Gallbladder and Bile Ducts

Development of Gallbladder and Bile Ducts

The foregut is the first segment of the gut tube within the abdomen. It is attached to the anterior body wall by a ventral/anterior mesentery and posteriorly by a dorsal/posterior mesentery, the latter supplying blood from the dorsal aorta via the celiac arterial trunk. Two diverticula extend from the foregut, one dorsally and the other ventrally. The dorsal pancreatic bud extends into the dorsal mesentery while the liver develops from the endodermal cells that line the foregut and extend into the ventral mesentery to create the hepatic diverticulum during the third week. The cells of the hepatic diverticulum proliferate and extend superiorly into the septum transversum, which separates the pericardial cavity from the developing peritoneal cavity. As the hepatic diverticulum expands within the septum transversum, its connection to the foregut narrows to become the bile duct, which will carry bile from the liver to the duodenum.

At approximately 30 days of development, another extension of endoderm projects inferiorly off of the bile duct. This diverticulum will develop into the gallbladder, and the connection between it and the bile duct will become the cystic duct. Just proximal to the developing gallbladder is yet another diverticulum extending from the bile duct, the ventral pancreatic bud. The two pancreatic buds will fuse to form the mature pancreas, and the gallbladder will associate with the inferior side of the liver. The bile duct superior to the departure point of the cystic duct will split to become the left and right hepatic ducts, and the region between the cystic duct and the duodenum becomes the common bile duct. The common bile duct shares a common chamber with the pancreatic duct, the hepatopancreatic ampulla, which opens into the second part of the duodenum at the major duodenal papilla and can be closed by the hepatopancreatic sphincter.

As do many other lumens in the gastrointestinal tract, the epithelium of the early cystic duct proliferates so quickly that it occludes the duct. The occlusion typically disappears and recanalizes by the 12th week, when the liver begins producing bile. If the duct fails to fully recanalize, congenital biliary atresia or stenosis will occur. Bile is released into the hepatic bile ducts, down to the duodenum through the common bile duct. When the hepatopancreatic sphincter closes the opening of the major duodenal papilla, the bile will back up into the cystic duct and gallbladder. The dark green color of bile gives the distinctive color to meconium, the early fecal products of newborns.

Anatomy and Histology of Gallbladder and Bile Ducts

The pear-shaped gallbladder is attached to the inferior surface of the right and quadrate lobes of the liver. Loose connective (areolar) tissue, in which blood vessels, lymphatics, and nerves run, fills the gallbladder bed, an impression it leaves on the surface of the liver. Otherwise, the gallbladder is covered by peritoneum, the reflection of which continues into the hepatic serosal surface. Usually about 10 cm long and 3 to 5 cm in diameter, the fundus of the gallbladder projects beyond the anterior liver margin to contact the inferior surface of the diaphragm. This is the part that is palpable in vivo and visible cholecystographically as the Phrygian cap when a kinking or folding of the fundus occurs. The corpus (body) is in contact with the second portion of the duodenum and the colon. The infundibulum, or Hartmann pouch, located at the free edge of the lesser omentum, bulges forward toward the cystic duct, hiding it from surgical exposure but serving as a landmark for its identification. The part between the body of the gallbladder and the cystic duct is called the neck of the gallbladder.

The microanatomy of the gallbladder is similar to that of the gastrointestinal tract but has several unique features. Its mucosal layer is thrown in folds and lined by a very distinctive simple columnar epithelium, and although there is a lamina propria, there is no muscularis mucosa or submucosa. The lamina propria is richly vascularized and contains lymphocytes. There is a significant muscularis externa, but it is not divided into longitudinal and circular layers. The fibers of the gallbladder muscle below the mucosa are discontinuous, separated by connective tissue, and they course longitudinally in the inner layer and diagonally in the outer layer. A subserous layer (in contact with the liver) and a serosal layer are present superficially. The irregular folds, easily seen in their contracted state, disappear on extreme distention.

Mucous glands are found only in the neck. Pocketlike invaginations of the surface epithelium occur normally and contribute to the formation of folds. As a result of inflammation, they may extend into and through the muscular layer as Rokitansky-Aschoff sinuses. Aberrant vestigial bile ducts (of Luschka) of the liver, not connected with the gallbladder lumen, may enter the adventitial layer and serve as a path for infections from the liver to the gallbladder bed.

The cystic duct, a few centimeters long, is tortuous in its first portion (pars spiralis) and smooth in its short end-piece (pars glabra). In the former, the spiral fold (of Heister) is produced by mucosal duplications that regulate filling and emptying of the gallbladder according to the pressure in the biliary system. The right and left hepatic ducts emerging from the liver unite to become the 2- to 3-cm–long common hepatic duct, which, in turn, combines with the cystic duct to form the common bile duct, also known as the ductus choledochus. The latter, 10 to 15 cm long, descends in the free margin of the lesser omentum and continues posterior to the pars superior of the duodenum and through the pancreas in a downward and slightly rightward direction to enter the descending part of the duodenum at the major papilla (of Vater). The common bile duct, thus, may be divided into supraduodenal, retroduodenal, infraduodenal, and intraduodenal portions.

The extrahepatic bile ducts are lined by high columnar epithelium, which is sometimes thrown into irregular folds. The subepithelial connective tissue is rich in elastic fibers but contains few and irregularly arranged smooth muscle fibers. Mucus-producing glands in the deep layers are connected with the lumen by long ducts . Their white viscous secretion, together with that of the neck glands, amounts to about 20 mL/day. It accounts for the mucous material admixed to the bile.

Variations of Extrahepatic Bile Ducts; Accessory Hepatic Ducts

During operation on the biliary system, it is of utmost importance to carefully identify each single structure, because anatomic variations in this field are common and because a series of dreaded consequences will ensue if such variations are overlooked. The course of the cystic duct varies frequently and may escape ligation, with resultant postoperative bile leakage. The common bile duct and, even more so, hepatic duct are exposed during surgery to unintended injuries, which may mean complete separation of the ducts or strictures at a later date.

The variation in sites at which the hepatic and cystic ducts unite determines the length of the common bile duct, which varies anywhere between a point close to the duodenum to almost the porta hepatis. If this union lies low, far away from the porta hepatis and near the duodenum, the supraduodenal portion of the common bile duct is very short or may be completely absent. In such cases, the cystic and common hepatic ducts run parallel for a considerable length, inviting difficulties during cholecystectomy. This situation is compounded if the two ducts are encircled by a common sheath of dense connective tissue; a stone in the cystic duct may lead not only to compression of the hepatic duct but also to added difficulties at surgery. The cystic duct may be duplicated or may be very short or absent, and then the gallbladder appears to empty directly into the hepatic duct. As a rule the cystic duct joins the right aspect of the hepatic duct, but sometimes its opening may be found on its anterior aspect and, in rare instances, on the left aspect of the duct. The cystic duct in such a situation crosses in a spiral fashion either the anterior or the posterior aspect of the common hepatic duct, again creating problems at surgical dissection.

Accessory hepatic ducts have been found in one fifth of all instances dissected. It has been pointed out that they are not actually accessory but rather aberrant, because the drainage of bile from a circumscribed portion of the liver depends upon them and no other collateral channels. They are regularly injured at cholecystectomy if they traverse the cystic triangle of Calot. In half of the cases in which an accessory duct is found, it joins the common hepatic duct somewhere along its course. Far less frequently, the accessory duct joins the right branch of the hepatic duct or the common bile duct. In the latter instance, it may cross the cystic duct. Sometimes the cystic duct may join an accessory hepatic duct, and both together combine with the common hepatic duct to form the common bile duct. Most accessory ducts are on the right side. Those on the left side enter the common bile duct. This may be associated with the presence of a right accessory duct joining the hepatic duct. An accessory hepatic duct may run through the gallbladder bed and may sometimes even enter the gallbladder itself. This duct is readily torn during cholecystectomy, and, if not recognized or if it is mistaken for fibrous strands, postoperative leakage into the gallbladder bed will occur. The relation of accessory vessels to the arteries also poses surgical predicaments, particularly with respect to a high cystic artery that may cross the low hepatic duct, and vice versa.

Choledochoduodenal Junction

The lumen of the second portion of the duodenum harbors the major duodenal papilla (of Vater) on its medial aspect, between the circular folds of the intestine (of Kerckring). This papilla and the longitudinal fold constitute the choledochoduodenal junction, an oblique passageway through the duodenal wall traversed by the common bile duct (ductus choledochus) and the main pancreatic duct (of Wirsung). These ducts may open separately or through the medium of a common chamber, the hepatopancreatic ampulla (of Vater). A minor duodenal papilla is often seen about 2 cm above the papilla of Vater, where the accessory pancreatic duct (of Santorini) empties into the duodenum. This duct typically communicates with the main pancreatic duct within the head of the pancreas.

The union between the common bile duct and the main pancreatic duct varies individually. Most frequently, both ducts join within the wall of the duodenum and have a short common terminal portion, the hepatopancreatic ampulla. In other instances, each duct has its own opening either at the papilla or, occasionally, at some distance away (as much as 2 cm). The third possibility is the union of both ducts before they enter the duodenum, in which case a long common terminal portion is formed that transverses the duodenal wall. A slightly elevated longitudinal fold in the duodenum is a projection of the hepatopancreatic ampulla, a dilated part of the common terminal portion of both ducts. It is this common portion that may rarely permit reflux of pancreatic juice into the biliary system or of bile into the pancreas. Obstruction of the papillary orifice by a biliary calculus or a muscular spasm, naturally, might facilitate reflux, except when the common portion is extremely short.

The common bile and pancreatic ducts with their sphincters pass through the duodenal wall in the form of an eye-shaped window, the size of which determines the influence of duodenal tonus and peristalsis upon bile flow as well as the passing of gallstones. Though the architecture of the sphincter muscles depends upon the various types of union discussed above, the prototype of this complex sphincter arrangement consists of the following parts:

• 1.

  The sphincter of the common bile duct surrounds the common bile duct from its entrance into the duodenal wall to its junction with the pancreatic duct; it regulates the bile flow and, retrogressively, the filling of the gallbladder.

• 2.

  The sphincter of the pancreatic duct, present only in a variable number of instances, surrounds the intraduodenal portion of the pancreatic duct.

• 3.

  The sphincter of the hepatopancreatic ampulla is an annular muscle extending from the junction of the ducts to the tip of the papilla; it is the muscle of the common channel and its relaxation allows the passage of bile and pancreatic enzymes to the duodenum.

• 4.

  Longitudinal muscle bundles, extending from the entrance of the ducts into the duodenal wall to the tip of the papilla, connect the ducts with each other as well as with the duodenal muscles; their activity retracts or erects the papilla.

• 5.

  Reinforcing fibers, extending from the duodenal muscles to the longitudinal fibers, enforce the duodenal window and prevent its dilatation.

Function of Gallbladder and Choledochoduodenal Sphincter

Under basal conditions, that is, with no food in the stomach or duodenum, no bile enters the duodenum, even though it is secreted continuously by the liver, because the sphincter of Oddi is contracted. Therefore, bile accumulates in the common bile duct and is diverted into the gallbladder when the pressure in the biliary system reaches about 200 mm H ₂ O. When food enters the duodenum, the sphincter relaxes, the gallbladder contracts, and bile enters the duodenum, and the biliary pressure drops to 100 mm H ₂ O or less. Then the gallbladder empties slowly and intermittently, being gradually reduced to the size of a thumb. The total evacuation period of the gallbladder varies from 15 minutes to several hours. The pattern of contraction exhibits great individual variation.

The natural stimuli for the release of bile into the duodenum (cholecystokinetic effect, i.e., the coordinated contraction of the gallbladder and dilatation of the sphincter of Oddi ) are food ingredients, of which fats are the most potent, followed by proteins. Carbohydrates have an inhibitory influence. Proteins are stronger than fats in exerting stimulation of bile production in the liver (choleretic effect), and carbohydrates, again, are inhibitors in this respect. The cholecystokinetic effect is mediated by the hormone cholecystokinin, which the intestinal mucosa releases when fats enter the duodenum. The dual (sympathetic and parasympathetic) innervation of the gallbladder and sphincter of Oddi also supports a coordinated effect. According to Meltzer's law of contrary innervation, sympathetic stimulation causes contraction of the sphincter and dilation of the gallbladder, whereas parasympathetic (vagus nerve) stimulation relaxes the sphincter and contracts the gallbladder, as do purified cholecystokinin or synthetic cholecystokinin analog, when administered intravenously, though this does not hold for excessive vagus stimulation, which leads to a contraction of both sites. In general, however, hormonal stimulation induced by cholekinetic food is more important than nervous stimulation. This effect is exploited in the so-called CCK-HIDA scan, the prevalent test used for clinical evaluation of gallbladder contractile function. The CCK-HIDA scan is a variant of the standard HIDA scan that is most often used to diagnose bile leaks, arising from fistulas and other disruptions of the bile duct, and cystic duct obstruction leading to acute cholecystitis (see HIDA scan). In the CCK-HIDA scan, a nuclear medicine assay, the radioactive scintigraphic agent hepatobiliary iminodiacetic acid (HIDA) is administered intravenously. It is taken up by the hepatocyte and excreted into bile, which collects in the gallbladder. In order to stimulate gallbladder contraction and ejection of bile, synthetic cholecystokinin analog (sincalide, a C-terminal octapeptide fragment of cholecystokinin) is then administered intravenously. The radioactive tracer, and therefore bile, remaining in the gallbladder after sincalide administration is calculated as a percentage of the initial amount present in the gallbladder prior to sincalide administration. This percentage is compared with the norm to determine if the gallbladder ejection fraction is abnormally low, indicating dysfunction.

In individuals with biliary fistulae, approximately 1000 mL of bile per day may be produced. Though this figure might not reflect the normal amount of bile, it may be assumed that the gallbladder may accumulate between 200 and 500 mL of bile between meals. Such a quantity of fluid in a region where the liver, intestine, kidney, and adrenal compete for space would create pressure difficulties were it not for the gallbladder's ability to concentrate the liver bile from four-fold to ten-fold. The gallbladder mucosa can reabsorb water and salts, leaving bile pigment, bile acid, and calcium salts in a concentrated solution. This concentrating power may be lost in certain pathologic conditions, or bile acids, which keep cholesterol and bile pigments in aqueous solution, may also be absorbed as in the presence of inflammatory processes. Such functional disturbances may contribute to the formation of gallstones. The gallbladder also secretes mucin and ions into bile.

Another function of the gallbladder is concerned with the regulation of the biliary pressure as it results from the secretion of the liver and the resistance offered by the sphincter of Oddi. The pressure would rise rapidly with spasms of the sphincter if the gallbladder, as an expansile side arm to the biliary system, would not dilate. If the gallbladder is removed surgically or is spontaneously eliminated by either cystic duct obstruction or chronic fibrosing cholecystitis, the same situation arises as in rats and horses, which have no gallbladder and also no sphincter of Oddi, so that bile trickles continuously into the duodenum. With the loss of the gallbladder, the regulative influence for the alternating contraction and relaxation is also lost, and the sphincter of Oddi remains permanently open until several months after cholecystectomy, when in some instances the extrahepatic bile ducts dilate and start concentrating bile, substituting in this way for one of the lost gallbladder functions. In time the sphincter regains its tone, and the normal economy of bile in the intestine is restored. Under these circumstances, however, the common and intrahepatic ducts may contain concentrated bile and thus become susceptible to stone formation by precipitation of biliary solids.

Sphincter of Oddi Dysfunction, Geenen's Classification, and Sphincter of Oddi Manometry

The sphincter of Oddi (SO) is a three- or four-part muscular structure surrounding the distal common bile duct (sphincter choledochus), the distal main pancreatic duct (sphincter pancreaticus), the combined (unified) ampullary biliopancreatic duct to the level of the papilla of Vater (sphincter ampullae), and, structurally, the surrounding duodenal muscularis. Through neuronal and peptide hormonal inputs not fully characterized, this sphincter muscle modulates outflow of bile and pancreatic succus via tonic and phasic contractions and relaxations. Anatomic alterations (stenosis, putatively resulting from chronic stone or sludge passage, or other inflammation or trauma) can result in mechanical obstruction of flow through the ampullary area of the biliary and pancreatic duct systems, as can alterations in contractile function of the SO, putatively. Both may result in pain and associated gastrointestinal symptoms. Both stenosis of the ampullary outlet and symptomatic obstruction attributed to SO dysmotility are typically included in the realm of dysfunction of the sphincter of Oddi.

Disorder of SO motility is termed sphincter of Oddi dysfunction (SOD), and is clinically described and categorized in the Rome III Criteria for Functional Gastrointestinal Disorders, section E, Functional Gallbladder and Sphincter of Oddi Disorders. This category is subdivided into Functional Gallbladder Disorder, Functional Biliary Sphincter of Oddi Disorder, and Functional Pancreatic Sphincter of Oddi Disorder. SOD encompasses the latter two. In summary, the Rome criteria for SOD characterize this pain syndrome as being epigastric or right upper abdominal in location, lasting 30 minutes or more, recurring, and not relieved by bowel movements, posture, or antacids, amongst other details. In these settings, elevated liver enzymes are considered supportive of biliary SOD, and elevated serum pancreatic enzymes are considered supportive of pancreatic SOD (1).

The original Milwaukee criteria classifies SOD into types I, II, and III, each with a biliary or pancreatic subgroup, SOD III demonstrating biliary or pancreatic pain alone (without objective criteria); SOD II with biliary or pancreatic pain plus one other criterion met (typically, liver enzyme or pancreatic serum enzyme elevation, or biliary or pancreatic ductal dilatation); and SOD I characterized by all three criteria, specifically pancreaticobiliary pain in the presence of biliary or pancreatic enzyme elevation as well as pancreatic or biliary ductal dilatation. The Rome III consensus statement revised these classifications, making them more specifically defined and detailed, with the aim of greater precision in diagnosis, of reducing misdiagnosis, and of discouraging unnecessary invasive investigation.

In general, entertaining the diagnosis of SOD involves a patient presenting with intermittent, recurrent upper abdominal pain, typically in the right upper quadrant or epigastrium. Clinically, more often than not, the pain investigated in this setting occurs following cholecystectomy, and may, to a greater or lesser degree, mimic the biliary pain that the patient experienced prior to cholecystectomy. The steps to diagnosing SOD begin with excluding other, non-SO causes of such pain, including other functional gastrointestinal disorders, such as gastroesophageal reflux disease or irritable bowel syndrome, which may present with similar symptoms in this anatomic distribution. The Rome III criteria summarize the workup in this way:

The initial diagnostic workup may approach SOD as a diagnosis of exclusion, after amply ruling out other potential causes of the patient's pain, while also determining if aminotransferase elevations or recurrent acute pancreatitis episodes are apparent, and if biliary and/or pancreatic ductal dilatation is visualized on ultrasound or radiologic imaging, which could add further support to a presumptive diagnosis of SOD if the above Rome III criteria are also met.

In biliary-type SOD, if liver enzyme elevations and biliary ductal dilatation are evident in the setting of appropriate symptoms, criteria for SOD I are met. Because these patients have a high likelihood of durable relief of pain episodes with biliary sphincterotomy, further investigation is usually considered unwarranted, and endoscopic sphincterotomy is undertaken as definitive treatment without the need to undertake sphincter of Oddi manometry (SOM).

In SOD II and III, different approaches may be used. Particularly in SOD III, empirical treatment using pharmacologic agents with anticholinergic or visceral neuromodulatory/analgesic effects, may be used in lieu of, or before considering, invasive diagnostic study with SOM or sphincterotomy without antecedent SOM.

SOM is performed during endoscopic retrograde cholangiopancreatography (ERCP). A typical SOM catheter is a multichannel perfusion-transducer device analogous to a perfusion-transducer type of esophageal manometry catheter. Perfusion ports are located on the side wall of the catheter and also at the distal lumen, which is frequently sacrificed to allow guidewire exchanges and/or negative-pressure aspiration in the case of pancreatic SOM. The tracing is zeroed in the duodenal lumen, the catheter inserted into the bile duct or pancreatic duct, and a station pull-through technique used, analogous to that employed in esophageal manometry using a perfusion manometry catheter. Basal SO pressures are measured and phasic pressures identified, although information from phasic contractions is not generally used in clinical decision making in SOD today.

SOM has been considered the definitive standard for the diagnosis of SOD. However, in clinical use, perhaps a more accurate characterization of its utility is as a stratification tool—to determine which cases of SOD are, or are not, likely to sustain a durable symptomatic response to sphincterotomy. Diagnosis, or presumptive diagnosis, of SOD, would be made based on the revised Milwaukee/Rome III criteria. If SOD II or III were then suspected, ERCP with SOM would be undertaken. SOM would be performed first, and if it demonstrates characteristic elevation of the basal (tonic) SO pressure (> 40 mm Hg), sphincterotomy would be undertaken.

The role of SOM in definitive diagnosis of SOD, or in the determination of indication for sphincterotomy, has been questioned in more recent trials, however; in such trials, SOM was not demonstrated to possess predictive value and sphincterotomy in SOD III subjects was not shown to be more effective than sham. Thus, the role of SOM in SOD is presently controversial, and in flux clinically.

Presumptive or empirical endoscopic treatment of SOD with noninvasive options can be effective and cost-effective, and may expose the patient to lower risk than endoscopic or surgical therapy. Such an approach does not preclude the option of escalating therapy to ERCP with sphincterotomy, with or without manometry, if pharmacologic therapy does not lead to successful symptom management. SOD I is tantamount to mechanical obstruction of bile flow and it therefore responds expectedly well to biliary sphincterotomy, but the durable response of SOD II or III to sphincterotomy has been historically lower, on the order of 70% and 50%, respectively, even if SOM is positive. Given that SOD II and SOD III are essentially pain syndromes without any additional sequelae, there is little to be lost in educating the patient and considering medical therapy first. Pharmacologic agents used in SOD are those typically finding utility in other visceral hyperalgesia syndromes, such as tricyclic (antidepressant) agents (in low doses, usually once daily), antispasmodic anticholinergic agents such as hyoscyamine or dicyclomine, and selective serotonin reuptake inhibitors.

Endoscopic therapy consists of sphincterotomy of either the biliary or pancreatic sphincter alone or in combination. Studies have differed regarding the need to undertake sphincterotomy of both the sphincter choledochus and the sphincter pancreaticus to obtain successful treatment of biliary or pancreatic SOD. In cases where symptoms remain or recur after endoscopic sphincterotomy, some experts recommend repeating endoscopic SOM to determine if any tonic or phasic activity is discernible, signifying residual sphincter function. If residual sphincter function is indeed demonstrated, surgical sphincteroplasty can be considered. In this procedure, typically undertaken through a duodenotomy, incision of the SO can be extended upstream from the point where the ampullary bile duct impression on the duodenal wall enters the retroperitoneum. As a result, the entire length of the sphincter is ablated, the defect above the duodenal reflection is sutured closed, and the edges of the surgical sphincterotomy are plicated over to reduce the likelihood of reannealing of the incision.

Noninvasive Imaging of Gallbladder and Bile Ducts

Most gallbladder stones are radiolucent and therefore are not detected by plain x-ray. As a result, a number of other imaging modalities are used to identify gallstones. Most imaging studies used to diagnose gallstones are noninvasive; in most cases, invasive modalities are reserved for treatment. Historically, radiopaque substances were introduced into the gallbladder and the bile duct by various means to enhance visualization of the biliary system. Today, transabdominal ultrasound is the primary, and most commonly performed, imaging study to visualize gallbladder anatomy. Ultrasound, in which images are acquired by exploiting variations in the reflective characteristics of sound waves between different tissues, is highly sensitive for detection of gallbladder stones and has excellent properties for assessing other anatomic evidence of gallbladder disease, such as wall thickening and fluid surrounding the gallbladder. It also visualizes the intrahepatic bile ducts and liver parenchyma well. However, because of air contained in intervening hollow viscera (duodenum, stomach, colon) and abdominal adipose tissue, transabdominal ultrasound is less sensitive in detecting bile duct stones and defining the anatomy of the extrahepatic bile duct. Magnetic resonance imaging (MRI) is a technology in which the patient is placed in a scanning apparatus that produces a strong oscillating magnetic field and radiofrequency pulses, which induce hydrogen protons in the nearby organs to generate a signal. The signal is received and processed into image data that can be reconstructed by a computer into various cross-sectional configurations, and even into three-dimensional images that can be rotated on more than one axis. Intravenous contrast agents can enhance these images, or provide more specific visualization of chosen target organs, and even provide information on physiologic function. Because MRI is a cross-sectional imaging modality, it not only visualizes the organ of interest but also can demonstrate spatial and other anatomic relationships of the target organ with surrounding structures. MRI that is optimized to visualize the biliary system and pancreatic duct is the most sensitive noninvasive imaging technology for visualizing the biliary and pancreatic duct systems, and is substantially more sensitive and specific than transabdominal ultrasound in detecting stones and other pathology in the extrahepatic bile duct. Cross-sectional imaging studies such as MRI and computed tomography (CT) also provide additional information by visualizing surrounding organs and their anatomic relationships. The MRI protocol specifically rendered to image the pancreaticobiliary ductal system in detail is called magnetic resonance cholangiopancreatography (MRCP). Such T2-weighted MRI sequences, which enhance visualization of still or slow-moving fluids such as bile, are routinely reconstructed to render the biliary tree in rotatable three-dimensional configurations. Enhanced imaging protocols combined with specialized contrast agents are used to enhance detection of biliary malignancies, such as cholangiocarcinoma, and bile duct leaks and fistulas.

Transabdominal ultrasound, CT, and MRI offer detailed anatomic imaging of the biliary system, but radioscintigraphy of the bile ducts (cholescintigraphy) is used to offer functional information by introducing a radioactive tracer to bile, thereby allowing for imaging of bile secretion from the liver into the bile duct, bile flow through the bile ducts and gallbladder into the duodenum, and bile extravasation into extrabiliary locations in the setting of a bile leak or fistula. The hepatobiliary iminodiacetic acid (HIDA) scan, and scans using related radioactive tracers, begin with the intravenous injection of the scintigraphic agent into a peripheral vein, wherein circulation to the liver leads to absorption by hepatocytes, which excrete the agent into the biliary system along with bile. In the setting of cystic duct obstruction (e.g., with a stone, the usual underlying cause of acute cholecystitis), the liver will excrete the HIDA into the bile, but the HIDA-laden bile cannot cross the cystic duct obstruction to enter the gallbladder. Thus, lack of visible radiotracer in the anatomic location of the gallbladder is a surrogate marker for cystic duct obstruction underlying acute cholecystitis. HIDA is also used in combination with administration of synthetic cholecystokinin analog to calculate the gallbladder ejection fraction to diagnose gallbladder dyskinesia in the CCK-HIDA scan, a gallbladder function test, as described in Plate 2-5 .

Invasive Imaging Modalities and Minimally Invasive Interventions of the Bile Duct

The proximity of the intrahepatic ducts to the abdominal wall and the accessibility of the biliary tree through the upper gastrointestinal tract render the biliary system highly amenable to a wide spectrum of minimally invasive approaches to visualization, tissue acquisition, and disease treatment via the peroral and transcutaneous routes. Percutaneous access to the intrahepatic ducts or gallbladder undertaken by the interventional radiologist is referred to as percutaneous transhepatic cholangiography (PTC) and percutaneous cholecystostomy, respectively. The transoral route is used by the gastrointestinal endoscopist to reach the biliary tree and pancreatic duct via a combined endoscopic and fluoroscopic approach in ERCP. In endoscopic ultrasound (EUS), the endoscopist can obtain a high-resolution ultrasound image of the pancreaticobiliary system via the peroral route using an endoscope with an ultrasound device incorporated into the tip of the instrument.