Biliary System

Chapter 55 Biliary System

Anatomy And Physiology

Biliary anatomy is extremely variable, and precise knowledge of the normal and anatomic variants is critical to surgical intervention in the biliary tree. The distal common bile duct (CBD) inserts into the duodenum via the ampulla of Vater, passing through the sphincter of Oddi. Ascending from the duodenum, the common bile duct may join with the pancreatic duct in the wall of the duodenum, within the pancreas prior to insertion into the duodenal wall, or may enter the duodenum separately from the pancreatic duct (Fig. 55-1). The most inferior portion of the CBD is encompassed by the head of the pancreas. Superior to this portion, the common bile duct is divided into retroduodenal and supraduodenal segments. The insertion of the cystic duct marks the differentiation of the common hepatic duct above and the common bile duct below.

The cystic duct drains the gallbladder, which is divided into the neck, infundibulum with Hartmann’s pouch, body, and fundus of the gallbladder. Roughly the size and shape of a common light bulb, the gallbladder holds 30 to 60 mL of bile as an extrahepatic reservoir. The gallbladder is attached to the inferior surface of the liver and is enveloped by liver for a variable portion of its circumference. Although some gallbladders are almost enveloped by liver parenchyma, others hang on a mesentery, predisposing to volvulus. The attachment of the gallbladder to the liver, known as the gallbladder fossa, identifies the separation of the left and right lobes of the liver (Fig. 55-2). Where the gallbladder attaches to the liver, Glisson’s capsule does not form, and this common surface provides the venous and lymphatic drainage of the gallbladder. The cystic duct drains at an acute angle into the common bile duct and can range from 1 to 5 cm in length. There are a number of anatomic variations in insertion of the cystic duct, including into the right hepatic duct (Fig. 55-3). Within the neck of the gallbladder and cystic ducts lie folds of mucosa oriented in a spiral pattern, known as the spiral valves of Heister, which act to keep gallstones from entering the common bile duct, in spite of distention and intraluminal pressure. The dependent portion of Hartmann’s pouch may overlie the common hepatic or right hepatic ducts, thus placing these structures at risk during the performance of a laparoscopic cholecystectomy.

Above the cystic duct lies the common hepatic duct, draining the left and right hepatic duct systems. The confluence of these structures lies at the hilar plate, which is an extension of Glisson’s capsule. The absence of any vascular structures overlying the bile ducts at this location allows exposure of the bifurcation by incising this layer at the base of the segment IV, lifting the liver off these structures, known as lowering the hilar plate, and is generally used to expose the remainder of the extrahepatic biliary tree for resection or reconstruction.

Vascular Anatomy

The segmental anatomy of the liver parenchyma is based on the vascular supply and drainage, and the biliary drainage is described by the corresponding vascular segment. The hepatic parenchyma is divided into lobes, each of which is divided into lobar segments (Fig. 55-4) to define the basic hepatic anatomic resections. The left lobe is comprised of medial and lateral segments. The right lobe is divided into posterior and anterior segments. Alternatively, the hepatic parenchyma can be divided into segments based on the specific hepatic venous drainage and portal inflow, allowing for a more precise description of anatomic pathology. In this classification system, as developed by Couinard,1 the liver is composed of eight segments. Segment I refers to the caudate lobe. The left lobe of the liver, supplied by the left portal vein, constitutes segments II through IV. The left lobe is further subdivided by the falciform ligament, which separates segments II and III, also known as the left lateral segment, from segment IV. Within the left lateral segment, segment II lies superior to the insertion of the portal vein and segment III lies inferior to it. Segment IV is similarly divided into segments IVA, above, and segment IVB, below the portal vein insertion. The right portal vein supplies the right lobe of the liver and divides into the posterior and anterior sector. Each sector is then subdivided based on its relative location compared with the portal vein. Segment V is supplied by the inferior branch of the anterior sector and segment VIII is supplied by the superior branch. In the posterior sector, segment VI is supplied by the inferior branch and segment VII is supplied by the superior branch. There are three major hepatic veins that drain into the inferior vena cava, in addition to a number of small veins that drain directly from the right lobe. The right hepatic vein constitutes most of the venous drainage from the right lobe and generally lies in the intersegmental fissure between the anterior and posterior sectors of the right lobe. The middle hepatic vein drains the medial segment of the left lobe and a small amount of the medial portions of segments V and VIII. In most cases, the middle hepatic vein fuses with the left hepatic vein that drains the left lateral segment.

As opposed to the liver, where most perfusion comes from portal venous flow, the entire biliary tree is supplied solely by the arterial anatomy. This anatomic arrangement makes it particularly susceptible to ischemic injury at the intrahepatic and extrahepatic levels. The inferior bile duct, below the level of the duodenal bulb, receives its perfusion from tributaries of the posterosuperior pancreaticoduodenal and gastroduodenal arteries. The small branches coalesce to form the two vessels that run along the common bile duct at the 3 and 9 o’clock positions. With close dissection of the areolar tissue surrounding the bile duct, these vessels can be damaged, leaving the bile duct at risk for ischemic injury. The superior common bile duct, from the duodenal bulb to the cystic duct, and common hepatic ducts receive their blood supply from the right hepatic and cystic arteries. As the proper hepatic artery ascends on the anterior medial side of the porta, it divides into right and left hepatic arteries. In most cases, the right hepatic artery passes posterior to the common hepatic duct to supply the right lobe of the liver. After crossing the duct, the right hepatic artery passes through the triangle of Calot, bordered by the cystic duct, common hepatic duct, and edge of liver. In this triangle, the right hepatic artery gives off the cystic artery to the gallbladder and is at risk for injury during a cholecystectomy. An accessory or replaced right hepatic artery, when present, passes through the portocaval space and ascends to the right lobe along the lateral aspect of the common bile duct. A pulsatile structure on the most lateral aspect of the porta during a Pringle maneuver identifies this anomaly.

Normally, the cystic artery arises from the right hepatic artery, which can pass posterior or anterior to the common bile duct to supply the gallbladder. Similar to the variability of the cystic duct, the cystic artery may arise from the right hepatic, left hepatic, proper hepatic, common hepatic, gastroduodenal, or superior mesenteric artery. Although variable, the cystic artery generally lies superior to the cystic duct and is usually associated with a lymph node, known as Calot’s node (Fig. 55-5). Because this node provides some of the lymphatic drainage of the gallbladder, it can be enlarged in the setting of gallbladder pathology, whether inflammatory or neoplastic.

Both within the liver and immediately outside the parenchyma, the bile ducts generally lie superior to the corresponding portal veins, which in turn are superior to the arterial supply (Fig. 55-6). Retaining a longer extrahepatic segment before inserting into the liver, the left hepatic duct travels under the edge of segment IV before slipping superior and posterior to the left portal vein. During this transverse portion, it can receive a few subsegmental branches from segment IV. The left duct drains segments II, III, and IV, with the most distal branch draining segment IVa. Further superolateral, the ducts draining segment IVb arise, and further up the left duct are the ducts for segments II and III. These fused ducts can generally be found just posterior and lateral to the umbilical recess. The caudate lobe drains via smaller ducts that enter the right and left hepatic duct systems. The drainage of the right duct system includes segments V, VI, VII, and VIII and is substantially shorter than the left duct, bifurcating almost immediately. The fusion of two sectoral ducts, posterior and anterior, creates this short right hepatic duct. The anterior sectoral duct runs in a vertical direction to drain segments V and VIII, whereas the posterior sectoral duct follows a horizontal course to drain segments VI and VII.


Bile secretion from the hepatocyte serves two major roles in human physiology. First, because the liver is a major site of detoxification and cellular recycling, bile transport allows excretion of toxins and normal cellular metabolites. Second, bile salts have a critical role in the absorption of most lipids. Bile is secreted into bile canaliculi, which encircle each hepatocyte. Within the hepatic lobule, these canaliculi coalesce to form small bile ducts, eventually entering a portal triad. Four to six portal triads combine to create a hepatic lobule, the smallest functional unit of the liver, identified by its central terminal hepatic venule. On the opposite aspect from the canalicular surface of the hepatocyte lies the sinusoidal surface, which contacts the space of Disse. In this contact area, the hepatocyte is responsible for the absorption of circulating components of bile, an important step in the enterohepatic circulation of bile. Once absorbed and secreted into the bile canaliculi, the tight junctions in the biliary tree keep these components within the bile secretory pathway. The secretion of bile components into the biliary tree form a major stimulus to bile flow, and the volume of bile flow is an osmotic process. Because bile salts combine to form spherical pockets, known as micelles, the salts themselves provide no osmotic activity. Instead, the cations that are secreted into the biliary tree along with the bile salt anion provide the osmotic load to draw water into the duct and increase flow to keep bile electrochemically neutral. For this reason, bile maintains an osmolality approximately comparable to that of plasma.

Although some bile flow is bile salt–independent, serving to expel toxins and metabolites from the body, much of the flow is dependent on neural, humoral, and chemical stimuli. Vagal activity induces bile secretion, as does the gastrointestinal hormone secretin. Cholecystokinin (CCK), secreted by the intestinal mucosa, serves to induce biliary tree secretion and gallbladder wall contraction, thereby augmenting excretion of bile into the intestines.

Bile salts, such as cholic acid and deoxycholic acid, are originally created from cholesterol and secreted into bile canaliculi as cholic acid and its metabolite, deoxycholic acid. The liver actually makes only a small amount of the total bile salt pool used on a daily basis, because most bile salts are recycled after use in the intestinal lumen (Fig. 55-7). After passage into the intestinal tract and reabsorption by the terminal ileum, bile acids are transported back to the liver for recycling bound to albumin. Less than 5% of bile salts are lost each day in the stool. When sufficient quantities of bile salts reach the colonic lumen, the powerful detergent activity of the bile salts can cause inflammation and diarrhea.

The passage of bound bile salts through the space of Disse allows uptake into the hepatocyte in an efficient process that involves sodium cotransport and sodium-independent pathways. In the less specific sodium-independent pathway, a number of organic anions are transported, including unconjugated or indirect bilirubin. The transport of bile salts across the canalicular membrane remains the rate-limiting step in bile salt excretion. Given the vast differences in concentration of bile salts, the transport of bile up an extreme concentration gradient is adenosine triphosphate (ATP)–dependent.

In addition to bile salts, bile contains proteins, lipids, and pigments. The major lipid components of bile are phospholipids and cholesterol. These lipids not only dispose of cholesterol from low- and high-density lipoproteins, but also serve to protect hepatocytes and cholangiocytes from the toxic nature of bile. The sources of most biliary cholesterol are circulating lipoproteins and hepatic synthesis. Therefore, the biliary secretion of cholesterol actually serves to excrete cholesterol from the body. These lipids form micelles and thereby allow absorption of dietary lipids.

Although cholesterol, bile salts, and phospholipids play an important role in nutritional homeostasis, bile also serves as a major route of exogenous and endogenous toxin disposal. One such example of the disposal system is that of bilirubin. Bile pigments, such as bilirubin, are breakdown products of hemoglobin and myoglobin. These are transported in the blood bound to albumin and transported into the hepatocyte. Here, they are transferred into the endoplasmic reticulum and conjugated to form bilirubin glucuronides, also known as conjugated or direct bilirubin. It is the bile pigments that give the color to bile and, when converted to urobilinogen by bacterial enzymes in the intestines, give stool its characteristic color.

In the fasting state, secreted bile will pass through the biliary tree into the intestine and be reabsorbed. Additionally, bile will collect in the gallbladder, which serves as an extrahepatic storage site of secreted bile. To store bile secretions, the gallbladder is extremely efficient in water absorption and thus concentration of bile components. This absorption is an osmotic process performed via the active NaCl transport. With the absorption of NaCl and water across the gallbladder epithelium, the chemical composition of bile changes in the gallbladder lumen. Increases in cholesterol concentration, in addition to calcium, which is not as efficiently absorbed, then lead to decreased stability of phospholipid cholesterol vesicles. The reduced vesicle stability predisposes to nucleation of this stagnant pool of cholesterol and thus to cholesterol stone formation. The gallbladder neck and cystic duct also secrete glycoproteins to help protect the gallbladder from the detergent activity of bile. These glycoproteins also promote cholesterol crystallization.

The gallbladder fills through a retrograde mechanism. With an increase in the tonic activity of the sphincter of Oddi in the fasting state, pressure increases in the common bile duct. This increased pressure allows filling of the lower intraluminal pressure gallbladder, which is capable of storing up to 600 mL of the daily production of bile. The passage of fat, protein, and acid into the duodenum induces CCK secretion from duodenal epithelial cells. Cholecystokinin, as its name suggests, then causes gallbladder contraction, with intraluminal pressures up to 300 mm Hg. Vagal activity also induces gallbladder emptying, but is a less powerful stimulus to gallbladder contraction than CCK.

The distal portion of the bile duct passes through the sphincter of Oddi (Fig. 55-8). The musculature of this sphincter is independent from that of the duodenal intestinal wall and responds differently to neurohumoral controls. This muscular sphincter, which normally maintains high tonic and phasic activity, is inhibited by CCK. With CCK-induced relaxation of the sphincter, bile flows more readily from the biliary tree. Coordinated with gallbladder contraction, the relaxation of this sphincter allows for evacuation of up to 70% of the gallbladder contents within 2 hours of CCK secretion. During the fasting state, the oblique passage of the bile duct through the duodenal wall and the tonic activity of the sphincter prevent duodenal contents from refluxing into the biliary tree.

General Considerations In Biliary Tree Pathophysiology


The common symptomatic manifestations of biliary tree disease are pain, fever, and jaundice. As is seen in other tubular structures, pain associated with other symptoms may be from obstruction with increased intraluminal pressure, infection with its associated inflammatory process, or both. Obstruction will generally precede infection, because stasis of bile is an inciting factor of biliary infection, along with sufficient quantity of infectious inoculum in a susceptible host.

Imaging Studies


Transabdominal ultrasound is a sensitive, inexpensive, reliable, and reproducible test to evaluate most of the biliary tree, being able to separate patients with medical jaundice from those with surgical jaundice. Therefore, this modality is seen as the study of choice for the initial evaluation of jaundice or symptoms of biliary disease. The finding of a dilated common bile duct in the setting of jaundice suggests an obstruction of the duct from stones, usually associated with pain, or from a tumor, which is commonly painless (Fig. 55-9). Gallbladder diseases are regularly diagnosed by ultrasound, because its superficial location with no overlying bowel gas enables its evaluation by sound waves. Ultrasound has a high specificity and sensitivity for cholelithiasis, or gallstones. The density of gallstones allows crisp reverberation of the sound wave, showing an echogenic focus with a characteristic shadowing behind the stone (Fig. 55-10). Most gallstones, unless impacted, will move with positional changes in the patient. This feature allows their differentiation from gallbladder polyps, which are fixed, and from sludge which will move more slowly and does not have the sharp echogenic pattern of gallstones. Pathologic changes seen in many gallbladder diseases can be identified by ultrasound. For example, the gallbladder wall thickening and pericholecystic fluid seen in cholecystitis are visible by ultrasound (Fig. 55-11). Porcelain gallbladder, with its calcified wall, will appear as a curvilinear echogenic focus along the entire gallbladder wall, with posterior shadowing (Fig. 55-12). In addition to division of medical versus surgical jaundice, ultrasound can sometimes identify the cause of obstructive jaundice, showing common bile duct stones or even cholangiocarcinoma.

Hepatic Iminodiacetic Acid Scan

Although incapable of providing precise anatomic delineation of pathophysiology, biliary scintigraphy, also known as a hepatic iminodiacetic acid scan (HIDA) scan, can be used to evaluate the physiologic secretion of bile. The injection of an iminodiacetic acid, which is processed in the liver and secreted with bile, allows identification of bile flow. Therefore, the failure to fill the gallbladder 2 hours after injection demonstrates obstruction of the cystic duct, as seen in acute cholecystitis (Figs. 55-13 and 55-14). In addition, the scan will identify obstruction of the biliary tree and bile leaks, which may be useful in the postoperative setting. HIDA scans can also be used to determine gallbladder function, because the injection of CCK during a scan will document physiologic ejection of the gallbladder. This may be useful in patients with biliary tract pain but without stones, because some patients have pain from impaired emptying, known as biliary dyskinesia. As a nuclear medicine test, the test demonstrates physiologic flow, but does not provide fine anatomic detail, nor can it identify gallstones.

Endoscopic Retrograde Cholangiopancreatography

Endoscopic retrograde cholangiopancreatography (ERCP) is an invasive test using endoscopy and fluoroscopy to inject contrast through the ampulla and image the biliary tree (Fig. 55-17). Although it does carry a complication rate of up to 10%, its usefulness lies in its ability to diagnose and treat many diseases of the biliary tree. For patients with malignant obstruction, ERCP can be used to provide tissue samples for diagnosis while also decompressing an obstruction, but does not stage patients accurately. Many benign diseases, such as choledocholithiasis, can be easily treated by endoscopic means. ERCP has also proven extremely useful in the diagnosis and treatment of complications of biliary surgery.

Benign Biliary Disease

Calculous Biliary Disease

Gallstones can be subclassified into two major subtypes, depending on the principle solute that precipitates into a stone. More than 70% of gallstones in America are formed by precipitation of cholesterol and calcium, with pure cholesterol stones accounting for only a small (<10%) portion. Pigment stones, further subclassified as black or brown stones, are caused by precipitation of concentrated bile pigments, the breakdown products of hemoglobin. Four major factors explain most gallstone formation—supersaturation of secreted bile, concentration of bile in the gallbladder, crystal nucleation, and gallbladder dysmotility. High concentrations of cholesterol and lipid in bile secretion from the liver constitute one predisposing condition to cholesterol stone formation, whereas increased hemoglobin processing is seen in most patients with pigment stones. Once in the gallbladder, bile is concentrated further through the absorption of water and NaCl, increasing the concentrations of the bile solutes and calcium. With respect to cholesterol stones (Fig. 55-20), cholesterol precipitates out into crystals when the concentration in vesicles exceeds the solubility of cholesterol (Fig. 55-21).2 This process of crystal formation is further accelerated by pronucleating agents, including glycoproteins and immunoglobulins. Finally, abnormal gallbladder motility can increase stasis in the gallbladder, allowing more time for solutes to precipitate in the gallbladder. Therefore, increased stone formation can be seen in conditions associated with impaired gallbladder emptying, such as prolonged fasting states, use of total parenteral nutrition, postvagotomy, and use of somatostatin analogues.

Pigment stones can be divided into black stones, as seen in hemolytic conditions and cirrhosis, or brown stones, which tend to be found in the bile ducts. The difference in color comes from incorporation of cholesterol into the brown stones. Because black pigment stones occur in hemolytic states from concentration of bilirubin, they are found almost exclusively in the gallbladder. Alternatively, brown stones occur within the biliary tree and suggest a disorder of biliary motility and associated bacterial infection.

Natural History

The vast majority of gallstones are asymptomatic, often being identified at time of abdominal imaging for other reasons or during laparotomy. To become symptomatic, the gallstone must obstruct a visceral structure, such as the cystic duct. Biliary colic, caused by temporary blockage of the cystic duct, tends to occur following a meal in which the secretion of CCK leads to gallbladder contraction. Stones that do not obstruct the cystic duct or pass through the entire biliary tree into the intestines without impaction do not cause symptoms. Only 20% to 30% of patients with asymptomatic stones will develop symptoms within 20 years and, because approximately 1% of patients with asymptomatic stones develop complications of their stones before onset of symptoms, prophylactic cholecystectomy is not warranted in asymptomatic patients.

Certain subsets of patients, however, constitute a higher risk pool, so prophylactic cholecystectomy should be considered. Among these are patients with hemolytic anemias, such as sickle cell anemia. These patients have an extremely high rate of pigment stone formation, and cholecystitis can precipitate a crisis. Patients with a calcified gallbladder wall, known as porcelain gallbladder, those with large (>2.5-cm) gallstones, and those with a long common channel of bile and pancreatic ducts all have a higher risk of gallbladder cancer and should consider cholecystectomy. Additionally, patients with asymptomatic gallstones undergoing bariatric surgery may also benefit from cholecystectomy. Not only does rapid weight loss favor stone formation but also, following gastric bypass, ERCP to remove common bile duct stones in ascending cholangitis is extremely challenging and usually unsuccessful. Finally, because severe infection can be life-threatening in the immunocompromised patient, some transplantation surgeons recommend prophylactic cholecystectomy prior to receipt of an organ transplant.

Chronic Cholecystitis

Recurrent attacks of biliary colic, which only temporarily occlude the cystic duct and do not cause acute cholecystitis, can cause some inflammation and scarring of the neck of the gallbladder and cystic duct. This process, called chronic cholecystitis, causes fibrosis as histologic evidence of repeated self-limited episodes of inflammation. The diagnosis of chronic cholecystitis lies along a continuum with biliary colic because it is results from recurrent attacks. Therefore, the presentation is that of symptomatic cholelithiasis, or biliary colic. Pain occurring after ingestion of a fatty meal, with the attendant increase in CCK secretion in response to duodenal intraluminal fat, is classic for biliary colic, although only 50% of patients will report an association with food. Pain from stones tends to locate in the epigastrium or right upper quadrant and may radiate around to the scapula. These attacks of pain generally last a few hours. Pain lasting longer than 24 hours or when associated with fever suggests acute cholecystitis. The pain of biliary colic, even in the absence of cholecystitis, may also cause other gastrointestinal symptoms such as bloating, nausea, or even vomiting.

Symptomatic stones constitute a different risk profile than the routine patient with asymptomatic stones, with a higher likelihood of complications from stones. Therefore, symptomatic cholelithiasis is an indication for cholecystectomy. To perform a cholecystectomy for symptomatic stones, one needs presence of symptoms and documentation of stones.

Acute Calculous Cholecystitis

Obstruction of the cystic duct from stone impaction eventually causes acute calculous cholecystitis. Temporary impaction, as seen with biliary colic, does not create inflammation as the obstruction resolves. If it does not resolve, however, inflammation ensues, with edema and subserosal hemorrhage, a process known as acute cholecystitis. Infection of the stagnant pool of bile is a secondary phenomenon; the primary pathophysiology is unresolved cystic duct obstruction. Without resolution of the obstruction, the gallbladder will progress to ischemia and necrosis. Eventually, acute cholecystitis becomes acute gangrenous cholecystitis and, when complicated by infection with a gas-forming organism, acute emphysematous cholecystitis (Fig. 55-23).


Transabdominal ultrasonography is a sensitive, inexpensive, and reliable tool for the diagnosis of acute cholecystitis, with a sensitivity of 85% and specificity of 95%. In addition to identifying gallstones, ultrasound can demonstrate pericholecystic fluid, gallbladder wall thickening, and even a sonographic Murphy’s sign, documenting tenderness specifically over the gallbladder (Fig. 55-24). In most cases, an accurate history and physical examination, along with supporting laboratory studies and an ultrasound, make the diagnosis of acute cholecystitis. In atypical cases, a HIDA scan may be used to demonstrate obstruction of the cystic duct, which definitively diagnoses acute cholecystitis. Filling of the gallbladder during a HIDA scan essentially eliminates the diagnosis of cholecystitis. CT may show similar findings to ultrasound with pericholecystic fluid, gallbladder wall thickening, and emphysematous changes, but CT is less sensitive than ultrasound for the diagnosis of acute cholecystitis.


Although infection is a secondary event following stasis and inflammation, most cases of acute cholecystitis are complicated by superinfection of the inflamed gallbladder. Therefore, patients are given nothing by mouth and IV fluids and parenteral antibiotics are started. Given that gram-negative aerobes are the most common organisms found in acute cholecystitis, followed by anaerobes and gram-positive aerobes, broad-spectrum antibiotics are warranted. Parenteral narcotics are usually required to control the pain.

Cholecystectomy, whether open or laparoscopic, is the treatment of choice for acute cholecystitis. The timing of operative intervention in acute cholecystitis has long been a source of debate. In the past, many surgeons advocated for delayed cholecystectomy, with patients managed nonoperatively during their initial hospitalization and discharged home with resolution of symptoms. An interval cholecystectomy was then performed at approximately 6 weeks following the initial episode. More recent studies have shown that when performed early in the disease process (within the first week), the operation can be performed laparoscopically with equivalent or improved morbidity, mortality, and length of stay, as well as a similar conversion rate to open cholecystectomy.3 Additionally, approximately 20% of patients initially admitted for nonoperative management failed medical treatment prior to the planned interval cholecystectomy and required surgical intervention. Initial nonoperative therapy remains a viable option for patients who present in a delayed fashion and should be decided on an individual basis.

Given the inflammatory process occurring in the porta hepatis, early conversion to open cholecystectomy should be considered when delineation of anatomy is not clear or when progress cannot be made laparoscopically. With substantial inflammation, a partial cholecystectomy, transecting the gallbladder at the infundibulum with cauterization of the remaining mucosa, is acceptable to avoid injury to the common bile duct. Some patients present with acute cholecystitis but have a prohibitively high operative risk. For these patients, a percutaneously placed cholecystostomy tube should be considered. Frequently performed using ultrasound guidance under local anesthesia with some sedation, cholecystostomy can act as a temporizing measure by draining the infected bile. Percutaneous drainage allows improvement in symptoms and physiology, allowing for a delayed cholecystectomy, 3 to 6 months after medical optimization.


Choledocholithiasis, or common bile duct stones, are classified by their point of origin, with primary common duct stones arising de novo in the bile duct and secondary common duct stones passing from the gallbladder into the bile duct. Primary choledocholithiasis is generally from brown pigment stones, which are a combination of precipitated bile pigments and cholesterol. Brown stones are more common in Asian populations and are associated with a bacterial infection of the bile duct. The bacteria secrete an enzyme that hydrolyzes bilirubin glucuronides to form free bilirubin, which then precipitates. Most common duct stones found in the United States are secondary, and are termed retained common duct stones when found within 2 years following cholecystectomy.

Many common duct stones are clinically silent and may be identified only during cholangiography, if performed routinely during cholecystectomy. Without pain or an abnormal liver function panel, a setting in which selective cholangiography is not performed, 1% to 2% of patients following cholecystectomy will present with a retained stone. When performed routinely, intraoperative cholangiography identifies choledocholithiasis in approximately 10% of asymptomatic patients, suggesting that most choledocholithiasis remains clinically silent.4,5

When not clinically silent, common duct stones may present with symptoms ranging from biliary colic to the clinical manifestations of obstructive jaundice, such as darkening of the urine, scleral icterus, and lightening of the stools. Jaundice with choledocholithiasis is more likely to be painful because the onset of obstruction is acute, causing rapid distention of the bile duct and activation of pain fibers. Fever, a common symptom, can be associated with right upper quadrant pain and jaundice, a constellation known as Charcot’s triad. This triad suggests ascending cholangitis and, if untreated, may progress to septic shock. The addition of hypotension and mental status changes, both evidence of shock, to Charcot’s triad is known as Reynolds pentad.


In the setting of choledocholithiasis, abnormalities of the hepatic function panel are common but neither sensitive nor specific and, with superinfection, leukocytosis may also be present. Ultrasound may show choledocholithiasis or only biliary ductal dilation. In patients with biliary pain, gallstones and jaundice, a dilated bile duct (>8 mm) is highly suggestive of choledocholithiasis, even if common duct stones are not documented ultrasonographically. Even without symptoms of biliary colic, a dilated bile duct in the presence of gallstones suggests choledocholithiasis.

ERCP is highly sensitive and specific for choledocholithiasis (Fig. 55-25) and can usually be therapeutic by clearing the duct of all stones in approximately 75% of patients during the first procedure and approximately 90% with repeat ERCP. During the endoscopic procedure, a sphincterotomy is performed with a balloon sweep and extraction of the stone, all of which have a complication rate of 5% to 8%. Indications for preoperative ERCP prior to cholecystectomy include cholangitis, biliary pancreatitis, limited surgeon experience with common duct exploration, and patients with multiple comorbidities.

Alternatively, magnetic resonance cholangiopancreatography (MRCP) is highly sensitive (>90%) with an almost 100% specificity for the diagnosis of common duct stones (Fig. 55-26). As a noninvasive test, MRCP provides accurate imaging of the biliary tree but, in the setting of choledocholithiasis, does not provide a therapeutic solution. A clear cholangiogram by MRCP eliminates the need for ERCP. However, choledocholithiasis identified by MRCP requires intervention by some other method. With more surgeons becoming adept at laparoscopic common duct exploration, the inability of MRCP to remove common duct stones may prove less clinically relevant.

PTC can also be used to diagnose and treat choledocholithiasis. PTC is an invasive test with a complication rate similar to ERCP. Although requiring less skill, and at a lower cost, PTC is as effective in patients with a dilated biliary ductal system but less effective in the setting of a nondilated biliary tree.

Ultrasound should be used routinely for evaluation of the gallbladder and biliary tree, but the remaining studies should be chosen selectively based on the likelihood of finding common duct stones. Patients with highest risk, such as those with cholangitis or a dilated biliary tree, should undergo ERCP. Those with lower risk can undergo laparoscopic cholecystectomy with cholangiography, and possible laparoscopic common duct exploration, or MRCP, depending on the surgeon’s expertise. Generally, choledocholithiasis identified but not removed during cholecystectomy mandates an ERCP for stone extraction.


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Aug 1, 2016 | Posted by in CARDIAC SURGERY | Comments Off on Biliary System

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