Acute cholecystitis complicated by obstructive jaundice. Calculous cholecystitis: symptoms and treatment Causes of changes in the size of the gallbladder

The gallbladder (GB) is an important organ in our digestive system. In infancy, it is located in the thickness of the liver. As the body develops, it forms and slightly descends, so that it begins to peek out from under the edge of the liver. In the normal state, the organ resembles a pear shape and measures 3-5 cm in diameter, depending on the weight and age of the person. An increase in the gallbladder in an adult or a child occurs for various reasons, but most often it is caused by the development of various diseases.

The main signs of organ enlargement

The size of the gallbladder during the day can vary quite a lot. The human liver constantly produces bile, which enters the gallbladder - a kind of temporary storage. When food enters the body, it contracts and secretes bile through the ducts into the duodenum, where it is actively involved in digestion. At the same time, the bubble significantly decreases, but after a short period of time, bile fills it again, increasing in size. And so several times a day. Only an excessive increase in the organ and the unpleasant symptoms that accompany it should disturb.

With an increase in the gallbladder, a person most often feels pain of varying intensity in the epigastric region (right hypochondrium). The nature of these pains can be different: from a barely noticeable tingling to severe attacks of stabbing or cutting pain, lasting several tens of minutes. In adults, the symptoms are usually more pronounced than in children. Symptoms may occur for no apparent reason, but the appearance of pain is preceded by eating fatty or spicy foods, drinking alcohol, skipping meals.

Reasons for changing the size of the gallbladder

A pathological change in the organ itself can occur against the background of other diseases of the gastrointestinal tract: gastritis, cholelithiasis, pancreatitis, cholecystitis, biliary dyskinesia. Often, violations are noted in a child in the period of growing up.

These diseases are caused by various factors:

  • irregular and malnutrition;
  • excessive consumption of food from semi-finished products;
  • bruises received in the abdomen or back;
  • high physical and mental stress;
  • penetration into the gastrointestinal tract of various infectious agents;
  • twisting of the bile ducts;
  • the use of certain drugs in the treatment of other pathologies;
  • congenital anomalies of the gallbladder;
  • the use of large doses of vitamins and calcium;
  • inflammation of the intestinal wall or the gallbladder itself.

If the above factors are completely excluded, it is necessary to be examined for the presence of other causes that influenced the pathological change in the size of the gallbladder. An increase in an organ may indicate various problems in the body in general and in the gastrointestinal tract in particular.

Diagnosis and treatment

Sometimes an enlarged gallbladder can be determined by palpation (palpation) of the right hypochondrium, but this method does not make it possible to accurately determine the size of the organ, especially in a child. The most informative will be instrumental types of research and testing.

To make an accurate diagnosis, ultrasound is performed and x-rays of the entire gastrointestinal tract are taken. They allow you to determine the exact dimensions of the gallbladder, the presence or absence of inflammation, stones, mechanical damage, etc.

By examining the symptoms and prescribing a series of blood and stool tests, the doctor will be able to get a more detailed picture of the condition of the enlarged organ. This will make it possible to more accurately diagnose one of the many causes that influenced the growth of the gallbladder.

Obstruction of the bile duct

This pathology often develops against the background of cholelithiasis, usually in adulthood or old age. The child is rarely diagnosed. At the same time, the organ itself stretches and swells from the contents that fill it, and its walls thicken quite a lot (sometimes by more than 5 mm), which indicates suppuration. On palpation, the patient feels moderate or severe pain.

An inflamed head of the pancreas can also lead to obstruction of the duct, when its tumor mechanically compresses the duct. In this case, an ultrasound of the pancreas and related blood tests are prescribed.

If the gallbladder is greatly stretched, but the thickness of its walls does not exceed normal values, a mucous cyst (mucocele) may occur. The phenomenon is relatively rare. Painful sensations on palpation are absent or mild. Treatment is operative.

Inflammation of the gallbladder (cholecystitis)

There are two types of cholecystitis: calculous and non-calculous. With calculous cholecystitis during the period of exacerbation, the patient is tormented by paroxysmal hepatic colic, nausea. Visually, yellowing of the skin is noted.

When examined on an ultrasound machine, an enlarged organ is clearly visible, as well as gallstones (stones), which caused its inflammation. In the presence of numerous large stones, an operation is prescribed for partial or complete resection (removal) of the gallbladder. After the operation, the patient must adhere to a strict diet for life. Non-surgical removal of calculi is possible only at the initial stage, provided that they are small in size. Treatment is carried out with drugs based on bile acids.

Non-calculous (stoneless) inflammation of the gallbladder is distinguished by the smoothness of all of the above manifestations inherent in calculous cholecystitis. Sometimes there may be no symptoms at all. The patient is concerned about weak pain in the epigastric region, which manifests itself after eating and disappears 1–2 hours after eating, aching pains in the right hypochondrium, the intensity of which increases after eating.

Dyskinesia of the gallbladder and bile ducts

By dyskinesia is meant a specific pathology of the bladder itself or its ducts, which is associated with impaired motility of the organ and biliary tract. In the normal state, the gallbladder contracts periodically, ejecting the accumulated bile through the ducts into the intestines. At the same time, the ducts themselves also contract, moving the contents of the gallbladder further into the duodenum.

With dyskinesia, the contractility of the bladder and its ducts either deteriorates or is completely absent. The accumulated bile in adults and children ceases to be normally excreted into the intestine, its flow into the gallbladder does not stop, because of which it begins to pathologically increase in size and become inflamed. A person feels heaviness in the epigastrium, dull, aching pain, he is tormented by insomnia, fatigue, and malaise. In some cases, on the contrary, an increased tone of the organ is noted, leading to a rapid emptying of the bladder even with an empty stomach. This negatively affects the state of both the gallbladder and the entire gastrointestinal tract.

The main causes of dyskinesia are stress, significant psychological and emotional stress, and allergies to certain foods.

Ultrasound is usually sufficient for diagnosis.

Treatment depends on the type of dyskinesia. With hypotension of the organ, that is, with a weak secretion of bile, frequent meals in small portions are prescribed. The diet should be rich in fiber, contain vegetable oils. A good effect is the use of mineral slightly carbonated water during the day.

With hypertonicity of the gallbladder, the patient should receive choleretic drugs of synthetic or herbal origin. Herbal decoctions from dandelion, chamomile, immortelle are considered safer and more effective. In the presence of psycho-emotional stress, sedatives of weak or moderate action are prescribed.

Cholelithiasis

Gallstone disease is one of the most common and most dangerous causes of disorders in the work of the gallbladder in adulthood or old age. The child has a minimal risk of developing.

Usually, symptoms appear gradually along with an increase in the number and size of stones in the bladder cavity. Calculi are pieces of hardened bile that form in adults due to the accumulation of large amounts of cholesterol in the bile, which is combined with calcium salts by bilirubin.

If you suspect the presence of stones in the gallbladder, you should immediately consult a doctor for appropriate examinations.

At first, the diameter of the stones is quite small (they are literally grains of sand), but gradually, while maintaining negative conditions, they begin to grow until they fill the bubble or clog one of its ducts. In this case, an emergency operation is required.

There can be several reasons for gallstone disease.

  • hereditary factor (the presence in the family of patients with this disease significantly increases the risk of cholelithiasis in descendants);
  • high blood sugar;
  • overweight;
  • unhealthy diet;
  • associated liver disease;
  • obstruction of the bile ducts;
  • hormonal imbalance (in pregnant women).

Gallstone disease manifests itself in different ways, which directly depends on the size of the formations, their total volume and the age of the patient. A typical symptom of cholelithiasis is a sharp stabbing pain in the liver (pain is caused by the passage of a calculus from the gallbladder into the bile ducts with further exit into the intestine). The pain in the right side is sharp and sharp, radiating to the right shoulder or shoulder blade.

The patient may have a fever, yellowing of the skin, the urine becomes dark, and the feces, on the contrary, become discolored. For the patient, these are very disturbing symptoms.

When the calculus enters the intestine, the symptoms are sharply weakened or disappear completely. If the stone gets stuck in the duct, completely blocking the exit of bile, the symptoms begin to increase. In this case, immediate surgical intervention is required. The bill can go to the clock!

The main methods of examination for suspected presence of gallstones are ultrasound and x-rays, which determine not only the size of the stones, but also their composition, size and quantity.

Treatment most often consists in the radical removal of all formations with the help of a surgical operation. Now, low-traumatic laparoscopic surgery has become widespread, in which stones or the entire bladder are completely removed through a puncture in the skin of the abdomen. Ultrasonic crushing of stones is also possible, but the procedure does not become mass, because it has its own contraindications.

Non-surgical removal of gallstones is allowed in rare cases when gallstone disease is diagnosed at an early stage, and the size of the stones does not exceed the size of the bile ducts. In this case, drugs that dissolve formations (for example, Ursofalk) may be prescribed, after which they enter the intestines in the form of sand and are excreted from the body naturally. Such treatment is long-term - medication should be taken for at least 6 months, and a strict diet and a sparing regimen are prescribed for the entire duration of therapy (the patient is prohibited from heavy physical and mental stress that can provoke a sharp release of stones with severe pain).

Postoperative reasons

An operation previously performed on it, the so-called postoperative syndrome, can also cause an increase in the gallbladder. It is understood as a complex of pathological changes to which the operation led. The performed laparoscopy or abdominal surgery can provoke inflammation of the stomach or pancreas, which negatively affects the condition of the gallbladder. After surgical procedures, there is a risk of impaired motility of the bile ducts and the bladder itself.

Treatment, as a rule, is conservative, consisting in taking choleretic drugs. In some cases, a second operation may be required (if not all calculi have been removed).

Tumors

Various kinds of tumors during ultrasound or X-ray are diagnosed most often in elderly patients. They are rare in a child or young person. Usually, a benign or malignant tumor contributes to the further development of gallstone disease or hepatitis.

Risk factors also include malnutrition, concomitant diseases of the gastrointestinal tract, decreased immunity, overweight, hormonal disorders. Symptoms, depending on the size of the tumor, are similar to those of calculous cholecystitis or gallstone disease. Treatment is only surgical.

Likely consequences and prognosis

Enlarged gallbladder is not an independent disease. It is most often caused by other disorders of the gastrointestinal tract. When they are eliminated, the size of the gallbladder returns to normal on its own. In some cases, symptomatic therapy is required.

The danger is only an increase in the gallbladder due to obstruction of the ducts or cholelithiasis. In this case, if left untreated, the most adverse consequences are possible, up to coma. With timely diagnosis and proper treatment, the risks are reduced to zero and the prognosis is favorable.

  • home
  • Liver disease
  • Jaundice

Jaundice. Symptoms, causes and treatment. Jaundice in children (newborns) and adults.

Jaundice (gospel disease) (lat. icterus) - icteric staining of the skin and visible mucous membranes, due to an increased content of bilirubin in the blood and tissues.

Jaundice (true) is a symptom complex characterized by icteric staining of the skin and mucous membranes, due to the accumulation of bilirubin in the tissues and blood. True jaundice can develop as a result of three main reasons:

  1. excessive destruction of red blood cells and increased production of bilirubin - hemolytic or suprahepatic jaundice;
  2. disturbances in the capture of bilirubin by liver cells and its binding to glucuronic acid - parenchymal or hepatocellular jaundice;
  3. the presence of an obstacle to the release of bilirubin with bile into the intestine and the reabsorption of conjugated bilirubin into the blood - mechanical or subhepatic jaundice.

False jaundice (pseudo-jaundice, carotene jaundice) - icteric coloration of the skin (but not the mucous membranes!) Due to the accumulation of carotenes in it during prolonged and abundant consumption of carrots, beets, oranges, pumpkins, as well as arising from the ingestion of quinacrine, picric acid and some other drugs.

Jaundice classification

Depending on the type of bilirubin metabolism disorders and the causes of hyperbilirubinemia, three types of jaundice can be distinguished: hemolytic (suprahepatic) jaundice, parenchymal (hepatic) jaundice, and mechanical (subhepatic) jaundice.

  • Prehepatic jaundice - occurs in connection with the intensification of the process of formation of bilirubin. At the same time, its indirect (non-conjugated) fraction increases.
  • Hepatic jaundice. The development of hepatic jaundice is associated with a violation of the consumption (capture) of bilirubin by hepatocytes. This increases the indirect (non-conjugated) fraction of bilirubin.
  • Subhepatic jaundice - occurs when there is a violation of the outflow of bile through the extrahepatic bile ducts (obstructive jaundice).

Jaundice Clinic

Jaundice is a symptom complex, which is a yellow coloration of the skin, sclera, mucous membranes. The intensity of staining can be completely different - from pale yellow to saffron-orange. Moderately severe jaundice without changing the color of urine is characteristic of unconjugated hyperbilirubinemia (with hemolysis or Gilbert's syndrome). More pronounced jaundice or jaundice with discoloration of the urine is indicative of hepatobiliary disease. Urine in patients with jaundice becomes dark in color due to hyperbilirubinemia. Sometimes a change in the color of urine precedes the onset of jaundice. All other clinical manifestations of jaundice depend on the causes that caused its development. In some cases, discoloration of the skin and sclera is the only complaint of the patient (for example, with Gilbert's syndrome), and in other cases, jaundice is only one of many clinical manifestations of the disease. Therefore, it is necessary to establish the cause of jaundice. True jaundice should be distinguished from hypercarotenemia in patients consuming large amounts of carrots. With the appearance of jaundice, one should first of all think about the presence of a hepatobiliary pathology in the patient, which occurs as a result of cholestasis or hepatocellular dysfunction. Cholestasis can be intra- and extrahepatic. Hemolysis, Gilbert's syndrome, viral, toxic liver damage, liver pathology in systemic diseases are intrahepatic causes of cholestasis. Gallstones are extrahepatic causes of cholestasis. Some clinical manifestations associated with jaundice (clinical symptoms are discussed in more detail in the sections on various diseases):

  • With cholestasis, jaundice is detected, urine of a dark color appears, and generalized skin itching occurs.
  • Chronic cholestasis can cause bleeding (due to malabsorption of vitamin K) or bone pain (osteoporosis due to malabsorption of vitamin D and calcium).
  • Chills, hepatic colic, or pain in the pancreas are pathognomonic for extrahepatic cholestasis.
  • In patients with cholestasis, xanthomas (subcutaneous deposits of cholesterol) and xanthelasmas (small, pale yellow formations in the upper eyelid due to the deposition of lipids) may be detected.
  • Symptoms of chronic liver damage (spider veins, splenomegaly, ascites) indicate intrahepatic cholestasis.
  • Symptoms of portal hypertension or portosystemic encephalopathy are pathognomonic of chronic liver disease.
  • In patients with hepatomegaly or ascites, swelling of the jugular veins is indicative of heart failure or constrictive pericarditis.
  • With liver metastases, a patient with jaundice may have cachexia.
  • A progressive increase in anorexia and an increase in body temperature are characteristic of alcoholic liver damage, chronic hepatitis, and malignant neoplasms.
  • Nausea and vomiting preceding the development of jaundice indicate acute hepatitis or obstruction of the common bile duct by a stone.
  • Clinical manifestations of hereditary syndromes, accompanied by the appearance of jaundice.

Jaundice parenchymal

Parenchymal jaundice (hepatic) - true jaundice that occurs with various lesions of the liver parenchyma. It is observed in severe forms of viral hepatitis, icterohemorrhagic leptospirosis, poisoning with hepatotoxic poisons, sepsis, chronic aggressive hepatitis, etc. Due to damage to hepatocytes, their function to capture free (indirect) bilirubin from the blood decreases, binding it to glucuronic acid with the formation of non-toxic water-soluble bilirubin -glucuronide (direct) and the release of the latter into the bile capillaries. As a result, the content of bilirubin in the blood serum increases (up to 50-200 µmol/l, rarely more). However, not only the content of free, but also bound bilirubin (bilirubin-glucuronide) increases in the blood - due to its reverse diffusion from the bile capillaries into the blood vessels during dystrophy and necrobiosis of the liver cells. There is icteric coloration of the skin, mucous membranes. Parenchymal jaundice is characterized by skin color - saffron-yellow, reddish ("red jaundice"). Initially, icteric coloration appears on the sclera and soft palate, then the skin stains. Parenchymal jaundice is accompanied by skin itching, but less pronounced than mechanical, since the affected liver produces less bile acids (the accumulation of which in the blood and tissues causes this symptom). With a prolonged course of parenchymal jaundice, the skin may acquire, as in mechanical, a greenish tint (due to the transformation of bilirubin deposited in the skin into biliverdin, which has a green color). The content of aldolase, aminotransferases, especially alanine aminotransferase, usually increases, other liver tests are changed. Urine acquires a dark color (beer color) due to the appearance of bound bilirubin and urobilin in it. Feces become discolored due to a decrease in the content of stercobilin in it. The ratio of the amount of stercobilin excreted with feces and urobilin bodies with urine (which is an important laboratory sign of jaundice differentiation), which is normally 10:1-20:1, decreases significantly with hepatocellular jaundice, reaching up to 1:1 with severe lesions.

… despite a noticeable improvement in treatment outcomes, mortality after emergency operations for acute cholecystitis remains several times higher than with elective surgical interventions.

Obstructive jaundice in patients with acute cholecystitis complicated by obstructive jaundice is caused by obstruction of the main bile ducts with stones, less often by stenosis of the Vater papilla, cholangitis, or compression of the terminal part of the common bile duct by the head of the pancreas.

Clinic and diagnostics. Complication of acute cholecystitis with mechanical jaundice leads to the development of a pronounced syndrome of endogenous intoxication. The clinical picture is extremely diverse. This is due to the intensity and duration of jaundice, as well as the combination of cholestasis with destructive cholecystitis or purulent cholangitis. With all the variety of clinical symptoms of acute cholecystitis with obstructive jaundice, a number of features characteristic of most patients can be traced.

Jaundice is the most striking symptom of the disease. It appears most often 12-14 hours after the pain attack subsides. In most cases, yellowness of the skin and sclera takes on a persistent and progressive character. With severe and prolonged jaundice, patients develop itching, scratching on the skin, weakness, decreased appetite, darkening of urine and discoloration of feces. Blood bilirubin increases due to the direct fraction.

In diagnostics, preference is given to ultrasound as a non-invasive and screening method.

Treatment in all patients with various forms of acute cholecystitis, it is aimed at eliminating the pain syndrome, using detoxification and anti-inflammatory therapy. An emergency operation (within 2-3 hours from the moment of admission) is performed in patients with signs of peritonitis. An urgent operation (24-48 hours) is performed in patients who have a clinical picture of obstructive cholecystitis, symptoms of the inflammatory process and endotoxicosis are growing. For a delayed operation - in the "interval" - they are preparing more painfully, in which, thanks to conservative therapy, an attack of acute cholecystitis is relieved (within 24-48 hours) and the outflow of bile into the duodenum is restored.

General principles of preparation for surgery: normalization of homeostasis, creation of functional reserves of vital organs, treatment of existing concomitant diseases, adaptation of the patient's psyche.

In cases where the attack of acute cholecystitis subsides, but the phenomena of obstructive jaundice persist, intensive preoperative preparation and topical diagnostics are carried out in the near future, not exceeding 5 days from the date of admission.

Surgical treatment. Adequate radical surgical intervention is cholecystectomy with revision of the extrahepatic bile ducts. Each operation for cholecystitis should be accompanied by a revision of the main extrahepatic ducts. Further tactics depend not only on the nature of the pathological process in the biliary tract, but also on the reserve capabilities of the patient. Sometimes, in a serious condition of the patient (senile age, concomitant diseases), cholecystolithostomy is performed. The most difficult and crucial moment is the operation on the choledochus. Indications for choledochotomy can be absolute and relative.

Absolute indications for choledochotomy: obstructive jaundice at the time of surgery; stones palpated in hepaticocholedochus; the presence of filling defects along the ducts on surgical radiographs; wedged stone of the large duodenal papilla; lack of evacuation of the contrast agent into the duodenum on the operating radiographs.

Relative indications for choledochotomy: history of jaundice or before surgery; shrunken gallbladder, wide cystic duct (more than 3 mm), small stones in the gallbladder; wide extrahepatic bile ducts (more than 10 mm); narrowing of the terminal section of the common bile duct with impaired evacuation of the contrast agent on radiographs.

The most common methods of external drainage of the bile ducts are: (1) according to Pikovsky: thin drainage is carried out into the cystic duct; (2) according to Vishnevsky: drainage, approximately equal in diameter to the choledochus and having an oval opening, retreating from the distal end by 2–4 cm, is carried out towards the porta of the liver; (3) according to Ker (at present, this drainage is recognized as the most successful): the drainage is a T-shaped tube, thanks to which bile flows naturally into the lumen of the duodenum 12, or when the pressure in the choledochus increases, it additionally flows out.

External choledochostomy is manageable at all stages of the postoperative period, does not introduce new anatomical relationships into the bile ducts. Along with external drainage in biliary tract surgery, internal drainage, most often for this purpose, choledochoduodenostomy is used. The main indications for it are extended tubular strictures of the terminal section of the common bile duct, as well as its expansion over 2 cm in diameter.

At strangulated stone duodenal papilla, cicatricial stenosis of the major duodenal papilla, if necessary, revision of the pancreatic duct, patients undergo transduodenal papillosphincterotomy with plasty. Along with transduodenal papillosphincterotomy, endoscopic papillosphincterotomy is also widely used.

Send your good work in the knowledge base is simple. Use the form below

Students, graduate students, young scientists who use the knowledge base in their studies and work will be very grateful to you.

Hosted at http://www.allbest.ru

Federal Agency for Health and Social Development

State educational institution of higher professional education

Saratov State Medical University named after V.I. Razumovsky

(GoU VPO Saratov State Medical University named after V.I. Razumovsky Roszdrav)

Department of Faculty Surgery of the Faculty of Medicine

Academic medical history

Patient: ____, 73 years old

The main diagnosis: Acute calculous cholecystitis. Mechanical jaundice

Complications: no

Concomitant diseases: ischemic heart disease, angina pectoris 2 f. Cl. Atherosclerosis of the aorta, coronary, cerebral vessels. Arterial hypertension grade 3, risk 4. Acquired rheumatic heart disease. mitral stenosis. Mitral insufficiency of severe degree. aortic insufficiency. Decompensation of blood circulation in the pulmonary circulation. Pulmonary hypertension. Persistent form of atrial fibrillation

Saratov 2011

General information about the patient

FULL NAME. patient: ______

Date of birth (age): 03/06/1938, 73 years old

Female gender

Education: secondary

Profession: salesperson

Place of residence: Saratov. _______

Received: 22.09.2011

Supervision date: 06.10.2011- 08.10.2011

Clinical diagnosis: Acute calculous cholecystitis. mechanical jaundice.

Complications: no

Concomitant diseases: ischemic heart disease, angina pectoris 2 f. Cl. Atherosclerosis of the aorta, coronary, cerebral vessels. Arterial hypertension grade 3, risk 4. Acquired rheumatic heart disease. mitral stenosis. Mitral insufficiency of severe degree. aortic insufficiency. Decompensation of blood circulation in the pulmonary circulation. Pulmonary hypertension. Persistent form of atrial fibrillation. Superficial gastritis. Duodenogastric reflux.

Complaints on the day of curation: the patient complains of a feeling of heaviness in the right hypochondrium, spreading to the epigastric region, nausea, dry mouth, weakness, fatigue.

The patient considers herself ill since December 2010, when for the first time she began to be disturbed by intense arching pains in the upper abdomen that occur after eating fatty foods and are accompanied by nausea, general malaise, elevated temperature to subfebrile numbers. She was in the hospital from 12/22/2010 to 12/29/2010, where, after ultrasound, calculi were found in the gallbladder. The operation was denied for health reasons (persistent form of atrial fibrillation, acquired rheumatic heart disease, mitral stenosis, severe mitral insufficiency, aortic insufficiency, circulatory decompensation in the pulmonary circulation, pulmonary hypertension). After the therapy, she was discharged with recommendations to follow a diet with the restriction of abundant consumption of fatty foods.

The last deterioration of the patient's condition was on September 16, 2011, when, after an error in the diet, intense pain appeared in the right hypochondrium, nausea, and vomiting. Similar episodes have been reported before. On an outpatient basis, ultrasound revealed gallbladder calculi. Independently the patient was treated with antispasmodics without a positive effect. 09/22/2011. noted yellowing of the skin and sclera, darkening of urine. She asked for medical help and was hospitalized in the 3rd City Clinical Hospital named after. Mirotvortseva S. R. SSMU in ECHO, where he is currently arriving. Thus, the disease

At first, spicy;

Downstream - progressive;

According to pathogenesis, exacerbation of chronic.

She was born on 03/06/1938 in Saratov in a working-class family. Material and living conditions in which developed satisfactory. In terms of physical and mental development, she did not lag behind her peers. Hygienic conditions and financial support are currently satisfactory. Married, has an adult daughter and grandchildren. Has no bad habits, denies drug use. Diseases transferred in childhood: SARS, tonsillitis. He denies any diseases he has had during his life (tuberculosis and contact with it; Botkin's disease; diabetes mellitus; venereal diseases - gonorrhea, syphilis, AIDS, malaria) in himself and in his relatives. Operations: amputation of the uterus in 1986. She has not traveled outside the region in the last year. There were no blood transfusions. Allergic reactions: does not note.

status preasens universalis

The general condition of the patient is of moderate severity, consciousness is clear, active position, physique of the hypersthenic type, height 164 cm, weight 91 kg. Body temperature 36.7°C.

The skin is icteric in color, dry, warm to the touch. The conjunctiva of the eyelids and sclera are icteric. The skin turgor is reduced, the hairline is normal, the hair is of the female type. Nails on the hands and feet are not changed.

Subcutaneous fat is overdeveloped, evenly distributed. Painless on palpation. There are no swelling in the legs.

Lymph nodes - accessible to palpation, not enlarged, densely elastic consistency, painless, mobile, not soldered to each other and to the surrounding tissue, the skin over them is not changed. The muscles are developed satisfactorily. Pain on palpation is not noted. Muscle tone is preserved.

The bones of the skull, chest, spine, pelvis, limbs of deformation, as well as pain during palpation and tapping are not noted.

Joints of normal configuration. The skin over them is of normal color. On palpation of the joints, their swelling and deformity, changes in the periarticular tissues, and pain are not noted. Full movement.

The thyroid gland is not visualized or palpated

RESPIRATORY SYSTEM

Makes no complaints.

Palpation

Without features.

Percussion

Topographic percussion:

Inferior borders of the lungs.

Right lung:

l. parasternalis - 6th rib;

l. medioclavicularis - 7th rib;

l. axillaris media - 8 rib;

l. axillaris posterior - 8th rib;

l. scapularis - 9th rib;

l. paravertebralis - at the level of the spinous process Th 10.

Left lung:

l. parasternalis - 6th rib;

l. medioclavicularis - 6th rib;

l. axillaris anterior - 7th rib;

l. axillaris media - 8 rib;

l. axillaris posterior - 9th rib;

l. scapularis - 10th rib;

l. paravertebralis - at the level of the spinous process Th 11.

Borders of the upper edge of the lungs:

Right lung:

Anteriorly 3.5 cm above the collarbone.

Behind at the level of the spinous process of the 7th cervical vertebra.

Left lung:

Anteriorly 3 cm above the collarbone; Behind at the level of the spinous process of the 7th cervical vertebra.

Comparative percussion.

Above the symmetrical areas of the lungs, a clear pulmonary sound is determined percussion.

Auscultation

Respiration is vesicular throughout the lung fields.

THE CARDIOVASCULAR SYSTEM

Makes no complaints.

Pulsations at the base of the heart, in the area of ​​the apical impulse, the epigastric region are not observed.

Palpation

The apex beat is determined by the 5th intercostal space 2 cm outward from the midclavicular line. Normal height, moderate strength, non-resistant. The pulse is symmetrical, with a frequency of 75 beats per minute, rhythmic, good filling.

Percussion

Limits of relative cardiac dullness:

Right - in the 4th intercostal space 2 cm outward from the right edge of the sternum

Upper - at the level of the 3rd rib between l. sternalis et l. Parasternalissinistrae

Left - in the 5th intercostal space, 2 cm outward from the left midclavicular line. The vascular bundle extends beyond the sternum in the 2nd intercostal space by 1.5 cm. The diameter of the vascular bundle is 8 cm.

Auscultation

Heart sounds are rhythmic, the sonority of tones is muffled. Heart rate - 60 beats. in min.

URINARY SYSTEM

Complaints of darkening of the color of urine.

No visible changes were found in the lumbar region. The kidneys could not be palpated. The symptom of tapping in the lumbar region is weakly positive on the right, negative on the left. Pain on palpation of the upper and lower ureteral points is absent. Percussion bladder does not protrude above the pubic joint. There are no dysuric phenomena.

NEUROPSYCHOLOGICAL RESEARCH

There are no complaints.

The mind is clear, the mood is calm. Pupillary reaction to light live D=S.

DIGESTIVE SYSTEM

Complaints (at the time of curation)

Complaints of intense, bursting pain in the right hypochondrium, epigastric region, nausea; general weakness. Acholic chair. Dark colored urine.

Examination of the oral cavity.

When examining the oral cavity, the lips are dry, without cracks, ulcerations and rashes. The oral mucosa is icteric, clean, moist. Tongue without white coating, moist. Swallowing is free, painless.

On examination, the abdomen is rounded, soft, painful in the right hypochondrium and epigastric region, does not participate in the act of breathing. There is no visible peristalsis, protrusions and retractions, expansion of the veins of the abdominal wall, the skin is icteric.

Examination of the abdomen.

The abdomen is rounded, swollen in the epigastric and paraumbilical region, asymmetric, collaterals on the anterior surface of the abdomen and its lateral surfaces are not expressed; there is no pathological peristalsis; the muscles of the abdominal wall are involved in the act of breathing; there are no limited protrusions of the abdominal wall during deep breathing and straining. Expansions of the veins of the abdominal wall are absent.

Percussion.

With percussion of the abdomen, tympanitis of varying severity is determined. Accumulation of fluid in the abdominal cavity is not observed. There is no splash noise. Ortner's sign is positive.

Approximate superficial palpation of the abdomen.

The abdomen is soft. Soreness is determined in the right hypochondrium, in the epigastric region. Kerr's sign is positive. Shchetkin-Blumberg's symptom is negative. When examining the "weak points" of the anterior abdominal wall (umbilical ring, aponeurosis of the white line of the abdomen, inguinal rings), no hernial protrusions are formed.

With deep palpation of the abdomen according to the Obraztsov-Strazhesko method:

The lower border of the stomach is determined by the method of percussion, by the method of stetoauscultic palpation, 3 cm above the navel.

Lesser curvature and pylorus are not palpable; splashing noise to the right of the midline of the abdomen (Vasilenko's symptom) is not detected.

Auscultation.

During auscultation of the abdomen, weakened peristaltic noises are heard. There are no noises of splashing and friction of the peritoneum.

The chair is aholic.

Borders of the liver according to Kurlov:

upper (along the right midclavicular line) - VI rib;

lower on the right midclavicular line - 2 cm below the edge of the costal arch;

the lower one along the anterior midline - 1 cm below the border of the upper and middle third of the distance from the navel to the xiphoid process;

lower along the left costal arch - 1.5 cm to the left of the left parasternal line.

Liver sizes according to Kurlov:

on the right midclavicular line - 11 cm;

along the anterior median line - 10 cm;

on the left costal arch - 8 cm.

Survey plan

General blood analysis

General urine analysis

Blood chemistry

Ultrasound of the abdominal organs

Fibrogastroduodenoscopy

Chest X-ray

Data from laboratory and additional research methods

Blood chemistry

Total protein 51.0 g/l

Albumin 39.0 g/l

Creatinine 76.2 mmol/l

Glucose 7.3 mmol/l

Urea 6.9 mmol/l

Total bilirubin 275.8 mmol/l

Direct bilirubin 117.8 mmol/l

ALT 100.9 units/l

AST 147.2 U/L

Alpha-amylase 34.0 U/l

General urine analysis.

Dirty yellow color

The reaction is sour

Specific Gravity 1009

Transparency cloudy

Protein 0.09 g/l

Sugar neg

Acetone neg

Leukocytes 8-10 in p. sp

Erythrocytes 4-6 in p. unchanged

Cylinders neg

Slime a little

no bacteria

General blood analysis.

HGB 13.3 g/dl

MCHC 35.2 g/dl

PL T 203*10 3 1 mm 3

ESR 13 mm/h

Ultrasound of the abdominal organs. (23.10.2011)

The liver is not enlarged, the contours are even, the parenchyma is homogeneous, there is an expansion of the intrahepatic ducts of the liver lobes. Gallbladder of irregular shape, dimensions 70*30 mm. The wall of 5 mm is doubled, compacted. Multiple calculi with a diameter of 0.5 to 1.1 cm. Choledoch expanded to 11-13 mm in the lumen, calculi up to 1.0 cm are determined.

Pancreas: dimensions: head 27 mm, body 11 mm, tail 23 mm; the contours are diffusely heterogeneous, the echogenicity is increased, the contours are not clear, the Wirsung duct is not visualized.

Spleen: dimensions 9.0×4.3 cm, homogeneous structure, not changed.

Conclusion: signs of acute calculous cholecystitis, chronic pancreatitis; obstructive jaundice, choledocholithiasis.

Fibrogastroduodenoscopy:

Esophagus: freely passable, pale pink mucosa, no varicose veins, no polyps, no diverticulum

Stomach: normal peristalsis, normal gastric contents, normal folds, atrophic mucosa, no erosions and ulcers, no polyps, no duodenogastric reflux, normal pylorus.

Bulb of duodenum: no deformities, normal lumen, normal contents, atrophic mucosa, no erosions and ulcers.

Conclusion: Chronic atrophic gastritis, duodenitis.

ECG: sinus rhythm, heart rate 60 in 1 minute, the electrical axis of the heart is horizontal. Hypertrophy of the left atrium, hypertrophy of the left and right ventricles. Signs of rheumatic damage to the mitral and aortic valves.

Chest X-ray: Conclusion. The lung pattern is not enhanced, the lung tissue is homogeneous, the sinuses are free from fluid; the heart shadow is not enlarged.

Endoscopy + endoscopic retrograde cholangiography

The duodenoscope was inserted into the duodenum, in the lumen of bile, mucous and large duodenal papilla were not changed. The mouth of the major duodenal papilla = 0.2 cm is contiguous; the catheter is inserted into the choledochus. The bile ducts are contrasted, they are dilated. Choledochus in the upper and middle thirds up to 1.5-1.8 cm, in its middle third the stone 1.5 to 2.0 cm is tightly attached to the walls, it is difficult to wrap around with contrast, it is impossible to hold the instrument above the stone. The distal part of the choledochus is up to 0.8 cm, which makes lithoextraction impossible, and papillotomy is not advisable

Summary of pathological symptoms

Acute. Prolonged, intense pain in the right hypochondrium and epigastric region, arising from errors in the diet.

General weakness.

Pressure increase 160/90 mm Hg.

Jaundice of the skin and mucous membranes, conjunctiva and sclera.

Sharp pain at the point of the gallbladder (Kera's symptom)

Soreness when tapping on the right costal arch (Ortner's symptom)

Leukocytosis.

Ultrasound showed acute calculous cholecystitis.

Differential Diagnosis

This disease can be differentiated from acute myocardial infarction in both cases, the pain is based in the epigastric region, radiates behind the sternum, accompanied by nausea, vomiting. In laboratory tests, there will be N blood sugar, urine diastasis and bilirubin are not elevated. However, in acute myocardial infarction, pain is associated with exercise. Stopped drugs NO. Bladder symptoms are not defined. Ultrasound showed no changes in the liver and biliary tract. Characteristic changes on the ECG. While this patient has a connection of pain with the use of fatty foods, vomiting of bile brings short-term relief. On admission, positive symptoms were noted: Grekov-Ortner, Kera. In the blood test, there is leukocytosis, which indicates an inflammatory process. Characteristic changes according to ultrasound.

This disease can also be differentiated from acute pancreatitis. In both cases, the pain is sharp constant (sometimes increasing) in the epigastric region. Characterized by irradiation of pain posteriorly - in the back, spine, lower back. Soon, repeated profuse vomiting appears, the connection of the disease with alcohol intake, there are no characteristic changes on the ECG. There is leukocytosis in the blood test. However, acute pancreatitis is characterized by: Cystic symptoms are not determined. A sharp increase in urinary diastase, and bilirubin is not elevated, vomiting does not relieve pain. While in this patient, vomiting of bile brought short-term relief. Upon admission, positive symptoms were noted: Grekov-Ortner, Kera. Diastasis is not increased. Detection of stones in the gallbladder according to ultrasound.

The presence in the clinical picture of the syndrome of a violation of the general condition, pain syndrome (pain in the parvo hypochondrium, radiating to the epigastric region), nausea, ultrasound data - pancreas of a heterogeneous structure, increased echogenicity with areas of reduced echogenicity. Along the lateral contour, there is a hyperechoic sickle 0.2 cm thick, the gland tissue is edematous. They allow us to think of acute pancreatitis as the main disease, but since there is no increase in the level of blood amylase, the pain syndrome is not pronounced, we can think of acute pancreatitis only as a complication of the underlying disease. But the level of amylase in the blood is not elevated, the diagnosis of acute pancreatitis can be refuted.

On the basis of pain (pain in the right hypochondrium and epigastric region, appearance after ingestion of fatty and spicy foods, bursting, girdle nature of pain) and dyspeptic (pain accompanied by nausea, vomiting that does not bring relief, heaviness in the right hypochondrium) syndromes, duodenal ulcer can be assumed intestines in a supervised patient. However, the distinctive features of the pain syndrome in duodenal ulcer are: connection with food intake, its quality and quantity, seasonality, increasing character, decrease after eating, applying heat, anticholinergic drugs. While in this patient, attacks of pain are deprived of a daily rhythm, occur after eating fatty foods, are accompanied by nausea, bitterness in the mouth, vomiting that does not bring relief, decrease after taking antispasmodics and analgesics. Soreness is determined on palpation at the point of the gallbladder, positive symptoms of Ortner, Murphy, Mussi-Georgievsky, which is absent in patients with duodenal ulcer. FGDS data also confirm the absence of a duodenal ulcer in the patient: the lumen of the duodenal bulb is normal, the contents are normal, the mucosa is atrophic, there are no ulcers and erosions.

Based on the patient's complaints about a feeling of heaviness and arching pains in the right hypochondrium, nausea, a diagnostic assumption can be made about the presence of chronic hepatitis. However, in chronic hepatitis, even with its benign course, an objective examination reveals a slight increase in the liver, and palpation has a moderately dense, slightly painful edge. In our patient, the edge of the liver is at the level of the lower edge of the costal arch, soft, rounded, moderately painful. With hepatitis of any form, a slight enlargement of the spleen is also detected, and with chronic active hepatitis, the spleen reaches a significant size. In this patient, the spleen is not palpable. Its dimensions are normal. When collecting an anamnesis for chronic hepatitis, either an infectious disease (brucellosis, syphilis, Botkin's disease) or toxic poisoning (industrial, household, drugs) is characteristic. When collecting an anamnesis, the patient denied contact with the above infectious diseases. Based on the nature of the disease (chronic hepatitis), one can expect the appearance of periods of exacerbation in the patient's clinical picture, during which he is disturbed by weakness, fever, pruritus, and yellowness of the skin. But in a supervised patient, pain appears after eating fatty foods. Also in the clinical picture of this patient, the greatest pain is observed at the Kera point, and in chronic hepatitis there is no most painful point, the entire region of the right hypochondrium hurts. Also, yellowness of the skin is not associated with chronic hepatitis, since endoscopic retrograde cholangiography revealed a stone from 1.5 to 2.0 cm in the middle third of the choledoch, which is tightly adjacent to the wall. Also, a biochemical blood test revealed an increase in the level of total bilirubin (275.8 mmol/l.) and fraction of direct bilirubin (117.8 mmol/l.). As a result of obstructive jaundice, the patient has acholic feces and dark urine, which is not typical for the clinic of chronic hepatitis. Due to the absence of a characteristic clinical picture, the absence of a history of contact with infectious diseases and poisoning with toxic substances, as well as periods of exacerbation, the assumption that the patient has chronic hepatitis can be refuted.

Final Diagnosis

The main one is Chronic calculous cholecystitis, exacerbation phase.

Complications - no.

Concomitant diseases - ischemic heart disease, angina pectoris 2 f. Cl. Atherosclerosis of the aorta, coronary, cerebral vessels. Arterial hypertension grade 3, risk 4. Acquired rheumatic heart disease. mitral stenosis. Mitral insufficiency of severe degree. aortic insufficiency. Decompensation of blood circulation in the pulmonary circulation. Pulmonary hypertension. Persistent form of atrial fibrillation.

Acute calculous cholecystitis is based on:

complaints of the patient: pain in the right hypochondrium, nausea, repeated vomiting of bile, bringing short-term relief.

Based on medical history: intake of fatty foods.

Clinical data: On palpation, the abdomen is soft, moderately painful in the right hypochondrium. Positive symptoms: Grekov-Ortner, Kera.

Laboratory data: leukocytosis, increased ESR, changes in biochemical parameters (preservation of a high level of bilirubin with a predominance of direct)

Ultrasound data: the size of the gallbladder is 70 * 30 mm, irregular in shape, the wall is up to 5 mm. doubled. Stones ranging in size from 0.5 to 1.0 cm.

Etiology and pathogenesis of cholelithiasis

There are two types of gallstones: cholesterol and pigment.

It is believed that the formation of stones contribute to the following factors:

Female;

Age 40 years and above;

Food rich in fats;

metabolic diseases;

Heredity;

Pregnancy;

Stagnation of bile;

Infection in the cavity of the gallbladder.

Cholesterol stones in the gallbladder are formed due to a violation of the relationship between the main bile lipids, which are cholesterol, phospholipids and bile acids. Due to cholesterol, cholesterol stones are formed, and due to bilirubin, pigment stones are formed.

Cholesterol is only able to be excreted into bile as micelles formed by phospholipids and bile acids, so its amount depends on the amount of secreted bile acids, which also increase its absorption in the intestine, thus regulating its level in bile.

C cholesterol is practically insoluble and forms crystals in the form of monohydrates. If the amount of bile acids and lecithin is not enough to form micelles, then such bile is considered supersaturated. Such bile is considered a factor predisposing to the formation of stones, as a result of which it was called lithogenic. C, they spontaneously form complex micelles formed on the outside by bile acids arranged so that cylinder-like structures arise, from the ends of which the hydrophilic groups of lecithin (phospholipid ). Inside the micelles are cholesterol molecules, which are isolated from the aqueous medium from all sides. In an aqueous medium at a temperature of 37, the molecules of all three main lipids are amphiphilic and, being in an aqueous medium at a temperature of 37

Theoretically, the following causes of bile supersaturation with cholesterol can be imagined:

1) its excessive secretion into bile;

2) reduced secretion of bile acids and phospholipids into bile;

3) a combination of these reasons.

Phospholipid deficiency is virtually non-existent. Their synthesis is always sufficient. Therefore, the first two reasons determine the frequency of occurrence of lithogenic bile. At the same time, most cholesterol stones have a pigment center, although the pigment is not the center of initiation, as it penetrates the stone a second time through cracks and pores.

Pigment stones can form when the liver is damaged, when it secretes pigments that are abnormal in structure, which immediately precipitate in the bile, or under the influence of pathological processes in the biliary tract that turn normal pigments into insoluble compounds. Most often this occurs under the influence of microflora. Fatty acids that enter the stone are products of the breakdown of lecithin under the influence of microbial lecithinases.

When studying the processes of initiation, it was found that the formation of stones requires the presence of an inflammatory process in the wall of the gallbladder. Moreover, it can be caused not only by a microorganism, but also by a certain composition of food, allergological and autoimmune processes. At the same time, the integumentary epithelium is rebuilt into goblet cells, which produce a large amount of mucus, the cylindrical epithelium flattens, microvilli are lost, and absorption processes are disrupted. In the niches of the mucosa, water and electrolytes are absorbed, and colloidal solutions of mucus turn into a gel. Lumps of the gel, when the bladder contracts, slip out of the niches and stick together, forming the beginnings of gallstones. Then the stones grow and impregnate the center with pigment. Depending on the degree and speed of impregnation, cholesterol or pigment stones are obtained.

The main reasons for the development of the inflammatory process in the wall of the gallbladder is the presence of microflora in the cavity of the gallbladder and a violation of the outflow of bile.

The focus is on infection. Pathogenic microorganisms can enter the bladder in three ways: hematogenous, lymphogenous, enterogenic. More often, the following organisms are found in the gallbladder: E. coli, Staphilococcus, Streptococcus.

The second reason for the development of the inflammatory process in the gallbladder is a violation of the outflow of bile and its stagnation. In this case, mechanical factors play a role - stones in the gallbladder or its ducts, kinks of the elongated and tortuous cystic duct, its narrowing. Against the background of cholelithiasis, according to statistics, up to 85-90% of cases of acute cholecystitis occur. If sclerosis or atrophy develops in the wall of the bladder, the contractile and drainage functions of the gallbladder suffer, which leads to a more severe course of cholecystitis with deep morphological disorders.

Vascular changes in the wall of the bladder play an unconditional role in the development of cholecystitis. The rate of development of inflammation, as well as morphological disorders in the wall, depend on the degree of circulatory disorders.

In this patient, it is possible to assume that the leading factors in the development of acute cholecystitis are the presence of stones in the gallbladder cavity, which clog the lumen of the duct. Thus, the patient has reasons for the development of cholelithiasis. female; over 40 years of age high-fat foods; a sedentary lifestyle leading to an increase in cholesterol levels.

Complications of calculous cholecystitis:

Empyema of the gallbladder (develops as a result of a bacterial infection).

Formation of a vesico-intestinal fistula. It develops as a result of erosion and breakthrough of the calculus through the wall of the gallbladder into neighboring organs (most often into the duodenum), while gallstone obstruction of the intestine may occur.

Emphysematous cholecystitis (develops in only 1% of cases as a result of the multiplication of gas-forming microorganisms, such as: E coli, Clostridia perfringens and Klebsiella species).

Pancreatitis.

Perforation of the gallbladder (develops in up to 15% of patients).

Tactics of treatment of acute cholecystitis complicated by obstructive jaundice

Therapeutic tactics for calculous cholecystitis complicated by obstructive jaundice is to eliminate jaundice before surgery, if the nature of the disease does not require emergency or urgent surgery. To eliminate jaundice, endoscopic operations have been widely used - papillosphinkerotomy and laparoscopic cholecystostomy, as well as transhepatic drainage of the bile ducts. The use of endoscopic and transhepatic interventions in this group of patients is aimed at eliminating jaundice and biliary hypertension and the causes of their development in order to perform the operation in more favorable conditions for the patient, with less risk for him and in a smaller volume. Thanks to modern diagnostic methods, which allow to speed up the examination of the patient and clarify the diagnosis, the time of the operation can be reduced to 3-5 days. During this relatively short period, it is possible to carefully examine the patient and evaluate the functional state of various body systems, as well as fully prepare the patient for surgery.

When obstructive jaundice is combined with acute cholecystitis, active tactics should be followed, which is determined not only by the presence of cholestasis and cholemia, but also by the addition of purulent intoxication. In these cases, the timing of the operation depends on the severity of the inflammatory process in the gallbladder and the severity of peritonitis. In the surgical treatment of acute cholecystitis, an intervention is simultaneously performed on the extrahepatic bile ducts, and after assessing the nature of the pathological process in them. In patients with a high operational risk for acute cholecystitis, laparoscopic cholecystostomy is performed, and to resolve jaundice, endoscopic transpapillary intervention is performed, combined with purulent cholangitis with nasobiliary drainage. Endoscopic operations on the gallbladder and bile ducts can stop the inflammatory process and eliminate jaundice.

When preparing patients for surgery and managing them in the postoperative period, one must first of all keep in mind the violation of protein metabolism with the development of hypoproteinemia and hypoalbuminemia. To eliminate these consequences, protein preparations are used, giving preference not to split proteins (dry plasma, protein, albumin), the half-life of which in the body is 14-30 days, but to amino acids that are used by the body for the synthesis of organ proteins. Such drugs include casein hydrolyzate, aminosol, alvesin, vamin, etc. Albumin deficiency must be replenished 3-4 days before surgery by transfusion of a 10-20% solution of it in an amount of 100-150 ml per day and continue for 3-5 days after her.

To provide the patient with energy material, as well as to stimulate regenerative processes in the liver, increase its antitoxic function and resistance of hepatocytes to hypoxia, it is recommended to administer concentrated glucose solutions in a volume of 500-1000 ml per day. In order to increase the efficiency of the metabolism of intravenously administered glucose, it is necessary to add insulin, while its dose must be slightly higher than the standard one in order for its metabolic effect to be manifested.

Mandatory components of the treatment program for obstructive jaundice are drugs that improve the functional state of hepatocytes and stimulate the process of their regeneration. These include Essentiale, legalon, carsil, sirepar, etc. They should be prescribed in the immediate postoperative period and refrained until the elimination of cholestasis, so as not to cause a breakdown in the adaptation of hepatocytes to the changes that have arisen in conditions of biliary hypertension and cholemia. Multicomponent therapy for obstructive jaundice should include vitamin therapy with vitamins A, B (B1, B6, B12), C, E.

Infusion therapy should be aimed at restoring the BCC, correcting the CBS. Antibacterial therapy should be aimed at preventing purulent-septic complications. The most effective regimen of antibiotic therapy is intraoperative administration of antibacterial drugs.

Carrying out pathogenetically substantiated infusion-drug therapy in patients with calculous cholecystitis and obstructive jaundice allows to ensure a favorable course of the postoperative period and prevent the development of acute hepatic, renal and cardiovascular failure.

Indications for surgery

The presence of stones in the gallbladder, even in the absence of clinical manifestations, is an indication for surgical treatment.

Taking into account the age, the presence of obesity and concomitant diseases, the patient chose the method of surgical intervention - cholecystectomy, choledocholithotomy.

Preoperative preparation

Chest x-ray

Infusion therapy

Operation

Operation protocol

Operation time 12.15 end 14.30

Date 09/28/2011

Operation No. 685

Name of operation: cholecystectomy, choledocholithotomy. Drainage of common bile duct according to Kehr, drainage of the abdominal cavity.

FULL NAME. Vanina A.A.

Diagnosis before surgery: Acute calculous cholecystitis. Choledocholithiasis. mechanical jaundice.

Diagnosis after surgery: Acute phlegmanous calculous cholecystitis. Choledocholithiasis. mechanical jaundice.

Surgeon: Cherkasova V.A.

Assistants: Dolgushin D.N., Osmanov R.

Anesthesiologist: Roshchina E.V.

Anesthetist: Knyazeva Yu.V.

Pain relief: ETH

Operating m / s: Bugrim S.S.

Operation description

A transrectal incision was made under the ETN in the right hypochondrium. In the subhepatic space, a pronounced adhesive process. The liver is not enlarged. During the revision, the entire gallbladder is filled with calculi, with a thickened wall. The choledochus is expanded up to 1.5 cm, a calculus is palpated in its lumen up to 1.5 cm, it is fixed. The gallbladder was opened, all stones were removed from it. Cystic duct is not defined, Merisi's syndrome is revealed. The defect in the hepatic duct is up to 0.5 cm, it is sutured. Produced choledochotomy over the stone, which is removed in parts. Choledoch is washed. The probe passes freely into the duodenum. Kera drain installed. The choledochotomy opening was sutured to drainage. Checking blood and bile flow - dry. Drainage is connected to the Winslow hole. Both drains were brought out through two separate punctures in the right hypochondrium. Layered suture of the wound. Aseptic bandage.

Preparation: gallbladder 10x4x3 cm, the wall is thickened up to 5 mm, there is pus in the lumen and a mass of stones with a diameter of 0.5 to 1.0 cm. There is no bile in the lumen.

Diseases associated directly and indirectly with the operation itself, as well as diseases progressing as a result of the operation, are included in the concept of postcholecystectomy syndrome.

Pathological changes in the body observed after surgery are very diverse and are not always limited to the biliary tract. Patients after surgery are concerned about epigastric pain of varying intensity, early or late relapses of hepatic colic, jaundice, dyspepsia, etc. The consequences of cholecystectomy (loss of the main function of the gallbladder) are observed only in isolated patients. Often the cause of suffering in these cases are diseases of the organs of the hepatoduodenal-pancreatic system.

Other authors suggest using a different definition of the disease - a true postcholecystectomy syndrome, including in this concept only relapses of hepatic colic due to an inferiorly performed cholecystectomy, i.e. a group of those complications that are caused by errors made during cholecystectomy. This group includes residual hepaticocholedochal stones, pathological changes in the stump of the cystic duct, stenosing papillitis, post-traumatic cicatricial stricture of the common bile duct, and the left part of the gallbladder.

A number of researchers recognize that there is no true postcholecystectomy syndrome. Complaints of patients after surgery are associated with the presence of diseases that were not recognized before cholecystectomy. With insufficient examination of the patient during the operation, insufficient surgeon technique, repeated stone formation, which may have nothing to do with surgical intervention.

Strictures most often develop due to damage to the biliary tract during surgery. An important role in the development of strictures is played by deformation at the confluence of the cystic duct and the common bile duct, so it is recommended to ligate the cystic duct at a distance of 0.5 cm from the common bile duct. Perhaps the occurrence of cicatricial strictures and as a result of external drainage of the ducts. The main clinical signs of stricture of the common bile duct are obstructive jaundice and recurrent cholangitis. However, with partial obstruction of the duct, a syndrome of moderately severe cholestasis is observed.

Bile duct stones are the most common cause of recurrence of pain after cholecystectomy and subsequent operations in connection with this.

It is customary to distinguish between true and false relapses of stone formation. True recurrence is understood as newly formed stones after cholecystectomy, under false recurrence - stones that are not recognized during surgery (residual).

A long stump of the cystic duct, gallbladder may be the cause of pain after cholecystectomy. The cause of a long stump is most often incomplete removal of the cystic duct in combination with stable biliary hypertension.

It is possible to expand the rest of the stump, develop small neuromas at the bottom of it, infection of its walls with the development of an inflammatory process.

In rare cases, the cause of an unsatisfactory outcome of surgical treatment of cholelithiasis is a choledochal cyst, most often an aneurysmal expansion of the walls of the choledochus between the gallbladder and duodenum. Much less often, the cyst comes from the side wall of the duct in the form of a diverticulum.

Cholangitis is one of the formidable complications after cholecystectomy. Most often, it develops with stenosis of the terminal choledochus, multiple stones in the extrahepatic bile ducts. The cause of the development of cholangitis, as a rule, is a violation of the evacuation of bile, leading to biliary hypertension, cholestasis. The development of cholestasis contributes to the upward spread of infection. Infection is the main factor leading to cholangitis in biliary tract surgery. Acute septic cholangitis is manifested by jaundice, chills, a sharp increase in body temperature, heavy sweat, thirst. On examination, there is severe pain in the right hypochondrium, aggravated by tapping along the costal arch (Ortner's symptom). The size of the liver is not significantly enlarged and quickly becomes normal as the patient's condition improves. The spleen may be enlarged, indicating parenchymal liver damage or spread of infection. Jaundice is accompanied by discolored stools and dark urine.

In a laboratory study, hyperbilirubinemia is noted due to the direct direct fraction, an increase in alkaline phosphatase activity, leukocytosis, and a stab shift to the left. The chronic form of cholangitis does not have a pronounced clinical picture. Weakness, constant sweating, periodically subfebrile temperature, slight chills can be noted. Characteristic of this disease is an increase in ESR.

Changes in the region of the major duodenal papilla, both organic and functional, are one of the etiological factors in the development of diseases of the hepatobiliary system and pancreas. With the defeat of the major duodenal papilla, the appearance of recurrence of pain, jaundice and cholangitis after cholecystectomy is associated.

Liver diseases are sometimes the cause of unsatisfactory well-being of patients after cholecystectomy.

6.10.11. The condition is stable, without negative dynamics. Pulse 72 beats/min, BP 120/80, body temperature 36.8° C. Stable hemodynamics. Respiration is vesicular. The tongue is moist and clean. The abdomen is soft, not swollen, moderately painful in the right hypochondrium. There are no peritoneal symptoms. Peristalsis is heard. Through the Kera drainage 150 ml of bile. Diuresis is not broken.

Appointments:

Bed mode.

Sol. Glucosae10% - 300 ml

Omez 20 mg × 2 times.

Erinit 1 tab 3 times.

Thrombo ACC 1 tab. 1 time.

Cardarone 100 mg × 1 time.

Egilok 12.5 mg × 2 times.

Panangin 1 tablet 3 times.

Prednisolone 30 mg 2 times / m.

The condition is stable without negative dynamics. The patient is more active. The jaundice is reduced. Pulse 68 beats/min, BP 110/70, body temperature 36.7° C. Stable hemodynamics. Respiration is vesicular. The tongue is wet. The abdomen is not swollen, soft, painless. The seam is clean. There was no chair. A cleansing enema was prescribed. Diuresis is normal. According to the drainage Kera 200 ml. bile.

Appointments:

Bed mode.

Sol. Glucosae10% - 300 ml

Sol. Kalii Chloridi 4% - 80 ml.

Sol/ Magnesii Sulfatis 25% - 10 ml.

Insulin 3 units IV drip slowly

Sol. Natrii Chloridi 0-9% - 200 ml. + Sol. Riboxyni 10.0 i.v.

Omez 20 mg × 2 times.

Erinit 1 tab 3 times.

Thrombo ACC 1 tab. 1 time.

Cardarone 100 mg × 1 time.

Egilok 12.5 mg × 2 times.

Panangin 1 tablet 3 times.

Prednisolone 30 mg 2 times / m.

8.10.11. The condition is stable, without negative dynamics. Pulse 68 beats/min, BP 110/70, body temperature 36.5° C. Stable hemodynamics. Respiration is vesicular. The tongue is moist and clean. The abdomen is soft, not swollen. Peristalsis is heard. Through the Kera drainage 150 ml of bile. Diuresis is not broken.

Appointments:

Bed mode.

Sol. Glucosae10% - 300 ml

Sol. Kalii Chloridi 4% - 80 ml.

Sol/ Magnesii Sulfatis 25% - 10 ml.

Insulin 3 units IV drip slowly

Sol. Natrii Chloridi 0-9% - 200 ml. + Sol. Riboxyni 10.0 i.v.

Omez 20 mg × 2 times.

Erinit 1 tab 3 times.

Thrombo ACC 1 tab. 1 time.

Cardarone 100 mg × 1 time.

Egilok 12.5 mg × 2 times.

Panangin 1 tablet 3 times.

Prednisolone 30 mg 2 times / m.

Patient _____, 73 years old, was urgently hospitalized in the 3rd City Clinical Hospital named after. Mirotvortsev SSMU. considers herself ill since December 2010, when for the first time she began to be disturbed by intense arching pains in the upper abdomen that occur after eating fatty foods and are accompanied by nausea, general malaise, elevated temperature to subfebrile numbers. She was in the hospital from 12/22/2010 to 12/29/2010, where, after ultrasound, calculi were found in the gallbladder. The operation was denied for health reasons. After the therapy, she was discharged with recommendations to follow a diet with the restriction of abundant consumption of fatty foods.

The last deterioration of the patient's condition was on September 16, 2011, when, after an error in the diet, intense pain appeared in the right hypochondrium, nausea, and vomiting. Similar episodes have been reported before. On an outpatient basis, ultrasound revealed gallbladder calculi. Independently the patient was treated with antispasmodics without a positive effect. 09/22/2011. noted yellowing of the skin and sclera, darkening of urine. She asked for medical help and was hospitalized in the 3rd City Clinical Hospital named after. Mirotvortseva S. R. SSMU in ECHO. An objective examination revealed: obesity of the 2nd degree, the tongue is covered with white coating, the abdomen is soft on palpation, painful in the right hypochondrium, a positive symptom of Ortner. In the hospital, as part of the examination, the patient was prescribed: Complete blood count, urinalysis, biochemical blood test, abdominal ultrasound, fibrogastroduodenoscopy, ECG, chest x-ray, endoscopy + endoscopic retrograde cholangiography.

Based on the above anamnesis, objective examination data, life history, ultrasound data of the abdominal organs (in the gallbladder lumen, stones with a diameter of 0.5 to 1.0 cm) were diagnosed with cholelithiasis. Acute calculous cholecystitis. mechanical jaundice.

Since the presence of stones in the gallbladder, even in the absence of clinical manifestations, is an indication for surgical treatment, it was decided to perform cholecystectomy.

Preoperative preparation included: conducting additional research methods, consulting a therapist, as well as preoperative drug preparation.

The operation was carried out: 28.09.11, without complications.

Postoperative treatment without features, stable condition, no negative dynamics, complaints of pain in the surgical area.

With a favorable course of the postoperative period after cholecystectomy:

visiting the surgeon of the polyclinic at least 1 time per week with an assessment of the general condition of the patient, assessment of the condition of the postoperative wound;

adherence to diet number 5; complaint cholecystitis biliary disease

removal of sutures on the 7-8th day;

In the complicated course of the postoperative period (after cholecystectomy):

a visit by the surgeon to the clinic at least once every 3 days (in the clinic, at home) with an assessment of the general condition of the patient, the effectiveness of the therapy; appointment of the necessary laboratory examination, consultations of specialists, correction of the therapy;

drug and non-drug treatment of complications;

limitation of heavy physical activity for 6 months;

symptomatic therapy (in the presence of concomitant diseases).

The prognosis for life and health is doubtful. The quality of life is reduced.

BIBLIOGRAPHY:

"Surgical Diseases" - a textbook for medical students. Moscow. "Medicine". 1997.

"Workshop on faculty surgery" - educational and methodological manual edited by prof. Rodionova V.V. Moscow 1994.

"The course of propaedeutics of internal diseases in diagrams and tables" V.V. Shedov. I.I. Shaposhnikov. Moscow 1995

The course of faculty surgery in tables and diagrams. K.I. Myshkin, L.A. Frankfurt, Saratov Medical Institute, 1998

General surgery. V.I.Struchkov - M.: Medicine, 2000

Korolev B.A., Pikovsky D.L. "Emergency surgery of the biliary tract", M., Medicine, 1996;

Savelyev V. S. "Guidelines for emergency surgery of the abdominal organs", M., 1990

Skripnichenko D.F. "Emergency abdominal surgery", Kyiv, "Health", 2001.

http://clinic-s.ru/catalog/3/25/

http://ru.wikipedia.org/wiki/

http://www.medicinarf.ru/medcatalog/?cid=156

http://el.sgmu.ru/mod/resource/view.php?id=1582

http://el.sgmu.ru/mod/resource/view.php?inpopup=true&id=7678

1. Posted on www.allbest.ru

Similar Documents

    Complaints of the patient upon admission to inpatient treatment for a feeling of heaviness and periodic paroxysmal pain in the right hypochondrium, radiating to the right shoulder, bitterness in the mouth. Data of laboratory and instrumental studies, diagnosis.

    case history, added 11/10/2015

    An objective examination of a patient with a preliminary diagnosis of "Chronic gastritis, exacerbation stage. Chronic calculous cholecystitis, without exacerbation". Survey plan. Data from laboratory and instrumental studies. Treatment. Observation diaries.

    case history, added 03/12/2015

    Substantiation of the clinical diagnosis of "chronic calculous cholecystitis" based on the patient's complaints, medical history, external examination, ultrasound examination results and laboratory tests. Development of a treatment plan and diary, preparation of an epicrisis.

    case history, added 01/25/2011

    Clinical diagnosis - cholelithiasis, acute calculous cholecystitis. The patient's condition at admission, the history of the disease. The results of laboratory tests, justification of the diagnosis, treatment. Preparing for a planned operation - cholecystectomy.

    case history, added 06/11/2009

    Establishment of a differential diagnosis based on the patient's complaints, the results of laboratory and instrumental studies, the clinical picture of the disease. Treatment plan for chronic calculous cholecystitis and cholelithiasis, operation protocol.

    case history, added 10/12/2011

    Chronic calculous cholecystitis. Diffuse changes in the liver, pancreas. Etiology of acute cholecystitis. Complaints of the patient, complications of the underlying disease. Operations on the extrahepatic bile ducts. Laboratory research methods.

    case history, added 12/19/2012

    Substantiation of the clinical diagnosis on the basis of physical examination data, the results of laboratory and instrumental methods of examination. Factors leading to the development of calculous cholecystitis. Operative and medical treatment of the disease.

    case history, added 09/11/2013

    Complaints upon admission of the patient. Determination of painful areas. Diagnosis of acute calculous cholecystitis. Contraindications for laparoscopic cholecystectomy. Surgical treatment of calculous cholecystitis. Prevention of acute cholecystitis.

    case history, added 06/14/2012

    Complaints of the patient at the time of curation. Genealogical and allergic history. The state of the patient by organs and functional systems. Results of laboratory, instrumental and other studies. Analysis of the clinical picture, identified syndromes.

    medical history, added 11/08/2011

    Characteristics of symptoms, complaints at the time of curation in a patient suffering from chronic calculous cholecystitis. Medical indicators at the time of the study of the respiratory, circulatory, digestion, urination, nervous system, rationale for treatment.

25.06.2013

Acute cholecystitis complicated by obstructive jaundice

… despite a noticeable improvement in treatment outcomes, mortality after emergency operations for acute cholecystitis remains several times higher than with elective surgical interventions.

Obstructive jaundice in patients with acute cholecystitis complicated by obstructive jaundice is caused by obstruction of the main bile ducts with stones, less often by stenosis of the Vater papilla, cholangitis, or compression of the terminal part of the common bile duct by the head of the pancreas.

Clinic and diagnostics. Complication of acute cholecystitis with mechanical jaundice leads to the development of a pronounced syndrome of endogenous intoxication. The clinical picture is extremely diverse. This is due to the intensity and duration of jaundice, as well as the combination of cholestasis with destructive cholecystitis or purulent cholangitis. With all the variety of clinical symptoms of acute cholecystitis with obstructive jaundice, a number of features characteristic of most patients can be traced.

Jaundice is the most striking symptom of the disease. It appears most often 12-14 hours after the pain attack subsides. In most cases, yellowness of the skin and sclera takes on a persistent and progressive character. With severe and prolonged jaundice, patients develop itching, scratching on the skin, weakness, decreased appetite, darkening of urine and discoloration of feces. Blood bilirubin increases due to the direct fraction.

In diagnostics, preference is given to ultrasound as a non-invasive and screening method.

Treatment in all patients with various forms of acute cholecystitis, it is aimed at eliminating the pain syndrome, using detoxification and anti-inflammatory therapy. An emergency operation (within 2-3 hours from the moment of admission) is performed in patients with signs of peritonitis. An urgent operation (24-48 hours) is performed in patients who have a clinical picture of obstructive cholecystitis, symptoms of the inflammatory process and endotoxicosis are growing. For a delayed operation - in the "interval" - they are preparing more painfully, in which, thanks to conservative therapy, an attack of acute cholecystitis is relieved (within 24-48 hours) and the outflow of bile into the duodenum is restored.

General principles of preparation for surgery: normalization of homeostasis, creation of functional reserves of vital organs, treatment of existing concomitant diseases, adaptation of the patient's psyche.

In cases where the attack of acute cholecystitis subsides, but the phenomena of obstructive jaundice persist, intensive preoperative preparation and topical diagnostics are carried out in the near future, not exceeding 5 days from the date of admission.

Surgical treatment. Adequate radical surgical intervention is cholecystectomy with revision of the extrahepatic bile ducts. Each operation for cholecystitis should be accompanied by a revision of the main extrahepatic ducts. Further tactics depend not only on the nature of the pathological process in the biliary tract, but also on the reserve capabilities of the patient. Sometimes, in a serious condition of the patient (senile age, concomitant diseases), cholecystolithostomy is performed. The most difficult and crucial moment is the operation on the choledochus. Indications for choledochotomy can be absolute and relative.

Absolute indications for choledochotomy: obstructive jaundice at the time of surgery; stones palpated in hepaticocholedochus; the presence of filling defects along the ducts on surgical radiographs; wedged stone of the large duodenal papilla; lack of evacuation of the contrast agent into the duodenum on the operating radiographs.

Relative indications for choledochotomy: history of jaundice or before surgery; shrunken gallbladder, wide cystic duct (more than 3 mm), small stones in the gallbladder; wide extrahepatic bile ducts (more than 10 mm); narrowing of the terminal section of the common bile duct with impaired evacuation of the contrast agent on radiographs.

The most common methods of external drainage of the bile ducts are: (1) according to Pikovsky: thin drainage is carried out into the cystic duct; (2) according to Vishnevsky: drainage, approximately equal in diameter to the choledochus and having an oval opening, retreating from the distal end by 2–4 cm, is carried out towards the porta of the liver; (3) according to Ker (at present, this drainage is recognized as the most successful): the drainage is a T-shaped tube, thanks to which bile flows naturally into the lumen of the duodenum 12, or when the pressure in the choledochus increases, it additionally flows out.

External choledochostomy is manageable at all stages of the postoperative period, does not introduce new anatomical relationships into the bile ducts. Along with external drainage in biliary tract surgery, internal drainage, most often for this purpose, choledochoduodenostomy is used. The main indications for it are extended tubular strictures of the terminal section of the common bile duct, as well as its expansion over 2 cm in diameter.

At strangulated stone duodenal papilla, cicatricial stenosis of the major duodenal papilla, if necessary, revision of the pancreatic duct, patients undergo transduodenal papillosphincterotomy with plasty. Along with transduodenal papillosphincterotomy, endoscopic papillosphincterotomy is also widely used.


Tags:
Description for announcement:
Start of activity (date): 06/25/2013 06:35:00
Created by (ID): 1

Federal Agency for Health and Social Development

State educational institution of higher professional education

Saratov State Medical University named after V.I. Razumovsky

(GoU VPO Saratov State Medical University named after V.I. Razumovsky Roszdrav)

Department of Faculty Surgery of the Faculty of Medicine

Academic medical history

Patient: ____, 73 years old

The main diagnosis: Acute calculous cholecystitis. Mechanical jaundice

Complications: no

Concomitant diseases: ischemic heart disease, angina pectoris 2 f. Cl. Atherosclerosis of the aorta, coronary, cerebral vessels. Arterial hypertension grade 3, risk 4. Acquired rheumatic heart disease. mitral stenosis. Mitral insufficiency of severe degree. aortic insufficiency. Decompensation of blood circulation in the pulmonary circulation. Pulmonary hypertension. Persistent form of atrial fibrillation

Saratov 2011

General information about the patient

FULL NAME. patient: ______

Date of birth (age): 03/06/1938, 73 years old

Female gender

Education: secondary

Profession: salesperson

Place of residence: Saratov. _______

Received: 22.09.2011

Supervision date: 06.10.2011- 08.10.2011

Clinical diagnosis: Acute calculous cholecystitis. mechanical jaundice.

Complications: no

Concomitant diseases: ischemic heart disease, angina pectoris 2 f. Cl. Atherosclerosis of the aorta, coronary, cerebral vessels. Arterial hypertension grade 3, risk 4. Acquired rheumatic heart disease. mitral stenosis. Mitral insufficiency of severe degree. aortic insufficiency. Decompensation of blood circulation in the pulmonary circulation. Pulmonary hypertension. Persistent form of atrial fibrillation. Superficial gastritis. Duodenogastric reflux.

Complaints on the day of curation: the patient complains of a feeling of heaviness in the right hypochondrium, spreading to the epigastric region, nausea, dry mouth, weakness, fatigue.

The patient considers herself ill since December 2010, when for the first time she began to be disturbed by intense arching pains in the upper abdomen that occur after eating fatty foods and are accompanied by nausea, general malaise, elevated temperature to subfebrile numbers. She was in the hospital from 12/22/2010 to 12/29/2010, where, after ultrasound, calculi were found in the gallbladder. The operation was denied for health reasons (persistent form of atrial fibrillation, acquired rheumatic heart disease, mitral stenosis, severe mitral insufficiency, aortic insufficiency, circulatory decompensation in the pulmonary circulation, pulmonary hypertension). After the therapy, she was discharged with recommendations to follow a diet with the restriction of abundant consumption of fatty foods.

The last deterioration of the patient's condition was on September 16, 2011, when, after an error in the diet, intense pain appeared in the right hypochondrium, nausea, and vomiting. Similar episodes have been reported before. On an outpatient basis, ultrasound revealed gallbladder calculi. Independently the patient was treated with antispasmodics without a positive effect. 09/22/2011. noted yellowing of the skin and sclera, darkening of urine. She asked for medical help and was hospitalized in the 3rd City Clinical Hospital named after. Mirotvortseva S. R. SSMU in ECHO, where he is currently arriving. Thus, the disease

At first, spicy;

Downstream - progressive;

According to pathogenesis, exacerbation of chronic.

She was born on 03/06/1938 in Saratov in a working-class family. Material and living conditions in which developed satisfactory. In terms of physical and mental development, she did not lag behind her peers. Hygienic conditions and financial support are currently satisfactory. Married, has an adult daughter and grandchildren. Has no bad habits, denies drug use. Diseases transferred in childhood: SARS, tonsillitis. He denies any diseases he has had during his life (tuberculosis and contact with it; Botkin's disease; diabetes mellitus; venereal diseases - gonorrhea, syphilis, AIDS, malaria) in himself and in his relatives. Operations: amputation of the uterus in 1986. She has not traveled outside the region in the last year. There were no blood transfusions. Allergic reactions: does not note.

preasens universalis

The general condition of the patient is of moderate severity, consciousness is clear, active position, physique of the hypersthenic type, height 164 cm, weight 91 kg. Body temperature 36.7°C.

The skin is icteric in color, dry, warm to the touch. The conjunctiva of the eyelids and sclera are icteric. The skin turgor is reduced, the hairline is normal, the hair is of the female type. Nails on the hands and feet are not changed.

Subcutaneous fat is overdeveloped, evenly distributed. Painless on palpation. There are no swelling in the legs.

Lymph nodes - accessible to palpation, not enlarged, densely elastic consistency, painless, mobile, not soldered to each other and to the surrounding tissue, the skin over them is not changed. The muscles are developed satisfactorily. Pain on palpation is not noted. Muscle tone is preserved.

The bones of the skull, chest, spine, pelvis, limbs of deformation, as well as pain during palpation and tapping are not noted.

Joints of normal configuration. The skin over them is of normal color. On palpation of the joints, their swelling and deformity, changes in the periarticular tissues, and pain are not noted. Full movement.

The thyroid gland is not visualized or palpated

RESPIRATORY SYSTEM

Makes no complaints.

Palpation

Without features.

Percussion

Topographic percussion:

Inferior borders of the lungs.

Right lung: parasternalis - 6th rib;. medioclavicularis - 7th rib; axillaris anterior - 7th rib; axillaris media - 8 rib;. axillaris posterior - 8th rib; scapularis - 9 rib;. paravertebralis - at the level of the spinous process Th 10.

Left lung: parasternalis - 6th rib;. medioclavicularis - 6th rib;. axillaris anterior - 7th rib; axillaris media - 8 rib;. axillaris posterior - 9th rib; scapularis - 10 rib;. paravertebralis - at the level of the spinous process Th 11.

Borders of the upper edge of the lungs:

Right lung:

Anteriorly 3.5 cm above the collarbone.

Behind at the level of the spinous process of the 7th cervical vertebra.

Left lung:

Anteriorly 3 cm above the collarbone; Behind at the level of the spinous process of the 7th cervical vertebra.

Comparative percussion.

Above the symmetrical areas of the lungs, a clear pulmonary sound is determined percussion.

Auscultation

Respiration is vesicular throughout the lung fields.

THE CARDIOVASCULAR SYSTEM

Makes no complaints.

Pulsations at the base of the heart, in the area of ​​the apical impulse, the epigastric region are not observed.

Palpation

The apex beat is determined by the 5th intercostal space 2 cm outward from the midclavicular line. Normal height, moderate strength, non-resistant. The pulse is symmetrical, with a frequency of 75 beats per minute, rhythmic, good filling.

Percussion

Right - in the 4th intercostal space 2 cm outward from the right edge of the sternum

Upper - at the level of the 3rd rib between l. sternalis et l. Parasternalissinistrae

Left - in the 5th intercostal space, 2 cm outward from the left midclavicular line. The vascular bundle extends beyond the sternum in the 2nd intercostal space by 1.5 cm. The diameter of the vascular bundle is 8 cm.

Auscultation

Heart sounds are rhythmic, the sonority of tones is muffled. Heart rate - 60 beats. in min.

URINARY SYSTEM

Complaints of darkening of the color of urine.

No visible changes were found in the lumbar region. The kidneys could not be palpated. The symptom of tapping in the lumbar region is weakly positive on the right, negative on the left. Pain on palpation of the upper and lower ureteral points is absent. Percussion bladder does not protrude above the pubic joint. There are no dysuric phenomena.

NEUROPSYCHOLOGICAL RESEARCH

There are no complaints.

The mind is clear, the mood is calm. Pupillary reaction to light live D=S.

DIGESTIVE SYSTEM

Complaints (at the time of curation)

Complaints of intense, bursting pain in the right hypochondrium, epigastric region, nausea; general weakness. Acholic chair. Dark colored urine.

Examination of the oral cavity.

When examining the oral cavity, the lips are dry, without cracks, ulcerations and rashes. The oral mucosa is icteric, clean, moist. Tongue without white coating, moist. Swallowing is free, painless.

On examination, the abdomen is rounded, soft, painful in the right hypochondrium and epigastric region, does not participate in the act of breathing. There is no visible peristalsis, protrusions and retractions, expansion of the veins of the abdominal wall, the skin is icteric.

Examination of the abdomen.

The abdomen is rounded, swollen in the epigastric and paraumbilical region, asymmetric, collaterals on the anterior surface of the abdomen and its lateral surfaces are not expressed; there is no pathological peristalsis; the muscles of the abdominal wall are involved in the act of breathing; there are no limited protrusions of the abdominal wall during deep breathing and straining. Expansions of the veins of the abdominal wall are absent.

Percussion.

With percussion of the abdomen, tympanitis of varying severity is determined. Accumulation of fluid in the abdominal cavity is not observed. There is no splash noise. Ortner's sign is positive.

Approximate superficial palpation of the abdomen.

The abdomen is soft. Soreness is determined in the right hypochondrium, in the epigastric region. Kerr's sign is positive. Shchetkin-Blumberg's symptom is negative. When examining the "weak points" of the anterior abdominal wall (umbilical ring, aponeurosis of the white line of the abdomen, inguinal rings), no hernial protrusions are formed.

With deep palpation of the abdomen according to the Obraztsov-Strazhesko method:

The lower border of the stomach is determined by the method of percussion, by the method of stetoauscultic palpation, 3 cm above the navel.

Lesser curvature and pylorus are not palpable; splashing noise to the right of the midline of the abdomen (Vasilenko's symptom) is not detected.

Auscultation.

During auscultation of the abdomen, weakened peristaltic noises are heard. There are no noises of splashing and friction of the peritoneum.

The chair is aholic.

Borders of the liver according to Kurlov:

upper (along the right midclavicular line) - VI rib;

lower on the right midclavicular line - 2 cm below the edge of the costal arch;

the lower one along the anterior midline - 1 cm below the border of the upper and middle third of the distance from the navel to the xiphoid process;

lower along the left costal arch - 1.5 cm to the left of the left parasternal line.

Liver sizes according to Kurlov:

on the right midclavicular line - 11 cm;

along the anterior median line - 10 cm;

on the left costal arch - 8 cm.

Survey plan

General blood analysis

General urine analysis

Blood chemistry

Ultrasound of the abdominal organs

Fibrogastroduodenoscopy

Chest X-ray

Endoscopy + endoscopic retrograde cholangiography

Data from laboratory and additional research methods

Blood chemistry

Total protein 51.0 g/l

Albumin 39.0 g/l

Creatinine 76.2 mmol/l

Glucose 7.3 mmol/l

Urea 6.9 mmol/l

Total bilirubin 275.8 mmol/l

Direct bilirubin 117.8 mmol/l

ALT 100.9 u/l 147.2 u/l

Alpha-amylase 34.0 U/l

General urine analysis.

Dirty yellow color

The reaction is sour

Specific Gravity 1009

Transparency cloudy

Protein 0.09 g/l

Sugar neg

Acetone neg

Erythrocytes 4-6 in p. unchanged

Cylinders neg

Slime a little

no bacteria

Salts neg

General blood analysis.

09.201113.0*10 33.86*10 613.3 g/dl33.2%

NEUT 91.9 %5.3 %86.0 1 mm 330.3 1 pg

MCHC 35.2 g/dlT 203*10 3 1 mm 3

ESR 13 mm/h

Ultrasound of the abdominal organs. (23.10.2011)

The liver is not enlarged, the contours are even, the parenchyma is homogeneous, there is an expansion of the intrahepatic ducts of the liver lobes. Gallbladder of irregular shape, dimensions 70*30 mm. The wall of 5 mm is doubled, compacted. Multiple calculi with a diameter of 0.5 to 1.1 cm. Choledoch expanded to 11-13 mm in the lumen, calculi up to 1.0 cm are determined.

Pancreas: dimensions: head 27 mm, body 11 mm, tail 23 mm; the contours are diffusely heterogeneous, the echogenicity is increased, the contours are not clear, the Wirsung duct is not visualized.

Spleen: dimensions 9.0 ×4.3 cm, the structure is homogeneous, not changed.

Conclusion: signs of acute calculous cholecystitis, chronic pancreatitis; obstructive jaundice, choledocholithiasis.

Fibrogastroduodenoscopy:

Esophagus: freely passable, pale pink mucosa, no varicose veins, no polyps, no diverticulum

Stomach: normal peristalsis, normal gastric contents, normal folds, atrophic mucosa, no erosions and ulcers, no polyps, no duodenogastric reflux, normal pylorus.

Bulb of duodenum: no deformities, normal lumen, normal contents, atrophic mucosa, no erosions and ulcers.

Conclusion: Chronic atrophic gastritis, duodenitis.

ECG: sinus rhythm, heart rate 60 in 1 minute, the electrical axis of the heart is horizontal. Hypertrophy of the left atrium, hypertrophy of the left and right ventricles. Signs of rheumatic damage to the mitral and aortic valves.

Chest X-ray: Conclusion. The lung pattern is not enhanced, the lung tissue is homogeneous, the sinuses are free from fluid; the heart shadow is not enlarged.

Endoscopy + endoscopic retrograde cholangiography

The duodenoscope was inserted into the duodenum, in the lumen of bile, mucous and large duodenal papilla were not changed. The mouth of the major duodenal papilla = 0.2 cm is contiguous; the catheter is inserted into the choledochus. The bile ducts are contrasted, they are dilated. Choledochus in the upper and middle thirds up to 1.5-1.8 cm, in its middle third the stone 1.5 to 2.0 cm is tightly attached to the walls, it is difficult to wrap around with contrast, it is impossible to hold the instrument above the stone. The distal part of the choledochus is up to 0.8 cm, which makes lithoextraction impossible, and papillotomy is not advisable

Summary of pathological symptoms

Acute. Prolonged, intense pain in the right hypochondrium and epigastric region, arising from errors in the diet.

General weakness.

Pressure increase 160/90 mm Hg.

Jaundice of the skin and mucous membranes, conjunctiva and sclera.

Sharp pain at the point of the gallbladder (Kera's symptom)

Soreness when tapping on the right costal arch (Ortner's symptom)

Leukocytosis.

Ultrasound showed acute calculous cholecystitis.

Differential Diagnosis

This disease can be differentiated from acute myocardial infarction in both cases, the pain is based in the epigastric region, radiates behind the sternum, accompanied by nausea, vomiting. In laboratory tests, there will be N blood sugar, urine diastasis and bilirubin are not elevated. However, in acute myocardial infarction, pain is associated with exercise. Stopped drugs NO. Bladder symptoms are not defined. Ultrasound showed no changes in the liver and biliary tract. Characteristic changes on the ECG. While this patient has a connection of pain with the use of fatty foods, vomiting of bile brings short-term relief. On admission, positive symptoms were noted: Grekov-Ortner, Kera. In the blood test, there is leukocytosis, which indicates an inflammatory process. Characteristic changes according to ultrasound.

This disease can also be differentiated from acute pancreatitis. In both cases, the pain is sharp constant (sometimes increasing) in the epigastric region. Characterized by irradiation of pain posteriorly - in the back, spine, lower back. Soon, repeated profuse vomiting appears, the connection of the disease with alcohol intake, there are no characteristic changes on the ECG. There is leukocytosis in the blood test. However, acute pancreatitis is characterized by: Cystic symptoms are not determined. A sharp increase in urinary diastase, and bilirubin is not elevated, vomiting does not relieve pain. While in this patient, vomiting of bile brought short-term relief. Upon admission, positive symptoms were noted: Grekov-Ortner, Kera. Diastasis is not increased. Detection of stones in the gallbladder according to ultrasound.

The presence in the clinical picture of the syndrome of a violation of the general condition, pain syndrome (pain in the parvo hypochondrium, radiating to the epigastric region), nausea, ultrasound data - pancreas of a heterogeneous structure, increased echogenicity with areas of reduced echogenicity. Along the lateral contour, there is a hyperechoic sickle 0.2 cm thick, the gland tissue is edematous. They allow us to think of acute pancreatitis as the main disease, but since there is no increase in the level of blood amylase, the pain syndrome is not pronounced, we can think of acute pancreatitis only as a complication of the underlying disease. But the level of amylase in the blood is not elevated, the diagnosis of acute pancreatitis can be refuted.

On the basis of pain (pain in the right hypochondrium and epigastric region, appearance after ingestion of fatty and spicy foods, bursting, girdle nature of pain) and dyspeptic (pain accompanied by nausea, vomiting that does not bring relief, heaviness in the right hypochondrium) syndromes, duodenal ulcer can be assumed intestines in a supervised patient. However, the distinctive features of the pain syndrome in duodenal ulcer are: connection with food intake, its quality and quantity, seasonality, increasing character, decrease after eating, applying heat, anticholinergic drugs. While in this patient, attacks of pain are deprived of a daily rhythm, occur after eating fatty foods, are accompanied by nausea, bitterness in the mouth, vomiting that does not bring relief, decrease after taking antispasmodics and analgesics. Soreness is determined on palpation at the point of the gallbladder, positive symptoms of Ortner, Murphy, Mussi-Georgievsky, which is absent in patients with duodenal ulcer. FGDS data also confirm the absence of a duodenal ulcer in the patient: the lumen of the duodenal bulb is normal, the contents are normal, the mucosa is atrophic, there are no ulcers and erosions.

Based on the patient's complaints about a feeling of heaviness and arching pains in the right hypochondrium, nausea, a diagnostic assumption can be made about the presence of chronic hepatitis. However, in chronic hepatitis, even with its benign course, an objective examination reveals a slight increase in the liver, and palpation has a moderately dense, slightly painful edge. In our patient, the edge of the liver is at the level of the lower edge of the costal arch, soft, rounded, moderately painful. With hepatitis of any form, a slight enlargement of the spleen is also detected, and with chronic active hepatitis, the spleen reaches a significant size. In this patient, the spleen is not palpable. Its dimensions are normal. When collecting an anamnesis for chronic hepatitis, either an infectious disease (brucellosis, syphilis, Botkin's disease) or toxic poisoning (industrial, household, drugs) is characteristic. When collecting an anamnesis, the patient denied contact with the above infectious diseases. Based on the nature of the disease (chronic hepatitis), one can expect the appearance of periods of exacerbation in the patient's clinical picture, during which he is disturbed by weakness, fever, pruritus, and yellowness of the skin. But in a supervised patient, pain appears after eating fatty foods. Also in the clinical picture of this patient, the greatest pain is observed at the Kera point, and in chronic hepatitis there is no most painful point, the entire region of the right hypochondrium hurts. Also, yellowness of the skin is not associated with chronic hepatitis, since endoscopic retrograde cholangiography revealed a stone from 1.5 to 2.0 cm in the middle third of the choledoch, which is tightly adjacent to the wall. Also, a biochemical blood test revealed an increase in the level of total bilirubin (275.8 mmol/l.) and fraction of direct bilirubin (117.8 mmol/l.). As a result of obstructive jaundice, the patient has acholic feces and dark urine, which is not typical for the clinic of chronic hepatitis. Due to the absence of a characteristic clinical picture, the absence of a history of contact with infectious diseases and poisoning with toxic substances, as well as periods of exacerbation, the assumption that the patient has chronic hepatitis can be refuted.

Final Diagnosis

The main one is Chronic calculous cholecystitis, exacerbation phase.

Complications - no.

Concomitant diseases - ischemic heart disease, angina pectoris 2 f. Cl. Atherosclerosis of the aorta, coronary, cerebral vessels. Arterial hypertension grade 3, risk 4. Acquired rheumatic heart disease. mitral stenosis. Mitral insufficiency of severe degree. aortic insufficiency. Decompensation of blood circulation in the pulmonary circulation. Pulmonary hypertension. Persistent form of atrial fibrillation.

Acute calculous cholecystitis is based on:

complaints of the patient: pain in the right hypochondrium, nausea, repeated vomiting of bile, bringing short-term relief.

Based on medical history: intake of fatty foods.

Clinical data: On palpation, the abdomen is soft, moderately painful in the right hypochondrium. Positive symptoms: Grekov-Ortner, Kera.

Laboratory data: leukocytosis, increased ESR, changes in biochemical parameters (preservation of a high level of bilirubin with a predominance of direct)

Ultrasound data: the size of the gallbladder is 70 * 30 mm, irregular in shape, the wall is up to 5 mm. doubled. Stones ranging in size from 0.5 to 1.0 cm.

Etiology and pathogenesis of cholelithiasis

There are two types of gallstones: cholesterol and pigment.

It is believed that the formation of stones contribute to the following factors:

female;

age 40 years and above;

fat-rich food;

metabolic diseases;

heredity;

pregnancy;

stagnation of bile;

infection in the gallbladder cavity.

Cholesterol stones in the gallbladder are formed due to a violation of the relationship between the main bile lipids, which are cholesterol, phospholipids and bile acids. Due to cholesterol, cholesterol stones are formed, and due to bilirubin, pigment stones are formed.

Cholesterol is only able to be excreted into bile as micelles formed by phospholipids and bile acids, so its amount depends on the amount of secreted bile acids, which also increase its absorption in the intestine, thus regulating its level in bile.

C cholesterol is practically insoluble and forms crystals in the form of monohydrates. If the amount of bile acids and lecithin is not enough to form micelles, then such bile is considered supersaturated. Such bile is considered a factor predisposing to the formation of stones, as a result of which it was called lithogenic. ° C, they spontaneously form complex micelles formed on the outside by bile acids arranged in such a way that cylinder-like structures arise, from the ends of which the hydrophilic groups of lecithin (phospholipid) face the aqueous medium. Inside the micelles are cholesterol molecules, which are isolated from the aqueous medium from all sides. In an aquatic environment at a temperature of 37 ° The molecules of all three main lipids are amphiphilic and, being in an aqueous medium at a temperature of 37

Theoretically, the following causes of bile supersaturation with cholesterol can be imagined:

) its excessive secretion into bile;

a) reduced secretion into bile of bile acids and phospholipids;

) a combination of these reasons.

Phospholipid deficiency is virtually non-existent. Their synthesis is always sufficient. Therefore, the first two reasons determine the frequency of occurrence of lithogenic bile. At the same time, most cholesterol stones have a pigment center, although the pigment is not the center of initiation, as it penetrates the stone a second time through cracks and pores.

Pigment stones can form when the liver is damaged, when it secretes pigments that are abnormal in structure, which immediately precipitate in the bile, or under the influence of pathological processes in the biliary tract that turn normal pigments into insoluble compounds. Most often this occurs under the influence of microflora. Fatty acids that enter the stone are products of the breakdown of lecithin under the influence of microbial lecithinases.

The main reasons for the development of the inflammatory process in the wall of the gallbladder is the presence of microflora in the cavity of the gallbladder and a violation of the outflow of bile.

The focus is on infection. Pathogenic microorganisms can enter the bladder in three ways: hematogenous, lymphogenous, enterogenic. More often, the following organisms are found in the gallbladder: E. coli, Staphilococcus, Streptococcus.

The second reason for the development of the inflammatory process in the gallbladder is a violation of the outflow of bile and its stagnation. In this case, mechanical factors play a role - stones in the gallbladder or its ducts, kinks of the elongated and tortuous cystic duct, its narrowing. Against the background of cholelithiasis, according to statistics, up to 85-90% of cases of acute cholecystitis occur. If sclerosis or atrophy develops in the wall of the bladder, the contractile and drainage functions of the gallbladder suffer, which leads to a more severe course of cholecystitis with deep morphological disorders.

Vascular changes in the wall of the bladder play an unconditional role in the development of cholecystitis. The rate of development of inflammation, as well as morphological disorders in the wall, depend on the degree of circulatory disorders.

In this patient, it is possible to assume that the leading factors in the development of acute cholecystitis are the presence of stones in the gallbladder cavity, which clog the lumen of the duct. Thus, the patient has reasons for the development of cholelithiasis. female; over 40 years of age high-fat foods; a sedentary lifestyle leading to an increase in cholesterol levels.

Complications of calculous cholecystitis<#"justify">"Surgical Diseases" - a textbook for medical students. Moscow. "Medicine". 1997.

"Workshop on faculty surgery" - educational and methodological manual edited by prof. Rodionova V.V. Moscow 1994.

"The course of propaedeutics of internal diseases in diagrams and tables" V.V. Shedov. I.I. Shaposhnikov. Moscow 1995

The course of faculty surgery in tables and diagrams. K.I. Myshkin, L.A. Frankfurt, Saratov Medical Institute, 1998

General surgery. V.I.Struchkov - M.: Medicine, 2000

Korolev B.A., Pikovsky D.L. "Emergency surgery of the biliary tract", M., Medicine, 1996;

Savelyev V. S. "Guidelines for emergency surgery of the abdominal organs", M., 1990

Skripnichenko D.F. "Emergency abdominal surgery", Kyiv, "Health", 2001.

<#"justify">1.

CATEGORIES

POPULAR ARTICLES

2023 "kingad.ru" - ultrasound examination of human organs