorable course of recurrence, especially in patients with a high surgical and anesthetic risk.

3. In 94.3% of patients with destructive forms of the disease, there is a decrease in the level of intrinsic APA below 35.6 with an increase in MDA above 2.8 μmol/l, which is an indication for the mandatory inclusion of AO (Reamberin at a dose of 400-800 ml/day) in the complex therapy of patients with ACC.

4. In case of local and diffuse peritonitis, complicating the course of destructive forms of ACC, it is possible to use video laparoscopic cholecystectomy, which allows for adequate sanitation of the abdominal cavity.

5. In patients with ACC, in the absence of pathology of the biliary tree requiring special correction, acute pancreatitis and peritonitis, it is advisable to perform LCE for destructive forms in the first 72 hours from the moment of the disease, and for catarrhal ones - at any time from the moment the symptoms of the disease appear.

6. For ACC complicated by peripysical infiltrate, it is advisable to use staged treatment, starting with MCS and parenteral administration of III-IV generation cephaloporins and fluoroquinolones.

7. In case of destructive cholecystitis, especially in elderly people with low surgical and anesthetic risk, it is advisable to use MCS followed by cholecystectomy (preferably LCE) no earlier than the 3rd week from the start of treatment.

8. In an effort to increase the number of radically treated patients with ACC and choosing the option of surgical treatment for stage IV surgical and anesthetic risk. according to ASA, after successful relief of acute phenomena, preference should be given to the non-surgical technique of transfistula sanitation of the gallbladder with obliteration of the organ mucosa.

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