Acute inflammation of the gallbladder is one of the most common complications of gallstone disease.
Etiology and pathogenesis. The disease occurs in approximately 25% of patients with chronic calculous cholecystitis. However, in 5-10% of patients with acute cholecystitis, stones in the gallbladder are not detected. The main reasons
The development of acute cholecystitis is caused by microflora in the lumen of the bladder, disruption of the outflow of bile (most often due to blockage of the neck or cystic duct by a calculus), stretching of the walls of the bladder and associated ischemia of its wall. The microflora enters the gallbladder via the ascending route from the duodenum, descending via the bile flow from the liver, where the infection enters via the bloodstream, and, less commonly, through the lymphogenous and hematogenous routes.
In the vast majority of patients with chronic calculous cholecystitis, bile contains microflora. However, an acute inflammatory process occurs only when the outflow of bile is disrupted. Of secondary importance are ischemia of the bladder wall and the damaging effect of pancreatic juice and the pancreas on the mucous membrane of the bladder during pancreatobiliary reflux.
Clinical picture and diagnosis. The following clinical and morphological forms of acute cholecystitis are distinguished: catarrhal, phlegmonous and gangrenous (with or without perforation of the gallbladder) cholecystitis.
Catarrhal cholecystitis is characterized by intense constant pain in the right hypochondrium, epigastric region with irradiation to the lumbar region, right shoulder blade, shoulder, and right half of the neck. At the onset of the disease, pain can be paroxysmal in nature due to increased contraction of the gallbladder wall. aimed at eliminating occlusion of the bladder neck or cystic duct. Vomiting of gastric and then duodenal contents often occurs, which does not bring relief to the patient. Body temperature rises to subfebrile levels. Moderate tachycardia develops up to 100 beats per minute. sometimes a slight increase in blood pressure. The tongue is moist and may be coated with a whitish coating. The abdomen participates in the act of breathing; there is some lag in the upper parts of the right half of the abdominal wall in the act of breathing. When palpating the abdomen, sharp pain occurs in the right hypochondrium, especially in the area of ​​​​the projection of the gallbladder. Tension of the abdominal wall muscles is absent or slightly expressed. Positive symptoms of Ortner, Murphy, Georgievsky-Mussi. In 20% of patients, an enlarged, moderately painful gallbladder can be felt. The blood test shows moderate leukocytosis (10-12*109/l).
Catarrhal cholecystitis, like hepatic colic, in most patients is provoked by errors in diet. Unlike colic, an attack of acute catarrhal cholecystitis is longer lasting (up to several days) and is accompanied by nonspecific symptoms of the inflammatory process (hyperthermia, leukocytosis, increased ESR).
Phlegmonous cholecystitis has more pronounced clinical symptoms. The pain is much more intense than with the catarrhal form of inflammation. They intensify when breathing, coughing, or changing body position. Nausea and repeated vomiting occur more often, the patient’s general condition worsens, body temperature reaches febrile levels, tachycardia increases to 110-120 beats per minute. The abdomen is somewhat swollen due to intestinal paresis; when breathing, the patient spares the right half of the abdominal wall, bowel sounds are weakened. On palpation, sharp pain occurs in the right hypochondrium, muscle protection is expressed: it is often possible to detect an inflammatory infiltrate or an enlarged, painful gallbladder. A positive Shchetkin-Blumberg sign is determined in the right upper quadrant of the abdomen. Ortner's and Murphy's symptoms. Georgievsky-Mussi are also positive. A blood test reveals leukocytosis up to 18-22"109/l with a shift of the formula to the left, an increase in ESR.
A distinctive feature of the phlegmonous process is the transition of inflammation to the parietal peritoneum. The gallbladder is enlarged in size, its wall is thickened, and has a purple-bluish color: there is fibrinous plaque on the peritoneum covering it, and purulent exudate in the lumen. If in the catarrhal form of acute cholecystitis, microscopic examination reveals only initial signs of inflammation (swelling of the bladder wall, hyperemia), then in phlegmonous cholecystitis, pronounced infiltration of the bladder wall with leukocytes, impregnation with purulent exudate, sometimes with the formation of ulcers, is revealed.
Gangrenous cholecystitis is characterized by a rapid clinical course, usually a continuation of the phlegmonous stage of inflammation, when the body's defenses are unable to cope with the virulent microflora. Symptoms of severe intoxication with symptoms of local or general purulent peritonitis come to the fore, which is especially pronounced with perforation of the gallbladder wall. The gangrenous form of inflammation is observed more often in elderly and senile people with reduced regenerative abilities of tissues, decreased reactivity of the body and impaired blood supply to the gallbladder wall due to atherosclerotic damage to the abdominal part of the aorta and its branches. When the inflammatory process transforms into a gangrenous form, there may be some reduction in pain and an apparent improvement in the general condition of the patient, which is associated with the death of sensory nerve fibers in the gallbladder. However, quite quickly this period of imaginary well-being is replaced by increasing intoxication and symptoms of widespread peritonitis. The condition of the patients is serious, they are lethargic and inhibited. The body temperature is febrile, severe tachycardia develops (up to 120 beats per minute or more). Breathing becomes rapid and shallow. The tongue is dry; the abdomen is swollen due to intestinal paresis, its right parts do not participate in the act of breathing, peristalsis is sharply suppressed, and in general peritonitis it is absent. The protective tension of the muscles of the anterior abdominal wall is expressed, symptoms of peritoneal irritation are revealed. Percussion sometimes detects dullness of sound over the right lateral canal of the abdomen. Blood and urine tests show high leukocytosis with a sharp shift in the leukocyte formula to the left, accelerated ESR, disturbances in the electrolyte composition of the blood and acid-base state, proteinuria, cylindriuria (signs of destructive inflammation and severe intoxication).
Acute cholecystitis in elderly and especially senile people with a decrease in the general reactivity of the body and the presence of concomitant diseases has a mild course. Gangrenous cholecystitis most often develops in this category of people. Old people often do not experience intense pain, the protective tension of the muscles of the anterior abdominal wall is erased, and there is no high leukocytosis. In this regard, elderly patients may experience quite serious difficulties in diagnosing acute cholecystitis, assessing their condition and choosing a treatment method.
In typical cases, the diagnosis of acute cholecystitis does not present serious problems. However, a similar clinical picture can occur in acute appendicitis, acute pancreatitis, perforated gastric and duodenal ulcers, renal colic and some other diseases of the abdominal organs.
Among the instrumental methods for diagnosing acute cholecystitis, the leading role belongs to ultrasound. In this case, it is possible to determine the thickening of the gallbladder wall, stones in its lumen, and exudate in the subhepatic space. Among the invasive research methods, laparoscopy has become widespread, allowing visual assessment of the nature of morphological changes in the gallbladder. Both of these methods can also be used as therapeutic procedures in combination with puncture of the gallbladder and its external drainage.
Treatment. All patients with acute cholecystitis should be in the hospital under constant supervision of a surgeon. If there are symptoms of local or widespread peritonitis, emergency surgery is indicated. In other cases, conservative treatment is carried out. Limit food intake, allowing only alkaline drinks (acidic gastric contents, proteins and fats stimulate the release of intestinal hormones that enhance the motor activity of the gallbladder and the secretory activity of the pancreas). Non-narcotic analgesics are used to reduce pain. It is not advisable to use narcotic analgesics, since due to their pronounced analyzing effect they can significantly reduce pain and objective signs of inflammation (peritoneal symptoms) and complicate diagnosis.
Narcotic analgesics, causing spasm of the sphincter of Oddi, contribute to the development of biliary hypertension and disruption of the outflow of pancreatic juice, which is extremely undesirable in acute cholecystitis. Pain can be reduced through the use of anticholinergic antispasmodics (atropine, platifillin, baralgin, no-spa, etc.) agents. An ice pack is placed on the area of ​​the right hypochondrium to reduce blood flow to the inflammatory organ. The use of a warm heating pad is absolutely unacceptable, since this significantly increases the blood supply to the gallbladder, which leads to further progression of the inflammatory process with the development of destructive changes. To suppress the activity of microflora, broad-spectrum antibiotics are prescribed, with the exception of tetracycline drugs that have hepatotoxic properties. For detoxification and parenteral nutrition, infusion therapy is prescribed in a total volume of at least 2.0-2.5 liters of solutions per day. During treatment, the patient is constantly monitored. Subjective sensations and objective symptoms of the disease are taken into account. It is advisable to keep an individual observation card, in which the pulse rate, blood pressure, body temperature, and the number of leukocytes in the blood are noted every 4-6 hours. This greatly facilitates monitoring of the patient, allows one to evaluate the effectiveness of the treatment, and judge the course of the inflammatory process.
In acute cholecystopancreatitis, the complex of drug therapy should also include drugs used to treat acute pancreatitis.
In most patients, it is possible to relieve an attack of acute cholecystitis. During the process of observation and treatment, it is necessary to examine the patient. To identify stones in the gallbladder, it is advisable to perform an ultrasound. If they are detected and there are no contraindications (severe diseases of vital organs), it is advisable to operate the patient as planned 24-72 hours or 2-3 weeks after the acute attack subsides.
If, against the background of the treatment of acute cholecystitis, the patient’s condition does not improve within 48-72 hours, abdominal pain and protective tension of the abdominal wall persist or intensify, the pulse quickens, remains at a high level or the temperature rises, leukocytosis increases, then urgent surgical intervention is indicated for prevention of peritonitis and other severe complications.
In recent years, punctures and external drainage of the gallbladder have been successfully used to treat acute cholecystitis in patients with increased surgical risk. Under the control of a laparoscope or ultrasound, the gallbladder is punctured, its infected contents (bile, pus) are evacuated through the liver tissue, after which a flexible plastic catheter is installed in the lumen of the bladder for aspiration of the contents and local administration of antibiotics. This allows you to stop the progression of the inflammatory process, including the development of destructive changes in the wall of the gallbladder, quickly achieve a positive clinical effect, and avoid forced surgical interventions that are risky for the patient at the height of acute cholecystitis and without proper preoperative preparation. This technique is appropriate for elderly and senile people with an extremely high operational risk.
The situation becomes significantly more complicated with the development of obstructive jaundice against the background of acute cholecystitis. This complication threatens the patient with cholangitis, damage to hepatocytes, further aggravation of intoxication with the possible development of hepatic-renal failure. Obstructive jaundice often develops in elderly and senile people, whose compensatory capabilities of the body are very limited. Surgery against the background of acute cholecystitis in such patients poses a fairly high risk. In this situation, urgent endoscopic papillotomy is a rather promising direction. Through the biopsy channel of the duodenoscope, a thin cannula is inserted into the major duodenal papilla, after which its upper wall is dissected using a special papillotome. In this case, the stones either leave the ducts on their own. or they are removed with special tweezers, using a Dormia loop (basket) or a Fogarty probe. This manipulation allows you to eliminate biliary and pancreatic hypertension, reduce jaundice and intoxication. Subsequently, gall bladder surgery is performed as planned.
Cholecystectomy is the main surgical intervention performed for acute cholecystitis. Removing the gallbladder can present significant difficulties due to pronounced inflammatory changes in it and the surrounding tissues. Therefore, it is recommended to remove the bubble “from the bottom”. Cholecystectomy should be supplemented by intraoperative examination of the extrahepatic bile ducts (cholangiography). If choledocholithiasis or stenosis of the terminal part of the common bile duct is detected, the same manipulations are performed that are usually done in similar cases during planned operations in patients with chronic calculous cholecystitis (choledochotomy, T-shaped drainage, etc.). Drainage is left in the abdominal cavity to control blood and bile leakage.
Choleistostomy with removal of stones and infected contents of the gallbladder is indicated in rare cases as a necessary measure in the general serious condition of the patient and massive inflammatory infiltrate around the gallbladder, especially in elderly and senile people. This operation only allows to eliminate acute inflammatory changes in the wall of the gallbladder. In the long term after surgery, as a rule, stones form in the gallbladder again and patients have to be operated on again.
Mortality after cholecystectomy performed for acute cholecystitis. is 6-8%, reaching 15-20% in elderly and senile people.

Acute cholecystitis- symptoms and treatment

What is acute cholecystitis? We will discuss the causes, diagnosis and treatment methods in the article by Dr. E. V. Razmakhnin, a surgeon with 22 years of experience.

Definition of disease. Causes of the disease

Acute cholecystitis is a rapidly progressing inflammatory process in the gallbladder. Stones located in this organ are the most common cause of this pathology.

About 20% of patients admitted to the emergency surgical hospital are patients with complicated forms, which include acute cholecystitis. In elderly patients, this disease occurs much more often and is more severe due to the large number of existing somatic diseases. In addition, with age, the incidence of gangrenous forms of acute cholecystitis increases. Acalculous acute cholecystitis is uncommon and is a consequence of infectious diseases, vascular pathology (cystic artery thrombosis) or sepsis.

The disease is usually provoked errors in diet - intake of fatty and spicy foods, which leads to intense bile formation, spasm of sphincters in the biliary tract and biliary hypertension.

Contributing factors are stomach diseases , and in particular gastritis with low acidity. They lead to a weakening of protective mechanisms and the penetration of microflora into the biliary tract.

At cystic artery thrombosis against the background of pathology of the blood coagulation system and atherosclerosis, the development of a primary gangrenous form of acute cholecystitis is possible.

Provoking factors if present cholelithiasis Physical activity, “shaky” riding, which leads to the displacement of the stone, blockage of the cystic duct and subsequent activation of the microflora in the lumen of the bladder, can also serve.

Existing cholelithiasis does not always lead to the development of acute cholecystitis; it is quite difficult to predict this. Throughout life, stones in the lumen of the bladder may not manifest themselves, or at the most inopportune moment they can lead to a serious complication that is life-threatening.

If you notice similar symptoms, consult your doctor. Do not self-medicate - it is dangerous for your health!

The clinical picture of the disease includes pain, dyspeptic and intoxication syndromes.

Typically, the onset of the disease is manifested by hepatic colic: intense pain in the right hypochondrium, radiating to the lumbar, supraclavicular region and epigastrium. Sometimes, in the presence of symptoms of pancreatitis, pain can become girdling. The epicenter of pain is usually localized at the so-called Kehr's point, located at the intersection of the outer edge of the right rectus abdominis muscle and the edge of the costal arch. At this point the gallbladder comes into contact with the anterior abdominal wall.

The appearance of hepatic colic is explained by sharply increasing biliary (biliary) hypertension against the background of a reflex spasm of the sphincters located in the biliary tract. Increased pressure in the biliary system leads to enlargement of the liver and stretching of the Glissonian capsule, which covers the liver. And since the capsule contains a huge number of pain receptors (i.e. noceroreceptors), this leads to the occurrence of pain syndrome.

The development of the so-called cholecystocardial Botkin syndrome is possible. In this case, with acute cholecystitis, pain occurs in the heart area, and even changes in the ECG may appear in the form of ischemia. Such a situation can mislead the doctor, and as a result of overdiagnosis (erroneous medical conclusion) of coronary disease, he runs the risk of not recognizing acute cholecystitis. In this regard, it is necessary to carefully understand the symptoms of the disease and evaluate the clinical picture as a whole, taking into account the anamnesis and paraclinical data. The occurrence of Botkin's syndrome is associated with the presence of a reflex parasympathetic connection between the gallbladder and the heart.

After relief of hepatic colic, the pain does not completely go away, as with chronic calculous cholecystitis. It becomes somewhat dull, takes on a constant bursting character and is localized in the right hypochondrium.

In the presence of complicated forms of acute cholecystitis, the pain syndrome changes. With the occurrence of perforation of the gallbladder and the development of peritonitis, the pain becomes diffuse throughout the abdomen.

Intoxication syndrome is manifested by increased temperature, tachycardia (increased heart rate), dry skin (or, conversely, sweating), lack of appetite, headache, muscle pain and weakness.

The degree of temperature rise depends on the severity of ongoing inflammation in the gallbladder:

• in the case of catarrhal forms, the temperature can be subfebrile - from 37°C to 38°C;
• for destructive forms of cholecystitis - above 38°C;
• when an empyema (ulcer) of the gallbladder or a perivesical abscess occurs, hectic temperature is possible with sharp rises and falls during the day and heavy sweat.

Dyspeptic syndrome is expressed in the form of nausea and vomiting. Vomiting can be either single or repeated with concomitant damage to the pancreas, which does not bring relief.

Pathogenesis of acute cholecystitis

Previously it was believed that the main factor leading to the development of acute cholecystitis was bacterial. In accordance with this, treatment was prescribed aimed at eliminating the inflammatory process. Currently, ideas about the pathogenesis of the disease have changed and treatment tactics have changed accordingly.

The development of acute cholecystitis is associated with a block of the gallbladder, which triggers all subsequent pathological reactions. The block is most often formed as a result of a stone wedging into the cystic duct. This is aggravated by a reflex spasm of the sphincters in the biliary tract, as well as increasing edema.

As a result of biliary hypertension, the microflora located in the biliary tract is activated, and acute inflammation develops. Moreover, the severity of biliary hypertension directly depends on the degree of destructive changes in the wall of the gallbladder.

Increased pressure in the biliary tract is a trigger for the development of many acute diseases of the hepatoduodenal zone (cholecystitis, cholangitis, pancreatitis). Activation of intravesical microflora leads to even greater edema and disruption of microcirculation, which, in turn, significantly increases pressure in the biliary tract - a vicious circle closes.

Classification and stages of development of acute cholecystitis

Based on morphological changes in the wall of the gallbladder, four forms of acute cholecystitis are distinguished:

• catarrhal;
• phlegmonous;
• gangrenous;
• gangrenous-perforative.

Different severity of inflammation suggests a different clinical picture.

With catarrhal form the inflammatory process affects the mucous membrane of the gallbladder. Clinically, this is manifested by pain of moderate intensity, intoxication syndrome is not expressed, and nausea occurs.

With phlegmonous form inflammation affects all layers of the gallbladder wall. A more intense pain syndrome, fever up to febrile levels, vomiting and flatulence occurs. An enlarged, painful gallbladder may be palpable. Symptoms are revealed:

• With. Murphy - interruption of inhalation when palpating the gallbladder;
• With. Mussi - Georgievsky, otherwise called phrenicus symptom - more painful palpation on the right between the legs of the sternocleidomastoid muscle (the exit point of the phrenic nerve);
• With. Ortner - pain when tapping on the right costal arch.

In gangrenous form intoxication syndrome comes to the fore: tachycardia, high temperature, dehydration (dehydration), symptoms of peritoneal irritation appear.

With perforation of the gallbladder(gangrenous-perforated form) the clinical picture of peritonitis prevails: muscle tension of the anterior abdominal wall, positive symptoms of peritoneal irritation (Mendel village, Voskresensky village, Razdolsky village, Shchetkina-Blumberg village), bloating and severe intoxication syndrome.

Forms of cholecystitis without appropriate treatment can flow from one to another (from catarrhal to gangrenous), and the initial development of destructive changes in the wall of the bladder is also possible.

Complications of acute cholecystitis

Complications can arise with a long course of untreated destructive forms of acute cholecystitis.

If inflammation is limited, it occurs perivesical infiltrate. Its obligatory component is the gallbladder, located in the center of the infiltrate. The composition most often includes the omentum, but may include the transverse colon, antrum of the stomach and duodenum. It usually occurs after 3-4 days of the disease. At the same time, pain and intoxication may decrease somewhat, and dyspeptic syndrome may be relieved. With correctly chosen conservative treatment, the infiltrate can resolve within 3-6 months; if unfavorable, it can abscess with development perivesical abscess(characterized by severe intoxication syndrome and increased pain). Diagnosis of infiltrate and abscess is based on anamnesis of the disease, objective examination data and is confirmed by ultrasound.

Peritonitis- the most dangerous complication of acute destructive cholecystitis. It occurs when the wall of the gallbladder is perforated and bile leaks into the free abdominal cavity. As a result of this, a sharp increase in pain occurs, the pain becomes diffused throughout the abdomen. The intoxication syndrome becomes more severe: the patient is initially excited, groans in pain, but as peritonitis progresses, he becomes apathetic. Peritonitis is also characterized by severe intestinal paresis, bloating and weakened peristalsis. Upon examination, defence (tension) of the anterior abdominal wall and positive symptoms of peritoneal irritation are determined. Ultrasound examination reveals the presence of free fluid in the abdominal cavity. An X-ray examination shows signs of intestinal paresis. Emergency surgical treatment is necessary after short-term preoperative preparation.

Another serious complication of acute cholecystitis is cholangitis- inflammation spreads to the biliary tree. In essence, this process is a manifestation of abdominal sepsis. The condition of the patients is severe, intoxication syndrome is pronounced, high hectic fever occurs with large daily temperature fluctuations, heavy sweats and chills. The liver increases in size, jaundice and cytolytic syndrome occur.

Ultrasound reveals dilation of the intra- and extrahepatic ducts. Blood tests show hyperleukocytosis, increased bilirubin levels due to both fractions, increased activity of aminotransferases and alkaline phosphatase. Without appropriate treatment, such patients quickly die from liver failure.

Diagnosis of acute cholecystitis

Diagnosis is based on a combination of medical history, objective data, laboratory and instrumental studies. In this case, the principle must be respected from simple to complex, from less invasive to more invasive.

When collecting anamnesis(during the survey) patients may indicate the presence of cholelithiasis, previous hepatic colic, diet violations in the form of consumption of fatty, fried or spicy foods.

Clinical data assessed by the manifestations of pain, dyspeptic and intoxication syndromes. In the presence of complications, concomitant choledocholithiasis and pancreatitis, cholestasis syndrome and moderate cytolytic syndrome are possible.

Of the instrumental diagnostic methods, the most informative and least invasive is ultrasound examination. At the same time, the size of the gallbladder, its contents, the condition of the wall, surrounding tissues, intra- and extrahepatic bile ducts, and the presence of free fluid in the abdominal cavity are assessed.

In the case of an acute inflammatory process in the gallbladder, ultrasound reveals an increase in its size (sometimes significant). Wrinkling of the bladder indicates the presence of chronic cholecystitis.

When assessing the contents, pay attention to the presence of stones (number, size and location) or flakes, which may indicate the presence of stagnation of bile (sludge) or pus in the lumen of the bladder. In acute cholecystitis, the wall of the gallbladder thickens (more than 3 mm), can reach 1 cm, and sometimes becomes layered (in destructive forms of cholecystitis).

With anaerobic inflammation, gas bubbles can be seen in the wall of the bladder. The presence of free fluid in the peri-vesical space and in the free abdominal cavity indicates the development of peritonitis. In the presence of biliary hypertension against the background of choledocholithiasis or pancreatitis, dilation of the intra- and extrahepatic bile ducts is observed.

Evaluation of ultrasound data makes it possible to decide on treatment tactics even at the admission stage: patient management conservatively, emergency, urgent or delayed surgery.

X-ray methods studies are carried out if a block of the biliary tract is suspected. Plain radiography is not very informative, since stones in the lumen of the gallbladder are usually non-contrast (about 80%) - they contain a small amount of calcium, and they can rarely be visualized.

With the development of such a complication of acute cholecystitis as peritonitis, signs of paresis of the gastrointestinal tract can be identified. To clarify the nature of the biliary tract block, contrast research methods are used:

• endoscopic retrograde cholangiopancreatography - the biliary tract is contrasted retrogradely through the papilla of Vater during duodenoscopy;
• percutaneous transhepatic cholecystocholangiography - antegrade contrast enhancement by percutaneous puncture of the intrahepatic duct.

If making a diagnosis and carrying out differential diagnosis is difficult, computed tomography belly. With its help, you can evaluate in detail the nature of changes in the gallbladder, surrounding tissues and bile ducts.

If differential diagnosis with other acute pathology of the abdominal organs is necessary, a diagnostic test can be performed. laparoscopy and visually assess existing changes in the gallbladder. This study can be performed either under local anesthesia or under endotracheal anesthesia (the latter is preferable). If necessary, the issue of switching to therapeutic laparoscopy, that is, performing cholecystectomy - removal of the gallbladder, is decided right on the operating table.

Laboratory diagnostics consists of performing general blood test, where leukocytosis is detected, a shift in the leukocyte formula to the left and an increase in ESR. The severity of these changes will depend on the severity of inflammatory changes in the gallbladder.

IN biochemical blood test there may be a slight increase in bilirubin levels and aminotransferase activity due to reactive hepatitis in the adjacent liver tissue. More pronounced changes in biochemical parameters occur with the development of complications and intercurrent diseases.

Treatment of acute cholecystitis

Patients with acute cholecystitis are subject to emergency hospitalization in the surgical department of the hospital. After carrying out the necessary diagnostic measures, further treatment tactics are determined. In the presence of severe complications - perivesical abscess, destructive cholecystitis with peritonitis - patients are subject to emergency surgery after short preoperative preparation.

Preparation consists of restoring the volume of circulating blood, detoxification therapy by infusion of crystalloid solutions in a volume of 2-3 liters. If necessary, correction of cardiac and respiratory failure is carried out. Perioperative antibiotic prophylaxis is performed (before, during and after surgery).

The surgical approach is selected depending on the technical capabilities of the clinic, the individual characteristics of the patient and the qualifications of the surgeon. The most commonly used is laparoscopic access, which is the least traumatic and allows for full inspection and sanitation.

The mini-access is not inferior to the laparoscopic approach in terms of morbidity and has the advantage of eliminating the need to apply pneumoperitoneum (limit the mobility of the diaphragm). If technical difficulties arise, pronounced adhesions in the abdominal cavity and diffuse peritonitis, it is more advisable to use a laparotomic approach: upper midline laparotomy, Kocher, Fedorov, Rio Branca access. In this case, the upper midline laparotomy is less traumatic, since in this case the muscles are not intersected, however, with oblique subcostal approaches, the subhepatic space is more adequately opened for surgical intervention.

The operation consists of performing a cholecystectomy. It should be taken into account that the presence of perivesical infiltrate implies certain technical difficulties in mobilizing the neck of the gallbladder. This leads to an increased risk of damage to the elements of the hepatoduodenal ligament. In this regard, we should not forget about the possibility of performing cholecystectomy from the fundus, which makes it possible to more clearly identify the elements of the cervix.

There is also the “Pribrama” operation, which consists of removing the anterior (lower) wall of the gallbladder, suturing the cystic duct in the neck area and mucoclasia (removal of the mucous membrane) by electrocoagulation of the posterior (upper) wall. Performing this operation with a pronounced infiltrate in the area of ​​the bladder neck will avoid the risk of iatrogenic damage. It is applicable for both laparotomic and laparoscopic approaches.

If there are no severe complications of acute cholecystitis, then upon admission of the patient to the hospital, conservative therapy aimed at unblocking the gallbladder. Antispasmodics, anticholinergics, infusion therapy are used to relieve intoxication, and antibiotics are prescribed.

An effective method is to block the round ligament of the liver with a solution of novocaine. The blockade can be performed either blindly using a special technique, or under the control of a laparoscope when performing diagnostic laparoscopy and under ultrasound guidance.

If conservative therapy is ineffective within 24 hours, the question of radical surgery is raised - cholecystectomy.

Of no small importance for determining treatment tactics is the time that has passed since the onset of the disease. If the interval is up to five days, then cholecystectomy is feasible; if it is more than five days, then it is better to adhere to the most conservative tactics in the absence of indications for emergency surgery. The fact is that in the early stages the perivesical infiltrate is still quite loose, it can be divided during surgery. Later, the infiltrate becomes dense, and attempts to separate it may result in complications. Of course, a period of five days is quite arbitrary.

If there is no effect from conservative treatment and there are contraindications for radical surgery - severe pathology of the cardiovascular and respiratory systems, five days have passed since the onset of the disease - it is better to resort to decompression of the gallbladder by cholecystostomy.

Cholecystoma can be applied in three ways: from a mini-access, under laparoscopic control and under ultrasound control. The most minimally traumatic procedure is to perform this operation under ultrasound guidance and local anesthesia. Single and double punctures of the gallbladder with sanitation of its lumen under ultrasound guidance are also effective. A necessary condition is the passage of the puncture channel through the liver tissue to prevent bile leakage.

After stopping the acute inflammatory process, radical surgery is performed in a cold period after three months. Usually this time is enough for the perivesical infiltrate to resolve.

Forecast. Prevention

The prognosis with timely and adequate treatment is usually favorable. After radical surgery, it is necessary for a certain period of time (at least three months) to adhere to diet No. 5 with the exception of fatty, fried and spicy foods. Food intake should be fractional - in small portions 5-6 times a day. It is necessary to take pancreatic enzymes and herbal choleretic agents (they are contraindicated before surgery).

Prevention consists of timely sanitation of stone carriers, that is, routine cholecystectomy for patients with chronic calculous cholecystitis. The founder of biliary surgery, Hans Kehr, said that “carrying a stone in the gall bladder is not the same as wearing an earring in the ear.” In the presence of cholecystolithiasis, factors leading to the development of acute cholecystitis should be avoided - do not break the diet.

MINISTRY OF HEALTH OF THE REPUBLIC OF UZBEKISTAN

ANDIJAN STATE MEDICAL INSTITUTE

DEPARTMENT OF SURGICAL DISEASES 6-7 COURSES WITH A COURSE OF ANESTHESIOLOGY-RESENIMATOLOGY AND UROLOGY

HEAD OF THE DEPARTMENT, PROFESSOR F.N. NISHANOV

LECTURE TOPIC:

ACUTE CHOLECYSTITIS

LECTURER: Doctor of Medical Sciences Professor NISHANOV F.N.

REVIEWER: Head of the Department of Surgery, Faculty of Internal Affairs of the ASMI, Professor

Khodzhimatov G.M.

Andijan 2005

PLAN AND CHRONOLOGY OF THE LECTURE:

1. 
   Introduction – 5 min.
2. 
   Etiology and pathogenesis - 10 min.
3. 
   Classification -5 min.
4. 
   Clinical semiotics-10 min.
5. 
   Laboratory and instrumental diagnostics - 15 min.

Break 5 min.

1. 
   Therapeutic tactics - 10 min.
2. 
   Surgical treatment - 10 min.
3. 
   Operations on extrahepatic bile ducts - 10 min.
4. 
   Postoperative period - 10 minutes.
5. 
   Questions and answers to reinforce the topic of the lecture - 5 min

Lecture No. X

ACUTE CHOLECYSTITIS

Acute cholecystitis is one of the most common diseases of the abdominal organs. In the last two decades, significant advances have been made in diagnosis and in improving methods of its treatment, which has reduced the mortality rate to 2.5%. At the same time, it remains high among elderly and senile patients, which makes this problem not only medical, but also socially significant.

Etiology and pathogenesis

The occurrence of acute cholecystitis is associated with the action of several etiological factors. The leading role in its development is played by infection and bile stagnation (biliary hypertension). Only if they are present, the necessary conditions are created for the development of the inflammatory process in the gallbladder.

It is believed that the infection enters the gallbladder in three ways - hematogenous, lymphogenous and enterogenous. In most cases, infection of the gallbladder occurs hematogenously - from the general circulation through the common hepatic artery system or from the gastrointestinal tract through the portal vein. When the phagocytic activity of the reticuloendothelial system of the liver decreases, microbes pass through the cell membranes into the bile capillaries and enter the gallbladder with the bile flow. Usually they “nest” in the wall of the gallbladder, in the passages of Lyushka, so microbial flora may not be detected in the gallbladder bile.

The bacteriological basis of acute cholecystitis are various microorganisms and their associations. Among them, the main importance belongs to gram-negative bacteria - these are enterobacteria (Escherichia coli, Klebsiella) and pseudomonas. In the general structure of the microbial flora that causes acute cholecystitis, gram-positive microorganisms (non-spore-forming anaerobes - bacteroides and anaerobic cocci) make up approximately one third, and are almost always in association with gram-negative aerobic bacteria.

The second decisive factor in the development of acute cholecystitis is an increase in intravesical pressure. Most often, the cause of its occurrence is obstruction of the bladder neck or cystic duct by a stone. Less commonly, a sudden increase in pressure in the gallbladder is caused by blockage of the duct with a lump of mucus, its narrowing and kinks, as well as dysfunction of the biliary tract - spasm of the sphincter of Oddi. Only from the moment of the onset of intravesical biliary hypertension do favorable conditions appear for the development of infection and destructive changes in the wall of the gallbladder. In approximately 70% of patients with acute cholecystitis, the cause of bile stagnation in the gallbladder is stones. Based on this fact, some authors call such cholecystitis “obstructive.”

In the pathogenesis of the inflammatory process in the wall of the gallbladder, importance is attached to lysolycetin. High concentrations of lysolycetin in bile appear when the gallbladder is blocked, which is accompanied by injury to its mucosa and the release of phospholipase A 2. This tissue enzyme converts bile lecithin into lysolycetin, which together with bile salts has a damaging effect on the mucous membrane of the gallbladder, causes disruption of the permeability of cell membranes and changes in the colloidal state of bile. The consequence of these tissue damages is aseptic inflammation of the gallbladder wall. In conditions of biliary hypertension and stretching of the gallbladder, mechanical compression of the vessels occurs, and microcirculation disturbances occur. This is manifested by slowing blood flow and stasis in both capillaries and venules and arterioles. It has been established that the degree of vascular disorders in the wall of the gallbladder is directly dependent on the magnitude of biliary hypertension. If the increase in pressure persists for a long time, then due to a decrease in hemoperfusion and ischemia of the gallbladder wall, as well as changes in the qualitative composition of bile, the endogenous infection becomes virulent. Exudation into the lumen of the gallbladder that occurs during inflammation leads to a further increase in intravesical hypertension and increased damage to the mucosa. In this case, we can talk about the formation of a pathophysiological vicious circle, in which the primary link in the development of the inflammatory process in the wall of the gallbladder is acute biliary hypertension, and the secondary link is infection.

It is well known that the timing and severity of the development of the inflammatory process in the gallbladder largely depend on vascular changes in its wall. Their consequence is foci of necrosis and perforation of the bladder wall, which most often occur in the bottom or neck area. In elderly patients, vascular disorders associated with atherosclerosis and hypertension especially often cause the development of destructive forms of acute cholecystitis. As a result of atherothrombosis or embolism of the cystic artery, they may have primary gangrene of the gallbladder.

Classification

The question of the classification of acute cholecystitis is not only theoretical, but also of great practical importance. A rationally compiled classification gives the surgeon the key to choosing treatment tactics, which should be adequate to the clinical situation.

The existing many classifications of acute cholecystitis, created by various authors, indicate that there is still no unity in the interpretation of the various aspects of this disease. In everyday practice, we use a classification that, from our point of view, corresponds to the modern diagnostic algorithm and choice of treatment method. It is extremely simple and convenient for clinical use.

It is based on a clinical and morphological principle - the dependence of the clinical manifestations of the disease on pathomorphological changes in the gallbladder, extrahepatic bile ducts and the abdominal cavity. This classification identifies two groups of acute cholecystitis: uncomplicated and complicated.

Clinical and morphological classification of acute cholecystitis

Uncomplicated acute cholecystitis includes all pathomorphological forms of inflammation of the gallbladder that are routinely encountered in clinical practice. Each of these forms should be considered as a natural development of the inflammatory process: a gradual transition from catarrhal inflammation to gangrene. An exception to this pattern is primary gangrenous cholecystitis, since its development is based on primary thrombosis (embolism) of the cystic artery.

Acute inflammation of the gallbladder can occur with or without stones in its lumen. The accepted division of acute cholecystitis into acalculous and calculous is rather arbitrary, since regardless of the presence or absence of stones, the clinical picture of the disease and treatment tactics in an urgent situation will be almost the same. We do not consider it appropriate to distinguish the so-called acute “obstructive” cholecystitis, since in most cases the development of acute cholecystitis is based on stone obstruction of the neck or duct of the gallbladder.

The group of complications consists of pathological processes directly related to inflammation of the gallbladder and the spread of infection beyond its boundaries, as well as those caused by cholelithiasis and its consequences.

Clinical semiotics

Acute cholecystitis occurs in people of all ages, but more often it affects people over 50 years of age. Elderly (60-74 years old) and senile (75-89 years old) patients make up 50% of the total number of cases. The ratio of men to women among them is 1:5.

Clinical manifestations of acute cholecystitis depend on the pathomorphological picture of inflammation of the gallbladder, the presence and prevalence of peritonitis, as well as concomitant changes in the bile ducts. Due to the diversity of the clinical picture of the disease, diagnostic difficulties and errors are possible.

Acute cholecystitis usually begins suddenly. The development of acute inflammatory phenomena in the gallbladder is often preceded by an attack of biliary colic caused by blockage of the neck of the gallbladder or cystic duct by a stone. An acute painful attack is relieved on its own or after the administration of antispasmodic drugs. A few hours after the attack of colic subsides, clinical signs of acute cholecystitis appear.

The leading symptom of acute cholecystitis is severe and constant stomach pain, the intensity of which increases as the disease progresses. Its distinctive feature is its localization in the right hypochondrium with irradiation to the right supraclavicular region, shoulder or scapula. Sometimes the pain radiates to the heart area, which can be regarded as an attack of angina (cholecystocoronary syndrome of S.P. Botkin).

Persistent symptoms of acute cholecystitis - nausea and repeated vomiting, which does not bring relief to the patient. Increased body temperature observed from the first days of the disease. Its nature largely depends on the depth of pathomorphological changes in the gallbladder.

The patient's condition may be different, depending on the form of the disease. The skin is usually of normal color. Moderate jaundice of the sclera can manifest itself in cases of local hepatitis and pericholedocheal lymphadenitis, occurring with stagnation of bile in the hepaticocholedochus. The appearance of bright jaundice of the skin and sclera indicates the mechanical nature of extrahepatic cholestasis, which may be associated with lithiasis of the bile ducts or with a stricture of the major duodenal papilla (MDP). The pulse rate ranges from 80 to 120 beats per minute and higher. A rapid pulse is an ominous symptom, indicating severe inflammatory changes in the gallbladder and abdominal cavity.

Specific signs of acute cholecystitis are described: Ortner's symptom - pain when tapping the right costal arch with the edge of the hand; Ker's symptom - pain in the area of ​​projection of the gallbladder onto the anterior abdominal wall upon palpation at the height of inspiration; Murphy's sign - involuntary holding of breath while inhaling when palpating this area; Mussi-Georgievsky(phrenicus symptom) - pain when pressing with a finger on the right supraclavicular fossa between the legs of the sternocleidomastoid muscle. The frequency of detection of the listed symptoms is not the same, which depends on the nature of the morphological changes in the gallbladder and the possible transition of inflammation to the parietal peritoneum.

In acute cholecystitis and its complications, significant structural changes occur in the liver. They are a consequence of the involvement of the liver segment adjacent to the gallbladder in the inflammatory process and toxic damage to hepatocytes. The degree of these changes is closely related to the duration of the disease and the severity of the inflammatory process. Depending on their depth in the patient’s blood, one can detect increased enzyme content: aminotransferase, aldolase, alkaline phosphatase, lactate dehydrolase, γ-glutamyl transferase. Determining the activity of liver enzymes, as well as bilirubin and its fractions, is important when detecting jaundice in a patient, which can be hepatocellular or obstructive in nature.

Significant changes in acute cholecystitis occur in the rheological state of the blood and the hemostatic system: increased blood viscosity, aggregation capacity of erythrocytes and platelets, and blood coagulation activity. Disturbances in hemorheology and hemostasis can lead to disorders of microcirculation and tissue metabolism in the liver and kidneys, creating preconditions for the development of acute hepatic-renal failure, as well as the occurrence of thromboembolic complications.

Catarrhal cholecystitis - the mildest form of the disease, characterized by moderate pain in the right hypochondrium, nausea and once or twice vomiting.

The general condition of the patient suffers little. The pulse can increase to 90 beats per minute. Tongue is wet. On palpation of the abdomen, local pain is noted in the right hypochondrium. Signs of acute inflammation of the gallbladder - symptoms of Ortner, Kehr, Murphy and Mussi-Georgievsky - are mild or absent; Shchetkin-Blumberg's symptom is not determined. The gallbladder is not palpable, but the area of ​​its projection is slightly painful. The number of leukocytes in the blood increases to 9-11∙10 9 /l. The mild clinical picture of catarrhal cholecystitis is often mistakenly regarded as a resolved attack of biliary colic.

With catarrh, the disease can result in complete clinical recovery. With active drug treatment, inflammatory phenomena in the gallbladder stop by 6-8 days from the onset of the disease. If, after the inflammatory process subsides, obstruction of the cystic duct with a stone persists, hydrocele of the gallbladder. In this case, the bubble reaches a large size due to the accumulation of colorless, mucus-like sterile liquid (“white bile”) in its lumen. It is palpated as an elastic and painless formation. Hydrocele of the gallbladder can exist for a long time and not cause any suffering. However, it may be complicated by the development empyema of the gallbladder. This is why elective surgery is indicated for such patients.

Phlegmonous cholecystitis characterized by constant intense abdominal pain with typical irradiation to the right shoulder or right supraclavicular region. Patients are concerned about nausea and repeated vomiting, which does not bring relief. Weakness and malaise are pronounced, and there may be chills. Body temperature rises to 37.8-38.0°C and above and lasts for several days.

The patient's condition is usually of moderate severity. The pulse quickens to 90-100 beats per minute. The tongue is dry. The abdomen is swollen, significantly painful in the right hypochondrium and, often, in the epigastric region. There are almost always symptoms of local peritonitis: tension of the abdominal muscles and the Shchetkin-Blumberg symptom are determined in the right hypochondrium. With mild tension in the abdominal wall, it is possible to palpate an enlarged and painful gallbladder. As a rule, the “sign” symptoms of acute cholecystitis are positive. The number of leukocytes in the blood reaches 12-15∙10 9 /l, in the leukocyte formula of the blood there is a neutrophil shift.

With phlegmonous inflammation of the gallbladder, different outcomes of the disease are possible. Clinical recovery is observed with timely hospitalization of the patient and active conservative therapy. Relief of the inflammatory process in the wall of the gallbladder and abdominal cavity can result in the formation empyema of the gallbladder. In this pathological condition, the gallbladder is palpated as a dense and moderately painful formation; symptoms of peritoneal irritation are not identified. As a result of the accumulation of purulent exudate in the “disabled” gallbladder, the patient periodically experiences chills and high fever. In blood taken during fever, high leukocytosis with a band shift is determined.

With phlegmonous cholecystitis, the inflammatory process extends beyond the gallbladder and spreads to the parietal peritoneum and adjacent organs, including the hepatoduodenal ligament. The transition of the inflammatory process to the organs and tissues surrounding the gallbladder leads to their dense adhesion and the formation of an inflammatory infiltrate. Peri-vesical infiltrate is detected on days 4-6 of the disease. Clinically, it is characterized by the presence of a dense, painful and immobile formation in the right hypochondrium. With a tendency for the inflammatory process to subside and the inflammatory infiltrate to resolve, abdominal pain decreases, peritoneal symptoms disappear, leukocytosis decreases, and temperature normalizes. With drug therapy, the infiltrate ceases to be palpable after 1.5-2 weeks, but it takes at least 1.5-2 months for the inflammatory process to completely subside.

In the absence of reliable limitation of the inflammatory process due to tight adhesions between the gallbladder and surrounding organs (transverse colon, greater omentum, stomach), the spread of infection beyond this focus leads to the development of peritonitis. In acute cholecystitis, the spread of the inflammatory process occurs predominantly along the right lateral canal and other parts of the right half of the abdominal cavity. It should be noted that widespread peritonitis with destructive damage to the gallbladder is not often observed. This is due to the typical reaction of limiting the inflammatory focus to surrounding organs, fusing them with the gallbladder.

Gangrenous cholecystitis. Depending on the mechanism of development of this form of cholecystitis, its clinical manifestations appear gradually or suddenly. The gradual appearance of clinical symptoms of the disease is observed during the transition of the phlegmonous form of cholecystitis to the gangrenous form (secondary gangrenous cholecystitis).

With the development of necrosis of the gallbladder wall, intoxication phenomena come to the fore in the clinical picture of the disease, while the pain syndrome may be mildly expressed. Patients are inhibited, adynamic, or, conversely, excited. The pulse quickens to 110-120 beats per minute. The tongue is dry. The abdomen becomes bloated and intestinal paresis increases. By palpation, one can note a slight decrease in pain in the right hypochondrium and the degree of tension in the abdominal muscles. Body temperature decreases and may be normal. At the same time, the number of leukocytes increases and the leukocyte formula of the blood shifts to the left. Severe intoxication, the appearance of tachycardia at normal temperature (symptom of “toxic scissors”) and leukocytosis with an increase in the number of band neutrophils indicate profound morphological changes in the gallbladder with the development of areas of necrosis or total gangrene.

For primary gangrenous cholecystitis, arising as a result of thrombosis of the cystic artery, a rapid course is characteristic from the first hours of the disease. It is manifested by severe intoxication and rapidly progressing symptoms of peritonitis.

Perforated cholecystitis develops in patients with a gangrenous form of the disease if they are not provided with surgical care or due to a pressure sore of the bladder wall with a gallstone. In the first case, perforation occurs most often in the area of ​​the bottom of the gallbladder, in the second - in the area of ​​the neck. A clear clinical picture of the disease is observed when the gallbladder is perforated into the free abdominal cavity, which leads to the spillage of purulent gallbladder bile throughout all its parts. Clinically, the moment of perforation is manifested by severe abdominal pain and repeated vomiting. The patient breaks out in a cold sweat, the skin turns pale. In the first minutes there is a decrease in pulse rate and hypotension. Subsequently, blood pressure stabilizes, and the pulse increases sharply as peritonitis develops. Examination of the abdomen reveals a picture of widespread peritonitis. Perforation of the gallbladder into the free abdominal cavity develops in 1-3% of cases of acute cholecystitis.

A less pronounced clinical picture is observed when the gallbladder is perforated, delimited by an inflammatory infiltrate. At the time of perforation, purulent bile enters the subhepatic space, which is accompanied by increased pain in the right hypochondrium and a gradual increase in symptoms of purulent intoxication (dry tongue, tachycardia, leukocytosis with a shift in the leukocyte formula to the left). There may be no symptoms of peritoneal irritation. Perforation of the gallbladder with accumulation of infected bile in the inflammatory infiltrate delimiting it leads to the formation subhepatic abscess with the development of systemic inflammatory response syndrome.

Purulent cholangitis, complicating the course of acute cholecystitis, can develop as a result of a direct transition of the inflammatory process from the gallbladder to the extrahepatic bile ducts. This is accompanied by thickening of their walls and narrowing of the lumen, which, in turn, leads to disruption of the outflow of bile into the intestines. However, in most cases, purulent cholangitis occurs in the presence of stones in the bile ducts and stricture of the major duodenal papilla. Obstructive cholangitis is the most severe due to persistent bile stasis and rapid spread of infection into the intrahepatic bile ducts. Purulent obstructive cholangitis can lead to cholangiogenic liver abscesses and biliary sepsis. Clinical signs of purulent cholangitis do not appear immediately, but 3-4 days after the onset of the attack, and sometimes later. It is characterized by three clinical signs (Charcot's triad): increasing icteric discoloration of the skin and sclera, high temperature up to 38-39°C, accompanied by chills and pain in the right hypochondrium. The patient's condition is serious, consciousness may be confused; Tachycardia and a tendency to hypotension are noteworthy. When palpating the abdomen, along with the symptoms of acute cholecystitis, an increase in the size of the liver and spleen can be detected. A blood test reveals high leukocytosis with a shift in the leukocyte formula to the left, a sharp increase in ESR, hyperbilirubinemia, as well as increased levels of transaminase, alkaline phosphatase, and gamma-glutamyl transferase. With the progressive course of purulent cholangitis, signs of hepatic-renal failure and disseminated intravascular coagulation appear. Purulent obstructive cholangitis, complicating the course of acute cholecystitis, is accompanied by high (up to 40%) mortality.

Laboratory and instrumental diagnostics

Correct and timely diagnosis of acute cholecystitis and its complications is the key to improving treatment results. In connection with an emergency situation, it involves the use of an optimal set of laboratory and instrumental methods (Fig. 10.1), which must be carried out within 24 hours from the moment of hospitalization of the patient.

Rice. 10.1. Diagnostic algorithm for acute cholecystitis and its complications.

This approach allows for an accurate diagnosis and development of adequate treatment tactics.

The figure shows a list of laboratory and instrumental studies, which, from our point of view, are the standard for diagnosing acute cholecystitis and its complications. When studying the composition of peripheral blood in patients with various forms of acute cholecystitis, significant changes are detected in the white blood. An increase in the number of leukocytes with a shift in the formula to the left (due to rod-nuclear neutrophils) indicates a destructive process in the bladder wall. The more severe the inflammatory process in the gallbladder and abdominal cavity, the more pronounced these changes are. However, in weakened and elderly patients, a clear pattern between the severity of changes in the gallbladder and the number of leukocytes in the blood may not be observed.

Determining the level of bilirubin in the blood in patients with acute cholecystitis is a mandatory study, which makes it possible to identify cholestasis in the early stages of the disease. A moderate increase in the content of bilirubin in the blood (25-40 µmol/l) is often found in patients with acute cholecystitis. Slight hyperbilirubinemia is explained by the development of concomitant toxic hepatitis with intrahepatic cholestasis. But even this level of hyperbilirubinemia should be considered as an alarming moment, indicating pronounced destructive changes in the gallbladder, or extrahepatic cholestasis due to lithiasis or the structure of the obstructive system. To determine the cause of hyperbilirubinemia, it is necessary to perform a detailed biochemical blood test, and in case of emergency surgery, use intraoperative cholangiography to assess the condition of the bile ducts.

The standard diagnostic examination of a patient with acute cholecystitis includes the study of amylase in the urine. Moderate increase in amylase in urine to 128-256 units. According to Wolgemut, acute cholecystitis is often noted, which is probably due to dysfunction of the gastrointestinal tract and evasion of the enzyme into the blood. Its higher level (512 units and above) requires clarification of the cause of amylasuria, since this is not typical for acute cholecystitis. Therefore, in such cases, it is necessary to conduct additional studies (determination of blood amylase, ultrasound, laparoscopy) to exclude or confirm the presence of acute pancreatitis, which can occur under the guise of acute cholecystitis and cause a diagnostic error. Experience shows that in acute pancreatitis, acute cholecystitis is most often mistakenly diagnosed. The list of mandatory studies in a patient with acute cholecystitis must include an ECG and chest x-ray. The results of these studies are extremely important for a comprehensive assessment of the patient’s physical condition, excluding acute myocardial infarction and right-sided pleuropneumonia, which can imitate the symptoms of an acute abdomen and cause diagnostic errors.

Ultrasound examination occupies a central place among special instrumental methods for diagnosing acute cholecystitis. The significance of ultrasound is determined by the high informativeness of the method for diseases of the pancreatohepatobiliary system, its non-invasive nature, the possibility of repeating the study many times and performing treatment procedures under its control. The availability of the ultrasound method for many medical institutions and high diagnostic accuracy (98%) allow us to consider this study standard for acute cholecystitis. To avoid unforgivable diagnostic errors, ultrasound should be performed in all patients suspected of having this disease, without exception, regardless of the severity of clinical symptoms. Based on ultrasound signs, it is necessary to determine the morphological form of acute cholecystitis, since the choice of treatment tactics depends on this.

Ultrasonic signs catarrhal cholecystitis are an increase in the size of the gallbladder, thickening of its walls to 4-5 mm, which have smooth, clear contours throughout. In addition, there are no structural changes in the tissues adjacent to the gallbladder. Reliable signs of destructive cholecystitis serve as an increase in the size of the gallbladder (more than 90.0 x 30.0 mm), significant thickening of the walls (6 mm or more), doubling (stratification) of the wall, uneven contours and the presence of suspended small hyperstructures without an acoustic shadow (Fig. 10.2) in the cavity gallbladder (pus). In addition, fluid is detected in the subhepatic space and areas of increased echogenicity of surrounding tissues - signs of inflammatory infiltration. Detection of the symptom of an echo-negative band (rim) of various shapes and widths adjacent to the gallbladder may indicate the formation of a perivesical abscess. Most often, in acute cholecystitis, stones are located in the cavity of the bladder: hyperechoic structures that give an echo shadow. Identification of a fixed echostructure with an acoustic shadow in the area of ​​the gallbladder neck is a sign of an impacted stone. An additional symptom of acute cholecystitis is a positive ultrasound Murphy sign - increased pain in the gallbladder area during inspiration under an ultrasound probe. When assessing the results of ultrasound, attention is paid to the condition of the extrahepatic bile ducts: normally, the width of the hepaticopedochus does not exceed 8 mm. An increase in the diameter of the hepaticopedochus to 9 mm or more may indicate biliary hypertension caused by a stone or stricture. Unfortunately, stones in the bile ducts are rarely detected by ultrasound, since they are usually located in the retroduodenal part of the common bile duct, which is inaccessible for ultrasound assessment.

Rice. 10.2. Ultrasound echogram of the gallbladder.

If it is impossible to obtain information about the condition of the gallbladder and bile ducts during an initial ultrasound due to severe flatulence, it must be repeated the next day after appropriate preparation of the patient (taking activated charcoal or espumizan, cleansing enema). A repeat examination (after 24-48 hours) is also necessary if the patient has signs of catarrhal inflammation of the gallbladder and is being treated conservatively. Ultrasound monitoring during patient monitoring allows one to evaluate the effectiveness of conservative therapy and identify signs of progressive inflammation of the gallbladder wall and its destruction.

The high diagnostic accuracy of ultrasound, the simplicity and harmlessness of the study, and the ability to conduct it at any time of the day allow us to consider ultrasound as the primary method in the diagnosis of acute cholecystitis.

Laparoscopy - an accurate and informative method for diagnosing acute cholecystitis. Previously, it was widely used to diagnose this disease, which made it possible to avoid diagnostic errors. Currently, due to the introduction of ultrasound into everyday practice, the indications for the use of laparoscopy for suspected acute cholecystitis are significantly limited. From our point of view, it is indicated when the diagnosis is unclear due to the inconclusive clinical picture of acute cholecystitis and the impossibility of establishing the cause of the acute abdomen using other (non-invasive) diagnostic methods.

Endoscopic retrograde cholangiopancreatography (ERCP) used for acute cholecystitis in cases of obstructive jaundice and obstructive cholangitis. In such situations it is very important before surgery have accurate information about the nature and level of bile duct obstruction. If the X-ray contrast study is successfully performed, the doctor is able to identify bile duct stones,

Determine their location and level of duct blockage, as well as establish the presence of stenosis and its extent. Determining the nature of the pathology in the bile ducts using the X-ray endoscopic method allows you to correctly resolve issues of treatment tactics.

ERCP should be performed in every case of acute cholecystitis, occurring with severe symptoms of extrahepatic cholestasis, if the severity of the inflammatory process in the abdominal cavity does not require urgent surgical intervention, and the endoscopic examination can be completed by performing endoscopic papillotomy and nasobiliary drainage to eliminate biliary stasis. It is necessary to refrain from performing ERCP in the group of patients in whom, due to the severity of the inflammatory process in the abdominal cavity, the operation should be performed in the next 12-24 hours, as well as when it is impossible to complete the diagnostic stage of the endoscopic examination by performing therapeutic measures. In these cases, to assess the condition of the bile ducts and identify the nature of the pathology, intraoperative cholangiography.

Treatment tactics

Despite the constant discussion on the issue of therapeutic tactics for acute cholecystitis, which takes place on the pages of the medical press, there is still no consensus on this issue. Some surgeons advocate a purely conservative method of treatment, while others take the position of active wait-and-see tactics. The failure of these positions affects the immediate results of treatment, which, unfortunately, cannot be considered favorable.

Modern advances in anesthesiology and the development of new medical technologies make it possible to radically reconsider the existing treatment tactics both for uncomplicated acute cholecystitis and for its complicated forms. The surgeon's tactics for acute cholecystitis should be active. The basic principles are as follows:

1. 
   Destructive cholecystitis with various variants of its course
   serves as an indication for surgical intervention - ho-
   lecystectomy or cholecystostomy, which must be performed in
   within 24-48 hours from the moment of hospitalization of the patient.
2. 
   Only catarrhal disease is subject to purely conservative treatment.
   cholecystitis, in which it is usually successful, allowing
   to stop the inflammatory process. Surgical intervention in
   these patients are performed routinely after a comprehensive examination
   dification, which makes it possible to assess the degree of surgical anesthesia
   physiological risk. In case of progression of inflammation and development

In case of destructive changes in the gallbladder (as detected during dynamic clinical observation and control ultrasound), active surgical tactics are used.

With this approach, the question of the need for surgery is resolved immediately when the final diagnosis of acute destructive cholecystitis is made, occurring both with and without symptoms of peritonitis. A distinctive feature of this treatment tactic is the timing of the operation. Depending on this, the operation may be emergency or urgent.

Emergency surgery is performed within the next 4-6 hours from the moment the patient is admitted to the hospital. Indications for it are all forms of destructive cholecystitis - phlegmonous, gangrenous or perforated, occurring with systemic inflammatory reaction syndrome, symptoms of local or diffuse peritonitis. Indications for urgent surgery, which is performed within the first 12-48 hours from the moment of hospitalization of the patient, are phlegmonous cholecystitis, occurring both with and without symptoms of local peritonitis.

The timing of the operation is not determined by the need to monitor the patient to make a decision: to operate or not to operate. They are dictated by the patient’s condition, the need for preoperative preparation and a minimum set of studies to assess the severity of his physical condition. Preoperative preparation should be aimed at correcting metabolic disorders and disorders of the cardiovascular and pulmonary systems, which are often found in patients with acute cholecystitis. The use of active treatment tactics and refusal of conservative treatment of acute destructive cholecystitis is advisable for the following reasons. Firstly, with conservative therapy, the clinical manifestations of the disease subside in approximately 50% of patients, while in the rest, the symptoms of the disease progress or persist for a long time, which delays their recovery. Secondly, conservative treatment of acute cholecystitis in elderly and senile patients often obscures clinical symptoms without preventing the progression of destructive changes in the gallbladder. Thirdly, postoperative mortality in early operations is significantly lower than in interventions performed at a later date. Based on the listed factors, we once again state that for all variants of the clinical manifestation of acute destructive cholecystitis, surgical treatment is indicated, which should be carried out in the first 12-48 hours from the moment of hospitalization of the patient.

Surgical diseases Tatyana Dmitrievna Selezneva

35. Acute cholecystitis

35. Acute cholecystitis

Acute cholecystitis– inflammation of the gallbladder. The following classification of acute cholecystitis is most acceptable.

I. Uncomplicated cholecystitis.

1) Catarrhal (simple) cholecystitis (calculous or acalculous), primary or exacerbation of chronic recurrent.

2) Destructive (calculous or acalculous), primary or exacerbation of chronic recurrent:

a) phlegmonous, phlegmonous-ulcerative;

b) gangrenous.

II. Complicated cholecystitis:

1) Occlusal (obstructive) cholecystitis (infected dropsy, phlegmon, empyema, gangrene of the gallbladder).

2) Perforated with symptoms of local or diffuse peritonitis.

3) Acute, complicated by damage to the bile ducts:

a) choledocholithiasis, cholangitis;

b) stricture of the common bile duct, papillitis, stenosis of the papilla of Vater.

4) Acute cholecystopancreatitis.

5) Acute cholecystitis, complicated by profuse bile peritonitis.

The main symptom of acute cholecystitis is pain, which usually occurs suddenly in the middle of full health, often after eating, or at night during sleep. The pain is localized in the right hypochondrium, but can also spread to the epigastric region with irradiation to the right shoulder, scapula, and supraclavicular region. In some cases, before its appearance, patients feel heaviness in the epigastric region, bitterness in the mouth, and nausea for several days, even weeks. Severe pain is associated with the reaction of the gallbladder wall to an increase in its contents as a result of outflow disturbance due to inflammatory edema, kinking of the cystic duct, or blockage of the latter by a stone.

Irradiation of pain to the heart area is often noted, then an attack of cholecystitis can occur as an attack of angina pectoris (Botkin cholecystocoronary syndrome). The pain intensifies with the slightest physical exertion - talking, breathing, coughing.

There is vomiting (sometimes repeated) of a reflex nature, which does not bring relief to the patient.

On palpation, sharp pain and muscle tension are detected in the right upper quadrant of the abdomen, especially sharp pain in the area where the gallbladder is located.

Objective symptoms are not expressed equally in all forms of acute cholecystitis. Increased heart rate to 100–120 beats per minute, symptoms of intoxication (dry, coated tongue) are characteristic of destructive cholecystitis. With complicated cholecystitis, the temperature reaches 38 °C and higher.

When analyzing blood, leukocytosis, neutrophilia, lymphopenia, and increased erythrocyte sedimentation rate are observed.

From the book Faculty Therapy: Lecture Notes author Yu. V. Kuznetsova

author Tatyana Dmitrievna Selezneva

From the book Paramedic's Handbook author Galina Yurievna Lazareva

From the book Pocket Guide to Symptoms author Konstantin Alexandrovich Krulev

From the book Surgical Diseases author Alexander Ivanovich Kirienko

From the book Dietetics: A Guide author Team of authors

From the book Emergency Care Directory author Elena Yurievna Khramova

by P. Vyatkin

From the book Complete Medical Diagnostics Guide by P. Vyatkin

From the book Complete Medical Diagnostics Guide by P. Vyatkin

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Surgery for acute cholecystitis

Acute cholecystitis

Acute cholecystitis, or inflammation of the gallbladder, remains one of the most common diseases encountered by the general surgeon.

In most cases (>90%), the cystic duct is obstructed by a stone. In contrast to biliary colic, constant (and not intermittent) pain in the hypochondrium, fever, leukocytosis are noted, and there is also a change in the level of liver enzymes in the blood test. Following cystic duct obstruction, the bladder dilates, resulting in subserosal edema, venous and lymphatic stasis, cellular infiltration, and localized areas of ischemia. In 50-75% of cases, bacteria play a role in the development of acute cholecystitis. Among them: Escherichia coli, Klebsiella aerogenes, Streptococcus fecalis, Clostridium spp., Enterobacter spp. and Proteus spp. Antibacterial drugs used in treatment must have a sufficient spectrum of action. If left untreated, acute gangrenous cholecystitis (most often developing in patients with diabetes) may develop gallbladder perforation or sepsis, and mortality increases. Another possible complication of cholecystitis is perforation of the gallbladder into the wall of adjacent hollow organs (duodenum, jejunum or colon). In this case, a vesicointestinal fistula is formed. If the stone migrates into the intestinal lumen, gallstone intestinal obstruction may develop. In cases of untreated acute cholecystitis, gangrenous cholecystitis may develop (most often in patients with diabetes), leading to gallbladder perforation or sepsis, thereby increasing morbidity and mortality.

Symptoms of acute cholecystitis

Most patients with acute cholecystitis will have a history of abdominal symptoms that can be attributed to the bile ducts, although in some cases acute cholecystitis is the first manifestation of cholelithiasis. In all observations of acute cholecystitis, the most characteristic sign is constant pain in the right hypochondrium, symptoms of peritoneal irritation (Blumberg's symptom, Murphy's symptom). Initially, pain develops due to obstruction of the cystic duct and dilatation of the gallbladder, although as inflammation, edema and ischemia develop, pain is caused by irritation of the peritoneum. As with biliary colic, pain is usually localized in the right hypochondrium, but can also develop in the epigastrium, and sometimes radiate to the shoulder and back. Unlike the pain of biliary colic, which usually lasts only a few hours, the pain of acute cholecystitis can last for several days. However, it is worth noting that patients with both acute cholecystitis and biliary colic experience nausea, vomiting and anorexia.

An objective examination of acute cholecystitis usually reveals an elevated temperature. Often an inflamed bladder may be palpated as a tender, swollen mass, but this is not always the case. Diabetic patients, in particular, may have severe cholecystitis with minimal findings on physical examination. Murphy's symptom is considered positive when there is a sudden increase in pain during palpation in the right hypochondrium during inspiration, which is caused by contact of the inflamed gallbladder with the anterior abdominal wall, deflected by the palpating hand. Patients often hold their breath mid-inhalation. A similar phenomenon during an ultrasound of the right upper quadrant is called an ultrasound Murphy sign (the role of the palpating hand is performed by the sensor).

Diagnosis of acute cholecystitis

Laboratory test data for acute cholecystitis reveal leukocytosis, increased AST and ALT, and alkaline phosphatase. Usually the level of total bilirubin increases slightly (1-2 times), although a significant increase (>2 times) may indicate concomitant obstruction of the common bile duct. Surprisingly, when the disease is detected in patients, even at a very late stage, the biochemical blood test can remain completely normal.

The two most common imaging modalities used in the diagnosis of acute cholecystitis are abdominal ultrasound and biliocintigraphy. Simple x-ray examination is of limited use because only about 15% of gallstones are radiopaque and the gallbladder is not visible at all. An ultrasound is usually performed first. It provides answers to the following questions: “Are gallstones present?”, “Is the gallbladder dilated?”, “Is there thickening of the gallbladder wall and/or the presence of peri-vesical fluid?” and “Are the intrahepatic or extrahepatic ducts dilated?” The main criterion for establishing the diagnosis of cholecystitis is often considered to be thickening of the bladder wall. As a result of such examination, many false positive and false negative results arise. For example, in patients with low serum albumin and a normal gallbladder, paravesical fluid may be detected as a result of anasarca in the absence of inflammation. In addition, patients with severe cholecystitis may have normal gallbladder wall thickness on ultrasound. The most reliable symptoms of the disease that can be detected using ultrasound are stones, enlarged gallbladder and ultrasound Murphy's sign. It is also necessary to always determine the diameter of the extrahepatic ducts to exclude choledocholithiasis.

For patients in whom the diagnosis of acute cholecystitis is questionable, a radioisotope study is performed. If there is no obstruction of the cystic duct, the extrahepatic bile ducts and bladder are identified). If there is an obstruction, the gallbladder will not be visible. The method is very sensitive in patients who have recently eaten, but has a 10-15% false positive rate when fasting for several days. Therefore, its use in the intensive care unit is somewhat limited. In patients with a typical clinical picture of acute cholecystitis, confirmed by ultrasound, this diagnostic method is not used.

Differential diagnosis

Acute cholecystitis can mimic a number of other acute abdominal diseases, such as appendicitis, perforated gastric ulcer, small bowel obstruction, hepatitis and acute pancreatitis. In addition, differential diagnosis is carried out with pneumonia, ischemic heart disease and herpes zoster (shingles). Usually, a careful history and examination can confirm the diagnosis. Increased serum amylase, sometimes occurring in acute cholecystitis, can make differential diagnosis with pancreatitis difficult. In this case, it is necessary to perform a CT scan of the abdominal organs.

Patients with suspected acute cholecystitis should be hospitalized. They are prescribed fasting and infusion therapy. If the diagnosis is confirmed, intravenous administration of broad-spectrum antibiotics is necessary.

In the absence of contraindications (ischemic heart disease, pancreatitis, cholangitis), cholecystectomy is performed within 24-36 hours. If the patient seeks help late (after 4-5 days), treatment should be started with antibiotics and laparoscopic surgery should be delayed for 6 weeks. Since the inflammatory process is most pronounced between 72 hours and 1 week from the onset of the disease, the success of laparoscopic cholecystectomy is questioned, and they are inclined to choose open surgery. Except in very low-risk patients, gallbladder removal is always necessary. Such patients can undergo percutaneous cholecystostomy under ultrasound guidance and local anesthesia.

Crushing stones

Extracorporeal shock wave lithotripsy has previously been used to treat gallstone disease. The essence of the method is the effect of a shock wave on the stone. The goal was to break the stones into pieces (approximately 5 mm) that could pass through the cystic duct and sphincter of Oddi. Unfortunately, the effectiveness rate was low and the complication rate was high, so the method was discontinued.

Treatment of acute cholecystitis complicated by biliary pancreatitis

The timing of cholecystectomy depends entirely on the clinical course of the disease. Patients with mild or moderate disease are usually evaluated first. If the symptoms of gallstone pancreatitis subside within the first 48 hours, laparoscopic cholecystectomy is usually performed. If pancreatitis is accompanied by jaundice, then ERCP is performed to exclude common bile duct stones. In addition, if the patient's condition worsens within 48 hours, ERCP is also performed to look for a stone in the ampulla of Vater's papilla. The procedure is performed carefully due to the risk of worsening pancreatitis. As soon as the obstruction (if it has been) is eliminated, treatment begins according to generally accepted principles. When the pancreatitis has resolved (this may take several weeks), the patient is discharged from the hospital and, to prevent future exacerbations of the disease, is prepared for a planned cholecystectomy in a few months.

Laparoscopic cholecystectomy for acute cholecystitis

At the 1992 NIH Consensus meeting, scientists concluded that laparoscopic cholecystectomy provides a safe and effective treatment for patients with gallstone disease and is the treatment of choice for these patients. This operation is widespread today, although the radical method in surgery of the biliary system has been used for more than a century. Previously, the procedure was very traumatic. Access was made through a midline or long incision in the right hypochondrium, which required a very long recovery period. Nowadays, minimally invasive methods are used. This allows patients to return to normal activities much sooner. With the exception of a few relative contraindications (portal hypertension, previous surgical interventions in the right hypochondrium, cirrhosis of the liver), laparoscopic removal of the gallbladder can be performed in most patients. The advent of laparoscopic methods has made surgery of the biliary system less traumatic. However, not all patients can undergo surgery laparoscopically. Sometimes during surgery it is necessary to additionally perform standard laparatomy. While the percentage of conversion to laparotomy for elective cholecystectomy is 1-2%, in patients with acute cholecystitis it varies from 5 to 10%. This number is even higher with concomitant diabetes mellitus.

Technical aspects of laparoscopic cholecystectomy

If planned laparoscopic cholecystectomy proceeds without complications, then same-day surgery can be used. No special bowel preparation is required before surgery. After induction of anesthesia, the patient is placed on the operating table in a supine position. The gastric tube should be inserted by the anesthesiologist for decompression and removed at the end of the operation. Bladder catheterization is not required if an open trocar placement method is used. The abdomen is processed and draped in the usual manner. A small incision is made under the navel down to the fascia. Next, the fascia is grasped with Kocher forceps, lifted and incised. A trocar (usually 10 mm) is inserted and secured. Carbon dioxide is injected at low pressure (15 mmHg). Then three trocars are inserted in the right hypochondrium. They use instruments designed exclusively for laparoscopic surgery. The gallbladder is retracted from the edge of the liver, and manipulations in Calot's triangle begin. After careful isolation, revision and clipping of the cystic duct and cystic artery, the bladder is cut off and removed from the abdominal cavity. Careful hemostasis is performed and all trocars are removed under eye control. Drainage of the abdominal cavity is not performed if there is no likelihood of postoperative bile leakage (from the bladder bed or unsuccessfully clipped cystic duct). Then the trocar insertion sites are sutured. The patient is taken to the recovery room where he is allowed to resume normal feeding as soon as he is fully conscious to prevent aspiration. After discharge, most patients can resume normal activities within 5 days after surgery.

The use of intraoperative cholangiography and laparoscopic cholecystectomy is controversial. Most surgeons use it when there is a suspicion of stones in the common bile duct, if ERCP was not performed before surgery, others use it in all cases. Chronic use increases the cost of surgery and is not indicated for the prevention of biliary lesions. If, however, the anatomy is unclear, cholangiography can help identify the extrahepatic bile ducts. If performed, the cholangiogram must be correctly interpreted by both the surgeon and the radiologist.

The technical aspects of identifying structures during open cholecystectomy correspond to those of the laparoscopic approach. The use of laparoscopic instrumentation and small incisions for trocars is preferable to the traditional surgical instrumentation and incision in the right upper quadrant of the abdomen or the midline approach used in open cholecystectomy.

surgeryzone.net

Surgery (Acute cholecystitis)

RUSSIAN STATE

MEDICAL UNIVERSITY

Department of Hospital Surgery

Topic: “Acute cholecystitis.”

Completed by a fifth year student

Faculty of Medicine

511a gr. Krat V.B.

Clinic of acute cholecystitis:

The temperature rises to 38-39°C, sometimes with chills. In elderly and senile people, severe destructive cholecystitis can occur with a slight increase in temperature and moderate leukocytosis. With simple cholecystitis, the pulse quickens according to the temperature; with destructive and, especially, perforative cholecystitis with the development of peritonitis, tachycardia is noted up to 100-120 beats per minute.

A blood test reveals neutrophilic leukocytosis (10 – 20 x 109 /l), with jaundice hyperbilirubinemia.

Differential diagnosis:

Accesses: 1) according to Kocher;

2) according to Fedorov;

From the second day they begin feeding liquid food through the mouth. On the 5th day, a narrow tampon facing the bed of the bladder is removed and replaced with others, leaving in place a wide delimiting tampon, which is tightened on the 5-6th day and removed with a smooth course on the 8-10th day. By day 14, the discharge from the wound usually stops, and the wound closes on its own. After removal of the gallbladder, patients are advised to follow a diet.

Literature:

1. Avdey L.V. “Clinic and treatment of cholecystitis”, Minsk, Gosizdat, 1963;

2. Galkin V.A., Lindenbraten L.A., Loginov A.S. “Recognition and treatment of cholecystitis”, M., Medicine, 1983;

3. Savelyev V. S. “Guide to emergency surgery of the abdominal organs,” M., 1986;

4. Smirnov E.V. “Surgical operations on the biliary tract”, Leningrad, Medicine, 1974

5. Skripnichenko D.F. “Emergency abdominal surgery”, Kyiv, “Zdorovya”, 1974;

6. Hegglin R. “Differential diagnosis of internal diseases”, M., 1991.

7. “Surgical diseases”, edited by Iuzin M.I., Medicine, 1986

mirznanii.com

Acute cholecystitis

Acute cholecystitis is an acute inflammation of the gallbladder of a bacterial nature.

ICD-10 CODE

K81.0. Acute cholecystitis. Acute cholecystitis is one of the most common diseases of the abdominal organs and ranks second after acute appendicitis. The high incidence is associated with an increase in the incidence of cholelithiasis (GSD) and an increase in people's life expectancy. The disease is more common in people over 50 years of age; elderly and senile patients account for more than 50%; The ratio of men to women among patients is approximately 1:5. The classification of acute cholecystitis is of practical importance for making the right tactical decision that is adequate to a specific clinical situation. The classification is based on the clinical and morphological principle of the dependence of the clinical manifestations of the disease on pathomorphological changes in the gallbladder, extrahepatic bile ducts and the abdominal cavity. In this classification, there are two groups of acute cholecystitis - uncomplicated and complicated.

Clinical and morphological classification of acute cholecystitis

Form of cholecystitis:

• catarrhal;
• phlegmonous;
• gangrenous.

Complications:

• peri-vesical infiltrate;
• perivesical abscess;
• perforation of the gallbladder;
• peritonitis;
• obstructive jaundice;
• cholangitis;
• external or internal bile fistula.

Uncomplicated acute cholecystitis includes all pathomorphological forms of inflammation of the gallbladder that are routinely encountered in clinical practice. This is catarrhal, phlegmonous and gangrenous inflammation. Each of these forms should be considered as a natural development of the inflammatory process: a gradual transition from the catarrhal process of inflammation to gangrene. With this mechanism of development of the pathological process, foci of necrosis of various sizes arise against the background of phlegmonous changes in the gallbladder as a result of vascular disorders. An exception to this pattern is primary gangrenous cholecystitis, since its origin is based on impaired blood circulation in the wall of the gallbladder (atherothrombosis). In primary gangrenous cholecystitis, the entire gallbladder undergoes necrosis at once, its walls are thinned, parchment-type and black in color. Enzymatic cholecystitis, which develops as a result of reflux of pancreatic secretions into the gallbladder, is relatively rare, which can occur in the presence of a common ampulla of the bile duct and the pancreatic duct. With enzymatic cholecystitis, the mucous membrane of the gallbladder is primarily damaged, and infection is secondary. The occurrence of acute cholecystitis is associated with two main factors: infection of the bile or gallbladder wall and bile stasis (biliary hypertension). Only when they are combined do conditions for the development of the inflammatory process are created. Infection enters the gallbladder in three ways - hematogenous, lymphogenous and enterogenous. In most cases, infection occurs hematogenously: from the general circulation through the common hepatic artery system or from the gastrointestinal tract through the portal vein. With a decrease in the phagocytic activity of the reticuloendothelial system of the liver, microorganisms enter the bile capillaries through the cell membranes and, with the flow of bile, into the gallbladder. Usually they are located in the wall of the gallbladder, in the ducts of Luschka, so often microbial flora may not be detected in the gallbladder bile. The main importance is given to gram-negative bacteria - enterobacteria (Escherichia coli, Klebsiella) and pseudomonads. In the general structure of the microbial flora that causes acute cholecystitis, gram-positive microorganisms (non-spore-forming anaerobes - bacteroides and anaerobic cocci) make up a third, and are almost always in association with gram-negative aerobic bacteria. The second decisive factor in the development of acute cholecystitis is bile stagnation, which most often occurs due to stone obstruction of the neck of the gallbladder or cystic duct. Stones, being in the cavity of the gallbladder, do not create an obstacle to the outflow of bile. However, if the diet is violated, the contractility of the gallbladder increases and obstruction of the neck or cystic duct may occur. Less commonly, biliary stasis is caused by blockage of the cystic duct with lumps of mucus, putty-like detritus, and stagnation can also occur when the gallbladder is narrowed and kinked. Intravesical biliary hypertension following the blockade causes the development of an inflammatory process in the gallbladder. In 70% of patients, stone obstruction leads to stagnation of bile and biliary hypertension, which allows us to consider cholelithiasis as the main factor predisposing to the development of acute “obstructive” cholecystitis.

Lysolecithin is of great importance in the pathogenesis of the inflammatory process, high concentrations of which are formed in the bile during blockade of the gallbladder, accompanied by damage to its mucosa and the release of phospholipase A2. This tissue enzyme converts bile lecithin into lysolecithin; together with bile salts, it damages the mucous membrane of the gallbladder, causes disruption of the permeability of cell membranes and changes in the colloidal state of bile. As a result of these processes, aseptic inflammation of the gallbladder wall occurs.

In conditions of biliary hypertension, when the gallbladder is stretched, mechanical compression of the vessels occurs, microcirculation disorders occur, blood flow slows down and stasis in the capillaries, venules, and arterioles. The degree of vascular disorders in the gallbladder wall is directly dependent on the severity of biliary hypertension. If elevated pressure persists, then due to ischemia of the gallbladder wall and changes in the qualitative composition of bile, the endogenous infection becomes virulent. Exudation into the lumen of the gallbladder that occurs during inflammation contributes to the progression of intravesical hypertension and even greater damage to the mucosa. In this case, we can talk about the formation of a pathophysiological vicious circle, in which the primary link in the development of the inflammatory process is considered to be acute biliary hypertension, and the secondary is infection. The timing and severity of the inflammatory process in the gallbladder largely depend on vascular disorders in its wall. They lead to the appearance of foci of necrosis, most often occurring in the fundus or neck, followed by perforation of the bladder wall. In elderly patients, impaired circulation in the gallbladder against the background of atherosclerosis and hypertension especially often causes the development of destructive forms of acute cholecystitis. With atherothrombosis or cystic artery embolism, such patients may develop primary gangrene of the gallbladder. Clinical symptoms of acute cholecystitis depend on pathomorphological changes in the gallbladder, the presence and prevalence of peritonitis, as well as the nature of the concomitant pathology of the bile ducts. The diversity of the clinical picture of the disease can create diagnostic difficulties and cause errors.

Acute cholecystitis occurs suddenly and manifests itself with severe constant pain in the abdomen, the intensity of the pain increases as the disease progresses. The development of acute inflammatory phenomena in the gallbladder is often preceded by an attack of biliary colic. The localization of pain in the right hypochondrium and epigastric region is typical. Irradiation to the right shoulder, supraclavicular region, interscapular space, or to the heart region is often noted. The latter localization can be regarded as an attack of angina (cholecystocoronary symptom of S.P. Botkin), and also provoke its occurrence.

Constant symptoms of acute cholecystitis are nausea and repeated vomiting, which does not bring relief to the patient. An increase in body temperature is noted from the first days of the disease, its nature depends on the pathomorphological changes in the gallbladder. Destructive forms of acute cholecystitis are characterized by chills. The general condition of the patient upon admission to the hospital depends on the form of the disease. The skin is usually of normal color. Moderate icterus of the sclera may be caused by the transition of the inflammatory process from the gallbladder to the liver and the development of local toxic hepatitis. The appearance of icterus in the sclera and skin is a sign of the mechanical nature of extrahepatic cholestasis (choledocholithiasis, stenosis of the major duodenal papilla). This must be taken into account when determining treatment tactics. The pulse rate ranges from 80 to 120 per minute and higher. A rapid pulse is a symptom indicating developing intoxication and inflammatory changes in the gallbladder and abdominal cavity. In acute cholecystitis, you can identify:

• Ortner's symptom - sharp pain in the projection of the gallbladder when lightly tapping the edge of the palm along the right costal arch;
• Murphy's symptom - involuntary holding of breath while inhaling when pressing on the area of ​​the right hypochondrium;
• Kehr's symptom - increased pain on inspiration with deep palpation of the right hypochondrium;
• Georgievsky-Mussi symptom (phrenicus symptom) - pain on the right when pressing between the legs of the sternocleidomastoid muscle;
• Shchetkin-Blumberg symptom - becomes positive if the peritoneum is involved in the inflammatory process.

The frequency of detection of the above symptoms depends on the severity of the inflammatory process in the gallbladder (a form of acute cholecystitis) and the involvement of the peritoneum. As the inflammatory process in the gallbladder progresses, structural changes occur in the liver, which is associated with toxic damage to hepatocytes. Depending on the severity of damage to hepatocytes and liver parenchyma, an increase in the level of enzyme activity (AST, alkaline phosphatase, lactate dehydrogenase, etc.) is detected in the blood. Determining the activity of liver enzymes, the level of bilirubin and its fractions is of particular importance when detecting jaundice, which can be hepatocellular or obstructive in nature. In acute cholecystitis, significant changes occur in the rheological state of the blood and the hemostasis system: an increase in blood viscosity, the aggregation ability of erythrocytes and platelets, and blood coagulation activity. These disorders can lead to disorders of microcirculation and metabolism in the liver and kidneys, creating preconditions for the development of acute liver failure and the occurrence of thromboembolic complications.

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Abstract: Surgery (Acute cholecystitis)

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RUSSIAN STATE

MEDICAL UNIVERSITY

Department of Hospital Surgery

Head Department Professor Nesterenko Yu.P.

Teacher Andreytseva O.I.

Completed by a fifth year student

Faculty of Medicine

511a gr. Krat V.B.

Acute cholecystitis is an inflammatory process in the extrahepatic tract with a predominant lesion of the gallbladder, in which there is a disruption of the nervous regulation of the production of the liver and biliary tract, as well as changes in the biliary tract themselves due to inflammation, bile stagnation and cholesterolemia.

Depending on the pathological changes, catarrhal, phlegmonous, gangrenous and perforated cholecystitis are distinguished.

The most common complications of acute cholecystitis are encysted and diffuse purulent peritonitis, cholangitis, pancreatitis, and liver abscesses. In acute calculous cholecystitis, partial or complete blockage of the common bile duct may occur with the development of obstructive jaundice.

There are acute cholecystitis that developed for the first time (primary acute cholecystitis) or due to chronic cholecystitis (acute recurrent cholecystitis). For practical use, the following classification of acute cholecystitis can be recommended:

I Acute primary cholecystitis (calculous, acalculous): a) simple; b) phlegmonous; c) gangrenous; d) perforative; e) complicated cholecystitis (peritonitis, cholangitis, bile duct obstruction, liver abscess, etc.).

II Acute secondary cholecystitis (calculous and acalculous): a) simple; b) phlegmonous; c) gangrenous; d) perforative; e) complicated (peritonitis, cholangitis, pancreatitis, bile duct obstruction, liver abscess, etc.).

Etiology and pathogenesis of acute cholecystitis:

The inflammatory process in the wall of the gallbladder 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 and mucous membranes, 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 mucus solutions 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.

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.

Clinic of acute cholecystitis:

The clinical picture of acute cholecystitis depends on the pathological changes in the gallbladder, the duration and course of the disease, the presence of complications and the reactivity of the body. The disease usually begins with an attack of pain in the gallbladder area. The pain radiates to the right shoulder, right supraclavicular space and right scapula, to the right subclavian region. A painful attack is accompanied by nausea and vomiting mixed with bile. As a rule, vomiting does not bring relief.

The temperature rises to 38-39°C, sometimes with chills. In elderly and senile people, severe destructive cholecystitis can occur with a slight increase in temperature and moderate leukocytosis. With simple cholecystitis, the pulse quickens according to the temperature; with destructive and, especially, perforative cholecystitis with the development of peritonitis, tachycardia is noted up to 100-120 beats per minute.

During examination, patients have icteric sclera; severe jaundice occurs when the patency of the common bile duct is impaired due to obstruction by a stone or inflammatory changes.

The abdomen is painful on palpation in the area of ​​the right hypochondrium. In the same area, muscle tension and symptoms of peritoneal irritation are determined, especially pronounced in destructive cholecystitis and the development of peritonitis.

There is pain when tapping along the right costal arch (Grekov-Ortner symptom), pain when pressing or tapping in the area of ​​the gallbladder (Zakharyin’s symptom) and with deep palpation when the patient inhales (Obraztsov’s symptom). The patient cannot take a deep breath with deep palpation in the right hypochondrium. Pain on palpation in the right supraclavicular region is characteristic (Georgievsky's symptom).

In the initial stages of the disease, careful palpation can reveal an enlarged, tense and painful gallbladder. The latter is especially well contoured during the development of acute cholecystitis due to hydrocele of the gallbladder. In case of gangrenous, perforated cholecystitis, due to severe tension in the muscles of the anterior abdominal wall, as well as in case of exacerbation of sclerosing cholecystitis, it is not possible to palpate the gallbladder. In severe destructive cholecystitis, sharp pain is observed during superficial palpation in the area of ​​the right hypochondrium, light tapping and pressing on the right costal arch.

A blood test reveals neutrophilic leukocytosis (10 – 20 x 109/l); with jaundice, hyperbilirubinemia.

The course of acute simple primary acalculous cholecystitis in 30-50% of cases ends with recovery within 5-10 days after the onset of the disease. Although acute cholecystitis can be very severe with the rapid development of gangrene and perforation of the bladder, especially in elderly and senile people. With exacerbation of chronic calculous cholecystitis, stones can contribute to faster destruction of the bladder wall due to stagnation and the formation of bedsores.

However, much more often, inflammatory changes increase gradually; within 2-3 days, the nature of the clinical course is determined with the progression or subsidence of inflammatory changes. Consequently, there is usually enough time to assess the course of the inflammatory process, the patient’s condition and a reasonable method of treatment.

Differential diagnosis:

Acute cholecystitis is differentiated from the following diseases:

1) Acute appendicitis. In acute appendicitis, the pain is not so intense, and, most importantly, does not radiate to the right shoulder, right scapula, etc. Also, acute appendicitis is characterized by migration of pain from the epigastrium to the right iliac region or throughout the abdomen; with cholecystitis, the pain is precisely localized in the right hypochondrium ; vomiting with appendicitis is one-time. Typically, palpation reveals a thickened consistency of the gallbladder and local tension in the muscles of the abdominal wall. Ortner's and Murphy's symptoms are often positive.

2) Acute pancreatitis. This disease is characterized by girdling pain and sharp pain in the epigastrium. A positive Mayo-Robson sign is noted. The patient's condition is characteristically grave; he assumes a forced position. The level of diastase in urine and blood serum is of decisive importance in diagnosis; figures above 512 units are conclusive. (in urine).

With stones in the pancreatic duct, the pain is usually localized in the left hypochondrium.

3) Acute intestinal obstruction. In acute intestinal obstruction, the pain is cramping and non-localized. There is no increase in temperature. Enhanced peristalsis, sound phenomena (“splashing noise”), and radiological signs of obstruction (Kloiber cups, arcades, symptom of pinnateness) are absent in acute cholecystitis.

4) Acute obstruction of the mesenteric arteries. With this pathology, severe pain of a constant nature occurs, but usually with distinct intensification, and is less diffuse in nature than with cholecystitis (more diffuse). A history of pathology of the cardiovascular system is required. The abdomen is easily accessible for palpation, without pronounced symptoms of peritoneal irritation. Fluoroscopy and angiography are decisive.

5) Perforated ulcer of the stomach and duodenum. Men are more likely to suffer from this, while cholecystitis most often affects women. Cholecystitis is characterized by intolerance to fatty foods, frequent nausea and malaise, which does not happen with a perforated ulcer of the stomach and duodenum; pain is localized in the right hypochondrium and radiates to the right scapula, etc., with an ulcer the pain radiates mainly to the back. Erythrocyte sedimentation is accelerated (with an ulcer - vice versa). The picture is clarified by the presence of a history of ulcers and tarry stools. X-ray reveals free gas in the abdominal cavity.

6) Renal colic. Pay attention to the urological history. The area of ​​the kidney is carefully examined, Pasternatsky's symptom is positive, a urine test, excretory urography, and chromocystography are performed to clarify the diagnosis, since renal colic often provokes biliary colic.

Correct assessment of the patient’s condition and the course of the disease in acute cholecystitis requires clinical experience and careful monitoring of the patient’s condition, repeated studies of the number of leukocytes and leukocyte formula, taking into account the dynamics of local and general symptoms.

In patients with a primary attack of acute cholecystitis, surgery is indicated only in cases of extremely severe disease and rapid development of destructive processes in the gallbladder. If the inflammatory process quickly subsides, or with catarrhal cholecystitis, surgery is not indicated.

Conservative treatment of patients consists of the use of broad-spectrum antibiotics and detoxification therapy. To relieve pain, it is advisable to carry out a course of therapy with atropine, no-shpa, papaverine, as well as blockade of the round ligament of the liver or perinephric novocaine blockade according to Vishnevsky.

Surgical treatment of cholecystitis is one of the most difficult sections of abdominal surgery, which is explained by the complexity of pathological processes, the involvement of the bile ducts in the inflammatory process, the development of angiocholitis, pancreatitis, paravesical and intrahepatic abscesses, peritonitis and the frequent combination of cholecystitis with choledocholithiasis, obstructive jaundice.

Within the first 24-72 hours after admission, emergency surgery is indicated for those patients with acute cholecystitis whose disease worsens despite vigorous treatment with antibiotics. Early surgery is indicated after the inflammatory process has subsided, 7-10 days after the onset of the attack, for patients suffering from acute calculous cholecystitis, exacerbation of chronic cholecystitis with severe and frequently recurring attacks of the disease. Early surgery contributes to the fastest recovery of patients and the prevention of possible complications during conservative treatment.

In acute cholecystitis, cholecystectomy is indicated; in the presence of bile duct obstruction, cholecystectomy in combination with choledochotomy is indicated. In very serious condition of patients, cholecystotomy is performed. Operations can be performed either laparoscopically or using standard methods with laparotomy.

Laparoscopic operations are performed under local anesthesia. An incision 4-6 cm long is made above the bottom of the gallbladder, parallel to the costal arch. The tissues of the abdominal wall are layered and pulled apart. The wall of the gallbladder is removed into the wound and the contents are punctured. The gallbladder is removed. The bladder cavity is inspected. In this case, after completing X-ray and endoscopic examinations, plastic drains are inserted and purse string sutures are applied. The wound is sutured.

Operations requiring standard laparotomy: cholecystotomy, cholecystostomy, choledochotomy, choledochoduodenostomy.

Accesses: 1) according to Kocher;

2) according to Fedorov;

3) transrectal mini-access 4 cm long.

Cholecystotomy is the application of an external fistula to the gallbladder. During this operation, the bottom of the gallbladder is sewn into the wound so that it is isolated from the abdominal cavity, and opened immediately or the next day, when adhesions of the walls of the bladder with the edges of the incision are formed.

This operation is performed as the first stage of surgery in elderly people for acute cholecystitis. Subsequently, cholecystectomy is required to eliminate the biliary fistula.

Cholecystostomy - opening the gallbladder, removing the gallbladder and suturing it tightly. This operation is performed on weakened patients with cardiac and respiratory problems, for whom a more complex operation may be life-threatening. This operation may cause subsequent relapses, since a pathologically altered gallbladder remains, serving as a site for the development of infection and the formation of new stones. To prevent complications after surgery, it is more advantageous to insert and seal tightly in the bladder a thin rubber drainage.

Cholecystectomy is the removal of the gallbladder; the operation is most often performed in typical cases in two ways: 1) from the cervix; 2) from the bottom.

Cholecystectomy from the fundus is technically simpler, but is used less frequently due to the possibility of purulent contents leaking into the common bile duct. When isolated from the bottom, the bladder is grabbed with a window clamp, its peritoneum is incised on the sides and the bladder is separated from the liver using a blunt or sharp method, capturing and tying up individual branches of a. cystica. After separating the bladder from the liver bed, the main branch of the cystic artery and the cystic duct are ligated. In the presence of powerful adhesions, the method of isolating from the bottom is simpler, but bleeding from the branches of the cystic artery somewhat complicates the operation, since when bleeding vessels are captured deep in the wound, the right hepatic duct passing near the cystic artery can be ligated.

Cholecystectomy from the cervix is ​​more difficult. First, the cystic duct and cystic artery are ligated in Calot's triangle. Then they begin to separate the bottom of the gallbladder, trying to preserve the peritoneum of the hepatic surface of the bladder, in order to then peritonize its bed. It is acceptable to leave parts of the bladder mucosa in its bed.

In cases where a gallbladder that is sclerotic and surrounded by powerful adhesions is discovered during an operation, when finding the neck and duct encounters insurmountable difficulties, the bladder is opened along its entire length and the mucous is burned out by electrocoagulation. After burning out the mucous membrane, the remaining wall of the bladder is turned inward and stitched with catgut sutures over the scab. In severe cases, burning out the mucous membrane is an advantage over acute removal of the bladder. This operation is called mucoclasis (according to Primbau).

Choledochotomy is an operation used for examination, drainage, and removal of stones from the duct. The duct is drained in case of cholangitis to drain the infected contents of the ducts out. There are three types of choledochotomy: supraduodenal, retroduodenal and transduodenal.

After removing the stone, the duct is carefully sutured with thin catgut sutures and closed with a second row of sutures placed on the peritoneum. A tampon is placed at the site of opening of the duct, since with the most careful suturing, bile can leak between the sutures and cause biliary peritonitis.

Choledochoduodenostomy is the formation of an anastomosis between the bile duct and the duodenum. This operation is performed for narrowing or impassable strictures of the bile duct. As a disadvantage of choledochoduodenostomy, it should be noted the possibility of duodenal contents entering the duct. However, experience shows that with normal outflow of bile this is not accompanied by dangerous consequences. Short-term outbreaks of biliary tract infections can be treated with antibiotics.

In the postoperative period, acute cholecystitis is prevented, the coagulation and fibrinolytic systems, water-salt and protein metabolism are corrected, and thromboembolic and cardiopulmonary complications are prevented.

From the second day they begin feeding liquid food through the mouth. On the 5th day, a narrow tampon facing the

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the bladder bed, leaving in place a wide delimiting tampon, which is tightened on the 5-6th day and removed with a smooth course on the 8-10th day. By day 14, the discharge from the wound usually stops, and the wound closes on its own. After removal of the gallbladder, patients are advised to follow a diet.

Improving the results of treatment of patients with acute cholecystitis depends on more active surgical treatment. Cholecystectomy, performed in a timely manner for sufficient indications, saves patients from severe complications and prolonged suffering.

Gall bladder symptoms and treatment with folk remedies