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Surgery_Schwartz. with right upper quadrant pain and tenderness, fever, and leukocytosis. In the sedated or unconscious patient, the clinical features are often masked, but fever and elevated WBC count, as well as eleva-tion of alkaline phosphatase and bilirubin, are indications for AIIIIIIEBFGCDFigure 32-25. Laparoscopic common bile duct exploration. I. Transcystic basket retrieval using fluoroscopy. A. The basket has been advanced past the stone and opened. B. The stone has been entrapped in the basket, and together, they are removed from the cystic duct. II. Transcystic choledochoscopy and stone removal. C. The basket has been passed through the working channel of the scope, and the stone is entrapped under direct vision. D. Entrapped stone. E. A view from the choledochoscope with stone captured in basket. III. Choledochotomy and stone removal. F. A small incision is made in the common bile duct. G. The common bile duct is cleared of stones.Brunicardi_Ch32_p1393-p1428.indd 141511/02/19 2:43 PM


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Surgery_Schwartz. III. Choledochotomy and stone removal. F. A small incision is made in the common bile duct. G. The common bile duct is cleared of stones.Brunicardi_Ch32_p1393-p1428.indd 141511/02/19 2:43 PM 1416SPECIFIC CONSIDERATIONSPART IIAIIIIIIBCDEFGFigure 32-26. Biliary enteric anastomoses. There are three types. I. Choledochoduodenostomy. A. The distal common bile duct is opened longitudinally, as is the duodenum. B. Interrupted sutures are placed between the common bile duct and the duodenum. C. Completed cho-ledochoduodenostomy. II. Choledochojejunostomy. D. The common bile duct and small bowel are divided. E. A limb of jejunum is brought up in a Roux-en-Y configuration and anastomosed to the bile duct. III. Hepaticojejunostomy. F. The entire extrahepatic biliary tree has been resected and the reconstruction completed with a Roux-en-Y limb of jejunum. G. Percutaneous transhepatic stents are placed across hepati-cojejunostomy (optional).Brunicardi_Ch32_p1393-p1428.indd 141611/02/19


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Surgery_Schwartz. the reconstruction completed with a Roux-en-Y limb of jejunum. G. Percutaneous transhepatic stents are placed across hepati-cojejunostomy (optional).Brunicardi_Ch32_p1393-p1428.indd 141611/02/19 2:43 PM 1417GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32further investigation. Ultrasonography is usually the diagnos-tic test of choice, as it can be done bedside in the intensive care unit. It can demonstrate the distended gallbladder with thickened wall, biliary sludge, pericholecystic fluid, and the presence or absence of abscess formation. CT scanning can aid in the diagnosis of acalculous cholecystitis and addition-ally allows a more general evaluation of the abdomen and chest to rule out other sources of infection. A HIDA scan can also be useful if it shows nonvisualization of the gallblad-der, but it is less sensitive and can have higher false-positive rates in patients who are in a prolonged fasting state, on total parenteral nutrition, or have liver disease. Once the


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Surgery_Schwartz. of the gallblad-der, but it is less sensitive and can have higher false-positive rates in patients who are in a prolonged fasting state, on total parenteral nutrition, or have liver disease. Once the diagnosis is confirmed, acalculous cholecystitis requires urgent inter-vention as rapid deterioration can occur. This should include early broad-spectrum antibiotics and fluid resuscitation. If the patient is stable to undergo an abdominal operation, lapa-roscopic cholecystectomy is the most definitive treatment, and it can be safely performed even in the setting of severe acute inflammation.64 However, if patients are critically ill and unfit for surgery, percutaneous cholecystostomy is the best treatment choice (see Fig. 32-18). About 90% of patients will improve with a percutaneous cholecystostomy tube. Interval cholecystectomy can be discussed with the patient after they have recovered from their acute illness, but it is not strictly required in the absence of gallstone or other


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Surgery_Schwartz. tube. Interval cholecystectomy can be discussed with the patient after they have recovered from their acute illness, but it is not strictly required in the absence of gallstone or other identi-fied gallbladder pathology.Choledochal (Biliary) CystsCholedochal cysts are congenital cystic dilatations of the extra-hepatic and/or intrahepatic biliary tree. They are rare, with an incidence of between 1:100,000 and 1:150,000 in populations of Western countries, but are more common in populations of Eastern countries occurring in as many as 1:1000 individuals. Choledochal cysts affect females three to eight times more often than males. Although frequently found in infancy or childhood, nearly one-half are diagnosed in adults. The cause is unknown, but it is believed that weakness of the bile duct wall and increased pressure secondary to partial biliary obstruction can contribute to biliary cyst formation. More than 90% of patients have an anomalous pancreaticobiliary duct junction, with the


Surgery_Schwartz

Surgery_Schwartz. wall and increased pressure secondary to partial biliary obstruction can contribute to biliary cyst formation. More than 90% of patients have an anomalous pancreaticobiliary duct junction, with the pancreatic duct joining the common bile duct outside the duode-nal wall, creating a long common channel (>1.5 cm). This may allow free reflux of pancreatic secretions into the biliary tract, leading to inflammatory changes, increased biliary pressure, and cyst formation. The cysts are lined with cuboidal epithelium and can vary in size from small dilations to giant cystic masses. The typical clinical triad of biliary cysts includes abdominal pain, jaundice, and a palpable mass, though this constellation is seen in less than one-half of patients. Adults may present with chol-angitis. Blood tests will often be normal though elevations of transaminases can be seen in cases of infection or obstruction. Ultrasonography or CT scanning will confirm the diagnosis, but ERCP or MRCP are essential to


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Surgery_Schwartz. will often be normal though elevations of transaminases can be seen in cases of infection or obstruction. Ultrasonography or CT scanning will confirm the diagnosis, but ERCP or MRCP are essential to formally assess the biliary anatomy and to plan the appropriate surgical treatment. The risk of cholangiocarcinoma in patients with choledochal cysts is 20to 30-fold higher than in the general population and varies with the patient’s age and type of cyst. For this reason, excision is recommended whenever possible when high-risk choledochal cysts are diagnosed.Choledochal cysts are classified into five types depend-ing on the location and structure of the cysts. The subcatego-ries of choledochal cysts are defined in Fig. 32-27. Type I cysts (fusiform CBD dilations) are the most common form, account-ing for approximately 50% of cases, and have the highest risk of malignancy (>60%). For types I and II (saccular diverticula of the common bile duct), excision of the cystic dilations in the


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Surgery_Schwartz. account-ing for approximately 50% of cases, and have the highest risk of malignancy (>60%). For types I and II (saccular diverticula of the common bile duct), excision of the cystic dilations in the extrahepatic biliary tree, including cholecystectomy, with either simple cyst excision or duct resection with Roux-en-Y hepaticojejunostomy is ideal. Type III cysts (intraduodenal) cre-ate a treatment challenge as full resection would require pan-creaticoduodenectomy. Given that type III cyst are associated with the lowest malignancy risk of any choledochal cyst (~2%), sphincterotomy and surveillance is generally recommended over formal excision.66 In Type IV (multiple cysts), excision of all cystic tissue and reconstruction is again recommended. For type IVa, which is characterized by multiple cysts with intrahe-patic involvement, additional segmental resection of the liver may be required if intrahepatic stones, strictures, or abscesses are present. Type V choledochal cysts (Caroli


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Surgery_Schwartz. cysts with intrahe-patic involvement, additional segmental resection of the liver may be required if intrahepatic stones, strictures, or abscesses are present. Type V choledochal cysts (Caroli disease) are very rare and account for less than 1% of patients with choledochal cysts. These cysts are multiple and can affect the entire liver. In advanced stages, this may result in cirrhosis and liver failure necessitating liver transplantation.Primary Sclerosing CholangitisPrimary sclerosing cholangitis (PSC) is an uncommon disease characterized by inflammatory strictures involving the intrahe-patic and extrahepatic biliary tree. It is a progressive disease that eventually results in secondary biliary cirrhosis. Sometimes, biliary strictures are clearly secondary to bile duct stones, acute cholangitis, previous biliary surgery, or toxic agents, and are termed secondary sclerosing cholangitis. However, primary sclerosing cholangitis is a disease entity of its own, with no clear attributing


Surgery_Schwartz

Surgery_Schwartz. previous biliary surgery, or toxic agents, and are termed secondary sclerosing cholangitis. However, primary sclerosing cholangitis is a disease entity of its own, with no clear attributing cause. Autoimmune reaction, chronic low-grade bac-terial or viral infection, toxic reaction, and genetic factors have all been suggested to play a role in its pathogenesis. PSC is commonly associated with other autoimmune diseases includ-ing ulcerative colitis in about two-thirds of patients, Riedel’s thyroiditis, and retroperitoneal fibrosis. The human leukocyte antigen haplotypes HLA-B8, DR3, DQ2, and DRw52A, com-monly found in patients with autoimmune diseases, also are more frequently seen in patients with primary sclerosing chol-angitis than in controls. The mean age of presentation for PSC is 30 to 45 years, and men are affected twice as often as women. Most patients are symptomatic when diagnosed, and may com-plain of intermittent jaundice, fatigue, weight loss, pruritus, or abdominal pain.


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Surgery_Schwartz. to 45 years, and men are affected twice as often as women. Most patients are symptomatic when diagnosed, and may com-plain of intermittent jaundice, fatigue, weight loss, pruritus, or abdominal pain. Initial presentation with acute cholangitis is rare without preceding biliary tract intervention or surgery. A minority of patients are diagnosed incidentally by elevated liver function tests, particular when found in a patient with ulcerative colitis. While the clinical presentation and laboratory results may suggest the PSC, ERCP revealing multiple dilatations and strictures (beading) of the intraand extrahepatic biliary tree confirms the diagnosis. The hepatic duct bifurcation is often the most severely affected segment. A liver biopsy may not be diagnostic, but it is important to determine the degree of hepatic fibrosis and the presence of cirrhosis.The clinical course in sclerosing cholangitis is highly vari-able, but cyclic remissions and exacerbations are typical. Some patients


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Surgery_Schwartz. the degree of hepatic fibrosis and the presence of cirrhosis.The clinical course in sclerosing cholangitis is highly vari-able, but cyclic remissions and exacerbations are typical. Some patients will remain asymptomatic for years, while others prog-ress rapidly with the obliterative inflammatory changes leading to secondary biliary cirrhosis and liver failure. In patients with associated ulcerative colitis, the course of each disease seems independent of the other and colectomy has no effect on the Brunicardi_Ch32_p1393-p1428.indd 141711/02/19 2:43 PM 1418SPECIFIC CONSIDERATIONSPART IIcourse of primary sclerosing cholangitis. Of the patients with sclerosing cholangitis, 10% to 15% will develop cholangio-carcinoma, which can present at any time during the disease process and does not necessarily correlate with the extent of the sclerosing cholangitis or the development of liver failure.67 Cholangiocarcinoma in the setting of PSC frequently follows an aggressive course. Patients


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Surgery_Schwartz. necessarily correlate with the extent of the sclerosing cholangitis or the development of liver failure.67 Cholangiocarcinoma in the setting of PSC frequently follows an aggressive course. Patients need to be followed by serial ERCP and liver biopsies to evaluate for the development of complica-tions such as strictures, cancers, or cirrhosis.There is no known curative treatment for primary scleros-ing cholangitis and medical management is largely supportive. Corticosteroids, immunosuppressants, ursodeoxycholic acid, and antibiotics have been attempted with disappointing results. If biliary strictures occur, they can be dilated and stented either endoscopically or percutaneously. These measures have given short-term improvements in symptoms and serum bilirubin lev-els but provide long-term results in less than half of patients. Surgical management with resection of the extrahepatic biliary tree and hepaticojejunostomy has produced reasonable results in patients with extrahepatic and


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Surgery_Schwartz. results in less than half of patients. Surgical management with resection of the extrahepatic biliary tree and hepaticojejunostomy has produced reasonable results in patients with extrahepatic and bifurcation strictures, but without cirrhosis or significant hepatic fibrosis.68 In patients with pri-mary sclerosing cholangitis and advanced liver disease, liver transplantation is the only option. It offers excellent results, with overall 5-year survival as high as 85%. Unfortunately, recur-rence of PSC can occur in 10% to 20% of patients and may require retransplantation.68Bile Duct StricturesBenign bile duct strictures can have numerous causes. However, the vast majority are related to operative injury, most commonly during cholecystectomy. Other causes include fibrosis due to chronic pancreatitis, common bile duct stones, acute cholan-gitis, biliary obstruction due to cholecystolithiasis (Mirizzi’s syndrome), sclerosing cholangitis, cholangiohepatitis, and stric-tures of a


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Surgery_Schwartz. pancreatitis, common bile duct stones, acute cholan-gitis, biliary obstruction due to cholecystolithiasis (Mirizzi’s syndrome), sclerosing cholangitis, cholangiohepatitis, and stric-tures of a biliary-enteric anastomosis. Bile duct strictures that go unrecognized or are improperly managed can lead to severe complications such as recurrent cholangitis, secondary biliary cirrhosis, and portal hypertension.69Bile duct strictures most commonly result in recurrent episodes of cholangitis but may present with isolated jaundice without infection. Liver function tests usually show evidence of cholestasis with elevations of bilirubin and alkaline phosphatase. Imaging with ultrasound or CT can show dilated bile ducts proximal to the stricture, as well as provide informa-tion about the level of the stenosis. MRCP gives more detailed anatomic information about the location and the degree of dilatation. If the diagnosis remains in question, cholangiog-raphy (endoscopic or more rarely


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Surgery_Schwartz. level of the stenosis. MRCP gives more detailed anatomic information about the location and the degree of dilatation. If the diagnosis remains in question, cholangiog-raphy (endoscopic or more rarely percutaneous) will outline the biliary tree, define the stricture and its location, and allow for therapeutic interventions (Fig. 32-28). The treatment of biliary strictures depends on the location and the cause of the stricture. Percutaneous or endoscopic dilatation and/or stent placement will provide good results in more than one half of Type IIIType IIType IType VType IVbType IVaFigure 32-27. Classification of choledochal cysts. Type I, fusiform or cystic dilations of the extrahepatic biliary tree, is the most common type, making up >50% of the choledochal cysts. Type II, saccular diverticulum of an extrahepatic bile duct. Rare, <5% of choledochal cysts. Type III, bile duct dilatation within the duodenal wall (choledochoceles), makes up about 5% of choledochal cysts. Types IVa and IVb,


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Surgery_Schwartz. of an extrahepatic bile duct. Rare, <5% of choledochal cysts. Type III, bile duct dilatation within the duodenal wall (choledochoceles), makes up about 5% of choledochal cysts. Types IVa and IVb, mul-tiple cysts, make up 5% to 10% of choledochal cysts. Type IVa affects both extrahepatic and intrahepatic bile ducts, whereas type IVb cysts affect the extrahepatic bile ducts only. Type V (Caroli disease), intrahepatic biliary cysts, is very rare and makes up 1% of choledochal cysts.Brunicardi_Ch32_p1393-p1428.indd 141811/02/19 2:44 PM 1419GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32patients. For persistent or complex strictures, surgical resec-tion and reconstruction with Roux-en-Y choledochojejunos-tomy or hepaticojejunostomy may be necessary and will result in good or excellent outcomes in 80% to 90% of patients.70 Choledochoduodenostomy may be a choice for strictures in the distal-most part of the common bile duct if a tension free repair can be achieved.INJURY TO THE


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Surgery_Schwartz. outcomes in 80% to 90% of patients.70 Choledochoduodenostomy may be a choice for strictures in the distal-most part of the common bile duct if a tension free repair can be achieved.INJURY TO THE BILIARY TRACTGallbladderInjuries to the gallbladder itself are uncommon but can occur in the setting of penetrating trauma (gunshot or stab wounds) or medical procedures (liver biopsy or surgery). Nonpenetrating trauma to the gallbladder is extremely rare but can cause con-tusion, avulsion, laceration, rupture, or traumatic cholecystitis. Regardless of the etiology of gallbladder injury, the treatment of choice is cholecystectomy. The prognosis is typically good but depends on the extent of related injury, as damage to nearby organs is not uncommon.Extrahepatic Bile DuctsRarely, penetrating trauma to the extrahepatic bile ducts does occur, and it is usually associated with trauma to other viscera. The vast majority of injuries to the extrahepatic bili-ary system, however, are iatrogenic,


Surgery_Schwartz

Surgery_Schwartz. to the extrahepatic bile ducts does occur, and it is usually associated with trauma to other viscera. The vast majority of injuries to the extrahepatic bili-ary system, however, are iatrogenic, usually occurring during cholecystectomy. These injuries are among the most feared and litigated complications in surgery, and can result in sig-nificant morbidity.71,72 Biliary tract injury can also occur during common bile duct exploration, division or mobilization of the duodenum during gastrectomy, or dissection of the hepatic hilum during liver resections.The incidence of bile duct injury during cholecystectomy is estimated to be relatively low (about 0.2%).73 While ini-tial experience with laparoscopic cholecystectomy appeared to show a higher rate of injury to the bile ducts compared to the open approach, these trends appear to be disappearing as lapa-roscopic technology and familiarity with the techniques of the procedure have improved.53 A number of different factors are thought to be


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Surgery_Schwartz. open approach, these trends appear to be disappearing as lapa-roscopic technology and familiarity with the techniques of the procedure have improved.53 A number of different factors are thought to be associated with bile duct injury during laparo-scopic cholecystectomy. These include acute or chronic inflam-mation, obesity, anatomic variations, and surgical technique. Inadequate exposure or failure to correctly identify structures before ligating or dividing them are the most common causes of significant biliary injury (see “Anatomic Variants” section). Excessive cephalad retraction of the gallbladder may align the cystic duct with the common bile duct, and the latter may then be mistakenly clipped and divided. Careless use of electrocau-tery can lead to thermal injury. Dissection deep into the liver parenchyma may cause injury to intrahepatic ducts, and poor clip placement close to the hilar area or to structures not well visualized can result in a clip across a bile


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Surgery_Schwartz. deep into the liver parenchyma may cause injury to intrahepatic ducts, and poor clip placement close to the hilar area or to structures not well visualized can result in a clip across a bile duct.74,75Techniques to avoid injury to the bile ducts during chole-cystectomy are important to understand. The use of an angled, 30° or 45° laparoscope instead of an end-viewing camera will help visualize the anatomic structures, in particular those around the triangle of Calot. An angled scope also will aid in the proper placement of clips. The routine use of intraoperative cholangi-ography during every cholecystectomy as a method to prevent bile duct injury remains controversial.55 Nonetheless, the fre-quency of bile duct injuries is cut by 50% when an intraop-erative cholangiogram is performed. Critical to the successful use of cholangiography is accurate interpretation of the imag-ing. It is important to check that the whole biliary system fills with contrast, including both major ducts on


Surgery_Schwartz

Surgery_Schwartz. Critical to the successful use of cholangiography is accurate interpretation of the imag-ing. It is important to check that the whole biliary system fills with contrast, including both major ducts on the right and the left hepatic duct, and that there is no extravasation of contrast. While routine use may reduce or limit the extent of injury, or help identify it early, it does not seem to prevent it entirely.76 No consensus recommendation exists on the use of selective versus routine cholangiography.Perhaps the most universally agreed upon method for mitigating the risk of bile duct injury during laparoscopic cholecystectomy is obtaining the critical view of safety. This requires that the hepatocystic triangle is dissected free of fat and fibrous tissue, the lower third of the gallbladder is sepa-rated from the cystic plate, and there are two and only two structures running into the gallbladder, the cystic duct, and the cystic artery (see Fig. 32-23).54 Newer technologies such as


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Surgery_Schwartz. is sepa-rated from the cystic plate, and there are two and only two structures running into the gallbladder, the cystic duct, and the cystic artery (see Fig. 32-23).54 Newer technologies such as fluorescence cholangiography to help identify biliary anatomy intraoperatively have shown promising early results, though large-scale applications remain to be seen.77Diagnosis. Only about 25% of major bile duct injuries (com-mon bile duct or hepatic duct) are recognized at the time of surgery. In these cases, intraoperative bile leakage, recognition of the correct anatomy, or an abnormal cholangiogram led to the diagnosis of a bile duct injury. In those that go unrecognized at the time of surgery, more than half will re-present within the first month postoperatively, though some can present months or years later with strictures, cholangitis, or cirrhosis from a remote bile duct injury.4Figure 32-28. An endoscopic retrograde cholangiography show-ing stricture of the common hepatic duct


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Surgery_Schwartz. months or years later with strictures, cholangitis, or cirrhosis from a remote bile duct injury.4Figure 32-28. An endoscopic retrograde cholangiography show-ing stricture of the common hepatic duct (arrow). The patient had recently had a laparoscopic cholecystectomy; clips from the opera-tion can be seen projected over the common bile duct.Brunicardi_Ch32_p1393-p1428.indd 141911/02/19 2:44 PM 1420SPECIFIC CONSIDERATIONSPART IIBile duct injuries typically result in either leaks or obstruc-tions related to strictures. Bile leak, most commonly from the cystic duct stump, a transected aberrant right hepatic duct, or a lateral injury to the main bile duct, usually presents with abdom-inal pain, fever, and a mild elevation of liver function tests. If a drain was placed at the time of surgery, bilious fluid may be seen. A CT scan or ultrasound can show either a fluid collection in the gallbladder fossa (biloma), or free fluid (bile) in the peri-toneum (Fig. 32-29A). ERCP (Fig. 32-29B) or


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Surgery_Schwartz. bilious fluid may be seen. A CT scan or ultrasound can show either a fluid collection in the gallbladder fossa (biloma), or free fluid (bile) in the peri-toneum (Fig. 32-29A). ERCP (Fig. 32-29B) or HIDA scan can be utilized to better localize the site of the bile leak.Obstruction or stricture should be suspected in patients with progressive elevations of liver function tests or jaundice after cholecystectomy. CT scan or ultrasound can demonstrate the dilated part of the biliary tree, and may identify the level of the bile duct obstruction. MRI cholangiography, if available, provides an excellent, noninvasive delineation of the biliary anatomy both proximal and distal to the injury. Endoscopic or percutaneous cholangiography may also be helpful to confirm the diagnosis, depending on the location and type of injury.Management. The management of bile duct injuries depends on the type, extent, and level of the injury, as well as the tim-ing of its diagnosis. Initial proper treatment of


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Surgery_Schwartz. location and type of injury.Management. The management of bile duct injuries depends on the type, extent, and level of the injury, as well as the tim-ing of its diagnosis. Initial proper treatment of bile duct injury can avoid the development of further complications or bile duct strictures. If an injury is discovered that exceeds the capacity of the available surgical expertise, the patient should be transferred to a tertiary care center. In these situations, drains should be placed in the surgical bed and antibiotics initiated. If a complete obstructive transection has occurred, it may also be necessary to place a percutaneous transhepatic drainage catheter to decom-press the biliary tree prior to transfer.If identified at the time of surgery, bile leaks from small bile ducts (<3 mm) or those draining a single hepatic segment can safely be ligated. If the injured duct is ≥4 mm, however, it is likely to drain multiple segments or an entire lobe and thus needs to be repaired or


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Surgery_Schwartz. mm) or those draining a single hepatic segment can safely be ligated. If the injured duct is ≥4 mm, however, it is likely to drain multiple segments or an entire lobe and thus needs to be repaired or reimplanted. Minor injuries to the com-mon bile duct or the common hepatic duct are traditionally managed with placement of a T-tube that has been modified by cutting the ends to allow for its placement in and removal from the bile duct (see Fig. 32-18). If the injury is small, the T-tube may be placed through it as if it were a formal choledochotomy. In more extensive injuries, the T-tube should be placed through a separate choledochotomy and the injury closed over the T-tube end to minimize the risk of subsequent stricture formation.Major bile duct injuries identified intraoperatively such as complete transection of the common hepatic or common bile duct are best managed at the time of injury. In many of these major injuries, the bile duct has not only been transected, but a variable


Surgery_Schwartz

Surgery_Schwartz. as complete transection of the common hepatic or common bile duct are best managed at the time of injury. In many of these major injuries, the bile duct has not only been transected, but a variable length of the duct may have been removed with the surgical specimen. This injury usually requires reconstruction with a biliary-enteric anastomosis, and is best performed as soon as possible following the injury. If there is no or minimal loss of ductal length, a duct-to-duct repair may be done over a T-tube that is placed through a separate incision. In any repair that is chosen, it is critical to perform a tension-free anastomosis to minimize the high risk of postoperative stricture formation.Bile leaks identified postoperatively can usually be man-aged with percutaneous drainage of intra-abdominal fluid col-lections followed by endoscopic biliary stenting. With most leaks, regardless of the location, stenting of the common bile duct will provide a low resistance route for bile flow into


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Surgery_Schwartz. fluid col-lections followed by endoscopic biliary stenting. With most leaks, regardless of the location, stenting of the common bile duct will provide a low resistance route for bile flow into the duodenum, decreasing flow through the leak and allowing it to heal. This is particularly effective for leaks from the cystic duct stump. Rarely, surgery is required to repair a large leak if endoscopic interventions have failed or peritonitis is present.Major bile duct injuries diagnosed in the later postopera-tive period may not be amenable to immediate reconstruction due to acute inflammation. They may need to be managed with transhepatic biliary catheter placement for biliary decompres-sion as well as percutaneous drainage of intra-abdominal bile collections, if any. When the acute inflammation has resolved 6 to 8 weeks later, operative repair is performed.Patients with bile duct stricture from an injury or as a sequela of previous repair usually present with either progres-sive elevation


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Surgery_Schwartz. has resolved 6 to 8 weeks later, operative repair is performed.Patients with bile duct stricture from an injury or as a sequela of previous repair usually present with either progres-sive elevation of liver function tests or cholangitis. The initial management usually includes endoscopic attempts at dilation or stenting. Balloon dilatation of a stricture usually requires multiple procedures and rarely provides long-term relief. Self-expanding metal or plastic stents can provide temporary or, in the high-risk patient, permanent drainage of the biliary tree. If the stricture is unable to be addressed endoscopically, ABFigure 32-29. A. Computed tomographic scan of a patient with bile leak after cholecystectomy. The short arrows indicate the intraperitoneal collections. Both air and bile are seen in the gallbladder bed (long arrow) as well as a surgical clip. B. An endoscopic retrograde cholangi-ography from the same patient showing contrast extravasation from the cystic duct stump


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Surgery_Schwartz. are seen in the gallbladder bed (long arrow) as well as a surgical clip. B. An endoscopic retrograde cholangi-ography from the same patient showing contrast extravasation from the cystic duct stump (arrow). Note the filling of the pancreatic duct.Brunicardi_Ch32_p1393-p1428.indd 142011/02/19 2:44 PM 1421GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32percutaneous transhepatic biliary drainage catheter placement may be necessary for decompression, and to define the anat-omy, location and extent of the damage. Definitive treatment of refractory biliary strictures entails resection of the affected segment and reconstruction with a biliary-enteric anastomosis.Outcome. Good results can be expected in the majority of patients with bile duct injuries, with the best results coming when the injury is recognized immediately and repaired by an experienced biliary tract surgeon.78 The perioperative mortality rate is reported to be less than 10%, but common morbidities associated with


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Surgery_Schwartz. the injury is recognized immediately and repaired by an experienced biliary tract surgeon.78 The perioperative mortality rate is reported to be less than 10%, but common morbidities associated with bile duct repairs include cholangitis, external biliary fistula, bile leak, subhepatic and subphrenic abscesses, and hemobilia. Restenosis of a biliary enteric anastomosis occurs in about 10% of patients, and typically presents within 2 years, but can manifest up to 20 years after the initial procedure. In general, treatment of proximal strictures is associated with a lower success rate than distal ones. The worst results are seen in patients with many operative revisions and in those who have evidence of liver failure or portal hypertension. However, previ-ous repair does not preclude a successful outcome, particularly in patients with good liver function. In the most severe cases, patients with refractory strictures and deteriorating liver func-tion may become candidates for liver


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Surgery_Schwartz. successful outcome, particularly in patients with good liver function. In the most severe cases, patients with refractory strictures and deteriorating liver func-tion may become candidates for liver transplant.TUMORSCarcinoma of the GallbladderCancer of the gallbladder is a rare malignancy that occurs pre-dominantly in the elderly. It is an aggressive tumor, with a poor prognosis that is usually not diagnosed until it has become advanced and is causing symptoms. The median survival for gallbladder cancer is around 6 months with a reported 5-year survival rate of 5%.79 In a minority of cases, early cancers are identified incidentally following cholecystectomy for cho-lelithiasis, in which case, 5-year survival is over 80%.80Incidence. Gallbladder cancer is the sixth most common GI malignancy in Western countries.80 It accounts for 2% to 4% of all malignant GI tumors, with about 4000 new cases diagnosed annually in the United States. It is two to six times more com-mon in females than


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Surgery_Schwartz. in Western countries.80 It accounts for 2% to 4% of all malignant GI tumors, with about 4000 new cases diagnosed annually in the United States. It is two to six times more com-mon in females than males, and the peak incidence is in the seventh decade of life. Its occurrence in random autopsy series is about 0.4%, but 0.3% to 3% of patients undergoing chole-cystectomy for gallstone disease are found incidentally to have gallbladder cancer.80 There are also significant ethnic variations in the incidence of gallbladder cancer, with rates being particu-larly high in native populations of the United States, Mexico, and Chile. The overall incidence of gallbladder cancer in the United States is approximately 1.5 cases per 100,000 residents. For Native American females with gallstones, the incidence is around 7.1 per 100,000. For women in the native populations of Chile, gallbladder cancer occurs in 27.3 per 100,000 individu-als. Asian populations, particularly those of Korean descent, are


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Surgery_Schwartz. is around 7.1 per 100,000. For women in the native populations of Chile, gallbladder cancer occurs in 27.3 per 100,000 individu-als. Asian populations, particularly those of Korean descent, are also at increased risk of developing gallbladder cancer.80Etiology. The pathogenesis of gallbladder cancer has not been fully defined but is likely related to a combination of chronic inflammation, infection, genetics, and environmental exposures such as heavy metals and tobacco. Cholelithiasis is the most important risk factor for gallbladder carcinoma, and up to 85% of patients with carcinoma of the gallbladder have gallstones. However, <3% of patients with gallstones have gallbladder cancer, and the 20-year risk of developing cancer remains low; <0.5% for the overall population and 1.5% for high-risk groups. Larger stones (>3 cm) are associated with a 10-fold increased risk of cancer.81 The risk of developing cancer of the gallblad-der is higher in patients with symptomatic than asymptomatic


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Surgery_Schwartz. groups. Larger stones (>3 cm) are associated with a 10-fold increased risk of cancer.81 The risk of developing cancer of the gallblad-der is higher in patients with symptomatic than asymptomatic gallstones, and it is more commonly seen in the setting of cho-lesterol stones.Polypoid lesions of the gallbladder, which are present in as many as 5% of adults, are also associated with increased risk of cancer. This is particularly true for polyps measuring >10 mm, which carry a 25% risk of malignancy.82 Solitary or sessile polys, or those showing rapid growth on serial imaging, particularly if in the presence of gallstones or age >50 are also concerning for malignancy. When such findings are identified, the patient should have their gallbladder removed, even if they are asymptomatic. Polyps that are not removed should be monitored on serial imaging. The finding of a “Porcelain” gallbladder, or dense circumferential calcifications of the gallbladder wall, is associated with an approximately


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Surgery_Schwartz. are not removed should be monitored on serial imaging. The finding of a “Porcelain” gallbladder, or dense circumferential calcifications of the gallbladder wall, is associated with an approximately 10% risk of gallbladder car-cinoma. While this condition was previously considered to be an absolute indication for cholecystectomy, more recent studies suggest that given the low rate of malignancy, observation is safe and acceptable. Nevertheless, resection remains a reason-able option, particularly if the patient is symptomatic, and the decision should ultimately be made only after discussing risks and benefits of each approach with the patient.97 Patients with certain types of choledochal cysts also have an increased risk of developing cancer anywhere in the biliary tree, but the inci-dence is highest in the gallbladder and cholecystectomy should be performed with any surgical intervention on the choledochal cyst. Primary sclerosing cholangitis, anomalous pancreatico-biliary duct


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Surgery_Schwartz. is highest in the gallbladder and cholecystectomy should be performed with any surgical intervention on the choledochal cyst. Primary sclerosing cholangitis, anomalous pancreatico-biliary duct junction, and exposure to carcinogens (azotoluene, nitrosamines) also are associated with cancer of the gallbladder, and screening with abdominal ultrasound should be considered in these patients.Pathology. Between 80% and 90% of gallbladder cancers are adenocarcinomas. Squamous cell, adenosquamous, oat cell, and other anaplastic lesions rarely occur. The histologic subtypes of gallbladder adenocarcinomas include papillary, nodular, and tubular. Less than 10% are of the papillary type, but these are associated with an overall better outcome, as they are most com-monly diagnosed while localized to the gallbladder. Cancer of the gallbladder can spread through lymphatics, venous drainage, or by direct invasion into the liver parenchyma. Lymphatic flow from the gallbladder drains first to the cystic


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Surgery_Schwartz. gallbladder. Cancer of the gallbladder can spread through lymphatics, venous drainage, or by direct invasion into the liver parenchyma. Lymphatic flow from the gallbladder drains first to the cystic duct node (Lund’s node or Calot’s node), then pericholedochal and hilar nodes, and finally to the peripancreatic, duodenal, periportal, celiac, and superior mes-enteric artery nodes. The gallbladder veins drain directly into the adjacent liver, usually segments IVb and V, where tumor inva-sion is common (Fig. 32-30). The gallbladder wall differs histo-logically from the intestines in that it lacks a muscularis mucosa and submucosa. Lymphatics are present in the subserosal layer only. Therefore, cancers that have not grown through the muscu-lar layer have minimal risk of nodal disease. Unfortunately, only a small portion of gallbladder cancers (10–25%) are identified while they are still localized to the gallbladder. The majority will already have nodal involvement, extension into adjacent


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Surgery_Schwartz. only a small portion of gallbladder cancers (10–25%) are identified while they are still localized to the gallbladder. The majority will already have nodal involvement, extension into adjacent liver, or distant metastasis at the time of diagnosis.80,83Clinical Manifestations and Diagnosis. Signs and symp-toms of carcinoma of the gallbladder are generally indistinguish-able from those associated with cholecystitis and cholelithiasis, and this can lead to delays in treatment or misdiagnosis. These include abdominal discomfort, right upper quadrant pain, nau-sea, and vomiting. Jaundice, weight loss, anorexia, ascites, 5Brunicardi_Ch32_p1393-p1428.indd 142111/02/19 2:44 PM 1422SPECIFIC CONSIDERATIONSPART IIand abdominal masses are less common presenting symptoms. Common misdiagnoses include chronic cholecystitis, acute cho-lecystitis, choledocholithiasis, hydrops of the gallbladder, and pancreatic cancer. Laboratory findings, if abnormal, are most often consistent with biliary


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Surgery_Schwartz. include chronic cholecystitis, acute cho-lecystitis, choledocholithiasis, hydrops of the gallbladder, and pancreatic cancer. Laboratory findings, if abnormal, are most often consistent with biliary obstruction. Ultrasonography often reveals a thickened, irregular gallbladder wall (>3mm) with hypervascularity or a mass replacing the gallbladder. It may also visualize tumor invasion of the liver, lymphadenopathy, or a dilated biliary tree. The sensitivity of ultrasonography in detect-ing gallbladder cancer ranges from 70% to 100%. A CT scan may be helpful in identifying a gallbladder mass and evaluating for nodal spread or local invasion into adjacent organs or vascu-lature. If questions about local invasion remain, MRCP allows for complete assessment of biliary, vascular, nodal, hepatic, and adjacent organ involvement.84 Endoscopic ultrasound (EUS) can be a useful tool in staging and evaluating for local invasion, as well as obtaining tissue diagnosis through fine needle aspiration


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Surgery_Schwartz. and adjacent organ involvement.84 Endoscopic ultrasound (EUS) can be a useful tool in staging and evaluating for local invasion, as well as obtaining tissue diagnosis through fine needle aspiration (FNA). Tissue diagnosis can also be obtained by CT or ultra-sound-guided biopsy of the tumor, though this is not required prior to cholecystectomy if the tumor appears resectable on imaging. In jaundiced patients, a percutaneous transhepatic or endoscopic cholangiogram may be helpful to delineate the extent of biliary tree involvement. The role of PET scanning in gallbladder cancer is yet to be fully defined but can be utilized in both staging and surveillance.Treatment. Surgical resection remains the only curative option for gallbladder cancer. While most patients are unresectable at the time of diagnosis, if preoperative staging suggests a potentially resectable tumor, exploration for tissue diagno-sis, formal pathologic staging, and possible curative resection are warranted.Tumors


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Surgery_Schwartz. time of diagnosis, if preoperative staging suggests a potentially resectable tumor, exploration for tissue diagno-sis, formal pathologic staging, and possible curative resection are warranted.Tumors limited to the lamina propria or muscular layer of the gallbladder (T1) are usually identified incidentally, after laparoscopic cholecystectomy for gallstone disease. There is near universal agreement that simple laparoscopic cholecys-tectomy is an adequate treatment for T1 lesions and results in a near 100% overall 5-year survival rate. When the tumor invades the perimuscular connective tissue without extension beyond the serosa or into the liver (T2 tumors), an extended cholecystectomy should be performed.85 This includes addi-tional resection of liver segments IVb and V, as well as lymph-adenectomy of the cystic duct and pericholedochal, portal, right celiac, and posterior pancreatoduodenal lymph nodes. Given the extent of this operation, an open approach is stan-dard. One-half of


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Surgery_Schwartz. of the cystic duct and pericholedochal, portal, right celiac, and posterior pancreatoduodenal lymph nodes. Given the extent of this operation, an open approach is stan-dard. One-half of patients with T2 tumors are found to have nodal disease on pathologic examination, highlighting the importance of regional lymphadenectomy as part of surgery for T2 cancers.86 For tumors that grow beyond the serosa, or invade the liver or other adjacent organs (T3), there is a higher likelihood of intraperitoneal or distant spread. However, if no peritoneal or nodal involvement is found, complete tumor excision with an extended right hepatectomy and possible cau-date lobectomy with lymphadenectomy must be performed for adequate tumor clearance. In addition, if a T2 or T3 tumor is identified incidentally after laparoscopic cholecystectomy, and the patient is returning to the OR for liver resection and lymph-adenectomy, the previous laparoscopic port sites must also be excised due to the high risk of


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Surgery_Schwartz. after laparoscopic cholecystectomy, and the patient is returning to the OR for liver resection and lymph-adenectomy, the previous laparoscopic port sites must also be excised due to the high risk of recurrence in these locations. T4 tumors are those that have grown into major blood vessels or two or more structures outside the liver, and they are typically considered unresectable.Due to the high frequency of late diagnosis, palliative procedures for unresectable cancer, jaundice, or duodenal obstructions remain the most frequently performed surgery for gallbladder cancers. Today, patients with obstructive jaundice can frequently be managed with either endoscopic or percutane-ously placed biliary stents. Various regimens of neoadjuvant, adjuvant, and definitive chemoradiotherapy have been trialed in gallbladder cancer. Overall, benefits have been marginal, but treatment may improve survival time by several months. These therapies can be offered to patients in conjunction with


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Surgery_Schwartz. been trialed in gallbladder cancer. Overall, benefits have been marginal, but treatment may improve survival time by several months. These therapies can be offered to patients in conjunction with resec-tion for curative intent or as definitive therapy, but no standard recommendation exists for their use.85-87Prognosis. Most patients with gallbladder cancer have unre-sectable disease at the time of diagnosis. The overall 5-year sur-vival rate of all patients with gallbladder cancer is <5%, with a median survival of 6 months.87 However, patients with T1 dis-ease treated with cholecystectomy have an excellent prognosis (85–100% 5-year survival rate). The 5-year survival rate for T2 lesions treated with an extended cholecystectomy (liver segment IVb/V resection) and lymphadenectomy is >70% compared to 25% to 40% for T2 patients treated with simple cholecystec-tomy. Patients with advanced (T3 or T4) but resectable gallblad-der cancer are reported to have 5-year survival rates of 20% to


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Surgery_Schwartz. compared to 25% to 40% for T2 patients treated with simple cholecystec-tomy. Patients with advanced (T3 or T4) but resectable gallblad-der cancer are reported to have 5-year survival rates of 20% to 50%, supporting aggressive resection in those patients who can tolerate surgery. The median survival for patients with distant metastasis at the time of presentation is only 1 to 3 months.Recurrence after resection of gallbladder cancer occurs most commonly in the liver or in the celiac or retropancreatic nodes. The prognosis for recurrent disease is very poor, and the main goal of follow-up is to provide palliative care. The most common problems are pruritus and cholangitis associated with obstructive jaundice, bowel obstruction secondary to carcino-matosis, and pain. Death occurs most commonly secondary to biliary sepsis or liver failure.6Figure 32-30. Computed tomography scan of a patient with gall-bladder cancer. The image shown is at the level of the liver hilum. The portal vein is


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Surgery_Schwartz. secondary to biliary sepsis or liver failure.6Figure 32-30. Computed tomography scan of a patient with gall-bladder cancer. The image shown is at the level of the liver hilum. The portal vein is bifurcating into the left and right portal branch. The tumor has invaded segment IV of the liver (arrowheads) and obstructed the common hepatic duct, resulting in intrahepatic ductal dilatation (arrows).Brunicardi_Ch32_p1393-p1428.indd 142211/02/19 2:44 PM 1423GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32CholangiocarcinomaCholangiocarcinoma is a rare tumor arising from the biliary epithelium and may occur anywhere along the biliary tree. About half are located at the hepatic duct bifurcation (Klatskin tumors), with 40% occurring more distally and 10% being intrahepatic.88 Surgical resection offers the only chance for cure, but unfortunately many patients have advanced disease at the time of diagnosis. Therefore, palliative procedures aimed to provide biliary drainage and


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Surgery_Schwartz. resection offers the only chance for cure, but unfortunately many patients have advanced disease at the time of diagnosis. Therefore, palliative procedures aimed to provide biliary drainage and prevent liver failure and cholangitis are often the only therapeutic possibilities available.Incidence. The autopsy incidence of bile duct carcinoma is about 0.3%. The overall incidence of cholangiocarcinoma in the United States is about 1 per 100,000 people per year, with approximately 2500 new cases diagnosed annually. The disease has a slight male predominance and an average age of presenta-tion between 50 and 70 years.88Etiology. Most cases of extrahepatic cholangiocarcinoma develop de novo with no identifiable risk factors. However, there is an increased risk of cholangiocarcinoma in patients with choledochal cysts, ulcerative colitis, hepatolithiasis, biliary-enteric anastomoses, hepatitis B and C, cirrhosis, bili-ary tract infections with Clonorchis (liver flukes), and chronic typhoid


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Surgery_Schwartz. with choledochal cysts, ulcerative colitis, hepatolithiasis, biliary-enteric anastomoses, hepatitis B and C, cirrhosis, bili-ary tract infections with Clonorchis (liver flukes), and chronic typhoid carriers. Exposure to dietary nitrosamines, Thorotrast, or dioxin also puts patients at increased risk for cholangiocar-cinoma.88 Patients with primary sclerosing cholangitis have a 5% to 10% lifetime risk of developing cholangiocarcinoma with typical disease onset in their 40s. For this reason, these patients require regular screening.67 Features common to most risk factors include biliary stasis, bile duct stones, and infection.Pathology. Over 95% of bile duct cancers are ductal adeno-carcinomas with the vast majority occurring in the extrahepatic biliary tree. Morphologically, they are divided into nodular (the most common type), scirrhous, diffusely infiltrating, or pap-illary. Anatomically, they are divided into distal, perihilar or intrahepatic tumors. Intrahepatic cholangiocarcinomas


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Surgery_Schwartz. into nodular (the most common type), scirrhous, diffusely infiltrating, or pap-illary. Anatomically, they are divided into distal, perihilar or intrahepatic tumors. Intrahepatic cholangiocarcinomas make up approximately 10% of cases and are typically treated like hepatocellular carcinoma, with hepatectomy when possible and transplant when unresectable. About half of all cholangiocar-cinomas are located in the perihilar region with the remaining 40% occurring more distally in the common bile duct.Perihilar cholangiocarcinomas, also referred to as Klatskin tumors, are further classified based on anatomic loca-tion by the Bismuth-Corlette classification (Fig. 32-31). Type I tumors are confined to the common hepatic duct, but type II tumors involve the bifurcation without involvement of the secondary intrahepatic ducts. Type IIIa and IIIb tumors extend into the right and left secondary intrahepatic ducts, respec-tively. Type IV tumors involve both the right and left secondary intrahepatic


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Surgery_Schwartz. intrahepatic ducts. Type IIIa and IIIb tumors extend into the right and left secondary intrahepatic ducts, respec-tively. Type IV tumors involve both the right and left secondary intrahepatic ducts.Clinical Manifestations and Diagnosis. Painless jaundice is the most common initial presentation in patients with cholangio-carcinoma. Pruritus, mild right upper quadrant pain, anorexia, fatigue, and weight loss may also be present. Cholangitis is the presenting symptom in about 10% of patients. Except for jaundice, physical examination is usually normal in patients with cholangiocarcinoma. Occasionally, asymptomatic patients are found to have cholangiocarcinoma while being evaluated for elevated liver function tests. Tumor markers, such as CA 125 and carcinoembryonic antigen (CEA), can be elevated in cholangiocarcinoma but tend to be nonspecific because they also increase in other GI and gynecologic malignancies. The tumor marker most commonly used to aid the diagnosis of


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Surgery_Schwartz. can be elevated in cholangiocarcinoma but tend to be nonspecific because they also increase in other GI and gynecologic malignancies. The tumor marker most commonly used to aid the diagnosis of chol-angiocarcinoma is CA 19-9, which has a sensitivity of 79% and specificity of 98% if the serum value is >129 U/mL.89 How-ever, mild elevations in CA 19-9 can also be seen in cholangitis, biliary obstruction, other GI and gynecologic neoplasms, and patients who lack the Lewis blood type antigen.90The initial workup for suspected cholangiocarcinoma includes abdominal imaging with ultrasound or CT scanning. Perihilar tumors will cause dilatation of the intrahepatic bili-ary tree, but a normal or collapsed gallbladder and extrahepatic bile ducts distal to the tumor. Distal bile duct cancer will lead to dilatation of the extraand intrahepatic bile ducts as well as the gallbladder. Initial imaging is important to determine the level of obstruction and to rule out the presence of bile duct stones


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Surgery_Schwartz. to dilatation of the extraand intrahepatic bile ducts as well as the gallbladder. Initial imaging is important to determine the level of obstruction and to rule out the presence of bile duct stones as the cause of the obstructive jaundice (Fig. 32-32). It is usually difficult to visualize the tumor itself on ultrasound, CT, or even MRCP, but any of these modalities can provide an outline of biliary anatomy, an estimate of the level of obstruc-tion, evaluation of portal vein patency, and screening for nearby lymphadenopathy. Detailed evaluation of the biliary anatomy and tumor itself is best completed through cholangiography. ERCP is generally adequate, but in cases where the proximal extent of the tumor remains in question, PTC may be required to determine resectability.Tissue diagnosis may be difficult to obtain. Current diag-nostic techniques including fine-needle aspiration (percutaneous or endoscopic), and biliary brushings have been shown to have a low sensitivity in detecting


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Surgery_Schwartz. may be difficult to obtain. Current diag-nostic techniques including fine-needle aspiration (percutaneous or endoscopic), and biliary brushings have been shown to have a low sensitivity in detecting malignancy, anywhere between 15% and 60%. Choledochoscopy with direct visualization and sam-pling of intraluminal masses may be able to improve diagnosis rates but is only available in specialized centers (see Fig. 32-10). Patients with potentially resectable disease should, therefore, be offered surgical exploration based on radiographic findings and clinical suspicion.91Type IIIbType IIType IType IVType IIIaFigure 32-31. Bismuth-Corlette classification of perihilar bile duct tumors (Klatskin tumors).Brunicardi_Ch32_p1393-p1428.indd 142311/02/19 2:44 PM 1424SPECIFIC CONSIDERATIONSPART IITreatment. Surgical excision is the only potentially cura-tive treatment for cholangiocarcinoma. In the past one to two decades, improvements in surgical techniques have resulted in lower mortality and


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Surgery_Schwartz. excision is the only potentially cura-tive treatment for cholangiocarcinoma. In the past one to two decades, improvements in surgical techniques have resulted in lower mortality and better outcomes for patients undergoing aggressive surgical excision for cholangiocarcinoma.92Despite improvements in ultrasonography, CT scanning, and MRI, more than one-half of patients who are explored are found to have peritoneal implants, nodal or hepatic metastasis, or locally advanced disease that precludes resection. Patients suspected of having resectable disease should first undergo diagnostic laparoscopy. Those who are found to have previously unidentified metastatic disease should undergo cholecystectomy and surgical bypass for biliary decompression.93For curative resection, the location and local exten-sion of the tumor dictates the extent of the surgery required. Distal bile duct tumors are often resectable but may require pancreaticoduodenectomy (Whipple procedure). For patients with distal


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Surgery_Schwartz. exten-sion of the tumor dictates the extent of the surgery required. Distal bile duct tumors are often resectable but may require pancreaticoduodenectomy (Whipple procedure). For patients with distal bile duct cancer found to be unresectable on sur-gical exploration, Roux-en-Y hepaticojejunostomy, chole-cystectomy, and gastrojejunostomy to prevent gastric outlet obstruction should be performed. Perihilar tumors involving the bifurcation or proximal common hepatic duct (Bismuth-Corlette type I or II) with no signs of vascular involvement are candidates for local tumor excision with portal lymphadenec-tomy, cholecystectomy, common bile duct excision, and bilat-eral Roux-en-Y hepaticojejunostomies. If the tumor involves the right or left hepatic duct (Bismuth-Corlette type IIIa or IIIb), right or left hepatic lobectomy, respectively, should also be performed. Frequently, resection of the adjacent caudate lobe is required because of direct extension into caudate bili-ary radicals or


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Surgery_Schwartz. right or left hepatic lobectomy, respectively, should also be performed. Frequently, resection of the adjacent caudate lobe is required because of direct extension into caudate bili-ary radicals or parenchyma.91 Type IV Klatskin tumors, those with more extensive involvement of both hepatic ducts and intrahepatic spread, are often considered unresectable or only treatable with liver transplantation.The best outcomes in perihilar cholangiocarcinoma are seen in patients who undergo neoadjuvant chemoradiation followed by liver transplantation. However, there are very strict inclusion criteria for transplantation, and few patients qualify.88 Patients with primary sclerosing cholangitis who develop chol-angiocarcinoma should be treated with liver transplant when-ever possible.Nonoperative biliary decompression can be performed for patients with unresectable disease on initial presentation. Endoscopic placement of expandable metal stents is often the preferred approach. For very proximal or


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Surgery_Schwartz. decompression can be performed for patients with unresectable disease on initial presentation. Endoscopic placement of expandable metal stents is often the preferred approach. For very proximal or intrahepatic tumors, percutaneous drainage catheters may be necessary to fully decompress the biliary tree (see Fig. 32-12). There is a sig-nificantly higher risk of cholangitis in patients with drainage catheters or stents compared to those with surgical bypasses. In addition, stent occlusion is not uncommon. Nevertheless, operative intervention is not warranted in patients with meta-static disease.94There is no proven role for adjuvant chemotherapy in the treatment of cholangiocarcinoma. Adjuvant radiation therapy has also not been shown to increase either quality of life or survival in resected patients. Patients with unresect-able disease can be offered palliative chemotherapy, typically with gemcitabine and cisplatin, but the response rates are low (10–20%), and the survival benefit is


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Surgery_Schwartz. patients. Patients with unresect-able disease can be offered palliative chemotherapy, typically with gemcitabine and cisplatin, but the response rates are low (10–20%), and the survival benefit is marginal. The combina-tion of radiation and chemotherapy may be more effective than either treatment alone for unresectable disease, but no data from randomized trials are available. Giving chemoradiation to these patients can be difficult because of the high incidence of cholangitis. External-beam radiation has not been shown to be an effective treatment for unresected disease. The use of interstitial (intraoperative) radiation, brachytherapy with iridium-192 via percutaneous or endoscopic stents, and com-bined interstitial and external-beam radiation for unresectable cholangiocarcinoma has been reported with some encouraging results. However, no randomized, prospective trials have been reported.91 Photodynamic therapy has been proposed as a palliative measure for patients with


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Surgery_Schwartz. has been reported with some encouraging results. However, no randomized, prospective trials have been reported.91 Photodynamic therapy has been proposed as a palliative measure for patients with unresectable disease and ABFigure 32-32. A. An endoscopic retrograde cholangiogram in a patient with cancer of the common hepatic duct (arrowheads). The common bile duct is of normal size, as is the cystic duct (arrow), but the proximal biliary tree is dilated. The gallbladder is not visualized because of tumor obstructing its neck. B. An ultrasound from the same patient showing dilated ducts and tumor obstructing the common hepatic duct (arrow). The walls of the bile ducts adjacent to the obstruction are thickened by tumor infiltration (arrowheads).Brunicardi_Ch32_p1393-p1428.indd 142411/02/19 2:44 PM 1425GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32has been found to prolong survival and improve quality of life in patients with biliary stents.95,96Prognosis. Most patients


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Surgery_Schwartz. 2:44 PM 1425GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32has been found to prolong survival and improve quality of life in patients with biliary stents.95,96Prognosis. Most patients with perihilar cholangiocarcinoma present with advanced, unresectable disease. Median survival in this population is between 5 and 8 months. The most common causes of death are hepatic failure and cholangitis. The overall 5-year survival rate for patients with resectable perihilar cholan-giocarcinoma is between 10% and 30%, but for patients with neg-ative margins, it may be as high as 40%. The operative mortality for perihilar cholangiocarcinoma is 6% to 8%. Patients with distal cholangiocarcinoma are more likely to have resectable disease and improved prognosis compared to perihilar cholangiocarci-noma. The overall 5-year survival rate for resectable distal dis-ease is 30% to 50%, and the median survival is 32 to 38 months. Patients who receive liver transplantation for cholangiocarcinoma


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Surgery_Schwartz. The overall 5-year survival rate for resectable distal dis-ease is 30% to 50%, and the median survival is 32 to 38 months. Patients who receive liver transplantation for cholangiocarcinoma can experience 5-year disease free survival rates as high as 68%.The greatest risk factors for recurrence after resection are the presence of positive margins and lymph node–positive tumors. Therapy for recurrent disease concentrates on palliation of symptoms and additional surgery is not recommended for patients with recurrent disease.REFERENCESEntries highlighted in bright blue are key references. 1. Clemente CD. Gray’s Anatomy. Philadelphia: Lea & Febiger; 1985:132. 2. Klein AS, Lillemoe KD, Yeo CJ, et al. Liver, biliary tract, and pancreas. In: O’Leary JP, ed. Physiologic Basis of Surgery. Baltimore: Williams & Wilkins; 1996:441. 3. Molmenti EP, Pinto PA, Klein J, et al. Normal and variant arte-rial supply of the liver and gallbladder. Pediatr Transplant. 2003;7:80-82. 4. Boyer J. Bile


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Surgery_Schwartz. Baltimore: Williams & Wilkins; 1996:441. 3. Molmenti EP, Pinto PA, Klein J, et al. Normal and variant arte-rial supply of the liver and gallbladder. Pediatr Transplant. 2003;7:80-82. 4. Boyer J. Bile secretion—models, mechanisms, and malfunc-tions. A perspective on the development of modern cellular and molecular concepts of bile secretion and cholestasis. J Gastro-enterol. 1996;31:475-481. 5. Geoghegan J, Pappas TN. Clinical uses of gut peptides. Ann Surg. 1997;225:145-154. 6. McDonnell CO, Bailey I, Stumpf T, et al. The effect of cho-lecystectomy on plasma cholecystokinin. Am J Gastroenterol. 2002;97:2189-2192. 7. Woods CM, Mawe GM, Toule J, Saccone GTP. The sphinc-ter of Oddi: understanding its control and function. Neuro-gastroenterol Motil. 2005;17(supp 1):31-40. 8. Yokohata K, Tanaka M. Cyclic motility of the sphincter of Oddi. J Hepato-Biliary-Pancreatic Surg. 2000;7:178-182. 9. Lee HJ, Choi BI, Han JK, et al. Three-dimensional ultraso-nography using the minimum transparent


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Surgery_Schwartz. M. Cyclic motility of the sphincter of Oddi. J Hepato-Biliary-Pancreatic Surg. 2000;7:178-182. 9. Lee HJ, Choi BI, Han JK, et al. Three-dimensional ultraso-nography using the minimum transparent mode in obstruc-tive biliary diseases: early experience. J Ultrasound Med. 2002;21:443-453. 10. Ralls PW, Jeffrey RB, Jr, Kane RA, et al. Ultrasonography. Gastroenterol Clin North Am. 2002;31:801-825. 11. O’Connor OJ, Maher MM. Imaging in cholecystitis. AJR Am J Roentgenol. 2011;196:W367-W374. 12. Wexler RS, Greene GS, Scott M. Left hepatic and common hepatic ductal bile leaks demonstrated by Tc-99m HIDA scan and percutaneous transhepatic cholangiogram. Clin Nucl Med. 1994;19:59-60. 13. Richmond BK, DiBaise J, Ziessman H. Utilization of cholecys-tokinin cholescintigraphy in clinical practice. J Am Coll Surg. 2013;217(2):317-323. 14. Magnuson TH, Bender JS, Duncan MD, et al. Utility of mag-netic resonance cholangiography in the evaluation of biliary obstruction. J Am Coll Surg.


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Surgery_Schwartz. practice. J Am Coll Surg. 2013;217(2):317-323. 14. Magnuson TH, Bender JS, Duncan MD, et al. Utility of mag-netic resonance cholangiography in the evaluation of biliary obstruction. J Am Coll Surg. 1999;189:63-72. 15. Liu TH, Consorti ET, Kawashima A, et al. Patient evaluation and management with selective use of magnetic resonance cholangiography and endoscopic retrograde cholangiopan-creatography before laparoscopic cholecystectomy. Ann Surg. 2001;234:33-40. 16. Glomsaker T, Hoff G, KvalØy JT, et al. Patterns and predictive factors of complications after endoscopic retrograde cholangio-pancreatography. Br J Surg. 2013;100(3):373-380. 17. Dumonceau JM, Andriulli A, Elmunzer BJ, et al. Prophylaxis of post-ERCP pancreatitis: European Society of Gastrointestinal Endoscopy (ESGE) Guideline—updated June 2014. Endoscopy. 2014;46(9):799-815. 18. Tischendorf JJ, Kruger M, Trautwein C, et al. Cholangioscopic characterization of dominant bile duct stenoses in patients with primary sclerosing


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Surgery_Schwartz. June 2014. Endoscopy. 2014;46(9):799-815. 18. Tischendorf JJ, Kruger M, Trautwein C, et al. Cholangioscopic characterization of dominant bile duct stenoses in patients with primary sclerosing cholangitis. Endoscopy. 2006;38:665-669. 19. Hui CK, Lai KC, Ng M, et al. Retained common bile duct stones: a comparison between biliary stenting and complete clearance of stones by electrohydraulic lithotripsy. Aliment Pharmacol Ther. 2003;17:289-296. 20. Tsuyuguchi T, Saisho H, Ishihara T, et al. Long-term follow-up after treatment of Mirizzi syndrome by peroral cholangioscopy. Gastrointest Endosc. 2000;52:639-644. 21. Fabbri C, Luigiano C, Lisotti A, et al. Endoscopic ultrasound-guided treatments: are we getting evidence based—a systematic review. World J Gastroenterol. 2014;20(26):8424-8448. 22. Stinton LM, Shaffer EA. Epidemiology of gallbladder disease: cholelithiasis and cancer. Gut Liver. 2012;6(2):172-187. 23. Nakeeb A, Comuzzie AG, Martin L, et al. Gallstones: genetics versus


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Surgery_Schwartz. LM, Shaffer EA. Epidemiology of gallbladder disease: cholelithiasis and cancer. Gut Liver. 2012;6(2):172-187. 23. Nakeeb A, Comuzzie AG, Martin L, et al. Gallstones: genetics versus environment. Ann Surg. 2002;235:842-849. 24. Sakorafas GH, Milingos D, Peros G. Asymptomatic choleli-thiasis: is cholecystectomy really needed? A critical reappraisal 15 years after the introduction of laparoscopic cholecystectomy. Dig Dis Sci. 2007;52:1313-1325. 25. Attili AF, De Santis A, Capri R, et al. The natural history of gallstones: the GREPCO experience. The GREPCO Group. Hepatology. 1995;21:655-660. 26. Strasberg SM. The pathogenesis of cholesterol gallstones a review. J Gastrointest Surg. 1998;2:109-125. 27. Stewart L, Oesterle AL, Erdan I, et al. Pathogenesis of pigment gallstones in Western societies: the central role of bacteria. J Gastrointest Surg. 2002;6:891-903. 28. Trowbridge RL, Rutkowski NK, Shojania KG. Does this patient have acute cholecystitis? JAMA. 2003;289:80-86. 29. Duncan CB,


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Surgery_Schwartz. the central role of bacteria. J Gastrointest Surg. 2002;6:891-903. 28. Trowbridge RL, Rutkowski NK, Shojania KG. Does this patient have acute cholecystitis? JAMA. 2003;289:80-86. 29. Duncan CB, Riall TS. Evidence-based current surgical prac-tice: calculous gallbladder disease. J Gastrointest Surg. 2012;16(11):2011-2025. 30. Menzo EL, Schnall R, Von Rueden D. Lithotripsy in the laparo-scopic era. JSLS. 2005;9(3):358-361. 31. Weber DM. Laparoscopic surgery: an excellent approach in elderly patients. Arch Surg. 2003;138:1083-1088. 32. Kaoutzanis C, Davies E, Leichtle SW, et al. Abdominal ultra-sound versus hepato-imino diacetic acid scan in diagnos-ing acute cholecystitis—what is the real benefit? J Surg Res. 2014:1;188(1):44-52. 33. Hunter JG. Acute cholecystitis revisited: get it while it’s hot. Ann Surg. 1998;227(4):468-469. 34. Ansaloni L, Pisano M, Coccolini F, et al. 2016 WSES guidelines on acute calculous cholecystitis. World J Emerg Surg. 2016;11:25. 35. Sakpal SV, Bindra SS,


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Surgery_Schwartz. it’s hot. Ann Surg. 1998;227(4):468-469. 34. Ansaloni L, Pisano M, Coccolini F, et al. 2016 WSES guidelines on acute calculous cholecystitis. World J Emerg Surg. 2016;11:25. 35. Sakpal SV, Bindra SS, Chamberlain RS. Laparoscopic cho-lecystectomy conversion rates two decades later. JSLS. 2010;14(4):476-483. 36. Cherng N, Witkowski E, Sneider EB, et al. Use of cholecystos-tomy tubes in the management of patients with primary diagno-sis of acute cholecystitis. JACS. 2012;214:196-201. 37. Chikamori F, Kuniyoshi N, Shibuya S, et al. Early scheduled laparoscopic cholecystectomy following percutaneous transhe-patic gallbladder drainage for patients with acute cholecystitis. Surg Endosc. 2002;16:1704-1707.Brunicardi_Ch32_p1393-p1428.indd 142511/02/19 2:44 PM 1426SPECIFIC CONSIDERATIONSPART II 38. Ko C, Lee S. Epidemiology and natural history of common bile duct stones and prediction of disease. Gastrointest Endosc. 2002;56:S165-169. 39. Giljaca V, Gurusamy KS, Takwoingi Y, et al.


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Surgery_Schwartz. C, Lee S. Epidemiology and natural history of common bile duct stones and prediction of disease. Gastrointest Endosc. 2002;56:S165-169. 39. Giljaca V, Gurusamy KS, Takwoingi Y, et al. Endoscopic ultra-sound versus magnetic resonance cholangiopancreatography for common bile duct stones. Cochrane Database Syst Rev. 2015:26;(2):CD011549. 40. Tranter S, Thompson M. Comparison of endoscopic sphincter-otomy and laparoscopic exploration of the common bile duct. Br J Surg. 2002;89:1495-1504. 41. Dasari BV, Tan CJ, Gurusamy KS, et al. Surgical versus endo-scopic treatment of bile duct stones. Cochrane Database Syst Rev. 2013;(12):CD003327. 42. Lilly MC, Arregui ME. A balanced approach to choledocholi-thiasis. Surg Endosc. 2001;15:467-472. 43. Lipsett PA, Pitt HA. Acute cholangitis. Front Biosci. 2003;8:S1229-S1239. 44. Lillemoe KD. Surgical treatment of biliary tract infections. Am Surg. 2000;66:138-144. 45. Li VK, Yum JL, Yeung YP. Optimal timing of elective lapa-roscopic cholecystectomy


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Surgery_Schwartz. 2003;8:S1229-S1239. 44. Lillemoe KD. Surgical treatment of biliary tract infections. Am Surg. 2000;66:138-144. 45. Li VK, Yum JL, Yeung YP. Optimal timing of elective lapa-roscopic cholecystectomy after acute cholangitis and sub-sequent clearance of choledocholithiasis. Am J Surg. 2010;200(4):483-488. 46. Johnstone M, Marriott P, Royle TJ, et al. The impact of timing of cholecystectomy following gallstone pancreatitis. Surgeon. 2014;12(3):134-140. 47. Nuño-Guzmán CM, Marín-Contreras ME, Figueroa-Sánchez M, Corona JL. Gallstone ileus, clinical presentation, diag-nostic and treatment approach. World J Gastrointest Surg. 2016;8(1):65-76. 48. Sperling RM, Koch J, Sandhu JS, et al. Recurrent pyogenic chol-angitis in Asian immigrants to the United States: natural history and role of therapeutic ERCP. Dig Dis Sci. 1997;42:865-871. 49. Thinh NC, Breda Y, Faucompret S, et al. Oriental biliary lithia-sis. Retrospective study of 690 patients treated surgically over 8 years at Hospital 108 in


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Surgery_Schwartz. ERCP. Dig Dis Sci. 1997;42:865-871. 49. Thinh NC, Breda Y, Faucompret S, et al. Oriental biliary lithia-sis. Retrospective study of 690 patients treated surgically over 8 years at Hospital 108 in Hanoi (Vietnam). Med Trop (Mars). 2001;61:509-511. 50. Akhan O, Akinci D, Ozmen MN. Percutaneous cholecystos-tomy. Eur J Radiol. 2002;43:229-236. 51. Khaitan L, Apelgren K, Hunter J, et al. A report on the Society of American Gastrointestinal Endoscopic Surgeons (SAGES) Outcomes Initiative: what have we learned and what is its potential? Surg Endosc. 2003;17:365-370. 52. Richards C, Edwards J, Culver D, et al. Does using a laparo-scopic approach to cholecystectomy decrease the risk of surgi-cal site infection? Ann Surg. 2003;237:358-362. 53. Halbert C, Pagkratis S, Yang J, et al. Beyond the learning curve: incidence of bile duct injuries following laparoscopic cholecys-tectomy normalize to open in the modern era. Surg Endosc. 2016;30(6):2239-2243. 54. The SAGES Safe Cholecystectomy Program.


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Surgery_Schwartz. curve: incidence of bile duct injuries following laparoscopic cholecys-tectomy normalize to open in the modern era. Surg Endosc. 2016;30(6):2239-2243. 54. The SAGES Safe Cholecystectomy Program. Strategies for minimizing bile duct injuries: adopting a universal culture of safety in cholecystectomy. Available at:https://www.sages.org/safe-cholecystectomy-program/. Accessed July 28, 2018. 55. Ford JA, Soop M, Du J, Loveday BP, Rodgers M. Systematic review of intraoperative cholangiography in cholecystectomy. Br J Surg. 2012;99(2):160-167. 56. Biffl W, Moore E, Offner P, et al. Routine intraoperative ultra-sonography with selective cholangiography reduces bile duct complications during laparoscopic cholecystectomy. J Am Coll Surg. 2001;193:272-280. 57. Ragulin-Coyne E, Witkowski ER, Chau Z, et al. Is routine intra-operative cholangiogram necessary in the twenty-first century? A national view. J Gastrointest Surg. 2013;17(3):434-442. 58. Flum DR, Dellinger EP, Cheadle A, et al.


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Surgery_Schwartz. Chau Z, et al. Is routine intra-operative cholangiogram necessary in the twenty-first century? A national view. J Gastrointest Surg. 2013;17(3):434-442. 58. Flum DR, Dellinger EP, Cheadle A, et al. Intraoperative chol-angiography and risk of common bile duct injury during chole-cystectomy. JAMA. 2003;289:1639-1644. 59. Halpin VJ, Dunnegan D, Soper NJ. Laparoscopic intracorporeal ultrasound versus fluoroscopic intraoperative cholangiography: after the learning curve. Surg Endosc. 2002;16:336-341. 60. Zheng C, Huang Y, Xie E, Xie D, Peng Y, Wang X. Laparo-scopic common bile duct exploration: a safe and definitive treat-ment for elderly patients. Surg Endosc. 2017;31(6):2541-2547. 61. Petelin JB. Laparoscopic common bile duct exploration. Surg Endosc. 2003:Nov;17(11):1705-1715. 62. George J, Baillie J. Biliary and gallbladder dyskinesia. Curr Treat Options Gastroenterol. 2007;10(4):322-327. 63. Linder JD, Klapow JC, Linder SD, et al. Incomplete response to endoscopic sphincterotomy in


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Surgery_Schwartz. J, Baillie J. Biliary and gallbladder dyskinesia. Curr Treat Options Gastroenterol. 2007;10(4):322-327. 63. Linder JD, Klapow JC, Linder SD, et al. Incomplete response to endoscopic sphincterotomy in patients with sphincter of Oddi dysfunction: evidence for a chronic pain disorder. Am J Gastro-enterol. 2003;98:1738-1743. 64. Huffman JL, Schenker S. Acute acalculous cholecystitis: a review. Clin Gastroenterol Hepatol. 2010;8(1):15-22. 65. Ryu JK, Ryu KH, Kim KH. Clinical features of acute acalcu-lous cholecystitis. J Clin Gastroenterol. 2003;36:166-169. 66. Lipsett PA, Pitt HA. Surgical treatment of choledochal cysts. J Hepatobiliary Pancreat Surg. 2003;10:352-359. 67. Hirschfield GM, Karlsen TH, Lindor KD, Adams DH. Primary sclerosing cholangitis. Lancet. 2013;382(9904):1587-1599. 68. Michales A, Levy C. Endoscopic and surgical manage-ment of primary sclerosing cholangitis. Medscape J Med. 2008;10(10):242. 69. Lillemoe KD, Melton GB, Cameron JL, et al. Postoperative bile duct


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Surgery_Schwartz. A, Levy C. Endoscopic and surgical manage-ment of primary sclerosing cholangitis. Medscape J Med. 2008;10(10):242. 69. Lillemoe KD, Melton GB, Cameron JL, et al. Postoperative bile duct strictures: Management and outcome in the 1990s. Ann Surg. 2000;232:430-431. 70. Melton GB, Lillemoe KD. The current management of postop-erative bile duct strictures. Adv Surg. 2002;36:193-221. 71. Archer SB, Brown DW, Smith CD, et al. Bile duct injury during laparoscopic cholecystectomy: results of a national survey. Ann Surg. 2001;234:549-558. 72. Halbert C, Altieri MS, Yang J, et al. Long-term outcomes of patients with common bile duct injury following laparoscopic cholecystectomy. Surg Endosc. 2016;30(10):4294-4299. 73. Barrett M, Asbun HJ, Chien HL, Brunt LM, Telem DA. Bile duct injury and morbidity following cholecystectomy: a need for improvement. Surg Endosc. 2017. Available at: https://doi .org/10.1007/s00464-017-5847-8. Accessed July 28, 2018. 74. Strasberg SM. Avoidance of biliary injury


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Surgery_Schwartz. following cholecystectomy: a need for improvement. Surg Endosc. 2017. Available at: https://doi .org/10.1007/s00464-017-5847-8. Accessed July 28, 2018. 74. Strasberg SM. Avoidance of biliary injury during laparoscopic cholecystectomy. J Hepatobiliary Pancreat Surg. 2002;9: 543-547. 75. Way LW, Stewart L, Gantert W, et al. Causes and preven-tion of laparoscopic bile duct injuries: analysis of 252 cases from a human factors and cognitive psychology perspective [Comment]. Ann Surg. 2003;237(4):460-469. 76. Halawani HM, Tamim H, Khalifeh F, Mailhac A, Jamali FR. Impact of intraoperative cholangiography on postoperative mor-bidity and readmission: analysis of the NSQIP database. Surg Endosc. 2016;30(12):5395-5403. 77. van den Bos J, Schols RM, Luyer MD, et al. Near-infrared fluorescence cholangiography assisted laparoscopic cholecys-tectomy versus conventional laparoscopic cholecystectomy (FALCON trial): study protocol for a multicentre randomised controlled trial. BMJ Open.


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Surgery_Schwartz. cholangiography assisted laparoscopic cholecys-tectomy versus conventional laparoscopic cholecystectomy (FALCON trial): study protocol for a multicentre randomised controlled trial. BMJ Open. 2016;26;6(8):e011668. 78. Melton GB, Lillemoe KD, Cameron JL, et al. Major bile duct injuries associated with laparoscopic cholecystectomy: effect of surgical repair on quality of life. Ann Surg. 2002;235:888-895. 79. Grobmyer SR, Lieberman MD, Daly JM. Gallbladder cancer in the twentieth century: single institution’s experience. World J Surg. 2004;28:47-49. 80. Hundal R, Shaffer EA. Gallbladder cancer: epidemiology and outcome. Clin Epidemiol. 2014;6:99-109. 81. Lowenfels AB, Walker AM, Althaus DP, et al. Gallstone growth, size, and risk of gallbladder cancer: an interracial study. Int J Epidemiol. 1998;18:50-54.Brunicardi_Ch32_p1393-p1428.indd 142611/02/19 2:44 PM 1427GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32 82. Csendes A, Burgos AM, Csendes P, et al. Late follow-up of


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Surgery_Schwartz. 1998;18:50-54.Brunicardi_Ch32_p1393-p1428.indd 142611/02/19 2:44 PM 1427GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEMCHAPTER 32 82. Csendes A, Burgos AM, Csendes P, et al. Late follow-up of polypoid lesions of the gallbladder smaller than 10 mm. Ann Surg. 2001;234:657-660. 83. Wagholikar G, Behari A, Krishnani N, et al. Early gallbladder cancer. J Am Coll Surg. 2002;194:137-141. 84. Kim JH, Kim TK, Eun HW. Preoperative evaluation of gall-bladder carcinoma: efficacy of combined use of MR imag-ing, MR cholangiography, and contrast-enhanced dual phase three dimensional MR angiography. J Magn Reson Imaging. 2002;16:676-684. 85. Bartlett DL, Fong Y, Fortner JG, et al. Long-term results after resection for gallbladder cancer. Implications for staging and management. Ann Surg. 1996;224:639-646. 86. Wakai T, Shirai Y, Hatakeyama K. Radical second resection provides survival benefit for patients with T2 gallbladder car-cinoma first discovered after laparoscopic cholecystectomy. World J


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Surgery_Schwartz. T, Shirai Y, Hatakeyama K. Radical second resection provides survival benefit for patients with T2 gallbladder car-cinoma first discovered after laparoscopic cholecystectomy. World J Surg. 2002;26:867-871. 87. Noshiro H, Chijiiwa K, Yamaguchi K, et al. Factors affecting surgical outcome for gallbladder carcinoma. Hepatogastroen-terology. 2003;50:939-944. 88. Razumilava N, Gores GJ. Cholangiocarcinoma. Lancet. 2014;383(9935):2168-2179. 89. Nehls O, Gregor M, Klump B. Serum and bile markers for chol-angiocarcinoma. Semin Liver Dis. 2004;24:139-154. 90. Siqueira E, Schoen RE, Silverman W, et al. Detecting cholan-giocarcinoma in patients with primary sclerosing cholangitis. Gastrointest Endosc. 2005;56:40-47. 91. Lillemoe KD, Cameron JL. Surgery for hilar cholangiocarci-noma: the Johns Hopkins approach. J Hepatobiliary Pancreat Surg. 2000;7:115-121. 92. Mulholland MW, Yahanda A, Yeo CJ. Multidisciplinary management of perihilar bile duct cancer. J Am Coll Surg.


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Surgery_Schwartz. the Johns Hopkins approach. J Hepatobiliary Pancreat Surg. 2000;7:115-121. 92. Mulholland MW, Yahanda A, Yeo CJ. Multidisciplinary management of perihilar bile duct cancer. J Am Coll Surg. 2001;193(4):440-447. 93. Vollmer CM, Drebin JA, Middleton WD, et al. Utility of staging laparoscopy in subsets of peripancreatic and biliary malignan-cies [Comment]. Ann Surg. 2002;235:1-7. 94. Strasberg SM. ERCP and surgical intervention in pancre-atic and biliary malignancies. Gastrointest Endosc. 2002;56: S213-S217. 95. Ortner ME, Caca K, Berr F, et al. Successful photodynamic therapy for nonresectable cholangiocarcinoma: a randomized prospective study. Gastroenterology. 2003;125:1355-1363. 96. Cheon YK, Lee TY, Lee SM, Yoon JY, Shim CS. Longterm out-come of photodynamic therapy compared with biliary stenting alone in patients with advanced hilar cholangiocarcinoma. HPB (Oxford). 2012;14(3):185-193.97. DesJardins H, Duy L, Scheirey C, Schnelldorfer T. Porcelain Gallbladder: Is Observation a Safe


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Surgery_Schwartz. stenting alone in patients with advanced hilar cholangiocarcinoma. HPB (Oxford). 2012;14(3):185-193.97. DesJardins H, Duy L, Scheirey C, Schnelldorfer T. Porcelain Gallbladder: Is Observation a Safe Option in Select Popula-tions? J Am Coll Surg. 2018 Jun;226(6):1064–1069.Brunicardi_Ch32_p1393-p1428.indd 142711/02/19 2:44 PM


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Surgery_Schwartz. PancreasWilliam E. Fisher, Dana K. Andersen, John A. Windsor, Vikas Dudeja, and F. Charles Brunicardi 33chapterANATOMYThe pancreas is perhaps the most unforgiving organ in the human body, leading most surgeons to avoid even palpating it unless necessary. Situated deep in the center of the abdomen, the pancreas is surrounded by numerous important structures and major blood vessels. Seemingly minor trauma to the pan-creas can result in the release of pancreatic enzymes and cause life-threatening pancreatitis. Therefore, knowledge of the rela-tionships of the pancreas to surrounding structures is critically important for all surgeons to ensure that pancreatic injury is avoided during abdominal surgery.Gross AnatomyThe pancreas is a retroperitoneal organ that lies in an oblique position, sloping upward from the C-loop of the duodenum to the splenic hilum (Fig. 33-1). In an adult, the pancreas weighs 75 to 100 g and is about 15 to 20 cm long. The fact that the pan-creas is situated so


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Surgery_Schwartz. sloping upward from the C-loop of the duodenum to the splenic hilum (Fig. 33-1). In an adult, the pancreas weighs 75 to 100 g and is about 15 to 20 cm long. The fact that the pan-creas is situated so deeply in the abdomen and is sealed in the retroperitoneum explains the poorly localized and sometimes ill-defined nature with which pancreatic pathology presents. Patients with pancreatic cancer without bile duct obstruction usually present after months of vague upper abdominal discom-fort, or no antecedent symptoms at all. Due to its retroperitoneal location, pain associated with pancreatitis often is characterized as penetrating through to the back.Regions of the PancreasSurgeons typically describe the location of pathology within the pancreas in relation to four regions: the head, neck, body, and tail. The head of the pancreas is nestled in the C-loop of the duodenum and is posterior to the transverse mesocolon. Just pos-terior to the head of the pancreas lie the vena cava, the right


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Surgery_Schwartz. and tail. The head of the pancreas is nestled in the C-loop of the duodenum and is posterior to the transverse mesocolon. Just pos-terior to the head of the pancreas lie the vena cava, the right renal artery, and both renal veins. The neck of the pancreas lies directly anterior to the portal vein. At the inferior border of the neck of the pancreas, the superior mesenteric vein joins the splenic vein and then continues toward the porta hepatis as the portal vein. The inferior mesenteric vein often joins the splenic vein near Anatomy1429Gross Anatomy / 1429Regions of the Pancreas / 1429Pancreatic Duct Anatomy / 1432Vascular and Lymphatic Anatomy / 1433Neuroanatomy / 1435Histology and Physiology1435Exocrine Pancreas / 1435Endocrine Pancreas / 1437Islet Distribution / 1439Acute Pancreatitis1439Definition, Incidence, and Epidemiology / 1439Etiology / 1440Gallstones / 1440Alcohol / 1440Iatrogenic / 1441Hereditary Pancreatitis / 1441Tumors / 1441Hyperlipidemia / 1441Drugs /


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Surgery_Schwartz. Pancreatitis1439Definition, Incidence, and Epidemiology / 1439Etiology / 1440Gallstones / 1440Alcohol / 1440Iatrogenic / 1441Hereditary Pancreatitis / 1441Tumors / 1441Hyperlipidemia / 1441Drugs / 1441Pathophysiology / 1441Precipitating Events / 1441Intrapancreatic Events / 1442Systemic Events / 1443Management of Acute Pancreatitis / 1443Diagnosis / 1444Pain Management / 1444Predicting Severity / 1444Classification of Severity / 1445Determining Etiology / 1446Fluid Resuscitation / 1446Nutritional Support / 1446Cross-Sectional Imaging / 1446Therapeutic Endoscopic Retrograde Cholangiopancreatography / 1447Antibiotics / 1447Managing Local Complications / 1447Managing Organ Failure / 1448Cholecystectomy / 1449Diabetes / 1449Chronic Pancreatitis1450Definition, Incidence, and Prevalence / 1450Etiology / 1450Genetic Causes / 1450Alcohol / 1451Hyperparathyroidism / 1452Hyperlipidemia / 1452Classification / 1452Chronic Calcific (Lithogenic) Pancreatitis / 1452Chronic Obstructive


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Surgery_Schwartz. / 1450Etiology / 1450Genetic Causes / 1450Alcohol / 1451Hyperparathyroidism / 1452Hyperlipidemia / 1452Classification / 1452Chronic Calcific (Lithogenic) Pancreatitis / 1452Chronic Obstructive Pancreatitis / 1453Chronic Inflammatory Pancreatitis / 1454Tropical (Nutritional) Pancreatitis / 1455Asymptomatic Pancreatic Fibrosis / 1455Idiopathic Pancreatitis / 1455Pathology / 1456Presentation, Natural History, and Complications / 1460Complications / 1465Treatment / 1468Pancreatic Neoplasms1480Neoplasms of the Endocrine Pancreas / 1480Insulinoma / 1480Noninsulinoma Hyperinsulinemia Hypoglycemia Syndrome / 1481Gastrinoma / 1481Vasoactive Intestinal Peptide-Secreting Tumor / 1482Glucagonoma / 1482Somatostatinoma / 1483Nonfunctioning Pancreatic Endocrine Tumors / 1483Neoplasms of the Exocrine Pancreas / 1484Workup of Asymptomatic Pancreatic Cystic Neoplasms / 1504Brunicardi_Ch33_p1429-p1516.indd 142901/03/19 6:44 PM 1430Key Points1 Incomplete fusion of the dorsal and ventral


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Surgery_Schwartz. Exocrine Pancreas / 1484Workup of Asymptomatic Pancreatic Cystic Neoplasms / 1504Brunicardi_Ch33_p1429-p1516.indd 142901/03/19 6:44 PM 1430Key Points1 Incomplete fusion of the dorsal and ventral pancreatic ducts results in pancreas divisum, but a variety of ductal anomalies can be seen. Magnetic resonance cholangiopancreatography as well as endoscopic retrograde cholangiopancreatography can identify these ductal anomalies, and clarification of the ductal pattern of the pancreas is important before attempts at interventions.2 The “replaced right hepatic artery” occurs in 15% of patients and needs to be identified preoperatively to prevent inadvertent injury with resulting hepatic necrosis. Anomalous hepatic arterial anatomy can result in hepatic ischemia during dissection of the porta hepatis as well. “Thin cut” multidetector computed tomographic images are usually able to identify the relevant arterial and venous patterns around the pancreas.3 Regardless of the etiology, the


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Surgery_Schwartz. hepatis as well. “Thin cut” multidetector computed tomographic images are usually able to identify the relevant arterial and venous patterns around the pancreas.3 Regardless of the etiology, the management of the early phase of acute pancreatitis is critical to achieve a success-ful outcome. Aggressive fluid resuscitation and early enteral feeding both reduce the risk of complications. It is no longer considered appropriate to “rest the pancreas” if the patient can tolerate enteral nutrients.4 Surgical intervention in acute pancreatitis is reserved for patients with infected collections or infected necrosis only, or to relieve an impacted gallstone in the ampulla if endo-scopic or radiologic treatments are unsuccessful. Infection is usually confirmed by a pattern of air in the retroperitoneum on computed tomographic scan or by documentation of bac-teria on Gram’s stain or culture from fine-needle aspiration of a suspected infected fluid collection. Fine-needle aspira-tion of


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Surgery_Schwartz. on computed tomographic scan or by documentation of bac-teria on Gram’s stain or culture from fine-needle aspiration of a suspected infected fluid collection. Fine-needle aspira-tion of suspicious fluid collections should not be converted to percutaneous drainage unless infection is confirmed and the consensus decision has been made that percutaneous drainage is appropriate for the individual patient.5 The appearance of chronic pancreatitis on computed tomo-graphic scan varies dramatically, and multiple diagnostic studies are usually needed to establish the extent of disease. Calcific pancreatitis is not a marker of alcoholic pancreati-tis alone, and it rarely indicates autoimmune pancreatitis. Endoscopic ultrasound provides a better assessment of the disease than computed tomography and is useful to disclose indolent or unsuspected cancer, which can occur in up to 10% of patients.6 The nidus of inflammation in chronic pancreatitis due to any cause is the head of the gland. Therefore,


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Surgery_Schwartz. useful to disclose indolent or unsuspected cancer, which can occur in up to 10% of patients.6 The nidus of inflammation in chronic pancreatitis due to any cause is the head of the gland. Therefore, treatment approaches that address the disease in the head have the best long-term results. The Whipple procedure, the Beger procedure, and the Frey procedure, with or without longitu-dinal duct drainage, are the best surgical options, as all three approaches remove all or most of the disease in the head of the gland. Although the limited pancreatic procedures (Beger/Frey) have a lower initial rate of endocrine dysfunc-tion, the long-term risk of diabetes is more related to the progression of the underlying disease than to the effects of operation. Level 1 studies confirm that the duodenum pre-serving options are associated with a lower immediate mor-bidity and mortality and therefore, in the absence of a mass or concerns about cancer, are better options than a Whipple procedure for chronic


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Surgery_Schwartz. options are associated with a lower immediate mor-bidity and mortality and therefore, in the absence of a mass or concerns about cancer, are better options than a Whipple procedure for chronic pancreatitis.7 The precursor lesion that probably leads to most cases of ductular adenocarcinoma is the ductal epithelial hyperplasia/dysplasia process described by the pancreatic intraepithelial neoplasia classification system. Pancreatic intraepithelial neoplasia 2 and pancreatic intraepithelial neoplasia 3 lesions may be associated with other, nonspecific changes in pancre-atic morphology seen on imaging studies, or they may only be seen histologically. Resection margins for pancreatic neo-plasms should be examined for advanced pancreatic intraep-ithelial neoplasia stage patterns of ductal hyperplasia to ensure adequate resection status.8 A low threshold for ordering a computed tomography scan with “pancreatic protocol” should be maintained for older adult patients with unexplained,


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Surgery_Schwartz. hyperplasia to ensure adequate resection status.8 A low threshold for ordering a computed tomography scan with “pancreatic protocol” should be maintained for older adult patients with unexplained, persistent, although vague, abdominal pain. New-onset diabetes in an older adult patient, especially if combined with vague abdominal pain, should prompt a search for pancreatic cancer.9 Intraductal papillary mucinous neoplasms are small macro-scopic polypoid or plaque-like adenomas that develop in the main pancreatic duct or in side-branch ducts, and secrete mucin. They are often silent symptomatically but cause char-acteristic appearances of small cyst-like collections of mucus or diffuse dilatation of the main pancreatic duct with mucus. These premalignant lesions may be multifocal or single and can evolve into invasive adenocarcinoma in a similar pattern as with other adenomatous polypoid lesions of the gastroin-testinal tract. They have been diagnosed with increasing fre-quency and


Surgery_Schwartz

Surgery_Schwartz. and can evolve into invasive adenocarcinoma in a similar pattern as with other adenomatous polypoid lesions of the gastroin-testinal tract. They have been diagnosed with increasing fre-quency and account for more than one-third of pancreatic resections at some centers. Main-duct intraductal papillary mucinous neoplasms are an indication for resection; side-branch intraductal papillary mucinous neoplasms have a lower incidence of malignancy and are sometimes followed with serial imaging surveillance.its junction with the portal vein. Sometimes, the inferior mesen-teric vein joins the superior mesenteric vein or merges with the superior mesenteric portal venous junction to form a trifurca-tion (Fig. 33-2). The superior mesenteric artery lies parallel to and just to the left of the superior mesenteric vein. The uncinate process and the head of the pancreas wrap around the right side of the portal vein and end posteriorly near the space between the superior mesenteric vein and superior


Surgery_Schwartz

Surgery_Schwartz. mesenteric vein. The uncinate process and the head of the pancreas wrap around the right side of the portal vein and end posteriorly near the space between the superior mesenteric vein and superior mesenteric artery. Venous branches draining the pancreatic head and uncinate process enter along the right lateral and posterior sides of the portal vein. There are usually no anterior venous tributaries, and a plane can usually be developed between the neck of the pancreas and the portal and superior mesenteric veins during pancreatic resection, unless the tumor is invading the vein anteriorly. The common bile duct runs in a deep groove on the posterior aspect of the pancreatic head until it passes through the pancreatic parenchyma to join the main pancreatic duct at the ampulla of Vater. The body and tail of the pancreas lie just anterior to the splenic artery and vein. The vein runs in a groove on the back of the pancreas and is fed by multiple fragile venous branches from the pancreatic


Surgery_Schwartz

Surgery_Schwartz. and tail of the pancreas lie just anterior to the splenic artery and vein. The vein runs in a groove on the back of the pancreas and is fed by multiple fragile venous branches from the pancreatic paren-chyma. These branches must be divided to perform a spleen-sparing distal pancreatectomy. The splenic artery runs parallel and just superior to the vein along the posterior superior edge of the body and tail of the pancreas. The splenic artery often is Brunicardi_Ch33_p1429-p1516.indd 143001/03/19 6:44 PM 1431PANCREASCHAPTER 33Body of pancreasTail of pancreasNeck of pancreasStomachLiverPortal veinSplenic veinGallbladderDuodenumHead of pancreasUncinate processof pancreasLeft kidneyVena cavaDuodenumAortaStomachHead of pancreasLeft kidneySMASMADuodenumJejunum4th portionof duodenumHead of pancreasPortal veinIMVSMVHead of pancreasDuodenumJejunumTail of pancreasStomachLiverPortal veinHead of pancreasDuodenumSMVFigure 33-1. Pancreatic anatomy as seen on computed tomography. Knowledge of the