Acute cholecystitis

　　One, etiology

　　The gallbladder is a blind sac that communicates with the bile duct through a curved, thin gallbladder duct. The main cause of the disease is obstruction of the cystic duct, bile stasis, and subsequent bacterial infection or chemical cholecystitis due to various factors. In a few cases, there is no obvious bile stasis in the gallbladder, and bacterial infection seems to be the only cause of acute cholecystitis.

　　1. Bile stasis is a precursor and basic factor causing acute cholecystitis, and its causes can be roughly divided into two categories:

　　(1) Mechanical obstruction: It is generally believed that more than 90% of patients with acute cholecystitis have calculi impacted in the cystic duct or gallbladder neck, leading to bile stasis; some authors believe that even if no calculi are found in the gallbladder during surgery or post-mortem examination, it cannot be proven that there were no calculi in the early stage of the disease, and it is possible that the calculi have been expelled into the common bile duct. In addition to calculi, obstruction and bile stasis can also occur at the junction of the cystic duct and the common bile duct due to a small angle, the cystic duct itself being too tortuous and malformed, or due to abnormal blood vessels, peripheral inflammation adhesions, ascaris invasion, and pressure from enlarged lymph nodes. Functional disorder research confirms that disordered gallbladder muscle and nerve function can impede the normal emptying activity of the gallbladder, causing transient bile stasis. When abdominal organs have lesions, such as gastric or duodenal ulcers, chronic appendicitis, or perinephritis, pathological stimulation impulses from visceral nerves are transmitted to the cerebral cortex, causing functional disorder of the cortex, which in turn reflexively leads to functional disorder of the cystic duct sphincter and the duodenal papilla sphincter, causing spasm and resulting in bile stasis throughout the biliary system. Long-term bile stasis and concentration in the gallbladder can stimulate the gallbladder mucosa, causing inflammatory changes, and with bacterial infection, acute cholecystitis can be formed.

　　2, Bacterial Infection The bacteria causing acute cholecystitis are about 70% Escherichia coli, with other bacteria including Klebsiella, Clostridium botulinum, Staphylococcus, Salmonella typhi, Paratyphi A, Streptococcus, and Pneumococcus, among others. About 50% of patients with acute cholecystitis have positive bile bacterial culture. The route of bacterial invasion generally passes through bile or lymphatic vessels, and sometimes can enter the biliary tract or spread hematogenously via the intestinal tract. In summary, there are many routes for bacteria to reach the gallbladder.

　　3, Other Causes There are a few cases in clinical practice that do not have bile retention or bacterial infection due to other reasons. These are mainly seen in trauma and pancreatic juice reflux. Trauma includes surgical operations, burns, and other factors that can lead to acute cholecystitis. During trauma, due to pain, fever, dehydration, emotional tension, and other factors, the viscosity of bile can increase, and the emptying can slow down. In addition, when the common channel between the pancreatic and bile ducts is obstructed, trypsin in the refluxed pancreatic juice is activated by bile, binds with bile acids, and can also activate phospholipase, converting lecithin into lysophosphatidylcholine. Both of these act on the gallbladder wall to cause damage.

　　Two, Pathogenesis

　　When the cystic duct or the cystic neck is obstructed suddenly due to the sudden lodgment of gallstones or other reasons, as the gallbladder is a blind sac, it can cause retention or concentration of bile. The concentrated bile salts stimulate and damage the gallbladder, leading to acute chemical cholecystitis. At the same time, bile retention and/or stone lodgment can cause phospholipase A to be released from the damaged gallbladder mucosal epithelium, hydrolyzing lecithin in bile into lysophosphatidylcholine, thereby altering the cell's biomembrane structure and leading to acute cholecystitis. Some authors have found that the gallbladder wall in inflammation contains high concentrations of prostaglandins, which they believe are also mediators that cause acute cholecystitis. If the cystic duct obstruction is not relieved in time, the pressure within the gallbladder cavity will continue to increase, causing the gallbladder wall to become congested and edematous due to impaired blood and lymphatic return, leading to ischemia. The ischemic gallbladder wall is prone to secondary bacterial infection, thereby aggravating the progression of acute cholecystitis, ultimately leading to complications such as gallbladder gangrene or perforation. For the elderly, those with diabetes and arteriosclerosis are more prone to ischemic necrosis of the gallbladder. Ischemia, exacerbation of inflammation, and gangrene of the gallbladder fundus are commonly seen in the second week of onset. If not treated promptly, perforation and peritonitis may occur quickly. If the gallbladder duct obstruction is simple without blood supply disorders or bacterial infection of the gallbladder wall, it may develop into cholecystasis.

　　According to the severity of inflammation and the duration of the course, the pathological manifestations of acute cholecystitis can vary greatly.

　　1. Simple cholecystitis belongs to the mildest type. Its characteristics are mild enlargement of the gallbladder, congestion of the gallbladder wall, edema of the mucosa, and slight thickening of the gallbladder wall; grossly, bile appears more viscous, slightly turbid, or without obvious abnormalities, and under the microscope, there may be leukocyte infiltration and desquamation of mucosal epithelium, but the bacterial culture is often negative.

　　2. Empyema cholecystitis is marked by significant enlargement of the gallbladder due to obvious obstruction of the cystic duct, presenting a blue-green or gray-red color, with the gallbladder wall being congested and thickened, and the serosal layer vessels dilated; the gallbladder surface often has purulent fibrinous deposits, and ulcers may form on the mucosa, with the entire gallbladder filled with pus. The inflammatory exudation of the gallbladder wall can lead to adhesion with adjacent peritoneum and lymph node enlargement. At this time, the bacterial culture of bile is often positive. Under the microscope, there may be a large number of mononuclear cell infiltrations, bilirubin calcium precipitation, and cholesterol crystals.

　　3. In severe cases of gangrenous cholecystitis, the gallbladder may become excessively dilated, the blood supply to the gallbladder wall is obstructed, causing ischemic gangrene of the gallbladder wall; gallstones may become impacted at the neck of the gallbladder, causing compression and necrosis of the gallbladder wall. These changes can ultimately lead to gallbladder perforation, or even the formation of an internal fistula between the gallbladder and the duodenum. Under the microscope, in addition to inflammatory cell infiltration, gallbladder wall edema, and hemorrhage, there may also be localized or extensive necrosis, ischemia, and even perforation; sometimes, there may be small artery atherosclerosis with lumen stenosis.

　　1. Acute emphysematous cholecystitis is a special type of cholecystitis, mainly caused by anaerobic bacteria, such as Clostridium perfringens, causing infection, often with mixed infection caused by Streptococcus, Escherichia coli, and other bacteria. The main cause of bacterial infection is that when acute cholecystitis develops to a certain degree, the gallbladder accumulates pus, the gallbladder wall becomes ischemic and necrotic, which not only causes a decrease in oxygen partial pressure in the tissue, but also makes anaerobic bacteria easy to thrive, and various bacteria continuously produce gas, thereby spreading to the surrounding tissues of the gallbladder. In recent years, foreign scholars in China believe that purulent bile in the gallbladder stimulates the gallbladder mucosa, releases lysozyme, causing further inflammation of the gallbladder mucosa. At the same time, phospholipase A can also promote the conversion of lecithin in bile into lysophosphatidylcholine, promoting mucosal hemolysis and bleeding.

　　The clinical manifestations of the patient are similar to acute severe cholangitis, and sometimes the patient may have jaundice and melena. Jaundice is mainly due to the compression of the enlarged gallbladder or gallstones on the bile duct. Most patients have significant abdominal distension. If gallbladder perforation is combined, bile peritonitis signs may appear, and in severe cases, it can cause multiple organ dysfunction syndrome.

　　Acute emphysematous cholecystitis can be seen on abdominal X-ray films 24 to 48 hours after onset, with thickening of the gallbladder wall and gas accumulation. With the progression of the disease, it can spread to the surrounding tissues of the gallbladder. If the gallbladder necrosis and perforation occur, free gas under the diaphragm and peritoneal effusion may appear. In X-ray signs, it should be distinguished from gallbladder gas accumulation when there is a gallbladder-enteric fistula. Ultrasound examination can show gallbladder wall and intracavity gas accumulation, as well as acute cholecystitis ultrasound signs. Due to the high mortality rate of the disease, rapid progression of the lesion, gallbladder gangrene and perforation can occur early, so early cholecystectomy or cholecystostomy should be performed, and abdominal drainage should be carried out.

　　15. 2. Gallbladder perforation Perforation of acute cholecystitis can have various clinical manifestations.

　　14. 3. Gallbladder fistula The main clinical manifestations of gallbladder fistula are mainly due to cholecystitis and gallstone disease. Due to the different locations of the fistula, there are different clinical manifestations. The most common is gallbladder gastrointestinal fistula, and a few are fistulas formed between the gallbladder and renal pelvis, bladder, ovary, or uterus. Clinically, it is more common to form fistulas between the gallbladder and the stomach, duodenum, colon, and common bile duct. The main clinical manifestations after fistula formation are recurrent biliary infections and reflux acute cholecystitis. After gallstones pass through the duodenal fistula, duodenal obstruction may occur, and if they reach the small intestine, they can cause mechanical obstruction at the lower end of the small intestine, which is clinically known as biliary enteric obstruction. Patients with gallbladder colon fistula often manifest with steatorrhea, hyponatremia, malnutrition, and other symptoms.

　　Ultrasound has a high diagnostic rate for gallstones, but it is difficult to detect internal fistulas. CT scan after oral contrast agent shows high-density shadows of the gallbladder that are of the same density as the intestines, indicating a diagnosis. Barium meal and X-ray abdominal film are important and practical clinical methods for diagnosing gallbladder fistula. The former can directly diagnose gallbladder gastrointestinal fistula, and the latter can show that there is gas filling in the gallbladder or bile duct, and some can even see the shadow of gallstones in the intestines, but it should be excluded that factors such as sphincter of Oddi relaxation, emphysematous cholecystitis, cholangitis, and biliary-enteric anastomosis are involved. PTC shows the bile ducts clearly, and if the contrast agent enters the intestines through an abnormal channel, a diagnosis can be made. ERCP shows an abnormal opening in the duodenum with bile efflux, which can confirm the diagnosis.

　　12. 4. Liver abscesses mostly occur in the V segment of the liver adjacent to the gallbladder bed, and a very few are abscesses in other parts of the liver. The cause may be the external invasion of the liver tissue by acute suppurative cholecystitis, with the abscess appearing and worsening as cholecystitis subsides, or it may be due to perforation of acute cholecystitis into the liver tissue. Patients have high fever, chills, and CT examination of the liver shows low-density and liquid shadow areas in the V segment of the liver.

　　10. 1. Sudden, persistent severe pain in the right upper quadrant, radiating to the subscapular area on the right, accompanied by nausea and vomiting.

　　9. 2. Chills, fever, poor appetite, abdominal distension.

　　8. 10% of patients may have mild jaundice.

　　7. In the past, there has been a similar history, and high-fat diet is prone to induce, gallstones are the cause, and nocturnal onset is a characteristic.

　　6. Right upper quadrant muscle tension, tenderness or rebound pain, Murphy (Murphy) sign positive, 30%-50% of patients can feel a swollen gallbladder with tenderness.

　　To prevent acute cholecystitis, the following measures should be taken:

　　1. Pay attention to diet, and it is advisable to eat light food. Eat less greasy and fried, and roasted food.

　　2. Maintain smooth defecation.

　　4. To maintain a harmonious family life, and to maintain a cheerful mood, those who are long-term family disharmony and unhappy can trigger or worsen this disease.

　　3. It is necessary to change the sedentary lifestyle, walk more, and exercise more.

　　Firstly, laboratory examination

　　1. Total white blood cell count and neutrophils

　　About 80% of patients have an increased white blood cell count, averaging (10-15)×10^9/L. The extent of increase is related to the severity of the lesion and the presence of complications. If the total white blood cell count is above 20×10^9/L, it should be considered that there may be gallbladder necrosis or perforation.

　　2. Serum total bilirubin

　　Clinically, about 10% of patients have jaundice, but about 25% have increased serum total bilirubin. The serum total bilirubin of patients with simple acute cholecystitis is generally not more than 34μmol/L. If it exceeds 85.5μmol/L, it should be considered that there may be gallstones in the common bile duct. When complicated with acute pancreatitis, the blood and urine amylase levels also increase.

　　3, Serum transaminase

　　About 40% of patients have abnormal serum transaminases, but most are below 400U, and rarely reach the level increased during acute hepatitis.

　　Secondly, imaging examination

　　1. B-ultrasound

　　Ultrasound is a rapid and non-invasive examination method for acute cholecystitis, with the main sonographic features being:

　　(1) The length and width of the gallbladder can be normal or slightly larger, often elliptical due to increased tension.

　　(2) The gallbladder wall thickens, and the contour is blurred; sometimes it presents as a double-loop shape, with a thickness greater than 3mm.

　　(3) The transmissibility of the gallbladder contents is reduced, and scattered echo points appear in a misty pattern.

　　(4) The enhancement effect at the inferior margin of the gallbladder is weakened or disappears.

　　2. X-ray examination

　　About 20% of acute gallstone cases can be visualized on X-ray films. Empyema cholecystitis or cholecystic effusion can also show the shadow of an enlarged gallbladder or inflammatory tissue mass.

　　3. CT examination

　　Ultrasound can sometimes replace CT, but patients with complications that cannot be diagnosed must undergo CT examination. CT can show a thickened gallbladder wall over 3mm. If gallstones are impacted in the cystic duct, causing the gallbladder to significantly enlarge, the subserosal tissues around the gallbladder and fat may present as a low-density halo due to secondary edema. A gallbladder perforation can be seen as a fluid-level abscess in the gallbladder fossa. If bubbles are visible in the gallbladder wall or inside the gallbladder, it suggests 'emphysematous cholecystitis'. In such patients, the gallbladder often has gangrene. During contrast-enhanced scanning, the density of the inflamed gallbladder wall is significantly increased.

　　4. Intravenous cholangiography

　　For difficult-to-diagnose acute cholecystitis, if the serum bilirubin is within 3mg％ (51μmol/L) and there is no severe liver damage, intravenous cholangiography can be performed within 24 hours after admission (the patient does not need to prepare, using 30% cholangiographic meglumine 20ml). If both the bile duct and gallbladder are visible, acute cholecystitis can be ruled out; if only the gallbladder shows delayed imaging, acute cholecystitis can also be ruled out. If the bile duct is visible but the gallbladder does not show imaging after 4 hours, acute cholecystitis can be diagnosed. If neither the gallbladder nor the bile duct shows imaging, most cases are acute cholecystitis. Currently, due to the popularity of ultrasound imaging as the first-line examination for biliary tract diseases, oral and intravenous cholangiography are rarely used.

　　5. Radioisotope imaging

　　After intravenous injection of 131I-rose bengal or 99mTc-2-methylaminoacetic acid (99mTc-HIDA), liver and gallbladder scanning is performed. Generally, if the gallbladder shows no radioactivity within 90 minutes after injection, it indicates that the cystic duct is obstructed, which is mostly due to acute cholecystitis. This method is safe and reliable with a high positive rate, so 99mTc-HIDA scintigraphy can be considered as the first-line examination method for acute cholecystitis.

　　What foods should acute cholecystitis patients avoid eating:

　　1. Avoid eating fried and fried foods, avoid eating eggs, meat soup, and drinking alcohol;

　　2. Eat less greasy and fried foods.

　　3. Avoid eating animal brain, kidneys, yolks, etc.

　　First, treatment

　　The treatment of acute cholecystitis should be differentiated according to different causes. For calculous acute cholecystitis, surgical treatment is generally advocated, but the choice of timing for surgery is currently controversial. It is generally believed that 60% to 80% of patients with calculous acute cholecystitis can be relieved under non-surgical treatment, and then scheduled surgery can be performed. The complications and mortality rate of scheduled surgery are much lower than those of acute surgery. Recently, several prospective randomized studies have shown that early cholecystectomy for acute cholecystitis (surgery is performed at the time of diagnosis) is superior to scheduled cholecystectomy after the acute attack is relieved, with the advantage that the incidence of complications is significantly reduced, the number of hospital days is reduced, and no recurrence occurs. For patients with non-calculous cholecystitis, as their conditions are often more complex and complications are more frequent, surgery should be performed early. Therefore, the choice of the timing of surgery for patients with acute cholecystitis is very important.

　　The main surgical methods are cholecystectomy or cholecystostomy. If the condition allows and there are no contraindications, cholecystectomy is generally performed. However, for critically ill patients, cholecystostomy should be performed under local anesthesia to achieve the purposes of decompression and drainage.

　　1. Cholecystectomy is the most thorough surgical method and is also relatively safe at present, with an overall surgical mortality rate

　　At this stage of dissection, careful distinction should be made to avoid injury to the right hepatic duct and right hepatic artery. If severe inflammation and unclear anatomical relationships are encountered, it is advisable to first locate the common bile duct, incise and explore it, and then place a catheter into the common hepatic duct to help identify the cystic duct. A simpler method is to separate the gallbladder retrogradely, starting from the bottom of the gallbladder, peeling it off from the liver surface, and finally dealing with the cystic duct and cystic artery. The residual end of the cystic duct is generally left 3 to 4 mm long, which can prevent the suture from slipping and also prevent the formation of a blind pouch after surgery. When encountering massive bleeding during the dissection of the gallbladder, do not blindly clamp in the blood pool to avoid accidental injury to important structures such as the common bile duct and portal vein. At this time, the left index finger can be inserted into the omental foramen, and together with the thumb, the proper hepatic artery in the hepatoduodenal ligament can be pinched to stop the bleeding, and then the surgical field can be cleared to locate the bleeding point and give a thorough hemostasis. When剥离胆囊 from the liver bed, it is necessary to carefully clamp and ligate the small blood vessels that directly enter the liver bed, and place a drain in the gallbladder fossa to prevent hematoma and infection.

　　II. Cholecystostomy is suitable for a small number of critically ill patients who cannot tolerate more complex surgery. These patients have severe local inflammation of the gallbladder, abundant bleeding, unclear anatomical boundaries. If they are forced to undergo a more complex cholecystectomy, complications or injury to the important structures of the hilum of the liver may occur, increasing the mortality rate of surgery. The purpose of cholecystostomy is to drain the infected focus by simple methods, prevent its necrosis and perforation, and for the根治 removal of the focus, it is left for delayed treatment. The surgery usually uses the nearest incision to the bottom of the gallbladder (ultrasound positioning is used when possible), such as an incision below the right rib margin. After making a double purse-string suture at the bottom of the gallbladder, it is aspirated and decompressed at the center, a small incision is made to explore the gallbladder and try to remove all the stones, and then an 18-22F mushroom-shaped catheter is inserted, the double purse-string suture is tightened and tied. Then, warm saline is used to rinse the gallbladder and observe for leakage. If possible, the bottom of the gallbladder is fixed to the abdominal wall, and a drainage tube is placed next to the gallbladder.

　　If the patient cannot tolerate surgery, percutaneous cholecystostomy under ultrasound guidance can be performed to some extent to alleviate the condition. Laparoscopic cholecystectomy can also be performed if conditions permit.

　　II. Prognosis

　　Acute cholecystitis can be cured or resolved in about 80% to 90% of patients with medical treatment, and another 10% to 20% of patients may require surgical treatment due to the progression of the disease. It is worth noting that patients who claim to have been 'cured' may have recurrent episodes or complications such as cholelithiasis or choledochitis, and ultimately require surgical treatment. The overall mortality rate of acute cholecystitis is 5%. The prognosis of surgical treatment is relatively good, with about 70% to 80% of patients achieving recovery. The prognosis mainly depends on the patient's age, the presence of complications, the timing of the disease, whether the preoperative preparation is sufficient, and the type of surgery.