Biliary Tract Chapter 27 PDF

EUROPEAN UNIVERSITY CYPRUS Access Provided by: Current Diagnosis & Treatment: Surgery, 15e Chapter 27: Biliary Tract David A. Harris; Eric G. Sheu EMBRYOLOGY & ANATOMY The anlage of the biliary ducts and liver is a diverticulum appearing on the ventral foregut in 3 mm embryos. The cranial portion becomes the liver; a caudal bud, the ventral pancreas; and an intermediate bud, the gallbladder. The hepatic diverticulum becomes a solid mass of cells that later recanalizes to form ducts. The smallest, the bile canaliculi, first appear as a basal network between the primitive hepatocytes (Figure 27–1). In most cases, the common hepatic duct is formed by the union of a single right and left duct. In 25% of individuals, the anterior and posterior divisions of the right duct join the left duct separately. The origin of the common hepatic duct is close to the liver but always outside its substance. It runs 4 cm before joining the cystic duct to form the common bile duct. The common duct begins in the hepatoduodenal ligament, passes behind the first portion of the duodenum, and runs in a groove on the posterior surface of the pancreas before entering the duodenum. Its terminal 1 cm is intimately adherent to the duodenal wall. The total length of the common duct is about 9 cm. Figure 27–1. Scanning electron photomicrograph of a hepatic plate with adjacent sinusoids and sinusoidal microvilli and a bile canaliculus running in the center of the liver cells. Although their boundaries are indistinct, about four hepatocytes constitute the section of the plate in the middle of the photograph. Occasional red cells are present within the sinusoids. (Reduced from ×2000.) In 80%90% of individuals, the main pancreatic duct joins the common duct to form a common channel about 1 cm long. The intraduodenal segment of the duct is called the hepatopancreatic ampulla, or ampulla of Vater. The gallbladder is a pearshaped organ adherent to the undersurface of liver segments 4b and 5 by a veil of peritoneum known as the, cystic plate. The fundus projects 12 cm below the hepatic edge. The gallbladder rarely has a complete peritoneal covering. The lumen of the cystic duct contains a thin mucosal septum, the spiral valve of Heister, that offers mild resistance to bile flow. The neck of the gallbladder tapers into the narrow cystic duct, which in 75% of people connects with the common duct. However, biliary anatomy is highly variable. The cystic duct can be short or long and can insert directly into the right hepatic duct, runs parallel to the hepatic duct, or winds around it before joining the common duct. An accessory right hepatic duct is also common (Figure 27–2). Figure 27–2. Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu ©2024 McGraw Hill. All Rights of Use Privacy Policy Notice Accessibility Anatomy of the gallbladder and Reserved. variations inTerms anatomy of the cystic duct. Page 1 / 32 mucosal septum, the spiral valve of Heister, that offers mild resistance to bile flow. The neck of the gallbladder tapers into the narrow cystic duct, which EUROPEAN UNIVERSITY CYPRUS in 75% of people connects with the common duct. However, biliary anatomy is highly variable. The cystic duct can be short or long and can insert Access Provided by: directly into the right hepatic duct, runs parallel to the hepatic duct, or winds around it before joining the common duct. An accessory right hepatic duct is also common (Figure 27–2). Figure 27–2. Anatomy of the gallbladder and variations in anatomy of the cystic duct. In the hepatoduodenal ligament, the hepatic artery is to the left of the common duct, and the portal vein is posterior and medial. The right hepatic artery usually passes behind the hepatic duct and then gives off the cystic artery before entering the right lobe of the liver, but variations are common. A replaced right hepatic artery is typically found coming off the superior mesenteric artery and will course along the lateral aspect of the common bile duct. The cystic artery can also have varied origins, but its termination is usually found by Calot’s node, which sits at the gallbladder infundibularcystic junction. PHYSIOLOGY Bile Flow Bile is produced from cholesterol at a rate of 5001500 mL/d, and bile salts are actively secreted into the biliary canaliculus. Na+ and water follow passively to establish isosmolality and electrical neutrality. Lecithin and cholesterol are secreted at rates that correlate with variations in bile salt output. In addition, bilirubin and a number of other organic anions are actively secreted by the hepatocytes. The columnar cells of the ducts add a fluid rich in HCO3– to that produced in the canaliculus. This involves active secretion stimulated by secretin, vasoactive intestinal peptide (VIP), and cholecystokinin (CCK). K+ and water are distributed passively across the ducts (Figure 27–3). Figure 27–3. Bile formation. Solid lines into the ductular lumen indicate active transport; dotted lines represent passive diffusion. Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Page 2 / 32 vasoactive intestinal peptide (VIP), and cholecystokinin (CCK). K+ and water are distributed passively across the ducts (Figure 27–3). EUROPEAN UNIVERSITY CYPRUS Figure 27–3. Access Provided by: Bile formation. Solid lines into the ductular lumen indicate active transport; dotted lines represent passive diffusion. Between meals, bile is stored in the gallbladder, where it is concentrated at rates of up to 20% per hour. Na+ and either HCO3– or Cl– are actively transported from its lumen during absorption. The changes in bile composition brought about by the act of concentration are shown in Figure 27–4. Figure 27–4. Changes in gallbladder bile composition with time. (Used wth permission from J Dietschy.) Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Page 3 / 32 transported from its lumen during absorption. The changes in bile composition brought about by the act of concentration are shown in Figure 27–4. EUROPEAN UNIVERSITY CYPRUS Figure 27–4. Access Provided by: Changes in gallbladder bile composition with time. (Used wth permission from J Dietschy.) Three factors regulate bile flow: hepatic secretion, gallbladder contraction, and choledochal sphincteric resistance. In the fasting state, pressure in the common bile duct is 510 cm H2O, and bile produced in the liver is diverted into the gallbladder. After a meal, the gallbladder contracts, reaching 25 cm H2O; the sphincter relaxes; and bile is forced into the duodenum as ductal pressure (1520 cm H2O) exceeds sphincteric resistance. CCK is the major physiologic stimulus for postprandial gallbladder contraction and relaxation of the sphincter, but vagal impulses facilitate its action. CCK is released into the bloodstream from the mucosa of the small bowel by fat or lipolytic products in the lumen. Amino acids and small polypeptides are weaker stimuli, and carbohydrates are ineffective. Bile flow during a meal is augmented by turnover of bile salts in the enterohepatic circulation and stimulation of ductal secretion by secretin, VIP, and CCK. Motilin stimulates episodic partial gallbladder emptying in the interdigestive phase. Bile Salts & the Enterohepatic Circulation Bile salts, lecithin, and cholesterol compose about 90% of the solids in bile, with the remainder consisting of bilirubin, fatty acids, and inorganic salts. Gallbladder bile contains about 10% solids and has a bile salt concentration between 200 and 300 mmol/L (Figure 27–4). Bile salts are steroid molecules formed from cholesterol by hepatocytes. The rate of synthesis is under feedback control and can be increased to a maximum of about 20fold. Two primary bile salts—cholate and chenodeoxycholate—are produced by the liver. Before excretion into bile, they are conjugated with either glycine or taurine, which enhances water solubility. Intestinal bacteria alter these compounds to produce the secondary bile salts, deoxycholate and lithocholate. Bile salts function to (1) induce the flow of bile, (2) transport lipids, (3) bind calcium ions in bile, and (4) regulate metabolic functions. The importance of the last of these is unknown, but it is clear that bile acid signaling is capable of affecting global glucose and fat metabolism and likely contributes to the metabolic benefits of bariatric operations such as RouxenY gastric bypass and sleeve gastrectomy. Bile acid molecules are amphipathic—ie, they have hydrophilic and hydrophobic poles. In bile, they form multimolecular aggregates called micelles in which the hydrophilic poles become aligned to face the aqueous medium. Waterinsoluble lipids, such as cholesterol, can be dissolved within the hydrophobic centers of bile salt micelles. Molecules of lecithin, which is water insoluble but polar lipid, aggregate into hydrated bilayers that form vesicles in bile, and they also become incorporated into bile acid micelles to form mixed micelles. Mixed micelles have an increased lipidcarrying capacity compared with pure bile acid micelles. Cholesterol in bile is transported within the phospholipid vesicles and the bile salt micelles. Bile salts remain in the intestinal lumen throughout the jejunum, where they participate in fat digestion and absorption (Figure 27–5). Upon reaching Downloaded 2024131 5:56 A Your IP is 82.116.202.56 the distal27: small bowel, theyDavid are reabsorbed by anG.active Pagefrom 4 / 32 Chapter Biliary Tract, A. Harris; Eric Sheutransport system located in the terminal 200 cm of ileum. Over 95% of bile salts arriving ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility the jejunum are transferred by this process into portal vein blood; the remainder enter the colon, where they are converted to secondary bile salts by colonic bacteria. The entire bile salt pool of 2.54 g circulates twice through the enterohepatic circulation during each meal, and six to eight cycles are made each day. The normal daily loss of bile salts in the stool amounts to 10%20% of the pool and is restored by hepatic synthesis. which the hydrophilic poles become aligned to face the aqueous medium. Waterinsoluble lipids, such as cholesterol, can be dissolved within the EUROPEAN UNIVERSITY CYPRUS hydrophobic centers of bile salt micelles. Molecules of lecithin, which is water insoluble but polar lipid, aggregate into hydrated bilayers that form Access Provided by: vesicles in bile, and they also become incorporated into bile acid micelles to form mixed micelles. Mixed micelles have an increased lipidcarrying capacity compared with pure bile acid micelles. Cholesterol in bile is transported within the phospholipid vesicles and the bile salt micelles. Bile salts remain in the intestinal lumen throughout the jejunum, where they participate in fat digestion and absorption (Figure 27–5). Upon reaching the distal small bowel, they are reabsorbed by an active transport system located in the terminal 200 cm of ileum. Over 95% of bile salts arriving from the jejunum are transferred by this process into portal vein blood; the remainder enter the colon, where they are converted to secondary bile salts by colonic bacteria. The entire bile salt pool of 2.54 g circulates twice through the enterohepatic circulation during each meal, and six to eight cycles are made each day. The normal daily loss of bile salts in the stool amounts to 10%20% of the pool and is restored by hepatic synthesis. Figure 27–5. Enterohepatic circulation of bile salts. (Used with permission from M Tyor.) Bilirubin About 250300 mg of bilirubin is excreted each day in the bile, 75% of it from breakdown of red cells in the reticuloendothelial system and 25% from turnover of hepatic heme and hemoproteins. First, heme is liberated from hemoglobin, and the iron and globin are removed for reuse by the organism. Biliverdin, the first pigment formed from heme, is reduced to unconjugated bilirubin, the indirectreacting bilirubin of the van den Bergh test. Unconjugated bilirubin is insoluble in water and is transported in plasma bound to albumin. Unconjugated bilirubin is extracted from blood by hepatocytes, where it is conjugated with glucuronic acid to form bilirubin diglucuronide, the water soluble direct bilirubin. Conjugation is catalyzed by glucuronyl transferase, an enzyme on the endoplasmic reticulum. Bilirubin is transported within the hepatocyte by cytosolic binding proteins, which rapidly deliver the molecule to the canalicular membrane for active secretion into bile. Within bile, conjugated bilirubin is largely transported in association with mixed lipid micelles. After entering the intestine, bilirubin is reduced by intestinal bacteria to several compounds known as urobilinogens, which are subsequently oxidized and converted to pigmented urobilins. The term urobilinogen is often used to refer to both urobilins and urobilinogens. PATHOGENESIS OF GALLSTONES Downloaded 2024131 5:56inAthe Your IP isStates 82.116.202.56 More than 20 million people United have gallstones in their gallbladders; about 300,000600,000 operations are performed annually for Page 5 / 32 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu this disease, and at least 6000 deaths result from itsof complications treatment. The incidence of gallstones increases with age, so that between 50 and ©2024 McGraw Hill. All Rights Reserved. Terms Use PrivacyorPolicy Notice Accessibility 65 years of age, about 20% of women and 5% of men are affected. After entering the intestine, bilirubin is reduced by intestinal bacteria to several compounds known as urobilinogens, which areUNIVERSITY subsequentlyCYPRUS oxidized EUROPEAN and converted to pigmented urobilins. The term urobilinogen is often used to refer to both urobilins and urobilinogens. Access Provided by: PATHOGENESIS OF GALLSTONES More than 20 million people in the United States have gallstones in their gallbladders; about 300,000600,000 operations are performed annually for this disease, and at least 6000 deaths result from its complications or treatment. The incidence of gallstones increases with age, so that between 50 and 65 years of age, about 20% of women and 5% of men are affected. The gallstones in 75% of patients are composed predominantly (70%95%) of cholesterol and are called cholesterol stones. The remaining 25% are pigment stones. Regardless of composition, all gallstones give rise to similar clinical sequelae. Cholesterol Gallstones Cholesterol gallstones result from secretion of bile supersaturated with cholesterol. Influenced by various factors present in bile, the cholesterol precipitates from solution, and the newly formed crystals grow to macroscopic stones. Except when the common bile duct is dilated or partially obstructed, the stones in this disease form exclusively within the gallbladder. Those found in the ducts usually reach that location after passing through the cystic duct. The incidence of cholesterol gallstone disease is highest in American Indians, lower in whites, and lowest in blacks, with a twofold gradient from one group to the next. More than 75% of American Indian women over age 40 are affected. Before puberty, the disease is rare but of equal frequency in both sexes. Thereafter, women are more commonly affected than men until after menopause, when the discrepancy lessens. Hormonal effects are also reflected in the increased incidence of gallstones with multiparity and the increased cholesterol saturation of bile and greater incidence of gallstones following ingestion of oral contraceptives. Obesity is the other major risk factor. The relative risk rises proportionately to the extent of overweight due to a progressively increasing output of cholesterol in bile. As noted previously, cholesterol is insoluble and, in bile, must be transported within bile salt micelles and phospholipid (lecithin) vesicles. When the amount of cholesterol in bile exceeds the cholesterol holding capacity, cholesterol crystals begin to precipitate from the phospholipid vesicles. The secretion of bile salt and cholesterol into bile is linked. Bile salt elutes cholesterol from the hepatocyte membrane during passage into the bile canaliculus. At higher bile salt output levels, the amount of cholesterol relative to bile salt entering bile decreases. This means that during low bile flow (eg, during fasting), bile holding capacity for cholesterol is more saturated than during high bile flow. In fact, almost half of persons in Western cultures have bile supersaturated with cholesterol in the morning after an overnight fast. The bile salt pool in patients with cholesterol gallstone disease is about half the size of that of normal subjects, but this is a result of the gallstone disease (eg, gallstones displace bile in the gallbladder) and not a cause. The occurrence of cholesterol gallstone disease requires cholesterol supersaturation of bile, but that in itself is not sufficient. Cholesterol in supersaturated bile from individuals without gallstone disease precipitates spontaneously at a much slower rate than does the cholesterol in similar bile from patients with gallstones. Furthermore, among individuals with supersaturated bile, only those with gallstone disease demonstrate cholesterol crystal formation in vivo. These observations are the result of specific bile proteins that either stabilize or destabilize cholesterolladen phospholipid vesicles. For gallstone formation, the pronucleating factors (eg, immunoglobulin, mucus glycoprotein, fibronectin, orosomucoid) appear to be more important than the antinucleating factors (eg, glycoprotein, apolipoprotein, cytokeratin). Variations in these proteins may be the critical factor determining which of the many individuals with saturated bile develop gallstones. The fact that gallstones form almost exclusively in the gallbladder, even though the composition of hepatic bile is abnormal, underscores the important role of the gallbladder in gallstone pathogenesis. This includes concentrating the bile, providing nidi (eg, small grains of pigment) for crystallization of cholesterol, supplying mucoprotein to paste the stones together, and serving as an area of stasis to allow stone formation and growth. Pigment Stones Pigment stones account for 25% of gallstones in the United States and 60% of those in Japan. Pigment stones are black to dark brown, 25 mm in diameter, and amorphous. They are composed of a mixture of calcium bilirubinate, complex bilirubin polymers, bile acids, and other unidentified substances. About 50% are radiopaque, and in the United States, they constitute twothirds of all radiopaque gallstones. The incidence is similar in men and women and in blacks and whites. Pigment stones are rare in American Indians. Predisposing factors are cirrhosis, bile stasis (eg, a strictured or markedly dilated common duct), and chronic hemolysis. Some patients with pigment stones have increased concentrations bilirubin in their bile. Scanning electron microscopy demonstrates that about 90% of pigment Downloaded 2024131 5:56 A Your of IP unconjugated is 82.116.202.56 stones are composed of dense mixtures of bacteria and bacterial glycocalyx along with pigment solids. This suggests that bacteria have a primary Page 6 role / 32 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu ©2024 McGraw Hill. formation, All Rights Reserved. Terms Use why Privacy Policy Notice Accessibility in pigment gallstone and it also helps to of explain patients with pigment gallstone disease have sepsis more often than do those with cholesterol gallstone disease. It seems likely that bacterial βglucuronidase is responsible for deconjugating the soluble bilirubindiglucuronide to insoluble unconjugated bilirubin, which subsequently becomes agglomerated by glycocalyx into macroscopic stones. diameter, and amorphous. They are composed of a mixture of calcium bilirubinate, complex bilirubin polymers, bile acids, and other unidentified EUROPEAN UNIVERSITY CYPRUS substances. About 50% are radiopaque, and in the United States, they constitute twothirds of all radiopaque gallstones. The incidence is similar in men and women and in blacks and whites. Pigment stones are rare in American Indians. Access Provided by: Predisposing factors are cirrhosis, bile stasis (eg, a strictured or markedly dilated common duct), and chronic hemolysis. Some patients with pigment stones have increased concentrations of unconjugated bilirubin in their bile. Scanning electron microscopy demonstrates that about 90% of pigment stones are composed of dense mixtures of bacteria and bacterial glycocalyx along with pigment solids. This suggests that bacteria have a primary role in pigment gallstone formation, and it also helps to explain why patients with pigment gallstone disease have sepsis more often than do those with cholesterol gallstone disease. It seems likely that bacterial βglucuronidase is responsible for deconjugating the soluble bilirubindiglucuronide to insoluble unconjugated bilirubin, which subsequently becomes agglomerated by glycocalyx into macroscopic stones. JAUNDICE Jaundice is categorized as prehepatic, hepatic, or posthepatic, depending on the site of the underlying disease. Hemolysis, the most common cause of prehepatic jaundice, involves increased production of bilirubin. Less common causes of prehepatic jaundice are Gilbert disease and the CriglerNajjar syndrome. Hepatic parenchymal jaundice is subdivided into hepatocellular and cholestatic types. The former includes acute viral hepatitis and chronic alcoholic cirrhosis. Some cases of intrahepatic cholestasis may be indistinguishable clinically and biochemically from cholestasis due to bile duct obstruction. Primary biliary cirrhosis, toxic drug jaundice, cholestatic jaundice of pregnancy, and postoperative cholestatic jaundice are the most common forms. Extrahepatic jaundice most often results from biliary obstruction by a malignant tumor, choledocholithiasis, or biliary stricture. Pancreatic pseudocyst, chronic pancreatitis, sclerosing cholangitis, metastatic cancer, and duodenal diverticulitis are less common causes. The cause of jaundice can be ascertained in the majority of patients from clinical and laboratory findings alone. In the remainder, transhepatic cholangiography (THC) or endoscopic retrograde cholangiopancreatography (ERCP) and ultrasound or computed tomography (CT) scans will be necessary. The indications for these tests are discussed in later sections. History The age, gender, and parity of the patient and possible deleterious habits should be noted. Most cases of infectious hepatitis occur in patients under age 30. A history of drug addiction may suggest serum hepatitis transmitted by shared hypodermic equipment. Chronic alcoholism can usually be documented in patients with cirrhosis, and acute jaundice in alcoholics usually follows a recent binge. Obstructing gallstones or tumors are more common in older people. Patients with jaundice due to choledocholithiasis may have associated biliary colic, fever, and chills and may report previous similar attacks. In contrast, pain is either absent in malignant obstruction or deepseated and dull. Pain in the region of the liver is frequently experienced in the early stages of viral hepatitis and acute alcoholic liver injury. The patient with extrahepatic obstruction may report that stools have become lighter in color and the urine dark. Cholestatic diseases are often accompanied by pruritus. The cause remains obscure; itching does not correlate with bile salt levels in the skin, as was once believed. Physical Examination Hepatomegaly is common in both hepatic and posthepatic jaundice. In some cases, palpation of the liver may suggest cirrhosis or metastatic cancer, but impressions of this kind are unreliable. Secondary stigmata of cirrhosis usually accompany acute alcoholic jaundice; palmar erythema, spider angiomas, ascites, collateral veins on the abdominal walls, and splenomegaly suggest cirrhosis. A nontender, palpable gallbladder in a jaundiced patient suggests malignant obstruction of the common duct (Courvoisier sign), but absence of a palpable gallbladder is of little significance in ruling out cancer. Laboratory Tests In hemolytic disease, the increased bilirubin is principally in the unconjugated indirect fraction. Because unconjugated bilirubin is insoluble in water, the jaundice in hemolysis is acholuric. The total bilirubin in hemolysis rarely exceeds 45 mg/dL because the rate of excretion increases as the bilirubin concentration rises and a plateau is quickly reached. Greater values suggest concomitant hepatic parenchymal disease. Jaundice due to hepatic parenchymal disease is characterized by elevations of both conjugated and unconjugated serum bilirubin. An increase in the conjugated fraction always signifies disease within the hepatobiliary system. The direct bilirubin predominates in about half of cases of hepatic parenchymal disease. Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Page 7 / 32 Chapter 27: Biliarycholestasis Tract, David Harris; Ericobstruction G. Sheu raise the direct bilirubin fraction, although the indirect fraction also increases somewhat. Both intrahepatic andA.extrahepatic ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Because direct bilirubin is water soluble, bilirubinuria develops. With complete extrahepatic obstruction, the total bilirubin rises to a plateau of 2530 mg/dL, at which point loss in the urine equals the additional daily production. Higher values suggest concomitant hemolysis or decreased renal the jaundice in hemolysis is acholuric. The total bilirubin in hemolysis rarely exceeds 45 mg/dL because the rate of excretion increases as the bilirubin EUROPEAN UNIVERSITY CYPRUS concentration rises and a plateau is quickly reached. Greater values suggest concomitant hepatic parenchymal disease. Access Provided by: Jaundice due to hepatic parenchymal disease is characterized by elevations of both conjugated and unconjugated serum bilirubin. An increase in the conjugated fraction always signifies disease within the hepatobiliary system. The direct bilirubin predominates in about half of cases of hepatic parenchymal disease. Both intrahepatic cholestasis and extrahepatic obstruction raise the direct bilirubin fraction, although the indirect fraction also increases somewhat. Because direct bilirubin is water soluble, bilirubinuria develops. With complete extrahepatic obstruction, the total bilirubin rises to a plateau of 2530 mg/dL, at which point loss in the urine equals the additional daily production. Higher values suggest concomitant hemolysis or decreased renal function. Obstruction of a single hepatic duct does not usually cause jaundice. In extrahepatic obstruction caused by neoplasms, the serum bilirubin usually exceeds 10 mg/dL, and the average concentration is about 18 mg/dL. Obstructive jaundice due to common duct stones often produces transient bilirubin increases in the range of 24 mg/dL, and the level rarely exceeds 15 mg/dL. Serum bilirubin values in patients with alcoholic cirrhosis and acute viral hepatitis vary widely in relation to the severity of the parenchymal damage. In extrahepatic obstruction, modest rises of aspartate aminotransferase (AST) levels are common, but levels as high as 1000 units/L are seen (although rarely) in patients with common duct stones and cholangitis. In the latter patients, the high values last for only a few days and are associated with increases in lactate dehydrogenase (LDH) concentrations. In general, AST levels above 1000 units/L suggest viral hepatitis. Serum alkaline phosphatase comes from three sites: liver, bone, and intestine. In normal subjects, liver and bone contribute about equally, and the intestinal contribution is small. Hepatic alkaline phosphatase is a product of the epithelial cells of the cholangioles, and increased alkaline phosphatase levels associated with liver disease result from increased enzyme production. Alkaline phosphatase levels increase with intrahepatic cholestasis, cholangitis, or extrahepatic obstruction. Because the elevation is from overproduction, it may occur with focal hepatic lesions in the absence of jaundice. For example, a solitary hepatic metastasis or pyogenic abscess in one lobe or a tumor obstructing only one hepatic duct may fail to obstruct enough hepatic parenchyma to cause jaundice but usually is associated with increased alkaline phosphatase. In cholangitis with incomplete extrahepatic obstruction, serum bilirubin levels may be normal or mildly elevated, but serum alkaline phosphatase may be very high. Bone disease may complicate the interpretation of abnormal alkaline phosphatase levels (Figure 27–6). If one suspects that the increased serum enzyme may be from bone, serum calcium, phosphorus, and 5′nucleotidase or leucine aminopeptidase levels should be determined. These last two enzymes are also produced by cholangioles and are elevated in cholestasis, but their serum concentrations remain unchanged with bone disease. Figure 27–6. Range of alkaline phosphatase values in various hepatobiliary disorders. Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Page 8 / 32 enzymes are also produced by cholangioles and are elevated in cholestasis, but their serum concentrations remain unchanged with bone disease. EUROPEAN UNIVERSITY CYPRUS Figure 27–6. Access Provided by: Range of alkaline phosphatase values in various hepatobiliary disorders. Changes in serum protein levels may reflect hepatic parenchymal dysfunction. In cirrhosis, the serum albumin falls and the globulins increase. Serum globulins reach high values in some patients with primary biliary cirrhosis. Biliary obstruction generally produces no changes unless secondary biliary cirrhosis has developed. Diagnosis The principal diagnostic objective is to distinguish surgical (obstructive) from nonsurgical jaundice. The history, physical examination, and basic laboratory data allow an accurate diagnosis to be made in most cases without invasive tests. Most patients with jaundice are not critically ill when first examined; thus, diagnosis and therapy may be conducted in a stepwise fashion. However, severe or worsening cholangitis requires urgent intervention. If the jaundice is mild and recent, it often passes within 2448 hours, at which time adjunct tests can be ordered to verify gallstone disease. A comprehensive discussion of available imaging modalities is found in the following sections. In patients with persistent jaundice, the first test is usually an abdominal ultrasound to allow for assessment of ductal dilation and cholelithiasis. Lesions may be further delineated by magnetic resonance cholangiopancreatography (MRCP), ERCP, endoscopic ultrasound (EUS), or THC. ERCP is preferable when the lower end of the duct is believed to be obstructed or if the presence of choledocholithiasis is likely. THC is usually preferred for proximal lesions because it gives better opacification of the ducts proximal to the obstruction and therefore provides more information that can be used in planning surgery. If the clinical presentation suggests neoplastic obstruction, magnetic resonance imaging (MRI) or multiphase, thinslice CT scan will allow improved definition of the mass, surrounding structures, and general location of bile duct obstruction. DIAGNOSTIC EXAMINATION OF THE BILIARY TREE Abdominal Ultrasound Due to its low risk and high sensitivity and specificity, transabdominal ultrasonography is the primary adjunct test of choice for the detection of cholelithiasis and cholecystitis and evaluation for bile duct dilation. Cholecystitis is suggested by distension of the gallbladder, the presence of stones, pericholecystic edema, and the presence of a sonographic Murphy sign. In the investigation of gallbladder disease, falsepositive diagnoses for stones Downloaded 2024131 5:56 A Your IP is 82.116.202.56 are rare, and falsenegative reports due to small stones or a contracted gallbladder occur in only 5% of patients examined by realtime ultrasound. Page 9 / 32 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu Ultrasound usually misses stones in the common duct, but aPrivacy dilated Policy common bile duct can hint toward the presence of choledocholithiasis and ©2024 McGraw Hill. All Rights Reserved. Terms of Use Notice Accessibility suggest the need for further intervention or imaging to confirm the presence of choledocholithiasis. Abdominal Ultrasound EUROPEAN UNIVERSITY CYPRUS Access Provided by: Due to its low risk and high sensitivity and specificity, transabdominal ultrasonography is the primary adjunct test of choice for the detection of cholelithiasis and cholecystitis and evaluation for bile duct dilation. Cholecystitis is suggested by distension of the gallbladder, the presence of stones, pericholecystic edema, and the presence of a sonographic Murphy sign. In the investigation of gallbladder disease, falsepositive diagnoses for stones are rare, and falsenegative reports due to small stones or a contracted gallbladder occur in only 5% of patients examined by realtime ultrasound. Ultrasound usually misses stones in the common duct, but a dilated common bile duct can hint toward the presence of choledocholithiasis and suggest the need for further intervention or imaging to confirm the presence of choledocholithiasis. The ultrasonographer occasionally reports that the gallbladder contains “sludge.” This material is sonographically opaque, does not cast an acoustic shadow, and forms a dependent layer in the gallbladder. On clinical analysis, it is a fine precipitate of calcium bilirubinate. Sludge may accompany gallstone disease or may be a solitary finding. It is observed in a variety of clinical settings, many of which are characterized by gallbladder stasis. By itself, sludge is not an indication for cholecystectomy. Abdominal Computed Tomography Patients presenting with abdominal pain with an unclear history and leukocytosis are often sent for abdominal CT. Although this is not the imaging modality of choice for evaluation of the gallbladder or biliary tree, it does have good specificity and sensitivity for the detection of acute cholecystitis. For the evaluation of the patient with persistent jaundice, it allows for superior detection of pancreatic and distal obstructive pathology. Radionuclide Scan (Hepatobiliary Iminodiacetic Acid Scan) Technetium99m–labeled derivatives of iminodiacetic acid (IDA) are excreted in high concentration in bile and produce excellent gamma camera images. Following intravenous injection of the radionuclide, imaging of the bile ducts and gallbladder normally appears within 1530 minutes and imaging of the intestine within 60 minutes. In patients with acute right upper quadrant pain and tenderness, a good image of the bile duct accompanied by no image of the gallbladder indicates cystic duct obstruction and strongly supports a diagnosis of acute cholecystitis. The test is easy to perform and is occasionally a useful method of confirming this diagnosis in patients with equivocal history and imaging for acute cholecystitis. In addition, if biliary dyskinesia is suspected, a hepatobiliary IDA (HIDA) scan can be used to measure the gallbladder ejection fraction after CCK stimulation. Finally, HIDA scanning is useful in the postcholecystectomy patient to diagnose a biliary leak, although the scan usually lacks the fidelity to determine the exact location of the leak. Magnetic Resonance Cholangiopancreatography MRCP and ERCP are the two most sensitive (approximately 90% for MRCP and near 100% for ERCP) and specific (approximately 90% for MRCP and 100% for ERCP) modalities for the evaluation of choledocholithiasis. MRCP has resolution to detect stones as small as 2 mm. In patients in whom choledocholithiasis is highly likely, forgoing MRCP for ERCP is prudent because ERCP affords the opportunity for intervention. However, if the diagnosis is in question, MRCP offers the advantage of being noninvasive, without the risk of ERCPrelated complications such as pancreatitis, bleeding, or perforation. Endoscopic Retrograde Cholangiopancreatography ERCP involves cannulating the sphincter of Oddi under direct vision through a sideviewing duodenoscope. It requires special training involving more than familiarity with the use of fiberoptic endoscopes. Usually it is possible to opacify the pancreatic and bile ducts. It is the preferred method of examining the biliary tree in patients with presumed choledocholithiasis or obstructing lesions in the periampullary region and provides access for therapeutic intervention. Endoscopic Ultrasound Using specialized echoendoscopes, EUS allows highresolution imaging of the biliary tree, pancreas, and stomach. EUS can be used to guide biopsy as well as more advanced interventions. For choledocholithiasis, EUS has a sensitivity of 89%94% and a specificity of 94%95%. For small stones in particular, EUS may be more sensitive than MRCP. If choledocholithiasis is detected on EUS, therapeutic ERCP can be immediately performed. Percutaneous Transhepatic Cholangiography Percutaneous THC is performed by passing a fine needle through the right lower rib cage and the hepatic parenchyma and into the lumen of a bile duct. Watersoluble contrast material is injected, and fluoroscopy is performed. Downloaded 2024131 5:56 A Your IP is 82.116.202.56 The technical success is related degree of G. dilatation Page 10 / 32 Chapter 27: Biliary Tract, DavidtoA.the Harris; Eric Sheu of the intrahepatic bile ducts. THC is especially valuable in demonstrating the biliary ©2024 McGraw Hill.with All Rights Termsmalignant of Use Privacy Notice bile Accessibility anatomy in patients benignReserved. biliary strictures, lesions Policy of the proximal duct, or when ERCP has been unsuccessful. Patients should be premedicated with antibiotics regardless of whether they have cholangitis—septic shock has been produced by sudden inoculation of organisms from bile into the systemic circulation. Otherwise, the contraindications are the same as for percutaneous liver biopsy. particular, EUS may be more sensitive than MRCP. If choledocholithiasis is detected on EUS, therapeutic ERCP can be immediately performed. EUROPEAN UNIVERSITY CYPRUS Percutaneous Transhepatic Cholangiography Access Provided by: Percutaneous THC is performed by passing a fine needle through the right lower rib cage and the hepatic parenchyma and into the lumen of a bile duct. Watersoluble contrast material is injected, and fluoroscopy is performed. The technical success is related to the degree of dilatation of the intrahepatic bile ducts. THC is especially valuable in demonstrating the biliary anatomy in patients with benign biliary strictures, malignant lesions of the proximal bile duct, or when ERCP has been unsuccessful. Patients should be premedicated with antibiotics regardless of whether they have cholangitis—septic shock has been produced by sudden inoculation of organisms from bile into the systemic circulation. Otherwise, the contraindications are the same as for percutaneous liver biopsy. Intraoperative Imaging Patients with cholecystitis and equivocal imaging or laboratory testing can undergo intraoperative imaging to assess for common bile duct stones. Intraoperative cholangiogram (IOC) is performed by direct cannulation of the cystic duct or gallbladder infundibulum during laparoscopic or open cholecystectomy. Contrast material is injected through the cannulation, and fluoroscopy is used to assess for common bile duct stones. Stones present in the duct can sometimes be cleared by flushing and glucagon administration to promote relaxation of the sphincter of Oddi. Some have recommended routine use of IOC as a means to limit and detect bile duct injuries during cholecystectomy. During routine use of IOC, 2%10% of patients will have a common bile duct stone, 10% of which will not have been suspected preoperatively, and the majority of incidentally detected common bile duct stones will pass spontaneously without clinical sequelae. Intraoperative ultrasound is another imaging modality that can be performed to define biliary and vascular anatomy and has a high sensitivity and specificity for the detection of common bile duct stones. However, unlike IOC, ultrasound does not afford the ability to intervene upon any identified pathology. The learning curve for this modality is steep, with upward of 100 cases needed for mastery. DISEASES OF THE GALLBLADDER & BILE DUCTS ASYMPTOMATIC GALLSTONES Data on the prevalence of gallstones in the United States indicate that only about 30% of people with cholelithiasis come to surgery. Symptoms of gallstone disease generally do not change in severity. Each year, about 2% of patients with asymptomatic gallstones develop symptoms, usually biliary colic rather than one of the complications of gallstone disease. Patients with chronic biliary colic tend to have symptoms of the same level of severity and frequency. The present practice of operating only on symptomatic patients, leaving the millions without symptoms alone, seems appropriate. A question is often raised about what to advise the asymptomatic patient found to have gallstones during the course of unrelated studies. The presence of the following portends a more serious course and should probably serve as a reason for consideration of prophylactic cholecystectomy in the asymptomatic patient: (1) large stones (> 1 cm in diameter), because they progress to symptomatic disease more often than small stones; (2) calcified gallbladder, as it may be associated with carcinoma; and (3) enlarging or > 1 cm gallbladder polyps, given the potential risk of malignancy. However, most asymptomatic patients have no special features. If coexistent cardiopulmonary or other problems increase the risk of surgery, operation should not be considered. For the average asymptomatic patient, it is not reasonable to make a strong recommendation for cholecystectomy. The tendency, however, is to operate on younger patients and temporize in the elderly. BILIARY DYSKINESIA Patients with histories consistent with biliary colic, but in the absence of stone disease may have a functional gallbladder disorder. Typically, after an overnight fast, a HIDA scan in the presence of CCK is performed over a 45minute period. A gallbladder ejection fraction less than 40% is considered evidence of gallbladder dyskinesia. Reproduction of symptoms with administration of CCK may also support the diagnosis of biliary dyskinesia. False positives are seen in patients on opioids, with diabetes, and on calcium channel blockers, oral contraceptives, or other medications. In patients with recurring, biliarytype pain and a HIDACCK test consistent with dyskinesia, cholecystectomy may be beneficial. GALLSTONES & CHRONIC CHOLECYSTITIS (BILIARY COLIC) ESSENTIALS OF DIAGNOSIS Episodic abdominal pain Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Dyspepsia Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Gallstones on cholecystography or ultrasound scan Page 11 / 32 evidence of gallbladder dyskinesia. Reproduction of symptoms with administration of CCK may also support the diagnosis of biliary dyskinesia. False positives are seen in patients on opioids, with diabetes, and on calcium channel blockers, oral contraceptives, or other medications. In patients with EUROPEAN UNIVERSITY CYPRUS recurring, biliarytype pain and a HIDACCK test consistent with dyskinesia, cholecystectomy may be beneficial. Access Provided by: GALLSTONES & CHRONIC CHOLECYSTITIS (BILIARY COLIC) ESSENTIALS OF DIAGNOSIS Episodic abdominal pain Dyspepsia Gallstones on cholecystography or ultrasound scan General Considerations Chronic cholecystitis is the most common form of symptomatic gallbladder disease and is associated with gallstones in nearly every case. In general, the term cholecystitis is applied whenever gallstones are present regardless of the histologic appearance of the gallbladder. Repeated minor episodes of obstruction of the cystic duct cause intermittent biliary colic and contribute to inflammation and subsequent scar formation. Gallbladders from symptomatic patients with gallstones who have never had an attack of acute cholecystitis are of two types: (1) In some, the mucosa may be slightly flattened, but the wall is thin and unscarred and, except for the stones, appears normal. (2) Others exhibit obvious signs of chronic inflammation, with thickening, cellular infiltration, loss of elasticity, and fibrosis. The clinical history in these two groups cannot always be distinguished, and inflammatory changes may also be found in patients with asymptomatic gallstones. Clinical Findings A. Symptoms and Signs Biliary colic, the most characteristic symptom, is caused by transient gallstone obstruction of the cystic duct. The pain usually begins abruptly and subsides gradually, lasting for a few minutes to several hours. The pain of biliary colic is usually steady—not intermittent, like that of intestinal colic. In some patients, attacks occur postprandially; in others, there is no relationship to meals. The frequency of attacks is quite variable, ranging from nearly continuous trouble to episodes many years apart. Nausea and vomiting may accompany the pain. Biliary colic is usually felt in the right upper quadrant, but epigastric and left abdominal pain are common, and some patients experience precordial pain. The pain may radiate around the costal margin into the back or may be referred to the region of the scapula. Pain on top of the shoulder is unusual and suggests direct diaphragmatic irritation. During an attack, there may be tenderness in the right upper quadrant, and rarely, the gallbladder is palpable. Fatty food intolerance, dyspepsia, indigestion, heartburn, flatulence, and nausea are other symptoms associated with gallstone disease. Because they are also frequent in the general population, their presence in any given patient may only be incidental to the gallstones. B. Laboratory Findings An ultrasound of the gallbladder should usually be the first test. Gallstones can be demonstrated in about 95% of cases, and a positive reading for gallstones is rarely in error. About 2% of patients with gallstone disease have normal ultrasound studies. Differential Diagnosis Gallbladder colic may be strongly suggested by the history, but the clinical impression should always be verified by an ultrasound study. Biliary colic may simulate the pain of duodenal ulcer, hiatal hernia, pancreatitis, and myocardial infarction. It has been suggested that biliary colic may sometimes aggravate cardiac disease, but angina pectoris or an abnormal electrocardiogram (ECG) should rarely be indications for cholecystectomy. Rightsided radicular pain in the T6T10 dermatomes may be confused with biliary colic. Osteoarthritic spurs, vertebral lesions, or tumors may be shown on xrays of the spine or may be suggested by hyperesthesia of the abdominal skin. A search for esophageal spasm, hiatal hernia, peptic ulcer, or gastric tumors may be warranted. In some patients, an irritable colon syndrome may be mistaken for gallbladder discomfort. Carcinoma of the cecum or ascending colon may be overlooked on the assumption that postprandial pain in these conditions is due to gallstones. Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Complications Page 12 / 32 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Chronic cholecystitis predisposes to acute cholecystitis, common duct stones, and adenocarcinoma of the gallbladder. The longer the stones have been present, the higher is the incidence of all of these complications. Complications are infrequent, however, and the presence of gallstones is not Rightsided radicular pain in the T6T10 dermatomes may be confused with biliary colic. Osteoarthritic spurs, vertebral lesions, or tumors may be shown on xrays of the spine or may be suggested by hyperesthesia of the abdominal skin. EUROPEAN UNIVERSITY CYPRUS Access Provided by: A search for esophageal spasm, hiatal hernia, peptic ulcer, or gastric tumors may be warranted. In some patients, an irritable colon syndrome may be mistaken for gallbladder discomfort. Carcinoma of the cecum or ascending colon may be overlooked on the assumption that postprandial pain in these conditions is due to gallstones. Complications Chronic cholecystitis predisposes to acute cholecystitis, common duct stones, and adenocarcinoma of the gallbladder. The longer the stones have been present, the higher is the incidence of all of these complications. Complications are infrequent, however, and the presence of gallstones is not reason enough for prophylactic cholecystectomy in a person with asymptomatic or mildly symptomatic disease. Treatment A. Medical Treatment Avoidance of offending foods may be helpful. Dissolution with ursodiol is generally not recommended due to poor efficacy. B. Surgical Treatment Cholecystectomy is indicated in most patients with symptoms. The procedure can be scheduled at the patient’s convenience, within weeks or months after diagnosis. Active concurrent disease that increases the risk of surgery should be treated before operation. In some chronically ill patients, surgery should be deferred indefinitely. Cholecystectomy is most often performed laparoscopically, but when the laparoscopic approach is contraindicated or unsuccessful, it may be performed through a laparotomy. The difference consists of 4 fewer days in the hospital and fewer weeks off work when done laparoscopically. Regardless of how it is done, operative cholangiography may be included to evaluate for common duct stones. If stones are found, common duct exploration may be performed (see section on choledocholithiasis). Prognosis Serious complications and deaths related to the operation itself are rare. The operative death rate is about 0.1% in patients under age 50 and about 0.5% in patients over age 50. Most deaths occur in patients recognized preoperatively to have increased risks. The operation relieves symptoms in 95% of cases. The historical risk of common bile duct injury is roughly 0.4%. To reduce this catastrophic event, many societies have advocated safe surgical dissection in the form of the “critical view of safety.” The goal of this method is to identify the cystic duct and artery prior to division of any tubular structures. The critical view of safety is obtained by dissection of the lower third of the gallbladder free from the liver and identifying two, and only two, tubular structures between the gallbladder and the hepatoduodenal ligament. Studies have shown a reduction in common bile duct injury to 0%0.03%. Gurusamy KS, Koti R, Fusai G, et al: Early versus delayed laparoscopic cholecystectomy for uncomplicated biliary colic. Cochrane Database Syst Rev. 2013;6:CD007196. ACUTE CHOLECYSTITIS ESSENTIALS OF DIAGNOSIS Acute right upper quadrant pain and tenderness Fever and leukocytosis Palpable gallbladder in onethird of cases Sonographic Murphy sign with gallbladder distension, wall thickening, stones, pericholecystic fluid Nonopacified gallbladder on radionuclide excretion scan Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility General Considerations Page 13 / 32 In 80% of cases, acute cholecystitis results from obstruction of the cystic duct by a gallstone impacted in the Hartmann pouch. The gallbladder 2013;6:CD007196. EUROPEAN UNIVERSITY CYPRUS Access Provided by: ACUTE CHOLECYSTITIS ESSENTIALS OF DIAGNOSIS Acute right upper quadrant pain and tenderness Fever and leukocytosis Palpable gallbladder in onethird of cases Sonographic Murphy sign with gallbladder distension, wall thickening, stones, pericholecystic fluid Nonopacified gallbladder on radionuclide excretion scan General Considerations In 80% of cases, acute cholecystitis results from obstruction of the cystic duct by a gallstone impacted in the Hartmann pouch. The gallbladder becomes inflamed and distended, creating abdominal pain and tenderness. The natural history of acute cholecystitis varies, depending on whether the obstruction becomes relieved, the extent of secondary bacterial invasion, the age of the patient, and the presence of other aggravating factors such as diabetes mellitus. Most attacks resolve spontaneously without surgery or other specific therapy, but some progress to abscess formation or free perforation with generalized peritonitis. The pathologic changes in the gallbladder evolve in a typical pattern. Subserosal edema and hemorrhage and patchy mucosal necrosis are the first changes. Later, polymorphonuclear leukocytes appear. The final stage involves development of fibrosis. Gangrene and perforation may occur as early as 3 days after onset, but most perforations occur during the second week. In cases that resolve spontaneously, acute inflammation has largely cleared by 4 weeks, but some residual evidence of inflammation may last for several months. About 90% of gallbladders removed during an acute attack show chronic scarring, although many of these patients deny having had any previous symptoms. The cause of acute cholecystitis is still partially conjectural. Obstruction of the cystic duct is present in most cases, but in experimental animals, cystic duct obstruction does not result in acute cholecystitis unless the gallbladder is filled with concentrated bile or bile saturated with cholesterol. There is also evidence that trauma from gallstones releases phospholipase from the mucosal cells of the gallbladder. This is followed by conversion of lecithin in bile to lysolecithin, which is a toxic compound that may cause more inflammation. Bacteria have a minor role in the early stages of acute cholecystitis, even though most complications of the disease involve suppuration. Clinical Findings A. Symptoms and Signs The first symptom is abdominal pain in the epigastrium or right upper quadrant, sometimes associated with referred pain in the region of the right scapula. In 75% of cases, the patient will have had previous attacks of biliary colic, at first indistinguishable from the present illness. However, in acute cholecystitis, the pain persists and becomes associated with abdominal tenderness. Nausea and vomiting are present in about half of patients, but the vomiting is rarely severe. Mild icterus occurs in 10% of cases. The temperature usually ranges from 38°C to 38.5°C. High fever and chills are uncommon and should suggest the possibility of complications or an incorrect diagnosis. Right upper quadrant tenderness is present, and in about a third of patients, the gallbladder is palpable (often in a position lateral to its normal one). Voluntary guarding during examination may prevent detection of an enlarged gallbladder. In others, the gallbladder is not enlarged because scarring of the wall restricts distention. If instructed to breathe deeply during palpation in the right subcostal region, the patient experiences accentuated tenderness and sudden inspiratory arrest (Murphy sign). B. Laboratory Findings The leukocyte count is usually elevated, but normal counts are common. A mild elevation of the serum bilirubin (in the range of 24 mg/dL) is common, presumably due to secondary inflammation of the common duct by the contiguous gallbladder. Bilirubin values above this range would most likely indicate the associated presence of common duct stones. A mild increase in alkaline phosphatase may accompany the attack. Occasionally, the serum amylase concentration reaches units/dL or more. Downloaded 2024131transiently 5:56 A Your IP is 1000 82.116.202.56 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu ©2024 McGraw C. Imaging StudiesHill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Page 14 / 32 As stated earlier, right upper quadrant ultrasound is the imaging modality of choice. The presence of stones or sludge, thickening of the gallbladder B. Laboratory Findings EUROPEAN UNIVERSITY CYPRUS Access Provided by: The leukocyte count is usually elevated, but normal counts are common. A mild elevation of the serum bilirubin (in the range of 24 mg/dL) is common, presumably due to secondary inflammation of the common duct by the contiguous gallbladder. Bilirubin values above this range would most likely indicate the associated presence of common duct stones. A mild increase in alkaline phosphatase may accompany the attack. Occasionally, the serum amylase concentration transiently reaches 1000 units/dL or more. C. Imaging Studies As stated earlier, right upper quadrant ultrasound is the imaging modality of choice. The presence of stones or sludge, thickening of the gallbladder wall, pericholecystic edema, and a sonographic Murphy sign are consistent with acute cholecystitis. Usually, along with a careful history and physical exam, ultrasound is the only test needed to make the diagnosis of acute cholecystitis. If additional diagnostic information is desirable (eg, if ultrasound is equivocal or negative), a radionuclide excretion scan (eg, HIDA scan) should be performed. This test cannot demonstrate gallstones, but if the gallbladder is imaged, acute cholecystitis is ruled out except in rare cases of acalculous cholecystitis (see later section; the test is positive in most cases of acute acalculous cholecystitis). Imaging of the duct but not the gallbladder supports the diagnosis of acute cholecystitis. A few false positives are seen in advanced gallstone disease without acute inflammation and in acute biliary pancreatitis. The presence of an elevated bilirubin and a dilated common bile duct should suggest the presence of choledocholithiasis (see later in chapter). Differential Diagnosis The differential diagnosis includes other common causes of acute upper abdominal pain and tenderness. An acute peptic ulcer with or without perforation might be suggested by a history of epigastric pain relieved by food or antacids. Most cases of perforated ulcer demonstrate free air under the diaphragm on xray. An abdominal CT could provide more anatomic detail. Acute pancreatitis can be confused with acute cholecystitis, especially if cholecystitis is accompanied by an elevated lipase level. Furthermore, HIDA scans fail to outline the gallbladder in most cases of acute biliary pancreatitis. Sometimes the two diseases coexist, but pancreatitis should not be accepted as a second diagnosis without specific findings. Acute appendicitis in patients with a high cecum may closely simulate acute cholecystitis. Severe right upper quadrant pain with high fever and local tenderness may develop in acute gonococcal perihepatitis (FitzHughCurtis syndrome). Clues to the proper diagnosis may be found in tenderness in the adnexa, vaginal discharge that shows gonococci on a gramstained smear, and a disparity between the patient’s high fever and her general lack of toxicity. Complications The major complications of acute cholecystitis are empyema and perforation. A. Empyema In empyema (suppurative cholecystitis), the gallbladder contains frank pus, and the patient becomes more toxic, with high spiking fever (3940°C), chills, and leukocytosis greater than 15,000/μL. Parenteral antibiotics should be given, and percutaneous cholecystostomy or cholecystectomy should be performed. B. Perforation Perforation may take any of three forms: (1) localized perforation with pericholecystic abscess; (2) free perforation with generalized peritonitis; and (3) perforation into an adjacent hollow viscus, with the formation of a fistula. Perforation may occur as early as 3 days after the onset of acute cholecystitis or not until late in the second week. The total incidence of perforation is about 10%. 1. Pericholecystic abscess Pericholecystic abscess, the most common form of perforation, should be suspected when the signs and symptoms progress, especially when accompanied by the appearance of a palpable mass. The patient often becomes toxic, with fever to 39°C and a leukocyte count above 15,000/μL, but sometimes there is no correlation between the clinical signs and the development of local abscess. Cholecystectomy and drainage of the abscess can be performed safely in many of these patients, but if the patient’s condition is unstable, percutaneous cholecystostomy is preferable. Downloaded 2024131 5:56 A Your IP is 82.116.202.56 2. Free perforation Page 15 / 32 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Free perforation occurs in only 1%2% of patients, most often early in the disease when gangrene develops before adhesions wall off the gallbladder. The diagnosis is made preoperatively in less than half of cases. In some patients with localized pain, sudden spread of pain and tenderness to other EUROPEAN UNIVERSITY Pericholecystic abscess, the most common form of perforation, should be suspected when the signs and symptoms progress, especially whenCYPRUS Access Provided by: accompanied by the appearance of a palpable mass. The patient often becomes toxic, with fever to 39°C and a leukocyte count above 15,000/μL, but sometimes there is no correlation between the clinical signs and the development of local abscess. Cholecystectomy and drainage of the abscess can be performed safely in many of these patients, but if the patient’s condition is unstable, percutaneous cholecystostomy is preferable. 2. Free perforation Free perforation occurs in only 1%2% of patients, most often early in the disease when gangrene develops before adhesions wall off the gallbladder. The diagnosis is made preoperatively in less than half of cases. In some patients with localized pain, sudden spread of pain and tenderness to other parts of the abdomen suggests the diagnosis. Whenever it is suspected, free perforation must be treated by emergency laparotomy. Abdominal paracentesis may be misleading and has proved to be of little diagnostic usefulness. Cholecystectomy should be performed if the patient’s condition will permit; otherwise, cholecystostomy is done. The death rate depends partly on whether the cystic duct remains obstructed or the stone becomes dislodged after perforation. The former leads to a purulent peritonitis that is lethal in 20% of cases. In the latter, a true bile peritonitis ensues and over 50% of patients die. The earlier source control is achieved, the better is the prognosis. 3. Cholecystenteric fistula If the acutely inflamed gallbladder becomes adherent to adjacent stomach, duodenum, or colon and necrosis develops at the site of one of these adhesions, perforation may occur into the lumen of the gut. The resulting decompression often allows the acute disease to resolve. If the gallbladder stones discharge through the fistula and if they are large enough, they may obstruct the small intestine (gallstone ileus; see later section). Rarely, patients vomit gallstones that have entered the stomach through a cholecystogastric fistula. In most patients, the acute attack subsides and the cholecystenteric fistula is clinically unsuspected. Fistulas arising from gallstones must be differentiated from those caused by perforated peptic ulcers. Cholecystenteric fistulas do not usually cause symptoms unless the gallbladder is still partially obstructed by stones or scarring. Malabsorption and steatorrhea have been reported in isolated cases of cholecystocolonic fistulas. Steatorrhea in this situation could be due either to absence of bile in the proximal bowel following diversion into the colon or, more rarely, to excess bacteria in the upper intestine. An upper gastrointestinal series or abdominal CT may delineate the fistula, but often, the fistula will be found intraoperatively. Treatment The two mainstays of therapy for acute cholecystitis are antibiotics and biliary decompression (Figure 27–7). Intravenous fluids should be given to correct dehydration and electrolyte imbalance. Antibiotics directed against enteric gramnegative rods and anaerobes should be given. Single therapy with piperacillintazobactam or imipenem or dual therapy with ceftriaxone plus metronidazole or ciprofloxacin plus metronidazole are appropriate options. Choice of antibiotics should account for known patient or regionspecific bacterial resistance patterns. Figure 27–7. Schema for the management of acute cholecystitis. CBC, complete blood count; ERCP, endoscopic retrograde cholangiopancreatography; HIDA, hepatobiliary iminodiacetic acid; LFTs, liver function tests; MRCP, magnetic resonance cholangiopancreatography; PTC, percutaneous transhepatic cholangiography; RUQ, right upper quadrant; US, ultrasound. The timing and approach to biliary decompression is dependent upon establishment of the diagnosis, the length of disease at presentation, and the patient’s preexisting health to undergo surgery. In patients who are reasonablerisk surgical candidates presenting early in their disease course (2472 Downloaded 2024131 5:56 of A treatment Your IP isis82.116.202.56 hours), the preferred method laparoscopic cholecystectomy. Four controlled trials have supported this approach with the following Page 16 / 32 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu data: (1)McGraw the incidence technical complications noUse greater with early surgery; (2) early surgery reduces the total duration of illness by ©2024 Hill. AllofRights Reserved. Termsisof Privacy Policy Notice Accessibility approximately 30 days, length of hospitalization by 57 days, and direct medical costs by several thousand dollars; and (3) the death rate is slightly lower with early surgery because of earlier treatment for some patients whose condition would have worsened during expectant management. EUROPEAN UNIVERSITY CYPRUS Access Provided by: The timing and approach to biliary decompression is dependent upon establishment of the diagnosis, the length of disease at presentation, and the patient’s preexisting health to undergo surgery. In patients who are reasonablerisk surgical candidates presenting early in their disease course (2472 hours), the preferred method of treatment is laparoscopic cholecystectomy. Four controlled trials have supported this approach with the following data: (1) the incidence of technical complications is no greater with early surgery; (2) early surgery reduces the total duration of illness by approximately 30 days, length of hospitalization by 57 days, and direct medical costs by several thousand dollars; and (3) the death rate is slightly lower with early surgery because of earlier treatment for some patients whose condition would have worsened during expectant management. In about 30% of cases, the diagnosis of acute cholecystitis is established but the general condition of the patient is unsatisfactory. If possible, surgery should be postponed in these cases until the ancillary disease is controlled. Percutaneous cholecystostomy can be performed in patients whose comorbidities preclude surgery. A catheter is inserted under ultrasound or CT guidance to decompress and drain the gallbladder of bile and/or pus. Along with antibiotics, cholecystostomy controls the acute disease, including any local infection, but the gallstones are not removed. Therefore, cholecystectomy should be considered to prevent recurrent disease once the patient recovers and attendant comorbidities are optimized. Alternatively, in nontoxic patients with less severe disease, cholecystitis can be temporized with antibiotics (60% success rate) alone, and an interval cholecystectomy can be performed after medical optimization. However, failure to promptly improve with antibiotics should lead to consideration of cholecystostomy or cholecystectomy. Prognosis The overall death rate of acute cholecystitis is about 5%. Nearly all of the deaths are in patients over age 60 or those with diabetes mellitus. In the older age group, secondary cardiovascular or pulmonary complications contribute substantially to the death rate. Uncontrolled sepsis with peritonitis and intrahepatic abscesses are the most important local conditions responsible for death. Common duct stones are present in about 15% of patients with acute cholecystitis, and some of the more seriously ill patients have simultaneous cholangitis from biliary obstruction. Acute pancreatitis may also complicate acute cholecystitis, and the combination carries a greater risk. Patients who develop the suppurative forms of gallbladder disease such as empyema or perforation are less likely to recover (Figure 27–8). Earlier admission to the hospital and early cholecystectomy reduce the chances of these complications. Figure 27–8. The natural history of gallbladder stones. The numbers approximate the percentage of patients in each category. Note that most patients with acute cholecystitis have previously had biliary colic. Gurusamy KS, Rossi M, Davidson BR: Percutaneous cholecystostomy for highrisk surgical patients with acute calculous cholecystitis. Cochrane Database Syst Rev. 2013;8:CD007088. Downloaded 2024131 5:56 AT,Your is 82.116.202.56 Okamoto K, Suzuki K, Takada et al:IPTokyo Guidelines 2018: flowchart for the management of acute cholecystitis. J Hepatobiliary Pancreat Sci. Page 17 / 32 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu 2018;25:55–72. 29045062] ©2024 McGraw[PubMed: Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility EUROPEAN UNIVERSITY CYPRUS Access Provided by: Gurusamy KS, Rossi M, Davidson BR: Percutaneous cholecystostomy for highrisk surgical patients with acute calculous cholecystitis. Cochrane Database Syst Rev. 2013;8:CD007088. Okamoto K, Suzuki K, Takada T, et al: Tokyo Guidelines 2018: flowchart for the management of acute cholecystitis. J Hepatobiliary Pancreat Sci. 2018;25:55–72. [PubMed: 29045062] ACALCULOUS CHOLECYSTITIS Acute cholecystitis can occur in the absence of cholelithiasis (acalculous cholecystitis). Some of these cases are due to cystic duct obstruction by another process such as a malignant tumor. More cases of acalculous cholecystitis result from primary bacterial infection by Escherichia coli, clostridia, or, occasionally, Salmonella typhi. Most cases occur in patients hospitalized with some other critical illness. Diagnosis is usually made after fever workup in otherwise critical patients reveals evidence for cholecystitis. Due to the nature of patients with this diagnosis, antecedent symptoms of disease are rare, save for a new fever and leukocytosis. Acute acalculous cholecystitis is particularly common in trauma victims, in patients receiving total parenteral nutrition, and in patients with other critical illness. Smallvessel occlusion occurs early, and unless treatment is given promptly, the disease progresses rapidly to gangrenous cholecystitis and septic complications, at which point the death rate is high. Antibiotics and biliary drainage via percutaneous cholecystostomy are the treatment modalities of choice. EMPHYSEMATOUS CHOLECYSTITIS Emphysematous cholecystitis is a rare condition in which bubbles of gas from anaerobic infection appear in the lumen of the gallbladder, its wall, the pericholecystic space, and, on occasion, the bile ducts. Clostridia species are the most commonly implicated organisms, but other gasforming anaerobes such as E coli or anaerobic streptococci may be found. Three times as many men as women are affected, and 20% of patients have diabetes mellitus. In contrast to the usual form of acute cholecystitis, the disease probably is a bacterial infection from the earliest moment. In many cases, the gallbladder contains no stones. The disease begins with sudden and rapidly progressive right upper quadrant pain. Fever and leukocytosis reach high levels quickly, and the patient is considerably more toxic than is usually the case in acute cholecystitis. On examination, a mass can usually be found in the right upper quadrant. The patient should be treated with antibiotics effective against clostridia and the other species mentioned earlier. Emergency surgical treatment should follow the initial resuscitative measures. Cholecystectomy can be safely performed in most cases, but the most critically ill might fare better with cholecystostomy. The types of complications are the same as in other forms of acute cholecystitis, but illness is more severe and death rates are higher. GALLSTONE ILEUS Gallstone ileus is mechanical intestinal obstruction caused by a large gallstone lodged in the ileal lumen. It occurs more often in women, and the average patient age is about 70 years. Clinical Findings A. Symptoms The patient usually presents with obvious small bowel obstruction, either partial or complete. The obstructing gallstone enters the intestine through a cholecystenteric fistula located in the duodenum, colon, or, rarely, the stomach or jejunum. The gallbladder may contain one or several stones, but stones that cause gallstone ileus are almost always 2.5 cm or more in diameter. The lumen in the proximal bowel will allow most of these large calculi to pass caudally until the ileum is reached. Obstruction of the large intestine may follow passage of a gallstone through a fistula at the hepatic flexure or may occur even after the stone has traversed the entire small bowel. B. Signs In most patients, the findings on physical examination are typical of distal small bowel obstruction. Obstruction of the duodenum or jejunum may give a perplexing clinical picture because of the lack of distention. Right upper quadrant tenderness and a mass may be present in some cases, but the distended abdomen may5:56 be difficult toIP examine accurately. Downloaded 2024131 A Your is 82.116.202.56 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu C. Imaging StudiesHill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility ©2024 McGraw Page 18 / 32 In addition to dilated small intestine, abdominal CT scan with oral and intravenous contrast can show air within the biliary tree and a cholecystenteric B. Signs EUROPEAN UNIVERSITY CYPRUS Access Provided by: In most patients, the findings on physical examination are typical of distal small bowel obstruction. Obstruction of the duodenum or jejunum may give a perplexing clinical picture because of the lack of distention. Right upper quadrant tenderness and a mass may be present in some cases, but the distended abdomen may be difficult to examine accurately. C. Imaging Studies In addition to dilated small intestine, abdominal CT scan with oral and intravenous contrast can show air within the biliary tree and a cholecystenteric fistula. Treatment The proper treatment is emergency laparotomy or laparoscopy with removal of the obstructing stone through a small enterotomy. The proximal intestine must be carefully inspected for the presence of a second calculus that might cause a postoperative recurrence. The gallbladder should be left undisturbed at the original operation. Once the patient has recovered, an elective cholecystectomy should be scheduled if the patient complains of chronic gallbladder symptoms. On this basis, interval cholecystectomy will be required in about 30% of patients. The fistula itself is rarely the source of trouble and closes spontaneously in most patients. Prognosis The death rate from gallstone ileus remains about 20%, largely because of the poor general condition of elderly patients at the time of laparotomy. In many cases, the patient has developed cardiac or pulmonary complications during a preoperative delay when the diagnosis was unclear. CHOLEDOCHOLITHIASIS ESSENTIALS OF DIAGNOSIS Biliary pain Jaundice Episodic cholangitis Gallstones in gallbladder or previous cholecystectomy General Considerations Approximately 15% of patients with stones in the gallbladder harbor calculi within the bile ducts. Common duct stones are usually accompanied by others in the gallbladder, but in 5% of cases, the gallbladder is empty. The number of duct stones may vary from 1 to more than 100. There are two possible origins for common duct stones. The evidence suggests that most cholesterol stones develop within the gallbladder and reach the duct after traversing the cystic duct. These are called secondary stones. Pigment stones may have a similar pedigree or, more often, develop de novo within the common duct. These are called primary common duct stones. About 60% of common duct stones are cholesterol stones and 40% are pigment stones. The latter are, on average, associated with more severe clinical manifestations. Patients may have one or more of the following principal clinical findings, all of which are caused by obstruction to the flow of bile or pancreatic juice: biliary colic, cholangitis, jaundice, and pancreatitis (Figure 27–9). It seems, however, that as many as 50% of patients with choledocholithiasis remain asymptomatic. Figure 27–9. The natural history of common duct stones. Of every 100 patients with gallbladder stones, 15 will have common duct stones, which will produce the spectrum of syndromes illustrated. Note that the individual syndromes overlap, indicating that they may appear together in various combinations. Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Page 19 / 32 Figure 27–9. EUROPEAN UNIVERSITY CYPRUS Access Provided by: The natural history of common duct stones. Of every 100 patients with gallbladder stones, 15 will have common duct stones, which will produce the spectrum of syndromes illustrated. Note that the individual syndromes overlap, indicating that they may appear together in various combinations. The common duct may dilate to 23 cm proximal to an obstructing lesion, and truly huge ducts develop in patients with biliary tumors. In choledocholithiasis or biliary stricture, the inflammatory reaction restricts dilation, so the dilatation is less marked. Dilation of the ductal system within the liver can also be limited by cirrhosis. Biliary colic is the result of rapid rises in biliary pressure whether the block is in the common duct or neck of the gallbladder. Gradual occlusion of the duct—as in cancer—rarely produces the same kind of pain as gallstone disease. Clinical Findings A. Symptoms Choledocholithiasis may be asymptomatic or may produce sudden toxic cholangitis, leading to a rapid demise. The seriousness of the disease parallels the degree of obstruction, the length of time it has been present, and the extent of secondary bacterial infection (see later section on cholangitis). Biliary colic, jaundice, and pancreatitis may be isolated findings or may occur in any combination along with signs of cholangitis. Biliary colic from common duct obstruction cannot be distinguished from that caused by stones in the gallbladder. The pain is felt in the right subcostal region, epigastrium, or even the substernal area. Referred pain to the region of the right scapula is common. Choledocholithiasis should be strongly suspected if intermittent chills, fever, or jaundice accompanies biliary colic. Some patients notice transient darkening of their urine during an attack even though jaundice is not evident. Pruritus is usually the result of persistent longstanding obstruction. The itching is more intense in warm weather when the patient perspires and is usually worse on the extremities than on the trunk. It is much more common with neoplastic obstruction than with gallstone obstruction. B. Signs The patient may be icteric and toxic, with high fever and chills, or may appear to be perfectly healthy. A palpable gallbladder is unusual in patients with obstructive jaundice from common duct stone because the obstruction is transient and partial, and scarring of the gallbladder renders it inelastic and Downloaded 2024131 5:56 A Your IP is 82.116.202.56 nondistensible. Tenderness may be present in the right upper quadrant but is not often as marked as in acute cholecystitis, perforated peptic ulcer, or Page 20 / 32 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu acute pancreatitis. Tender hepatic enlargement may occur. ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility C. Laboratory Findings usually worse on the extremities than on the trunk. It is much more common with neoplastic obstruction than with gallstone obstruction. EUROPEAN UNIVERSITY CYPRUS B. Signs Access Provided by: The patient may be icteric and toxic, with high fever and chills, or may appear to be perfectly healthy. A palpable gallbladder is unusual in patients with obstructive jaundice from common duct stone because the obstruction is transient and partial, and scarring of the gallbladder renders it inelastic and nondistensible. Tenderness may be present in the right upper quadrant but is not often as marked as in acute cholecystitis, perforated peptic ulcer, or acute pancreatitis. Tender hepatic enlargement may occur. C. Laboratory Findings In cholangitis, leukocytosis of 15,000/μL is usual, and values above 20,000/μL are common. A rise in serum bilirubin often appears within 24 hours after the onset of symptoms. The absolute level usually remains under 10 mg/dL, and most levels are in the range of 24 mg/dL. The direct fraction exceeds the indirect, but the latter becomes elevated in most cases. Bilirubin levels do not ordinarily reach the high values seen in malignant tumors because the obstruction is usually incomplete and transient. The serum alkaline phosphatase level usually rises and may be the only chemical abnormality in patients without jaundice. When the obstruction is relieved, the alkaline phosphatase and bilirubin levels should return to normal within 12 weeks, with the exception that the former may remain elevated longer if the obstruction was prolonged. Mild increases in AST and alanine aminotransferase (ALT) are often seen with extrahepatic obstruction of the ducts. D. Imaging Studies Ultrasound will usually show gallbladder stones and, depending on the degree of obstruction, dilatation of the bile duct. Ultrasound and CT scans are insensitive in the search for stones in the common duct. Strong predictors of choledocholithiasis are cholangitis, bilirubin > 4 mg/dL, and a dilated common bile duct on ultrasound and are indications for ERCP. Intermediate evidence of choledocholithiasis warrants evaluation with intraoperative cholangiogram or ultrasound or preoperative MRCP. EUS is another sensitive technique for detection of choledocholithiasis and a costeffective technique to guide subsequent ERCP. Differential Diagnosis The workup should consider the same possibilities in the differential diagnosis as for cholecystitis. Elevated serum lipase levels are diagnostic of pancreatitis, which may be the result of choledocholithiasis in the appropriate clinical setting. Alcoholic cirrhosis or acute alcoholic hepatitis may present with jaundice, right upper quadrant tenderness, and leukocytosis. The differentiation from cholangitis may be impossible from clinical data. A history of a recent binge suggests acute liver disease. A percutaneous liver biopsy may be specific. Intrahepatic cholestasis from drugs, pregnancy, chronic active hepatitis, or primary biliary cirrhosis may be difficult to distinguish from extrahepatic obstruction. MRCP/ERCP would be appropriate to make the distinction, particularly if other studies (eg, ultrasound scan) failed to provide evidence of gallstone disease. If jaundice has persisted for 46 weeks, a mechanical cause is probable. Because most patients improve during this interval, persistent jaundice should never be assumed to be the result of parenchymal disease unless imaging rules out obstruction of the major ducts. Intermittent jaundice and cholangitis after cholecystectomy are compatible with biliary stricture or a retained common bile duct stone, and the distinction requires MRCP/ERCP. Biliary tumors usually produce intense jaundice without biliary colic or fever, and once it begins, the jaundice rarely remits. Complications Longstanding ductal infection can produce intrahepatic abscesses. Hepatic failure or secondary biliary cirrhosis may develop in unrelieved obstruction of long duration. Because the obstruction is usually incomplete and intermittent, cirrhosis develops only after several years in untreated disease. Acute pancreatitis, a fairly common complication of calculous biliary disease, is discussed in Chapter 28. In brief, patients should undergo supportive care for pancreatitis and undergo cholecystectomy with symptomatic improvement on the indexed operation. There is a nearly 25% recurrence of gallstone pancreatitis treated without cholecystectomy within the following 3 months. Rarely, a stone in the common duct may erode through the ampulla, resulting in gallstone ileus. Hemorrhage (hemobilia) is also a rare complication. Treatment 2024131 5:56 A Your IP is 82.116.202.56 Downloaded Page 21 / 32 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu PatientsMcGraw with acute be treated with systemic antibiotics other measures, as described in the following section, followed by ©2024 Hill.cholangitis All Rights should Reserved. Terms of Use Privacy Policy and Notice Accessibility urgent or emergent, depending on the patient’s condition, decompression of the bile duct through either endoscopic sphincterotomy or surgical common bile duct exploration. disease. Acute pancreatitis, a fairly common complication of calculous biliary disease, is discussed in Chapter 28. In brief, patients should undergo supportive care for pancreatitis and undergo cholecystectomy with symptomatic improvement on the indexed operation. ThereUNIVERSITY is a nearly 25% EUROPEAN CYPRUS recurrence of gallstone pancreatitis treated without cholecystectomy within the following 3 months. Access Provided by: Rarely, a stone in the common duct may erode through the ampulla, resulting in gallstone ileus. Hemorrhage (hemobilia) is also a rare complication. Treatment Patients with acute cholangitis should be treated with systemic antibiotics and other measures, as described in the following section, followed by urgent or emergent, depending on the patient’s condition, decompression of the bile duct through either endoscopic sphincterotomy or surgical common bile duct exploration. The typical patient presents with mild cholangitis and evidence on ultrasound scans of gallbladder stones. Laparoscopic cholecystectomy is indicated along with, depending on the experience of the surgeon, laparoscopic exploration of the common duct if an operative cholangiogram or laparoscopic ultrasound demonstrates the expected common duct stones. Laparoscopic common duct exploration is usually accomplished through the cystic duct (which may have to be dilated), but when the common duct is enlarged (> 1.5 cm), it may be accomplished through a choledochotomy incision, just as in open surgery. If the surgeon thinks the common duct stones cannot be removed laparoscopically, it is probably best to remove the gallbladder laparoscopically and the common duct stones by endoscopic sphincterotomy. If the stones cannot be removed by sphincterotomy, a second (open) operation may be necessary. To avoid the need for a second operation, ERCP to remove common duct stones may be considered prior to proceeding to the operating room for cholecystectomy. There is also a lack of consensus regarding the importance of operative cholangiography or ultrasound during cholecystectomy when there are no clues suggesting stones in the duct. In such cases, the chances of finding a stone are only 3%5%, and because many of these stones will pass spontaneously without clinical sequelae, some consider the effort unwarranted. However, operative cholangiograms also provide confirmation of the biliary anatomy, which contributes to avoidance of bile duct injuries and allows prompt treatment of those stones that would go on to cause symptoms. When the common duct is explored through the cystic duct and gallstones are removed, the cystic duct must be ligated, but a drainage catheter is not usually left within the common duct. When the common duct is explored through a choledochotomy (either during a laparoscopic or open operation), a T tube is usually left in the duct, and cholangiograms are taken a week or so postoperatively. Any residual stones discovered on these postoperative xrays can be extracted 46 weeks later through the T tube tract. Patients with common duct stones who have had a previous cholecystectomy are best treated by endoscopic sphincterotomy. Using a sideviewing duodenoscope, the ampulla is cannulated, and a 1cm incision is made in the sphincter with an electrocautery wire. The opening created in the sphincter permits stones to pass from the duct into the duodenum. Endoscopic sphincterotomy is less likely to be successful in patients with large stones (eg, > 2 cm), and it is contraindicated in the presence of stenosis of the bile duct proximal to the sphincter. In these cases, common duct exploration is required. Stones in the intrahepatic branches of the bile duct can usually be removed without difficulty during common duct exploration. In some cases, however, one or more of the intrahepatic ducts have become packed with stones, and the associated chronic inflammation has produced stenosis of the duct near its junction with the common hepatic duct. It is often impossible in these cases to clear the duct of stones, and if the disease involves only one lobe (usually the left lobe), hepatic lobectomy is indicated. ASGE Standards of Practice Committee: The role of endoscopy in the evaluation of suspected choledocholithiasis. Gastrointest Endosc. 2010;71:1–9. [PubMed: 20105473] CHOLANGITIS (BACTERIAL CHOLANGITIS) Bacterial infection of the biliary ducts always signifies biliary obstruction because, in the absence of obstruction, even heavy bacterial contamination of the ducts fails to produce symptoms or pathologic changes. The block to flow may be partial or, less commonly, complete. The principal causes are choledocholithiasis, biliary stricture, and neoplasm. Less common causes are chronic pancreatitis, ampullary stenosis, pancreatic pseudocyst, duodenal diverticulum, congenital cyst, and parasitic invasion. Iatrogenic cholangitis may complicate transhepatic or T tube cholangiography. Not all obstructing lesions are followed by cholangitis, however. For example, biliary infection develops in only 15% of patients with neoplastic obstruction. The likelihood of cholangitis is greatest when the obstruction occurs after the duct has acquired a resident bacterial population. With obstruction, ductal pressure rises, and bacteria proliferate and escape into the systemic circulation via the hepatic sinusoids. Experimentally, the incidence of positive blood cultures with ductal infection is directly proportionate to the absolute height of the pressure in the duct. Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Pagetriad 22 / is 32 Chapter 27: Biliary Tract, David A. Harris;referred Eric G.to Sheu The symptoms of cholangitis (sometimes as the Charcot triad) are biliary colic, jaundice, and chills and fever, although a complete ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility present in only 70% of cases. Laboratory findings include leukocytosis and elevated serum bilirubin and alkaline phosphatase levels. The predominant organisms in bile (in approximately decreasing frequency) are E coli, Klebsiella, Pseudomonas, enterococci, and Proteus. Bacteroides fragilis and other anaerobes (eg, Clostridium perfringens) can be detected in about 25% of cases, and their presence correlates with multiple previous biliary operations duodenal diverticulum, congenital cyst, and parasitic invasion. Iatrogenic cholangitis may complicate transhepatic or T tube cholangiography. Not all EUROPEAN UNIVERSITY CYPRUS obstructing lesions are followed by cholangitis, however. For example, biliary infection develops in only 15% of patients with neoplastic obstruction. Access Provided by: The likelihood of cholangitis is greatest when the obstruction occurs after the duct has acquired a resident bacterial population. With obstruction, ductal pressure rises, and bacteria proliferate and escape into the systemic circulation via the hepatic sinusoids. Experimentally, the incidence of positive blood cultures with ductal infection is directly proportionate to the absolute height of the pressure in the duct. The symptoms of cholangitis (sometimes referred to as the Charcot triad) are biliary colic, jaundice, and chills and fever, although a complete triad is present in only 70% of cases. Laboratory findings include leukocytosis and elevated serum bilirubin and alkaline phosphatase levels. The predominant organisms in bile (in approximately decreasing frequency) are E coli, Klebsiella, Pseudomonas, enterococci, and Proteus. Bacteroides fragilis and other anaerobes (eg, Clostridium perfringens) can be detected in about 25% of cases, and their presence correlates with multiple previous biliary operations (often including a biliary enteric anastomosis), severe symptoms, and a high incidence of postoperative suppurative complications. Anaerobes are nearly always seen in the company of aerobes. Two species of bacteria can be cultured in about 50% of cases. Bacteremia probably occurs in most cases, and blood cultures obtained at the appropriate time contain the same organisms as the bile. An ultrasound will often give useful diagnostic information suggestive of biliary obstruction. The term suppurative cholangitis has been used for the most severe form of this disease, when manifestations of sepsis overshadow those of hepatobiliary disease. The diagnostic pentad of suppurative cholangitis consists of abdominal pain, jaundice, fever and chills, mental confusion or lethargy, and shock. The diagnosis is often missed because the signs of biliary disease are overlooked. Most cases of cholangitis can be controlled with intravenous antibiotics, as stated earlier, followed by prompt ERCP with sphincterotomy and bile duct decompression. In the uncommon case where this is unsuccessful, laparotomy is indicated in order to decompress the bile duct through a formal common bile duct exploration or, in the most extreme instances, direct common bile duct decompression. Cholangitis accompanying neoplastic obstruction may be managed by insertion of a transhepatic drainage catheter into the bile duct. Miura F, Okamoto K, Takada T, et al: Tokyo Guidelines 2018: initial management of acute biliary infection and flowchart for acute cholangitis. J Hepatobiliary Pancreat Sci. 2018;25:31–40. [PubMed: 28941329] POSTCHOLECYSTECTOMY SYNDROME The term postcholecystectomy syndrome has been used to signify the heterogeneous group of disorders affecting patients who continue to complain of symptoms after cholecystectomy. It is not really a syndrome, and the term is confusing. The usual reason for incomplete relief after cholecystectomy is that the preoperative diagnosis of chronic cholecystitis was incorrect. The only symptom entirely characteristic of chronic cholecystitis is biliary colic. When a calculous gallbladder is removed in the hope that the patient will gain relief from dyspepsia, fatty food intolerance, belching, and other symptoms, the operation may leave the symptoms unchanged. The presenting symptom may be dyspepsia or pain. An organic cause for the symptoms is more likely to be discovered in patients with severe episodic pain than in those with other complaints. Abnormal liver function studies, jaundice, and cholangitis are other manifestations that indicate residual biliary disease. Patients with suspicious findings should be studied by MRCP, ERCP, or THC. Choledocholithiasis, biliary stricture, and chronic pancreatitis are the most common causes of symptoms. Occasionally, there is sufficient evidence to implicate sphincter of Oddi dysmotility as a cause of pain. Relief of pain may follow endoscopic sphincterotomy. Stenosis of the hepatobiliary ampulla, a long cystic duct remnant, and neuromas have been blamed for continued symptoms. CARCINOMA OF THE GALLBLADDER Carcinoma of the gallbladder is an uncommon neoplasm that occurs in elderly patients. It is associated with gallstones in 70% of cases, and the risk of malignant degeneration correlates with the length of time gallstones have been present. The tumor is twice as common in women as in men, as one would expect from the association with gallstones. Most primary tumors of the gallbladder are adenocarcinomas that appear histologically to be scirrhous (60%), papillary (25%), or mucoid (15%). Dissemination of the tumor occurs early by direct invasion of the liver and hilar structures and by metastases to the common duct lymph nodes, liver, and lungs. In an occasional case, where carcinoma is an incidental finding after cholecystectomy for gallstone disease, the tumor is confined to the gallbladder as a carcinoma in situ or an early invasive lesion. Most invasive carcinomas, however, have spread by the time of surgery, and spread is virtually certain if the tumor has progressed to the point where it causes symptoms. Clinical Findings Downloaded 2024131 5:56 A Your IP is 82.116.202.56 Chapter 27: Biliary Tract, David A. Harris; Eric G. Sheu A. Symptoms and Signs ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Page 23 / 32 The most common presenting complaint is of right upper quadrant pain similar to previous episodes of biliary colic but more persistent. Obstruction Dissemination of the tumor occurs early by direct invasion of the liver and hilar structures and by metastases to the common duct lymph nodes, liver, EUROPEAN UNIVERSITY CYPRUS and lungs. In an occasional case, where carcinoma is an incidental finding after cholecystectomy for gallstone disease, the tumor is confined to the Access Provided by: gallbladder as a carcinoma in situ or an early invasive lesion. Most invasive carcinomas, however, have spread by the time of surgery, and spread is virtually certain if the tumor has progressed to the point where it causes symptoms. Clinical Findings A. Symptoms and Signs The most common presenting complaint is of right upper quadrant pain similar to previous episodes of biliary colic but more persistent. Obstruction of the cystic duct by tumor sometimes ini

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