Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

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fraction of <35% suggests chronic cholecystitis. Infusion over 30 or 60 minutes is required to establish reproducible results; shorter infusions lead to erratic results. One should keep in mind that a number of pharmacologic agents affect gallbladder ejection fraction; for instance, morphine decreases gallbladder ejection fraction.

It is unusual to see gallbladder uptake of bone-seeking radiopharmaceutical agents. Some patients undergoing whole-body bone scanning during chemotherapy, however, have an intense gallbladder uptake; after completion of chemotherapy, gallbladder uptake ceases. Presumably such uptake is secondary to the chemotherapy regimen employed rather than to underlying gallbladder disease.

Some patients undergoing lung perfusion studies with Tc-99m–macroaggregated albumin (MAA) have measurable gallbladder activity.

Occasionally delayed whole-body iodine 131 imaging visualizes focal radioactivity in a dilated intrahepatic duct, suggesting a metastasis; other imaging should differentiate these conditions.

Biliary Drainage

The biocompatibility of catheter material and bile mucosa is an ongoing research topic and beyond the scope of this book. The main problems encountered in clinical practice are erosions, mucosal hyperplasia, catheter encrustation, and obstruction during chronic drainage.

Biliary drainage is performed primarily to relieve an obstruction. In acute cholangitis urgent biliary drainage is generally initiated using an endoscopic approach and, if necessary, a sphincterotomy and stone extraction are performed during the same procedure. Some critically ill patients, deemed potentially unstable to be moved to a fluoroscopy suite, have had endoscopic biliary drainage performed either under sonographic guidance or blindly. Drainage through a nasobiliary catheter is preferred; the bile ducts are decompressed manually and ready catheter access allows cholangiography.

Controversy continues on the relative merits of endoscopic versus percutaneous biliary decompression for biliary obstruction. In a number of hospitals the choice depends on the

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relative expertise of the interventionalists and endoscopists involved and on the suspected obstruction etiology. Especially with high biliary obstructions (at porta hepatis or hepatic duct), percutaneous drainage tends to have an overall greater success rate than endoscopic drainage. Also, percutaneous biliary drainage can achieve decompression after failed endoscopic drainage, but endoscopic drainage is not often attempted after failed percutaneous drainage.

Most percutaneous biliary drainage is performed using fluoroscopic or US guidance (or both) and a right lateral approach. Left lobe biliary drainage is also feasible if a bile duct can be localized with US guidance. An open lowfield strength MR unit using near real-time imaging also provides needle positioning guidance. Percutaneous biliary drainage can achieve a high success rate in patients even with nondilated bile ducts. Success rates range from 50% to 90%. Only one puncture is necessary in most patients during percutaneous transhepatic biliary drainage when color Doppler US provides guidance.

Percutaneous cholecystostomy consists of percutaneous catheter insertion into the gallbladder using imaging guidance. It is an alternative to surgical cholecystostomy, especially in high risk patients with acalculous cholecystitis.

At times biliary access is necessary in a patient after creation of a choledochojejunostomy and Roux-en-Y jejunojejunostomy and an antegrade approach is not feasible. In these patients percutaneous retrograde transjejunal cholangiography is an option, especially if the surgeon has provided superficial Roux-en-Y loop fixation. In fact, surgeons should be encouraged to perform superficial fixation of Roux-en-Y loops for biliary-enteric anastomoses to allow future access for biliary interventions.

Most duct localization is performed with an iodinated contrast agent. CO2 cholangiography can also be performed and occasionally a duct segment not visualized with iodinated contrast is outlined by CO2. In most studies,however,CO2 offers little advantage.

An MRCP is feasible with a stent in place, but the results are often unsatisfactory. An indwelling polyethylene stent lumen is visible

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with MRCP, but artifacts obliterate cobalt alloy and most nitinol stent lumina (5).

In a setting of distal bile duct obstruction, percutaneous biliary drainage diverts bile away from the gut. A patient’s nutritional status can be improved by reintroducing this bile to the jejunum through either a nasogastric tube or a jejunal catheter passed through a gastrostomy.

Bile cytology obtained at the time of biliary drainage is a useful adjunct. In consecutive patients with presumed malignant biliary strictures undergoing percutaneous biliary drainage, single specimen bile cytology achieved a sensitivity of 15% and specificity of 100% (6); in spite of the low sensitivity, the simplicity of this procedure argues for its continued use. Bile culture is also useful during percutaneous biliary drainage. Fever, previous biliary instrumentation, and bile duct surgery are predictors of a positive bile culture, with the most common organisms being enterococcal species.

Hemobilia is a complication of percutaneous transhepatic biliary drainage. This complication is decreased if during initial needle passage the needle tract is opacified with contrast, and, if a major vascular structure communicates with this tract, it should be abandoned and another tract established.

Whether catheter tract embolization should be performed after transhepatic biliary drainage is not clear. Some interventionalists do embolize drainage tracts. Surgeons do not embolize T-tube tracts. Sufficient fibrosis ensues after long-term drainage that free peritoneal spill and peritonitis rarely are issues (except after liver transplantation). Whether embolization has any effect in a setting of distal biliary tract obstruction is arguable.

Biopsy

Fluoroscopically guided percutaneous transhepatic intraductal biopsy, usually performed as part of a percutaneous biliary drainage procedure, is useful with a suspected primary bile duct malignancy. Multiple forceps biopsies, using intraductal US guidance, achieve high tumor detection sensitivities.

Mucosal brushing is feasible either during ERCP or through a percutaneous biliary

catheter. All other factors being equal, a biopsy achieves a greater sensitivity than brushings. Pain and transient hemobilia are complications.

Congenital Abnormalities

Gallbladder

Agenesis of Gallbladder

Gallbladder agenesis is rare. An absent gallbladder is found in left-sided isomerism (asplenia). Most patients with gallbladder agenesis also have an absent cystic duct, and often other gastrointestinal anomalies are evident. An association exists between gallbladder agenesis and duodenal atresia.

Some patients have symptoms clinically compatible with gallbladder disease and some even have a false-positive US study. Bile duct stones are relatively common in these patients. Gallbladder agenesis has only been diagnosed at laparoscopy for presumed cholecystitis in some of these patients.

Multiple Gallbladders

Most gallbladder duplications are discovered in a setting of either cholelithiasis or acute cholecystitis. Gallbladder duplication is more common in right-sided isomerism (polysplenia). Anecdotal reports describe not only stones in a duplicated gallbladder but also a carcinoma.

Gallbladder duplication can usually be identified with US or any type of cholangiography. Magnetic resonance imaging (MRI) is also helpful in defining the underlying anatomy. Some double gallbladders are not detected either with preoperative imaging or even during cholecystectomy and a second operation is then necessary.

Multiseptate Gallbladder

A congenital multiseptate gallbladder is rare. More common are gallbladder folds mimicking septa.

Ultrasonography should detect a multiseptate gallbladder. Endoscopic retrograde cholangiopancreatography is helpful only if sufficient

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contrast fills the gallbladder to outline the septa. These patients also have impaired gallbladder function.

Ectopic Gallbladder

An abnormal gallbladder location is more common than agenesis. Congenitally lax mesenteric attachments allow gallbladder migration to unusual sites. An ectopic gallbladder can be intrahepatic, extraperitoneal, in the lesser omentum, within the falciform ligament, or in other locations. It can be located just inferior to the right hemidiaphragm. Subcutaneous gallbladder herniation through the abdominal wall is rare (7). Also rare is internal gallbladder herniation through the adjacently located foramen of Winslow and obstruction to either bile or blood flow. Some patients also have associated hepatic lobe, portal vein, and pancreaticobiliary duct anomalies.

Imaging does not identify the gallbladder in its usual position. Endoscopic retrograde cholangiopancreatography is useful in defining this condition and identifying any associated ductal anomalies prior to laparoscopic cholecystectomy.

With an intrahepatic gallbladder, Tc-99m– sulfur colloid scintigraphy reveals a focal intrahepatic defect.

Anomalous Bile Ducts

Intrahepatic bile ducts develop from liver progenitor cells in contact with portal vein mesenchyme and form ductal plates that evolve into mature ducts. Failure of evolution leads to ductal plate malformation and congenital intrahepatic bile duct disorders characterized by dilated biliary segments and surrounding fibrosis.

Considerable variation exists in intrahepatic bile duct anatomy (Fig. 8.2). A right lobe duct draining into the cystic duct, in particular, has bedeviled surgeons during apparent routine cholecystectomy.

More complex intraand extrahepatic bile duct anomalies are rare. One rather extreme example consists of the hepatic duct draining into the gallbladder and the cystic duct then draining the entire biliary system. Some preduodenal common bile ducts are associated with a preduodenal portal vein. These

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and other related anomalies need to be considered to prevent bile duct injury during cholecystectomy.

Computed tomographic cholangiography detects major bile duct anomalies. Both 2D and 3D images are necessary to fully evaluate these anomalies. Whether aberrant bile ducts are better identified by CT cholangiography or MRCP is detectable; the latter images are degraded by overlapping duodenum and other ductal structures. Complicating this issue is that MRCP rather than CT cholangiography has achieved a superior role as a preferred preoperative imaging modality. What preoperative role MRCP has in alerting the surgeon to possible bile duct anomalies and thus potentially decreasing intraoperative duct injury remains to be determined.

Sphincter of Oddi Region Anomalies

Numerous anomalous biliary and pancreatic duct insertions are possible, including a long common channel (called anomalous arrangement of the pancreaticobiliary duct and anomalous pancreaticobiliary ductal union by some authors). This latter congenital variant (depending on viewpoint, considered an anomaly, maljunction, or disease) consists of pancreatic and biliary duct union outside the duodenal wall. Such a long common pancreaticobiliary channel presumably leads to pancreatic juice reflux into bile ducts. It is a common finding in patients with a choledochal cyst and gallbladder carcinoma and is also associated with gallstone-induced acute pancreatitis (discussed in Chapter 9). Several patients with an anomalous pancreaticobiliary duct junction and pancreatic carcinoma have been reported. Whether such an association is fortuitous or not is conjecture.

The prevalence of an anomalous pancreaticobiliary duct connection is unknown.Anomalous insertions are associated with dilated bile ducts (choledochal cyst), a tendency toward gallstone formation, and possibly gallbladder adenomyomatosis. Even in childhood, anomalous pancreaticobiliary ducts are associated with increased gallbladder epithelial cellular proliferation, manifesting as epithelial hyperplasia. Ultrasonography, including endoscopic US, reveals a diffuse thickened hypoechoic inner gallbladder wall layer, indicative of mucosal

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A

B

C D

Figure 8.2. Illustration of common bile duct anomalies. A: A right lobe branch inserts into the cystic duct. B: A right lobe branch inserts into the hepatic duct. C: A right lobe duct communicates with the main left lobe duct. D: A short cystic duct inserts close to the porta hepatis and the hepatic duct is very short. In such a setting the common bile duct is readily confused with the cystic duct.

hyperplasia; this characteristic sonographic finding of gallbladder mucosal hyperplasia is found only in those who have associated anomalous pancreaticobiliary ducts. An increased risk of gallbladder cancer has been suggested in affected patients.

Computed tomographic cholangiography is useful in evaluating pancreaticobiliary duct

anomalous junctions; at times pancreatic juice is identified refluxing into the bile duct. The reverse is also true—in some patients contrast refluxes from the common bile duct into the pancreatic duct.

Many of these maljunctions are readily identified with ERCP. Endoscopic US and intraductal US are helpful in defining surrounding

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structures. An MRCP identifies an anomalous pancreaticobiliary duct junction in most patients, less so in children than in adults.

Regardless of whether bile ducts are dilated or not, whether a prophylactic cholecystectomy should be recommended to patients with a pancreatic or biliary maljunction because of increased gallbladder cancer risk is not clear.

Cholestatic Conditions

Especially in the very young, jaundice has a broad differential diagnosis ranging from a benign, transient event to a lethal hereditary condition. It is associated with biliary atresia, a dysplasia such as Alagille’s syndrome, an acute hepatic insult such as viral hepatitis, and a choledochal cyst, and it is a manifestation of a hereditary hyperbilirubinemia. Some cholestatic conditions are a result of gene coding mutations.A number of these conditions first manifest in childhood rather than in neonates.

Neonatal Cholestasis

Clinical

The prior thinking was that a majority of neonates with persistent jaundice had either biliary atresia or sequelae of neonatal viral hepatitis. Whether these are different entities or simply different manifestations of the same condition is conjecture. Their clinical findings are indistinguishable in most neonates. Currently, other conditions have emerged in the differential diagnosis, including Alagille’s syndrome. Aside from intrahepatic causes, occasional neonatal jaundice is secondary to a choledochal cyst, sepsis, hemolysis, infection, juvenile xanthogranulomatosis, or metabolic disorders such as a1-antitrypsin deficiency, cystic fibrosis, and others.

Congenital biliary atresia ranges from a rare isolated, focal atretic segment, mostly intrahepatic atresia, to mostly extrahepatic atresia. Disrupted intrahepatic bile ducts lead to bile ductule proliferation and periportal fibrosis, with residual bile ducts replaced by fibrosis and rapid progression to cirrhosis. In a minority of neonates, extrahepatic atresia is associated with other systemic abnormalities.

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Viral hepatitis can be confirmed in some neonates with clinical follow-up until jaundice resolves, although one often does not have the luxury of time. Prognosis in neonates with congenital biliary atresia is better with early intervention, generally within the first month of life.

A liver biopsy in infants with neonatal cholestasis often is not diagnostic. A high falsenegative rate is evident in biliary atresia. The presence of giant cells is found in several entities.

Imaging

Most of these neonates have marked hepatomegaly and some degree of splenomegaly.With the exception of scintigraphy,most noninterventional imaging studies are of limited use in differentiating biliary atresia and neonatal hepatitis. Intrahepatic US findings are nonspecific, although if a gallbladder is identified, neonatal hepatitis is somewhat more likely. Yet about 20% of neonates with biliary atresia have an intact gallbladder, in others it is atretic or elongated. And, to add more confusion, US detected gallbladder contractions after oral feeding in 9% of 34 children with biliary atresia (8); surgery in these children revealed patency between the gallbladder and duodenum. Still, US is useful in detecting any associated cysts and other congenital anomalies, because these neonates have an increased prevalence of polysplenia, situs inversus, malrotation, and a number of vascular anomalies.

Magnetic resonance cholangiopancreatography shows promise in differentiating between biliary atresia and neonatal hepatitis by detecting extrahepatic bile ducts in the latter entity. Successful duct visualization is difficult in infants with jaundice and small ducts even when normal, but biliary atresia can be excluded if normal-appearing extrahepatic bile ducts are visualized. In some neonates and infants with biliary atresia, MRCP shows a triangular hyperintense region in the porta hepatis; histopathology reveals a cystic structure without ductal epithelium surrounded by myxoid mesenchyme and plate-like fetal bile ducts.

Technetium-99m-IDA scintigraphy differentiates among biliary atresia, neonatal hepatitis, and other causes of jaundice in most infants. If

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