Gallbladder stones

　　1. Causes of onset

　　The onset of gallstones is related to age, gender, obesity, reproduction, race, and diet, and is also affected by medication history, surgical history, and other diseases.

　　1. Age of onset

　　Most epidemiological studies show that the incidence of gallstones increases with age. This disease is rare in childhood, and its occurrence may be related to hemolytic disease or congenital bile duct disease. A survey shows that the 5-year incidence rate among people aged 40 to 69 is four times higher than that of the younger age group, and the boundary between high incidence and low incidence is 40 years old. Although there are certain differences in the reports of various countries, the peak age of onset is generally between 40 and 50 years old.

　　2. Gender of onset

　　In recent years, the results of ultrasound diagnosis have shown that the ratio of male to female onset is about 1:2, and the difference in gender ratio is mainly reflected in the incidence of cholesterol stones, and there is no significant gender difference in the incidence of gallbladder pigment stones. The high incidence of cholesterol stones in women may be related to the decrease of estrogen in bile flow, the increase of cholesterol secretion in bile, the decrease of the total amount and activity of bile acids, as well as the influence of progesterone on gallbladder motility, causing bile stasis.

　　3. The relationship between onset and obesity

　　Clinical and epidemiological studies have shown that obesity is an important risk factor for the onset of gallbladder cholesterol stones, and the incidence rate of obese people is three times higher than that of people with normal weight. The reason why obese people are more prone to gallstones lies in the absolute increase of cholesterol synthesis in their bodies, or the relative increase of bile acids and phospholipids, leading to cholesterol oversaturation.

　　4. The relationship between onset and reproduction

　　Pregnancy can promote the formation of gallstones, and the number of pregnancies is positively correlated with the incidence of gallstones, which has been proven by clinical and epidemiological research. The reasons for the easy occurrence of gallstones during pregnancy include: ① The increase of estrogen during pregnancy changes the composition of bile, which can increase the saturation of cholesterol in bile. ② The gallbladder emptying is delayed during pregnancy, as shown by ultrasound, when pregnant women are fasting, the volume of the gallbladder increases, and the residual volume after contraction increases, and the contraction rate of the gallbladder decreases. ③ Changes in body weight during pregnancy and postpartum also affect the composition of bile, changing the enterohepatic circulation of bile acids, and promoting the formation of cholesterol crystals.

　　5. Differences in the regions of onset

　　There are certain differences in the incidence of gallstones between different countries and regions. The incidence of gallstones is high in Western Europe, North America, and Australia, while gallstones are rare in many places in Africa; the incidence of gallbladder stones is relatively high in Beijing, Shanghai, the northwestern and north China. The types of gallstones between countries and regions are also different. In countries such as Sweden and Germany, cholesterol stones are the main type, while in the UK, the incidence of calcium carbonate stones is higher than in other countries.

　　6. Onset and dietary factors dietary habits

　　It is one of the main factors affecting the formation of gallstones. The incidence of gallbladder stones in people who eat refined foods and high-cholesterol foods is significantly higher. This is because refined carbohydrates increase the saturation of cholesterol in bile. With the improvement of living standards in China, the incidence of gallbladder stones has already accounted for a major part of biliary lithiasis, and they are mainly cholesterol stones.

　　7. Onset and genetic factors

　　The difference in the incidence of gallbladder stones among races also suggests that genetic factors are one of the pathogenesis of biliary lithiasis. People with Indian genetic factors have a higher incidence of gallstones. Research on monozygotic twins has shown that the risk of gallstones in relatives of patients with cholelithiasis is also high, and the incidence rate in families with cholelithiasis is also higher, and the onset age is earlier, so it supports the possibility that cholelithiasis may have a genetic predisposition.

　　8. Other factors

　　The onset of gallbladder stones is also related to liver cirrhosis, diabetes, hyperlipidemia, parenteral nutrition, surgical trauma, and the use of certain drugs. For example, the incidence rate of biliary lithiasis in patients with liver cirrhosis is three times higher than that in patients without liver cirrhosis, and the incidence rate of biliary lithiasis in patients with diabetes is twice as high as that in patients without diabetes.

　　The composition of gallbladder stones is mainly cholesterol, and the formation reasons of gallbladder stones are not yet completely clear. Currently, it is considered that they are closely related to various factors such as lipid metabolism, nucleation time, gallbladder motor function, bacterial gene fragments, and many other factors.

　　2. Pathogenesis

　　1. Pathogenesis of gallbladder stones

　　The formation mechanism of gallbladder stones varies with the type of stone, and the formation mechanism is not the same. Among gallbladder stones, about 70% to 80% are cholesterol stones, and the exact formation mechanism is not yet clear. However, most researchers currently believe that it may be related to the following factors.

　　(1) Cholesterol supersaturation in bile to form 'calculus-forming bile': 'Calculus-forming bile' was first proposed by Smiall and Admirand in 1968. They applied the theory of mutual equilibrium between physics and chemistry to represent the relationship among bile salts, lecithin, and cholesterol with an equilateral triangle. Through simulating bile experiments, they found the region in this equilateral triangle where cholesterol is dissolved in the form of 'micelles'. Within this region, the 'micelles' in bile are not sufficient to dissolve all cholesterol, resulting in bile being in a supersaturated state. Consequently, cholesterol crystals precipitate, forming the so-called 'calculus-forming bile' region. However, recent studies have shown that the bile of most normal people is supersaturated, and the degree of supersaturation in liver bile is much higher than that in gallbladder bile, but cholesterol stones do not form. It has also been proposed that the cholesterol supersaturation index cannot distinguish between the bile of normal people and patients with cholesterol stones. Recent research also suggests that 'calculus-forming bile must meet two conditions at the same time': ① Cholesterol supersaturation in bile; ② Abnormal nucleation factors in bile. The cause of cholesterol supersaturation in bile is often due to normal secretion of bile salts with excessive cholesterol secretion, or due to normal cholesterol secretion with insufficient bile salt secretion.

　　(2) The existence of promoting nucleation factors: Recent research has found that there are particle structures with a size of 50-100 nm in fresh liver bile and gallbladder bile. These particles have a basic size similar to that in different bile specimens, and these particles are 10-20 times larger in diameter than the mixed 'microspheres'. And it has been confirmed that these particles are single-layer lipid 'bubbles' structures, and the main components of the 'bubbles' are cholesterol and lecithin, without bile salts, which confirms that the 'bubbles' in bile are another form of cholesterol solubility and transport.

　　After the bile of normal people is ultra-centrifuged, the number of 'bubbles' formed 2 hours later is more, with equal size and even distribution. This state can be maintained and stable for up to 168 hours, and then the aggregation and fusion of 'bubbles' and the formation of cholesterol monohydrate crystals occur. In the gallbladder bile of patients with cholesterol gallstones, the aggregation and fusion start 2 hours after ultra-centrifugation, and multiple-layer 'bubble' structures can be seen from 4 to 6 hours, and typical cholesterol monohydrate crystals can be found at 8 hours.

　　Under the condition of low degree of cholesterol supersaturation, cholesterol spontaneously precipitates and forms crystals from the solid-phase substances of other non-lipid components in the dissolved state. During the formation process, it is affected by nucleation factors. The influence of nucleation factors on nucleation is often divided into two types, one is the antinucleation factor, which can delay the occurrence of nucleation; the other is the promoting nucleation factor, which can promote the occurrence of nucleation.

　　Under normal circumstances, there are promoting/antagonistic nucleation factors in the gallbladder bile, and the two factors are relatively balanced. In the case of cholesterol gallstones, the force of promoting nucleation increases, disrupting the balance of promoting/antagonistic nucleation forces, leading to a rapid nucleation process. Studies have shown that the glycoprotein components in the gallbladder bile of patients with cholesterol gallstones have a significant shortening effect on the nucleation time of artificial simulated bile, and it has also been found that gallbladder mucin and calcium also have a significant promoting effect on nucleation, and they are important promoting nucleation factors in bile.

　　(3) Abnormal function of the gallbladder:

　　①Abnormal function of gallbladder mucosa, under normal circumstances, gallbladder mucosa can absorb water, electrolytes, and organic matter, while also secreting mucus. In the initial stage of cholesterol gallstones in the gallbladder mucosa, the main manifestations are: A, increased absorption of water and electrolytes by the mucosa, which improves the solubility of cholesterol 'microspheres', while reducing the stability of phospholipid cholesterol 'bubbles', thereby promoting the nucleation of cholesterol; B, the core of cholesterol gallstones often contains calcium, and normal gallbladder mucosa can absorb 50% of bile calcium, thus reducing the concentration of free calcium in bile, and the gallbladder mucosa also secretes hydrogen ions to acidify bile, increasing the solubility of free calcium. When the absorption and secretion functions of the mucosa change, it can lead to calcium supersaturation in bile, resulting in calcium salt precipitation; C, excessive secretion of mucin by the gallbladder mucosa.

　　② Abnormal gallbladder contraction function, the weakened gallbladder contraction function increases the retention time of bile in the gallbladder, providing an opportunity for the formation of cholesterol monohydrate crystals. In patients with complete parenteral nutrition, diabetes, pregnancy, and those using somatostatin, the formation of stones is all related to the weakened gallbladder emptying.

　　③ Cholestasis and bile sludge formation, due to the weakened contraction and emptying of bile movement of the gallbladder, the result is the cholestasis of cholesterol “bubbles” in the gallbladder into cholesterol monohydrate crystals, which are composed of bilirubin calcium ions and mucoprotein to form bile sludge. Most of the bile sludge will disappear, and about 15% of the bile sludge will continue to develop into gallstones.

　　2. Formation mechanism of bilirubin stones

　　The characteristics of bilirubin stones are mainly composed of “bilirubin calcium,” with a lower cholesterol content than bilirubin content. The bilirubin stones in the gallbladder are further divided into two types according to their clinical characteristics, namely black bilirubin stones and brown bilirubin stones.

　　(1) Characteristics and formation mechanism of black bilirubin stones:

　　① The patients have no history of recurrent biliary tract infection, bile culture is sterile, and it occurs in gallbladders without infection.

　　② The stones have a small volume, hard texture, black and shiny appearance and section, and irregular shape.

　　③ The oversaturation of “bilirubin calcium” in bile has nothing to do with the enhanced activity of bacterial β-G.

　　④ The incidence of black bilirubin stones in patients with hemolytic anemia is higher than that in normal people.

　　⑤ The content of glycoproteins and other proteins in black bilirubin stones is higher than that in brown bilirubin stones.

　　⑥ Chronic alcoholism can induce the formation of black bilirubin stones.

　　(2) The formation mechanism of brown bilirubin stones: Repeated biliary tract infection is an indispensable cause of the formation of brown bilirubin stones. The bacteria in the infected bile include anaerobic bacteria and aerobic bacteria, which can produce β-G and phospholipase A1. β-G hydrolyzes the bound bilirubin into unbound bilirubin, which combines with calcium in bile to form “bilirubin calcium,” leading to the oversaturation and precipitation of “bilirubin calcium.” Phospholipase A1 hydrolyzes phospholipids, releasing hemolytic phospholipids and free fatty acids, which can cause calcium fatty acid oversaturation and precipitation.

　　In addition, biliary tract infection can also cause the secretion of a large amount of glycoproteins by the mucosa of the biliary tract, which can aggregate various precipitates to form the matrix of stones.

　　“Bilirubin calcium” is a high molecular polymer, which is almost insoluble in various solvents. Moreover, due to its combination with glycoproteins in gallstones, direct perfusion dissolution becomes a difficult problem in treatment.

　　3. Classification of gallbladder stones

　　The analysis results of gallstone specimens in China show that cholesterol stones account for 70% of gallbladder stones, 23.8% are bilirubin stones, and the rest are mixed stones.

　　Currently, the classification of gallstones is often based on the similar components and the剖面 and surface observation of gallstones.

　　The clinical classification of gallstones based on their main components usually includes: ① Pure cholesterol stones; ② Pure bilirubin stones; ③ Mixed stones (mixed cholesterol-bilirubin or bilirubin calcium-cholesterol); ④ Rare stones, mainly composed of fatty acids, bilirubin fatty acids, polysaccharides, proteins, and so on.

　　1, Trotman, Soloway, and others proposed a relatively simple and practical classification method in 1974 and 1997. It is simply to divide them into cholesterol stones and pigment stones. Cholesterol stones are light brown, single or multiple, and the cross-section of the stones shows a radiating, layered, and crystalline appearance. Pigment stones are brownish black, the shape depending on the anatomical location, and the cross-section is amorphous. This classification method is relatively practical, but it is too simple, because the vast majority of gallstones are mixed.

　　2, Fu Peibin and others, based on the surface and cross-sectional observations of the stones, divided the stones into 8 types: ① Radiating stone: Grayish white and transparent, with a cross-sectional shape of a radiating column, composed of crystals, and the core is mostly a small amount of pigment granule clusters. ② Radiating annular stone: Most are brownish yellow, with a cross-sectional shape of a radiating pattern, as well as multiple concentric dark brown annular stripes. ③ Stratified rock: Light yellow or grayish white, dense and smooth, layered, with bilirubin granules or black substances between layers. ④ Casting amorphous stone: Deep brown, the shape of the stone is determined by the anatomical location, and the cross-sectional structure is amorphous. ⑤ Sand layer stone: The cross-section shows relaxed concentric circular layers, composed of similar-sized bilirubin granules, with white granules separating layers. ⑥ Mud and sand stone: Brown, fragile, in small pieces or mud and sand shape, all are loose aggregates of bilirubin granules. ⑦ Black stone: Seen in the gallbladder, about 0.5 cm in diameter, black, with luster, hard, and the cross-section is like asphalt. ⑧ Composite structure stone: A combination of the two structures mentioned above, such as the core part being a radiating stone, and the surrounding part being a stratified rock structure (Figure 1).

　　Gallstones can sometimes be the sequelae of chronic cholecystitis, but more often, they are formed first, and then acute and chronic cholecystitis develop secondarily. Due to the stimulation of the stones on the gallbladder mucosa, not only can chronic inflammation of the gallbladder be caused, but when stones become lodged in the gallbladder neck or cystic duct, they can also cause secondary infection due to the inability of bile to be excreted, leading to acute inflammation of the gallbladder, and further complications such as gallbladder empyema and gallbladder perforation. Occasionally, due to the long-term stimulation of gallstones on the gallbladder mucosa, gallbladder cancer may also occur.

　　1. Acute complications

　　1, Biliary colic: Sudden onset of paroxysmal severe pain in the hypochondrium or below the right rib, with heavy sweating and restlessness in severe cases. The pain often occurs at night or after eating greasy food, and it naturally subsides after several minutes to several hours or is relieved after taking antispasmodic drugs. There is no fever, but nausea and vomiting may occur. The gallbladder area may have tenderness but no muscle tension. When the severe pain is caused by gallstones lodging in the gallbladder neck, an ultrasound can show gallstones located in the gallbladder neck and an enlarged gallbladder; when the severe pain is caused by gallstones of about 0.5 cm in diameter falling into the common bile duct, an ultrasound can show not only gallstones but also a slight expansion of the common bile duct. If echoes of gallstones can be seen within the common bile duct, the diagnosis can be confirmed, but the absence of gallstone echoes does not exclude the possibility of gallstones hiding behind the duodenum in the common bile duct. Simple biliary colic does not accompany fever, jaundice, or increased blood and urine amylase levels. Biliary colic that does not resolve after 5 to 6 hours may lead to secondary infection and transform into one of the following three complications.

　　2. Acute cholecystitis: Caused by gallstones blocking the cystic duct orifice, leading to increased white blood cells and systemic inflammatory manifestations, as well as peritoneal irritation signs in the gallbladder area such as right upper quadrant tenderness and muscle tension. It is not accompanied by jaundice or increased blood and urine amylase levels.

　　3. Acute empyema of the bile duct: Caused by gallstones descending into the common bile duct (secondary bile duct stones) blocking the outlet of the bile duct, plus infection, leading to acute suppurative inflammation of the entire biliary tract, including the gallbladder. The onset is similar to acute cholecystitis but with more severe systemic inflammatory manifestations and jaundice. It is manifested as Schick's triad: upper abdominal pain, chills, and jaundice; shock is prone to occur. Serum ALT and AST levels increase. If blood and urine amylase levels also increase, it indicates the presence of acute pancreatitis. B-ultrasound examination shows small stones in the gallbladder and widened bile duct. If the echo of stones in the bile duct is seen, the diagnosis can be confirmed, but the absence of stone echoes does not exclude the possibility that there may be stones in the posterior segment of the bile duct duodenum.

　　4. Biliary acute pancreatitis: Sometimes, gallstones descending into the common bile duct can trigger pancreatitis without acute empyema of the bile duct when passing through or staying at the outlet of the bile duct, known as biliary pancreatitis. The onset is similar to biliary colic, but the pain is wider in the upper abdomen above the umbilicus and below the xiphoid process. At the same time, blood or urine amylase levels may increase. Jaundice may or may not be present. B-ultrasound examination shows not only gallstones and dilated bile ducts but also signs of pancreatic swelling and peripancreatic effusion; however, stones may not always be seen in the bile duct.

　　Two, chronic obstructive complications

　　1. Obstructive jaundice: The common bile duct is blocked by secondary bile duct stones without secondary infection or biliary colic. Patients seek medical attention due to jaundice.

　　2. Cholecystic hydrops: Patients seek medical attention due to palpable mass in the upper right abdomen or an enlarged gallbladder detected by B-ultrasound. This is the result of gallstone obstruction of the cystic duct orifice without secondary infection or biliary colic. After a long-term obstruction of the cystic duct orifice, the bile pigments in the gallbladder bile are absorbed, leaving colorless and transparent fluid, known as 'white bile'.

　　After gallstones cause biliary obstruction, it can lead to the dilation of the gallbladder or bile duct upstream, and the stones may become loose or float upwards to relieve the obstruction. Alternatively, if the obstructing stone is not large, it may be driven through the cystic duct or Oddi's sphincter to relieve the obstruction. Subsequently, inflammation subsides and symptoms disappear. After a period of quiet interval, it usually recurs. During the interval period, patients may either have no clinical symptoms or only the so-called 'chronic gastric disease symptoms' as before the obstruction.

　　The clinical symptoms of gallstone disease are often atypical. For gallstones with a history of acute attacks, diagnosis can usually be made based on clinical symptoms and signs; but without a history of acute attacks, diagnosis mainly relies on auxiliary examinations, with the following key points for diagnosis:

　　1. Recurrent acute cholecystitis, chronic cholecystitis, gallbladder effusion, or biliary colic, without jaundice of the skin and mucous membranes or mild jaundice.

　　2. Recurrent cholecystitis for many years without jaundice, this time accompanied by jaundice, should consider gallstones accompanied by secondary common bile duct stones.

　　3. Ultrasound shows gallstones in the gallbladder, gallbladder enlargement, effusion, wall thickening, or atrophy; oral gallbladder contrast confirms gallstones in the gallbladder, and the accuracy of ultrasound diagnosis can reach over 95%.

　　4. Mirizzi syndrome: In some patients, the gallbladder duct and common hepatic duct run parallel for a segment before merging into the common bile duct. If there is a calculus impacted in the gallbladder neck or gallbladder duct, the common bile duct may become partially obstructed or narrowed due to the pressure and inflammation from the calculus, causing recurrent cholangitis. The patients may experience right upper quadrant pain, fever, and jaundice. Ultrasound and laparotomy can confirm the diagnosis.

　　1. The proposal and concept of gallstone disease prevention The epidemiological survey of gallstone disease shows that the type of gallstones in China has shifted to cholesterol stones in large cities and wealthy rural areas. Although surgical operations can effectively treat gallstones, there are also new developments in laparoscopic surgery and many non-surgical methods available for the treatment of gallstones, yet gallstone disease remains a major issue in medicine and society. The symptoms of gallstone disease may recur repeatedly, with the risk of complications such as acute cholecystitis, cholecystitis, pancreatitis, and gallbladder cancer; surgical treatment may cause damage to the bile duct; and gallstone disease also has a certain mortality rate. The United States spends 5 billion US dollars on medical expenses for the treatment of gallstones each year. According to 5% of China's 1.2 billion population, there are 60 million patients waiting for treatment, and new cases of gallstones continue to appear every year. Therefore, the only way to solve gallstone disease is prevention.

　　In 1987, the first world conference on the prevention of gallstones was held in the United States, which proposed the concept of three-level prevention of gallstones, namely primary prevention, preventing the formation of gallstones; secondary prevention, preventing asymptomatic gallstones from transforming into symptomatic gallstones; and tertiary prevention, preventing the recurrence of gallstones after non-surgical treatment. Recently, Hofmann has once again emphasized the primary and secondary prevention of gallbladder calculi. Ruijin Hospital of the Second Military Medical University of Shanghai has proposed a four-level prevention of cholesterol gallstones, namely preventing the formation of gallstones; preventing the occurrence of gallstone symptoms; preventing recurrence after treatment; and preventing complications of gallstones. The emphasis is on primary prevention, and a series of studies on high-risk populations for gallstone disease have been carried out for primary prevention.

　　2. Prognosis

　　Severe complications and deaths caused by surgery are rare, and the mortality rate of surgery is about 0.1% in patients under 50 years old and 0.5% in those over 50. Death from surgery is often seen in patients considered to be at high risk before surgery. In about 95% of cases, symptoms can be relieved after surgery.

　　1. Simple gallbladder stones generally do not cause jaundice and liver dysfunction, so laboratory tests related to jaundice and liver function often have no positive results.

　　2. Imaging examinations are the main means of diagnosing gallbladder stone disease at present. Ultrasound is often the first-line examination method, which can find gallbladder stones, thickened gallbladder wall, and lack of gallbladder contraction. The results are often accurate and reliable. Other examination methods are often determined based on the results of ultrasound examination.

　　3. On X-ray films, about 20% of gallbladder stones, due to high calcium content, can present as positive images. Since the positive rate of stones is low, X-ray films of the liver and gallbladder area are no longer required for clinical diagnosis, but X-ray films can show the soft tissue shadow of an enlarged gallbladder and inflammatory mass, and in emphysematous cholecystitis, gas shadows inside and around the gallbladder can be seen. In addition, some indirect X-ray signs often help in the diagnosis of acute cholecystitis: (1) distension and aerophagia of the small intestine below the gallbladder, reflexive intestinal stasis; (2) increase in soft tissue shadow in the gallbladder area; (3) stimulation signs of the peritoneum, such as blurred or disappeared right peritoneal fat line, or elevated right diaphragm; (4) reactive pleural effusion or discoid atelectasis of the lower lobe of the right lung, etc.

　　① When the cystic duct is unobstructed and the gallbladder has good concentration function, oral cholecystography can show the negative shadow of stones inside the gallbladder, with an accuracy rate of up to 95%.

　　② If the cystic duct is unobstructed, intravenous cholecystography can show the negative shadow of stones inside the gallbladder.

　　4. On CT images, the gallbladder wall can be seen thickened, with stones and bile sedimentation inside the gallbladder. Oral gallbladder contrast agent CT scan can increase the resolution of stones.

　　First, Gallbladder Stone Food Therapy Formula:

　　1. Stewed Clam Meat with Corn Silk: 50 grams of corn silk, 200 grams of clam meat. Put corn silk and clam meat in a pot, add an appropriate amount of water, and simmer over low heat until tender. Take once every other day.

　　2. Egg and Cucumber Vine Drink: 100 grams of cucumber vine, 1 fresh egg. Wash the cucumber vine, boil it in water to 100 milliliters, then take the juice to mix with the egg. Take once a day, for clearing heat and benefiting the gallbladder, but not suitable for those with deficiency-cold.

　　3. Four-Flavor Drink: Boil 10 grams of loofah seeds, fried radish seeds, lychee kernel, and orange peel in water, and take the juice. Take once a day, served warm.

　　4. Stewed Lean Pork with Jin Qian Hua and Jin Yin Hua: 80 grams of Jin Qian Hua (200 grams fresh), 60 grams of Jin Yin Hua (150 grams fresh), 600 grams of lean pork, and 20 grams of yellow wine. Wrap Jin Qian Hua and Jin Yin Hua in gauze, immerse them with pork pieces in water, bring to a boil with yellow wine, then simmer over low heat for 2 hours, and remove the medicinal bag. Drink the soup and eat the meat, 1 small bowl per time, twice a day. Boil overnight, finish within 3 days.

　　II. Foods that are good for gallbladder stones:

　　1. Choose foods rich in high-quality protein and relatively low in cholesterol, such as fish, lean meat, dairy products, and soy products, and control the intake of animal liver, kidney, brain, or fish roe and other foods.

　　2. Ensure the supply of fresh vegetables and fruits. Leafy vegetables can provide necessary vitamins and a certain amount of fiber, which should be ensured. Yogurt, hawthorn, brown rice, and other foods are also beneficial to patients.

　　3. Drink more water, do not hold urine. Do not hold urine, drinking more and urinating more can help bacteria, carcinogens, and substances prone to forming stones be quickly excreted from the body, reducing the chance of kidney and bladder damage.

　　4. Eat bile-promoting foods Vegetables, spinach, bamboo shoots, onions, tomatoes, soybeans, corn, green peppers, pumpkins, red-skinned radishes, lotus roots, etc., all have varying degrees of stone-dissolving effects. Japanese researchers have also found that the gingerol in ginger can inhibit the synthesis of prostaglandins, reducing the formation of mucus in bile, and has a strong bile-promoting effect. Eating more of these foods is beneficial to prevent the formation of gallstones.

　　5. Eat more fiber-rich foods Foods rich in fiber can stimulate peristalsis and stimulate bile to flow into the intestinal cavity, preventing bile stasis. Foods rich in fiber include vegetables, fruits, and coarse grains.

　　6. Eat foods rich in vitamin A Foods rich in vitamin A can prevent the shedding of gallbladder epithelial cells, which can form stones, and also help in the digestion and absorption of fats, so they should be eaten regularly. Foods rich in vitamin A include corn, dairy products, fish, tomatoes, carrots, etc.

　　III. Foods to avoid eating for gallbladder stones:

　　1. Drink less beer

　　Some people think that beer can diuretic and prevent the occurrence of kidney stones. In fact, the malt juice in beer contains acidic substances such as calcium, oxalic acid, uridine nucleotides, and purine nucleotides, which interact with each other to increase uric acid in the body, making it an important cause of kidney stones.

　　2. Eat less meat and animal internal organs

　　Control the intake of meat and animal internal organs, because meat metabolism produces uric acid, and animal internal organs are high-purine foods, which also produce high blood uric acid during metabolism. Uric acid is a component of kidney stone formation. Therefore, daily diet should be mainly vegetarian, and more fiber-rich foods should be eaten.

　　3. Reduce salt intake

　　Too salty diets will increase the workload of the kidneys, and salt and calcium have a synergistic effect in the body, which can interfere with the metabolism process of drugs for the prevention and treatment of kidney stones. The daily intake of salt should be less than 5 grams.

　　4. Be cautious when eating spinach

　　According to statistics, more than 90% of kidney stones contain calcium, and about 87.5% of calcium oxalate stones. If the intake of oxalates in food is too high, and the calcium oxalate in urine is in a supersaturated state, excess calcium oxalate crystals may precipitate from the urine to form stones. In food, spinach has the highest oxalate content, and it is also one of the vegetables commonly eaten by people.

　　5. Do not drink milk before going to bed

　　Due to the high calcium content in milk, and most kidney stones contain calcium salts. The most dangerous factor in the formation of kidney stones is the sudden increase in calcium concentration in urine over a short period of time. Two to three hours after drinking milk, it is the peak time for calcium to be excreted by the kidneys. If one is in a state of sleep at this time, the urine becomes concentrated, and more calcium passes through the kidneys, thus making it easier to form stones.

　　6. It is not advisable to eat too much sugar

　　After taking sugar, the concentration of calcium ions in urine, oxalic acid, and the acidity of urine will increase. Increased uric acid can make calcium urate and calcium oxalate more prone to precipitation, promoting stone formation.

　　7. Avoid spicy foods such as chili, curry, and mustard greens, as well as alcohol, coffee, and strong tea.

　　1. Surgical treatment for gallstones

　　In recent years, many non-surgical treatment methods for gallstone disease have emerged, some of which were popular for a time, but ultimately failed to pass the test of practice. These include oral medication for dissolving stones, contact dissolution therapy, extracorporeal shock wave lithotripsy, and so on. Some interventional treatments aim to remove stones while preserving the gallbladder, such as percutaneous cholecystoscopy with ultrasound lithotripsy and stone extraction, small incision cholecystotomy for stone extraction, etc. Since the pathological gallbladder, the bed for stone formation, is preserved, there is the drawback of a high recurrence rate of stones. So-called small incision cholecystectomy requires the establishment of a series of delicate work procedures to achieve better results, not just making the incision smaller. After many years of practical testing, surgical treatment remains the preferred method for treating symptomatic gallstones today. Minimally invasive surgery is the current trend in surgery, and laparoscopic cholecystectomy conforms to this trend.

　　1. Indications for open surgery for gallstones

　　(1) Gallstones accompanied by acute cholecystitis, onset within 72 hours, with clear surgical indications (suppurative, gangrenous, obstructive).

　　(2) Recurrent chronic cholecystitis that does not respond to non-surgical treatment, and ultrasound indicates thickening of the gallbladder wall.

　　(3) Gallstones with symptoms, especially small stones that are prone to impaction.

　　(4) Atrophy of the gallbladder with no function.

　　(5) Internal and external fistulas in the gallbladder, especially mucinous fistulas after cholecystostomy.

　　(6) Gallstones in diabetic patients.

　　2. Contraindications for open surgery for gallstone

　　(1) Chronic pain in the upper right abdomen that cannot be explained by gallbladder lesions, and ultrasound and gallbladder imaging did not find any abnormalities in the gallbladder.

　　(2) The gallbladder should not be removed blindly before the etiology of obstructive jaundice is clarified.

　　(3) Patients with severe heart, lung, liver, kidney dysfunction or other serious internal diseases that cannot tolerate cholecystectomy.

　　3. Precautions

　　Patients with acute cholecystitis who meet the following conditions can be treated with non-surgical methods first, and elective surgery can be performed after the acute phase.

　　(1) Young patients with mild symptoms during the first attack.

　　(2) Patients whose condition rapidly improves after conservative treatment.

　　(3) Patients with atypical clinical symptoms.

　　(4) Patients with onset of disease for more than 3 days, without urgent surgical indications, and symptoms improved with conservative treatment.

　　4. Common surgical methods include open cholecystectomy and laparoscopic cholecystectomy. Traditional open surgery is divided into two types: conventional and retrograde resection. If the gallbladder triangle anatomy is abnormal or there is inflammation, edema, severe adhesion that is difficult to separate, the method of combined forward and backward resection can also be used to remove the gallbladder.

　　(1) Conventional cholecystectomy:

　　①Exposing and handling the cystic duct: Incise the peritoneum on the left side of the cystic neck along the lateral margin of the hepatoduodenal ligament, carefully separate the cystic duct, and ligate and cut the cystic duct with a clamp 0.5cm away from the common bile duct.

　　② Treatment of the cystic artery: Anatomize the cystic triangle, find the cystic artery, and pay attention to its relationship with the right hepatic artery. After confirming its distribution to the gallbladder, clamp, cut, and ligate it close to the gallbladder side, and ligate the proximal end in duplicate. If the local anatomical relationship can be clearly identified, the cystic artery can be ligated and cut first in the gallbladder triangle area, and then the cystic duct can be handled. This makes the surgical field clean and bleeding less, allowing the gallbladder duct to be safely pulled to straighten the twisted and spiraling gallbladder duct, making it easy to recognize the relationship with the common bile duct. If the cystic artery is not cut and ligated, it is likely to tear or break the cystic artery when pulling the gallbladder, causing massive bleeding.

　　③ Removing the gallbladder: At a distance of 1 to 1.5 cm from the liver edge at the subserosal junction between the gallbladder and the liver surface, incise the gallbladder serosa. If there has been recent acute inflammation, the gallbladder can be separated using fingers or a gauze ball along the subserosal loose space under the incised serosa. If the gallbladder wall is thickened and it is difficult to peel off due to adhesion with surrounding tissues, a small amount of sterile normal saline or 0.25% procaine can be injected under the gallbladder serosa, and then the separation is performed. When separating the gallbladder, it can be converged from both ends of the gallbladder bottom and neck to the middle to remove the gallbladder. If there are communicating vessels and wandering bile ducts between the gallbladder and the liver, they should be ligated and cut to prevent postoperative bleeding or bile fistula.

　　④ Treatment of the liver: After removing the gallbladder, a small amount of oozing bleeding in the gallbladder fossa can be stopped by pressing with a hot saline gauze pad for 3 to 5 minutes. Active bleeding points should be ligated or sutured to stop bleeding. After hemostasis, the serosa on both sides of the gallbladder fossa is sutured with silk thread in an interrupted manner to prevent oozing or adhesion. However, if the gallbladder fossa is wide and the serosa is less, it is not necessarily sutured.

　　(2) Retrograde cholecystectomy:

　　① Incision of the gallbladder bottom serosa: Clamp the bottom of the gallbladder with a forceps to pull it, inject a small amount of normal saline under the serosa at a distance of 1 cm from the gallbladder margin around the liver, causing the serosa to swell and float up, and incise the serosa at that location.

　　② Separation of the gallbladder: Starting from the bottom of the gallbladder, separate the gallbladder from the subserosal space to the body. The ligation and incision during separation must be close to the gallbladder wall. If adhesions are tight and separation is difficult, the bottom of the gallbladder can be incised, and the left index finger can be inserted into the gallbladder as a guide for sharp dissection around the gallbladder wall.

　　③ Exposure and ligation of the cystic artery: When the separation reaches the neck of the gallbladder, find the cystic artery above and inside, clamp, cut, and ligate the artery close to the gallbladder wall, and ligate the proximal end in duplicate.

　　④ Separation and ligation of the cystic duct: Clamp the neck of the gallbladder and pull it outward, separate the covering serosa, find the cystic duct, and separate and trace it to the junction with the common bile duct. After seeing the relationship between the two, clamp, cut, and ligate 0.5 cm away from the common bile duct, and then remove the gallbladder. The residual end of the cystic duct is ligated with a medium-sized silk thread and then reinforced with a suture.

　　(3) Laparoscopic cholecystectomy:

　　Laparoscopic cholecystectomy has become a mature surgical technique, characterized by minimal trauma, less patient pain, and rapid recovery, which is widely accepted by patients. In 1992, the Department of Surgery of the Chinese Medical Association conducted a survey of 3,986 cases of laparoscopic cholecystectomy in China, and the surgical complications were slightly higher than those of open surgery, so strict control of the indications and contraindications for surgery should be exercised, and technical training should be strengthened.

　　① Indications:

　　A, gallstones with symptoms. B, chronic cholecystitis with symptoms. C, gallstones with a diameter greater than 3cm. D, gallstones of the filling type. E, gallbladder protrusive lesions with symptoms and surgical indications. F, acute cholecystitis with symptoms relieved after treatment and surgical indications. G, estimated to be well tolerated by the patient for surgery.

　　② Contraindications:

　　B, relative contraindications include: a, Acute attack of calculous cholecystitis. b, Chronic atrophic calculous cholecystitis. c, Secondary common bile duct stones. d, History of upper abdominal surgery. e, Obesity. f. Hernia.

　　B, absolute contraindications: a, Acute cholecystitis with severe complications, such as empyema, gangrene, perforation, etc. b, Acute pancreatitis due to gallstones. c. Acute cholangitis. d. Primary common bile duct stones and intrahepatic bile duct stones. e, Obstructive jaundice. f, Cholecystoma. g, Suspicious cholecystic protrusive lesions for possible malignancy. h, Liver cirrhosis with portal hypertension. i, Middle and late pregnancy. j, Abdominal infection, peritonitis. Other conditions include chronic atrophic cholecystitis, gallbladder less than 4.5cm×1.5cm, wall thickness >0.5cm (ultrasound measurement). With bleeding disorders, coagulation dysfunction. Incomplete function of important organs, difficult to tolerate surgery and anesthesia, and those with a pacemaker (prohibition of electrocoagulation and electrosection). Poor general condition not suitable for surgery or elderly patients without strong indications for cholecystectomy, diaphragmatic hernia.

　　The scope of indications for laparoscopic surgery continues to expand with the development of technology. Certain diseases that were originally relative contraindications for surgery are also increasingly being attempted to be completed by laparoscopy. For example, secondary common bile duct stones can already be partially solved by laparoscopic surgery. After gaining the necessary experience, more diseases will be available for laparoscopic surgical treatment.

　　③ Surgical steps:

　　A, creating pneumoperitoneum: Make an arc-shaped incision along the inferior margin of the umbilical fossa, about 10mm long. If there has been previous surgery in the lower abdomen, the incision can be made above the umbilicus to avoid the original surgical scar and cut the skin. The operator and the first assistant each hold a towel clamp to lift the abdominal wall from both sides of the umbilical fossa. The operator holds the pneumoperitoneum needle (Veress needle) with the thumb and index finger of the right hand, applies force with the wrist, and inserts the needle vertically or slightly obliquely into the peritoneal cavity. There are two breakthrough sensations when the needle head breaks through the fascia and peritoneum during the puncture process; judge whether the tip of the needle has entered the peritoneal cavity. A syringe filled with physiological saline can be connected, and a negative pressure is present when the needle tip is in the peritoneal cavity. Connect the pneumoperitoneum machine, if the inflation pressure display does not exceed 1.73kPa, it indicates that the pneumoperitoneum needle is in the peritoneal cavity. When starting to inflate, it should not be too fast, use low-flow inflation, 1-2L/min. At the same time, observe the intraperitoneal pressure on the pneumoperitoneum machine; the pressure should not exceed 1.73kPa during inflation. If it is too high, it indicates that the position of the pneumoperitoneum needle is incorrect or the anesthesia is too shallow and the muscles are not sufficiently relaxed, and appropriate adjustments should be made. When the abdomen begins to swell and the liver dullness boundary disappears, high-flow automatic inflation can be changed to until reaching the predetermined value (1.73-2.00kPa), at this time, inflate 3-4L, the patient's abdomen is completely swollen, and the operation can begin.

　　At the umbilical pneumoperitoneum needle site, lift the abdominal wall with a towel clip, puncture with a 10mm trocar, the first puncture has a certain degree of 'blindness' and is one of the more dangerous steps in laparoscopy, requiring extra caution. Rotate the trocar slowly and insert it evenly, feeling a sudden disappearance of resistance when entering the abdominal cavity. Open the sealed gas valve and gas will escape, indicating successful puncture. Connect the pneumoperitoneum machine to maintain a constant pressure in the abdominal cavity. Then insert the laparoscope and perform punctures at various points under the laparoscope. Generally, puncture 2cm below the xiphoid process and insert a 10mm trocar for the electrocoagulation hook and clip applicator. At 2cm below the right midclavicular line rib margin or 2cm below the lateral edge of the rectus muscle and axillary前线 rib margin, puncture with a 5mm trocar to insert the irrigator and gallbladder fixation forceps. At this point, artificial pneumoperitoneum and preparation are complete.

　　Due to the risk of accidentally injuring major blood vessels and intestines in the abdominal cavity during the creation of pneumoperitoneum and the first trocar puncture, and the difficulty in discovery during surgery, recently, many people have changed to making a small incision at the umbilicus, finding the peritoneum, and directly inserting the trocar into the abdominal cavity for inflation.

　　After successful creation of pneumoperitoneum, start the surgical operation. The division of labor in surgery varies from hospital to hospital; in the General Hospital of the People's Liberation Army, the surgeon holds the gallbladder fixation forceps and electrocoagulation hook, responsible for all surgical operations; the first assistant holds the irrigator, responsible for irrigation, aspiration, and assisting in exposing the surgical field; the second assistant holds the laparoscope to ensure that the surgical field is always displayed in the center of the television screen.

　　B. Dissection of the Calot triangle: Grasp the gallbladder neck or Hartmann's pouch with a forceps and pull it upwards to the right. It is best to pull the gallbladder duct perpendicular to the common bile duct to clearly distinguish the two, but be careful not to angle the common bile duct. Cut the serosa on the gallbladder duct with an electrocoagulation hook, bluntly separate the gallbladder duct and gallbladder artery, and identify the common bile duct and common hepatic duct. Since it is close to the common bile duct, use as little electrocoagulation as possible to avoid accidental injury to the common bile duct. Free the gallbladder duct with an electrocoagulation hook. Make sure to see the relationship between the gallbladder duct and the common bile duct. Place titanium clips as close as possible to the gallbladder neck, ensuring there is enough distance between the clips, with a minimum distance of 0.5cm from the common bile duct. Cut between the clips with scissors, not using electrocautery or electrocoagulation to prevent heat conduction and injury to the common bile duct. Then find the gallbladder artery behind it and place a titanium clip to cut it. After cutting the gallbladder artery, do not pull it too hard to avoid breaking the gallbladder artery, and pay attention to the posterior branch of the gallbladder artery. Carefully剥离 the gallbladder, use electrocoagulation or place titanium clips to stop bleeding.

　　C. Cholecystectomy: Clamp the gallbladder neck and pull it upwards, carefully剥离 along the gallbladder wall. The assistant should assist in pulling to create a certain tension between the gallbladder and the liver bed. Remove the gallbladder completely and place it above the right lobe of the liver. Stop bleeding on the liver bed with electrocoagulation, rinse carefully with saline, and check for bleeding and bile leakage (place a gauze pad at the hilum of the liver, remove it and check for bile staining). After removing the accumulated fluid in the abdominal cavity, switch the laparoscope to the subxiphoid trocar, leave the umbilical incision open for the next step, which is to remove a gallbladder larger than 1cm containing stones from the relatively loose and easily dilated umbilical incision. If the stones are small, they can also be removed through the puncture hole below the xiphoid process.

　　D, Removing the gallbladder: Insert a toothed forceps through the trocar at the umbilicus into the peritoneal cavity, grasp the residual end of the gallbladder duct under the monitor, slowly pull the gallbladder into the trocar sheath, and remove it together with the trocar sheath. When gripping the gallbladder, pay attention to place the gallbladder above the liver to avoid the sharp teeth of the forceps from accidentally injuring the intestines. If the stone is large or the gallbladder tension is high, do not pull it out with force to avoid rupture of the gallbladder, leakage of stones and bile into the abdominal cavity. At this time, it can be removed by expanding the incision with a hemostat or by using an expander to expand the incision to 2.0cm, if the stone is too large, the incision can be extended. If bile leaks into the abdominal cavity, use a moist gauze to enter the umbilical incision to absorb the bile clean. If the stone is too large to be removed from the incision, first open the gallbladder, dry the bile in the gallbladder with a suction device, crush the stones and remove them one by one. If stones are found to have fallen into the abdominal cavity, they should be removed thoroughly.

　　After checking that there is no blood and fluid in the abdominal cavity, remove the laparoscope, open the valve of the trocar to exhaust the carbon dioxide gas in the abdominal cavity, and then remove the trocar. Suture the fascia layer with a fine thread at the incision for the 10mm trocar 1 to 2 times, and close all incisions with sterile adhesive film.

　　④ Points to note during surgery:

　　A, Precautions for establishing pneumoperitoneum: When puncturing the abdominal wall in obese patients, the sense of breakthrough is not obvious twice, to confirm that the needle tip is indeed in the peritoneal cavity, connect a syringe filled with saline to the pneumoperitoneum needle, if the saline in the syringe flows into the peritoneal cavity naturally under gravity, it indicates that the puncture needle has entered the peritoneal cavity. Always watch the gas flow gauge during inflation, the pressure should not exceed 1.73kPa at 4L/min, and the abdomen should rise evenly during inflation, and the liver dullness boundary should disappear.

　　After the pneumoperitoneum is established, to further confirm whether there is adhesion of the intestines at the umbilicus, a Palmer aspiration test can be performed: connect a 10ml syringe filled with normal saline to an 18-gauge needle, puncture into the peritoneal cavity through the umbilicus, at this time the carbon dioxide gas in the peritoneal cavity will push the saline out of the syringe, and only gas enters the needle, indicating that there is no intestine here. If blood is aspirated or fluid cannot be aspirated, it indicates local adhesion. If intestinal fluid is aspirated, it indicates adhesion of the intestines.

　　B, Precautions for the use of high-frequency electrosurgical knives: The most common injury to the common bile duct and intestines in laparoscopic organ injury should be noted.

　　The insulating layer of laparoscopic instruments such as electrocoagulation hooks should be intact, and timely replacement should be made when damaged; preoperative preparation should be sufficient, and enema should be performed to eliminate intestinal bloating; low-voltage high-frequency electrocoagulation is safe at 200V, and no ionized sparks should be produced during cutting; for intestinal injury, the operator often fails to find it at the time, so the electrocoagulation instrument should always be placed on the monitor screen during the operation; when the operator uses the electrocoagulation hook, the force should be kept upward (abdominal wall) to prevent the electrocoagulation hook from rebounding and burning surrounding organs.

　　C, Anatomy of the Calot triangle: It is mainly to prevent biliary duct injury. Abnormal course of the bile duct is common, so special care should be taken. It is not allowed to use electrocoagulation during dissection to prevent injury to the common bile duct, and it is best to use electrocoagulation hooks or dissectors carefully. When the adhesion of the Calot triangle is very severe or congestion and edema are obvious, and the common bile duct cannot be distinguished, it is wise to switch to open surgery.

　　D, Handling the cystic duct: One of the causes of bile leakage is improper handling of the cystic duct. The cystic duct is short or the cystic duct is thick, the clip is not fully closed, which often makes the handling of the cystic duct difficult. When encountering a short cystic duct, try to clamp the clip on the side of the common bile duct well, keep the gallbladder side open, and drain the bile. The distal end of the gallbladder should be left with sufficient length to prevent the clip from slipping off. When encountering a thick cystic duct, it is first tied with silk thread, and then the clip is applied. Now there are large clips that work well for thick cystic ducts.

　　E, Intraoperative cholangiography: There are many methods for cholangiography during bile duct surgery. The method used by the General Hospital of the People's Liberation Army is to clamp the cystic duct on the side of the gallbladder during cholangiography, then cut a small incision on the cystic duct, clamp the opening of the catheter with a hemostat, inject contrast agent and take a film, and monitor the operation with a laparoscope during the process. There are now special hemostats for cholangiography, which are very convenient to use.

　　F, Removal of the gallbladder: The abdominal muscle at the umbilical trocar hole is relatively weak and can be easily separated with hemostats. When the gallbladder stone is large, the neck of the gallbladder is first pulled out through the abdominal wall, the gallbladder is opened to drain the bile, and the stone is removed from the gallbladder with a stone forceps. If the stone is large, it can be crushed inside the gallbladder first and then removed. After removal, the accumulated blood and bile in the incision should be wiped dry. It is absolutely forbidden to pull out the gallbladder with force when the incision is not large enough, which may cause the gallbladder to rupture and the stones to fall into the abdominal cavity. If stones fall into the abdominal cavity, they should be removed in full, otherwise, residual stones may cause abdominal infection and adhesion.

　　G, Laparoscopic cholecystectomy is a surgery with risks. The entire process of the surgery should be recorded so that the cause can be found in case of surgical complications.

　　⑤ Main complications:

　　A, Biliary duct injury: Biliary duct injury is one of the most common and serious complications of laparoscopic cholecystectomy. The incidence of biliary duct injury and bile leakage is about 10%. It should be given sufficient attention. The main cause is the unclear anatomy of the Calot triangle, especially the lack of vigilance for common variations of the common bile duct or the cystic duct. Unintentional thermal injury to the bile duct during the separation of the cystic duct can lead to bile leakage, as there is no bile leakage during the operation. Postoperative necrosis and shedding of tissue in the area of thermal injury can also cause bile leakage. In addition, the gallbladder bed often has a large wandering bile duct, and the electrocoagulation during the operation cannot be completely coagulated, which can also lead to bile leakage. The main manifestations of biliary duct injury are severe upper abdominal pain, high fever, and jaundice. Patients with typical symptoms generally receive timely treatment after surgery; however, a small number of patients may only present with abdominal distension, lack of appetite, and low fever, which may progressively worsen. Close observation of such patients is necessary, as there have been reports of bile accumulation in the abdominal cavity months after surgery. The judgment of whether there is bile leakage mainly relies on ultrasound or CT examination, and then fine needle puncture or radioactive liver and gallbladder scintigraphy is used to confirm under the guidance of ultrasound or CT.

　　B. Vascular Injury: One type is massive hemorrhage caused by the tip of the needle damaging the abdominal aorta, iliac artery, or mesenteric artery during the creation of pneumoperitoneum and the insertion of the trocar, with reports of deaths due to trocar puncture. Therefore, after the success of pneumoperitoneum, the laparoscope should scan the entire abdomen to prevent the omission of vascular injuries; another type is unclear anatomy at the porta hepatis or accidental clamping of the right hepatic artery or proper hepatic artery due to bleeding from the gallbladder artery, as well as reports of portal vein injury during dissection. There was a report of right liver necrosis caused by accidental clamping of the hepatic artery.

　　C. Intestinal Injury: Intestinal injury is mostly caused by accidental injury during electrocoagulation, mainly due to the electrocoagulation hook not being placed on the television monitoring screen and not being discovered, leading to postoperative abdominal pain, distension, fever, and severe peritonitis, with a high mortality rate.

　　D. Postoperative Intraperitoneal Hemorrhage: Postoperative intraperitoneal hemorrhage is also one of the serious complications of laparoscopic surgery. The main damaged areas are the blood vessels near the gallbladder, such as the hepatic artery, portal vein, and abdominal aorta or vena cava damaged during umbilical puncture. It is manifested as hemorrhagic shock, abdominal swelling, and circulatory failure. Immediate laparotomy should be performed to stop the bleeding.

　　E. Subcutaneous Emphysema: The causes of subcutaneous emphysema are: one is that when creating pneumoperitoneum, the needle of the pneumoperitoneum does not penetrate the abdominal wall, and high-pressure carbon dioxide enters the subcutaneous tissue; the other is that due to a small skin incision, the trocar is inserted very tightly, and the puncture hole of the peritoneum is relatively loose, carbon dioxide gas leaks into the subcutaneous layer of the abdominal wall during surgery. Postoperative examination can find crepitus under the abdomen, which generally does not require special treatment.

　　F. Others: Such as incisional hernia, incisional infection, and peritoneal abscess, etc.

　　2. Other Special Therapies

　　Non-surgical treatment for cholecystolithiasis includes litholysis, stone expulsion, extracorporeal shock wave lithotripsy, and endoscopic stone removal. The first three are non-invasive, and the last one is invasive. Clinical practice has shown that the lesions of cholecystolithiasis are located in the gallbladder. Simply using the aforementioned non-surgical treatments can temporarily remove stones in some patients, but cannot cure the intrinsic lesions of the gallbladder itself. The recurrence of gallstones in the long term is inevitable, so caution should be exercised when choosing non-surgical treatment for cholecystolithiasis.

　　1. Litholysis Therapy: Currently, the main drugs for litholysis therapy are ursodeoxycholic acid (ursodeoxycholic acid) and chenodeoxycholic acid (chenodeoxycholic acid). Chenodeoxycholic acid (chenodeoxycholic acid) (chenodeoxycholic acid, CDCA) is obtained by processing and extracting from cow bile, with a structure similar to that synthesized physiologically in human liver. It is taken orally in the form of capsules, with a daily dose of 250-1000mg, and the absorption rate reaches 80%-90%. After absorption, it is transported to the liver, where it combines with glycine and bilirubinate and is secreted into the bile ducts through bile. The mechanism of action of chenodeoxycholic acid can be summarized as follows: ① By inhibiting the biosynthesis of cholesterol by restricting the activity of liver HMG-CoA (hepatichydroxymethylglutaryl, coenzyme A); ② Reducing the absorption of cholesterol in the intestines; ③ Reducing the activity of 7α-hydroxylase (7α-hydroxylase) to inhibit the biosynthesis of endogenous bile acids, while also reducing the entry of cholesterol into the exchangeable cholesterol pool; ④ Chenodeoxycholic acid has the effect of increasing low-density lipoprotein in the blood.

　　However, there are also side effects of chenodeoxycholic acid treatment, mainly including three points: ①Serum transaminase levels increase, usually temporarily, rarely exceeding twice the normal level; ②Serum cholesterol levels continue to rise; ③Diarrhea occurs at high doses. The dosage of chenodeoxycholic acid is: 10-20 mg/kg/day, then most patients' bile is in a non-saturated state of cholesterol, and the ratio of bile acids plus lecithin/cholesterol reaches about 20. The course of chenodeoxycholic acid treatment is 6 months to 2 years, suitable for most small cholesterol stones, patients with gallbladder contraction function, and has little effect on large single stones. Most gallstones in China are mixed stones, and the efficacy of drug treatment is worse. The biggest problem of chenodeoxycholic acid treatment is the recurrence of gallstones after stopping treatment, with 25% to 50% of patients experiencing recurrence, often within 3 months after treatment, with an annual recurrence rate of 10%.

　　Ursodeoxycholic acid (ursodeoxycholic acid, ursodiol UDCA) is a 7-β isomer of chenodeoxycholic acid. Its effect is better than that of chenodeoxycholic acid, and it has no side effects of chenodeoxycholic acid. The mechanisms of action of the two are different, UDCA has no inhibitory effect on the biosynthesis of cholesterol and bile acids, which can increase the content of UDCA in bile. The side effects of UDCA are few, and the effect may be better. The dosage of UDCA is: 8-13 mg per kilogram of body weight per day, taken in three doses.

　　The combined application of ursodeoxycholic acid (chenodeoxycholic acid) and ursodeoxycholic acid in equal proportions can enhance the effectiveness of dissolution, while reducing the side effects of each drug when used separately.

　　In summary, ursodeoxycholic acid and/or UDCA are only effective for cholesterol stones, and are suitable for stones with a diameter less than 1 cm, which can be single or multiple, X-ray permeable, and for patients with good gallbladder function. Continuous medication for half a year to 2 years is effective. Due to the long course of treatment, less than 10% of patients can persist with the treatment. The recurrence rate is high, the drug has side effects, and the drug price is expensive, which limits its application. In recent years, it is often used in combination with shock wave lithotripsy treatment, becoming part of the systemic treatment for gallstones.

　　2. Extracorporeal Shock Wave Lithotripsy (ESWL): China held the first national academic symposium on extracorporeal shock wave lithotripsy for bile duct diseases in January 1991, reporting 6357 cases of extracorporeal shock wave lithotripsy. ESWL treatment for gallstones has not been widely conducted in China for a long time, but its impact is significant, and the third-generation extracorporeal shock wave lithotripsy machines with high automation have emerged. It is divided into three types according to the different extracorporeal shock wave generators: ①Electrohydraulic shock wave; ②Electromagnetic shock wave, which uses the working principle of electromagnetic pulse generators to crush stones; ③Piezoelectric shock wave, which uses the principle of inverse piezoelectric effect to crush stones.

　　To completely expel broken gallstone fragments, it is necessary to rely on: ①Natural excretion of fragments; ②Stone expulsion therapy; ③Stone dissolution therapy. The natural excretion rate of gallstones in the gallbladder is less than 1%, and to improve the curative effect of ESWL to a considerable extent, it depends on the progress of stone dissolution and stone expulsion therapy.

　　3. Stone expulsion therapy: It is mainly based on the effects of some traditional Chinese medicine on increasing bile secretion, promoting gallbladder contraction, and dilating the Oddi sphincter, combined with the understanding of modern medicine to form a combination of traditional Chinese and Western medicine for stone expulsion. The main medicine for stone expulsion using traditional Chinese medicine preparations is Jin Qian Cao, Yin Chen. Secondly, there are Da Huang, Mang Xiao; Western medicine has magnesium sulfate, which has the effects of promoting bile secretion and reducing the tension of the Oddi sphincter, the latter effect is the strongest at 40 minutes after administration. The dosage of magnesium sulfate is 33% solution 10-20ml, taken orally 3 times a day. The main effective method of the combination of traditional Chinese and Western medicine for stone expulsion therapy is mainly in the common bile duct.

　　4. Contact dissolution: Thistle first reported percutaneous gallbladder catheterization, injection of dissolution agent methyl叔丁醚 (methylten-butylether, MTBE) for contact dissolution. MTBE can quickly and effectively dissolve cholesterol gallstones, with a boiling point of 55.2°C, higher than that of ether, and will not volatilize immediately after entering the human body. Cholesterol gallstones can be dissolved after contacting for about 24 hours.

　　Application conditions require a small number of gallstones, able to penetrate X-rays, good gallbladder function, no acute inflammation. It must be noted that as much bile as possible should be drained before injection, the specific gravity of MTBE is 0.74, and if bile is present, it will stratify, which will affect the effect of dissolution. The MTBE solution should be changed regularly to ensure effective contact with gallstones. According to comprehensive literature data, the side effects of using this drug to dissolve gallstones include: ①Burning pain in the upper abdomen; ②Inducing enteritis and hemolysis, which often occurs when the drug infusion is too fast; ③Localized liver necrosis and hemorrhagic pneumonia. Animal experiments show that MTBE has a strong hemolytic effect and can produce acute inflammation on the gallbladder mucosa. Therefore, there is a certain risk in using MTBE to dissolve gallstones, and it must be handled with great caution. MTBE cannot be used for bile duct dissolution. So far, dozens of dissolution drugs have been reported, and the dissolution drugs for cholesterol gallstones discussed more often include: compound lauric acid glyceride monostearate, compound citrus oil mixture, etc.