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

The gallbladder (GB) is an important organ of our digestive system. In infancy, it is located deep in the liver. As the body develops, it forms and moves down slightly, so that it begins to peek out from under the edge of the liver. In its 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 enlarged gallbladder in an adult or child occurs for various reasons, but most often it is caused by the development of various diseases.

Main signs of organ enlargement

The size of the gallbladder can change quite a lot during the day. The human liver constantly produces bile, which enters the gallbladder - a kind of temporary storage facility. When food enters the body, it contracts and secretes bile through the ducts into the duodenum, where it actively participates in digestion. At the same time, the bladder decreases significantly, but after a short period of time, bile fills it again, increasing in size. And so several times a day. The only thing to worry about is the excessive enlargement of the organ and the unpleasant symptoms that accompany it.

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 sensation to severe attacks of stabbing or cutting pain, lasting several tens of minutes. In adults, symptoms are usually more severe than in children. Symptoms may occur for no apparent reason, but the onset of pain is preceded by eating fatty or spicy foods, drinking alcohol, or skipping meals.

Reasons for changing the size of the gastrointestinal tract

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 disorders are observed in a child as he grows up.

These diseases are caused by various factors:

irregular and poor nutrition;
excessive consumption of processed foods;
bruises received in the abdomen or back;
high physical and mental stress;
penetration of various infectious agents into the gastrointestinal tract;
twisting of the bile ducts;
the use of certain medications in the treatment of other pathologies;
congenital anomalies of the gallbladder;
consuming large doses of vitamins and calcium;
inflammation of the intestinal walls or the gallbladder itself.

If the above factors are completely excluded, it is necessary to be examined for the presence of other reasons that influenced the pathological change in the size of the gallbladder. An enlarged 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 (feeling) 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, an ultrasound is performed and X-rays of the entire gastrointestinal tract are taken. They allow you to determine the exact size of the gallbladder, the presence or absence of inflammation, stones, mechanical damage, etc.

By studying the symptoms and ordering 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 reasons that influenced the growth of the gallbladder.

Bile duct obstruction

This pathology often develops against the background of cholelithiasis, usually in adulthood or old age. It is rarely diagnosed in a child. In this case, the organ itself stretches and swells from the contents filling it, and its walls thicken quite strongly (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 duct obstruction when its tumor mechanically compresses the duct. In this case, an ultrasound of the pancreas and accompanying 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 surgical.

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 suffers from paroxysmal hepatic colic and nausea. Yellowing of the skin is visually observed.

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

Non-calculous (acalculous) 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 bothered by mild pain in the epigastric region, which appears after eating and disappears 1-2 hours after eating, aching pain in the right hypochondrium, the intensity of which increases after eating.

Dyskinesia of the gallbladder and bile ducts

Dyskinesia refers to a specific pathology of the bladder itself or its ducts, which is associated with impaired motility of the organ and bile ducts. Normally, the gallbladder contracts periodically, releasing accumulated bile through the ducts into the intestines. The ducts themselves also contract, pushing the contents of the gallbladder further into the duodenum.

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

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

An ultrasound is usually sufficient for diagnosis.

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

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

Cholelithiasis

Gallstone disease is one of the most common and most dangerous causes of gallstone dysfunction in adulthood or old age. The child has a minimal risk of development.

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

If you suspect the presence of gallstones, you should immediately consult a doctor to undergo appropriate examinations.

At first, the diameter of the stones is very small (these are literally grains of sand), but gradually, as negative conditions persist, they begin to grow until they fill the bladder or clog one of its ducts. In this case, emergency surgery is required.

There may be several causes for cholelithiasis

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;
concomitant liver diseases;
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 considered to be a sharp stabbing pain in the liver area (pain caused by the passage of stones from the gallbladder into the bile ducts with further exit into the intestines). The pain in the right side is sharp and acute, radiating to the right shoulder or shoulder blade.

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

When the stone passes into the intestines, 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 clock can count!

The main methods of examination if the presence of gallstones is suspected 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 of radical removal of all formations through surgery. Nowadays, low-traumatic laparoscopic surgery has become widespread, in which stones or the entire bladder are removed through a puncture in the skin of the abdomen. Ultrasonic crushing of stones is also possible, but the procedure does not become widespread because it has its contraindications.

Non-surgical removal of gallstones is allowed in rare cases when cholelithiasis 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 can be prescribed that dissolve the formations (for example, Ursofalk), after which they enter the intestines in the form of sand and are eliminated from the body naturally. Such treatment is long-term - medication must be taken for at least 6 months, and for the entire duration of therapy a strict diet and a gentle regime are prescribed (the patient is prohibited from heavy physical and mental stress, which can provoke a sudden release of stones with severe pain).

Post-operative reasons

A previous operation on it can also cause an enlargement of the gallbladder - the so-called postoperative syndrome. It is understood as a complex of pathological changes that the operation led to. Laparoscopy or abdominal surgery can provoke inflammation of the stomach or pancreas, which also negatively affects the condition of the gastrointestinal tract. After surgical manipulations, there is a risk of impaired motility of the bile ducts and the bladder itself.

Treatment is usually conservative, consisting of taking choleretic drugs. In some cases, a repeat operation may be required (if not all stones were removed).

Tumors

Various types of tumors are most often diagnosed in elderly patients using ultrasound or x-rays. They are rare in a child or young person. Typically, a benign or malignant tumor contributes to the further development of gallstone disease or hepatitis.

Risk factors also include poor nutrition, concomitant gastrointestinal diseases, decreased immunity, excess weight, and hormonal disorders. Symptoms, depending on the size of the tumor, are similar to those of calculous cholecystitis or cholelithiasis. Treatment is only surgical.

Likely consequences and prognosis

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

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

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Liver diseases
Jaundice

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

Jaundice (gospel disease) (lat. icterus) is an icteric discoloration of the skin and visible mucous membranes, caused by an increased content of bilirubin in the blood and tissues.

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

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

False jaundice (pseudo-jaundice, carotene jaundice) - icteric staining 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, pumpkin, and also occurs when ingesting quinine, picric acid and some other drugs.

Classification of jaundices

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

Prehepatic jaundice - occurs due to increased bilirubin formation. At the same time, its indirect (unconjugated) fraction increases.
Hepatic jaundice. The development of hepatic jaundice is associated with a violation of the consumption (uptake) of bilirubin by hepatocytes. At the same time, the indirect (unconjugated) fraction of bilirubin increases.
Subhepatic jaundice - occurs when the outflow of bile through the extrahepatic bile ducts is impaired (obstructive jaundice).

Jaundice Clinic

Jaundice is a symptom complex that is a yellow discoloration of the skin, sclera, and mucous membranes. The intensity of color can be completely different - from pale yellow to saffron orange. Moderate jaundice without change in urine color is characteristic of unconjugated hyperbilirubinemia (with hemolysis or Gilbert's syndrome). More pronounced jaundice or jaundice with a change in urine color indicates hepatobiliary pathology. Urine in patients with jaundice becomes dark in color due to hyperbilirubinemia. Sometimes a change in urine color precedes the onset of jaundice. All other clinical manifestations of jaundice depend on the reasons that caused its development. In some cases, a change in the color 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 determine the cause of jaundice. True jaundice should be distinguished from hypercarotenemia in patients who consume large amounts of carrots. When jaundice appears, you 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 accompanying jaundice (clinical symptoms are discussed in more detail in the sections devoted to various diseases):

With cholestasis, jaundice is detected, dark-colored urine appears, and generalized skin itching occurs.
Chronic cholestasis may 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.
Patients with cholestasis may have xanthomas (subcutaneous cholesterol deposits) and xanthelasmas (small pale yellow formations in the upper eyelid caused by the deposition of lipids).
Symptoms of chronic liver damage (spider veins, splenomegaly, ascites) indicate intrahepatic cholestasis.
Symptoms of portal hypertension or portosystemic encephalopathy are pathognomonic for chronic liver damage.
In patients with hepatomegaly or ascites, distension of the jugular veins suggests 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 is 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.

Parenchymal jaundice

Parenchymal (hepatic) jaundice is true jaundice that occurs with various lesions of the liver parenchyma. 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 of capturing free (indirect) bilirubin from the blood, binding it with glucuronic acid to form non-toxic water-soluble bilirubin is reduced. -glucuronide (direct) and the release of the latter into the bile capillaries. As a result, the bilirubin content 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. A icteric discoloration of the skin and mucous membranes occurs. Parenchymal jaundice is characterized by skin color - saffron-yellow, reddish (“red jaundice”). Initially, the icteric color appears on the sclera and soft palate, then the skin becomes colored. Parenchymal jaundice is accompanied by itching of the skin, but less pronounced than mechanical jaundice, since the affected liver produces less bile acids (the accumulation of which in the blood and tissues causes this symptom). With a long course of parenchymal jaundice, the skin can acquire, as with mechanical jaundice, a greenish tint (due to the conversion of bilirubin deposited in the skin into biliverdin, which has a green color). The content of aldolase and aminotransferases, especially alanine aminotransferase, usually increases, and other liver tests are changed. Urine acquires a dark color (the color of beer) 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 secreted in feces and urobilin bodies in urine (which is an important laboratory sign for differentiating jaundice), which is normally 10:1-20:1, is significantly reduced in hepatocellular jaundice, reaching 1:1 in severe lesions.

... despite a noticeable improvement in treatment results, mortality after emergency operations for acute cholecystitis remains several times higher than during planned 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 commonly by stenosis of the papilla of Vater, cholangitis or compression of the terminal portion of the common bile duct by the head of the pancreas.

Clinic and diagnostics. Complication of acute cholecystitis with obstructive jaundice leads to the development of a pronounced syndrome of endogenous intoxication. The clinical picture is extremely diverse. This is explained by 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 that are characteristic of most patients can be traced.

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

In diagnosis, 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. Emergency surgery (within 2 - 3 hours from the moment of admission) is performed on patients with signs of peritonitis. Urgent surgery (24 – 48 hours) is performed on patients whose clinical picture of obstructive cholecystitis persists and the symptoms of the inflammatory process and endotoxicosis increase. For a delayed operation - in the “interval” - they are preparing for the sick, in whom, thanks to conservative therapy, an attack of acute cholecystitis is stopped (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 an attack of acute cholecystitis subsides, but obstructive jaundice persists, intensive preoperative preparation and topical diagnostics are carried out as soon as possible, not exceeding 5 days from the moment of admission.

Surgical treatment. An adequate radical surgical intervention is cholecystectomy with revision of the extrahepatic bile ducts. Each operation for cholecystitis should be accompanied by 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 patient’s reserve capabilities. Sometimes, if the patient’s condition is serious (senile age, concomitant diseases), cholecystolithostomy is performed. The most difficult and crucial moment is surgery on the common bile duct. Indications for choledochotomy can be absolute and relative.

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

Relative indications for choledochotomy: history of jaundice or before surgery; wrinkled 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 part 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 common bile duct and having an oval opening, retreating from the distal end by 2 - 4 cm, is carried out towards the porta hepatis; (3) according to Kehr (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, or when the pressure in the common bile duct increases, it additionally flows out.

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

At pinched stone duodenal nipple, cicatricial stenosis of the large duodenal nipple, if revision of the pancreatic duct is necessary, patients undergo transduodenal papillosphincterotomy with plastic surgery. Along with transduodenal papillosphincterotomy, endoscopic papillosphincterotomy is also widely used.

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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 of Roszdrav)

Department of Faculty Surgery, Faculty of Medicine

Academic medical history

Patient: ____, 73 years old

Main diagnosis: Acute calculous cholecystitis. Obstructive jaundice

Complications: no

Concomitant diseases: ischemic heart disease, angina pectoris 2 f. Cl. Atherosclerosis of the aorta, coronary and cerebral vessels. Arterial hypertension stage 3, risk 4. Acquired rheumatic heart disease. Mitral stenosis. Severe mitral insufficiency. 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: salesman

Place of residence: Saratov. _______

Received: 09/22/2011

Date of supervision: 06.10.2011- 08.10.2011

Clinical diagnosis: Acute calculous cholecystitis. Mechanical jaundice.

Complications: no

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

The patient has considered herself sick since December 2010, when she first began to experience intense, bursting pain in the upper abdomen, occurring after eating fatty foods and accompanied by nausea, general malaise, and a low-grade fever. She was in the hospital from December 22, 2010 to December 29, 2010, where after an ultrasound scan they discovered stones in the gall bladder. The operation was refused for health reasons (persistent form of atrial fibrillation, acquired rheumatic heart disease, mitral stenosis, severe mitral regurgitation, aortic insufficiency, circulatory decompensation in the pulmonary circulation, pulmonary hypertension). After the therapy, she was discharged with recommendations to follow a diet with limited consumption of fatty foods.

At first it’s spicy;

The flow is progressive;

According to pathogenesis, exacerbation of chronic.

Born on March 6, 1938 in Saratov in a working-class family. The material and living conditions in which it developed were satisfactory. In terms of physical and mental development, she did not lag behind her peers. Hygienic conditions and material support are currently satisfactory. Married, has an adult daughter and grandchildren. He has no bad habits and denies drug use. Diseases suffered in childhood: ARVI, tonsillitis. Denies diseases suffered during life (tuberculosis and contact with it; Botkin's disease; diabetes mellitus; sexually transmitted diseases - gonorrhea, syphilis, AIDS, malaria). Operations: uterine amputation in 1986. I have not traveled outside the region over the past year. There were no blood transfusions. Allergic reactions: not noted.

Status preasens universalis

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

The skin is icteric in color, dry, and warm to the touch. The conjunctiva of the eyelids and sclera are icteric. Skin turgor is reduced, hair growth is normal, female-type hair growth. The fingernails and toenails are unchanged.

Subcutaneous fat is overdeveloped and evenly distributed. It is painless on palpation. There is no swelling in the legs.

Lymph nodes are accessible to palpation, not enlarged, densely elastic consistency, painless, mobile, not fused to each other or to the surrounding tissue, the skin over them is not changed. The muscles are developed satisfactorily. There is no pain when palpated. Muscle tone is preserved.

There are no deformities in the bones of the skull, chest, spine, pelvis, limbs, as well as pain when palpating or tapping.

Joints of normal configuration. The skin over them is of normal color. When palpating the joints, their swelling and deformation, changes in the periarticular tissues, and pain are not noted. Full movements.

The thyroid gland is not visualized or palpated

RESPIRATORY SYSTEM

He makes no complaints.

Palpation

Without features.

Percussion

Topographic percussion:

The lower borders of the lungs.

Right lung:

l. parasternalis - 6th rib;

l. medioclavicularis - 7th rib;

l. axillaris media - 8th rib;

l. axillaris posterior - 8th rib;

l. scapularis - 9th rib;

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

Left lung:

l. parasternalis - 6th rib;

l. medioclavicularis - 6th rib;

l. axillaris anterior - 7th rib;

l. axillaris media - 8th rib;

l. axillaris posterior - 9th rib;

l. scapularis - 10th rib;

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

Boundaries of the upper edge of the lungs:

Right lung:

In front 3.5 cm above the collarbone.

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

Left lung:

In front 3 cm above the collarbone; Posteriorly at the level of the spinous process of the 7th cervical vertebra.

Comparative percussion.

A clear pulmonary sound is determined by percussion over symmetrical areas of the lungs.

Auscultation

Vesicular breathing throughout the lung fields.

THE CARDIOVASCULAR SYSTEM

He makes no complaints.

There is no pulsation at the base of the heart, in the area of the apex beat, or in the epigastric region.

Palpation

The apical impulse is determined along the 5th intercostal space 2 cm outward from the midclavicular line. Normal height, moderate strength, non-resistant. The pulse is symmetrical, frequency 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 the tones is muffled. Heart rate - 60 beats. per minute

URINARY SYSTEM

Complaints of darkening 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. There is no pain on palpation of the upper and lower ureteral points. On percussion, the bladder does not protrude above the pubic symphysis. There are no dysuric phenomena.

NEUROPSYCHOLOGICAL STUDY

No complaints.

Consciousness is clear, mood is calm. The reaction of the pupils to light is lively D=S.

DIGESTIVE SYSTEM

Complaints (at the time of supervision)

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 or rashes. The oral mucosa is icteric in color, clean, moist. The tongue is without a white coating, moist. Swallowing is free and painless.

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

Abdominal examination.

The abdomen is round in shape, swollen in the epigastric and paraumbilical region, asymmetrical, collaterals on the anterior surface of the abdomen and its lateral surfaces are not pronounced; 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. There are no dilations of the veins of the abdominal wall.

Percussion.

Percussion of the abdomen reveals tympanitis of varying severity. There is no accumulation of fluid in the abdominal cavity. There is no splashing noise. Ortner's sign is positive.

Approximate superficial palpation of the abdomen.

The stomach is soft. Pain is detected in the right hypochondrium, in the epigastric region. Ker's symptom is positive. The Shchetkin-Blumberg symptom is negative. When examining the “weak spots” of the anterior abdominal wall (umbilical ring, aponeurosis of the white line of the abdomen, inguinal rings), no hernial protrusions are formed.

For deep palpation of the abdomen using the Obraztsov-Strazhesko method:

Using percussion and stetoauscultic palpation, the lower border of the stomach is determined 3 cm above the navel.

The lesser curvature and the pylorus are not palpable; a splashing noise to the right of the midline of the abdomen (Vasilenko's symptom) is not detectable.

Auscultation.

When auscultating the abdomen, weakened peristaltic sounds are heard. There are no sounds of splashing or friction of the peritoneum.

The chair is aholic.

Boundaries of the liver according to Kurlov:

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

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

lower 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 dimensions according to Kurlov:

along the right midclavicular line - 11 cm;

along the anterior midline - 10 cm;

along the left costal arch - 8 cm.

Survey plan

General blood analysis

General urine analysis

Blood chemistry

Ultrasound of the abdominal organs

Fibrogastroduodenoscopy

X-ray of the chest organs

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

AST 147.2 units/l

Alpha amylase 34.0 units/l

General urine analysis.

Color dirty yellow

The reaction is acidic

Specific gravity 1009

Transparency is cloudy

Protein 0.09 g/l

Sugar negative

Acetone neg

Leukocytes 8-10 in p.s.

Red blood cells 4-6 in p.s. unchanged

Negative cylinders

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.(10/23/2011)

The liver is not enlarged, the contours are smooth, the parenchyma is homogeneous, there is an expansion of the intrahepatic ducts of the liver lobes. The gallbladder is irregularly shaped, dimensions 70*30 mm. The 5 mm wall is doubled and compacted. Multiple stones with a diameter of 0.5 to 1.1 cm. The common bile duct is expanded to 11-13 mm; stones up to 1.0 cm are identified in the lumen.

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 9.0x4.3 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 diverticula

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

Duodenal bulb: no deformations, normal lumen, normal contents, atrophic mucosa, no erosions or ulcers.

Conclusion: Chronic atrophic gastritis, duodenitis.

ECG: sinus rhythm, heart rate 60 per minute, the electrical axis of the heart is horizontal. Left atrial hypertrophy, left and right ventricular hypertrophy. Signs of rheumatic damage to the mitral and aortic valves.

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

Endoscopy + endoscopic retrograde cholangiography

The duodenoscope is inserted into the duodenum, in the lumen the bile, mucous membrane and large duodenal papilla are not changed. The orifice of the major duodenal papilla = 0.2 cm is fixed; the catheter is passed into the common bile duct. The bile ducts are contrasted and dilated. The common bile duct in the upper and middle third is up to 1.5-1.8 cm, in its middle third the stone is 1.5 to 2.0 cm. It is tightly adjacent to the walls, it is difficult to flow around with contrast, it is impossible to carry the instrument above the stone. The distal part of the common bile duct is up to 0.8 cm, making lithoextraction impossible and papilotomy not advisable

Summary of pathological symptoms

Spicy. Prolonged, intense pain in the right hypochondrium and epigastric region, which occurs when there is an error in diet.

General weakness.

Pressure increase 160/90 mmHg.

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

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

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

Leukocytosis.

Ultrasound shows 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 beyond the sternum, and is accompanied by nausea and vomiting. Laboratory tests will show N blood sugar, urine diastasis and bilirubin are not elevated. However, in acute MI there is a relationship between pain and exercise. Treated with NO drugs. Bladder symptoms are not detected. Ultrasound showed no changes in the liver and biliary tract. Characteristic changes on the ECG. While this patient has a connection between pain and consumption of fatty foods, vomiting bile brings short-term relief. Upon admission, positive symptoms were noted: Grekov-Ortner, Kera. The blood test shows leukocytosis, which indicates an inflammatory process. Characteristic changes according to ultrasound data.

This disease can also be differentiated from acute pancreatitis. In both cases, the pain is sharp, constant (sometimes increasing) in the epigastric region. The pain radiates posteriorly - into the back, spine, and lower back. Soon repeated profuse vomiting appears. The disease is associated with alcohol intake, there are no characteristic changes on the ECG. The blood test shows leukocytosis. However, acute pancreatitis is characterized by: No blistering symptoms are detected. A sharp increase in urine diastasis, but bilirubin is not increased, vomiting does not relieve pain. While in this patient, vomiting 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 a syndrome of impaired general condition, pain syndrome (pain in the lower 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 falx 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 main disease. But the level of amylase in the blood is not elevated and the diagnosis of acute pancreatitis can be refuted.

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

Based on the patient’s complaints of a feeling of heaviness and bursting pain in the right hypochondrium, nausea, it is possible to make a diagnostic assumption about the presence of chronic hepatitis. However, with chronic hepatitis, even with its benign course, an objective examination reveals a slight enlargement of the liver, and upon palpation 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. Her dimensions are normal. When collecting an anamnesis, chronic hepatitis is characterized by either a previous infectious disease (brucellosis, syphilis, Botkin's disease) or toxic poisoning (industrial, household, drugs). When collecting anamnesis, the patient denied contact with the above infectious diseases. Based on the nature of the disease (chronic hepatitis), we can expect the patient to experience periods of exacerbation in the clinical picture, during which he is bothered by weakness, fever, itching, and yellowness of the skin. But in the 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 with chronic hepatitis the most painful point does not exist; the entire area of the right hypochondrium hurts. Also, the jaundice of the skin is not associated with chronic hepatitis, since endoscopic retrograde cholangiography revealed a stone of 1.5 to 2.0 cm in the middle third of the common bile duct, 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 the direct bilirubin fraction (117.8 mmol/l.). As a result of obstructive jaundice, the patient has acholic stool and dark-colored urine, which is not typical for the clinic of chronic hepatitis. Due to the absence of a characteristic clinical picture, the absence of contact with infectious diseases and poisoning with toxic substances in the anamnesis, as well as periods of exacerbation, the assumption that the supervised patient has chronic hepatitis can be refuted.

Final diagnosis

Main - Chronic calculous cholecystitis, exacerbation phase.

Complications - no.

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

Acute calculous cholecystitis is diagnosed on the basis of:

The patient's complaints: 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 and moderately painful in the right hypochondrium. Positive symptoms: Grekov-Ortner, Kera.

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

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

Etiology and pathogenesis of cholelithiasis

There are two types of gallstones: cholesterol and pigment.

The following factors are believed to contribute to the formation of stones:

Female;

Age 40 years and above;

Fat-rich foods;

Metabolic diseases;

Heredity;

Pregnancy;

Stagnation of bile;

Infection in the cavity of the gallbladder.

Cholesterol stones in the gall bladder are formed due to disruption of the relationship between the main lipids of bile, which are cholesterol, phospholipids and bile acids. Cholesterol stones are formed due to cholesterol, and pigment stones are formed due to bilirubin.

Cholesterol is able to be released into bile exclusively in the form of 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 is called lithogenic. C, they spontaneously form complex micelles formed externally by bile acids located so that cylinder-like structures arise, from the ends of which the hydrophilic groups of lecithin (phospholipid) face the aqueous environment ). Inside the micelle there are cholesterol molecules, which are isolated from the aqueous environment on all sides. In an aqueous environment at a temperature of 37, the molecules of all three main lipids are amphiphilic and, being in an aqueous environment at a temperature of 37

Theoretically, the following reasons for the occurrence of bile oversaturation 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 practically never occurs. Their synthesis always turns out to be sufficient. Therefore, the first two reasons determine the frequency of lithogenic bile. Moreover, most cholesterol stones have a pigment center, although the pigment is not the center of initiation, since 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, turning normal pigments into insoluble compounds. More often this happens 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 initiation processes, it was found that for the formation of stones, the presence of an inflammatory process in the wall of the gallbladder is necessary. Moreover, it can be caused not only by a microorganism, but also by a certain composition of food, allergic and autoimmune processes. In this case, the integumentary epithelium is reconstructed into goblet cells, which produce a large amount of mucus, the cylindrical epithelium is flattened, microvilli are lost, and absorption processes are disrupted. In the niches of the mucosa, water and electrolytes are absorbed, and colloidal solutions of mucus are converted into a gel. When the bladder contracts, lumps of gel slip out of their niches and stick together, forming the rudiments of gallstones. The stones then grow and saturate 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 are the presence of microflora in the cavity of the bladder and a violation of the outflow of bile.

The main importance is given to infection. Pathogenic microorganisms can enter the bladder in three ways: hematogenous, lymphogenous, enterogenous. The following organisms are most often 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 in the elongated and tortuous cystic duct, and its narrowing. According to statistics, up to 85-90% of cases of acute cholecystitis occur against the background of cholelithiasis. If sclerosis or atrophy develops in the bladder wall, the contractile and drainage functions of the gallbladder suffer, which leads to a more severe course of cholecystitis with profound morphological disorders.

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

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 cavity of the gallbladder, which block the lumen of the duct. Thus, the patient has reasons for the development of cholelithiasis. female; age above 40 years, foods rich in fats; A sedentary lifestyle leads to an increase in cholesterol levels.

Complications of calculous cholecystitis:

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

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

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

Pancreatitis.

Gallbladder perforation (occurs in up to 15% of patients).

Treatment tactics for 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 are widely used - papilosphinkerotomy 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 speed up the examination of the patient and clarify the diagnosis, the time of the operation can be reduced to 3-5 days. In this relatively short period of time, it is possible to thoroughly examine the patient and assess the functional state of various body systems, as well as fully prepare the patient for surgery.

When obstructive jaundice is combined with acute cholecystitis, one should adhere to active tactics, 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. During 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 surgical risk for acute cholecystitis, laparoscopic cholecystostomy is performed, and to resolve jaundice, endoscopic transpapillary intervention is performed, combined with nasobiliary drainage in case of purulent cholangitis. Endoscopic operations on the gallbladder and bile ducts make it possible to 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 disturbance 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), whose half-life in the body is 14-30 days, but to amino acids, which are used by the body for the synthesis of organ proteins. Such drugs include casein hydrolyzate, aminosol, alvezin, vamin, etc. Albumin deficiency must begin to be replenished 3-4 days before surgery by transfusion of a 10-20% solution in the 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 the resistance of hepatocytes to hypoxia, it is recommended to administer concentrated glucose solutions in a volume of 500-1000 ml per day. To increase the efficiency of metabolism of intravenously administered glucose, it is necessary to add insulin, and its dose must be slightly higher than the standard one in order for its metabolic effect to manifest itself.

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, Karsil, Sirepar, etc. They should be prescribed in the immediate postoperative period and should be abstained until cholestasis is eliminated, so as not to cause a disruption 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 BCC and correcting ABS. Antibacterial therapy should be aimed at preventing purulent-septic complications. The most effective regimen of antibacterial therapy is the intraoperative administration of antibacterial drugs.

Carrying out pathogenetically based infusion-drug therapy in patients with calculous cholecystitis and obstructive jaundice makes it possible to ensure a favorable course of the postoperative period and prevent the development of acute liver, kidney and cardiovascular failure.

Indications for surgery

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

Taking into account the patient’s age, obesity and concomitant diseases, the surgical method chosen was 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 the operation: cholecystectomy, choledocholithotomy. Drainage of the 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: ETN

Operating room m/s: Bugrim S.S.

Operation description

Under the ETN, a transrectal incision was made in the right hypochondrium. There is a pronounced adhesive process in the subhepatic space. The liver is not enlarged. During inspection, the entire gallbladder is filled with stones, with a thickened wall. The common bile duct is dilated to 1.5 cm; a calculus is palpated in its lumen up to 1.5 cm; it is fixed. The gallbladder was opened and all stones were removed. Cholecystectomy from the fundus with ligation of the cystic artery and suture on the gallbladder bed. The cystic duct is not identified, Merisi syndrome is detected. The defect in the hepatic duct is up to 0.5 cm, it is sutured. A choledochotomy was performed over the stone, which was removed in parts. The common bile duct is washed. The probe passes freely into the duodenum. Kera drainage installed. The choledochotomy opening is sutured to drainage. Checking blood and bile flow - dry. Drainage is connected to the Winslov hole. Both drains were removed through two separate punctures in the right hypochondrium. Layered suture of the wound. Aseptic dressing.

Specimen: gallbladder 10×4×3 cm, the wall is thickened 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 only 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 a few patients. Often the cause of suffering in these cases is diseases of the hepatoduodenal-pancreatic system.

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

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

Strictures most often develop due to damage to the bile ducts 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, therefore ligation of the cystic duct is recommended to be carried out at a distance of 0.5 cm from the common bile duct. Cicatricial strictures may also occur as a result of external drainage of the ducts. The main clinical signs of a stricture of the common bile duct are obstructive jaundice and the phenomenon of recurrent cholangitis. However, with partial obstruction of the duct, a syndrome of moderate cholestasis is observed.

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

It is customary to distinguish between true and false relapses of stone formation. True relapse refers to newly formed stones after cholecystectomy; false relapse refers to stones that were not recognized during surgery (residual).

A long stump of the cystic duct or gallbladder may cause the development 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 that the rest of the stump may expand, small neuromas may develop at its bottom, and its walls may become infected with the development of an inflammatory process.

In rare cases, the cause of an unsatisfactory outcome of surgical treatment of cholelithiasis is a common bile duct cyst, most often an aneurysmal dilatation of the walls of the common bile duct between the gallbladder and the 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 serious complications after cholecystectomy. Most often it develops with stenosis of the terminal part of the common bile duct, 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 and cholestasis. The development of cholestasis contributes to the ascending spread of infection. Infection is the main factor leading to cholangitis during biliary tract surgery. Acute septic cholangitis is manifested by jaundice, chills, a sharp increase in body temperature, heavy sweat, and thirst. On examination, severe pain is noted in the right hypochondrium, which intensifies with tapping along the costal arch (Ortner's symptom). The size of the liver is not significantly increased and quickly becomes normal as the patient’s condition improves. The spleen may be enlarged, indicating parenchymal liver damage or spreading infection. Jaundice is accompanied by discolored stool and dark urine.

Laboratory tests reveal hyperbilirubinemia due to the direct direct fraction, increased alkaline phosphatase activity, leukocytosis, and a band shift to the left. The chronic form of cholangitis does not have a pronounced clinical picture. You may note weakness, constant sweating, periodically low-grade fever, and mild chills. A characteristic feature of this disease is an increase in ESR.

Changes in the area 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. Damage to the major duodenal papilla is associated with the appearance of relapse of pain, jaundice and cholangitis after cholecystectomy.

Liver diseases are sometimes the cause of unsatisfactory health of patients after cholecystectomy.

6.10.11. The condition is stable, without negative dynamics. Pulse 72 beats/min, blood pressure 120/80, body temperature 36.8° C. Hemodynamics are stable. Vesicular breathing. 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 impaired.

Destination:

Bed rest.

Sol. Glucosae10% - 300 ml

Omez 20 mg 2 times.

Erinite 1 tablet 3 times.

Thrombo ACC 1 tablet 1 time.

Cardarone 100 mg 1 time.

Egilok 12.5 mg 2 times.

Panangin 1 tablet 3 times.

Prednisolone 30 mg 2 times IM.

The condition is stable without negative dynamics. The patient is more active. Jaundice decreases. Pulse 68 beats/min, blood pressure 110/70, body temperature 36.7° C. Hemodynamics are stable. Vesicular breathing. 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. By Kera drainage 200 ml. bile.

Destination:

Bed rest.

Sol. Glucosae10% - 300 ml

Sol. Kalii Chloridi 4% - 80 ml.

Sol/ Magnesii Sulfatis 25% - 10 ml.

Insulin 3 units. slow intravenous drip

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

Omez 20 mg 2 times.

Erinite 1 tablet 3 times.

Thrombo ACC 1 tablet 1 time.

Cardarone 100 mg 1 time.

Egilok 12.5 mg 2 times.

Panangin 1 tablet 3 times.

Prednisolone 30 mg 2 times IM.

8.10.11. The condition is stable, without negative dynamics. Pulse 68 beats/min, blood pressure 110/70, body temperature 36.5° C. Hemodynamics are stable. Vesicular breathing. The tongue is moist and clean. The abdomen is soft and not swollen. Peristalsis is heard. Through the Kera drainage 150 ml of bile. Diuresis is not impaired.

Destination:

Bed rest.

Sol. Glucosae10% - 300 ml

Sol. Kalii Chloridi 4% - 80 ml.

Sol/ Magnesii Sulfatis 25% - 10 ml.

Insulin 3 units. slow intravenous drip

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

Omez 20 mg 2 times.

Erinite 1 tablet 3 times.

Thrombo ACC 1 tablet 1 time.

Cardarone 100 mg 1 time.

Egilok 12.5 mg 2 times.

Panangin 1 tablet 3 times.

Prednisolone 30 mg 2 times IM.

Patient _____, 73 years old, was urgently hospitalized at City Clinical Hospital No. 3 named after. Peacemakers SSMU. considers herself sick since December 2010, when she first began to be bothered by intense, bursting pain in the upper abdomen, occurring after eating fatty foods and accompanied by nausea, general malaise, and a fever elevated to subfebrile levels. She was in the hospital from December 22, 2010 to December 29, 2010, where after an ultrasound scan they discovered stones in the gall bladder. The operation was refused due to health reasons. After the therapy, she was discharged with recommendations to follow a diet with limited consumption of fatty foods.

The last deterioration of the patient’s condition was on September 16, 2011, when, after an error in diet, intense pain appeared in the right hypochondrium, nausea, and vomiting. Similar attacks have been reported previously. An outpatient ultrasound revealed gallbladder stones. The patient was treated independently with antispasmodics without a positive effect. 09/22/2011. noted yellowing of the skin and sclera, darkening of the urine. She sought medical help and was hospitalized in the 3rd City Clinical Hospital named after. Mirotvortseva S. R. SSMU in ECHO. An objective examination revealed: grade 2 obesity, the tongue is covered with a white coating, the abdomen is soft on palpation, painful in the right hypochondrium, positive Ortner’s sign. In the hospital, as part of the examination, the patient was prescribed: General blood test, general urinalysis, biochemical blood test, ultrasound of the abdominal organs, fibrogastroduodenoscopy, ECG, chest radiography, endoscopy + endoscopic retrograde cholangiography.

Based on the above-described anamnesis, objective examination data, life history, and ultrasound data of the abdominal organs (there are stones with a diameter of 0.5 to 1.0 cm in the lumen of the gallbladder), a diagnosis was made: cholelithiasis. Acute calculous cholestitis. Mechanical jaundice.

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

Preoperative preparation included: additional research methods, consultation with a therapist, as well as preoperative drug preparation.

The operation was performed on September 28, 2011, without complications.

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

If the postoperative period after cholecystectomy is favorable:

visiting a surgeon at the clinic at least once a week to assess the general condition of the patient and assess the condition of the postoperative wound;

compliance with diet No. 5; complaint cholecystitis bile disease

removal of sutures on the 7-8th day;

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

visits 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 and the effectiveness of the therapy; appointment of the necessary laboratory examination, consultation with specialists, correction of the therapy;

drug and non-drug treatment of complications;

limiting heavy physical activity for 6 months;

symptomatic therapy (in the presence of concomitant diseases).

The prognosis for life and health is questionable. Quality of life is reduced.

BIBLIOGRAPHY:

“Surgical Diseases” - a textbook for students of medical universities. Moscow. "Medicine". 1997.

“Workshop on Faculty Surgery” - educational and methodological manual edited by prof. Rodionova V.V. Moscow 1994.

“Course of propaedeutics of internal diseases in diagrams and tables” V.V. Shedov. I.I. Shaposhnikov. Moscow 1995

Faculty surgery course 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. “Guide to emergency surgery of the abdominal organs”, M., 1990

Skripnichenko D.F. “Emergency abdominal surgery”, Kyiv, “Health”, 2001.

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Acute cholecystitis complicated by obstructive jaundice

... despite a noticeable improvement in treatment results, mortality after emergency operations for acute cholecystitis remains several times higher than during planned surgical interventions.

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

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Start of activity (date): 06/25/2013 06:35:00
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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 of Roszdrav)

Department of Faculty Surgery, Faculty of Medicine

Academic medical history

Patient: ____, 73 years old

Main diagnosis: Acute calculous cholecystitis. Obstructive jaundice

Complications: no

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: salesman

Place of residence: Saratov. _______

Received: 09/22/2011

Date of supervision: 06.10.2011- 08.10.2011

Clinical diagnosis: Acute calculous cholecystitis. Mechanical jaundice.

Complications: no

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

At first it’s spicy;

The flow is progressive;

According to pathogenesis, exacerbation of chronic.

preasens universalis

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

Subcutaneous fat is overdeveloped and evenly distributed. It is painless on palpation. There is no swelling in the legs.

There are no deformities in the bones of the skull, chest, spine, pelvis, limbs, as well as pain when palpating or tapping.

The thyroid gland is not visualized or palpated

RESPIRATORY SYSTEM

He makes no complaints.

Palpation

Without features.

Percussion

Topographic percussion:

The lower borders of the lungs.

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

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

Boundaries of the upper edge of the lungs:

Right lung:

In front 3.5 cm above the collarbone.

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

Left lung:

In front 3 cm above the collarbone; Posteriorly at the level of the spinous process of the 7th cervical vertebra.

Comparative percussion.

A clear pulmonary sound is determined by percussion over symmetrical areas of the lungs.

Auscultation

Vesicular breathing throughout the lung fields.

THE CARDIOVASCULAR SYSTEM

He makes no complaints.

There is no pulsation at the base of the heart, in the area of the apex beat, or in the epigastric region.

Palpation

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

Auscultation

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

URINARY SYSTEM

Complaints of darkening the color of urine.

NEUROPSYCHOLOGICAL STUDY

No complaints.

Consciousness is clear, mood is calm. The reaction of the pupils to light is lively D=S.

DIGESTIVE SYSTEM

Complaints (at the time of supervision)

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

Examination of the oral cavity.

Abdominal examination.

Percussion.

Percussion of the abdomen reveals tympanitis of varying severity. There is no accumulation of fluid in the abdominal cavity. There is no splashing noise. Ortner's sign is positive.

Approximate superficial palpation of the abdomen.

For deep palpation of the abdomen using the Obraztsov-Strazhesko method:

Using percussion and stetoauscultic palpation, the lower border of the stomach is determined 3 cm above the navel.

The lesser curvature and the pylorus are not palpable; a splashing noise to the right of the midline of the abdomen (Vasilenko's symptom) is not detectable.

Auscultation.

When auscultating the abdomen, weakened peristaltic sounds are heard. There are no sounds of splashing or friction of the peritoneum.

The chair is aholic.

Boundaries of the liver according to Kurlov:

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

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

lower 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 dimensions according to Kurlov:

along the right midclavicular line - 11 cm;

along the anterior midline - 10 cm;

along the left costal arch - 8 cm.

Survey plan

General blood analysis

General urine analysis

Blood chemistry

Ultrasound of the abdominal organs

Fibrogastroduodenoscopy

X-ray of the chest organs

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/L147.2 U/L

Alpha amylase 34.0 units/l

General urine analysis.

Color dirty yellow

The reaction is acidic

Specific gravity 1009

Transparency is cloudy

Protein 0.09 g/l

Sugar negative

Acetone neg

Red blood cells 4-6 in p.s. unchanged

Negative cylinders

Slime a little

No bacteria

Salts negative

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.(10/23/2011)

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 diverticula

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

Duodenal bulb: no deformations, normal lumen, normal contents, atrophic mucosa, no erosions or ulcers.

Conclusion: Chronic atrophic gastritis, duodenitis.

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

Endoscopy + endoscopic retrograde cholangiography

Summary of pathological symptoms

Spicy. Prolonged, intense pain in the right hypochondrium and epigastric region, which occurs when there is an error in diet.

General weakness.

Pressure increase 160/90 mmHg.

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

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

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

Leukocytosis.

Ultrasound shows acute calculous cholecystitis.

Differential diagnosis

Final diagnosis

Main - Chronic calculous cholecystitis, exacerbation phase.

Complications - no.

Acute calculous cholecystitis is diagnosed on the basis of:

The patient's complaints: 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 and moderately painful in the right hypochondrium. Positive symptoms: Grekov-Ortner, Kera.

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

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

Etiology and pathogenesis of cholelithiasis

There are two types of gallstones: cholesterol and pigment.

The following factors are believed to contribute to the formation of stones:

female;

age 40 years and above;

foods rich in fats;

metabolic diseases;

heredity;

pregnancy;

bile stagnation;

infection in the gallbladder cavity.

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 is called lithogenic. ° C, they spontaneously form complex micelles formed externally by bile acids arranged so that cylinder-like structures arise, with the hydrophilic groups of lecithin (phospholipid) facing the aqueous medium at their ends. Inside the micelle there are cholesterol molecules, which are isolated from the aqueous environment on 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 environment at a temperature of 37

Theoretically, the following reasons for the occurrence of bile oversaturation with cholesterol can be imagined:

) its excessive secretion into bile;

) decreased secretion of bile acids and phospholipids into bile;

) a combination of these reasons.

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

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

“Workshop on Faculty Surgery” - educational and methodological manual edited by prof. Rodionova V.V. Moscow 1994.

“Course of propaedeutics of internal diseases in diagrams and tables” V.V. Shedov. I.I. Shaposhnikov. Moscow 1995

Faculty surgery course 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. “Guide to emergency surgery of the abdominal organs”, M., 1990

Skripnichenko D.F. “Emergency abdominal surgery”, Kyiv, “Health”, 2001.

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

Main signs of organ enlargement

Reasons for changing the size of the gastrointestinal tract

Diagnosis and treatment

Bile duct obstruction

Inflammation of the gallbladder (cholecystitis)

Dyskinesia of the gallbladder and bile ducts

Cholelithiasis

Post-operative reasons

Tumors

Likely consequences and prognosis

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

Classification of jaundices

Jaundice Clinic

Parenchymal jaundice

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Acute cholecystitis complicated by obstructive jaundice