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The creation of a sonographic image (sonogram) depends on three major components: the production of a high frequency sound wave,

the reception of a reflected wave or echo, and the conversion of that echo into the actual image.

Signs of acute cholecystitis on ultrasound: o The presence of gallstones, possibly impacted in the neck of the gallbladder or cystic duct. o Thickening of the gallbladder wall (>3 mm) (Fig. 19-5A). o Pericholecystic fluid (fluid around the gallbladder) (Fig. 19-5B). o A positive Murphy sign (pain that is elicited by compression of the gallbladder with the ultrasound probe).

Figure 19-5 Acute cholecystitis, sagittal views, two patients. A, Thickening of gallbladder (GB) wall. The wall should be 3 mm or less. This wall is markedly thickened at 6 mm (solid white arrows). B, There is an echo-free crescent (dotted white arrow) surrounding a thickened gallbladder (GB) wall representing pericholecystic fluid. The patient had a positive sonographic Murphy sign.

page 196 page 197 Ultrasound plays a key role in evaluation of the intrahepatic and extrahepatic bile

ducts and pancreatic duct. The intrahepatic biliary radicals drain into the left and right hepatic ducts, which join to form the common hepatic duct (CHD). Where the cystic duct from the gallbladder joins the CHD is the origin of the common bile duct (CBD), which drains either within or adjacent to the head of the pancreas via the ampulla of Vater into the second portion of the duodenum. The CBD lies anterior to the portal vein and lateral to the hepatic artery in the porta hepatis (Fig. 19-7). Normal intrahepatic bile ducts are not visible. When the CBD is obstructed, the extrahepatic ducts dilate before the intrahepatic ducts. Over time, both the intrahepatic and extrahepatic ducts will be dilated (Fig. 19-8). Causes of bile duct obstruction include gallstones, pancreatic carcinoma, strictures, sclerosing cholangitis, cholangiocarcinoma, and metastatic disease.

Figure 19-8 Dilated intrahepatic and extrahepatic ducts in two different patients, sagittal images. A, The intrahepatic (L = liver) biliary ducts are normally not visible by ultrasound. In this case, they are dilated (solid white arrow) from obstruction by a pancreatic carcinoma (not shown). B, The CBD is dilated at 15 mm (dotted white arrows) and the gallbladder (GB) is distended from an obstructing stone (not shown).

A transducer converts electric energy into ultrasonic energy.

Tissues with large differences in acoustic impedance (i.e., physical density or velocity) produce reflections of almost 100%. Tissueair and musclebone interfaces always give large reflections. A coupling fluid must be used between the

ultrasonic transducer and the patients skin to avoid 100% reflection from the transducerair interface.


Multiple imaging modalities are available for investigating the biliary system. Methods vary in cost and invasiveness; all modalities can contribute to the goal of correct diagnosis. Because not all are needed in each patient, a careful evaluation of the clinical needs is required before proceeding. Also, it is important to tailor the diagnostic algorithm to local skills and equipment. Imaging Techniques The abdominal plain film (abdominal radiograph) is of value in finding gas or calcium in the biliary tract. Approximately 10% to 15% of gallstones are calcified and readily identifiable on plain films. At times there may be an accumulation of calcium in the gallbladder that simulates contrast material (milk of calcium bile) ( Fig. 14-20). Occasionally, the gallbladder wall is calcified (porcelain gallbladder), which is important because of the association of this abnormality with gallbladder carcinoma Gas may be seen in the center of gallstones in a triangular pattern (Mercedes-Benz sign). Gas in the biliary ducts implies an abnormal connection between the gut and the gallbladder or common bile duct. This may be caused by penetration of a duodenal ulcer into the biliary tract or by gallstone erosion into the stomach, duodenum, or colon. Biliary air is more centrally located in the liver compared with portal venous air, which is peripheral. Most commonly, biliary air is a consequence of surgical anastomosis of the gut to the biliary tract or sphincterotomy of the sphincter of Oddi ( Fig. 14-21; Table 14-6). FIG.

Gas is occasionally seen in the ducts as a manifestation of cholangitis caused by a gasforming organism. Gas in the gallbladder and its wall (emphysematous cholecystitis) is the manifestation of a similar infection. Gas in the portal vein, seen peripherally in the liver, implies necrotic bowel, but it may occur with severe cholecystitis or cholangitis. Oral cholecystography (OCG) is based on hepatobiliary function. Ingestion of an iodinated compound that is absorbed by

the small bowel, conjugated, excreted by the liver, and concentrated in the gallbladder by water absorption provides the opportunity to discover noncalcified gallstones as filling defects. In addition to gallstones, other intraluminal abnormalities of the gallbladder can be detected on OCG ( Fig. 14-22). OCG has essentially been replaced by US.

Gallbladder ultrasonography is the preferred screening method for biliary and gallbladder disease because of cost and convenience. After 6 hours of fasting, imaging is performed with the patient in the supine and decubitus positions. Jaundice does not interfere with the examination. The ability to detect biliary dilatation, wall thickening, and stones and to evaluate the parenchyma of the liver and pancreas is enormously beneficial. US can detect smaller stones than can OCG.

A hepatobiliary scan or cholescintigraphy is a dynamic study of the pathophysiology of the biliary system. IV injection of technetium-labeled iminodiacetic acid compounds allows imaging of the gallbladder, and the radioactivity can be followed into the duodenum. A lack of filling of the gallbladder is indicative of cystic duct obstruction and is a highly reliable sign of acute cholecystitis. Delayed filling of the gallbladder (within 4 hours) is seen in chronic cholecystitis. The sensitivity and specificity are comparable to those of US for the diagnosis of acute cholecystitis. Cholescintigraphy has also been advocated as a procedure that can detect bile duct obstruction before duct dilatation occurs and is visible by US. It is useful to detect biliary leaks and to demonstrate the patency of biliary-enteric anastomoses. Cholangiography can be performed percutaneously, endoscopically, or directly, either intraoperatively or through a T tube. Endoscopic retrograde cholangiopancreatography (ERCP) allows direct injection of the common bile duct lumen with contrast material. It is of special value in detecting common bile duct stones and both inflammatory and neoplastic duct abnormalities. Sphincterotomy, biopsy, mucosal brushings, stone retrieval from the bile ducts, stricture dilation, and placement of stents to relieve obstruction are all possible by ERCP. Percutaneous transhepatic cholangiography is accomplished by injecting contrast material, with fluoroscopic guidance,

through a narrow-gauge needle placed into the parenchyma of the liver and withdrawing the needle slowly, observing for bile duct opacification (see Chapter 15). It is valuable for the same reasons as ERCP and has the advantage of allowing the operator to institute biliary drainage if necessary. It is reserved for patients with biliary obstruction who need permanent or temporary biliary drainage. Needle biopsy of masses, drainage of fluid collections, and placement of external and internal drainage (choledochoduodenal) stents all can be accomplished percutaneously. Operative cholangiography is used to visualize nonpalpable common duct stones during surgery and T-tube cholangiography is used to visualize retained common duct stones after surgery ( Fig. 14-23).

Computed tomography can detect gallstones and dilated biliary ducts but is less sensitive than sonography. CT is useful in evaluating the liver parenchyma and pancreas for neoplasm. It also is more sensitive than abdominal plain films in detecting biliary and portal vein gas. CT is useful in the diagnosis and staging of gallbladder carcinoma. Biliary and gallbladder disease can be an incidental finding on CT of the abdomen. Magnetic resonance imaging of the gallbladder and ducts is relatively recent. MRI may be better than CT or US in biliary dilatation. Ionizing radiation is not used in this examination, which is an important consideration. Anatomy The gallbladder is a thin-walled, cystic structure attached to the inferior and medial aspect of the right lobe of the liver. The fossa is at the junction of the right and left lobes of the liver, but occasionally it is intrahepatic in location. The neck of the gallbladder has a consistent relationship to the porta hepatis. The gallbladder measures approximately 10 cm in length and 3 to 5 cm in diameter when distended. A gallbladder with a diameter of more than 5 cm is enlarged or hydropic. The cystic duct is approximately 2 to 4 cm in length. The initial segment has characteristic tortuous mucosal folds, known as the spiral valves of Heister. The gallbladder wall should be less than 4 mm thick. Normal variants include a phrygian cap and septation of the fundus. The gallbladder may be congenitally absent, or it may be intrahepatic in location. CT is the best imaging modality for making these diagnoses ( Fig. 14-24).

FIG. 14-24. Intrahepatic gallbladder. Computed tomographic scan demonstrates the gallbladder ( arrow) to be well within the parenchyma of the liver. The right and left hepatic ducts join to form the common hepatic duct, which courses with the hepatic artery and portal vein in the porta hepatis. The common bile duct is anterior to the portal vein and right of the hepatic artery in the hepatoduodenal ligament. The cystic duct joins the common hepatic duct to form the common bile duct. The site of the junction of cystic and common hepatic ducts can vary considerably. Additionally, the right hepatic duct may join the cystic duct rather than joining directly with the left hepatic duct. The common bile duct courses caudally in close relationship to the head of the pancreas and tapers distally as it ends in the sphincter of Oddi, which protrudes into the duodenum as the papilla of Vater. A slight dilatation of the distal lumen is called the ampulla of Vater. In 60%, the pancreatic duct merges with the common bile duct proximal to the ampulla ( Fig. 14-25). Tumors of the region of the ampulla often obstruct both ducts. The common duct is less than 6 mm in diameter but can be a few millimeters larger in the elderly.

The most common malady of the gallbladder is cholelithiasis. Ten percent of the population have gallstones. Women and people with hemolytic anemia, cirrhosis, diabetes, or disease of the ileum are more commonly afflicted. Most stones are comprised of cholesterol. US, the most common screening procedure for cholelithiasis, detects 95% of stones; those in the gallbladder neck may be missed. Stones are diagnosed by echogenic, shadowing foci within the gallbladder that move when the patient changes position. If the foci are not mobile, the sonographic differential diagnosis includes biliary sludge from concentrated bile, cholesterol or adenomatous polyps, adenomyomatosis, and gallbladder carcinoma ( Table 14-7). CT is less sensitive for the detection of gallstones, with 85% seen on CT. However, stones have a variable density, ranging from that of fat to that of calcium. Some may be the same density as bile (

TABLE 14-7. Causes of gallbladder filling defect

FIG. 14-26. Cholelithiasis. A: A longitudinal ultrasound scan shows multiple stones in the gallbladder that cause shadowing of the ultrasound beam below them. B: Ultrasonogram shows large echogenic defect in the gallbladder ( open arrow) with acoustical shadowing ( black arrowheads). C: Cholesterol stones are seen as lucent areas in the gallbladder on computed tomogram (CT). D: Large, laminated stone on CT. The stone has a central calcification and a peripheral rim of calcification.

The most common cause of acute cholecystitis is obstruction of the cystic duct by a stone. Five percent to 10% of cases are acalculous. Acalculous cholecystitis occurs most commonly in critically ill patients, especially after surgery, trauma, or burns, or in patients receiving hyperalimentation. Acute cholecystitis is usually diagnosed clinically or by US or hepatobiliary scan. Normally, the gallbladder fills in 30 minutes on a hepatobiliary scan. Nonvisualization at 1 hour is consistent with acute cholecystitis. Other causes of nonvisualization include chronic cholecystitis, stasis, and hyperalimentation (Fig. 14-27). The sonographic findings include cholelithiasis, wall thickeningoften with a lucent band in the wall (edema)and a positive Murphys sign or pinpoint tenderness over the gallbladder. Generally, CT is employed only in atypical or complicated situations. The most common CT findings are wall thickening, stones, and pericholecystic fluid.

Complications, which occur in 25% to 30% of patients with acute cholecystitis, include gangrenous cholecystitis, gallbladder perforation, emphysematous cholecystitis, and hemorrhagic cholecystitis. Gangrenous cholecystitis is necrosis of the wall. Sonographically the gallbladder wall is asymmetrically thickened, often with multiple sonolucent layers. Gallbladder perforation has a 25% mortality. Most wall off the lesion, forming a pericholecystic abscess. Emphysematous cholecystitis is secondary infection with a gas-forming organism. Diabetics are most commonly affected (Fig. 14-28). The US appearance can be confusingbright echoes with dirty posterior shadows from the wall or lumen.

The imaging findings in chronic cholecystitis are similar to those of acute cholecystitis except that the gallbladder is often contracted. Patients have gallstones, chronic inflammation, and recurrent biliary colic. The gallbladder is visualized at between 1 and 4 hours on a hepatobiliary scan.

Biliary Dilatation Biliary dilatation is not synonymous with biliary obstruction. Biliary dilatation can be present with or without biliary obstruction. Additionally, early biliary obstruction can be present without biliary dilatation. US is usually the initial modality unless the patient is obese or there is a high likelihood of malignancy. The findings on CT and US include branching tubular structures in the liver, a common bile duct larger than 5 mm in diameter, and a gallbladder diameter greater than 5 cm (Fig. 14-29). Normal intrahepatic ducts can be seen on newer, highresolution CT scans; the intrahepatic ducts should be few, scattered, and less than 3 mm in diameter. If biliary obstruction is suspected, an attempt should be made to determine the presence, level, and cause of obstruction.

FIG. 14-29. Biliary dilatation. A: Dilated intrahepatic biliary ducts. Ultrasonogram through the right lobe of the liver shows numerous tubular structures representing dilated bile duct ( arrows) secondary to impacted stone in common bile duct. B: Intrahepatic biliary dilatation is shown on contrast-enhanced computed tomogram in a patient with pancreatic cancer obstructing the distal common bile duct. Two peripheral liver metastases also are seen ( arrows). CT is approximately 95% accurate in determining the presence, level, and cause of biliary obstruction. Benign causes of biliary dilatation are more common than malignant ones. The major causes of biliary obstruction are gallstones, tumor, stricture, and pancreatitis ( Table 14-8). A rare but interesting cause of biliary obstruction is Mirizzis syndrome. A gallstone impacted in the gallbladder neck, cystic duct, or cystic duct remnant obstructs the common hepatic duct. Secondary inflammation is contributory. It occurs more frequently with low insertion of the cystic duct

Abrupt termination of a dilated extrahepatic biliary duct is characteristic of a malignant process even in the absence of a visible mass. Common tumors causing biliary obstruction are pancreatic carcinoma, ampullary carcinoma, and cholangiocarcinoma. A mass is often visible on CT at the point of biliary obstruction. Gradual tapering of a dilated duct is seen most commonly with benign disease such as inflammatory stricture, surgical or iatrogenic trauma, or pancreatitis. Calcifications in the pancreas are a clue to the presence of chronic pancreatitis. Gallstones obstructing the bile ducts are seen as calcific or soft-tissue density structures within the bile duct surrounded by a crescent of fluid-density bile. Some stones are isodense with bile and are not detected by CT. US detects 65% of choledocholithiasis. A contrast-enhanced cholangiogram is the best detector of choledocholithiasis. Stones appear as filling defects ( Fig. 14-30). The disadvantage is that it is invasive unless a previously inserted biliary tube is present

Ascending cholangitis is acute infection of the biliary tree. Most cases are secondary to partial or complete biliary obstruction. Escherichia coli is frequently one of the organisms responsible. Cholangitis is being reported with increasing frequency in association with human immunodeficiency virus (HIV) infection. Cryptosporidia and cytomegalovirus are implicated pathogens. Manifestations include thickening of the wall of the bile ducts and gallbladder and intrahepatic changes such as sclerosing cholangitis. An important clue to the diagnosis is papillary stenosis. ERCP is useful to confirm the diagnosis because the duct can be directly evaluated and biopsied and a papillotomy can be performed. Recurrent pyogenic cholangitis (Oriental cholangiohepatitis) is endemic to areas of Asia. Patients present with acute abdominal pain, recurrent jaundice, and fever and chills. The intrahepatic and extrahepatic ducts are dilated and contain soft, pigmented stones and infection. The most common location is the intrahepatic ducts of the left lobe of the liver. CT is considered better than US for diagnosis because some stones do not shadow on US. The diagnosis can be confirmed by cholangiography, which reveals ductal dilatation, strictures, and stones ( Fig. 14-32).

Cholangiocarcinoma is a slow-growing carcinoma of the bile ducts that is almost uniformly fatal and occurs in older

patients. A common site is at the junction of the right and left hepatic ducts (Klatskins tumor) ( Fig. 14-39). Patients present with dilated intrahepatic ducts. Cholangiocarcinoma may be too small to identify on CT, or it may infiltrate surrounding tissues. Cholangiography most commonly demonstrates an intraluminal filling defect, frequently with an irregular surface, in the proximal biliary system. Predisposing factors include sclerosing cholangitis; hepatolithiasis; the liver flukes Clonorchis sinesis and Opisthorchis viverrini; Carolis disease; choledochal cysts; and, rarely, familial polyposis coli.

Choledocholithiasis refers to the presence of one or more gallstones in the common bile duct. Usually, this occurs when a gallstone passes from the gallbladder into the common bile duct (see the image below).

Common bile duct stone (choledocholithiasis). The sensitivity of transabdominal ultrasonography for choledocholithiasis is approximately 75% in the presence of dilated ducts and 50% for nondilated ducts. Image courtesy of DT Schwartz.

A gallstone in the common bile duct may impact distally in the ampulla of Vater, the point where the common bile duct and pancreatic duct join before opening into the duodenum. Obstruction of bile flow by a stone at this critical point may lead to abdominal pain and jaundice. Stagnant bile above an obstructing bile duct stone often becomes infected, and bacteria can spread rapidly back up the ductal system into the liver to produce a life-threatening infection called ascending cholangitis. Obstruction of the pancreatic duct by a gallstone in the ampulla of Vater also can trigger activation of pancreatic digestive enzymes within the pancreas itself, leading to acute pancreatitis.[1, 2] Chronically, gallstones in the gallbladder may cause progressive fibrosis and loss of function of the gallbladder, a condition known as chronic cholecystitis. Chronic cholecystitis predisposes to gallbladder cancer. Ultrasonography is the initial diagnostic procedure of choice in most cases of suspected gallbladder or biliary tract disease (see Workup). The treatment of gallstones depends upon the stage of disease. Asymptomatic gallstones may be managed expectantly. Once gallstones become symptomatic, definitive surgical intervention with excision of the gallbladder (cholecystectomy) is usually indicated. Cholecystectomy is among the most frequently performed abdominal surgical procedures (see Treatment). Complications of gallstone disease may require specialized management to relieve obstruction and infection. Gallstone formation occurs because certain substances in bile are present in concentrations that approach the limits of their solubility. When bile is concentrated in the gallbladder, it can become

supersaturated with these substances, which then precipitate from solution as microscopic crystals. The crystals are trapped in gallbladder mucus, producing gallbladder sludge. Over time, the crystals grow, aggregate, and fuse to form macroscopic stones. Occlusion of the ducts by sludge and/or stones produces the complications of gallstone disease. The 2 main substances involved in gallstone formation are cholesterol and calcium bilirubinate.

Cholesterol gallstones
More than 80% of gallstones in the United States contain cholesterol as their major component. Liver cells secrete cholesterol into bile along with phospholipid (lecithin) in the form of small spherical membranous bubbles, termed unilamellar vesicles. Liver cells also secrete bile salts, which are powerful detergents required for digestion and absorption of dietary fats. Bile salts in bile dissolve the unilamellar vesicles to form soluble aggregates called mixed micelles. This happens mainly in the gallbladder, where bile is concentrated by reabsorption of electrolytes and water. Compared with vesicles (which can hold up to 1 molecule of cholesterol for every molecule of lecithin), mixed micelles have a lower carrying capacity for cholesterol (about 1 molecule of cholesterol for every 3 molecules of lecithin). If bile contains a relatively high proportion of cholesterol to begin with, then as bile is concentrated, progressive dissolution of vesicles may lead to a state in which the cholesterol-carrying capacity of the micelles and residual vesicles is exceeded. At this point, bile is supersaturated with cholesterol, and cholesterol monohydrate crystals may form. Thus, the main factors that determine whether cholesterol gallstones will form are (1) the amount of cholesterol secreted by liver cells, relative to lecithin and bile salts, and (2) the degree of concentration and extent of stasis of bile in the gallbladder.

Calcium, bilirubin, and pigment gallstones

Bilirubin, a yellow pigment derived from the breakdown of heme, is actively secreted into bile by liver cells. Most of the bilirubin in bile is in the form of glucuronide conjugates, which are quite water soluble and stable, but a small proportion consists of unconjugated bilirubin. Unconjugated bilirubin, like fatty acids, phosphate, carbonate, and other anions, tends to form insoluble precipitates with calcium. Calcium enters bile passively along with other electrolytes. In situations of high heme turnover, such as chronic hemolysis or cirrhosis, unconjugated bilirubin may be present in bile at higher than normal concentrations. Calcium bilirubinate may then crystallize from solution and eventually form stones. Over time, various oxidations cause the bilirubin precipitates to take on a jet-black color, and stones formed in this manner are termed black pigment gallstones. Black pigment stones represent 10-20% of gallstones in the United States. Bile is normally sterile, but in some unusual circumstances (eg, above a biliary stricture), it may become colonized with bacteria. The bacteria hydrolyze conjugated bilirubin, and the resulting increase in unconjugated bilirubin may lead to precipitation of calcium bilirubinate crystals. Bacteria also hydrolyze lecithin to release fatty acids, which also may bind calcium and precipitate from solution. The resulting concretions have a claylike consistency and are termed brown pigment stones. Unlike cholesterol or black pigment gallstones, which form almost exclusively in the gallbladder, brown pigment gallstones often form de novo in the bile ducts. Brown pigment gallstones are unusual in the United States but are fairly common in some parts of Southeast Asia, possibly related to liver fluke infestation.

Mixed gallstones
Cholesterol gallstones may become colonized with bacteria and can elicit gallbladder mucosal inflammation. Lytic enzymes from bacteria and leukocytes hydrolyze bilirubin conjugates and fatty acids. As a result, over time, cholesterol stones may accumulate a substantial proportion of calcium bilirubinate

and other calcium salts, producing mixed gallstones. Large stones may develop a surface rim of calcium resembling an eggshell that may be visible on plain x-ray films. Cholesterol gallstones, black pigment gallstones, and brown pigment gallstones have different pathogeneses and different risk factors.

Cholesterol gallstones
Cholesterol gallstones are associated with female sex, European or Native American ancestry, and increasing age. Other risk factors include the following: Obesity Pregnancy Gallbladder stasis Drugs Heredity The metabolic syndrome of truncal obesity, insulin resistance, type II diabetes mellitus, hypertension, and hyperlipidemia is associated with increased hepatic cholesterol secretion and is a major risk factor for the development of cholesterol gallstones. Cholesterol gallstones are more common in women who have experienced multiple pregnancies. A major contributing factor is thought to be the high progesterone levels of pregnancy. Progesterone reduces gallbladder contractility, leading to prolonged retention and greater concentration of bile in the gallbladder. Other causes of gallbladder stasis associated with increased risk of gallstones include high spinal cord injuries, prolonged fasting with total parenteral nutrition, and rapid weight loss associated with severe caloric and fat restriction (eg, diet, gastric bypass surgery). A number of medications are associated with formation of cholesterol gallstones. Estrogens administered for contraception or for treatment of prostate cancer increase the risk of cholesterol gallstones by increasing biliary cholesterol secretion. Clofibrate and other fibrate hypolipidemic drugs increase hepatic elimination of cholesterol via biliary secretion and appear to increase the risk of cholesterol gallstones. Somatostatin analogues appear to predispose to gallstones by decreasing gallbladder emptying. About 25% of the predisposition to cholesterol gallstones appears to be hereditary, as judged from studies of identical and fraternal twins. At least a dozen genes may contribute to the risk.[3] A rare syndrome of low phospholipidassociated cholelithiasis occurs in individuals with a hereditary deficiency of the biliary transport protein required for lecithin secretion.

Black and brown pigment gallstones

Black pigment gallstones occur disproportionately in individuals with high heme turnover. Disorders of hemolysis associated with pigment gallstones include sickle cell anemia, hereditary spherocytosis, and beta-thalassemia. In cirrhosis, portal hypertension leads to splenomegaly. This, in turn, causes red cell sequestration, leading to a modest increase in hemoglobin turnover. About half of all cirrhotic patients have pigment gallstones. Prerequisites for formation of brown pigment gallstones include intraductal stasis and chronic colonization of bile with bacteria. In the United States, this combination is most often encountered in patients with postsurgical biliary strictures or choledochal cysts. In rice-growing regions of East Asia, infestation with biliary flukes may produce biliary strictures and predispose to formation of brown pigment stones throughout intrahepatic and extrahepatic bile ducts. This condition, termed hepatolithiasis, causes recurrent cholangitis and predisposes to biliary cirrhosis andcholangiocarcinoma.

Other comorbidities

Crohn disease, ileal resection, or other diseases of the ileum decrease bile salt reabsorption and increase the risk of gallstone formation. Other illnesses or states that predispose to gallstone formation include burns, use of total parenteral nutrition, paralysis, ICU care, and major trauma. This is due, in general, to decreased enteral stimulation of the gallbladder with resultant biliary stasis and stone formation.

Race-, sex-, and age-related demographics

Women are more likely to develop cholesterol gallstones than men, especially during their reproductive years, when the incidence of gallstones in women is 2-3 times that in men. The difference appears to be attributable mainly to estrogen, which increases biliary cholesterol secretion. [6] Risk of developing gallstones increases with age. Gallstones are uncommon in children in the absence of congenital anomalies or hemolytic disorders. Beginning at puberty, the concentration of cholesterol in bile increases. After age 15 years, the prevalence of gallstones in US women increases by about 1% per year; in men, the rate is less, about 0.5% per year. Gallstones continue to form throughout adult life, and the prevalence is greatest at advanced age. The incidence in women falls with menopause, but new stone formation in men and women continues at a rate of about 0.4% per year until late in life.

Less than half of patients with gallstones become symptomatic. The mortality rate for an elective cholecystectomy is 0.5% with less than 10% morbidity. The mortality rate for an emergent cholecystectomy is 3-5% with 30-50% morbidity. Following cholecystectomy, stones may recur in the bile duct. Approximately 10-15% of patients have an associated choledocholithiasis. The prognosis in patients with choledocholithiasis depends on the presence and severity of complications. Of all patients who refuse surgery or are unfit to undergo surgery, 45% remain asymptomatic from choledocholithiasis, while 55% experience varying degrees of complications.

Patient Education
Patients with asymptomatic gallstones should be educated to recognize and report the symptoms of biliary colic and acute pancreatitis. Alarm symptoms include persistent epigastric pain lasting for greater than 20 minutes, especially if accompanied by nausea, vomiting, or fever. If pain is severe or persists for more than an hour, the patient should seek immediate medical attention. For patient education information, see the Liver, Gallbladder, and Pancreas Centerand Cholesterol Center, as well as Gallstones. Choledocholithiasis with acute common bile duct (CBD) obstruction initially produces an acute increase in the level of liver transaminases (alanine and aspartate aminotransferases), followed within hours by a rising serum bilirubin level. The higher the bilirubin level, the greater the predictive value for CBD obstruction. CBD stones are present in approximately 60% of patients with serum bilirubin levels greater than 3 mg/dL. If obstruction persists, a progressive decline in the level of transaminases with rising alkaline phosphatase and bilirubin levels may be noted over several days. Prothrombin time may be elevated in patients with prolonged CBD obstruction, secondary to depletion of vitamin K (the absorption of which is bile-dependent).Concurrent obstruction of the pancreatic duct by a stone in the ampulla of Vater may be accompanied by increases in serum lipase and amylase levels.

Repeated testing over hours to days may be useful in evaluating patients with gallstone complications. Improvement of the levels of bilirubin and liver enzymes may indicate spontaneous passage of an obstructing stone. Conversely, rising levels of bilirubin and transaminases with progression of leukocytosis in the face of antibiotic therapy may indicate ascending cholangitis with need for urgent intervention. Blood culture results are positive in 30-60% of patients with cholangitis. Common bile duct (CBD) stones are missed frequently on transabdominal ultrasonography (sensitivity, 15-40%). The detection of CBD stones is impeded by the presence of gas in the duodenum, possible reflection and refraction of the sound beam by curvature of the duct, and the location of the duct beyond the optimal focal point of the transducer. On the other hand, dilatation of the CBD on ultrasonographic images is an indirect indicator of CBD obstruction. CBD dilatation is identified accurately, with up to 90% accuracy. However, this finding may be absent if the obstruction is of recent onset. The usefulness of ultrasonography findings as a predictor of CBD stones is at best 15-20%. Go to Imaging of Cholelithiasis for complete information on this topic.

Endoscopic ultrasound
Endoscopic ultrasound (EUS) is also an accurate and relatively noninvasive technique to identify stones in the distal common bile duct. Sensitivity and specificity of CBD stone detection are reported in range of 85-100%. The treatment of gallstones depends upon the stage of disease. Ideally, interventions in the lithogenic state could prevent gallstone formation, although, currently, this option is limited to a few special circumstances. Asymptomatic gallstones may be managed expectantly. Once gallstones become symptomatic, definitive surgical intervention with cholecystectomy is usually indicated, although, in some cases, medical dissolution may be considered. In uncomplicated cholelithiasis with biliary colic, medical management may be a useful alternative to cholecystectomy in selected patients, particularly those for whom surgery would pose high risk. Medical treatment, beyond pain control, is not initiated in the emergency department. Medical treatments for gallstones, used alone or in combination, include the following: Oral bile salt therapy (ursodeoxycholic acid) Contact dissolution Extracorporeal shockwave lithotripsy Medical management is more effective in patients with good gallbladder function who have small stones (< 1 cm) with a high cholesterol content. Bile salt therapy may be required for more than 6 months and has a success rate less than 50%. Surgical treatment of asymptomatic gallstones without medically complicating diseases is discouraged. The risk of complications arising from interventions is higher than the risk of symptomatic disease. Approximately 25% of patients with asymptomatic gallstones develop symptoms within 10 years. Persons with diabetes and women who are pregnant should have close follow-up to determine if they become symptomatic or develop complications. However, cholecystectomy for asymptomatic gallstones may be indicated in the following patients: Patients with large gallstones greater than 2 cm in diameter Patients with nonfunctional or calcified (porcelain) gallbladder observed on imaging studies and who are at high risk of gallbladder carcinoma Patients with spinal cord injuries or sensory neuropathies affecting the abdomen

Patients with sickle cell anemia in whom the distinction between painful crisis and cholecystitis may be difficult Patients with risk factors for complications of gallstones may be offered elective cholecystectomy, even if they have asymptomatic gallstones. These groups include persons with the following conditions and demographics: Cirrhosis Portal hypertension Children Transplant candidates Diabetes with minor symptoms Patients with a calcified or porcelain gallbladder should consider elective cholecystectomy due to the possibly increased risk of carcinoma (25%). Refer to a surgeon for removal as an outpatient procedure.

Medical dissolution of gallstones

Ursodeoxycholic acid (ursodiol) is a gallstone dissolution agent. In humans, long-term administration of ursodeoxycholic acid reduces cholesterol saturation of bile, both by reducing liver cholesterol secretion and by reducing the detergent effect of bile salts in the gallbladder (thereby preserving vesicles that have a high cholesterol carrying capacity). Desaturation of bile prevents crystals from forming and, in fact, may allow gradual extraction of cholesterol from existing stones. In patients with established cholesterol gallstones, treatment with ursodeoxycholic acid at a dose of 8-10 mg/kg/d PO divided bid/tid may result in gradual gallstone dissolution. This intervention typically requires 6-18 months and is successful only with small, purely cholesterol stones. Patients remain at risk for gallstone complications until dissolution is completed. The recurrence rate is 50% within 5 years. Moreover, after discontinuation of treatment, most patients form new gallstones over the subsequent 5-10 years. In patients with symptomatic gallstones, discuss the options for surgical and nonsurgical intervention; emergency physicians should refer patients to their primary care provider and surgical consultant for outpatient follow-up.

Removal of the gallbladder (cholecystectomy) is generally indicated in patients who have experienced symptoms or complications of gallstones, unless the patient's age and general health make the risk of surgery prohibitive. In some cases of gallbladder empyema, temporary drainage of pus from the gallbladder (cholecystostomy) may be preferred to allow stabilization and to permit later cholecystectomy under elective circumstances. In patients with gallbladder stones who are suspected to have concurrent common bile duct stones, the surgeon can perform intraoperative cholangiography at the time of cholecystectomy. The common bile duct can be explored using a choledochoscope. If common duct stones are found, they can usually be extracted intraoperatively. Alternatively, the surgeon can create a fistula between the distal bile duct and the adjacent duodenum (choledochoduodenostomy), allowing stones to pass harmlessly into the intestine.

Open versus laparoscopic cholecystectomy

The first cholecystectomy was performed in the late 1800s. The open approach pioneered by Langenbuch remained the standard until the late 1980s, when laparoscopic cholecystectomy was introduced.[14, 15] Laparoscopic cholecystectomy was the vanguard of the minimally invasive revolution, which has affected all areas of modern surgical practice. Currently, open cholecystectomy is mainly reserved for special situations.

The traditional open approach to cholecystectomy employed a large, right subcostal incision. In contrast, laparoscopic cholecystectomy employs 4 very small incisions. Recovery time and postoperative pain are diminished markedly by the laparoscopic approach. Currently, laparoscopic cholecystectomy is commonly performed in an outpatient setting. By reducing inpatient stay and time lost from work, the laparoscopic approach has also reduced the cost of cholecystectomy. In its 2010 guidelines for the clinical application of laparoscopic biliary tract surgery, the Society of American Gastrointestinal and Endoscopic Surgeons (SAGES) states that patients with symptomatic cholelithiasis are eligible for laparoscopic surgery. Cholelithiasis patients whose laparoscopic cholecystectomy was uncomplicated may be sent home the same day if postoperative pain and nausea are well controlled. Patients older than 50 years may be at greater risk of readmission. [16] During laparoscopic cholecystectomy, a surgeon must retrieve stones that might escape through a perforated gallbladder. Conversion to an open procedure might be required in certain cases. In patients in whom gallstones have been lost in the peritoneal cavity, the current recommendation is follow-up with ultrasonographic examinations for 12 months. Most of the complications (usually, abscess formation around the stone) occur within this time frame. The most dreaded and morbid complication of cholecystectomy is damage to the common bile duct. Bile duct injuries increased in incidence with the advent of laparoscopic cholecystectomy, but the incidence of this complication has since declined as experience and training in minimally invasive surgery have improved.[17] Routine cholangiography is only of minimal help in preventing common bile duct injury. However, good evidence indicates that it leads to intraoperative detection of such injuries.

In patients who are critically ill with gallbladder empyema and sepsis, cholecystectomy can be treacherous. In this circumstance, the surgeon may elect to perform cholecystostomy, a minimal procedure involving placement of a drainage tube in the gallbladder. This usually results in clinical improvement. Once the patient stabilizes, definitive cholecystectomy can be performed under elective circumstances. Cholecystostomy also can be performed in some cases by invasive radiologists under CT-scan guidance. This approach eliminates the need for anesthesia and is especially appealing in a patient who is clinically unstable.

Endoscopic sphincterotomy
If surgical removal of common bile duct stones is not immediately feasible, endoscopic retrograde sphincterotomy can be used. In this procedure, the endoscopist cannulates the bile duct via the papilla of Vater. Using an electrocautery sphincterotome, the endoscopist makes an incision measuring approximately 1 cm through the sphincter of Oddi and the intraduodenal portion of the common bile duct, creating an opening through which stones can be extracted. Endoscopic retrograde sphincterotomy is especially useful in patients who are critically ill with ascending cholangitis caused by impaction of a gallstone in the ampulla of Vater. Other indications for the procedure are as follows: Removal of common bile duct stones inadvertently left behind during previous cholecystectomy Preoperative clearing of stones from the common bile duct to eliminate the need for intraoperative common bile duct exploration, especially in situations where the surgeon's expertise in laparoscopic bile duct exploration is limited or the patient's anesthesia risk is high

Preventing recurrence of acute gallstone pancreatitis or other complications of choledocholithiasis in patients who are too sick at present to undergo elective cholecystectomy or whose long-term prognosis is poor Intraoperative endoscopic sphincterotomy (IOES) during laparoscopic cholecystectomy has been suggested as an alternative treatment to preoperative endoscopic sphincterotomy (POES) followed by laparoscopic cholecystectomy; this is because IOES is as effective and safe as POES and results in a significantly shorter hospital stay.[18] Ursodeoxycholic acid treatment can prevent gallstone formation. This has been demonstrated in the setting of rapid weight loss caused by very low-calorie diets or by bariatric surgery, which are associated with a high risk of new cholesterol gallstones (20-30% within 4 mo). Administration of ursodeoxycholic acid at a dose of 600 mg daily for 16 weeks reduces the incidence of gallstones by 80% in this setting. Recommending dietary changes of decreased fat intake is prudent; this may decrease the incidence of biliary colic attacks. However, it has not been shown to cause dissolution of stones. Little evidence suggests that dietary composition affects the natural history of gallstone disease in humans. Obese patients who undertake aggressive weight-loss programs or undergo bariatric surgery are at risk to develop gallstones; short-term prophylaxis with ursodeoxycholic acid should be considered. Regular exercise may reduce the frequency of cholecystectomy. Following cholecystectomy, about 5-10% of patients develop chronic diarrhea. This is usually attributed to bile salts. The frequency of enterohepatic circulation of bile salts increases after the gallbladder is removed, resulting in more bile salt reaching the colon. In the colon, bile salts stimulate mucosal secretion of salt and water. Postcholecystectomy diarrhea is usually mild and can be managed with occasional use of over-thecounter antidiarrheal agents, such as loperamide. More frequent diarrhea can be treated with daily administration of a bile acid-binding resin (eg, colestipol, cholestyramine, colesevelam). Following cholecystectomy, a few individuals experience recurrent pain resembling biliary colic. The term postcholecystectomy syndrome is sometimes used for this condition. Many patients with postcholecystectomy syndrome have long-term functional pain that was originally misdiagnosed as being of biliary origin.[19] Persistence of symptoms following cholecystectomy is unsurprising. Diagnostic and therapeutic efforts should be directed at the true cause. Some individuals with postcholecystectomy syndrome have an underlying motility disorder of the sphincter of Oddi, termed biliary dyskinesia, in which the sphincter fails to relax normally following ingestion of a meal. The diagnosis can be established in specialized centers by endoscopic biliary manometry. In established cases of biliary dyskinesia, endoscopic retrograde sphincterotomy is usually effective in relieving the symptoms.

The goal of treatment is to relieve the blockage. Treatment may involve: Surgery to remove the gallbladder and stones ERCP and a procedure called a sphincterotomy, which makes a surgical cut into the muscle in the common bile duct to allow stones to pass or be removed

Stones may be described as

Primary stones (usually brown pigment stones), which form in the bile ducts Secondary stones (usually cholesterol), which form in the gallbladder but migrate to the bile ducts Residual stones, which are missed at the time of cholecystectomy (evident < 3 yr later) Recurrent stones, which develop in the ducts > 3 yr after surgery

Diagnosis Liver function tests


Common duct stones should be suspected in patients with jaundice and biliary colic. Fever and leukocytosis further suggest acute cholangitis. Elevated levels of bilirubin, alkaline phosphatase, ALT, and -glutamyltransferase are consistent with extrahepatic obstruction, suggesting stones, particularly in patients with features of acute cholecystitis or cholangitis. Ultrasonography may show stones in the gallbladder and occasionally in the common duct (less accurate). The common duct is dilated (> 6 mm in diameter if the gallbladder is intact; >10 mm after a cholecystectomy). If the ducts are not dilated early in the presentation (eg, first day), stones have probably passed. If doubt exists, magnetic resonance cholangiopancreatography (MRCP) is highly accurate for retained stones. ERCP is done if MRCP is equivocal; it can be therapeutic as well as diagnostic. CT, though less accurate than ultrasonography, can detect liver abscesses. For suspected acute cholangitis, CBC and blood cultures are essential. Leukocytosis is common, and aminotransferases may reach 1000 IU/L, suggesting acute hepatic necrosis, often due to microabscesses. Blood cultures guide antibiotic choice. Treatment ERCP and sphincterotomy If biliary obstruction is suspected, ERCP and sphincterotomy are necessary to remove the stone. Success rate exceeds 90%; up to 7% of patients have complications (eg, bleeding pancreatitis, infection with fibrosis and subsequent duct stricture). Laparoscopic cholecystectomy, which is not as well suited for operative cholangiography or common duct exploration, can be done electively following ERCP and sphincterotomy. Mortality and morbidity after open cholecystectomy with common duct exploration are higher. In patients at high risk of complications with cholecystectomy (eg, the elderly), sphincterotomy alone is an alternative. Acute cholangitis is an emergency requiring aggressive supportive care and urgent removal of the stones, endoscopically or surgically. Antibiotics are given, similar to those used for acute cholecystitis (see Gallbladder and Bile Duct Disorders: Treatment) An alternative regimen for very ill patients is imipenem

and ciprofloxacin

, plus metronidazole

to cover anaerobes. For recurrent pyogenic cholangitis, management aims to provide supportive care (eg, broad-spectrum antibiotics), eradicate any parasites, and mechanically clear the ducts of stones and debris endoscopically (via ERCP) or surgically.