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ЗмістThe Bile Ducts
Sphincter of Oddi
Biliary Radionuclide Scanning (HIDA Scan)
Percutaneous Transhepatic Cholangiography
Magnetic Resonance Imaging
Endoscopic Retrograde Cholangiography and Endoscopic Ultrasound
Operative interventions for gallstone disease
Choledochal Drainage Procedures
Other benign diseases and lesions
The gallbladder is a pear-shaped sac, about 7–10 cm long with an average capacity of 30–50 mL. When obstructed, the gallbladder can distend markedly and contain up to 300 mL. The same peritoneal lining that covers the liver covers the fundus and the inferior surface of the gallbladder. The gallbladder is lined by a single, highly folded, tall columnar epithelium that contains cholesterol and fat globules. The epithelial lining of the gallbladder is supported by a lamina propria. The muscle layer has circular longitudinal and oblique fibers, but without well-developed layers. The perimuscular subserosa contains connective tissue, nerves, vessels, lymphatics, and adipocytes. It is covered by the serosa except where the gallbladder is embedded in the liver. The gallbladder differs histologically from the rest of the gastrointestinal tract in that it lacks a muscularis mucosa and submucosa. The cystic artery that supplies the gallbladder usually is a branch of the right hepatic artery (>90 % of the time). The course of the cystic artery may vary, but it nearly always is found within the hepatocystic triangle, the area bound by the cystic duct, common hepatic duct, and the liver margin (triangle of Calot). Venous return is carried either through small veins that enter directly into the liver, or rarely to a large cystic vein that carries blood back to the portal vein. Gallbladder lymphatics drain into nodes at the neck of the gallbladder. Frequently, a visible lymph node overlies the insertion of the cystic artery into the gallbladder wall. The nerves of the gallbladder arise from the vagus and from sympathetic branches that pass through the celiac plexus.
The extrahepatic bile ducts consist of the right and left hepatic ducts, the common hepatic duct, the cystic duct, and the common bile duct or choledochus. The common bile duct enters the second portion of the duodenum through a muscular structure, the sphincter of Oddi. The left hepatic duct is longer than the right and has a greater propensity for dilatation as a consequence of distal obstruction. The two ducts join to form a common hepatic duct, close to their emergence from the liver. The common hepatic duct is 1–4 cm in length and has a diameter of approximately 4 mm. It lies in front of the portal vein and to the right of the hepatic artery. The common hepatic duct is joined at an acute angle by the cystic duct to form the common bile duct. Variations of the cystic duct and its point of union with the common hepatic duct are surgically important. The segment of the cystic duct adjacent to the gallbladder neck bears a variable number of mucosal folds called the spiral valves of Heister. The common bile duct is about 7–11 cm in length and 5–10 mm in diameter. The common bile duct runs obliquely downward within the wall of the duodenum for 1–2 cm before opening on a papilla of mucous membrane (ampulla ofVater), about 10 cm distal to the pylorus. The pancreatic duct frequently joins the common bile duct outside the duodenal wall and traverses the duodenal wall as a single duct. The sphincter of Oddi controls the flow of bile, and in some cases pancreatic juice, into the duodenum. The extrahepatic bile ducts are lined by a columnar mucosa with numerous mucous glands in the common bile duct. A fibroareolar tissue containing scant smooth muscle cells surrounds the mucosa. The arterial supply to the bile ducts is derived from the gastroduodenal and the right hepatic arteries, with major trunks running along the medial and lateral walls of the common duct.
The classic description of the extrahepatic biliary tree and its arteries applies only in about one third of patients. The gallbladder may have abnormal positions, be intrahepatic, be rudimentary, have anomalous forms, or be duplicated. Isolated congenital absence of the gallbladder is rare. Duplication of the gallbladder with two separate cavities and two separate cystic ducts has an incidence of about one in every 4000 persons. A partial or totally intrahepatic gallbladder is associated with an increased incidence of cholelithiasis. Small ducts (of Luschka) may drain directly from the liver into the body of the gallbladder. If present, but not recognized at the time of a cholecystectomy, a bile leak with the accumulation of bile (biloma) may occur in the abdomen. An
accessory right hepatic duct occurs in about 5 % of patients. Anomalies of the hepatic artery and the cystic artery are quite common, occurring in as many as 50 % of patients.
Bile Formation and Composition
The liver produces bile continuously and excretes it into the bile canaliculi. The normal adult consuming an average diet produces within the liver 500–1000 mL of bile a day. The secretion of bile is responsive to neurogenic, humoral, and chemical stimuli. With an intact sphincter of Oddi, bile flow is directed into the gallbladder. Bile is mainly composed of water, electrolytes, bile salts, proteins, lipids, and bile pigments. Sodium, potassium, calcium, and chlorine have the same concentration in bile as in plasma or extracellular fluid. The primary bile salts, cholate and chenodeoxycholate, are synthesized in the liver from cholesterol. They are conjugated there with taurine and glycine, and act within the bile as anions (bile acids) that are balanced by sodium. Bile salts are excreted into the bile by the hepatocyte and aid in the digestion and absorption of fats in the intestines. About 95 % of the bile acid pool is reabsorbed and returned via the portal venous system to the liver, the so-called enterohepatic circulation. Five % is excreted in the stool, leaving the relatively small amount of bile acids to have maximum effect. Cholesterol and phospholipids synthesized in the liver are the principal lipids found in bile. The synthesis of phospholipids and cholesterol by the liver is in part regulated by bile acids. The color of the bile is because of the presence of the pigment bilirubin diglucuronide, which is the metabolic product from the breakdown of hemoglobin, and is present in bile in concentrations 100 times greater than in plasma. Once in the intestine, bacteria convert it into urobilinogen, a small fraction of which is absorbed and secreted into the bile.
The gallbladder, the bile ducts, and the sphincter of Oddi act together to store and regulate the flow of bile. The main function of the gallbladder is to concentrate and store hepatic bile and to deliver bile into the duodenum in response to a meal.
Absorption and Secretion
In the fasting state, approximately 80 % of the bile secreted by the liver is stored in the gallbladder. It rapidly absorbs sodium, chloride, and water against significant concentration gradients, concentrating the bile as much as tenfold and leading to a marked change in bile composition. The epithelial cells of the gallbladder secrete at least two important products into the gallbladder lumen: glycoproteins and hydrogen ions. The mucosal glands in the infundibulum and the neck of the gallbladder secrete mucus glycoproteins. This mucus makes up the colorless “white bile” seen in hydrops of the gallbladder resulting from cystic duct obstruction. The transport of hydrogen ions by the gallbladder epithelium leads to a decrease in the gallbladder bile pH. The acidification promotes calcium solubility, thereby preventing its precipitation as calcium salts.
Gallbladder filling is facilitated by tonic contraction of the sphincter of Oddi, which creates a pressure gradient between the bile ducts and the gallbladder. In response to a meal, the gallbladder empties by a coordinated motor response of gallbladder contraction and sphincter of Oddi relaxation. One of the main stimuli to gallbladder emptying is the hormone cholecystokinin (CCK).CCK is released endogenously from the duodenal mucosa in response to a meal. When
stimulated by eating, the gallbladder empties 50–70 % of its contents
within 30–40 min. Over the following 60–90 min the gallbladder gradually
refills. This is correlated with a reduced CCK level.
The vagus nerve stimulates contraction of the gallbladder, and splanchnic sympathetic stimulation is inhibitory to its motor activity. Antral distention of the stomach causes both gallbladder contraction and relaxation of the sphincter of Oddi. Hormonal receptors are located on the smooth muscles, vessels, nerves, and epithelium of the gallbladder. CCK is a peptide that comes from epithelial cells of the upper gastrointestinal tract and is found in the highest concentrations in the duodenum. CCK acts directly on smooth muscle receptors of the gallbladder and stimulates gallbladder contraction. It also relaxes the terminal bile duct, the sphincter of Oddi, and the duodenum. VIP inhibits contraction and causes gallbladder relaxation. Somatostatin and its analogues are potent inhibitors of gallbladder contraction.
The sphincter of Oddi regulates flow of bile (and pancreatic juice) into the duodenum, prevents the regurgitation of duodenal contents into the biliary tree, and diverts bile into the gallbladder. The sphincter of Oddi is about 4–6mmin length and has a basal resting pressure of about 13 mmHg above the duodenal pressure. Relaxation occurs with a rise in CCK, allowing increased flow of bile into the duodenum.
An elevated white blood cell (WBC) count may indicate or raise suspicion of cholecystitis. If associated with an elevation of conjugated bilirubin, alkaline phosphatase, and aminotransferase, cholangitis should be suspected. Cholestasis, an obstruction to bile flow, is characterized by an elevation of bilirubin and a rise in alkaline phosphatase. Serum aminotransferases may be normal or mildly elevated. In patients with biliary colic, blood tests typically will be normal.
An ultrasound is the initial investigation of any patient suspected of disease of the biliary tree. It is dependent on the skills and the experience of the operator and it is dynamic. Adjacent organs can frequently be examined at the same time. Obese patients, patients with ascites, and patients with distended bowel may be difficult to examine satisfactorily with an ultrasound. An ultrasound will show stones in the gallbladder with sensitivity and specificity of over 90 %. Stones are acoustically dense and reflect the ultrasound waves back to the ultrasonic transducer. Because stones block the passage of sound waves to the region behind them, they also produce an acoustic shadow. Stones also move with changes in position. Some stones form a layer in the gallbladder; others a sediment or sludge. A thickened gallbladder wall and local tenderness indicate cholecystitis. The patient has acute cholecystitis if a layer of edema is seen within the wall of the gallbladder or between the gallbladder and the liver. When a stone obstructs the neck of the gallbladder, the gallbladder may become very large, but thinwalled.Acontracted, thick-walled gallbladder indicates chronic cholecystitis. The extrahepatic bile ducts also are well visualized by ultrasound, except for the retroduodenal portion. Dilation of the ducts in a patient with jaundice establishes an extrahepatic obstruction as a cause for the jaundice. Frequently the site, and sometimes the cause of obstruction, can be determined by ultrasound. Small stones in the common bile duct frequently get lodged at the distal end of it, behind the duodenum, and are therefore difficult to detect. Periampullary tumors can be difficult to diagnose on ultrasound, but beyond the retroduodenal portion, the level of obstruction and the cause may be visualized quite well. Ultrasound can be helpful in evaluating tumor invasion and flow in the portal vein, an important guideline for resectability of periampullary tumors.
Oral Cholecystography involves oral administration of a radiopaque compound that is absorbed, excreted by the liver, and passed into the gallbladder. Stones are noted on a film as filling defects in a visualized, opacified gallbladder. Oral cholecystography is of no value in patients with intestinal malabsorption, vomiting, obstructive jaundice, and hepatic failure.
Biliary scintigraphy provides a noninvasive evaluation of the liver, gallbladder, bile ducts, and duodenum with both anatomic and functional information. 99m-Technetium-labeled derivatives of dimethyl iminodiacetic acid (HIDA) are injected intravenously, cleared by theKupffer cells in the liver, and excreted in the bile. Uptake by the liver is detected within 10 min, and the gallbladder, the bile ducts, and the duodenum are visualized within 60 min in fasting subjects. The primary use of biliary scintigraphy is in the diagnosis of acute cholecystitis, which appears as a nonvisualized gallbladder, with prompt filling of the common bile duct and duodenum. Filling of the gallbladder and common bile duct with delayed or absent filling of the duodenum indicates an obstruction at the ampulla. Biliary leaks as a complication of surgery of the gallbladder or the biliary tree can be confirmed and frequently localized by biliary scintigraphy.
Abdominal computed tomography (CT) scans are inferior to ultrasonography in diagnosing gallstones. CT scan is the test of choice in evaluating the patient with suspected malignancy of the gallbladder, the extrahepatic biliary system, or nearby organs, in particular the head of the pancreas. Use of CT scan is an integral part of the differential diagnosis of obstructive jaundice. Spiral CT scanning provides additional staging information, including vascular involvement in patients with periampullary tumors.
An intrahepatic bile duct is accessed percutaneously with a small needle under fluoroscopic guidance. Once the position in a bile duct has been confirmed, a guidewire is passed and subsequently a catheter passed over the wire. Through the catheter, a cholangiogram can be performed and therapeutic interventions done, such as biliary drain insertions and stent placements. Percutaneous transhepatic cholangiography is particularly useful in patients with bile duct strictures and tumors, as it defines the anatomy of the biliary tree proximal to the affected segment.
Using magnetic resonance imaging (MRI) with newer techniques and contrast materials, accurate anatomic images can be obtained of the bile ducts and the pancreatic duct. It has a sensitivity and specificity of 95 and 89 %, respectively, at detecting choledocholithiasis. If available, MRI with magnetic resonance cholangiopancreatography (MRCP) offers a single noninvasive test for the diagnosis of biliary tract and pancreatic disease.
Using a side-viewing endoscope, the common bile duct can be cannulated and a cholangiogram performed using fluoroscopy. Endoscopic retrograde cholangiography (ERC) provides direct visualization of the ampullary region and direct access to the distal common bile duct, with the possibility of therapeutic intervention. The test rarely is needed for uncomplicated gallstone disease. Once the endoscopic cholangiogram has shown ductal stones, sphincterotomy and stone extraction can be performed, and the common bile duct cleared of stones. In the hands of experts, the success rate of common bile duct cannulation and cholangiography is more than 90 %. Complications of diagnostic ERC include pancreatitis and cholangitis, and occur in up to 5 % of patients. An endoscopic ultrasound requires a special endoscope with an ultrasound transducer at its tip. It offers noninvasive imaging of the bile ducts and adjacent structures. It is of particular value in the evaluation of tumors and their resectability. The ultrasound endoscope has a biopsy channel, allowing needle biopsies of a tumor under ultrasonic guidance.
Prevalence and Incidence
Gallstone disease is one of the most common problems affecting the digestive tract. Autopsy reports have shown a prevalence of gallstones from 11–36 %. Obesity, pregnancy, dietary factors, Crohn disease, terminal ileal resection, gastric surgery, hereditary spherocytosis, sickle cell disease, and thalassemia all are associated with an increased risk of developing gallstones. Women are three times more likely to develop gallstones than men, and first-degree relatives of patients with gallstones have a 2-fold greater prevalence.
Most patients will remain asymptomatic from their gallstones throughout life. For unknown reasons some patients progress to a symptomatic stage, with biliary colic caused by a stone obstructing the cystic duct. Symptomatic gallstone disease may progress to complications related to the gallstones. Rarely, complication of gallstones is the presenting picture. Gallstones in patients without biliary symptoms are commonly diagnosed incidentally. Approximately 3 % of asymptomatic individuals develop biliary colic each year. Once symptomatic, patients tend to have recurring bouts of biliary colic. Complicated gallstone disease develops in 3–5 % of symptomatic patients per year. Over a 20-year period, about two-thirds of asymptomatic patients with gallstones remain symptom free. Since few patients develop complications without previous biliary symptoms, prophylactic cholecystectomy in asymptomatic persons with gallstones rarely is indicated. For older adult patients with diabetes, for individuals who will be isolated from medical care for extended periods of time, and in populations with increased risk of gallbladder cancer, a prophylactic cholecystectomy may be advisable. Porcelain gallbladder, a rare premalignant condition in which the wall of the gallbladder becomes calcified, is an absolute indication for cholecystectomy.
Gallstones form as a result of solids settling out of solution. Gallstones are classified by their cholesterol content as either cholesterol stones or pigment stones. Pigment stones can be further classified as either black or brown. In Western countries, about 80 % of gallstones are cholesterol stones and about 15–20 % are black pigment stones. Brown pigment stones account for only a small %age. Both types of pigment stones are more common in Asia.
Pure cholesterol stones are uncommon and account for less than 10 % of all stones. They usually occur as single large stones with smooth surfaces. Most other cholesterol stones contain variable amounts of bile pigments and calcium, but are always more than 70 % cholesterol by weight. These stones are usually multiple, of variable size, and may be hard and faceted or irregular, mulberry-shaped and soft. Colors range from whitish yellow and green to black. Most cholesterol stones are radiolucent. Whether pure or of mixed nature, the common primary event in the formation of cholesterol stones is supersaturation of bile with cholesterol.
Pigment stones contain less than 20 % cholesterol and are dark because of the presence of calcium bilirubinate. Otherwise, black and brown pigment stones have little in common and should be considered as separate entities. Black pigment stones are usually small, brittle, black, and sometimes spiculated. They are formed by supersaturation of calcium bilirubinate, carbonate, and phosphate, most often secondary to hemolytic disorders such as hereditary spherocytosis and sickle cell disease, and in those with cirrhosis. Like cholesterol stones, they almost always form in the gallbladder. When altered conditions lead to increased levels of deconjugated bilirubin in bile, precipitation with calcium occurs. In Asian countries such as Japan, black stones account for a much higher %age of gallstones than in the Western hemisphere. Brown stones are usually less than 1 cm in diameter, brownish-yellow, soft, and often mushy. They may form either in the gallbladder or in the bile ducts, usually secondary to bacterial infection caused by bile stasis. Precipitated calcium bilirubinate and bacterial cell bodies compose the major part of the stone. Brown stones are typically found in the biliary tree of Asian populations and are associated with stasis secondary to parasite infection. In Western populations, brown stones occur as primary bile duct stones in patients with biliary strictures or other common bile duct stones that cause stasis and bacterial contamination.
About two thirds of patients with gallstone disease present with chronic cholecystitis characterized by recurrent attacks of pain, often inaccurately labelled biliary colic. The pain develops when a stone obstructs the cystic duct, resulting in a progressive increase of tension in the gallbladder wall. The pathologic changes, vary from an apparently normal gallbladder with minor chronic inflammation in the mucosa, to a shrunken, nonfunctioning gallbladder with gross transmural fibrosis and adhesions to nearby structures.
Clinical presentation. The chief symptom associated with symptomatic gallstones is pain. The pain is constant and increases in severity over the first half hour or so and typically lasts 1–5 h. It is located in the epigastrium or right upper quadrant and frequently radiates to the right upper back or between the scapulae. The pain is severe and comes on abruptly, typically during the night or after a fatty meal. It often is associated with nausea and sometimes vomiting. The pain is episodic. The patient suffers discrete attacks of pain, between which they feel well. Physical examination may reveal mild right upper quadrant tenderness during an episode of pain. If the patient is pain free, the physical exam usually is unremarkable. Laboratory values, such as white blood cell count and liver function tests, usually are normal in patients with uncomplicated gallstones. Atypical presentation of gallstone disease is common. In patients with atypical presentation, other conditions with upper abdominal pain should be sought out, even in the presence of gallstones. When the pain lasts more than 24 h, an impacted stone in the cystic duct or acute cholecystitis (see below) should be suspected. An impacted stone will result in what is called hydrops of the gallbladder. The bile gets absorbed, but the gallbladder epithelium continues to secrete mucus and the gallbladder becomes distended with mucinous material. Early cholecystectomy generally is indicated to avoid complications.
Diagnosis. An abdominal ultrasound is the standard diagnostic test for gallstones. Sometimes only sludge in the gallbladder is demonstrated on ultrasonography. If the patient has recurrent attacks of typical biliary pain and sludge is detected on two or more occasions, cholecystectomy is warranted. In addition to sludge and stones, cholesterolosis and adenomyomatosis of the gallbladder may cause typical biliary symptoms and may be detected on ultrasonography. In symptomatic patients, cholecystectomy is the treatment of choice for patients with these conditions.
Management. Patients with symptomatic gallstones should be advised to have elective laparoscopic cholecystectomy. While waiting for surgery, or if surgery has to be postponed, the patient should be advised to avoid dietary fats and large meals. Diabetic patients with symptomatic gallstones should have a cholecystectomy promptly, as they are more prone to develop acute cholecystitis that often is severe. Pregnant women with symptomatic gallstones who cannot be managed expectantly with diet modifications can safely undergo laparoscopic cholecystectomy during the second trimester. Laparoscopic cholecystectomy is safe and effective in children and in older adults. holecystectomy, open or laparoscopic, for patients with symptomatic gallstones offers excellent longterm results. About 90 % of patients with typical biliary symptoms and stones are rendered symptom free after cholecystectomy. For patients with atypical symptoms or dyspepsia (flatulence, belching, bloating, and dietary fat intolerance) the results are not as favorable.
Pathogenesis. Acute cholecystitis is secondary to gallstones in 90–95 % of cases. Acute acalculous cholecystitis is a condition that typically occurs in patients with other acute systemic diseases (see acalculous cholecystitis section, below). In less than 1 % of acute cholecystitis, the cause is a tumor obstructing the cystic duct. Obstruction of the cystic duct by a gallstone is the initiating event that leads to gallbladder distention, inflammation, and edema of the gallbladder wall. Initially, acute cholecystitis is an inflammatory process. Secondary bacterial contamination is documented in over one half of patients undergoing early cholecystectomy for acute uncomplicated cholecystitis. In acute cholecystitis the gallbladder wall becomes grossly thickened and reddish with subserosal hemorrhages. Pericholecystic fluid often is present. The mucosa may show hyperemia and patchy necrosis. In severe cases, about 5–10 %, the inflammatory process progresses and leads to ischemia and necrosis of the gallbladder wall. More frequently, the gallstone is dislodged and the inflammation resolves. When the gallbladder remains obstructed and secondary bacterial infection supervenes, an acute gangrenous cholecystitis develops and an abscess or empyema forms within the gallbladder. Rarely, perforation of ischemic areas occurs. The perforation usually is contained in the subhepatic space by the omentum and adjacent organs.
Clinical manifestations. About 80 % of patients with acute cholecystitis give a history compatible with chronic cholecystitis. Acute cholecystitis begins as an attack of biliary colic, but in contrast to biliary colic, the pain does not subside; it is unremitting and may persist for several days. The patient often is febrile, complains of anorexia, nausea, and vomiting, and is reluctant to move, as the inflammatory process affects the parietal peritoneum. On physical exam, focal tenderness and guarding are usually present in the right upper quadrant. A mass, the gallbladder and adherent omentum, is occasionally palpable; however, guarding may prevent this. A Murphy’s sign, an inspiratory arrest with deep palpation in the right subcostal area, is characteristic of acute cholecystitis. A mild to moderate leukocytosis (12,000–15,000 cells/mm3) usually is present. However, some patients may have a normal WBC. Serum liver chemistries usually are normal, but a mild elevation of serum bilirubin, less than 4 mg/mL, may be present along with mild elevation of alkaline phosphatase, transaminases, and amylase. Severe jaundice is suggestive of common bile duct stones or obstruction of the bile ducts by severe pericholecystic inflammation secondary to impaction of a stone in the infundibulum of the gallbladder that mechanically obstructs the bile duct (Mirizzi syndrome). In older adult patients and in those with diabetes mellitus, acute cholecystitis may have a subtle presentation resulting in a delay in diagnosis. The incidence of complications is higher in these patients, who also have approximately tenfold the mortality rate compared to that of younger and healthier patients.
Diagnosis. Ultrasonography is the most useful radiologic test for diagnosing acute cholecystitis. It has a sensitivity and specificity of 95 %. It will show the thickening of the gallbladder wall and the pericholecystic fluid. Focal tenderness over the gallbladder when compressed by the sonographic probe (sonographic Murphy sign) also is suggestive of acute cholecystitis. Biliary radionuclide scanning (HIDA scan) may be of help in the atypical case. A normal HIDA scan excludes acute cholecystitis. CT scan is frequently performed on patients with acute abdominal pain. It demonstrates thickening of the gallbladder wall, pericholecystic fluid, and the presence of gallstones and air in the gallbladder wall, but is less sensitive than ultrasonography.
Treatment. Patients who present with acute cholecystitis will need intravenous fluids, antibiotics, and analgesia. The antibiotics should cover Gramnegative aerobes and anaerobes. Although the inflammation in acute cholecystitis may be sterile in some patients, more than one half will have positive cultures from the gallbladder bile. Cholecystectomy is the definitive treatment for acute cholecystitis. Early cholecystectomy performed within 2–3 days of the illness is preferred over interval or delayed cholecystectomy that is performed 6–10 weeks after initial medical treatment and recuperation. Early cholecystectomy offers the patient a definitive solution in one hospital admission, quicker recovery times, and an earlier return to work. Laparoscopic cholecystectomy is the procedure of choice for acute cholecystitis. The conversion rate to an open cholecystectomy is higher (10–15 %) in the setting of acute cholecystitis than with chronic cholecystitis. The procedure is more tedious and takes longer than in the elective setting. When patients present late, after 3–4 days of illness, or are for some reason unfit for surgery, they are treated with antibiotics with laparoscopic cholecystectomy scheduled for approximately 2 months later. Approximately 20 % of patients will fail to respond to initial medical therapy and require an intervention. For those unfit for surgery, a percutaneous cholecystostomy or an open cholecystostomy under local analgesia can be performed. Failure to improve after cholecystostomy usually is because of gangrene of the gallbladder or perforation. For these patients, surgery is unavoidable. For those who respond after cholecystostomy, the tube can be removed once cholangiography through it shows a patent ductus cysticus. Laparoscopic cholecystectomy may then be scheduled in the near future.
Common bile duct stones may be small or large, single or multiple, and are found in 6–12 % of patients with stones in the gallbladder. The incidence increases with age. About 20–25 % of patients older than the age of 60 with symptomatic gallstones have stones in the common bile duct and in the gallbladder. The vast majority of ductal stones inWestern countries are formed within the gallbladder and migrate down the cystic duct to the common bile duct. These are classified as secondary common bile duct stones, in contrast to the primary stones that form in the bile ducts.
Clinical manifestations. Choledochal stones may be silent and often are discovered incidentally. They may cause obstruction, complete or incomplete, or they may manifest with cholangitis or gallstone pancreatitis. The pain caused by a stone in the bile duct is similar to that of biliary colic. Nausea and vomiting are common. Physical exam may be normal, but mild epigastric or right upper quadrant tenderness and mild icterus are common. The symptoms may also be intermittent, such as pain and transient jaundice caused by a stone that temporarily impacts the ampulla but subsequently moves away, acting as a ball valve. A small stone may pass through the ampulla spontaneously with resolution of symptoms. Finally the stones may become completely impacted, causing severe progressive jaundice. Elevation of serum bilirubin, alkaline phosphatase, and transaminases are commonly seen in patients with bile duct stones. However, in about one third of patients with common bile duct stones, the liver chemistries are normal. Commonly the first test, ultrasonography is useful for documenting stones in the gallbladder, and determining the size of the common bile duct. As stones in the bile ducts tend to move down to the distal part of the common duct, bowel gas can preclude their demonstration on ultrasonography. A dilated common bile duct (>8mmin diameter) on ultrasonography in a patient with gallstones, jaundice, and biliary pain is highly suggestive of common bile duct stones. Magnetic resonance cholangiography (MRC) provides excellent anatomic detail and has a sensitivity and specificity of 95 and 89 %, respectively, at detecting choledocholithiasis. Endoscopic cholangiography is the gold standard for diagnosing common bile duct stones. It has the distinct advantage of providing a therapeutic option at the time of diagnosis. In experienced hands, cannulation of the ampulla of Vater and diagnostic cholangiography are achieved in over 90 % of cases, with associated morbidity of less than 5 % (mainly cholangitis and pancreatitis). Percutaneous transhepatic cholangiography (PTC) rarely is needed in patients with secondary common bile duct stones, but frequently is performed for both diagnostic and therapeutic reasons in patients with primary bile duct stones.
Treatment. For patients with symptomatic gallstones and suspected common bile duct stones, either preoperative endoscopic cholangiography or an intraoperative cholangiogram will document the bile duct stones. If an endoscopic cholangiogram reveals stones, sphincterotomy and ductal clearance of the stones is appropriate, followed by a laparoscopic cholecystectomy. An intraoperative cholangiogram at the time of cholecystectomy also will document the presence or absence of bile duct stones. Laparoscopic common bile duct exploration via the cystic duct or with formal choledochotomy allows the stones to be retrieved in the same setting (see following section). If the expertise and/or the instruments for laparoscopic common bile duct exploration are not available, a drain should be left adjacent to the cystic duct and the patient scheduled for endoscopic sphincterotomy the following day. An open common bile duct exploration is an option if the endoscopic method has already been tried or is for some reason not feasible. If a choledochotomy is performed, a ? tube is left in place. Stones impacted in the ampulla may be difficult for both endoscopic ductal clearance and common bile duct exploration (open or laparoscopic). In these cases the common bile duct usually is quite dilated (about 2 cm in diameter). A choledochoduodenostomy or a Roux-en-Y choledochojejunostomy may be the best option for these circumstances. Retained or recurrent stones following cholecystectomy are best treated endoscopically. If a common bile duct exploration was performed and a ? tube left in place, a ?-tube cholangiogram is obtained prior to its removal. Retained stones can be retrieved either endoscopically or via the ?-tube tract once it has matured (2–4 weeks). Under fluoroscopic guidance the stones are retrieved with baskets or balloons. Recurrent stones may be multiple and large. A generous endoscopic sphincterotomy will allow stone retrieval and spontaneous passage of retained and recurrent stones.
Cholangitis is one of the two main complications of choledochal stones, the other being gallstone pancreatitis. Acute cholangitis is an ascending bacterial infection in association with partial or complete obstruction of the bile ducts. Hepatic bile is sterile, and bile in the bile ducts is kept sterile by continuous bile flow and by the presence of antibacterial substances in bile such as immunoglobulin. The combination of both significant bacterial contamination and biliary obstruction is required for its development. Gallstones are the most common cause of obstruction in cholangitis. The most common organisms cultured from bile in patients with cholangitis include Escherichia coli, Klebsiella pneumoniae, Streptococcus faecalis, and Bacteroides fragilis.
Clinical presentation. Cholangitis may present as anything from a mild, intermittent, and self-limited disease to a fulminant, potentially life-threatening septicemia. The most common presentation is fever, epigastric or right upper quadrant pain, and jaundice. These classic symptoms, well known as Charcot triad, are present in about two thirds of patients. The illness may progress rapidly with septicemia and disorientation, known as Reynolds pentad (e.g., fever, jaundice, right upper quadrant pain, septic shock, and mental status changes). However, the presentation may be atypical, with little if any fever, jaundice, or pain. This occurs most commonly in older adults, who may have unremarkable symptoms until they collapse with septicemia. On abdominal examination, the findings are indistinguishable from those of acute cholecystitis.
Diagnosis and management. Leukocytosis, hyperbilirubinemia, and elevation of alkaline phosphatase and transaminases are common, and when present, support the clinical diagnosis of cholangitis. Ultrasonography is helpful if the patient has not been diagnosed previously with gallstones, as it will document the presence of gallbladder stones and demonstrate dilated ducts. The definitive diagnostic test is ERC. In cases in which ERC is not available, PTC is indicated. Both ERC and PTC will show the level and the reason for the obstruction, allow culture of the bile, possibly allow the removal of stones if present, and drainage of the bile ducts with drainage catheters or stents. CT scanning and MRI will show pancreatic and periampullary masses, if present, in addition to the ductal dilatation. The initial treatment of patients with cholangitis includes intravenous antibiotics and fluid resuscitation. Most patients will respond to these measures. However, the obstructed bile duct must be drained as soon as the patient has been stabilized. About 15 % of patients will not respond to antibiotics and fluid resuscitation, and an emergency biliary decompression may be required. Biliary decompression may be accomplished endoscopically, via the percutaneous transhepatic route, or surgically. Patients with choledocholithiasis or periampullary malignancies are best approached endoscopically, with sphincterotomy and stone removal, or by placement of an endoscopic biliary stent. In patients in whom the obstruction is more proximal or perihilar, percutaneous transhepatic drainage is used. Where neither ERC nor PTC is possible, an emergent operation and decompression of the common bile duct with a ? tube may be necessary and life-saving. Definitive operative therapy should be deferred until the cholangitis has been treated and the proper diagnosis established. Patients with indwelling stents and cholangitis usually require repeated imaging and exchange of the stent over a guidewire. Acute cholangitis is associated with an overall mortality rate of approximately 5 %.
Gallstones in the common bile duct are associated with acute pancreatitis. Obstruction of the pancreatic duct by an impacted stone or temporary obstruction by a stone passing through the ampulla may lead to pancreatitis. An ultrasonogram of the biliary tree in patients with pancreatitis is essential. If gallstones are present and the pancreatitis is severe, an ERC with sphincterotomy and stone extraction may abort the episode of pancreatitis. Once the pancreatitis has subsided, the gallbladder should be removed during the same admission. When gallstones are present and the pancreatitis is mild and self-limited, the stone has probably passed. For these patients a cholecystectomy and an intraoperative cholangiogram or a preoperative ERC is indicated.
Cholangiohepatitis, also known as recurrent pyogenic cholangitis, is endemic to the Orient. It also has been encountered in the Chinese population in the United States and in Europe and Australia. Cholangiohepatitis is caused by bacterial contamination (commonly E. coli, Klebsiella species, Bacteroides species, or Enterococcus faecalis) of the biliary tree, and often is associated with biliary parasites such as Clonorchis sinensis, Opisthorchis viverrini, and Ascaris lumbricoides. Bacterial enzymes cause deconjugation of bilirubin, which precipitates as bile sludge. The sludge and dead bacterial cell bodies form brown pigment stones. These stones are formed throughout the biliary tree and cause partial obstruction that contributes to the repeated bouts of Cholangitis The patient usually presents with pain in the right upper quadrant and epigastrium, fever, and jaundice. Recurrence of symptoms is one of the most characteristic features of the disease. An ultrasound will detect stones in the biliary tree, pneumobilia from infection because of gas-forming organisms, liver abscesses, and occasionally strictures. MRCP and PTC are the mainstays of biliary imaging for cholangiohepatitis. The long-term goal of therapy is to extract stones and debris and relieve strictures. It may take several procedures and require a Roux-en-Y hepaticojejunostomy to establish biliary-enteric continuity.
Acholecystostomy decompresses and drains the distended, inflamed, hydropic, or purulent gallbladder. Ultrasound guided percutaneous drainage with a pigtail catheter is the procedure of choice. By passing the catheter through the liver, the risk of bile leak around the catheter is minimized. The catheter can be removed when the inflammation has resolved and the patient’s condition improved.
Cholecystectomy is the most common major abdominal procedure performed in Western countries. Open cholecystectomy is a safe and effective treatment for both acute and chronic cholecystitis. In 1987, laparoscopic cholecystectomy was introduced. Today laparoscopic cholecystectomy is the treatment of choice for symptomatic gallstones. Symptomatic gallstones are the main indication for cholecystectomy. Absolute contraindications for the procedure are uncontrolled coagulopathy and end-stage liver disease. When important anatomic structures cannot be clearly identified or when no progress is made over a set period of time, a conversion to an open procedure usually is indicated. In the elective setting, conversion to an open procedure is needed in about 5 % of patients. Emergent procedures may require more skill on the part of the surgeon, and be needed in patients with complicated gallstone disease; the incidence of conversion is 10–30 %. Serious complications are rare. The mortality rate for laparoscopic cholecystectomy is about 0.1 %. Wound infection and cardiopulmonary complication rates are considerably lower following laparoscopic cholecystectomy than are those for an open procedure, in which injury to the bile ducts is slightly more frequent. Patients undergoing cholecystectomy should have a complete blood count (CBC) and liver function tests preoperatively. Prophylaxis against deep venous thrombosis with either low-molecular-weight heparin or compression stockings is indicated.
The patient is placed supine on the operating table with the surgeon standing at the patient’s left side. The pneumoperitoneum is created with carbon dioxide gas, either with an open technique or by closed needle technique. Once an adequate pneumoperitoneum is established, a 10-mm trocar is inserted through the supraumbilical incision. The laparoscope with the attached video camera is passed through the umbilical port and the abdomen inspected. Three additional ports are placed under direct vision. Through the lateral-most port a grasper is used to grasp the gallbladder fundus. The dissection starts at the junction of the gallbladder and the cystic duct. A helpful anatomic landmark is the cystic artery lymph node. The peritoneum, fat, and loose areolar tissue around the gallbladder and the cystic duct-gallbladder junction is dissected off toward the bile duct. The next step is the identification of the cystic artery, which usually runs parallel to and somewhat behind the cystic duct. A wide cystic duct may be too big for clips, requiring the placement of a pretied loop ligature to close. The cystic artery is then clipped and divided. Finally, the gallbladder is dissected out of the gallbladder fossa, using either a hook or scissors with electrocautery. The gallbladder is removed through the umbilical incision. If the gallbladder is acutely inflamed or gangrenous, or if the gallbladder is perforated, it is placed in a retrieval bag before it is removed from the abdomen. A closed suction drain can be placed through one of the 5-mm ports and left underneath the right liver lobe close to the gallbladder fossa.
Open cholecystectomy has become an uncommon procedure, usually performed either as a conversion from laparoscopic cholecystectomy or as a second procedure in patients who require laparotomy for another reason. After the cystic artery and cystic duct have been identified, the gallbladder is dissected free from the liver bed, starting at the fundus. The dissection is carried proximally toward the cystic artery and the cystic duct, which are then ligated and divided.
Intraoperative Cholangiogram or Ultrasound
The bile ducts are visualized under fluoroscopy by injecting contrast through a catheter placed in the cystic duct. Routine intraoperative cholangiography will detect stones in approximately 7 % of patients, and outlining the anatomy and detecting injury. A selective intraoperative cholangiogram can be performed when the patient has a history of abnormal liver function tests, pancreatitis, jaundice, a large duct and small stones, a dilated duct on preoperative ultrasonography, and if preoperative endoscopic cholangiography for the above reasons was unsuccessful. Laparoscopic ultrasonography is as accurate as intraoperative cholangiography in detecting common bile duct stones and it is less invasive; however, it requires more skill to perform and interpret.
Common bile duct stones that are detected intraoperatively on Intraoperative cholangiography or ultrasonography may be managed with laparoscopic choledochal exploration as a part of the laparoscopic cholecystectomy procedure. Patients with common bile duct stones detected preoperatively, but endoscopic clearancewas either not available or unsuccessful, should also have their ductal stones managed during the cholecystectomy. If the stones in the duct are small, they may sometimes be flushed into the duodenum with saline irrigation via the cholangiography catheter after the sphincter of Oddi has been relaxed with glucagon. By managing common bile duct stones at the time of the cholecystectomy, the patients can have all of their gallstone disease treated with one invasive procedure. It does, however, depend on the available surgical expertise.
Rarely, when the stones cannot be cleared and/or when the duct is very dilated (larger than 1.5 cm in diameter), a choledochal drainage procedure is performed.
In the majority of cases, endoscopic sphincterotomy has replaced open transduodenal sphincterotomy. If an open procedure for common bile duct stones is being done in which the stones are impacted, recurrent, or multiple, the transduodenal approach may be feasible. The duodenum is incised transversely. The sphincter then is incised at the 11 o’clock position to avoid injury to the pancreatic duct. The impacted stones are removed as are large stones from the duct.
Acute inflammation of the gallbladder can occur without gallstones. Acalculous cholecystitis typically develops in critically ill patients in the intensive care unit. The cause is unknown, but gallbladder distention with bile stasis and ischemia have been implicated as causative factors. The symptoms and signs depend on the condition of the patient, but in the alert patient they are similar to acute calculous cholecystitis. In the sedated or unconscious patient the clinical features often are masked, but fever and elevated white blood cell count, and elevation of alkaline phosphatase and bilirubin are indications for further investigation. Ultrasonography is usually the diagnostic test of choice. Abdominal CT scan is as sensitive as ultrasonography and additionally allows imaging of the abdominal cavity and chest. A HIDA scan will not visualize the gallbladder. Acalculous cholecystitis requires urgent intervention. Percutaneous ultrasound- or CT-guided cholecystostomy is the treatment of choice for these patients, as they usually are unfit for surgery. About 90 % of patients will improve with the percutaneous cholecystostomy. However, if they do not improve, other steps, such as open cholecystostomy or cholecystectomy, may be required.
Choledochal cysts are congenital cystic dilatations of the extrahepatic and/or intrahepatic biliary tree. They are rare—the incidence is between 1:100,000 and 1:150,000. Choledochal cysts affect females three to eight times more often than males. Although frequently diagnosed in infancy or childhood, as many as one half of the patients have reached adulthood when diagnosed. The cause is unknown. Choledochal cysts are classified into five types. The cysts are lined with cuboidal epithelium and can vary in size from 2 cm in diameter to giant cysts. Adults commonly present with jaundice or cholangitis. Less than one half of patients present with the classic clinical triad of abdominal pain, jaundice, and a mass. Ultrasonography or CT scanning will confirm the diagnosis, but endoscopic, transhepatic, or MRC is required to assess the biliary anatomy and to plan the appropriate surgical treatment. For types I, II, and IV, excision of the extrahepatic biliary tree, including cholecystectomy, with a Roux-en-Y hepaticojejunostomy are ideal. In type IV, additional segmental resection of the liver may be appropriate, particularly if intrahepatic stones, strictures, or abscesses are present, or if the dilatations are confined to one lobe. The risk of cholangiocarcinoma developing in choledochal cysts is as high as 15 % in adults, and supports complete excision when they are diagnosed. For type III, sphincterotomy is recommended.
Sclerosing cholangitis is an uncommon disease characterized by inflammatory strictures involving the intrahepatic and extrahepatic biliary tree. It is a progressive disease that eventually results in secondary biliary cirrhosis. Sometimes, biliary strictures are clearly secondary to bile duct stones, acute cholangitis, previous biliary surgery, or toxic agents, and are termed secondary sclerosing cholangitis. However, primary sclerosing cholangitis is a disease entity of its own, with no known attributing cause. It is associated with ulcerative colitis in about two thirds of patients. Other diseases associated with sclerosing cholangitis include Riedel thyroiditis and retroperitoneal fibrosis. Patients with sclerosing cholangitis are at risk for developing cholangiocarcinoma Eventually 10–20 % of the patients will develop cancer. The mean age of presentation is 30–45 years and men are affected twice as commonly as women. The usual presentation is intermittent jaundice, fatigue, weight loss, pruritus, and abdominal pain. In several patients with ulcerative colitis, abnormal liver function tests found on routine testing lead to the diagnosis. The clinical course in sclerosing cholangitis is highly variable, but cyclic remissions and exacerbations are typical. However, some patients remain asymptomatic for years, although others progress rapidly with the obliterative inflammatory changes leading to secondary biliary cirrhosis and liver failure. The median survival for patients with primary sclerosing Cholangitis from the time of diagnosis ranges from 10 to 12 years, and most die from hepatic failure. The clinical presentation and elevation of alkaline phosphatase and bilirubin may suggest the diagnosis, but ERC, revealing multiple dilatations and strictures (beading) of both the intra- and extrahepatic biliary tree confirms it. The hepatic duct bifurcation is often the most severely affected segment. Sclerosing cholangitis is followed by ERC and liver biopsies to provide appropriate management. There is no known effective medical therapy for primary sclerosing Cholangitis and no known curative treatment. Corticosteroids, immunosuppressants, ursodeoxycholic acid, and antibiotics have been disappointing. Biliary strictures can be dilated and stented either endoscopically or percutaneously. Surgical management with resection of the extrahepatic biliary tree and hepaticojejunostomy has produced reasonable results in patients with extrahepatic and bifurcation strictures. In patients with sclerosing cholangitis and advanced liver disease, liver transplantation is the only option. It offers excellent results with overall 5-year survival as high as 85 %. Primary sclerosing Cholangitis recurs in 10–20 % of patients and may require retransplantation. Stenosis of the Sphincter of Oddi A benign stenosis of the outlet of the common bile duct usually is associated with inflammation, fibrosis, or muscular hypertrophy. Episodic pain of the biliary type with abnormal liver function tests is a common presentation. However, recurrent jaundice or pancreatitis also may play a role. A dilated common bile duct that is difficult to cannulate with delayed emptying of the contrast are useful diagnostic features. If the diagnosis is well established, endoscopic or operative sphincterotomy will yield good results.
Benign bile duct strictures can have numerous causes. However, the vast majority are caused by operative injury, most commonly by laparoscopic cholecystectomy (see below). Other causes include fibrosis because of chronic pancreatitis, common bile duct stones, acute cholangitis, biliary obstruction because of cholecystolithiasis (Mirizzi syndrome), sclerosing cholangitis, cholangiohepatitis, and strictures of a biliary-enteric anastomosis. Bile duct strictures that go unrecognized or are improperly managed may lead to recurrent cholangitis, secondary biliary cirrhosis, and portal hypertension. Patients with bile duct strictures most commonly present with episodes of cholangitis. An ultrasound or a CT scan will show dilated bile ducts proximal to the stricture, and provide some information about the level of the stenosis. MRC will also provide good anatomic information about the location and the degree of dilatation. In patients with intrahepatic ductal dilatation, a percutaneous transhepatic cholangiogram will outline the proximal biliary tree, define the stricture and its location, and allow decompression of the biliary tree with transhepatic catheters or stents. An endoscopic cholangiogram will outline the distal bile duct. Percutaneous or endoscopic dilatation and/or stent placement give good results in more than one half of patients. Surgery with Roux-en-Y choledochojejunostomy or hepaticojejunostomy is the standard of care with good or excellent results in 80–90 % of patients. Choledochoduodenostomy may be a choice for strictures in the distal-most part of the common bile duct.
|Acute cholecistitis anatomy the Gallbladder|
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|Workshop 5 Topographic anatomy of the lateral part of the face. Surgical anatomy of parotid gland. Surgical anatomy of the facial nerve|
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