Gallstone

Introduction

Introduction to gallstones Cholelithiasis is the most common lesion in the biliary system. Depending on the location, it may have gallstones, primary or secondary common bile duct stones, extrahepatic bile duct or intrahepatic bile duct stones, but clinically, single The stones in the site are possible but not common. Stones in several sites often exist in the same patient. The gallstones in cholelithiasis in Europe and the United States occur in the gallbladder. Only a few cases (10% to 25%) are primary. In the bile duct. However, in East Asia, Southeast Asian countries including China, especially in China's vast coastal areas, most of the gallstones (50% to 90%) are primary bile pigment stones of bile ducts, gallstones of different parts, their morphology, size and Ingredients and the like generally have obvious differences, so it can be assumed that the mechanism of their formation is also different, and the clinical symptoms and pathological manifestations will vary from person to person. basic knowledge The proportion of illness: 0.001% (incidence increased with age after age 40, about 70%) Susceptible people: no specific people Mode of infection: non-infectious Complications: acute cholecystitis, acute suppurative cholangitis, jaundice

Cause

Cause of gallstone

Most epidemiological studies have shown that the incidence of gallstones increases with age, and the disease is rare in childhood, which may be related to hemolysis or congenital biliary disease. A survey shows that ages range from 40 to 69. The 5-year incidence rate is 4 times that of the low-age group, and the boundary between high-incidence and low-risk is 40 years old. Although there are some differences in reports from various countries, the peak age of the disease is in the age range of 40-50 years old.

Sex difference in incidence (15%):

In recent years, the ratio of male and female onset of ultrasound diagnosis is about 1:2. The difference in sex ratio is mainly reflected in the incidence of cholesterol stones. There is no significant gender difference in the incidence of gallstones in gallbladder. The high incidence of cholesterol in women may reduce the gallbladder with estrogen. Flow, increase cholesterol secretion in bile, reduce total bile acid volume and activity, and progesterone affect gallbladder motility, which is related to bile stasis.

Relationship between onset and obesity (10%):

Clinical and epidemiological studies have shown that obesity is an important risk factor for the incidence of cholesterol gallstones in the gallbladder. Obesity is three times higher than that of normal-weight people. Obese people are more susceptible to gallstones because of the absolute increase in cholesterol synthesis. Or compare the relative increase of bile acids and phospholipids to make the cholesterol supersaturated.

Relationship between onset and fertility (7%):

Pregnancy can promote the formation of gallstones, and the number of pregnancies is positively correlated with the incidence of gallstones. This view has been proved by clinical and epidemiological studies. The causes of stones in pregnancy are: 1 increase in estrogen during pregnancy to make bile components Changes can increase the saturation of cholesterol in the bile, 2 stagnation of gallbladder emptying during pregnancy, B-ultrasound shows that when the pregnant woman is fasting, the gallbladder volume increases, the residual volume after contraction increases, the gallbladder contraction rate decreases, 3 pregnancy And postpartum weight changes also affect bile composition, altering the bile acid enterohepatic circulation, and promoting the formation of cholesterol crystals.

Regional differences in incidence (5%):

There are some differences in the incidence rates in different countries and regions. The prevalence of cholelithiasis is high in Western Europe, North America and Australia, and cholelithiasis is rare in many parts of Africa. The incidence of gallstones in Beijing, Shanghai, Northwest and North China is high. There are also different types of gallstones between the regions. In Sweden, Germany and other countries, cholesterol gallstones are dominant, while in the UK, calcium carbonate stones are more common than other countries.

Incidence and dietary factors (10%):

Eating habits are the main factors affecting the formation of gallstones. The incidence of gallstones is significantly increased in high-cholesterol foods, because refined carbohydrates increase bile cholesterol saturation. With the improvement of living standards in China, the incidence of gallstones has accounted for cholelithiasis. The main position is mainly cholesterol gallstones.

Incidence and genetic factors The difference in the incidence of gallstones in the race also suggests that genetic factors are one of the pathogenesis of cholelithiasis. For those with Indian genes, the incidence of gallstones is high, and the study of single-oval twins It is proved that the risk of gallstone occurrence in relatives of patients with cholelithiasis is also high, and the incidence rate in the family of cholelithiasis is also advanced, so support for cholelithiasis may have a genetic predisposition.

Other factors The incidence of gallstones is also related to cirrhosis, diabetes, hyperlipidemia, parenteral nutrition, surgical trauma and the application of certain drugs. For example, the incidence of cholelithiasis in patients with cirrhosis is 3 times that of cirrhosis without liver cirrhosis. The incidence of cholelithiasis in diabetic patients is twice that of patients without diabetes.

The main components of gallstones are mainly cholesterol, and the cause of gallstone formation has not yet been fully understood. At present, it is closely related to lipid metabolism, nucleation time, gallbladder motor function, bacterial gene fragment and other factors.

Pathogenesis

1. The pathogenesis of gallstones

The formation mechanism of gallstones is different due to the different types of stones.

In gallstones, about 70% to 80% are cholesterol-like stones. The exact mechanism of formation is still unclear, but most researchers believe that it may be related to the following factors.

(1) Cholesterol supersaturation to form "stone-forming bile": "stone-forming bile" was first proposed by Smiall and Admirand in 1968, they applied the theory of physical and chemical balance, which would be bile salts, lecithin and cholesterol. The relationship is represented by an equilateral triangle, and by simulating a bile experiment, a region in which bile cholesterol is dissolved in the form of "microcapsules" is found in this equilateral triangle, in which "microcapsules" in bile Not enough to dissolve all cholesterol, bile is supersaturated, which precipitates cholesterol crystals, the so-called "stone-forming bile" area, but recent studies have shown that most normal human gallbladder bile is supersaturated, and liver bile is supersaturated. The degree is much higher than that of gallbladder bile, but it does not form cholesterol stones. It is suggested that the cholesterol supersaturation index does not distinguish the bile of normal people and patients with cholesterol stones. In recent years, studies have also suggested that "stone-forming bile must have two conditions at the same time": 1 bile cholesterol hypersaturation; 2 bile nucleation factor abnormalities, resulting in bile cholesterol supersaturation often due to bile acid Salt secretion is normal and excessive cholesterol secretion, or due to normal cholesterol secretion and bile acid secretion is too small.

(2) Promoting the presence of nuclear factors: In recent years, studies have found that there are 50-100 nm particle structures in fresh liver bile and gallbladder bile. These particles are basically the same size in different bile samples, and the particles are more mixed than The "microcapsules" are 10 to 20 times larger in diameter, and it has been confirmed that these particles are a single-layered lipid "bubble" structure, and the main components of the "bubble" are measured as cholesterol and lecithin, and do not contain bile salts. It was confirmed that "bubble" in bile is another form of cholesterol lysis transport.

After ultracentrifugation of gallbladder bile in normal people, the number of "bubbles" formed after 2 hours is larger, the size is equal, and the distribution is uniform. This state can be stabilized for 168 hours, and then the "bubble" aggregation and formation of cholesterol is formed. Water crystallizes, and aggregation and fusion begin in the second hour after ultracentrifugation of gallbladder bile in patients with cholesterol stones. The multi-layered "bubble" structure of aggregation and fusion can be seen in the 4th to 6th hours. Typical cholesterol monohydrate crystals can be found.

In the case of low degree of supersaturation of cholesterol, the cholesterol in the dissolved state is self-precipitated by other solid components of non-lipid components to form crystals, which are affected by nucleation factors during the formation process, and nucleated by nucleation factors. The effects are often divided into two types, one is anti-nucleation factor, which can delay the occurrence of nucleation process; the other is to promote nuclear factor, which can promote the occurrence of nucleation process.

Under normal circumstances, there is a pro-/anti-nucleating factor in the gallbladder bile, and the two factors are relatively balanced in strength. In the case of cholesterol stones, the force that promotes nucleation increases, and the balance of the pro-/nuclear nucleus is destroyed. In the nucleation process, studies have shown that the glycoprotein component of gallbladder bile in patients with cholesterol stones significantly shortens the nucleation time of artificially simulated bile, and also found that gallbladder mucin and calcium also significantly promote nucleation. It is an important nucleating factor in bile.

(3) Abnormalities in gallbladder function:

1 gallbladder mucosal dysfunction, under normal circumstances, gallbladder mucosa can absorb water, electrolytes and organic matter, while secreting mucus, and the primary gallbladder mucosa in cholesterol stones mainly manifests as: A. mucous membrane to water, electrolyte absorption increased, thereby improving The "microcapsule" solubility of cholesterol, while reducing the stability of phospholipid cholesterol "bubble", thereby promoting cholesterol nucleation; B. the core of cholesterol stones often contain calcium, the normal gallbladder mucosa can absorb 50% of bile calcium, thereby reducing The concentration of bile free calcium, and the gallbladder mucosa also secretes hydrogen ions to acidify bile, increase the solubility of free calcium, when the mucous membrane absorption and secretion function changes, the calcium in the bile can be supersaturated to produce calcium salt precipitation; C. excessive secretion of gallbladder mucosa Mucin.

2 gallbladder contraction dysfunction, gallbladder systolic function increased bile retention time in the gallbladder, providing the opportunity to form cholesterol monohydrate crystallized in patients with complete parenteral nutrition, gallbladder, diabetes, pregnancy and the use of somatostatin The formation of their stones is related to the weakening of gallbladder emptying.

3 cholestasis and bile formation, as the gallbladder shrinks and the movement of the empty bile is weakened, the result is that the cholesterol "bubble" in the gallbladder is converted into cholesterol monohydrate crystals, and the bilirubin calcium ion mucin is composed of bile. Most of the biliary mud will disappear, and about 15% of the biliary sludge will continue to develop into gallstones.

2. Formation mechanism of pigment stones

The characteristics of bile pigment stones are "bilirubin calcium" as the main component, and its cholesterol content is lower than that of bilirubin. The gallstones in the gallbladder are divided into two categories according to their clinical characteristics, namely black bile pigment stones and Brown bile pigment stones.

(1) Characteristics and formation mechanism of black bile pigment stones:

1 The patient has no history of recurrent episodes of biliary tract infection, bile culture is sterile, and occurs in the gallbladder without infection.

2 The stone is small in size and hard in texture. The appearance and profile of the stone are black and shiny, and the shape is irregular.

3 The "bilirubin calcium" supersaturation in its bile has nothing to do with the increase of bacterial -G activity.

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

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

6 chronic alcoholism can induce the formation of black bile pigment stones.

(2) The formation mechanism of brown pigment stones: repeated biliary infection is an essential cause of the formation of brown pigment stones. Bacteria in the infected bile include anaerobic bacteria and aerobic bacteria, which can produce -G and phospholipase. A1, -G hydrolyzes bound bilirubin to unbound bilirubin, which combines with calcium in bile to form bilirubin calcium, which leads to supersaturation of bilirubin calcium and precipitation, phospholipase A1 The phospholipids are hydrolyzed to release lysophospholipids and free fatty acids which can be supersaturated and precipitated.

In addition, biliary infection can also secrete a large amount of glycoproteins in the biliary mucosa, which can aggregate various precipitates to form a matrix of stones.

"Bilirubin calcium" is a high molecular polymer which is hardly soluble in various solvents, and because it is combined with glycoproteins in gallstones, direct perfusion of dissolved stone becomes a problem of treatment.

3. Classification of gallstones

According to the analysis of gallstone specimens in China, cholesterol gallstones account for 70% of gallstones, 23.8% are bile pigment stones, and others are mixed stones.

Similar components of gallstones and gallstone profiles and surface observations are often classified.

According to the main components of the stone, it is often divided into: 1 pure cholesterol stones; 2 pure bilirubin stones; 3 mixed stones (cholesterol-bilirubin mixed or bilirubin calcium-cholesterol mixed); 4 rare stones, mainly Fatty acid, fatty acid bilirubin, polysaccharides, protein and other components.

Trotman, Soloway et al. proposed a relatively simple and practical classification in 1974 and 1997 respectively, that is, they were simply divided into cholesterol stones and pigment stones. The cholesterol stones were light brown, single or multiple, and the stone profiles were radial. The layered and crystalline appearance, the pigmented stone is brownish black, the shape depends on the anatomical part, and the profile is amorphous. This classification is more practical, but it is too simple, because most of the gallstones are Mixed.

Fu Peibin et al. According to the surface and section observation of the stone, the stones are divided into 8 categories: 1 radial stone: gray and transparent, the section is radioactive column, composed of crystal, the core is mostly a small amount of pigment particles, 2 radiation years of round stones: It is brownish yellow, the cut surface is radial, and there are many concentric circles of dark brown annual ring pattern. 3 rock layered stones: light yellow or grayish white, showing a dense and smooth laminate, with bilirubin sandwiched between layers. Granular or black matter, 4 cast amorphous stone: dark brown, the shape of the stone depends on the anatomical part, the cut surface has an amorphous structure, 5 sand layered stone: the profile is a relaxed concentric circle, which is a similar size of bilirubin Particle composition, separated by white particles between layers, 6 mud-like stones: brown, brittle, small or silty, all loosely aggregated bilirubin particles, 7 black stones: found in the gallbladder, diameter about 0.5cm , black, shiny, hard, cut surface like asphalt, 8 composite structure stone: the above two structures are combined, such as the core is radial stone, surrounded by rock layer structure.

Gallstones are sometimes a follow-up lesion of chronic cholecystitis, but more often it is the formation of gallstones, and then secondary to acute, chronic cholecystitis, due to the stimulation of the gallbladder mucosa, can not only cause chronic inflammation of the gallbladder, but Once the stone is incarcerated in the neck of the gallbladder or the cystic duct, it can also cause secondary infection due to the inability of the bile to be discharged, resulting in acute inflammation of the gallbladder, and then complications such as gallbladder empyema, gallbladder perforation, occasionally due to gallstones on the gallbladder Long-term stimulation of the mucosa may also lead to gallbladder cancer.

Prevention

Gallstone prevention

1. Proposal and concept of prevention of cholelithiasis

Epidemiological investigation of gallstones shows that China's gallstone type has turned to cholesterol stones in large cities and rural rich areas, although surgical treatment can effectively treat gallstone disease, new development of laparoscopic surgery and many non-surgical methods for treatment of cholelithiasis Choosing, however, cholelithiasis remains a major medical and social problem, recurrent seizures of gallstone disease, complicated with acute cholecystitis, gallbladder empyema, pancreatitis, gallbladder cancer risk; surgical treatment may damage the biliary tract; cholelithiasis There is also a certain mortality rate. In the United States, it costs 5 billion US dollars per year to treat cholelithiasis. In China, 1.2 billion people have 60 million patients waiting for treatment according to 5%, and new gallstone patients are still appearing every year. The only way to solve gallstone disease is prevention.

In 1987, the first worldwide conference on prevention of cholelithiasis was held in the United States, and the concept of prevention of cholelithiasis was proposed, namely primary prevention to prevent gallstone formation; secondary prevention to prevent asymptomatic gallstones from being converted into symptomatic gallstones; tertiary prevention, prevention After non-surgical treatment, gallstone recurrence. Recently, Hofmann once again emphasized primary prevention and secondary prevention of gallstones. Shanghai Second Medical University Ruijin Hospital proposed four levels of prevention of cholesterol gallstone disease, namely prevention of gallstone formation; prevention of gallstone symptoms; prevention and treatment Post-recurrence and prevention of gallstone complications, with emphasis on primary prevention, and a series of studies to predict high-risk groups of cholelithiasis for primary prevention.

2. Primary prevention of cholelithiasis

(1) Universal prevention: The purpose of primary prevention of gallstones is to prevent the formation of gallstones. Ruijin Hospital uses hamster diet regulation experiments to prove that dietary changes and gallstone formation, induced gallstone type (cholesterol stones or bile pigment stones) and gallstone dissolution, gallstone The occurrence of both genetic and environmental factors, the former is more difficult to change, while the latter can be adjusted, the study of risk factors for cholesterol stone disease also confirmed this: high calorie and fat intake, increased incidence of cholelithiasis; intake The incidence of gallstones is reduced, and the following preventive measures are recommended based on epidemiological and stone-forming mechanisms.

1 Prevention of cholesterol over-saturated bile: Obesity has excessive cholesterol and bile discharge. On the other hand, obese patients use various methods to reduce weight and consume body fat tissue. The cholesterol is discharged into bile and also increases the amount of bile cholesterol. Avoiding obesity is positive.

2 increase the intake of calcium and cellulose: DCA increased bile cholesterol secretion, inhibited the activity of bile acid synthesis rate-limiting enzyme, induced nucleation accelerated, Shanghai Second Medical University Ruijin Hospital analyzed more than 400 cases of gallstone patients, found that serum DCA content was significantly greater than Normal people, foods high in calcium and cellulose can reduce DCA and prevent gallstone formation.

3 Reduce the intake of saturated fatty acids: Animal experiments have shown that the reduction of saturated fatty acids in food can not only reduce the cholesterol content of bile, but also reduce the nucleation activity of bile.

4 regular meals and increased exercise: recently in the animal model with a mixture of lipids and proteins or exogenous cholecystokinin (CCK) to stimulate gallbladder emptying, prevent bile stasis, significantly reduce the occurrence of gallstones, recommended on time to eat, avoid two The meal interval is too long, reducing the blocking time of bile acid enterohepatic circulation. When the liver secretes bile acid, the ratio of cholesterol/phospholipid in the bile bubble decreases. It is recommended to add a small meal before going to sleep after three meals, shortening the fasting overnight. Time, often emptying the gallbladder, not only promotes the circulation of bile acids, but also reduces the residence time of bile in the gallbladder. This diet may increase the intake of calories and the risk of obesity, so it is necessary to increase physical activity and promote energy consumption.

(2) Prevention of high-risk groups: In addition to primary prevention for the general population, it is also necessary to selectively prevent some high-risk groups who are about to form gallstones. People with high risk of gallstones are those with risk factors for forming gallstones, epidemiology. It is pointed out that age, female, multi-partum, ethnic Indians, and hyperlipidemia are all risk factors. Ruijin Hospital of Shanghai Second Medical University has passed gallstones for animals, hospitalized patients with cholelithiasis and natural populations. Predictive studies of high-risk factors suggest that in addition to the characteristics of age, obesity, and hyperlipidemia, high-risk factors include increased serum DCA, decreased gallbladder contraction, and thickening of the gallbladder wall. Among all these factors, prediction of gallbladder morphology and function changes The most obvious meaning is that the prevention of gallstones in high-risk groups requires not only the above dietary adjustment and physical activity, but also the planned administration of drugs to correct early pathological changes. Ursodeoxycholic acid (ursodeoxycholic acid) is currently the most effective. Drugs that reduce bile cholesterol saturation, expensive for long-term use, and possibly Was added and the volume reduced gallbladder gallbladder unfavorable surface tension, to the attention of the clinical application of gallbladder dysfunction may be administered to promote the cholecystokinin CCK like medicament.

3. Secondary prevention of cholelithiasis

Secondary prevention of cholelithiasis is to prevent asymptomatic gallstone disease from being converted into symptomatic cholelithiasis. In the past 20 years, a variety of non-surgical treatments for gallstones have been established and improved, such as oral dissolution of stone, gravel, oral dissolution of stone, perfusion of dissolved stone and gravel. Infusion of dissolved stone therapy, etc., can remove gallstones for prevention purposes. In addition to considering the efficacy, in addition to considering the efficacy, we should consider safe and less complication methods. Secondly, we should further study the natural history of asymptomatic gallstones and understand the conversion to The proportion and clinical characteristics of symptomatic gallstones, as well as the risk of symptoms of gallstones and the risk of complications from non-surgical or surgical treatment, to establish a more complete treatment of asymptomatic gallstones, to achieve secondary prevention.

4. Three-level prevention of cholelithiasis

Non-surgical treatment of gallstones in the presence of functional gallbladder, there is a problem of recurrence of gallstones, so the content of tertiary prevention is to use a primary prevention program to correct the pathological basis of gallstone formation in patients, avoid gallstone recurrence, doctors and patients It is necessary to recognize that there may be recurrence of gallstone after non-surgical treatment, pay attention to regular review, adjust the type of diet, avoid obesity, strengthen physical exercise, and once the early changes of gallstones are discovered, that is, the formation of gallbladder mud, it will be treated early. To a very good effect.

5. Four-level prevention of cholelithiasis

The fourth-grade prevention of cholelithiasis is to treat symptomatic gallstones and prevent gallstone complications. When gallstones develop into symptomatic gallstones, the possibility of reversing to asymptomatic gallstones is extremely small, and acute cholecystitis occurs, followed by bile duct stones. The risk of complications such as acute pancreatitis and gallbladder cancer is cholecystectomy.

The fourth-level prevention of gallstones, from high-risk groups to symptomatic gallstones; the method is to adjust diet, lifestyle change, non-surgical and surgical treatment. The ultimate goal of cholelithiasis research is to change patients with gallstones from treatment to prevention. Objects, with the development of cholelithia epidemiology, the content of cholelithiasis will be increasingly rich and perfect.

Complication

Gallbladder stone complications Complications acute cholecystitis acute suppurative cholangitis jaundice

Once the stone causes obstruction of the biliary tract, it will cause acute or chronic complications, prompting the patient to see a doctor. Acute obstructive complications are common, and chronic obstructive complications are rare.

Acute complication

(1) biliary colic: sudden onset of severe pain in the heart or right rib margin, severe sweating, uneasiness, pain more often occurs at night or after greasy food, lasting for ten minutes to several hours Natural relief or relief after antispasmodic, without fever, may have nausea, vomiting, gallbladder area may have tenderness but no muscle tension, colic is caused by gallstones embedded in the gallbladder neck, B ultrasound can be seen in the gallbladder The stone in the neck and the enlarged gallbladder; when the colic is caused by the gallbladder stone with a diameter of about 0.5cm, it is caused by the bile duct. In addition to the gallbladder stone, the superficial common bile duct is seen, and the common bile duct can be seen. The echo of the stone can definitely confirm the diagnosis, but the echo of the stone can not exclude the stones that are hidden in the posterior segment of the common bile duct. The simple biliary colic is not accompanied by fever, jaundice or blood, and the urinary amylase is increased, 5~6h or more. Relieved biliary colic can be converted into one of the following three complications by secondary infection.

(2) acute cholecystitis: obstruction of gallbladder ducts caused by gallbladder ducts and other systemic inflammatory manifestations, as well as right upper quadrant tenderness, muscle tension and other peritoneal irritation of the gallbladder area, without jaundice or blood, increased urine amylase.

(3) acute suppurative cholangitis: obstruction of the common bile duct by the gallbladder stones (secondary bile duct stones) descending into the common bile duct, and infection, the entire biliary tree, including the gallbladder, has acute suppurative inflammation. The disease is similar to acute cholecystitis but the systemic inflammation is more severe, and there is jaundice, which is characterized by Charcol triad: upper abdominal pain, chills, jaundice; prone to shock, serum ALT, AST increased, such as blood, urine Increased amylase, indicating acute pancreatitis, B-mode ultrasound showed small stones in the gallbladder, widened common bile duct, if you see the echo in the common bile duct stone can be surely diagnosed, but no stone echo can not rule out the common bile duct There is the possibility of stones in the back of the intestine.

(4) biliary acute pancreatitis: sometimes, gallbladder stones falling into the common bile duct can induce pancreatitis without acute suppurative cholangitis when passing or staying at the exit of the common bile duct, called biliary pancreatitis, The disease is similar to biliary colic, but on the umbilicus, the range of tenderness under the xiphoid is wider, and the blood or urine amylase is elevated, and the jaundice is optional. In addition to seeing gallbladder stones and dilatation of the common bile duct, B-mode ultrasound examination It can also be seen that the pancreas is swollen, and there are signs of exudate around the pancreas; however, stones may not be seen in the common bile duct.

2. Chronic obstructive complications

(1) obstructive jaundice: the common bile duct was blocked by secondary bile duct stones but not secondary infection, nor did it cause biliary colic, and presented with jaundice.

(2) hydronephrosis: due to the upper right abdomen mass or B-mode ultrasound examination of the enlarged gallbladder and seeing, is the result of gallbladder stones obstructing the cystic duct but not causing secondary infection or biliary colic, gallbladder orifice After long-term obstruction, the bile pigment in the gallbladder bile is absorbed, leaving a colorless and transparent liquid called "white bile".

After the biliary obstruction caused by the stone, the gallbladder or bile duct in the upper reaches of the obstruction is dilated, the stone can be loosened, the upward floating causes the obstruction to be relieved, or the stone causing the obstruction is not large, and may be driven over the cystic duct or Oddi sphincter to relieve the obstruction. Then the inflammation subsides and the symptoms disappear. After a period of calm interval, it usually recurs. The patient in the interstitial period, like before the obstruction, has no clinical symptoms, or only the so-called "chronic stomach symptoms."

Symptom

Gallbladder stones symptoms Common symptoms Gallbladder dyskinesia biliary colic bloating bile duct stones cysts gallbladder hydrops abdominal pain jaundice liver bile duct stones bilirubin calcium stones

About 60% of patients with gallstones have no obvious clinical manifestations. They were found in other cases of physical examination or upper abdominal surgery. When the incarceration of the stones caused obstruction of the cystic duct, they often showed upset discomfort in the right upper quadrant, similar to symptoms of gastritis, but taking treatment. Gastritis drugs are ineffective, patients are more tired of greasy food; some patients in bed at night to change position, the stone blocked in the cystic duct temporarily obstructed and the right upper abdomen and upper abdomen pain, so some patients with gallstones often have nighttime abdominal pain.

The clinical symptoms of gallstone disease are often atypical. Gallbladder stones with a history of acute exacerbation are generally difficult to diagnose according to clinical symptoms and signs; however, if there is no history of acute attacks, the diagnosis depends mainly on auxiliary examination. The main points of diagnosis are as follows:

1. Repeated episodes of acute cholecystitis, chronic cholecystitis, gallbladder effusion or biliary colic, while the skin mucosa is not yellow or jaundice.

2. Repeated cholecystitis for many years without jaundice. This episode is accompanied by jaundice. Gallstones with secondary choledocholithiasis should be considered.

3. Ultrasound found gall stones in the gallbladder, gallbladder enlargement, effusion, wall thickening or atrophy; oral gallbladder angiography confirmed gallstones in the gallbladder, the accuracy of ultrasound diagnosis can reach more than 95%.

4.Mirizzi syndrome: In some patients, the cystic duct and the common hepatic duct are merged into the common bile duct for a period of time. If the gallbladder neck or the cystic duct is incarcerated, the common bile duct may cause partial obstruction or stenosis due to stone compression and inflammatory edema. This leads to recurrent cholangitis, patients with right upper quadrant pain, fever and jaundice, ultrasound and laparotomy can confirm the diagnosis.

Examine

Examination of gallstones

Simple gallbladder stones generally do not have jaundice and liver dysfunction, so there is no positive test results for laboratory tests on jaundice and liver function.

Imaging examination is currently the main means of diagnosis of gallstone disease. Ultrasound is often the first line of examination. It can be found in gallbladder stones, thickened gallbladder wall, and lack of gallbladder contraction. The results are often accurate and reliable. Other tests The method often determines whether to use it further based on the results of the ultrasound examination.

On X-ray films, about 20% of gallstones are positive because of high calcium content. Because of the low positive rate of stones, X-ray films in the liver and gallbladder area are not required for clinical diagnosis, but X-ray films can be displayed. The soft tissue shadow of the enlarged gallbladder and inflammatory mass and the gas shadow around the gallbladder and gallbladder in the case of gas cholecystitis. In addition, some indirect X-ray signs often contribute to the diagnosis of acute cholecystitis: 1 below the gallbladder Intestinal dilatation, inflated and other reflex intestinal fistula; 2 soft tissue shadow in the gallbladder area; 3 peritoneal stimulation signs, such as the right peritoneal fat line blurred or disappeared, right iliac muscle elevation; 4 right pleural reactive product Fluid or discoid lung atelectasis in the lower right lobe.

When the cystic duct is patency and the concentrating function of the gallbladder is still good, oral cholecystography can show the negative shadow of stones in the gallbladder with an accuracy of 95%.

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

The wall thickness of the gallbladder is visible on the CT image. There are stones and bile deposits in the capsule. The CT scan of the oral gallbladder contrast agent can increase the resolution of the stone.

Diagnosis

Diagnosis and diagnosis of gallstones

Diagnosis of gallstones

The clinical symptoms of gallstone disease are often atypical. Gallbladder stones with a history of acute exacerbation are generally difficult to diagnose according to clinical symptoms and signs; however, if there is no history of acute attacks, the diagnosis depends mainly on auxiliary examination. The main points of diagnosis are as follows:

1. Repeated episodes of acute cholecystitis, chronic cholecystitis, gallbladder effusion or biliary colic, while the skin mucosa is not yellow or jaundice.

2. Repeated cholecystitis for many years without jaundice. This episode is accompanied by jaundice. Gallstones with secondary choledocholithiasis should be considered.

3. Ultrasound found gall stones in the gallbladder, gallbladder enlargement, effusion, wall thickening or atrophy; oral gallbladder angiography confirmed gallstones in the gallbladder, the accuracy of ultrasound diagnosis can reach more than 95%.

4.Mirizzi syndrome: In some patients, the cystic duct and the common hepatic duct are merged into the common bile duct for a period of time. If the gallbladder neck or the cystic duct is incarcerated, the common bile duct may cause partial obstruction or stenosis due to stone compression and inflammatory edema. This leads to recurrent cholangitis, patients with right upper quadrant pain, fever and jaundice, ultrasound and laparotomy can confirm the diagnosis.

Differential diagnosis

1. Chronic gastritis: The main symptoms are upper abdominal bloating pain, hernia, loss of appetite and history of dyspepsia. Fiber gastroscopy is extremely important for the diagnosis of chronic gastritis. It can be found that gastric mucosal edema, congestion, mucous membrane color turns yellow or grayish yellow Mucosal atrophy, hypertrophic gastritis can be seen mucosal folds hypertrophy, or nodules and visible erosion and superficial ulcers.

2. Peptic ulcer: a history of ulcers, upper abdominal pain is related to regular diet, while gallstones and chronic cholecystitis often increase pain after eating, especially into high-fat foods. Ulcers often occur in acute spring and autumn, and gallstones Chronic cholecystitis is more common than nighttime onset, and barium meal examination and fiber gastroscopy have obvious discriminating value.

3. Gastric neurosis: Although there is a long history of recurrent episodes, it has no obvious relationship with eating greasy, and is often closely related to mood fluctuations. It often has neurological vomiting. Every time after eating, sudden vomiting occurs, generally no nausea, vomiting is not More and less effort, you can eat after vomiting, does not affect appetite and food intake, this disease is often accompanied by systemic neurological symptoms, with suggestive therapy can relieve symptoms, identification is not difficult.

4. Gastroptosis: This disease may have liver, kidney and other organs drooping, upper abdominal discomfort is aggravated after meals, symptoms are relieved in the lying position, standing position examination can be seen in the lower abdomen fullness, while the upper abdomen is empty, sometimes visible stomach type There is also a sound of water, and a meal check can confirm the diagnosis.

5. Renal ptosis: often have poor appetite, nausea and vomiting, and more common on the right side, but the right upper abdomen and lower back pain are aggravated when standing and walking, colic may appear, and radiate to the lower abdomen, Physical examination was performed in the supine position, sitting position and standing position. If the right upper quadrant was found to be displaced due to the change of body position, it would be meaningful for the identification. The horizontal and standing kidney X-ray film and intravenous urography can help. For diagnosis.

6. Prolonged hepatitis and chronic hepatitis: This disease has a history of acute hepatitis, and there are symptoms such as chronic dyspepsia and right upper quadrant discomfort. There may be liver and liver dysfunction, and splenomegaly, spider mites and liver may occur in chronic hepatitis. Palm, B-ultrasound examination of the gallbladder function.

7. Chronic pancreatitis: often the sequela of acute pancreatitis, the upper abdominal pain is radiated to the left shoulder and back, X-ray plain film sometimes shows pancreatic calcification or pancreatic stones, fiber duodenoscopy and retrograde cholangiopancreatography for diagnosis Chronic pancreatitis has a certain value.

8. Gallbladder cancer: This disease can be combined with gallstones, the disease has a short history, rapid development of the disease, and soon hepatic lymph node metastasis and direct invasion of nearby liver tissue, so persistent jaundice occurs, and the right upper quadrant is persistent. When the symptoms are obvious, most patients can reach a hard mass under the cost of the right upper abdomen. B-ultrasound and CT examination can help diagnose.

9. Liver cancer: Primary liver cancer, such as the right upper abdomen or upper abdominal pain, has been late, often can reach the swollen and nodular liver, B-ultrasound, radionuclide scanning and CT examination can be found in the liver The alpha-fetoprotein was positive in the image and radiographic defect or density reduction zone.

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