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Surgery_Schwartz_9402 | 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 | 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 |
Surgery_Schwartz_9403 | 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 | 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 |
Surgery_Schwartz_9404 | 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 | 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 |
Surgery_Schwartz_9405 | 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 | 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 |
Surgery_Schwartz_9406 | 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 | 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 |
Surgery_Schwartz_9407 | 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 | 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 |
Surgery_Schwartz_9408 | 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 | 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 |
Surgery_Schwartz_9409 | 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 | 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 |
Surgery_Schwartz_9410 | 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 | 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 |
Surgery_Schwartz_9411 | 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 | 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 |
Surgery_Schwartz_9412 | 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 | 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 |
Surgery_Schwartz_9413 | 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 | 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 |
Surgery_Schwartz_9414 | 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 | 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 |
Surgery_Schwartz_9415 | 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 | 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 |
Surgery_Schwartz_9416 | 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 | 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 |
Surgery_Schwartz_9417 | 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 | 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 |
Surgery_Schwartz_9418 | 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 | 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 |
Surgery_Schwartz_9419 | 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 | 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 |
Surgery_Schwartz_9420 | 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 | 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 |
Surgery_Schwartz_9421 | 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 | 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 |
Surgery_Schwartz_9422 | 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 | 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 |
Surgery_Schwartz_9423 | 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 | 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 |
Surgery_Schwartz_9424 | 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 | 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 |
Surgery_Schwartz_9425 | 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 | 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 |
Surgery_Schwartz_9426 | 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 | 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 |
Surgery_Schwartz_9427 | 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 | 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 |
Surgery_Schwartz_9428 | 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 | 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 |
Surgery_Schwartz_9429 | 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 | 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 |
Surgery_Schwartz_9430 | 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 | 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 |
Surgery_Schwartz_9431 | 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 | 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 |
Surgery_Schwartz_9432 | 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 | 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 |
Surgery_Schwartz_9433 | 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 | 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 |
Surgery_Schwartz_9434 | 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 | 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 |
Surgery_Schwartz_9435 | 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 | 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 |
Surgery_Schwartz_9436 | 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 | 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 |
Surgery_Schwartz_9437 | 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 | 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 |
Surgery_Schwartz_9438 | 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 | 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 |
Surgery_Schwartz_9439 | 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. | 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. |
Surgery_Schwartz_9440 | 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 | 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 |
Surgery_Schwartz_9441 | 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 | 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 |
Surgery_Schwartz_9442 | 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, | 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, |
Surgery_Schwartz_9443 | 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, | 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, |
Surgery_Schwartz_9444 | 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. | 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_9446 | 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 | 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_9457 | 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 | 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_9459 | 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 | 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 |
Surgery_Schwartz_9460 | 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 | 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 |
Surgery_Schwartz_9461 | 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 / | 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 / |
Surgery_Schwartz_9462 | 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 | 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 |
Surgery_Schwartz_9463 | 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 | 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 |
Surgery_Schwartz_9464 | 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 | 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 |
Surgery_Schwartz_9465 | 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 | 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 |
Surgery_Schwartz_9466 | 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, | 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, |
Surgery_Schwartz_9467 | 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 | 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 |
Surgery_Schwartz_9468 | 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, | 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, |
Surgery_Schwartz_9469 | 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. 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_9470 | 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. 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_9471 | 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. 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_9472 | 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 | 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 |
Surgery_Schwartz_9473 | Surgery_Schwartz | veinIMVSMVHead of pancreasDuodenumJejunumTail of pancreasStomachLiverPortal veinHead of pancreasDuodenumSMVFigure 33-1. Pancreatic anatomy as seen on computed tomography. Knowledge of the relationship of the pancreas with surrounding structures is important to ensure that injury is avoided during abdominal surgery. IMV = inferior mesenteric vein; SMA = superior mesenteric artery; SMV = superior mesenteric vein.PortalveinSplenicveinInferiormesentericveinSuperiormesentericveinSuperiormesentericveinSuperiormesentericveinInferiormesentericveinInferiormesentericveinSplenicveinSplenicveinPortalveinPortalveinFigure 33-2. Variations in portal venous anatomy. 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 its junction with the portal vein, but sometimes joins the superior mesenteric vein; or the three veins merge as a trifurcation to form the portal | Surgery_Schwartz. veinIMVSMVHead of pancreasDuodenumJejunumTail of pancreasStomachLiverPortal veinHead of pancreasDuodenumSMVFigure 33-1. Pancreatic anatomy as seen on computed tomography. Knowledge of the relationship of the pancreas with surrounding structures is important to ensure that injury is avoided during abdominal surgery. IMV = inferior mesenteric vein; SMA = superior mesenteric artery; SMV = superior mesenteric vein.PortalveinSplenicveinInferiormesentericveinSuperiormesentericveinSuperiormesentericveinSuperiormesentericveinInferiormesentericveinInferiormesentericveinSplenicveinSplenicveinPortalveinPortalveinFigure 33-2. Variations in portal venous anatomy. 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 its junction with the portal vein, but sometimes joins the superior mesenteric vein; or the three veins merge as a trifurcation to form the portal |
Surgery_Schwartz_9474 | Surgery_Schwartz | mesenteric vein often joins the splenic vein near its junction with the portal vein, but sometimes joins the superior mesenteric vein; or the three veins merge as a trifurcation to form the portal vein.Brunicardi_Ch33_p1429-p1516.indd 143101/03/19 6:44 PM 1432SPECIFIC CONSIDERATIONSPART IIBlindaccessory duct30%60%Minor papilla10%Dorsal anlageVentral anlageVentral budLiver budLesser oraccessorypapillaGreaterpapillaFusion oftwo ductsBile ductDorsal budDuct ofsantoriniDuct ofwirsungFigure 33-3. Embryology of pancreas and duct variations. The duct of Wirsung from the ventral bud connects to the bile duct, while the duct of Santorini from the larger dorsal bud connects to the duodenum. With gut rotation, the two ducts fuse in most cases such that the majority of the pancreas drains through the duct of Wirsung to the major papilla. The duct of Santorini can persist as a blind accessory duct or drain through the lesser papilla. In a minority of patients, the ducts remain separate, and | Surgery_Schwartz. mesenteric vein often joins the splenic vein near its junction with the portal vein, but sometimes joins the superior mesenteric vein; or the three veins merge as a trifurcation to form the portal vein.Brunicardi_Ch33_p1429-p1516.indd 143101/03/19 6:44 PM 1432SPECIFIC CONSIDERATIONSPART IIBlindaccessory duct30%60%Minor papilla10%Dorsal anlageVentral anlageVentral budLiver budLesser oraccessorypapillaGreaterpapillaFusion oftwo ductsBile ductDorsal budDuct ofsantoriniDuct ofwirsungFigure 33-3. Embryology of pancreas and duct variations. The duct of Wirsung from the ventral bud connects to the bile duct, while the duct of Santorini from the larger dorsal bud connects to the duodenum. With gut rotation, the two ducts fuse in most cases such that the majority of the pancreas drains through the duct of Wirsung to the major papilla. The duct of Santorini can persist as a blind accessory duct or drain through the lesser papilla. In a minority of patients, the ducts remain separate, and |
Surgery_Schwartz_9475 | Surgery_Schwartz | the duct of Wirsung to the major papilla. The duct of Santorini can persist as a blind accessory duct or drain through the lesser papilla. In a minority of patients, the ducts remain separate, and the majority of the pancreas drains through the duct of Santorini, a condition referred to as pancreas divisum.tortuous. The anterior surface of the body of the pancreas is cov-ered by peritoneum. Once the gastrocolic omentum is divided, the body and tail of the pancreas can be seen along the floor of the lesser sac, just posterior to the stomach.Pancreatic pseudocysts commonly develop in this area, and the posterior aspect of the stomach can form the anterior wall of the pseudocyst, allowing drainage into the stomach. The base of the transverse mesocolon attaches to the inferior margin of the body and tail of the pancreas. The transverse mesoco-lon often forms the inferior wall of pancreatic pseudocysts or inflammatory processes, allowing surgical drainage through the transverse mesocolon. | Surgery_Schwartz. the duct of Wirsung to the major papilla. The duct of Santorini can persist as a blind accessory duct or drain through the lesser papilla. In a minority of patients, the ducts remain separate, and the majority of the pancreas drains through the duct of Santorini, a condition referred to as pancreas divisum.tortuous. The anterior surface of the body of the pancreas is cov-ered by peritoneum. Once the gastrocolic omentum is divided, the body and tail of the pancreas can be seen along the floor of the lesser sac, just posterior to the stomach.Pancreatic pseudocysts commonly develop in this area, and the posterior aspect of the stomach can form the anterior wall of the pseudocyst, allowing drainage into the stomach. The base of the transverse mesocolon attaches to the inferior margin of the body and tail of the pancreas. The transverse mesoco-lon often forms the inferior wall of pancreatic pseudocysts or inflammatory processes, allowing surgical drainage through the transverse mesocolon. |
Surgery_Schwartz_9476 | Surgery_Schwartz | and tail of the pancreas. The transverse mesoco-lon often forms the inferior wall of pancreatic pseudocysts or inflammatory processes, allowing surgical drainage through the transverse mesocolon. The body of the pancreas is anterior to the aorta at the origin of the superior mesenteric artery. The neck of the pancreas is anterior to the vertebral body of L1 and L2, and blunt anteroposterior trauma can compress the neck of the pancreas against the spine, causing parenchymal and, sometimes, ductal injury. The neck divides the pancreas into approximately two equal halves. The small portion of the pan-creas anterior to the left kidney is referred to as the tail and is nestled in the hilum of the spleen near the splenic flexure of the left colon. Awareness of these anatomic relationships is impor-tant to avoid injury to the pancreatic tail during left colectomy or splenectomy.Pancreatic Duct AnatomyAn understanding of embryology is required to appreciate the common variations in pancreatic | Surgery_Schwartz. and tail of the pancreas. The transverse mesoco-lon often forms the inferior wall of pancreatic pseudocysts or inflammatory processes, allowing surgical drainage through the transverse mesocolon. The body of the pancreas is anterior to the aorta at the origin of the superior mesenteric artery. The neck of the pancreas is anterior to the vertebral body of L1 and L2, and blunt anteroposterior trauma can compress the neck of the pancreas against the spine, causing parenchymal and, sometimes, ductal injury. The neck divides the pancreas into approximately two equal halves. The small portion of the pan-creas anterior to the left kidney is referred to as the tail and is nestled in the hilum of the spleen near the splenic flexure of the left colon. Awareness of these anatomic relationships is impor-tant to avoid injury to the pancreatic tail during left colectomy or splenectomy.Pancreatic Duct AnatomyAn understanding of embryology is required to appreciate the common variations in pancreatic |
Surgery_Schwartz_9477 | Surgery_Schwartz | to avoid injury to the pancreatic tail during left colectomy or splenectomy.Pancreatic Duct AnatomyAn understanding of embryology is required to appreciate the common variations in pancreatic duct anatomy. The pancreas is formed by the fusion of a ventral and dorsal bud (Fig. 33-3). The duct from the smaller ventral bud, which arises from the hepatic diverticulum, connects directly to the common bile duct. The duct from the larger dorsal bud, which arises from the duodenum, drains directly into the duodenum. The duct of the ventral anlage becomes the duct of Wirsung, and the duct from the dorsal anlage becomes the duct of Santorini. With gut rotation, the ventral anlage rotates to the right and around the posterior side of the duodenum to fuse with the dorsal bud. The ventral anlage becomes the inferior portion of the pancreatic head and the unci-nate process, while the dorsal anlage becomes the body and tail of the pancreas. The ducts from each anlage usually fuse together in the | Surgery_Schwartz. to avoid injury to the pancreatic tail during left colectomy or splenectomy.Pancreatic Duct AnatomyAn understanding of embryology is required to appreciate the common variations in pancreatic duct anatomy. The pancreas is formed by the fusion of a ventral and dorsal bud (Fig. 33-3). The duct from the smaller ventral bud, which arises from the hepatic diverticulum, connects directly to the common bile duct. The duct from the larger dorsal bud, which arises from the duodenum, drains directly into the duodenum. The duct of the ventral anlage becomes the duct of Wirsung, and the duct from the dorsal anlage becomes the duct of Santorini. With gut rotation, the ventral anlage rotates to the right and around the posterior side of the duodenum to fuse with the dorsal bud. The ventral anlage becomes the inferior portion of the pancreatic head and the unci-nate process, while the dorsal anlage becomes the body and tail of the pancreas. The ducts from each anlage usually fuse together in the |
Surgery_Schwartz_9478 | Surgery_Schwartz | the inferior portion of the pancreatic head and the unci-nate process, while the dorsal anlage becomes the body and tail of the pancreas. The ducts from each anlage usually fuse together in the pancreatic head such that most of the pancreas drains through the duct of Wirsung, or main pancreatic duct, into the common channel formed from the bile duct and pancreatic duct. The length of the common channel is variable. In about one-third of patients, the bile duct and pancreatic duct remain distinct to the end of the papilla, the two ducts merge at the end of the papilla in another one-third, and in the remaining one-third, a true common channel is present for a distance of several millimeters. Commonly, the duct from the dorsal anlage, the duct of Santorini, persists as the lesser pancreatic duct, and sometimes drains directly into the duo-denum through the lesser papilla just proximal to the major papilla. In approximately 30% of patients, the duct of Santorini ends as a blind accessory | Surgery_Schwartz. the inferior portion of the pancreatic head and the unci-nate process, while the dorsal anlage becomes the body and tail of the pancreas. The ducts from each anlage usually fuse together in the pancreatic head such that most of the pancreas drains through the duct of Wirsung, or main pancreatic duct, into the common channel formed from the bile duct and pancreatic duct. The length of the common channel is variable. In about one-third of patients, the bile duct and pancreatic duct remain distinct to the end of the papilla, the two ducts merge at the end of the papilla in another one-third, and in the remaining one-third, a true common channel is present for a distance of several millimeters. Commonly, the duct from the dorsal anlage, the duct of Santorini, persists as the lesser pancreatic duct, and sometimes drains directly into the duo-denum through the lesser papilla just proximal to the major papilla. In approximately 30% of patients, the duct of Santorini ends as a blind accessory |
Surgery_Schwartz_9479 | Surgery_Schwartz | duct, and sometimes drains directly into the duo-denum through the lesser papilla just proximal to the major papilla. In approximately 30% of patients, the duct of Santorini ends as a blind accessory duct and does not empty into the duodenum. In 10% of patients, the ducts of Wirsung and Santorini fail to fuse.1 This results in the majority of the pancreas draining through the duct of Santorini and the lesser papilla, while the inferior portion of the pancreatic head and uncinate process drains through the duct of Wirsung and major papilla. This nor-mal anatomic variant, which occurs in one out of 10 patients, is referred to as pancreas divisum (see Fig. 33-3). In a minority of these patients, the minor papilla can be inadequate to handle the flow of pancreatic juices from the majority of the gland. This rela-tive outflow obstruction can result in pancreatitis and is some-times treated by sphincteroplasty of the minor papilla.The main pancreatic duct is usually only 2 to 3 mm in | Surgery_Schwartz. duct, and sometimes drains directly into the duo-denum through the lesser papilla just proximal to the major papilla. In approximately 30% of patients, the duct of Santorini ends as a blind accessory duct and does not empty into the duodenum. In 10% of patients, the ducts of Wirsung and Santorini fail to fuse.1 This results in the majority of the pancreas draining through the duct of Santorini and the lesser papilla, while the inferior portion of the pancreatic head and uncinate process drains through the duct of Wirsung and major papilla. This nor-mal anatomic variant, which occurs in one out of 10 patients, is referred to as pancreas divisum (see Fig. 33-3). In a minority of these patients, the minor papilla can be inadequate to handle the flow of pancreatic juices from the majority of the gland. This rela-tive outflow obstruction can result in pancreatitis and is some-times treated by sphincteroplasty of the minor papilla.The main pancreatic duct is usually only 2 to 3 mm in |
Surgery_Schwartz_9480 | Surgery_Schwartz | of the gland. This rela-tive outflow obstruction can result in pancreatitis and is some-times treated by sphincteroplasty of the minor papilla.The main pancreatic duct is usually only 2 to 3 mm in diameter and runs midway between the superior and inferior borders of the pancreas, usually closer to the posterior than to the anterior surface. Pressure inside the pancreatic duct is about twice that in the common bile duct, which is thought to prevent reflux of bile into the pancreatic duct. The main pancreatic duct joins with the common bile duct and empties at the ampulla of Vater or major papilla, which is located on the medial aspect of the second portion of the duodenum. The muscle fibers around the ampulla form the sphincter of Oddi, which controls the flow of pancreatic and biliary secretions into the duodenum. Contrac-tion and relaxation of the sphincter is regulated by complex neu-ral and hormonal factors. When the accessory pancreatic duct or lesser duct drains into the | Surgery_Schwartz. of the gland. This rela-tive outflow obstruction can result in pancreatitis and is some-times treated by sphincteroplasty of the minor papilla.The main pancreatic duct is usually only 2 to 3 mm in diameter and runs midway between the superior and inferior borders of the pancreas, usually closer to the posterior than to the anterior surface. Pressure inside the pancreatic duct is about twice that in the common bile duct, which is thought to prevent reflux of bile into the pancreatic duct. The main pancreatic duct joins with the common bile duct and empties at the ampulla of Vater or major papilla, which is located on the medial aspect of the second portion of the duodenum. The muscle fibers around the ampulla form the sphincter of Oddi, which controls the flow of pancreatic and biliary secretions into the duodenum. Contrac-tion and relaxation of the sphincter is regulated by complex neu-ral and hormonal factors. When the accessory pancreatic duct or lesser duct drains into the |
Surgery_Schwartz_9481 | Surgery_Schwartz | secretions into the duodenum. Contrac-tion and relaxation of the sphincter is regulated by complex neu-ral and hormonal factors. When the accessory pancreatic duct or lesser duct drains into the duodenum, a lesser papilla can be identified approximately 2 cm proximal to the ampulla of Vater.1Brunicardi_Ch33_p1429-p1516.indd 143201/03/19 6:44 PM 1433PANCREASCHAPTER 33BileductPortalveinAbdominal aortaCeliac trunkSplenic arteryDorsalpancreatic arteryGreatpancreaticarteryCaudalarteryInferiorpancreatic arteryAnterior inferiorpancreaticoduodenal arteryAnterior superiorpancreatico-duodenalarteryPosterior inferiorpancreaticoduodenal arteryPosterior superiorpancreatico-duodenalarteryGastroduodenalarteryHepatic arteryproperCommon hepaticarterySuperiormesenteric arterySpleenDuodenumFigure 33-4. Arterial supply to the pancreas. Multiple arcades in the head and body of the pancreas provide a rich blood supply. The head of the pancreas cannot be resected without devascularizing the duodenum | Surgery_Schwartz. secretions into the duodenum. Contrac-tion and relaxation of the sphincter is regulated by complex neu-ral and hormonal factors. When the accessory pancreatic duct or lesser duct drains into the duodenum, a lesser papilla can be identified approximately 2 cm proximal to the ampulla of Vater.1Brunicardi_Ch33_p1429-p1516.indd 143201/03/19 6:44 PM 1433PANCREASCHAPTER 33BileductPortalveinAbdominal aortaCeliac trunkSplenic arteryDorsalpancreatic arteryGreatpancreaticarteryCaudalarteryInferiorpancreatic arteryAnterior inferiorpancreaticoduodenal arteryAnterior superiorpancreatico-duodenalarteryPosterior inferiorpancreaticoduodenal arteryPosterior superiorpancreatico-duodenalarteryGastroduodenalarteryHepatic arteryproperCommon hepaticarterySuperiormesenteric arterySpleenDuodenumFigure 33-4. Arterial supply to the pancreas. Multiple arcades in the head and body of the pancreas provide a rich blood supply. The head of the pancreas cannot be resected without devascularizing the duodenum |
Surgery_Schwartz_9482 | Surgery_Schwartz | supply to the pancreas. Multiple arcades in the head and body of the pancreas provide a rich blood supply. The head of the pancreas cannot be resected without devascularizing the duodenum unless a rim of pancreas containing the pancreaticoduodenal arcade is preserved.Vascular and Lymphatic AnatomyThe blood supply to the pancreas comes from multiple branches from the celiac and superior mesenteric arteries (Fig. 33-4). The common hepatic artery gives rise to the gastroduodenal artery before continuing toward the porta hepatis as the proper hepatic artery. The right gastric artery branches off the gastroduodenal artery just superior to the duodenum. The gastroduodenal artery also supplies the superior pancreaticoduodenal artery which divides into the anterior and superior pancreaticoduodenal arteries. These travel inferiorly within the pancreaticoduodenal groove giving off small branches to the duodenum and head of the pancreas. The superior pancreaticoduodenal arteries join the | Surgery_Schwartz. supply to the pancreas. Multiple arcades in the head and body of the pancreas provide a rich blood supply. The head of the pancreas cannot be resected without devascularizing the duodenum unless a rim of pancreas containing the pancreaticoduodenal arcade is preserved.Vascular and Lymphatic AnatomyThe blood supply to the pancreas comes from multiple branches from the celiac and superior mesenteric arteries (Fig. 33-4). The common hepatic artery gives rise to the gastroduodenal artery before continuing toward the porta hepatis as the proper hepatic artery. The right gastric artery branches off the gastroduodenal artery just superior to the duodenum. The gastroduodenal artery also supplies the superior pancreaticoduodenal artery which divides into the anterior and superior pancreaticoduodenal arteries. These travel inferiorly within the pancreaticoduodenal groove giving off small branches to the duodenum and head of the pancreas. The superior pancreaticoduodenal arteries join the |
Surgery_Schwartz_9483 | Surgery_Schwartz | arteries. These travel inferiorly within the pancreaticoduodenal groove giving off small branches to the duodenum and head of the pancreas. The superior pancreaticoduodenal arteries join the inferior pancreaticoduodenal arteries to complete the arcade. The inferior pancreaticoduodenal artery is a branch off the supe-rior mesenteric artery. Therefore, it is impossible to resect the head of the pancreas without devascularizing the duodenum, unless a rim of pancreas containing the pancreaticoduodenal arcade is preserved. The inferior pancreaticoduodenal artery needs to be controlled when dissecting the head of the pancreas off the SMA during a Whipple procedure. The gastroduodenal artery travels inferiorly anterior to the neck of the pancreas and posterior to the duodenal bulb. A posterior ulcer in the duodenal bulb can erode into the gastroduodenal artery in this location. At the inferior border of the duodenum, the gastroduodenal artery then gives rise to the right gastroepiploic | Surgery_Schwartz. arteries. These travel inferiorly within the pancreaticoduodenal groove giving off small branches to the duodenum and head of the pancreas. The superior pancreaticoduodenal arteries join the inferior pancreaticoduodenal arteries to complete the arcade. The inferior pancreaticoduodenal artery is a branch off the supe-rior mesenteric artery. Therefore, it is impossible to resect the head of the pancreas without devascularizing the duodenum, unless a rim of pancreas containing the pancreaticoduodenal arcade is preserved. The inferior pancreaticoduodenal artery needs to be controlled when dissecting the head of the pancreas off the SMA during a Whipple procedure. The gastroduodenal artery travels inferiorly anterior to the neck of the pancreas and posterior to the duodenal bulb. A posterior ulcer in the duodenal bulb can erode into the gastroduodenal artery in this location. At the inferior border of the duodenum, the gastroduodenal artery then gives rise to the right gastroepiploic |
Surgery_Schwartz_9484 | Surgery_Schwartz | ulcer in the duodenal bulb can erode into the gastroduodenal artery in this location. At the inferior border of the duodenum, the gastroduodenal artery then gives rise to the right gastroepiploic artery then can con-tinue on to join the inferior pancreaticoduodenal artery.Variations in the arterial anatomy occur in one out of five patients. The right hepatic artery, common hepatic artery, or gas-troduodenal arteries can arise from the superior mesenteric artery. In 15% to 20% of patients, the right hepatic artery will arise from the superior mesenteric artery and travel upwards toward the liver along the posterior aspect of the head of the pancreas (referred to as a replaced right hepatic artery). It is important to look for this variation on preoperative com-puted tomographic (CT) scans and in the operating room so the 2replaced hepatic artery is recognized and injury is avoided. The body and tail of the pancreas are supplied by multiple branches of the splenic artery. The splenic | Surgery_Schwartz. ulcer in the duodenal bulb can erode into the gastroduodenal artery in this location. At the inferior border of the duodenum, the gastroduodenal artery then gives rise to the right gastroepiploic artery then can con-tinue on to join the inferior pancreaticoduodenal artery.Variations in the arterial anatomy occur in one out of five patients. The right hepatic artery, common hepatic artery, or gas-troduodenal arteries can arise from the superior mesenteric artery. In 15% to 20% of patients, the right hepatic artery will arise from the superior mesenteric artery and travel upwards toward the liver along the posterior aspect of the head of the pancreas (referred to as a replaced right hepatic artery). It is important to look for this variation on preoperative com-puted tomographic (CT) scans and in the operating room so the 2replaced hepatic artery is recognized and injury is avoided. The body and tail of the pancreas are supplied by multiple branches of the splenic artery. The splenic |
Surgery_Schwartz_9485 | Surgery_Schwartz | and in the operating room so the 2replaced hepatic artery is recognized and injury is avoided. The body and tail of the pancreas are supplied by multiple branches of the splenic artery. The splenic artery arises from the celiac trunk and travels along the posterior-superior border of the body and tail of the pancreas toward the spleen. The inferior pancreatic artery usually arises from the superior mesenteric artery and runs to the left along the inferior border of the body and tail of the pancreas, parallel to the splenic artery. Three vessels run perpen-dicular to the long axis of the pancreatic body and tail and con-nect the splenic artery and inferior pancreatic artery. They are, from medial to lateral, the dorsal, great, and caudal pancreatic arteries. These arteries form arcades within the body and tail of the pancreas and account for the rich blood supply of the organ.The venous drainage of the pancreas follows a pattern similar to that of the arterial supply (Fig. 33-5). The | Surgery_Schwartz. and in the operating room so the 2replaced hepatic artery is recognized and injury is avoided. The body and tail of the pancreas are supplied by multiple branches of the splenic artery. The splenic artery arises from the celiac trunk and travels along the posterior-superior border of the body and tail of the pancreas toward the spleen. The inferior pancreatic artery usually arises from the superior mesenteric artery and runs to the left along the inferior border of the body and tail of the pancreas, parallel to the splenic artery. Three vessels run perpen-dicular to the long axis of the pancreatic body and tail and con-nect the splenic artery and inferior pancreatic artery. They are, from medial to lateral, the dorsal, great, and caudal pancreatic arteries. These arteries form arcades within the body and tail of the pancreas and account for the rich blood supply of the organ.The venous drainage of the pancreas follows a pattern similar to that of the arterial supply (Fig. 33-5). The |
Surgery_Schwartz_9486 | Surgery_Schwartz | the body and tail of the pancreas and account for the rich blood supply of the organ.The venous drainage of the pancreas follows a pattern similar to that of the arterial supply (Fig. 33-5). The veins are usually superficial to the arteries within the parenchyma of the pancreas. There is an anterior and posterior venous arcade within the head of the pancreas. Typically, the superior vein drains directly into the portal vein just above the neck of the pancreas and is often a larger branch of the portal vein which is divided during the Whipple procedure. The posterior infe-rior arcade drains directly into the inferior mesenteric vein at the inferior border of the neck of the pancreas and this is also divided during a Whipple procedure. The anterior inferior pan-creaticoduodenal vein joins the right gastroepiploic vein and the middle colic vein to form a common venous trunk, which enters into the superior mesenteric vein. Traction on the trans-verse colon during colectomy can tear these | Surgery_Schwartz. the body and tail of the pancreas and account for the rich blood supply of the organ.The venous drainage of the pancreas follows a pattern similar to that of the arterial supply (Fig. 33-5). The veins are usually superficial to the arteries within the parenchyma of the pancreas. There is an anterior and posterior venous arcade within the head of the pancreas. Typically, the superior vein drains directly into the portal vein just above the neck of the pancreas and is often a larger branch of the portal vein which is divided during the Whipple procedure. The posterior infe-rior arcade drains directly into the inferior mesenteric vein at the inferior border of the neck of the pancreas and this is also divided during a Whipple procedure. The anterior inferior pan-creaticoduodenal vein joins the right gastroepiploic vein and the middle colic vein to form a common venous trunk, which enters into the superior mesenteric vein. Traction on the trans-verse colon during colectomy can tear these |
Surgery_Schwartz_9487 | Surgery_Schwartz | right gastroepiploic vein and the middle colic vein to form a common venous trunk, which enters into the superior mesenteric vein. Traction on the trans-verse colon during colectomy can tear these fragile veins, which then retract into the parenchyma of the pancreas, making control tedious. There also are numerous small venous branches com-ing from the pancreatic parenchyma directly into the lateral and posterior aspect of the portal vein. Venous return from the body and tail of the pancreas drains into the splenic vein.The lymphatic drainage from the pancreas is diffuse and widespread (Fig. 33-6). The profuse network of lymphatic Brunicardi_Ch33_p1429-p1516.indd 143301/03/19 6:44 PM 1434SPECIFIC CONSIDERATIONSPART IIBileductPortal veinLeft gastric veinSplenic veinInferior mesenteric veinMiddle colic veinAnteroinferiorpancreatico-duodenalveinAnterosuperiorpancreatico-duodenalveinPosterosuperiorpancreatico-duodenalveinRightgastroepiploicveinSuperior mesenteric | Surgery_Schwartz. right gastroepiploic vein and the middle colic vein to form a common venous trunk, which enters into the superior mesenteric vein. Traction on the trans-verse colon during colectomy can tear these fragile veins, which then retract into the parenchyma of the pancreas, making control tedious. There also are numerous small venous branches com-ing from the pancreatic parenchyma directly into the lateral and posterior aspect of the portal vein. Venous return from the body and tail of the pancreas drains into the splenic vein.The lymphatic drainage from the pancreas is diffuse and widespread (Fig. 33-6). The profuse network of lymphatic Brunicardi_Ch33_p1429-p1516.indd 143301/03/19 6:44 PM 1434SPECIFIC CONSIDERATIONSPART IIBileductPortal veinLeft gastric veinSplenic veinInferior mesenteric veinMiddle colic veinAnteroinferiorpancreatico-duodenalveinAnterosuperiorpancreatico-duodenalveinPosterosuperiorpancreatico-duodenalveinRightgastroepiploicveinSuperior mesenteric |
Surgery_Schwartz_9488 | Surgery_Schwartz | mesenteric veinMiddle colic veinAnteroinferiorpancreatico-duodenalveinAnterosuperiorpancreatico-duodenalveinPosterosuperiorpancreatico-duodenalveinRightgastroepiploicveinSuperior mesenteric veinAbdominalaortaSpleenFigure 33-5. Venous drainage from the pancreas. The venous drainage of the pancreas follows a pattern similar to the arterial supply, with the veins usually superficial to the arteries. Anterior traction on the transverse colon can tear fragile branches along the inferior border of the pancreas, which then retract into the parenchyma of the pancreas. 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.Celiaclymph nodeHepaticlymph nodePyloriclymph nodeAnteriorpancreatico-duodenallymph nodePosteriorpancreaticoduodenallymph | Surgery_Schwartz. mesenteric veinMiddle colic veinAnteroinferiorpancreatico-duodenalveinAnterosuperiorpancreatico-duodenalveinPosterosuperiorpancreatico-duodenalveinRightgastroepiploicveinSuperior mesenteric veinAbdominalaortaSpleenFigure 33-5. Venous drainage from the pancreas. The venous drainage of the pancreas follows a pattern similar to the arterial supply, with the veins usually superficial to the arteries. Anterior traction on the transverse colon can tear fragile branches along the inferior border of the pancreas, which then retract into the parenchyma of the pancreas. 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.Celiaclymph nodeHepaticlymph nodePyloriclymph nodeAnteriorpancreatico-duodenallymph nodePosteriorpancreaticoduodenallymph |
Surgery_Schwartz_9489 | Surgery_Schwartz | between the neck of the pancreas and the portal and superior mesenteric veins.Celiaclymph nodeHepaticlymph nodePyloriclymph nodeAnteriorpancreatico-duodenallymph nodePosteriorpancreaticoduodenallymph nodeSuperior mesentericlymph nodeInferiorbodySuperior body Splenic lymphnodeDuodenumSpleenFigure 33-6. Lymphatic supply to the pancreas. The lymphatic drainage from the pancreas is diffuse and widespread, which explains the high incidence of lymph node metastases and local recurrence of pancreatic cancer. The pancreatic lymphatics also communicate with lymph nodes in the transverse mesocolon and mesentery of the proximal jejunum. Tumors in the body and tail of the pancreas are often unresect-able because they metastasize to these lymph nodes. (Reproduced with permission from Bell RH, Rikkers LF, Mulholland M: Digestive Tract Surgery: A Text and Atlas. Philadelphia, PA: Lippincott Williams & Wilkins; 1996.)Brunicardi_Ch33_p1429-p1516.indd 143401/03/19 6:44 PM 1435PANCREASCHAPTER | Surgery_Schwartz. between the neck of the pancreas and the portal and superior mesenteric veins.Celiaclymph nodeHepaticlymph nodePyloriclymph nodeAnteriorpancreatico-duodenallymph nodePosteriorpancreaticoduodenallymph nodeSuperior mesentericlymph nodeInferiorbodySuperior body Splenic lymphnodeDuodenumSpleenFigure 33-6. Lymphatic supply to the pancreas. The lymphatic drainage from the pancreas is diffuse and widespread, which explains the high incidence of lymph node metastases and local recurrence of pancreatic cancer. The pancreatic lymphatics also communicate with lymph nodes in the transverse mesocolon and mesentery of the proximal jejunum. Tumors in the body and tail of the pancreas are often unresect-able because they metastasize to these lymph nodes. (Reproduced with permission from Bell RH, Rikkers LF, Mulholland M: Digestive Tract Surgery: A Text and Atlas. Philadelphia, PA: Lippincott Williams & Wilkins; 1996.)Brunicardi_Ch33_p1429-p1516.indd 143401/03/19 6:44 PM 1435PANCREASCHAPTER |
Surgery_Schwartz_9490 | Surgery_Schwartz | LF, Mulholland M: Digestive Tract Surgery: A Text and Atlas. Philadelphia, PA: Lippincott Williams & Wilkins; 1996.)Brunicardi_Ch33_p1429-p1516.indd 143401/03/19 6:44 PM 1435PANCREASCHAPTER 33SpleenPancreasEsophagusCeliac ganglionRight vagus nerveLeft vagus nerveSplanchnic nervesDuodenumAbdominal aortaFigure 33-7. Innervation of the pancreas. The pancreas has a rich supply of afferent sensory fibers that travel superiorly to the celiac ganglia. Interruption of these somatic fibers with a celiac plexus block can interfere with transmission of pancreatic pain. (Reproduced with permission from Bell RH, Rikkers LF, Mulholland M: Digestive Tract Surgery: A Text and Atlas. Philadelphia, PA: Lippincott Williams & Wilkins; 1996.)vessels and lymph nodes draining the pancreas provides egress to tumor cells arising from the pancreas. This diffuse lymphatic drainage contributes to the fact that pancreatic cancer often presents with positive lymph nodes and a high incidence of local recurrence | Surgery_Schwartz. LF, Mulholland M: Digestive Tract Surgery: A Text and Atlas. Philadelphia, PA: Lippincott Williams & Wilkins; 1996.)Brunicardi_Ch33_p1429-p1516.indd 143401/03/19 6:44 PM 1435PANCREASCHAPTER 33SpleenPancreasEsophagusCeliac ganglionRight vagus nerveLeft vagus nerveSplanchnic nervesDuodenumAbdominal aortaFigure 33-7. Innervation of the pancreas. The pancreas has a rich supply of afferent sensory fibers that travel superiorly to the celiac ganglia. Interruption of these somatic fibers with a celiac plexus block can interfere with transmission of pancreatic pain. (Reproduced with permission from Bell RH, Rikkers LF, Mulholland M: Digestive Tract Surgery: A Text and Atlas. Philadelphia, PA: Lippincott Williams & Wilkins; 1996.)vessels and lymph nodes draining the pancreas provides egress to tumor cells arising from the pancreas. This diffuse lymphatic drainage contributes to the fact that pancreatic cancer often presents with positive lymph nodes and a high incidence of local recurrence |
Surgery_Schwartz_9491 | Surgery_Schwartz | tumor cells arising from the pancreas. This diffuse lymphatic drainage contributes to the fact that pancreatic cancer often presents with positive lymph nodes and a high incidence of local recurrence after resection. Lymph nodes can be palpated along the distal bile duct and posterior aspect of the head of the pan-creas in the pancreaticoduodenal groove, where the mesenteric vein passes under the neck of the pancreas, along the inferior border of the body, at the celiac axis and along the hepatic artery ascending into the porta hepatis, and along the splenic artery and vein. The pancreatic lymphatics also communicate with lymph nodes in the transverse mesocolon and mesentery of the proxi-mal jejunum. Tumors in the body and tail of the pancreas often metastasize to these nodes and lymph nodes along the splenic vein and in the hilum of the spleen.NeuroanatomyThe pancreas is innervated by the sympathetic and parasympathetic nervous systems. The acinar cells responsible for exocrine | Surgery_Schwartz. tumor cells arising from the pancreas. This diffuse lymphatic drainage contributes to the fact that pancreatic cancer often presents with positive lymph nodes and a high incidence of local recurrence after resection. Lymph nodes can be palpated along the distal bile duct and posterior aspect of the head of the pan-creas in the pancreaticoduodenal groove, where the mesenteric vein passes under the neck of the pancreas, along the inferior border of the body, at the celiac axis and along the hepatic artery ascending into the porta hepatis, and along the splenic artery and vein. The pancreatic lymphatics also communicate with lymph nodes in the transverse mesocolon and mesentery of the proxi-mal jejunum. Tumors in the body and tail of the pancreas often metastasize to these nodes and lymph nodes along the splenic vein and in the hilum of the spleen.NeuroanatomyThe pancreas is innervated by the sympathetic and parasympathetic nervous systems. The acinar cells responsible for exocrine |
Surgery_Schwartz_9492 | Surgery_Schwartz | nodes along the splenic vein and in the hilum of the spleen.NeuroanatomyThe pancreas is innervated by the sympathetic and parasympathetic nervous systems. The acinar cells responsible for exocrine secretion, the islet cells responsible for endocrine secretion, and the islet vasculature are innervated by both systems. The parasympathetic system stimulates endocrine and exocrine secretion and the sympathetic system inhibits secretion.2 The pancreas is also innervated by neurons that secrete amines and peptides, such as somatostatin, vasoactive intestinal peptide (VIP), calcitonin gene-related peptide (CGRP), and galanin. The exact role of these neurons in pancreatic physiology is uncertain, but they do appear to affect both exocrine and endocrine function. The pancreas also has a rich supply of afferent sensory fibers, which are responsible for the intense pain associated with advanced pancreatic cancer, as well as acute and chronic pancreatitis. These somatic fibers travel superiorly | Surgery_Schwartz. nodes along the splenic vein and in the hilum of the spleen.NeuroanatomyThe pancreas is innervated by the sympathetic and parasympathetic nervous systems. The acinar cells responsible for exocrine secretion, the islet cells responsible for endocrine secretion, and the islet vasculature are innervated by both systems. The parasympathetic system stimulates endocrine and exocrine secretion and the sympathetic system inhibits secretion.2 The pancreas is also innervated by neurons that secrete amines and peptides, such as somatostatin, vasoactive intestinal peptide (VIP), calcitonin gene-related peptide (CGRP), and galanin. The exact role of these neurons in pancreatic physiology is uncertain, but they do appear to affect both exocrine and endocrine function. The pancreas also has a rich supply of afferent sensory fibers, which are responsible for the intense pain associated with advanced pancreatic cancer, as well as acute and chronic pancreatitis. These somatic fibers travel superiorly |
Surgery_Schwartz_9493 | Surgery_Schwartz | of afferent sensory fibers, which are responsible for the intense pain associated with advanced pancreatic cancer, as well as acute and chronic pancreatitis. These somatic fibers travel superiorly to the celiac ganglia (Fig. 33-7). Interruption of these somatic fibers with a celiac plexus block can stop transmission of pain sensation.HISTOLOGY AND PHYSIOLOGYThe exocrine pancreas accounts for about 85% of the pancreatic mass; 10% of the gland is accounted for by extracellular matrix, and 4% by blood vessels and the major ducts, whereas only 2% of the gland is comprised of endocrine tissue. The endocrine and exocrine pancreas are sometimes thought of as function-ally separate, but these different components of the organ are coordinated to allow an elegant regulatory feedback system for digestive enzyme and hormone secretion. This complex system regulates the type of digestion, its rate, and the processing and distribution of absorbed nutrients. This coordination is facili-tated by the | Surgery_Schwartz. of afferent sensory fibers, which are responsible for the intense pain associated with advanced pancreatic cancer, as well as acute and chronic pancreatitis. These somatic fibers travel superiorly to the celiac ganglia (Fig. 33-7). Interruption of these somatic fibers with a celiac plexus block can stop transmission of pain sensation.HISTOLOGY AND PHYSIOLOGYThe exocrine pancreas accounts for about 85% of the pancreatic mass; 10% of the gland is accounted for by extracellular matrix, and 4% by blood vessels and the major ducts, whereas only 2% of the gland is comprised of endocrine tissue. The endocrine and exocrine pancreas are sometimes thought of as function-ally separate, but these different components of the organ are coordinated to allow an elegant regulatory feedback system for digestive enzyme and hormone secretion. This complex system regulates the type of digestion, its rate, and the processing and distribution of absorbed nutrients. This coordination is facili-tated by the |
Surgery_Schwartz_9494 | Surgery_Schwartz | enzyme and hormone secretion. This complex system regulates the type of digestion, its rate, and the processing and distribution of absorbed nutrients. This coordination is facili-tated by the physical approximation of the islets and the exo-crine pancreas, the presence of specific islet hormone receptors on the plasma membranes of pancreatic acinar cells, and the existence of an islet-acinar portal blood system.Although patients can live without a pancreas when insu-lin and digestive enzyme replacement are administered, the loss of this islet-acinar coordination leads to impairments in diges-tive function. Although only approximately 20% of the normal pancreas is required to prevent insufficiency, in many patients undergoing pancreatic resection, the remaining pancreas is not normal, and pancreatic endocrine and exocrine insufficiency can develop with removal of smaller portions of the gland.Exocrine PancreasThe pancreas secretes approximately 500 to 800 mL per day of colorless, | Surgery_Schwartz. enzyme and hormone secretion. This complex system regulates the type of digestion, its rate, and the processing and distribution of absorbed nutrients. This coordination is facili-tated by the physical approximation of the islets and the exo-crine pancreas, the presence of specific islet hormone receptors on the plasma membranes of pancreatic acinar cells, and the existence of an islet-acinar portal blood system.Although patients can live without a pancreas when insu-lin and digestive enzyme replacement are administered, the loss of this islet-acinar coordination leads to impairments in diges-tive function. Although only approximately 20% of the normal pancreas is required to prevent insufficiency, in many patients undergoing pancreatic resection, the remaining pancreas is not normal, and pancreatic endocrine and exocrine insufficiency can develop with removal of smaller portions of the gland.Exocrine PancreasThe pancreas secretes approximately 500 to 800 mL per day of colorless, |
Surgery_Schwartz_9495 | Surgery_Schwartz | and pancreatic endocrine and exocrine insufficiency can develop with removal of smaller portions of the gland.Exocrine PancreasThe pancreas secretes approximately 500 to 800 mL per day of colorless, odorless, alkaline, isosmotic pancreatic juice. Pan-creatic juice is a combination of acinar cell and duct cell secre-tions. The acinar cells secrete amylase, proteases, and lipases, enzymes responsible for the digestion of all three food types: carbohydrate, protein, and fat. The acinar cells are pyramid-shaped, with their apices facing the lumen of the acinus. Near the apex of each cell are numerous enzyme-containing zymogen Brunicardi_Ch33_p1429-p1516.indd 143501/03/19 6:44 PM 1436SPECIFIC CONSIDERATIONSPART IIAcinar cellsCentroacinar cellsIntercalated ductFigure 33-8. Acinar cell. Zymogen granules fuse with the apical membrane and release multiple enzymes to digest carbohydrates, proteins, and fat. (Reproduced with permission from Bloom W, Fawcett DW: A Textbook of Histology, 10th | Surgery_Schwartz. and pancreatic endocrine and exocrine insufficiency can develop with removal of smaller portions of the gland.Exocrine PancreasThe pancreas secretes approximately 500 to 800 mL per day of colorless, odorless, alkaline, isosmotic pancreatic juice. Pan-creatic juice is a combination of acinar cell and duct cell secre-tions. The acinar cells secrete amylase, proteases, and lipases, enzymes responsible for the digestion of all three food types: carbohydrate, protein, and fat. The acinar cells are pyramid-shaped, with their apices facing the lumen of the acinus. Near the apex of each cell are numerous enzyme-containing zymogen Brunicardi_Ch33_p1429-p1516.indd 143501/03/19 6:44 PM 1436SPECIFIC CONSIDERATIONSPART IIAcinar cellsCentroacinar cellsIntercalated ductFigure 33-8. Acinar cell. Zymogen granules fuse with the apical membrane and release multiple enzymes to digest carbohydrates, proteins, and fat. (Reproduced with permission from Bloom W, Fawcett DW: A Textbook of Histology, 10th |
Surgery_Schwartz_9496 | Surgery_Schwartz | granules fuse with the apical membrane and release multiple enzymes to digest carbohydrates, proteins, and fat. (Reproduced with permission from Bloom W, Fawcett DW: A Textbook of Histology, 10th ed. Philadelphia, PA: Saunders; 1975.)granules that fuse with the apical cell membrane (Fig. 33-8). Unlike the endocrine pancreas, where islet cells specialize in the secretion of one hormone type, individual acinar cells secrete all types of enzymes. However, the ratio of the different enzymes released is adjusted to the composition of digested food through nonparallel regulation of secretion.Pancreatic amylase is secreted in its active form and com-pletes the digestive process already begun by salivary amylase. Amylase is the only pancreatic enzyme secreted in its active form, and it hydrolyzes starch and glycogen to glucose, malt-ose, maltotriose, and dextrins. These simple sugars are trans-ported across the brush border of the intestinal epithelial cells by active transport mechanisms. | Surgery_Schwartz. granules fuse with the apical membrane and release multiple enzymes to digest carbohydrates, proteins, and fat. (Reproduced with permission from Bloom W, Fawcett DW: A Textbook of Histology, 10th ed. Philadelphia, PA: Saunders; 1975.)granules that fuse with the apical cell membrane (Fig. 33-8). Unlike the endocrine pancreas, where islet cells specialize in the secretion of one hormone type, individual acinar cells secrete all types of enzymes. However, the ratio of the different enzymes released is adjusted to the composition of digested food through nonparallel regulation of secretion.Pancreatic amylase is secreted in its active form and com-pletes the digestive process already begun by salivary amylase. Amylase is the only pancreatic enzyme secreted in its active form, and it hydrolyzes starch and glycogen to glucose, malt-ose, maltotriose, and dextrins. These simple sugars are trans-ported across the brush border of the intestinal epithelial cells by active transport mechanisms. |
Surgery_Schwartz_9497 | Surgery_Schwartz | starch and glycogen to glucose, malt-ose, maltotriose, and dextrins. These simple sugars are trans-ported across the brush border of the intestinal epithelial cells by active transport mechanisms. Gastric hydrolysis of protein yields peptides that enter the intestine and stimulate intestinal endocrine cells to release cholecystokinin (CCK)-releasing pep-tide, CCK, and secretin, which then stimulate the pancreas to secrete enzymes and bicarbonate into the intestine.The proteolytic enzymes are secreted as proenzymes that require activation. Trypsinogen is converted to its active form, trypsin, by another enzyme, enterokinase, which is produced by the duodenal mucosal cells. Trypsin, in turn, activates the other proteolytic enzymes. Trypsinogen activation within the pancreas is prevented by the presence of inhibitors that are also secreted by the acinar cells. A failure to express a normal tryp-sinogen inhibitor, pancreatic secretory trypsin inhibitor (PSTI), also known as serine | Surgery_Schwartz. starch and glycogen to glucose, malt-ose, maltotriose, and dextrins. These simple sugars are trans-ported across the brush border of the intestinal epithelial cells by active transport mechanisms. Gastric hydrolysis of protein yields peptides that enter the intestine and stimulate intestinal endocrine cells to release cholecystokinin (CCK)-releasing pep-tide, CCK, and secretin, which then stimulate the pancreas to secrete enzymes and bicarbonate into the intestine.The proteolytic enzymes are secreted as proenzymes that require activation. Trypsinogen is converted to its active form, trypsin, by another enzyme, enterokinase, which is produced by the duodenal mucosal cells. Trypsin, in turn, activates the other proteolytic enzymes. Trypsinogen activation within the pancreas is prevented by the presence of inhibitors that are also secreted by the acinar cells. A failure to express a normal tryp-sinogen inhibitor, pancreatic secretory trypsin inhibitor (PSTI), also known as serine |
Surgery_Schwartz_9498 | Surgery_Schwartz | by the presence of inhibitors that are also secreted by the acinar cells. A failure to express a normal tryp-sinogen inhibitor, pancreatic secretory trypsin inhibitor (PSTI), also known as serine protease inhibitor Kazal type 1 (SPINK1), is a cause of familial pancreatitis. Inhibition of trypsinogen activation ensures that the enzymes within the pancreas remain in an inactive precursor state and are activated only within the duodenum. Trypsinogen is expressed in several isoforms, and a missense mutation on the cationic trypsinogen, or PRSS1, results in premature, intrapancreatic activation of trypsinogen. This accounts for about two-thirds of cases of hereditary pan-creatitis. Chymotrypsinogen is activated to form chymotrypsin. Elastase, carboxypeptidase A and B, and phospholipase are also activated by trypsin. Trypsin, chymotrypsin, and elastase cleave bonds between amino acids within a target peptide chain, and carboxypeptidase A and B cleave amino acids at the end of peptide | Surgery_Schwartz. by the presence of inhibitors that are also secreted by the acinar cells. A failure to express a normal tryp-sinogen inhibitor, pancreatic secretory trypsin inhibitor (PSTI), also known as serine protease inhibitor Kazal type 1 (SPINK1), is a cause of familial pancreatitis. Inhibition of trypsinogen activation ensures that the enzymes within the pancreas remain in an inactive precursor state and are activated only within the duodenum. Trypsinogen is expressed in several isoforms, and a missense mutation on the cationic trypsinogen, or PRSS1, results in premature, intrapancreatic activation of trypsinogen. This accounts for about two-thirds of cases of hereditary pan-creatitis. Chymotrypsinogen is activated to form chymotrypsin. Elastase, carboxypeptidase A and B, and phospholipase are also activated by trypsin. Trypsin, chymotrypsin, and elastase cleave bonds between amino acids within a target peptide chain, and carboxypeptidase A and B cleave amino acids at the end of peptide |
Surgery_Schwartz_9499 | Surgery_Schwartz | also activated by trypsin. Trypsin, chymotrypsin, and elastase cleave bonds between amino acids within a target peptide chain, and carboxypeptidase A and B cleave amino acids at the end of peptide chains. Individual amino acids and small dipeptides are then actively transported into the intestinal epithelial cells. Pancreatic lipase hydrolyzes triglycerides to 2-monoglyceride and fatty acid. Pancreatic lipase is secreted in an active form. Colipase is also secreted by the pancreas and binds to lipase, changing its molecular configuration and increasing its activity. Phospholipase A2 is secreted by the pancreas as a proenzyme that becomes activated by trypsin. Phospholipase A2 hydrolyzes phospholipids and, as with all lipases, requires bile salts for its action. Carboxylic ester hydrolase and cholesterol esterase hydrolyze neutral lipid substrates like esters of cholesterol, fat-soluble vitamins, and triglycerides. The hydrolyzed fat is then packaged into micelles for transport into | Surgery_Schwartz. also activated by trypsin. Trypsin, chymotrypsin, and elastase cleave bonds between amino acids within a target peptide chain, and carboxypeptidase A and B cleave amino acids at the end of peptide chains. Individual amino acids and small dipeptides are then actively transported into the intestinal epithelial cells. Pancreatic lipase hydrolyzes triglycerides to 2-monoglyceride and fatty acid. Pancreatic lipase is secreted in an active form. Colipase is also secreted by the pancreas and binds to lipase, changing its molecular configuration and increasing its activity. Phospholipase A2 is secreted by the pancreas as a proenzyme that becomes activated by trypsin. Phospholipase A2 hydrolyzes phospholipids and, as with all lipases, requires bile salts for its action. Carboxylic ester hydrolase and cholesterol esterase hydrolyze neutral lipid substrates like esters of cholesterol, fat-soluble vitamins, and triglycerides. The hydrolyzed fat is then packaged into micelles for transport into |
Surgery_Schwartz_9500 | Surgery_Schwartz | and cholesterol esterase hydrolyze neutral lipid substrates like esters of cholesterol, fat-soluble vitamins, and triglycerides. The hydrolyzed fat is then packaged into micelles for transport into the intestinal epithelial cells, where the fatty acids are reassembled and packaged inside chylomicrons for transport through the lymphatic system into the bloodstream (Table 33-1).The centroacinar and intercalated duct cells secrete the water and electrolytes present in the pancreatic juice. About 40 acinar cells are arranged into a spherical unit called an acinus. Centroacinar cells are located near the center of the acinus and are responsible for fluid and electrolyte secretion. These cells contain the enzyme carbonic anhydrase, which is needed for bicarbonate secretion. The amount of bicarbonate secreted varies with the pancreatic secretory rate, with greater concen-trations of bicarbonate being secreted as the pancreatic secre-tory rate increases. Chloride secretion varies inversely | Surgery_Schwartz. and cholesterol esterase hydrolyze neutral lipid substrates like esters of cholesterol, fat-soluble vitamins, and triglycerides. The hydrolyzed fat is then packaged into micelles for transport into the intestinal epithelial cells, where the fatty acids are reassembled and packaged inside chylomicrons for transport through the lymphatic system into the bloodstream (Table 33-1).The centroacinar and intercalated duct cells secrete the water and electrolytes present in the pancreatic juice. About 40 acinar cells are arranged into a spherical unit called an acinus. Centroacinar cells are located near the center of the acinus and are responsible for fluid and electrolyte secretion. These cells contain the enzyme carbonic anhydrase, which is needed for bicarbonate secretion. The amount of bicarbonate secreted varies with the pancreatic secretory rate, with greater concen-trations of bicarbonate being secreted as the pancreatic secre-tory rate increases. Chloride secretion varies inversely |
Surgery_Schwartz_9501 | Surgery_Schwartz | secreted varies with the pancreatic secretory rate, with greater concen-trations of bicarbonate being secreted as the pancreatic secre-tory rate increases. Chloride secretion varies inversely with bicarbonate secretion such that the sum of these two remains constant. In contrast, sodium and potassium concentrations are kept constant throughout the spectrum of secretory rates3 (Fig. 33-9). The hormone secretin is released from cells in the duodenal mucosa in response to acidic chyme passing through the pylorus into the duodenum. Secretin is the major stimulant for bicarbonate secretion, which buffers the acidic fluid entering the duodenum from the stomach. CCK also stimulates bicarbon-ate secretion, but to a much lesser extent than secretin. CCK potentiates secretin-stimulated bicarbonate secretion. Gastrin and acetylcholine, both stimulants of gastric acid secretion, are also weak stimulants of pancreatic bicarbonate secretion.4 Truncal vagotomy produces a myriad of complex effects | Surgery_Schwartz. secreted varies with the pancreatic secretory rate, with greater concen-trations of bicarbonate being secreted as the pancreatic secre-tory rate increases. Chloride secretion varies inversely with bicarbonate secretion such that the sum of these two remains constant. In contrast, sodium and potassium concentrations are kept constant throughout the spectrum of secretory rates3 (Fig. 33-9). The hormone secretin is released from cells in the duodenal mucosa in response to acidic chyme passing through the pylorus into the duodenum. Secretin is the major stimulant for bicarbonate secretion, which buffers the acidic fluid entering the duodenum from the stomach. CCK also stimulates bicarbon-ate secretion, but to a much lesser extent than secretin. CCK potentiates secretin-stimulated bicarbonate secretion. Gastrin and acetylcholine, both stimulants of gastric acid secretion, are also weak stimulants of pancreatic bicarbonate secretion.4 Truncal vagotomy produces a myriad of complex effects |
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