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Surgery_Schwartz_9102
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Bayer-Schering, Berlin, Germany), hepatic adenomas can be better distinguished from FNH by their enhancement characteristics during the hepa-tobiliary phase of imaging. The new MRI contrast agent, gado-benate dimeglumine (MultiHance, Bracco Diagnostics, Milan, Italy), is eliminated through both renal and biliary excretion. Therefore, liver lesions that contain hepatocytes with intact bili-ary excretion mechanism will take up this contrast agent and be easily distinguished from lesions that do not. This contrast agent has improved our ability to differentiate hepatic adenoma from FNH with a high degree of accuracy.Hepatic adenomas carry a significant risk of spontaneous rupture with intraperitoneal bleeding. The clinical presentation may be abdominal pain, and in 10% to 25% of cases, hepatic adenomas present with spontaneous intraperitoneal hemorrhage. Hepatic adenomas also have a risk of malignant transformation to a well-differentiated HCC. Therefore, it usually is recom-mended that
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Surgery_Schwartz. Bayer-Schering, Berlin, Germany), hepatic adenomas can be better distinguished from FNH by their enhancement characteristics during the hepa-tobiliary phase of imaging. The new MRI contrast agent, gado-benate dimeglumine (MultiHance, Bracco Diagnostics, Milan, Italy), is eliminated through both renal and biliary excretion. Therefore, liver lesions that contain hepatocytes with intact bili-ary excretion mechanism will take up this contrast agent and be easily distinguished from lesions that do not. This contrast agent has improved our ability to differentiate hepatic adenoma from FNH with a high degree of accuracy.Hepatic adenomas carry a significant risk of spontaneous rupture with intraperitoneal bleeding. The clinical presentation may be abdominal pain, and in 10% to 25% of cases, hepatic adenomas present with spontaneous intraperitoneal hemorrhage. Hepatic adenomas also have a risk of malignant transformation to a well-differentiated HCC. Therefore, it usually is recom-mended that
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Surgery_Schwartz_9103
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Surgery_Schwartz
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adenomas present with spontaneous intraperitoneal hemorrhage. Hepatic adenomas also have a risk of malignant transformation to a well-differentiated HCC. Therefore, it usually is recom-mended that large hepatic adenomas (>4–5 cm) be surgically resected.Focal Nodular HyperplasiaFNH is a solid, benign lesion of the liver believed to be a hyper-plastic response to an anomalous artery. Similar to adenomas, they are more common in women of childbearing age, although the link to oral contraceptive use is not as clear as with adeno-mas. A good-quality biphasic CT scan usually is diagnostic of FNH, on which such lesions appear well circumscribed with a typical central scar (see Fig. 31-18). They show intense homo-geneous enhancement on arterial phase contrast images and are often isodense or invisible compared with background liver on the venous phase. On MRI scans, FNH lesions are hypoin-tense on T1-weighted images and isointense to hyperintense on T2-weighted images. After gadolinium
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Surgery_Schwartz. adenomas present with spontaneous intraperitoneal hemorrhage. Hepatic adenomas also have a risk of malignant transformation to a well-differentiated HCC. Therefore, it usually is recom-mended that large hepatic adenomas (>4–5 cm) be surgically resected.Focal Nodular HyperplasiaFNH is a solid, benign lesion of the liver believed to be a hyper-plastic response to an anomalous artery. Similar to adenomas, they are more common in women of childbearing age, although the link to oral contraceptive use is not as clear as with adeno-mas. A good-quality biphasic CT scan usually is diagnostic of FNH, on which such lesions appear well circumscribed with a typical central scar (see Fig. 31-18). They show intense homo-geneous enhancement on arterial phase contrast images and are often isodense or invisible compared with background liver on the venous phase. On MRI scans, FNH lesions are hypoin-tense on T1-weighted images and isointense to hyperintense on T2-weighted images. After gadolinium
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Surgery_Schwartz_9104
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invisible compared with background liver on the venous phase. On MRI scans, FNH lesions are hypoin-tense on T1-weighted images and isointense to hyperintense on T2-weighted images. After gadolinium administration, lesions are hyperintense but become isointense on delayed images. The fibrous septa extending from the central scar are also more readily seen with MRI. Unlike adenomas, FNH lesions usually do not rupture spontaneously and have no significant risk of malignant transformation. Therefore, the management of FNH is usually reassurance and prospective observation irrespective of size. Surgical resection can be recommended, however, when patients are symptomatic or when hepatic adenoma or HCC can-not be definitively excluded. Oral contraceptive or estrogen use should be stopped when either FNH or adenoma is diagnosed.Bile Duct HamartomaBile duct hamartomas are typically small liver lesions, 2 to 4 mm in size, visualized on the surface of the liver at laparotomy. They are firm,
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Surgery_Schwartz. invisible compared with background liver on the venous phase. On MRI scans, FNH lesions are hypoin-tense on T1-weighted images and isointense to hyperintense on T2-weighted images. After gadolinium administration, lesions are hyperintense but become isointense on delayed images. The fibrous septa extending from the central scar are also more readily seen with MRI. Unlike adenomas, FNH lesions usually do not rupture spontaneously and have no significant risk of malignant transformation. Therefore, the management of FNH is usually reassurance and prospective observation irrespective of size. Surgical resection can be recommended, however, when patients are symptomatic or when hepatic adenoma or HCC can-not be definitively excluded. Oral contraceptive or estrogen use should be stopped when either FNH or adenoma is diagnosed.Bile Duct HamartomaBile duct hamartomas are typically small liver lesions, 2 to 4 mm in size, visualized on the surface of the liver at laparotomy. They are firm,
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Surgery_Schwartz_9105
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either FNH or adenoma is diagnosed.Bile Duct HamartomaBile duct hamartomas are typically small liver lesions, 2 to 4 mm in size, visualized on the surface of the liver at laparotomy. They are firm, smooth, and whitish yellow in appearance. They can be difficult to differentiate from small metastatic lesions, and excisional biopsy often is required to establish the diagnosis.MALIGNANT LIVER TUMORSMalignant tumors in the liver can be classified as primary (cancers that originate in the liver) or metastatic (cancers that spread to the liver from an extrahepatic primary site) (see Table 31-6). Primary cancers in the liver that originate from hepato-cytes are known as hepatocellular carcinomas (HCCs or hepa-tomas), whereas cancers arising in the bile ducts are known as cholangiocarcinomas.In the United States, approximately 150,000 new cases of colorectal cancer are diagnosed each year, and the majority of patients (approximately 60%) will develop hepatic metas-tases over their lifetime.
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Surgery_Schwartz. either FNH or adenoma is diagnosed.Bile Duct HamartomaBile duct hamartomas are typically small liver lesions, 2 to 4 mm in size, visualized on the surface of the liver at laparotomy. They are firm, smooth, and whitish yellow in appearance. They can be difficult to differentiate from small metastatic lesions, and excisional biopsy often is required to establish the diagnosis.MALIGNANT LIVER TUMORSMalignant tumors in the liver can be classified as primary (cancers that originate in the liver) or metastatic (cancers that spread to the liver from an extrahepatic primary site) (see Table 31-6). Primary cancers in the liver that originate from hepato-cytes are known as hepatocellular carcinomas (HCCs or hepa-tomas), whereas cancers arising in the bile ducts are known as cholangiocarcinomas.In the United States, approximately 150,000 new cases of colorectal cancer are diagnosed each year, and the majority of patients (approximately 60%) will develop hepatic metas-tases over their lifetime.
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Surgery_Schwartz_9106
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the United States, approximately 150,000 new cases of colorectal cancer are diagnosed each year, and the majority of patients (approximately 60%) will develop hepatic metas-tases over their lifetime. Hence, the most common tumor seen in the liver is metastatic colorectal cancer. This compares with approximately 30,000 new cases of HCC diagnosed annually in the United States. Interestingly, in a Western series of 1000 con-secutive new liver cancer patients seen at a university medical center, 47% had HCC, 17% had colorectal cancer metastases, 11% had cholangiocarcinomas, 7% had neuroendocrine metas-tases, and 18% had other tumors.77 Although these figures do not reflect the incidence or prevalence of these liver cancers, they are indicative of referral patterns in a tertiary academic medical center with a large liver transplantation team and active hepatology clinic.Hepatocellular CarcinomaHCC is the fifth most common malignancy worldwide, with an estimated 750,000 new cases diagnosed
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Surgery_Schwartz. the United States, approximately 150,000 new cases of colorectal cancer are diagnosed each year, and the majority of patients (approximately 60%) will develop hepatic metas-tases over their lifetime. Hence, the most common tumor seen in the liver is metastatic colorectal cancer. This compares with approximately 30,000 new cases of HCC diagnosed annually in the United States. Interestingly, in a Western series of 1000 con-secutive new liver cancer patients seen at a university medical center, 47% had HCC, 17% had colorectal cancer metastases, 11% had cholangiocarcinomas, 7% had neuroendocrine metas-tases, and 18% had other tumors.77 Although these figures do not reflect the incidence or prevalence of these liver cancers, they are indicative of referral patterns in a tertiary academic medical center with a large liver transplantation team and active hepatology clinic.Hepatocellular CarcinomaHCC is the fifth most common malignancy worldwide, with an estimated 750,000 new cases diagnosed
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Surgery_Schwartz_9107
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center with a large liver transplantation team and active hepatology clinic.Hepatocellular CarcinomaHCC is the fifth most common malignancy worldwide, with an estimated 750,000 new cases diagnosed annually. Because of its high fatality, it is the third most common cause of cancer death worldwide.78 Major risk factors are viral hepatitis (B or C), alcoholic cirrhosis, hemochromatosis, and NASH. In Asia, the risk is as high as 35 to 117 per 100,000 persons per year, whereas in the United States, the risk is only 7 per 100,000 per-sons per year.78 Although cirrhosis is not present in all cases, it has been estimated to be present 70% to 90% of the time. In a person with cirrhosis, the annual conversion rate to HCC is 2% to 6%.79 In patients with chronic HCV infection, cirrhosis usually is present before the HCC develops; however, in cases of hepatitis B virus infection, HCC tumors can occur before the onset of cirrhosis. HCCs are typically hypervascular with blood supplied predominantly
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Surgery_Schwartz. center with a large liver transplantation team and active hepatology clinic.Hepatocellular CarcinomaHCC is the fifth most common malignancy worldwide, with an estimated 750,000 new cases diagnosed annually. Because of its high fatality, it is the third most common cause of cancer death worldwide.78 Major risk factors are viral hepatitis (B or C), alcoholic cirrhosis, hemochromatosis, and NASH. In Asia, the risk is as high as 35 to 117 per 100,000 persons per year, whereas in the United States, the risk is only 7 per 100,000 per-sons per year.78 Although cirrhosis is not present in all cases, it has been estimated to be present 70% to 90% of the time. In a person with cirrhosis, the annual conversion rate to HCC is 2% to 6%.79 In patients with chronic HCV infection, cirrhosis usually is present before the HCC develops; however, in cases of hepatitis B virus infection, HCC tumors can occur before the onset of cirrhosis. HCCs are typically hypervascular with blood supplied predominantly
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Surgery_Schwartz_9108
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before the HCC develops; however, in cases of hepatitis B virus infection, HCC tumors can occur before the onset of cirrhosis. HCCs are typically hypervascular with blood supplied predominantly from the hepatic artery. Thus, the lesion often appears hypervascular during the arterial phase of CT studies (Fig. 31-19) and relatively hypodense during the delayed phases due to early washout of the contrast medium by the arterial blood. MRI imaging also is effective in character-izing HCC. HCC is variable on T1-weighted images and usu-ally hyperintense on T2-weighted images. As with contrast CT, HCC enhances in the arterial phase after gadolinium injection because of its hypervascularity and becomes hypointense in the delayed phases due to contrast washout. HCC has a tendency to invade the portal vein, and the presence of an enhancing portal vein thrombus is highly suggestive of HCC.The treatment of HCC is complex and is best managed by a multidisciplinary liver transplant team. A complete
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Surgery_Schwartz. before the HCC develops; however, in cases of hepatitis B virus infection, HCC tumors can occur before the onset of cirrhosis. HCCs are typically hypervascular with blood supplied predominantly from the hepatic artery. Thus, the lesion often appears hypervascular during the arterial phase of CT studies (Fig. 31-19) and relatively hypodense during the delayed phases due to early washout of the contrast medium by the arterial blood. MRI imaging also is effective in character-izing HCC. HCC is variable on T1-weighted images and usu-ally hyperintense on T2-weighted images. As with contrast CT, HCC enhances in the arterial phase after gadolinium injection because of its hypervascularity and becomes hypointense in the delayed phases due to contrast washout. HCC has a tendency to invade the portal vein, and the presence of an enhancing portal vein thrombus is highly suggestive of HCC.The treatment of HCC is complex and is best managed by a multidisciplinary liver transplant team. A complete
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Surgery_Schwartz_9109
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vein, and the presence of an enhancing portal vein thrombus is highly suggestive of HCC.The treatment of HCC is complex and is best managed by a multidisciplinary liver transplant team. A complete algorithm for the evaluation and management of HCC is shown in Fig. 31-20. For patients without cirrhosis who develop HCC, resection is the treatment of choice. For patients with Child’s class A cirrhosis with preserved liver function and no portal hypertension, resection also is considered. If resection is not possible because of poor liver function and the HCC meets transplant criteria (discussed later), liver transplantation is the treatment of choice.80,81The Barcelona-Clinic Liver Cancer Group has refined its HCC management strategy and has developed the American Association for the Study of Liver Diseases Practice Guidelines.82 Management guidelines vary slightly in Asia, Europe, the 7Brunicardi_Ch31_p1345-p1392.indd 137620/02/19 2:36 PM 1377LIVERCHAPTER 31United States, and
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Surgery_Schwartz. vein, and the presence of an enhancing portal vein thrombus is highly suggestive of HCC.The treatment of HCC is complex and is best managed by a multidisciplinary liver transplant team. A complete algorithm for the evaluation and management of HCC is shown in Fig. 31-20. For patients without cirrhosis who develop HCC, resection is the treatment of choice. For patients with Child’s class A cirrhosis with preserved liver function and no portal hypertension, resection also is considered. If resection is not possible because of poor liver function and the HCC meets transplant criteria (discussed later), liver transplantation is the treatment of choice.80,81The Barcelona-Clinic Liver Cancer Group has refined its HCC management strategy and has developed the American Association for the Study of Liver Diseases Practice Guidelines.82 Management guidelines vary slightly in Asia, Europe, the 7Brunicardi_Ch31_p1345-p1392.indd 137620/02/19 2:36 PM 1377LIVERCHAPTER 31United States, and
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Surgery_Schwartz_9110
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Surgery_Schwartz
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of Liver Diseases Practice Guidelines.82 Management guidelines vary slightly in Asia, Europe, the 7Brunicardi_Ch31_p1345-p1392.indd 137620/02/19 2:36 PM 1377LIVERCHAPTER 31United States, and other countries based in part on availability of organ donors for liver transplantation. Living donor liver trans-plantation also is an alternative for patients with HCC awaiting transplantation to avoid dropout as a candidate for cadaveric donor liver transplantation due to tumor progression.81 Specific treatment options are described in the next section.CholangiocarcinomaCholangiocarcinoma, or bile duct cancer, is the second most common primary malignancy of the liver. Cholangiocarcinoma is an adenocarcinoma of the bile ducts; it forms in the biliary epithelial cells and can be subclassified into peripheral (intra-hepatic) bile duct cancer and central (extrahepatic) bile duct cancer. Extrahepatic bile duct cancer can be located distally or proximally. When proximal, it is referred to as a
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Surgery_Schwartz. of Liver Diseases Practice Guidelines.82 Management guidelines vary slightly in Asia, Europe, the 7Brunicardi_Ch31_p1345-p1392.indd 137620/02/19 2:36 PM 1377LIVERCHAPTER 31United States, and other countries based in part on availability of organ donors for liver transplantation. Living donor liver trans-plantation also is an alternative for patients with HCC awaiting transplantation to avoid dropout as a candidate for cadaveric donor liver transplantation due to tumor progression.81 Specific treatment options are described in the next section.CholangiocarcinomaCholangiocarcinoma, or bile duct cancer, is the second most common primary malignancy of the liver. Cholangiocarcinoma is an adenocarcinoma of the bile ducts; it forms in the biliary epithelial cells and can be subclassified into peripheral (intra-hepatic) bile duct cancer and central (extrahepatic) bile duct cancer. Extrahepatic bile duct cancer can be located distally or proximally. When proximal, it is referred to as a
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Surgery_Schwartz_9111
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Surgery_Schwartz
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peripheral (intra-hepatic) bile duct cancer and central (extrahepatic) bile duct cancer. Extrahepatic bile duct cancer can be located distally or proximally. When proximal, it is referred to as a hilar chol-angiocarcinoma (Klatskin’s tumor). Hilar cholangiocarcinoma originates in the wall of the bile duct at the hepatic duct conflu-ence and usually presents with obstructive jaundice rather than an actual liver mass. In contrast, a peripheral (or intrahepatic) cholangiocarcinoma represents a tumor mass within a hepatic lobe or at the periphery of the liver. A biopsy specimen from the cholangiocarcinoma will show adenocarcinoma, but patholo-gists are often unable to differentiate metastatic adenocarcinoma to the liver from primary bile duct adenocarcinoma. Therefore, a search for a primary site should be undertaken in cases in which an incidentally discovered liver lesion is proven to be an adenocarcinoma on biopsy.Hilar cholangiocarcinoma is difficult to diagnose and typi-cally
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Surgery_Schwartz. peripheral (intra-hepatic) bile duct cancer and central (extrahepatic) bile duct cancer. Extrahepatic bile duct cancer can be located distally or proximally. When proximal, it is referred to as a hilar chol-angiocarcinoma (Klatskin’s tumor). Hilar cholangiocarcinoma originates in the wall of the bile duct at the hepatic duct conflu-ence and usually presents with obstructive jaundice rather than an actual liver mass. In contrast, a peripheral (or intrahepatic) cholangiocarcinoma represents a tumor mass within a hepatic lobe or at the periphery of the liver. A biopsy specimen from the cholangiocarcinoma will show adenocarcinoma, but patholo-gists are often unable to differentiate metastatic adenocarcinoma to the liver from primary bile duct adenocarcinoma. Therefore, a search for a primary site should be undertaken in cases in which an incidentally discovered liver lesion is proven to be an adenocarcinoma on biopsy.Hilar cholangiocarcinoma is difficult to diagnose and typi-cally
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Surgery_Schwartz_9112
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site should be undertaken in cases in which an incidentally discovered liver lesion is proven to be an adenocarcinoma on biopsy.Hilar cholangiocarcinoma is difficult to diagnose and typi-cally presents as a stricture of the proximal hepatic duct causing painless jaundice. It preferentially grows along the length of the bile ducts, often involving the periductal lymphatics with frequent lymph node metastases. Surgical resection offers the only chance for cure of cholangiocarcinoma.83 The location and extent of tumor dictate the operative approach. In one series of 225 patients with hilar cholangiocarcinoma, 65 (29%) were deemed to have unresectable tumors by initial imaging.84 Of the remaining 160 patients who underwent exploratory surgery with curative intent, 80 (50%) were found to have inoperable tumors. Histologically negative margins, concomitant hepatic resection, and well-differentiated tumor histology were associ-ated with improved outcome after resection. In another series of
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Surgery_Schwartz. site should be undertaken in cases in which an incidentally discovered liver lesion is proven to be an adenocarcinoma on biopsy.Hilar cholangiocarcinoma is difficult to diagnose and typi-cally presents as a stricture of the proximal hepatic duct causing painless jaundice. It preferentially grows along the length of the bile ducts, often involving the periductal lymphatics with frequent lymph node metastases. Surgical resection offers the only chance for cure of cholangiocarcinoma.83 The location and extent of tumor dictate the operative approach. In one series of 225 patients with hilar cholangiocarcinoma, 65 (29%) were deemed to have unresectable tumors by initial imaging.84 Of the remaining 160 patients who underwent exploratory surgery with curative intent, 80 (50%) were found to have inoperable tumors. Histologically negative margins, concomitant hepatic resection, and well-differentiated tumor histology were associ-ated with improved outcome after resection. In another series of
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Surgery_Schwartz_9113
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inoperable tumors. Histologically negative margins, concomitant hepatic resection, and well-differentiated tumor histology were associ-ated with improved outcome after resection. In another series of 61 patients undergoing surgical exploration for hilar cholangio-carcinoma, the 5-year actuarial survival rates for an R0 or R1 resection were 45% and 26%, respectively.85 In a large series reported by Nagino and colleagues, 132 patients with hilar chol-angiocarcinoma underwent extended hepatectomy with resec-tion of the caudate lobe and extrahepatic bile duct, and/or portal vein resection (n = 63) after portal vein embolization.86 The 3and 5-year survival rates were 41.7% and 26.8%, respectively.In the absence of associated primary sclerosing cholangi-tis (PSC), surgical resection is the treatment of choice for hilar cholangiocarcinoma. However, approximately 10% of patients with cholangiocarcinoma have PSC.87 Furthermore, cholangio-carcinoma in the setting of PSC is frequently
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Surgery_Schwartz. inoperable tumors. Histologically negative margins, concomitant hepatic resection, and well-differentiated tumor histology were associ-ated with improved outcome after resection. In another series of 61 patients undergoing surgical exploration for hilar cholangio-carcinoma, the 5-year actuarial survival rates for an R0 or R1 resection were 45% and 26%, respectively.85 In a large series reported by Nagino and colleagues, 132 patients with hilar chol-angiocarcinoma underwent extended hepatectomy with resec-tion of the caudate lobe and extrahepatic bile duct, and/or portal vein resection (n = 63) after portal vein embolization.86 The 3and 5-year survival rates were 41.7% and 26.8%, respectively.In the absence of associated primary sclerosing cholangi-tis (PSC), surgical resection is the treatment of choice for hilar cholangiocarcinoma. However, approximately 10% of patients with cholangiocarcinoma have PSC.87 Furthermore, cholangio-carcinoma in the setting of PSC is frequently
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Surgery_Schwartz_9114
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the treatment of choice for hilar cholangiocarcinoma. However, approximately 10% of patients with cholangiocarcinoma have PSC.87 Furthermore, cholangio-carcinoma in the setting of PSC is frequently multicentric and often is associated with underlying liver disease, with eventual cirrhosis and portal hypertension. As a result, experience has shown that resection of cholangiocarcinoma in patients with PSC yields dismal results. This led transplant centers to con-sider OLT for patients with hilar cholangiocarcinoma. The ini-tial results of transplantation were disappointing, however, with high recurrence and overall 3-year survival rates of <30%.88Because the growth of hilar cholangiocarcinoma indicates that this disease spreads in a locoregional manner, a rationale for the use of neoadjuvant chemoradiation was developed by the transplant team at the University of Nebraska in the late 1980s. This was adapted in 1993 by the transplant team at the Mayo Clinic, which led to the current Mayo
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Surgery_Schwartz. the treatment of choice for hilar cholangiocarcinoma. However, approximately 10% of patients with cholangiocarcinoma have PSC.87 Furthermore, cholangio-carcinoma in the setting of PSC is frequently multicentric and often is associated with underlying liver disease, with eventual cirrhosis and portal hypertension. As a result, experience has shown that resection of cholangiocarcinoma in patients with PSC yields dismal results. This led transplant centers to con-sider OLT for patients with hilar cholangiocarcinoma. The ini-tial results of transplantation were disappointing, however, with high recurrence and overall 3-year survival rates of <30%.88Because the growth of hilar cholangiocarcinoma indicates that this disease spreads in a locoregional manner, a rationale for the use of neoadjuvant chemoradiation was developed by the transplant team at the University of Nebraska in the late 1980s. This was adapted in 1993 by the transplant team at the Mayo Clinic, which led to the current Mayo
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Surgery_Schwartz_9115
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Surgery_Schwartz
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chemoradiation was developed by the transplant team at the University of Nebraska in the late 1980s. This was adapted in 1993 by the transplant team at the Mayo Clinic, which led to the current Mayo Clinic protocol.89 The pretransplant Mayo protocol consists of external-beam radiation therapy plus a protracted course of intravenous 5-fluorouracil followed by iridium-192 brachytherapy.90 Patients then undergo an abdominal exploration with staging. If findings are negative, patients are given capecitabine for 2 of every 3 weeks until transplantation. Even after restaging with CT/MRI and endo-scopic ultrasonography, approximately 15% to 20% of patients will have positive findings for tumor on abdominal Figure 31-19. Computed tomographic (CT) images of hepato-cellular carcinoma (HCC) and peripheral cholangiocarcinoma. CT scans reveal a large (upper panel) and small (middle panel) hypervascular HCC. A hypovascular left lobe peripheral cholangio-carcinoma (CholangioCA) is also shown (lower
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Surgery_Schwartz. chemoradiation was developed by the transplant team at the University of Nebraska in the late 1980s. This was adapted in 1993 by the transplant team at the Mayo Clinic, which led to the current Mayo Clinic protocol.89 The pretransplant Mayo protocol consists of external-beam radiation therapy plus a protracted course of intravenous 5-fluorouracil followed by iridium-192 brachytherapy.90 Patients then undergo an abdominal exploration with staging. If findings are negative, patients are given capecitabine for 2 of every 3 weeks until transplantation. Even after restaging with CT/MRI and endo-scopic ultrasonography, approximately 15% to 20% of patients will have positive findings for tumor on abdominal Figure 31-19. Computed tomographic (CT) images of hepato-cellular carcinoma (HCC) and peripheral cholangiocarcinoma. CT scans reveal a large (upper panel) and small (middle panel) hypervascular HCC. A hypovascular left lobe peripheral cholangio-carcinoma (CholangioCA) is also shown (lower
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Surgery_Schwartz_9116
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cholangiocarcinoma. CT scans reveal a large (upper panel) and small (middle panel) hypervascular HCC. A hypovascular left lobe peripheral cholangio-carcinoma (CholangioCA) is also shown (lower panel).Brunicardi_Ch31_p1345-p1392.indd 137720/02/19 2:36 PM 1378SPECIFIC CONSIDERATIONSPART IIexploration.87,90 The 5-year survival rate for those undergoing transplantation for cholangiocarcinoma at the Mayo Clinic is approximately 70% and compares favorably with the rate for resection.87,90 Current eligibility criteria for this Mayo Clinic protocol include unresectable hilar cholangiocarcinoma or hilar cholangiocarcinoma with PSC. The tumor must have a radial dimension of ≤3 cm with no intrahepatic or extrahepatic metastases, and the patient must not have undergone prior radiation therapy or transperitoneal biopsy.90 Many centers have adopted similar protocols with comparable results.91Peripheral, or intrahepatic, cholangiocarcinoma is less common than hilar cholangiocarcinoma. In a
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Surgery_Schwartz. cholangiocarcinoma. CT scans reveal a large (upper panel) and small (middle panel) hypervascular HCC. A hypovascular left lobe peripheral cholangio-carcinoma (CholangioCA) is also shown (lower panel).Brunicardi_Ch31_p1345-p1392.indd 137720/02/19 2:36 PM 1378SPECIFIC CONSIDERATIONSPART IIexploration.87,90 The 5-year survival rate for those undergoing transplantation for cholangiocarcinoma at the Mayo Clinic is approximately 70% and compares favorably with the rate for resection.87,90 Current eligibility criteria for this Mayo Clinic protocol include unresectable hilar cholangiocarcinoma or hilar cholangiocarcinoma with PSC. The tumor must have a radial dimension of ≤3 cm with no intrahepatic or extrahepatic metastases, and the patient must not have undergone prior radiation therapy or transperitoneal biopsy.90 Many centers have adopted similar protocols with comparable results.91Peripheral, or intrahepatic, cholangiocarcinoma is less common than hilar cholangiocarcinoma. In a
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or transperitoneal biopsy.90 Many centers have adopted similar protocols with comparable results.91Peripheral, or intrahepatic, cholangiocarcinoma is less common than hilar cholangiocarcinoma. In a series of 53 patients at Memorial Sloan-Kettering Cancer Center who underwent surgical exploration for a diagnosis of intrahepatic cholangiocarcinoma, 33 (62%) were found to have resectable tumors.92 Actuarial 3-year survival for patients undergoing resection was 55%. Factors predictive of poor survival included vascular invasion, histologically positive margins, and multiple tumors. In a large series in Taiwan, 373 patients with peripheral cholangiocarcinoma underwent surgical treatment from 1977 to 2001. Absence of mucobilia, nonpapillary tumor type, tumor of advanced stage, nonhepatectomy, and lack of postoperative chemotherapy were five independent prognostic factors that adversely affected overall survival.93 Liver transplantation has been performed for peripheral
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Surgery_Schwartz. or transperitoneal biopsy.90 Many centers have adopted similar protocols with comparable results.91Peripheral, or intrahepatic, cholangiocarcinoma is less common than hilar cholangiocarcinoma. In a series of 53 patients at Memorial Sloan-Kettering Cancer Center who underwent surgical exploration for a diagnosis of intrahepatic cholangiocarcinoma, 33 (62%) were found to have resectable tumors.92 Actuarial 3-year survival for patients undergoing resection was 55%. Factors predictive of poor survival included vascular invasion, histologically positive margins, and multiple tumors. In a large series in Taiwan, 373 patients with peripheral cholangiocarcinoma underwent surgical treatment from 1977 to 2001. Absence of mucobilia, nonpapillary tumor type, tumor of advanced stage, nonhepatectomy, and lack of postoperative chemotherapy were five independent prognostic factors that adversely affected overall survival.93 Liver transplantation has been performed for peripheral
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nonhepatectomy, and lack of postoperative chemotherapy were five independent prognostic factors that adversely affected overall survival.93 Liver transplantation has been performed for peripheral cholangiocarcinoma94; however, currently all but one center in the United States have eschewed this approach because of organ shortages and relatively high recurrence rates.Gallbladder CancerGallbladder cancer is a rare aggressive tumor with a very poor prognosis. Over 90% of patients have associated cholelithia-sis. In one study examining the mode of presentation over a 10-year period from 1990 to 2000 in 44 patients diagnosed with gallbladder cancer, the diagnosis was found to be made preoperatively in 57%, intraoperatively in 11%, and inciden-tally after cholecystectomy in 32%.95 Surgical approaches can be classified into (a) reoperation for an incidental finding of gallbladder cancer after cholecystectomy, and (b) radical resec-tion in patients with advanced disease. The results are
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Surgery_Schwartz. nonhepatectomy, and lack of postoperative chemotherapy were five independent prognostic factors that adversely affected overall survival.93 Liver transplantation has been performed for peripheral cholangiocarcinoma94; however, currently all but one center in the United States have eschewed this approach because of organ shortages and relatively high recurrence rates.Gallbladder CancerGallbladder cancer is a rare aggressive tumor with a very poor prognosis. Over 90% of patients have associated cholelithia-sis. In one study examining the mode of presentation over a 10-year period from 1990 to 2000 in 44 patients diagnosed with gallbladder cancer, the diagnosis was found to be made preoperatively in 57%, intraoperatively in 11%, and inciden-tally after cholecystectomy in 32%.95 Surgical approaches can be classified into (a) reoperation for an incidental finding of gallbladder cancer after cholecystectomy, and (b) radical resec-tion in patients with advanced disease. The results are
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Surgery_Schwartz_9119
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approaches can be classified into (a) reoperation for an incidental finding of gallbladder cancer after cholecystectomy, and (b) radical resec-tion in patients with advanced disease. The results are dismal for radical resection in patients with advanced disease and positive hilar lymph nodes.96,97 For incidental gallbladder can-cer beyond stage T1, reoperation with central liver resection, hilar lymphadenectomy, and evaluation of cystic duct stump is most commonly performed.98,99 The role of formal lobectomy or extended lobectomy as well as common bile duct resection is more controversial. In a single-center study of 23 patients undergoing attempted curative treatment by surgical resec-tion, survival was 85% at 1 year, 63% at 2 years, and 55% at 3 years.99 In a multicenter study encompassing 115 patients with incidentally discovered gallbladder cancer who underwent re-resection,98 residual disease in the liver was identified in 46% of patients (0% of those with stage T1 disease, 10%
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Surgery_Schwartz. approaches can be classified into (a) reoperation for an incidental finding of gallbladder cancer after cholecystectomy, and (b) radical resec-tion in patients with advanced disease. The results are dismal for radical resection in patients with advanced disease and positive hilar lymph nodes.96,97 For incidental gallbladder can-cer beyond stage T1, reoperation with central liver resection, hilar lymphadenectomy, and evaluation of cystic duct stump is most commonly performed.98,99 The role of formal lobectomy or extended lobectomy as well as common bile duct resection is more controversial. In a single-center study of 23 patients undergoing attempted curative treatment by surgical resec-tion, survival was 85% at 1 year, 63% at 2 years, and 55% at 3 years.99 In a multicenter study encompassing 115 patients with incidentally discovered gallbladder cancer who underwent re-resection,98 residual disease in the liver was identified in 46% of patients (0% of those with stage T1 disease, 10%
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115 patients with incidentally discovered gallbladder cancer who underwent re-resection,98 residual disease in the liver was identified in 46% of patients (0% of those with stage T1 disease, 10% of those with T2 tumors, and 36% of those with T3 disease). T stage also was associated with the risk of metastasis to locoregional lymph nodes (lymph node metastasis for T1 of 13%; for T2, 31%; and for T3, 46%). In another study, a German registry of incidental gallbladder cancer identified 439 patients. Patients with tumors staged as T2 or T3 after cholecystectomy had better survival if they underwent reoperation than if they were managed with observation.100 Hence, reoperation should be considered for all patients who have T2 or T3 tumors or for whom the accuracy of staging is in question.Metastatic Colorectal CancerOver 50% to 60% of patients diagnosed with colorectal cancer will develop hepatic metastases during their lifetime. Resection for hepatic metastases has been a routine part of
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Surgery_Schwartz. 115 patients with incidentally discovered gallbladder cancer who underwent re-resection,98 residual disease in the liver was identified in 46% of patients (0% of those with stage T1 disease, 10% of those with T2 tumors, and 36% of those with T3 disease). T stage also was associated with the risk of metastasis to locoregional lymph nodes (lymph node metastasis for T1 of 13%; for T2, 31%; and for T3, 46%). In another study, a German registry of incidental gallbladder cancer identified 439 patients. Patients with tumors staged as T2 or T3 after cholecystectomy had better survival if they underwent reoperation than if they were managed with observation.100 Hence, reoperation should be considered for all patients who have T2 or T3 tumors or for whom the accuracy of staging is in question.Metastatic Colorectal CancerOver 50% to 60% of patients diagnosed with colorectal cancer will develop hepatic metastases during their lifetime. Resection for hepatic metastases has been a routine part of
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Colorectal CancerOver 50% to 60% of patients diagnosed with colorectal cancer will develop hepatic metastases during their lifetime. Resection for hepatic metastases has been a routine part of treatment for 8ResectionNoncirrhotic/Child’s ASingle lesionNo metastasisOLTx evaluation1 lesion ˜5 cm3 lesions ˜3 cmChild’s A/B/CNo gross vasc. invasionNo metastasisNot Tx candidateComorbid factors°4 lesionsGross vasc. invasionLN (+) or metastasisLDLT ?Suitable donorPalliative careChild’s CBili °3 HCC IdentifiedResection candidate?Transplant candidate?YesYesNoSorafenibYesYesNoOLTxClinicaltrialsNeoadjuvant therapyRFA/TACE/90 YttriumUNOS list (cadaver)MELD score (? >3 mos)Perc/lap. RFASingle lesion<5 cmChild’s A/BTace/90 YttriumMulti-focal >5 cmChild’s A/B/CBili <3NewagentsFigure 31-20. Algorithm for the management of hepatocellular carcinoma (HCC). The treatment algorithm for HCC begins with determining whether the patient is a resection candidate or liver transplant candidate. Bili = bilirubin
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Surgery_Schwartz. Colorectal CancerOver 50% to 60% of patients diagnosed with colorectal cancer will develop hepatic metastases during their lifetime. Resection for hepatic metastases has been a routine part of treatment for 8ResectionNoncirrhotic/Child’s ASingle lesionNo metastasisOLTx evaluation1 lesion ˜5 cm3 lesions ˜3 cmChild’s A/B/CNo gross vasc. invasionNo metastasisNot Tx candidateComorbid factors°4 lesionsGross vasc. invasionLN (+) or metastasisLDLT ?Suitable donorPalliative careChild’s CBili °3 HCC IdentifiedResection candidate?Transplant candidate?YesYesNoSorafenibYesYesNoOLTxClinicaltrialsNeoadjuvant therapyRFA/TACE/90 YttriumUNOS list (cadaver)MELD score (? >3 mos)Perc/lap. RFASingle lesion<5 cmChild’s A/BTace/90 YttriumMulti-focal >5 cmChild’s A/B/CBili <3NewagentsFigure 31-20. Algorithm for the management of hepatocellular carcinoma (HCC). The treatment algorithm for HCC begins with determining whether the patient is a resection candidate or liver transplant candidate. Bili = bilirubin
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the management of hepatocellular carcinoma (HCC). The treatment algorithm for HCC begins with determining whether the patient is a resection candidate or liver transplant candidate. Bili = bilirubin level (in milligrams per deciliter); Child’s = Child-Turcotte-Pugh class; lap = laparoscopic; LDLT = living-donor liver transplantation; LN = lymph node; MELD = Model for End-Stage Liver Disease; OLTx = orthotopic liver transplantation; Perc = percutaneous; RFA = radiofrequency ablation; TACE = transarterial chemoemboli-zation; Tx = transplantation; UNOS = United Network for Organ Sharing; vasc. = vascular.Brunicardi_Ch31_p1345-p1392.indd 137820/02/19 2:36 PM 1379LIVERCHAPTER 31colorectal cancer since the publication of a large single-center experience demonstrating its safety and efficacy.101 Predictors of poor outcome in that study included node-positive primary, disease-free interval <12 months, more than one tumor, tumor size >5 cm, and carcinoembryonic antigen level >200 ng/mL.
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Surgery_Schwartz. the management of hepatocellular carcinoma (HCC). The treatment algorithm for HCC begins with determining whether the patient is a resection candidate or liver transplant candidate. Bili = bilirubin level (in milligrams per deciliter); Child’s = Child-Turcotte-Pugh class; lap = laparoscopic; LDLT = living-donor liver transplantation; LN = lymph node; MELD = Model for End-Stage Liver Disease; OLTx = orthotopic liver transplantation; Perc = percutaneous; RFA = radiofrequency ablation; TACE = transarterial chemoemboli-zation; Tx = transplantation; UNOS = United Network for Organ Sharing; vasc. = vascular.Brunicardi_Ch31_p1345-p1392.indd 137820/02/19 2:36 PM 1379LIVERCHAPTER 31colorectal cancer since the publication of a large single-center experience demonstrating its safety and efficacy.101 Predictors of poor outcome in that study included node-positive primary, disease-free interval <12 months, more than one tumor, tumor size >5 cm, and carcinoembryonic antigen level >200 ng/mL.
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Predictors of poor outcome in that study included node-positive primary, disease-free interval <12 months, more than one tumor, tumor size >5 cm, and carcinoembryonic antigen level >200 ng/mL. Traditional teaching suggested that hepatic resection for meta-static colorectal cancer to the liver, if technically feasible, should be performed only for fewer than four metastases.102 However, later studies challenged this paradigm. In a series of 235 patients who underwent hepatic resection for metastatic colorectal cancer, the 10-year survival rate of patients with four or more nodules was 29%, nearly comparable to the 32% sur-vival rate of patients with only a solitary tumor metastasis.103 In the Memorial Sloan-Kettering Cancer Center series of 98 patients with four or more colorectal hepatic metastases who underwent resection between 1998 and 2002, the 5-year actu-arial survival was 33%.104 Furthermore, improved chemothera-peutic regimens and surgical techniques have produced aggressive
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Surgery_Schwartz. Predictors of poor outcome in that study included node-positive primary, disease-free interval <12 months, more than one tumor, tumor size >5 cm, and carcinoembryonic antigen level >200 ng/mL. Traditional teaching suggested that hepatic resection for meta-static colorectal cancer to the liver, if technically feasible, should be performed only for fewer than four metastases.102 However, later studies challenged this paradigm. In a series of 235 patients who underwent hepatic resection for metastatic colorectal cancer, the 10-year survival rate of patients with four or more nodules was 29%, nearly comparable to the 32% sur-vival rate of patients with only a solitary tumor metastasis.103 In the Memorial Sloan-Kettering Cancer Center series of 98 patients with four or more colorectal hepatic metastases who underwent resection between 1998 and 2002, the 5-year actu-arial survival was 33%.104 Furthermore, improved chemothera-peutic regimens and surgical techniques have produced aggressive
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metastases who underwent resection between 1998 and 2002, the 5-year actu-arial survival was 33%.104 Furthermore, improved chemothera-peutic regimens and surgical techniques have produced aggressive strategies for the management of this disease. Many groups now consider volume of future liver remnant and the health of the background liver, and not actual tumor number, as the primary determinants in selection for an operative approach.105,106 Hence, resectability is no longer defined by what is actually removed, but indications for hepatic resection now center on what will remain after resection.107 Use of neo-adjuvant chemotherapy, portal vein embolization, two-stage hepatectomy, simultaneous ablation, and resection of extrahepatic tumor in select patients have increased the number of patients eligible for a surgical approach.108,109Neuroendocrine TumorsHepatic metastases from neuroendocrine tumors have a protracted natural history and commonly are associated with debilitating
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Surgery_Schwartz. metastases who underwent resection between 1998 and 2002, the 5-year actu-arial survival was 33%.104 Furthermore, improved chemothera-peutic regimens and surgical techniques have produced aggressive strategies for the management of this disease. Many groups now consider volume of future liver remnant and the health of the background liver, and not actual tumor number, as the primary determinants in selection for an operative approach.105,106 Hence, resectability is no longer defined by what is actually removed, but indications for hepatic resection now center on what will remain after resection.107 Use of neo-adjuvant chemotherapy, portal vein embolization, two-stage hepatectomy, simultaneous ablation, and resection of extrahepatic tumor in select patients have increased the number of patients eligible for a surgical approach.108,109Neuroendocrine TumorsHepatic metastases from neuroendocrine tumors have a protracted natural history and commonly are associated with debilitating
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of patients eligible for a surgical approach.108,109Neuroendocrine TumorsHepatic metastases from neuroendocrine tumors have a protracted natural history and commonly are associated with debilitating endocrinopathies. Several groups have advocated an aggressive surgical approach of debulking surgery, both to control symp-toms and to extend survival.110,111 In a series of 170 patients undergoing resection of hepatic metastases from neuroendocrine tumors between 1977 and 1998 at the Mayo Clinic, overall sur-vival was 61% and 35% at 5 and 10 years, respectively.112 There was no difference in survival between patients with carcinoid tumors and those with islet cell tumors. Major hepatectomy was performed in 91 patients (54%), and recurrence rate was 84% at 5 years. Belghiti’s group has described a two-stage strategy used in 41 patients with a primary neuroendocrine tumor and synchronous bilobar liver metastases.113 In the first stage, the primary tumor is resected and limited resection of
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Surgery_Schwartz. of patients eligible for a surgical approach.108,109Neuroendocrine TumorsHepatic metastases from neuroendocrine tumors have a protracted natural history and commonly are associated with debilitating endocrinopathies. Several groups have advocated an aggressive surgical approach of debulking surgery, both to control symp-toms and to extend survival.110,111 In a series of 170 patients undergoing resection of hepatic metastases from neuroendocrine tumors between 1977 and 1998 at the Mayo Clinic, overall sur-vival was 61% and 35% at 5 and 10 years, respectively.112 There was no difference in survival between patients with carcinoid tumors and those with islet cell tumors. Major hepatectomy was performed in 91 patients (54%), and recurrence rate was 84% at 5 years. Belghiti’s group has described a two-stage strategy used in 41 patients with a primary neuroendocrine tumor and synchronous bilobar liver metastases.113 In the first stage, the primary tumor is resected and limited resection of
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a two-stage strategy used in 41 patients with a primary neuroendocrine tumor and synchronous bilobar liver metastases.113 In the first stage, the primary tumor is resected and limited resection of metastases in the left hemiliver, combined with right portal vein ligation, is performed. After 8 weeks of hypertrophy, a right hepatec-tomy or extended right hepatectomy (also referred to as a right trisectionectomy; resection of Couinaud’s segments IV, V, VI, VII, and VIII of the liver) is performed.113 In patients treated using this strategy, the 2-, 5-, and 8-year Kaplan-Meier over-all survival rates were 94%, 94%, and 79%, respectively, and disease-free survival rates were 85%, 50%, and 26%, respec-tively. Because systemic therapy has had little success in the treatment of advanced tumors, a broader approach using multi-modal therapy has been used to increase survival and improve hormone-related symptoms. These therapies include radiofre-quency or microwave ablation and intra-arterial
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Surgery_Schwartz. a two-stage strategy used in 41 patients with a primary neuroendocrine tumor and synchronous bilobar liver metastases.113 In the first stage, the primary tumor is resected and limited resection of metastases in the left hemiliver, combined with right portal vein ligation, is performed. After 8 weeks of hypertrophy, a right hepatec-tomy or extended right hepatectomy (also referred to as a right trisectionectomy; resection of Couinaud’s segments IV, V, VI, VII, and VIII of the liver) is performed.113 In patients treated using this strategy, the 2-, 5-, and 8-year Kaplan-Meier over-all survival rates were 94%, 94%, and 79%, respectively, and disease-free survival rates were 85%, 50%, and 26%, respec-tively. Because systemic therapy has had little success in the treatment of advanced tumors, a broader approach using multi-modal therapy has been used to increase survival and improve hormone-related symptoms. These therapies include radiofre-quency or microwave ablation and intra-arterial
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a broader approach using multi-modal therapy has been used to increase survival and improve hormone-related symptoms. These therapies include radiofre-quency or microwave ablation and intra-arterial therapy with chemoembolization or radioembolization (yttrium-90). Some centers perform liver transplantation for selected patients (carci-noid histology; primary tumor removed with curative resection; primary tumor drained by portal system; ≤50% hepatic paren-chyma involved; good response or stable disease for at least 6 months during pretransplantation period; and age 55 years or younger), although this is not routine.114Other Metastatic TumorsNearly every cancer has the propensity to metastasize to the liver. Historically, enthusiasm was low for resecting metastases other than those from a colorectal cancer primary. This was due in part to the recognition that many other primary cancers (such as breast cancer) represent a systemic disease when liver metas-tases are present. However, more
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Surgery_Schwartz. a broader approach using multi-modal therapy has been used to increase survival and improve hormone-related symptoms. These therapies include radiofre-quency or microwave ablation and intra-arterial therapy with chemoembolization or radioembolization (yttrium-90). Some centers perform liver transplantation for selected patients (carci-noid histology; primary tumor removed with curative resection; primary tumor drained by portal system; ≤50% hepatic paren-chyma involved; good response or stable disease for at least 6 months during pretransplantation period; and age 55 years or younger), although this is not routine.114Other Metastatic TumorsNearly every cancer has the propensity to metastasize to the liver. Historically, enthusiasm was low for resecting metastases other than those from a colorectal cancer primary. This was due in part to the recognition that many other primary cancers (such as breast cancer) represent a systemic disease when liver metas-tases are present. However, more
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cancer primary. This was due in part to the recognition that many other primary cancers (such as breast cancer) represent a systemic disease when liver metas-tases are present. However, more recent studies have shown acceptable 5-year survival rates in the 20% to 40% range for resection of hepatic metastases from breast, renal, and other GI tumors.115,116 In a large study of hepatic resection for non-colorectal, nonendocrine liver metastases in 1452 patients, neg-ative prognostic factors were nonbreast origin, age >60 years, disease-free interval of <12 months, need for major hepatec-tomy, performance of R2 resection, and presence of extrahe-patic metastases.115TREATMENT OPTIONS FOR LIVER CANCERIn general, the major treatment options for liver cancer can be categorized as shown in Table 31-7. The decision making for any given patient is complex and is best managed by a multidis-ciplinary liver tumor board. The treatments listed in Table 31-7 are not mutually exclusive; the important
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Surgery_Schwartz. cancer primary. This was due in part to the recognition that many other primary cancers (such as breast cancer) represent a systemic disease when liver metas-tases are present. However, more recent studies have shown acceptable 5-year survival rates in the 20% to 40% range for resection of hepatic metastases from breast, renal, and other GI tumors.115,116 In a large study of hepatic resection for non-colorectal, nonendocrine liver metastases in 1452 patients, neg-ative prognostic factors were nonbreast origin, age >60 years, disease-free interval of <12 months, need for major hepatec-tomy, performance of R2 resection, and presence of extrahe-patic metastases.115TREATMENT OPTIONS FOR LIVER CANCERIn general, the major treatment options for liver cancer can be categorized as shown in Table 31-7. The decision making for any given patient is complex and is best managed by a multidis-ciplinary liver tumor board. The treatments listed in Table 31-7 are not mutually exclusive; the important
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31-7. The decision making for any given patient is complex and is best managed by a multidis-ciplinary liver tumor board. The treatments listed in Table 31-7 are not mutually exclusive; the important point is to select the most appropriate initial treatment after a complete evaluation. In general, surveillance imaging (CT or MRI) is performed every 3 to 4 months during the first year after diagnosis to observe for response, progression, or recurrence. The treatment plan is indi-vidualized and modified according to the response of the patient.Hepatic ResectionFor primary liver cancers or hepatic metastases, hepatic resection is the gold standard and treatment of choice. Although there are anecdotal reports of long-term survival after ablation and other regional liver therapies, liver resection remains the only real option for cure. For HCC in the setting of cirrhosis, liver trans-plantation also offers the potential for long-term survival, albeit with the consequences of
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Surgery_Schwartz. 31-7. The decision making for any given patient is complex and is best managed by a multidis-ciplinary liver tumor board. The treatments listed in Table 31-7 are not mutually exclusive; the important point is to select the most appropriate initial treatment after a complete evaluation. In general, surveillance imaging (CT or MRI) is performed every 3 to 4 months during the first year after diagnosis to observe for response, progression, or recurrence. The treatment plan is indi-vidualized and modified according to the response of the patient.Hepatic ResectionFor primary liver cancers or hepatic metastases, hepatic resection is the gold standard and treatment of choice. Although there are anecdotal reports of long-term survival after ablation and other regional liver therapies, liver resection remains the only real option for cure. For HCC in the setting of cirrhosis, liver trans-plantation also offers the potential for long-term survival, albeit with the consequences of
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liver resection remains the only real option for cure. For HCC in the setting of cirrhosis, liver trans-plantation also offers the potential for long-term survival, albeit with the consequences of immunosuppression. Hepatic resection 9Table 31-7Treatment options for liver cancerHepatic resectionLiver transplantationAblation techniquesRadiofrequency ablation• Ethanol ablation• Cryoablation• Microwave ablationRegional liver therapies• Chemoembolization/embolization• Hepatic artery pump chemoperfusion• Internal radiation therapy (yttrium-90 internal radiation)External-beam radiation therapy• Stereotactic radiosurgery (CyberKnife, Trilogy, Synergy)• Intensity-modulated radiation therapySystemic chemotherapyMultimodality approachBrunicardi_Ch31_p1345-p1392.indd 137920/02/19 2:36 PM 1380SPECIFIC CONSIDERATIONSPART IIalso has been advocated for HCC in select patients with cirrho-sis before secondary liver transplantation, although not without some controversy.117 Many large series of
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Surgery_Schwartz. liver resection remains the only real option for cure. For HCC in the setting of cirrhosis, liver trans-plantation also offers the potential for long-term survival, albeit with the consequences of immunosuppression. Hepatic resection 9Table 31-7Treatment options for liver cancerHepatic resectionLiver transplantationAblation techniquesRadiofrequency ablation• Ethanol ablation• Cryoablation• Microwave ablationRegional liver therapies• Chemoembolization/embolization• Hepatic artery pump chemoperfusion• Internal radiation therapy (yttrium-90 internal radiation)External-beam radiation therapy• Stereotactic radiosurgery (CyberKnife, Trilogy, Synergy)• Intensity-modulated radiation therapySystemic chemotherapyMultimodality approachBrunicardi_Ch31_p1345-p1392.indd 137920/02/19 2:36 PM 1380SPECIFIC CONSIDERATIONSPART IIalso has been advocated for HCC in select patients with cirrho-sis before secondary liver transplantation, although not without some controversy.117 Many large series of
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CONSIDERATIONSPART IIalso has been advocated for HCC in select patients with cirrho-sis before secondary liver transplantation, although not without some controversy.117 Many large series of patients undergoing major hepatectomy now report mortality rates of <5%.118-121 Pre-viously, a 1-cm tumor margin was considered desirable; how-ever, recent studies have reported comparable survival rates with smaller margins.122-124 Technical innovation in liver surgery and a better understanding of perioperative care have even allowed surgeons to perform resections in cases with IVC involvement with extracorporeal liver surgery.125 The technical aspects of anatomic hepatic lobectomies are described later.Liver TransplantationThe rationale supporting OLT for HCC includes the fact that most HCCs (>80%) arise in the setting of cirrhosis.88,126 The cirrhotic liver often does not have enough reserve to tolerate a formal resection. Also, HCC tumors are commonly multifo-cal and are underestimated by
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Surgery_Schwartz. CONSIDERATIONSPART IIalso has been advocated for HCC in select patients with cirrho-sis before secondary liver transplantation, although not without some controversy.117 Many large series of patients undergoing major hepatectomy now report mortality rates of <5%.118-121 Pre-viously, a 1-cm tumor margin was considered desirable; how-ever, recent studies have reported comparable survival rates with smaller margins.122-124 Technical innovation in liver surgery and a better understanding of perioperative care have even allowed surgeons to perform resections in cases with IVC involvement with extracorporeal liver surgery.125 The technical aspects of anatomic hepatic lobectomies are described later.Liver TransplantationThe rationale supporting OLT for HCC includes the fact that most HCCs (>80%) arise in the setting of cirrhosis.88,126 The cirrhotic liver often does not have enough reserve to tolerate a formal resection. Also, HCC tumors are commonly multifo-cal and are underestimated by
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arise in the setting of cirrhosis.88,126 The cirrhotic liver often does not have enough reserve to tolerate a formal resection. Also, HCC tumors are commonly multifo-cal and are underestimated by current CT or MRI imaging.127 Furthermore, recurrence rates are high at 5 years after resec-tion (>50%). Hence, OLT is an appealing treatment because it removes both the cancer and the cirrhotic liver that leads to can-cer. More than 7000 liver transplantations are performed each year in the United States, with 1-year survival rates approaching 90%. In May 2017, approximately 14,463 patients were on the waiting list for liver transplantation.128Initial series of OLT for HCC reported in the 1990s included advanced cases of HCC, and the 5-year survival rates were only 20% to 50%.88 This compared poorly with overall 5-year survival rates of 70% to 75% for OLT in the Organ Pro-curement and Transplantation Network/United Network for Organ Sharing (OPTN/UNOS) database. Mazzaferro and col-leagues at
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Surgery_Schwartz. arise in the setting of cirrhosis.88,126 The cirrhotic liver often does not have enough reserve to tolerate a formal resection. Also, HCC tumors are commonly multifo-cal and are underestimated by current CT or MRI imaging.127 Furthermore, recurrence rates are high at 5 years after resec-tion (>50%). Hence, OLT is an appealing treatment because it removes both the cancer and the cirrhotic liver that leads to can-cer. More than 7000 liver transplantations are performed each year in the United States, with 1-year survival rates approaching 90%. In May 2017, approximately 14,463 patients were on the waiting list for liver transplantation.128Initial series of OLT for HCC reported in the 1990s included advanced cases of HCC, and the 5-year survival rates were only 20% to 50%.88 This compared poorly with overall 5-year survival rates of 70% to 75% for OLT in the Organ Pro-curement and Transplantation Network/United Network for Organ Sharing (OPTN/UNOS) database. Mazzaferro and col-leagues at
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with overall 5-year survival rates of 70% to 75% for OLT in the Organ Pro-curement and Transplantation Network/United Network for Organ Sharing (OPTN/UNOS) database. Mazzaferro and col-leagues at Milan subsequently showed that survival rates were markedly improved when OLT was limited to patients with early-stage HCC (stage I or stage II) with one tumor ≤5 cm, or up to three tumors no larger than 3 cm, along with the absence of gross vascular invasion or extrahepatic spread.129 Multiple studies have validated these findings, and many groups have proposed an expansion of the Milan criteria.81As noted previously, the 6to 40-point MELD score was adopted by OPTN/UNOS in 2002 for allocation of deceased donor liver organs in the United States. In an attempt to pri-oritize patients with preserved liver function and progressive HCC, patients with stage II HCC are allocated exception points (currently 28 MELD points which activates 6 months after liver transplant listing, increasing every 3
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Surgery_Schwartz. with overall 5-year survival rates of 70% to 75% for OLT in the Organ Pro-curement and Transplantation Network/United Network for Organ Sharing (OPTN/UNOS) database. Mazzaferro and col-leagues at Milan subsequently showed that survival rates were markedly improved when OLT was limited to patients with early-stage HCC (stage I or stage II) with one tumor ≤5 cm, or up to three tumors no larger than 3 cm, along with the absence of gross vascular invasion or extrahepatic spread.129 Multiple studies have validated these findings, and many groups have proposed an expansion of the Milan criteria.81As noted previously, the 6to 40-point MELD score was adopted by OPTN/UNOS in 2002 for allocation of deceased donor liver organs in the United States. In an attempt to pri-oritize patients with preserved liver function and progressive HCC, patients with stage II HCC are allocated exception points (currently 28 MELD points which activates 6 months after liver transplant listing, increasing every 3
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liver function and progressive HCC, patients with stage II HCC are allocated exception points (currently 28 MELD points which activates 6 months after liver transplant listing, increasing every 3 months and capping at 34 points as long as they continue to meet transplant criteria). This allocation has had a positive effect for HCC liver transplant can-didates, leading to decreased waiting list dropout and increased transplant rates with excellent long-term outcomes.130 The goal is to better equate death rates on the liver transplant waiting list for patients with stage I or stage II HCC with rates for patients with chronic liver disease without HCC. Although indications for liver transplantation have increased, the supply of donor liv-ers has failed to keep pace with the numbers of potential recipi-ents. A partial solution has been the use of living donor grafts. This is especially true in Asia where the incidence of HCC is high and the rate of cadaveric donation is low. Living donor
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Surgery_Schwartz. liver function and progressive HCC, patients with stage II HCC are allocated exception points (currently 28 MELD points which activates 6 months after liver transplant listing, increasing every 3 months and capping at 34 points as long as they continue to meet transplant criteria). This allocation has had a positive effect for HCC liver transplant can-didates, leading to decreased waiting list dropout and increased transplant rates with excellent long-term outcomes.130 The goal is to better equate death rates on the liver transplant waiting list for patients with stage I or stage II HCC with rates for patients with chronic liver disease without HCC. Although indications for liver transplantation have increased, the supply of donor liv-ers has failed to keep pace with the numbers of potential recipi-ents. A partial solution has been the use of living donor grafts. This is especially true in Asia where the incidence of HCC is high and the rate of cadaveric donation is low. Living donor
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recipi-ents. A partial solution has been the use of living donor grafts. This is especially true in Asia where the incidence of HCC is high and the rate of cadaveric donation is low. Living donor grafts include right and left lobes, as well as dual grafts from separate donors to provide adequate hepatic mass to the recipi-ent. The use of living donor grafts also allows for transplant programs to push the boundaries by accepting patients beyond the Milan criteria with good results.112Radiofrequency AblationIn 1891, d’Arsonval discovered that radiofrequency (RF) waves delivered as an alternating electric current (>10 kHz) could pass through living tissue without causing pain or neuromuscular excitation. The resistance of the tissue to the rapidly alternating current produced heat. This discovery contributed to the devel-opment of the surgical application of electrocautery. In 1908, Beer used RF coagulation to destroy urinary bladder tumors. Cushing and Bovie later applied RF ablation to
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Surgery_Schwartz. recipi-ents. A partial solution has been the use of living donor grafts. This is especially true in Asia where the incidence of HCC is high and the rate of cadaveric donation is low. Living donor grafts include right and left lobes, as well as dual grafts from separate donors to provide adequate hepatic mass to the recipi-ent. The use of living donor grafts also allows for transplant programs to push the boundaries by accepting patients beyond the Milan criteria with good results.112Radiofrequency AblationIn 1891, d’Arsonval discovered that radiofrequency (RF) waves delivered as an alternating electric current (>10 kHz) could pass through living tissue without causing pain or neuromuscular excitation. The resistance of the tissue to the rapidly alternating current produced heat. This discovery contributed to the devel-opment of the surgical application of electrocautery. In 1908, Beer used RF coagulation to destroy urinary bladder tumors. Cushing and Bovie later applied RF ablation to
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contributed to the devel-opment of the surgical application of electrocautery. In 1908, Beer used RF coagulation to destroy urinary bladder tumors. Cushing and Bovie later applied RF ablation to intracranial tumors. In 1961, Lounsberry studied the histologic changes of the liver after RF ablation (RFA) in animal models. He found that RF caused local tissue destruction with uniform necrosis. In the early 1990s, two groups proposed that RFA can be an effective method for destroying unresectable malignant liver tumors.132,133 Both groups found that RFA produced lesions with well-demarcated areas of necrosis without viable tumor cells present. Clinical reports after short-term follow-up sug-gested that RFA was safe and effective in the treatment of liver tumors.134-136 However, Abdalla and colleagues exam-ined data for 358 consecutive patients with colorectal liver metastases treated with curative intent over a 10-year period (1992 to 2002).137 Liver-only recurrence after RFA was four
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Surgery_Schwartz. contributed to the devel-opment of the surgical application of electrocautery. In 1908, Beer used RF coagulation to destroy urinary bladder tumors. Cushing and Bovie later applied RF ablation to intracranial tumors. In 1961, Lounsberry studied the histologic changes of the liver after RF ablation (RFA) in animal models. He found that RF caused local tissue destruction with uniform necrosis. In the early 1990s, two groups proposed that RFA can be an effective method for destroying unresectable malignant liver tumors.132,133 Both groups found that RFA produced lesions with well-demarcated areas of necrosis without viable tumor cells present. Clinical reports after short-term follow-up sug-gested that RFA was safe and effective in the treatment of liver tumors.134-136 However, Abdalla and colleagues exam-ined data for 358 consecutive patients with colorectal liver metastases treated with curative intent over a 10-year period (1992 to 2002).137 Liver-only recurrence after RFA was four
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colleagues exam-ined data for 358 consecutive patients with colorectal liver metastases treated with curative intent over a 10-year period (1992 to 2002).137 Liver-only recurrence after RFA was four times the rate after resection (44% vs. 11% of patients), and RFA alone or in combination with resection did not provide survival rates comparable to those with resection alone. None-theless, RFA remains a common procedure that can be per-formed by a percutaneous, minimally invasive laparoscopic, or open approach.138,139 It also has been used successfully to ablate small HCCs as a bridge to liver transplantation.140 Results were reported for the first randomized clinical trial involving RFA treatment for HCC in 291 Chinese patients with three or fewer HCC tumors ranging in size from 3 to 7.5 cm.141 Patients were randomly assigned to treatment arms of RFA alone (n = 100), transarterial chemoembolization (TACE) alone (n = 95), or combined TACE plus RFA (n = 96). At a median follow-up of 28.5
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Surgery_Schwartz. colleagues exam-ined data for 358 consecutive patients with colorectal liver metastases treated with curative intent over a 10-year period (1992 to 2002).137 Liver-only recurrence after RFA was four times the rate after resection (44% vs. 11% of patients), and RFA alone or in combination with resection did not provide survival rates comparable to those with resection alone. None-theless, RFA remains a common procedure that can be per-formed by a percutaneous, minimally invasive laparoscopic, or open approach.138,139 It also has been used successfully to ablate small HCCs as a bridge to liver transplantation.140 Results were reported for the first randomized clinical trial involving RFA treatment for HCC in 291 Chinese patients with three or fewer HCC tumors ranging in size from 3 to 7.5 cm.141 Patients were randomly assigned to treatment arms of RFA alone (n = 100), transarterial chemoembolization (TACE) alone (n = 95), or combined TACE plus RFA (n = 96). At a median follow-up of 28.5
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Patients were randomly assigned to treatment arms of RFA alone (n = 100), transarterial chemoembolization (TACE) alone (n = 95), or combined TACE plus RFA (n = 96). At a median follow-up of 28.5 months, median survival was 22 months in the RFA group, 24 months in the TACE group, and 37 months in the TACE plus RFA group. Patients treated with TACE plus RFA had sig-nificantly better overall survival than those treated with TACE alone (P <.001) or RFA alone (P <.001). Sucandy and col-leagues examined long-term 5and 10-year overall survival in 320 patients that had hepatic RFA for HCC or colorectal cancer liver metastases (CLM).142 The majority of patients (71%) had a single tumor ablation. Minimum 5-year follow-up was available in 89% patients, with a median follow-up of 115.3 months. In the HCC group, the 5and 10-year overall survivals were 38.5% and 23.4%, respectively, while in the CLM group, the 5and 10-year overall survivals were 27.6% and 15%, respectively.Ethanol Ablation,
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Surgery_Schwartz. Patients were randomly assigned to treatment arms of RFA alone (n = 100), transarterial chemoembolization (TACE) alone (n = 95), or combined TACE plus RFA (n = 96). At a median follow-up of 28.5 months, median survival was 22 months in the RFA group, 24 months in the TACE group, and 37 months in the TACE plus RFA group. Patients treated with TACE plus RFA had sig-nificantly better overall survival than those treated with TACE alone (P <.001) or RFA alone (P <.001). Sucandy and col-leagues examined long-term 5and 10-year overall survival in 320 patients that had hepatic RFA for HCC or colorectal cancer liver metastases (CLM).142 The majority of patients (71%) had a single tumor ablation. Minimum 5-year follow-up was available in 89% patients, with a median follow-up of 115.3 months. In the HCC group, the 5and 10-year overall survivals were 38.5% and 23.4%, respectively, while in the CLM group, the 5and 10-year overall survivals were 27.6% and 15%, respectively.Ethanol Ablation,
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In the HCC group, the 5and 10-year overall survivals were 38.5% and 23.4%, respectively, while in the CLM group, the 5and 10-year overall survivals were 27.6% and 15%, respectively.Ethanol Ablation, Cryosurgery, and Microwave AblationPercutaneous ethanol injection has been shown to be a safe and effective treatment for small HCCs.136 The ethanol usually is delivered by percutaneous injection under ultrasound or CT guidance. Percutaneous ethanol injection also is used to treat small HCC tumors as a bridge to liver transplantation in some centers to avoid patient dropout.80 Although cryosurgery was used in the late 1980s and 1990s for ablation of liver tumors, many have abandoned this approach in favor of RFA because of the latter’s fewer side effects and ease of use. Microwave ablation is a thermal ablative technique used in the management of unresectable liver tumors to produce a coagulation necrosis. Brunicardi_Ch31_p1345-p1392.indd 138020/02/19 2:36 PM 1381LIVERCHAPTER 31In a
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Surgery_Schwartz. In the HCC group, the 5and 10-year overall survivals were 38.5% and 23.4%, respectively, while in the CLM group, the 5and 10-year overall survivals were 27.6% and 15%, respectively.Ethanol Ablation, Cryosurgery, and Microwave AblationPercutaneous ethanol injection has been shown to be a safe and effective treatment for small HCCs.136 The ethanol usually is delivered by percutaneous injection under ultrasound or CT guidance. Percutaneous ethanol injection also is used to treat small HCC tumors as a bridge to liver transplantation in some centers to avoid patient dropout.80 Although cryosurgery was used in the late 1980s and 1990s for ablation of liver tumors, many have abandoned this approach in favor of RFA because of the latter’s fewer side effects and ease of use. Microwave ablation is a thermal ablative technique used in the management of unresectable liver tumors to produce a coagulation necrosis. Brunicardi_Ch31_p1345-p1392.indd 138020/02/19 2:36 PM 1381LIVERCHAPTER 31In a
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a thermal ablative technique used in the management of unresectable liver tumors to produce a coagulation necrosis. Brunicardi_Ch31_p1345-p1392.indd 138020/02/19 2:36 PM 1381LIVERCHAPTER 31In a multicenter phase 2 U.S. trial using a 915-MHz micro-wave generator, 87 patients underwent 94 ablation procedures for 224 hepatic tumors.143 Forty-five percent of the procedures were performed using an open approach, 7% laparoscopically, and 48% percutaneously. The average tumor size was 3.6 cm (range, 0.5 to 9.0 cm). At a mean follow-up of 19 months, 47% of the patients were alive with no evidence of disease. Local recurrence at the ablation site occurred in 2.7% of tumors, and regional recurrence occurred in 43% of patients. There were no procedure-related deaths. Further studies are required to define the role of this technology in relation to the other abla-tion options available.Chemoembolization and Hepatic Artery Pump ChemoperfusionChemoembolization is the process of injecting
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Surgery_Schwartz. a thermal ablative technique used in the management of unresectable liver tumors to produce a coagulation necrosis. Brunicardi_Ch31_p1345-p1392.indd 138020/02/19 2:36 PM 1381LIVERCHAPTER 31In a multicenter phase 2 U.S. trial using a 915-MHz micro-wave generator, 87 patients underwent 94 ablation procedures for 224 hepatic tumors.143 Forty-five percent of the procedures were performed using an open approach, 7% laparoscopically, and 48% percutaneously. The average tumor size was 3.6 cm (range, 0.5 to 9.0 cm). At a mean follow-up of 19 months, 47% of the patients were alive with no evidence of disease. Local recurrence at the ablation site occurred in 2.7% of tumors, and regional recurrence occurred in 43% of patients. There were no procedure-related deaths. Further studies are required to define the role of this technology in relation to the other abla-tion options available.Chemoembolization and Hepatic Artery Pump ChemoperfusionChemoembolization is the process of injecting
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to define the role of this technology in relation to the other abla-tion options available.Chemoembolization and Hepatic Artery Pump ChemoperfusionChemoembolization is the process of injecting chemotherapeu-tic drugs combined with embolization particles into the hepatic artery that supplies the liver tumor using a percutaneous, trans-femoral approach. It is most commonly used for treatment of unresectable HCC. Three randomized trials and a meta-analysis have shown a survival benefit with chemoembolization.144-147 In a study by Lo and colleagues, 80 Asian patients were randomly assigned to receive either chemoembolization with cisplatin in lipiodol or symptomatic treatment only.144 Chemoembolization resulted in a marked tumor response, and the actuarial survival was significantly better in the chemoembolization group (1and 3-year survival of 57% and 26%, respectively) than in the con-trol group (1and 3-year survival of 32% and 3%, respectively). In another randomized trial, a
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Surgery_Schwartz. to define the role of this technology in relation to the other abla-tion options available.Chemoembolization and Hepatic Artery Pump ChemoperfusionChemoembolization is the process of injecting chemotherapeu-tic drugs combined with embolization particles into the hepatic artery that supplies the liver tumor using a percutaneous, trans-femoral approach. It is most commonly used for treatment of unresectable HCC. Three randomized trials and a meta-analysis have shown a survival benefit with chemoembolization.144-147 In a study by Lo and colleagues, 80 Asian patients were randomly assigned to receive either chemoembolization with cisplatin in lipiodol or symptomatic treatment only.144 Chemoembolization resulted in a marked tumor response, and the actuarial survival was significantly better in the chemoembolization group (1and 3-year survival of 57% and 26%, respectively) than in the con-trol group (1and 3-year survival of 32% and 3%, respectively). In another randomized trial, a
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better in the chemoembolization group (1and 3-year survival of 57% and 26%, respectively) than in the con-trol group (1and 3-year survival of 32% and 3%, respectively). In another randomized trial, a Barcelona group compared chemoembolization with doxorubicin versus supportive care and showed that chemoembolization significantly improved survival.145 Finally, in a large prospective cohort study of 8510 patients with unresectable HCC in Japan who received trans-catheter arterial lipiodol chemoembolization, the 5-year survival rate was 26% and median survival time was 34 months.146 The TACE-related mortality rate after the initial therapy was 0.5%. Complications of TACE include liver dysfunction or liver fail-ure, hepatic abscess, and hepatic artery thrombosis. Multiple studies also have shown promising results for chemoemboliza-tion with drug-eluting beads in treatment of HCC.148In the 1990s, hepatic artery pump chemoperfusion with floxuridine for colorectal cancer metastases to the
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Surgery_Schwartz. better in the chemoembolization group (1and 3-year survival of 57% and 26%, respectively) than in the con-trol group (1and 3-year survival of 32% and 3%, respectively). In another randomized trial, a Barcelona group compared chemoembolization with doxorubicin versus supportive care and showed that chemoembolization significantly improved survival.145 Finally, in a large prospective cohort study of 8510 patients with unresectable HCC in Japan who received trans-catheter arterial lipiodol chemoembolization, the 5-year survival rate was 26% and median survival time was 34 months.146 The TACE-related mortality rate after the initial therapy was 0.5%. Complications of TACE include liver dysfunction or liver fail-ure, hepatic abscess, and hepatic artery thrombosis. Multiple studies also have shown promising results for chemoemboliza-tion with drug-eluting beads in treatment of HCC.148In the 1990s, hepatic artery pump chemoperfusion with floxuridine for colorectal cancer metastases to the
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shown promising results for chemoemboliza-tion with drug-eluting beads in treatment of HCC.148In the 1990s, hepatic artery pump chemoperfusion with floxuridine for colorectal cancer metastases to the liver was used both for treatment of inoperable disease and in the adjuvant setting.149 However, in the modern era of improved chemothera-peutic options, this treatment modality is seldom used outside of a clinical trial.Yttrium-90 MicrospheresSelective internal radioembolization or transarterial radioem-bolization (TARE) is a promising new treatment modality for patients with inoperable primary or metastatic liver tumors. The treatment is a minimally invasive transcatheter therapy in which radioactive microspheres are infused into the hepatic arteries via a transfemoral percutaneous approach. The yttrium-90 micro-spheres are directly injected into the hepatic artery branches that supply the tumor. Once infused, the microspheres deliver doses of high-energy, low-penetration radiation
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Surgery_Schwartz. shown promising results for chemoemboliza-tion with drug-eluting beads in treatment of HCC.148In the 1990s, hepatic artery pump chemoperfusion with floxuridine for colorectal cancer metastases to the liver was used both for treatment of inoperable disease and in the adjuvant setting.149 However, in the modern era of improved chemothera-peutic options, this treatment modality is seldom used outside of a clinical trial.Yttrium-90 MicrospheresSelective internal radioembolization or transarterial radioem-bolization (TARE) is a promising new treatment modality for patients with inoperable primary or metastatic liver tumors. The treatment is a minimally invasive transcatheter therapy in which radioactive microspheres are infused into the hepatic arteries via a transfemoral percutaneous approach. The yttrium-90 micro-spheres are directly injected into the hepatic artery branches that supply the tumor. Once infused, the microspheres deliver doses of high-energy, low-penetration radiation
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The yttrium-90 micro-spheres are directly injected into the hepatic artery branches that supply the tumor. Once infused, the microspheres deliver doses of high-energy, low-penetration radiation selectively to the tumor. The main indications are inoperable HCC150 and colorec-tal cancer hepatic metastases for which systemic chemotherapy has failed.151,152 In a study involving 137 patients with unresect-able chemorefractory liver metastases treated with radioembo-lization, there was a response rate of 42.8% (2.1% complete response, 40.7% partial response) according to World Health Organization criteria.152 One-year survival rate was 47.8%, and 2-year survival rate was 30.9%. Median survival was 457 days for patients with colorectal tumor metastases, 776 days for those with neuroendocrine tumor metastases, and 207 days for those with noncolorectal, nonneuroendocrine tumor metastases. The two products available in the United States are SIR-Spheres (Sirtex, Sydney, Australia) and
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Surgery_Schwartz. The yttrium-90 micro-spheres are directly injected into the hepatic artery branches that supply the tumor. Once infused, the microspheres deliver doses of high-energy, low-penetration radiation selectively to the tumor. The main indications are inoperable HCC150 and colorec-tal cancer hepatic metastases for which systemic chemotherapy has failed.151,152 In a study involving 137 patients with unresect-able chemorefractory liver metastases treated with radioembo-lization, there was a response rate of 42.8% (2.1% complete response, 40.7% partial response) according to World Health Organization criteria.152 One-year survival rate was 47.8%, and 2-year survival rate was 30.9%. Median survival was 457 days for patients with colorectal tumor metastases, 776 days for those with neuroendocrine tumor metastases, and 207 days for those with noncolorectal, nonneuroendocrine tumor metastases. The two products available in the United States are SIR-Spheres (Sirtex, Sydney, Australia) and
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tumor metastases, and 207 days for those with noncolorectal, nonneuroendocrine tumor metastases. The two products available in the United States are SIR-Spheres (Sirtex, Sydney, Australia) and TheraSphere (Nordian, Ottawa, Canada).Stereotactic Radiosurgery and Intensity-Modulated Radiation TherapyAlthough stereotactic radiosurgery (with CyberKnife and other systems) is in widespread use for brain and spinal tumors, body application to HCC or metastatic liver tumors has only recently occurred. In a phase 1 study, 31 patients with unresectable HCCs and 10 with unresectable cholangiocarcinomas completed a six-fraction course of stereotactic body radiotherapy.153 The treat-ment was well tolerated, and median survival was 11.7 and 15.0 months for the two groups, respectively. A similar safety profile was observed in a study in the Netherlands.154 Further clinical trials are required to define the future role of stereo-tactic radiosurgery in treatment of HCC and metastatic tumors.
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Surgery_Schwartz. tumor metastases, and 207 days for those with noncolorectal, nonneuroendocrine tumor metastases. The two products available in the United States are SIR-Spheres (Sirtex, Sydney, Australia) and TheraSphere (Nordian, Ottawa, Canada).Stereotactic Radiosurgery and Intensity-Modulated Radiation TherapyAlthough stereotactic radiosurgery (with CyberKnife and other systems) is in widespread use for brain and spinal tumors, body application to HCC or metastatic liver tumors has only recently occurred. In a phase 1 study, 31 patients with unresectable HCCs and 10 with unresectable cholangiocarcinomas completed a six-fraction course of stereotactic body radiotherapy.153 The treat-ment was well tolerated, and median survival was 11.7 and 15.0 months for the two groups, respectively. A similar safety profile was observed in a study in the Netherlands.154 Further clinical trials are required to define the future role of stereo-tactic radiosurgery in treatment of HCC and metastatic tumors.
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safety profile was observed in a study in the Netherlands.154 Further clinical trials are required to define the future role of stereo-tactic radiosurgery in treatment of HCC and metastatic tumors. Intensity-modulated radiation therapy (IMRT) is another tech-nologic advancement that facilitates the targeted delivery of external-beam radiation. Early clinical data suggested favorable outcomes with IMRT for the treatment of patients with unre-sectable HCC, and ongoing trials are further examining the role of IMRT for these locally advanced tumors.DownstagingIn more advanced-stage patients not eligible for MELD excep-tion points, hepatic-directed therapy including TACE and tumor ablation with radiofrequency, microwave, and ethanol ablation have been found to be effective in shrinking tumors to meet Milan criteria (downstaging). Multiple centers have used down-staging to allow for OLT in patients whose tumors responded and shrank to meet eligibility criteria.155,156Systemic
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Surgery_Schwartz. safety profile was observed in a study in the Netherlands.154 Further clinical trials are required to define the future role of stereo-tactic radiosurgery in treatment of HCC and metastatic tumors. Intensity-modulated radiation therapy (IMRT) is another tech-nologic advancement that facilitates the targeted delivery of external-beam radiation. Early clinical data suggested favorable outcomes with IMRT for the treatment of patients with unre-sectable HCC, and ongoing trials are further examining the role of IMRT for these locally advanced tumors.DownstagingIn more advanced-stage patients not eligible for MELD excep-tion points, hepatic-directed therapy including TACE and tumor ablation with radiofrequency, microwave, and ethanol ablation have been found to be effective in shrinking tumors to meet Milan criteria (downstaging). Multiple centers have used down-staging to allow for OLT in patients whose tumors responded and shrank to meet eligibility criteria.155,156Systemic
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tumors to meet Milan criteria (downstaging). Multiple centers have used down-staging to allow for OLT in patients whose tumors responded and shrank to meet eligibility criteria.155,156Systemic ChemotherapyChemotherapy has not demonstrated great efficacy in patients with HCC, especially in patients with significant cirrhosis. For treatment of HCC, the multikinase inhibitor sorafenib has shown some efficacy in a phase 3 randomized international multicenter trial. The SHARP trial (Sorafenib HCC Assessment Random-ized Protocol) enrolled 602 patients with Child’s class A cir-rhosis and inoperable HCC. At interim analysis, the trial was discontinued because a survival benefit was found in the treat-ment group. The median overall survival for patients receiv-ing sorafenib was 10.7 months versus 7.9 months for patients in the control arm. Based on these findings, sorafenib received accelerated Food and Drug Administration approval for the treatment of advanced unresectable HCC.157 Future
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Surgery_Schwartz. tumors to meet Milan criteria (downstaging). Multiple centers have used down-staging to allow for OLT in patients whose tumors responded and shrank to meet eligibility criteria.155,156Systemic ChemotherapyChemotherapy has not demonstrated great efficacy in patients with HCC, especially in patients with significant cirrhosis. For treatment of HCC, the multikinase inhibitor sorafenib has shown some efficacy in a phase 3 randomized international multicenter trial. The SHARP trial (Sorafenib HCC Assessment Random-ized Protocol) enrolled 602 patients with Child’s class A cir-rhosis and inoperable HCC. At interim analysis, the trial was discontinued because a survival benefit was found in the treat-ment group. The median overall survival for patients receiv-ing sorafenib was 10.7 months versus 7.9 months for patients in the control arm. Based on these findings, sorafenib received accelerated Food and Drug Administration approval for the treatment of advanced unresectable HCC.157 Future
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7.9 months for patients in the control arm. Based on these findings, sorafenib received accelerated Food and Drug Administration approval for the treatment of advanced unresectable HCC.157 Future studies will likely examine the role of other molecularly targeted agents and combinations of sorafenib with other treatment modalities.HEPATIC RESECTION SURGICAL TECHNIQUESNomenclatureDue to the confusion in language with regard to anatomic descrip-tions of hepatic resections, a common nomenclature was intro-duced at the International Hepato-Pancreato-Biliary Association Brunicardi_Ch31_p1345-p1392.indd 138120/02/19 2:36 PM 1382SPECIFIC CONSIDERATIONSPART IImeeting in Brisbane, Australia, in 2000 (Table 31-8).158,159 The goal was to provide universal terminology for liver anatomy and hepatic resections because there was much overlap among the designations for hepatic lobes, sections, sectors, and segments used by surgeons worldwide (Fig. 31-21). The most common or prevailing anatomic
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Surgery_Schwartz. 7.9 months for patients in the control arm. Based on these findings, sorafenib received accelerated Food and Drug Administration approval for the treatment of advanced unresectable HCC.157 Future studies will likely examine the role of other molecularly targeted agents and combinations of sorafenib with other treatment modalities.HEPATIC RESECTION SURGICAL TECHNIQUESNomenclatureDue to the confusion in language with regard to anatomic descrip-tions of hepatic resections, a common nomenclature was intro-duced at the International Hepato-Pancreato-Biliary Association Brunicardi_Ch31_p1345-p1392.indd 138120/02/19 2:36 PM 1382SPECIFIC CONSIDERATIONSPART IImeeting in Brisbane, Australia, in 2000 (Table 31-8).158,159 The goal was to provide universal terminology for liver anatomy and hepatic resections because there was much overlap among the designations for hepatic lobes, sections, sectors, and segments used by surgeons worldwide (Fig. 31-21). The most common or prevailing anatomic
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resections because there was much overlap among the designations for hepatic lobes, sections, sectors, and segments used by surgeons worldwide (Fig. 31-21). The most common or prevailing anatomic pattern was used as the basis for naming liver anatomy, and the surgical procedure nomenclature adopted for hepatic resections was based on the assigned anatomic ter-minology.160 Adoption of a common language should enable hepatic surgeons to better understand and interpret liver surgery publications from different continents and disseminate their knowledge to the next generation of hepatobiliary surgeons. Nonetheless, even today, the literature is full of both old and new liver resection terminology, so the surgeon in training must be familiar with all the various classifications.Techniques and Devices for Dividing the Hepatic ParenchymaHepatic resection surgery has evolved over the past 50 years. A better understanding of liver anatomy and physiology, coupled with improved anesthesia
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Surgery_Schwartz. resections because there was much overlap among the designations for hepatic lobes, sections, sectors, and segments used by surgeons worldwide (Fig. 31-21). The most common or prevailing anatomic pattern was used as the basis for naming liver anatomy, and the surgical procedure nomenclature adopted for hepatic resections was based on the assigned anatomic ter-minology.160 Adoption of a common language should enable hepatic surgeons to better understand and interpret liver surgery publications from different continents and disseminate their knowledge to the next generation of hepatobiliary surgeons. Nonetheless, even today, the literature is full of both old and new liver resection terminology, so the surgeon in training must be familiar with all the various classifications.Techniques and Devices for Dividing the Hepatic ParenchymaHepatic resection surgery has evolved over the past 50 years. A better understanding of liver anatomy and physiology, coupled with improved anesthesia
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and Devices for Dividing the Hepatic ParenchymaHepatic resection surgery has evolved over the past 50 years. A better understanding of liver anatomy and physiology, coupled with improved anesthesia techniques and widespread use of intraoperative ultrasound, has led to virtually “bloodless” liver surgery in the modern era (the year 2000 to the present). Innova-tions in technology have expanded the list of liver parenchymal transection devices161-163 and hemostatic agents (Table 31-9). Use of each device or agent has a learning curve, and undoubt-edly every experienced hepatic surgeon has his or her personal preferences.One major trend has been the application of vascular sta-pling devices for division of the hepatic and portal veins.164-166 Based on early reports of successful stapling of extrahepatic Table 31-8Brisbane 2000 liver terminologyOLDER HEPATIC RESECTION TERMINOLOGYBRISBANE 2000 HEPATIC RESECTION TERMINOLOGY Right hepatic lobectomy Left hepatic lobectomy Right hepatic
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Surgery_Schwartz. and Devices for Dividing the Hepatic ParenchymaHepatic resection surgery has evolved over the past 50 years. A better understanding of liver anatomy and physiology, coupled with improved anesthesia techniques and widespread use of intraoperative ultrasound, has led to virtually “bloodless” liver surgery in the modern era (the year 2000 to the present). Innova-tions in technology have expanded the list of liver parenchymal transection devices161-163 and hemostatic agents (Table 31-9). Use of each device or agent has a learning curve, and undoubt-edly every experienced hepatic surgeon has his or her personal preferences.One major trend has been the application of vascular sta-pling devices for division of the hepatic and portal veins.164-166 Based on early reports of successful stapling of extrahepatic Table 31-8Brisbane 2000 liver terminologyOLDER HEPATIC RESECTION TERMINOLOGYBRISBANE 2000 HEPATIC RESECTION TERMINOLOGY Right hepatic lobectomy Left hepatic lobectomy Right hepatic
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of extrahepatic Table 31-8Brisbane 2000 liver terminologyOLDER HEPATIC RESECTION TERMINOLOGYBRISBANE 2000 HEPATIC RESECTION TERMINOLOGY Right hepatic lobectomy Left hepatic lobectomy Right hepatic trisegmentectomy Left hepatic trisegmentectomy Left lateral segmentectomy Right posterior lobectomy Caudate lobectomy Right hepatectomy or right hemihepatectomy (V, VI, VII, VIII) Left hepatectomy or left hemihepatectomy (II, III, IV) Right trisectionectomy or extended right hepatectomy (or hemihepatectomy, IV, V, VI, VII, VIII) Left trisectionectomy or extended left hepatectomy (or hemihepatectomy, II, III, IV, V, VIII) Left lateral sectionectomy or bisegmentectomy (II, III) Right posterior sectionectomy (VI, VII) Caudate lobectomy or segmentectomy (I)ALTERNATIVE “SECTOR” TERMINOLOGY Right anterior sectorectomy Right posterior sectorectomy or right lateral sectorectomy Left medial sectorectomy or left paramedian sectorectomy (bisegmentectomy, III, IV) Left lateral sectorectomy
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Surgery_Schwartz. of extrahepatic Table 31-8Brisbane 2000 liver terminologyOLDER HEPATIC RESECTION TERMINOLOGYBRISBANE 2000 HEPATIC RESECTION TERMINOLOGY Right hepatic lobectomy Left hepatic lobectomy Right hepatic trisegmentectomy Left hepatic trisegmentectomy Left lateral segmentectomy Right posterior lobectomy Caudate lobectomy Right hepatectomy or right hemihepatectomy (V, VI, VII, VIII) Left hepatectomy or left hemihepatectomy (II, III, IV) Right trisectionectomy or extended right hepatectomy (or hemihepatectomy, IV, V, VI, VII, VIII) Left trisectionectomy or extended left hepatectomy (or hemihepatectomy, II, III, IV, V, VIII) Left lateral sectionectomy or bisegmentectomy (II, III) Right posterior sectionectomy (VI, VII) Caudate lobectomy or segmentectomy (I)ALTERNATIVE “SECTOR” TERMINOLOGY Right anterior sectorectomy Right posterior sectorectomy or right lateral sectorectomy Left medial sectorectomy or left paramedian sectorectomy (bisegmentectomy, III, IV) Left lateral sectorectomy
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anterior sectorectomy Right posterior sectorectomy or right lateral sectorectomy Left medial sectorectomy or left paramedian sectorectomy (bisegmentectomy, III, IV) Left lateral sectorectomy (segmentectomy, II)IVCRHVMHVVIIVIIIIVaIIVIVIVbIIIFalciform lig.Portal veinIVCLHVIFigure 31-21. Hepatic anatomy. Hepatic segments removed in the formal major hepatic resections are indicated. IVC = inferior vena cava; LHV = left hepatic vein; MHV = middle hepatic vein; RHV = right hepatic vein.Table 31-9Techniques and devices for dividing liver parenchyma and achieving hemostasisBlunt fracture and clipsMonopolar cautery (Bovie)Bipolar cauteryArgon beam coagulatorCUSA ultrasonic dissectorHydro-Jet water-jet dissectorHarmonic Scalpel, AutoSonix ultrasonic transector-coagulatorLigaSure tissue fusion systemSurgRx EnSeal tissue sealing and transection systemGyrus PK cutting forcepsEndovascular staplersTissueLink sealing devicesHabib 4X Laparoscopic sealerInLine bipolar linear coagulatorTopical agents
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Surgery_Schwartz. anterior sectorectomy Right posterior sectorectomy or right lateral sectorectomy Left medial sectorectomy or left paramedian sectorectomy (bisegmentectomy, III, IV) Left lateral sectorectomy (segmentectomy, II)IVCRHVMHVVIIVIIIIVaIIVIVIVbIIIFalciform lig.Portal veinIVCLHVIFigure 31-21. Hepatic anatomy. Hepatic segments removed in the formal major hepatic resections are indicated. IVC = inferior vena cava; LHV = left hepatic vein; MHV = middle hepatic vein; RHV = right hepatic vein.Table 31-9Techniques and devices for dividing liver parenchyma and achieving hemostasisBlunt fracture and clipsMonopolar cautery (Bovie)Bipolar cauteryArgon beam coagulatorCUSA ultrasonic dissectorHydro-Jet water-jet dissectorHarmonic Scalpel, AutoSonix ultrasonic transector-coagulatorLigaSure tissue fusion systemSurgRx EnSeal tissue sealing and transection systemGyrus PK cutting forcepsEndovascular staplersTissueLink sealing devicesHabib 4X Laparoscopic sealerInLine bipolar linear coagulatorTopical agents
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EnSeal tissue sealing and transection systemGyrus PK cutting forcepsEndovascular staplersTissueLink sealing devicesHabib 4X Laparoscopic sealerInLine bipolar linear coagulatorTopical agents (fibrin glues, Surgicel, Gelfoam, Avitene, Tisseel, Floseal, Crosseal)Brunicardi_Ch31_p1345-p1392.indd 138220/02/19 2:36 PM 1383LIVERCHAPTER 31vessels, stapling devices are now being used in the parenchymal transection phase, which remains a source of potential blood loss due to back bleeding from the middle hepatic vein.167,168 One advantage of the stapling technique is the speed with which the transection can be performed, which minimizes surface bleeding and period of ischemia for the remnant liver. How-ever, a major disadvantage of the stapling technique is the cost of multiple stapler cartridges. This is balanced by the decreased expenses reported with avoidance of ICU admission and blood transfusion, as well as shortened operating room time. Another consideration in the use of staplers
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Surgery_Schwartz. EnSeal tissue sealing and transection systemGyrus PK cutting forcepsEndovascular staplersTissueLink sealing devicesHabib 4X Laparoscopic sealerInLine bipolar linear coagulatorTopical agents (fibrin glues, Surgicel, Gelfoam, Avitene, Tisseel, Floseal, Crosseal)Brunicardi_Ch31_p1345-p1392.indd 138220/02/19 2:36 PM 1383LIVERCHAPTER 31vessels, stapling devices are now being used in the parenchymal transection phase, which remains a source of potential blood loss due to back bleeding from the middle hepatic vein.167,168 One advantage of the stapling technique is the speed with which the transection can be performed, which minimizes surface bleeding and period of ischemia for the remnant liver. How-ever, a major disadvantage of the stapling technique is the cost of multiple stapler cartridges. This is balanced by the decreased expenses reported with avoidance of ICU admission and blood transfusion, as well as shortened operating room time. Another consideration in the use of staplers
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This is balanced by the decreased expenses reported with avoidance of ICU admission and blood transfusion, as well as shortened operating room time. Another consideration in the use of staplers for parenchymal transec-tion is the potential for bile leaks. However, in a large series of 101 consecutive right hemihepatectomies performed using the stapling technique, there was only one reported bile leak (1%), which sealed after ERCP.168Steps in Commonly Performed Hepatic ResectionsA fundamental understanding of hepatic anatomy is vital for any surgeon with the desire to perform hepatobiliary surgery. Each hepatic resection surgery can be broken down into a series of orderly steps. The key to being a proficient hepatic surgeon is not to operate swiftly but rather to accomplish the operation by completing the steps in an orchestrated fashion. Mastery of the operative steps coupled with knowledge of liver anatomy and the common anatomic variants provides the foundation for safe hepatic
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Surgery_Schwartz. This is balanced by the decreased expenses reported with avoidance of ICU admission and blood transfusion, as well as shortened operating room time. Another consideration in the use of staplers for parenchymal transec-tion is the potential for bile leaks. However, in a large series of 101 consecutive right hemihepatectomies performed using the stapling technique, there was only one reported bile leak (1%), which sealed after ERCP.168Steps in Commonly Performed Hepatic ResectionsA fundamental understanding of hepatic anatomy is vital for any surgeon with the desire to perform hepatobiliary surgery. Each hepatic resection surgery can be broken down into a series of orderly steps. The key to being a proficient hepatic surgeon is not to operate swiftly but rather to accomplish the operation by completing the steps in an orchestrated fashion. Mastery of the operative steps coupled with knowledge of liver anatomy and the common anatomic variants provides the foundation for safe hepatic
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by completing the steps in an orchestrated fashion. Mastery of the operative steps coupled with knowledge of liver anatomy and the common anatomic variants provides the foundation for safe hepatic surgery. There are many different techniques and sequences for accomplishing each of the anatomic (and nonana-tomic) hepatic operations. The authors present their preferred approach in a stepwise fashion for right hepatic lobectomy (right hemihepatectomy), left hepatic lobectomy (left hemihepa-tectomy), and left lateral segmentectomy (left lateral sectionec-tomy). Provision of a detailed approach for every type of liver resection is beyond the scope of this chapter, and readers are referred to several excellent descriptions.169Steps Common to All Open Major Hepatic Resections 1. Make the skin incision—right subcostal with or without a partial or complete left subcostal extension across the mid-line, depending on the patient’s habitus and liver/tumor anatomy.2. Open and explore the abdomen,
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Surgery_Schwartz. by completing the steps in an orchestrated fashion. Mastery of the operative steps coupled with knowledge of liver anatomy and the common anatomic variants provides the foundation for safe hepatic surgery. There are many different techniques and sequences for accomplishing each of the anatomic (and nonana-tomic) hepatic operations. The authors present their preferred approach in a stepwise fashion for right hepatic lobectomy (right hemihepatectomy), left hepatic lobectomy (left hemihepa-tectomy), and left lateral segmentectomy (left lateral sectionec-tomy). Provision of a detailed approach for every type of liver resection is beyond the scope of this chapter, and readers are referred to several excellent descriptions.169Steps Common to All Open Major Hepatic Resections 1. Make the skin incision—right subcostal with or without a partial or complete left subcostal extension across the mid-line, depending on the patient’s habitus and liver/tumor anatomy.2. Open and explore the abdomen,
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subcostal with or without a partial or complete left subcostal extension across the mid-line, depending on the patient’s habitus and liver/tumor anatomy.2. Open and explore the abdomen, and place a fixed table retractor (e.g., Thompson or Bookwalter).3. Examine the liver with bimanual palpation. Perform liver ultrasound, and confirm the operation to be performed.4. Take down the round and falciform ligaments, and expose the anterior surface of the hepatic veins.5. For a left hepatectomy, divide the left triangular ligament; for a right hepatectomy, mobilize the right lobe from the right coronary and triangular ligaments.6. Open the gastrohepatic ligament, palpate the porta hepatis, and assess for accessory or replaced hepatic arteries.7. Perform a cholecystectomy; leave the gallbladder with the cystic duct intact if the gallbladder is involved by the tumor.Right Hepatic Lobectomy (Right Hepatectomy or Hemihepatectomy) 8. Mobilize the liver from the anterior aspect of the IVC in
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Surgery_Schwartz. subcostal with or without a partial or complete left subcostal extension across the mid-line, depending on the patient’s habitus and liver/tumor anatomy.2. Open and explore the abdomen, and place a fixed table retractor (e.g., Thompson or Bookwalter).3. Examine the liver with bimanual palpation. Perform liver ultrasound, and confirm the operation to be performed.4. Take down the round and falciform ligaments, and expose the anterior surface of the hepatic veins.5. For a left hepatectomy, divide the left triangular ligament; for a right hepatectomy, mobilize the right lobe from the right coronary and triangular ligaments.6. Open the gastrohepatic ligament, palpate the porta hepatis, and assess for accessory or replaced hepatic arteries.7. Perform a cholecystectomy; leave the gallbladder with the cystic duct intact if the gallbladder is involved by the tumor.Right Hepatic Lobectomy (Right Hepatectomy or Hemihepatectomy) 8. Mobilize the liver from the anterior aspect of the IVC in
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with the cystic duct intact if the gallbladder is involved by the tumor.Right Hepatic Lobectomy (Right Hepatectomy or Hemihepatectomy) 8. Mobilize the liver from the anterior aspect of the IVC in “piggyback” fashion; ligate the short hepatic veins up to the right hepatic vein (RHV).9. Perform a right hilar dissection—gently lower the hilar plate, then doubly ligate and divide the right hepatic artery (RHA), superior to the right side of the common bile duct.10. Doubly ligate and divide a replaced or accessory RHA if present.11. Expose the portal vein, identifying its right and left branches. There is a small lateral portal vein branch off the right portal vein (RPV) to the caudate lobe that should be controlled and ligated to allow the exposure of additional length on the RPV. Divide the RPV either with a vascular stapler or between vascular clamps.12. Dissect the avascular tissue along the suprahepatic vena cava between the right and middle hepatic veins. Pass a silastic tube of a
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Surgery_Schwartz. with the cystic duct intact if the gallbladder is involved by the tumor.Right Hepatic Lobectomy (Right Hepatectomy or Hemihepatectomy) 8. Mobilize the liver from the anterior aspect of the IVC in “piggyback” fashion; ligate the short hepatic veins up to the right hepatic vein (RHV).9. Perform a right hilar dissection—gently lower the hilar plate, then doubly ligate and divide the right hepatic artery (RHA), superior to the right side of the common bile duct.10. Doubly ligate and divide a replaced or accessory RHA if present.11. Expose the portal vein, identifying its right and left branches. There is a small lateral portal vein branch off the right portal vein (RPV) to the caudate lobe that should be controlled and ligated to allow the exposure of additional length on the RPV. Divide the RPV either with a vascular stapler or between vascular clamps.12. Dissect the avascular tissue along the suprahepatic vena cava between the right and middle hepatic veins. Pass a silastic tube of a
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RPV either with a vascular stapler or between vascular clamps.12. Dissect the avascular tissue along the suprahepatic vena cava between the right and middle hepatic veins. Pass a silastic tube of a Jackson-Pratt drain through this gap.13. Notch or divide the caudate process crossing to the right hepatic lobe, and bring the drain up and through this notch.14. Hang the liver over the drain by pulling up as you divide through the liver parenchyma.15. Repeat ultrasound and confirm the transection plane, staying just to the right of the middle hepatic vein (MHV) unless the tumor extends over it.16. Cauterize approximately 1 cm into the liver parenchyma, then switch to a hydro-jet dissection device in combination with Bovie electrocautery and suture ligation.17. Continue parenchymal division until the RHV is encoun-tered. During this division, identification, control, ligation, and transection of the right hepatic duct (RHD) are obtained late in the parenchymal transection
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Surgery_Schwartz. RPV either with a vascular stapler or between vascular clamps.12. Dissect the avascular tissue along the suprahepatic vena cava between the right and middle hepatic veins. Pass a silastic tube of a Jackson-Pratt drain through this gap.13. Notch or divide the caudate process crossing to the right hepatic lobe, and bring the drain up and through this notch.14. Hang the liver over the drain by pulling up as you divide through the liver parenchyma.15. Repeat ultrasound and confirm the transection plane, staying just to the right of the middle hepatic vein (MHV) unless the tumor extends over it.16. Cauterize approximately 1 cm into the liver parenchyma, then switch to a hydro-jet dissection device in combination with Bovie electrocautery and suture ligation.17. Continue parenchymal division until the RHV is encoun-tered. During this division, identification, control, ligation, and transection of the right hepatic duct (RHD) are obtained late in the parenchymal transection
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division until the RHV is encoun-tered. During this division, identification, control, ligation, and transection of the right hepatic duct (RHD) are obtained late in the parenchymal transection process.18. Divide the RHV between vascular clamps and suture ligate the RHV.19. Examine the transected liver edge for bleeding; place a figure-of-eight ligating vascular suture if bleeding is encountered.20. Ensure hemostasis of the transected liver edge with an argon beam coagulator and suture ligation.21. Inspect the transection surface for bile leaks. These should be clipped or suture ligated. Applying a dilute solution of hydro-gen peroxide can facilitate the visualization of bile leaks.22. Inspect the IVC and right retroperitoneal space for hemostasis.23. Perform completion ultrasound to confirm left portal vein (LPV) inflow and outflow in the remaining hepatic veins.24. Fix the proximal falciform ligament back to the diaphragm side with figure-of-eight sutures.25. Apply tissue sealant to
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Surgery_Schwartz. division until the RHV is encoun-tered. During this division, identification, control, ligation, and transection of the right hepatic duct (RHD) are obtained late in the parenchymal transection process.18. Divide the RHV between vascular clamps and suture ligate the RHV.19. Examine the transected liver edge for bleeding; place a figure-of-eight ligating vascular suture if bleeding is encountered.20. Ensure hemostasis of the transected liver edge with an argon beam coagulator and suture ligation.21. Inspect the transection surface for bile leaks. These should be clipped or suture ligated. Applying a dilute solution of hydro-gen peroxide can facilitate the visualization of bile leaks.22. Inspect the IVC and right retroperitoneal space for hemostasis.23. Perform completion ultrasound to confirm left portal vein (LPV) inflow and outflow in the remaining hepatic veins.24. Fix the proximal falciform ligament back to the diaphragm side with figure-of-eight sutures.25. Apply tissue sealant to
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left portal vein (LPV) inflow and outflow in the remaining hepatic veins.24. Fix the proximal falciform ligament back to the diaphragm side with figure-of-eight sutures.25. Apply tissue sealant to the cut surface of the liver, and place a Jackson-Pratt drain in the right subphrenic space and close the abdomen (Fig. 31-22).Comments Although some liver surgeons advocate a one-step division of the entire intrahepatic Glissonian pedicle as described by Launois and Jamieson,170 it is the authors’ prefer-ence to divide the RHA, RHD, and RPV in an extrahepatic fash-ion. As for the transection plane, the key is to perform accurate ultrasound visualization and mapping of the MHV and to stay just to the right of it. Weaving in and out or bisecting the MHV can leading to torrential back bleeding. Also, for bulky right lobe tumors adherent to the diaphragm or retroperitoneum, an anterior approach with division of the parenchyma can be per-formed before right lobe mobilization.152,153Left Hepatic
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Surgery_Schwartz. left portal vein (LPV) inflow and outflow in the remaining hepatic veins.24. Fix the proximal falciform ligament back to the diaphragm side with figure-of-eight sutures.25. Apply tissue sealant to the cut surface of the liver, and place a Jackson-Pratt drain in the right subphrenic space and close the abdomen (Fig. 31-22).Comments Although some liver surgeons advocate a one-step division of the entire intrahepatic Glissonian pedicle as described by Launois and Jamieson,170 it is the authors’ prefer-ence to divide the RHA, RHD, and RPV in an extrahepatic fash-ion. As for the transection plane, the key is to perform accurate ultrasound visualization and mapping of the MHV and to stay just to the right of it. Weaving in and out or bisecting the MHV can leading to torrential back bleeding. Also, for bulky right lobe tumors adherent to the diaphragm or retroperitoneum, an anterior approach with division of the parenchyma can be per-formed before right lobe mobilization.152,153Left Hepatic
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for bulky right lobe tumors adherent to the diaphragm or retroperitoneum, an anterior approach with division of the parenchyma can be per-formed before right lobe mobilization.152,153Left Hepatic Lobectomy (Left Hepatectomy or Hemihepatectomy) 8. Widely open the gastrohepatic ligament flush with the undersurface of the left lateral section and the caudate lobe. 9. Doubly ligate and divide a replaced or accessory left hepatic artery (LHA) if present.Brunicardi_Ch31_p1345-p1392.indd 138320/02/19 2:36 PM 1384SPECIFIC CONSIDERATIONSPART II10. Clamp the round ligament (ligament teres) and pull it ante-riorly as a handle to expose the left hilum.11. Divide any existing parenchymal bridge between segments III and IVB.12. Dissect the left hilum at the base of the umbilical fissure and lower the hilar plate anterior to the left portal pedicle.13. Incise the peritoneum overlying the hilum from the left side, and doubly ligate the LHA (after test clamping and confirming a palpable pulse in
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Surgery_Schwartz. for bulky right lobe tumors adherent to the diaphragm or retroperitoneum, an anterior approach with division of the parenchyma can be per-formed before right lobe mobilization.152,153Left Hepatic Lobectomy (Left Hepatectomy or Hemihepatectomy) 8. Widely open the gastrohepatic ligament flush with the undersurface of the left lateral section and the caudate lobe. 9. Doubly ligate and divide a replaced or accessory left hepatic artery (LHA) if present.Brunicardi_Ch31_p1345-p1392.indd 138320/02/19 2:36 PM 1384SPECIFIC CONSIDERATIONSPART II10. Clamp the round ligament (ligament teres) and pull it ante-riorly as a handle to expose the left hilum.11. Divide any existing parenchymal bridge between segments III and IVB.12. Dissect the left hilum at the base of the umbilical fissure and lower the hilar plate anterior to the left portal pedicle.13. Incise the peritoneum overlying the hilum from the left side, and doubly ligate the LHA (after test clamping and confirming a palpable pulse in
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the hilar plate anterior to the left portal pedicle.13. Incise the peritoneum overlying the hilum from the left side, and doubly ligate the LHA (after test clamping and confirming a palpable pulse in the RHA).14. Dissect the portal vein at the base of the umbilical fissure (it will take a nearly 90° bend from the transverse to the umbilical portion).15. Expose the portal vein, identifying the right and left branches. Control the small portal vein branch off the LPV to the caudate lobe to allow the exposure of additional length. Divide the LPV either with a vascular stapler or between vascular clamps.16. Ligate and divide the ligamentum venosum caudally.17. Identify the long extrahepatic course of the left hepatic duct (LHD) behind the portal vein. Ligate and divide the LHD at the umbilical fissure.18. Fold the left lateral segment up and back to the right, expos-ing the window at the base of the left hepatic vein (LHV) as it enters the IVC. This is facilitated by dividing any loose
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Surgery_Schwartz. the hilar plate anterior to the left portal pedicle.13. Incise the peritoneum overlying the hilum from the left side, and doubly ligate the LHA (after test clamping and confirming a palpable pulse in the RHA).14. Dissect the portal vein at the base of the umbilical fissure (it will take a nearly 90° bend from the transverse to the umbilical portion).15. Expose the portal vein, identifying the right and left branches. Control the small portal vein branch off the LPV to the caudate lobe to allow the exposure of additional length. Divide the LPV either with a vascular stapler or between vascular clamps.16. Ligate and divide the ligamentum venosum caudally.17. Identify the long extrahepatic course of the left hepatic duct (LHD) behind the portal vein. Ligate and divide the LHD at the umbilical fissure.18. Fold the left lateral segment up and back to the right, expos-ing the window at the base of the left hepatic vein (LHV) as it enters the IVC. This is facilitated by dividing any loose
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fissure.18. Fold the left lateral segment up and back to the right, expos-ing the window at the base of the left hepatic vein (LHV) as it enters the IVC. This is facilitated by dividing any loose areolar tissue overlying the ligamentum venosum, which is divided proximally.19. Pass a large, blunt right-angle clamp in the window between the RHV and the MHV, and hug the back of the MHV, aim-ing for the deep edge of the LHV. Do not force it or perfo-rate the IVC or MHV.20. Pass the silastic tube of a Jackson-Pratt drain through this window.21. Notch or divide the caudate process crossing to the left hepatic lobe and bring the drain up and through this notch.22. Hang the liver over the drain by pulling up as you divide through the liver parenchyma.23. Repeat ultrasound and confirm the transection plane on the anterior surface, staying close to the demarcated line. Do not bisect the MHV as it passes tangentially from the left to the right lobe.24. Cauterize down approximately 1 cm in the
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Surgery_Schwartz. fissure.18. Fold the left lateral segment up and back to the right, expos-ing the window at the base of the left hepatic vein (LHV) as it enters the IVC. This is facilitated by dividing any loose areolar tissue overlying the ligamentum venosum, which is divided proximally.19. Pass a large, blunt right-angle clamp in the window between the RHV and the MHV, and hug the back of the MHV, aim-ing for the deep edge of the LHV. Do not force it or perfo-rate the IVC or MHV.20. Pass the silastic tube of a Jackson-Pratt drain through this window.21. Notch or divide the caudate process crossing to the left hepatic lobe and bring the drain up and through this notch.22. Hang the liver over the drain by pulling up as you divide through the liver parenchyma.23. Repeat ultrasound and confirm the transection plane on the anterior surface, staying close to the demarcated line. Do not bisect the MHV as it passes tangentially from the left to the right lobe.24. Cauterize down approximately 1 cm in the
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plane on the anterior surface, staying close to the demarcated line. Do not bisect the MHV as it passes tangentially from the left to the right lobe.24. Cauterize down approximately 1 cm in the liver paren-chyma, then switch to a hydro-jet dissection device in com-bination with Bovie electrocautery and suture ligation.25. Continue parenchymal division until the left/middle hepatic veins are encountered.26. Divide the LHV and MHV between vascular clamps and suture the ligate the LHV/MHV.27. Check the transected edge of the liver for surgical bleed-ing; ensure hemostasis of the transected edge with an argon beam coagulator and suture ligation.28. Inspect the transection surface for bile leaks. These should be clipped or suture ligated. Apply dilute solution of hydro-gen peroxide to facilitate the visualization of bile leaks.29. Perform completion ultrasound to confirm RPV inflow and RHV outflow.30. Apply tissue sealant to the transected surface of the liver. Place a Jackson-Pratt drain
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Surgery_Schwartz. plane on the anterior surface, staying close to the demarcated line. Do not bisect the MHV as it passes tangentially from the left to the right lobe.24. Cauterize down approximately 1 cm in the liver paren-chyma, then switch to a hydro-jet dissection device in com-bination with Bovie electrocautery and suture ligation.25. Continue parenchymal division until the left/middle hepatic veins are encountered.26. Divide the LHV and MHV between vascular clamps and suture the ligate the LHV/MHV.27. Check the transected edge of the liver for surgical bleed-ing; ensure hemostasis of the transected edge with an argon beam coagulator and suture ligation.28. Inspect the transection surface for bile leaks. These should be clipped or suture ligated. Apply dilute solution of hydro-gen peroxide to facilitate the visualization of bile leaks.29. Perform completion ultrasound to confirm RPV inflow and RHV outflow.30. Apply tissue sealant to the transected surface of the liver. Place a Jackson-Pratt drain
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the visualization of bile leaks.29. Perform completion ultrasound to confirm RPV inflow and RHV outflow.30. Apply tissue sealant to the transected surface of the liver. Place a Jackson-Pratt drain in the left subphrenic space and close the abdomen (Fig. 31-23).Comments Because the right posterior duct arises from the left hepatic duct (LHD) in approximately 20% of cases (see Fig. 31-9) and the right anterior duct comes off the LHD in approximately 5% of cases,6 it is vital to divide the LHD at the base of the umbilical fissure and not more centrally in the hilum as it bifurcates. If the LHD were divided as it appears to bifurcate from the right hepatic duct, then approximately 20% to Figure 31-22. Completed right hepatic lobectomy (right hepa-tectomy) with the right portal vein, right hepatic artery, and right bile duct ligated and divided. The right hepatic vein is ligated and divided. Middle hepatic vein branches inside the liver are divided.Figure 31-23. Completed left hepatic
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Surgery_Schwartz. the visualization of bile leaks.29. Perform completion ultrasound to confirm RPV inflow and RHV outflow.30. Apply tissue sealant to the transected surface of the liver. Place a Jackson-Pratt drain in the left subphrenic space and close the abdomen (Fig. 31-23).Comments Because the right posterior duct arises from the left hepatic duct (LHD) in approximately 20% of cases (see Fig. 31-9) and the right anterior duct comes off the LHD in approximately 5% of cases,6 it is vital to divide the LHD at the base of the umbilical fissure and not more centrally in the hilum as it bifurcates. If the LHD were divided as it appears to bifurcate from the right hepatic duct, then approximately 20% to Figure 31-22. Completed right hepatic lobectomy (right hepa-tectomy) with the right portal vein, right hepatic artery, and right bile duct ligated and divided. The right hepatic vein is ligated and divided. Middle hepatic vein branches inside the liver are divided.Figure 31-23. Completed left hepatic
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hepatic artery, and right bile duct ligated and divided. The right hepatic vein is ligated and divided. Middle hepatic vein branches inside the liver are divided.Figure 31-23. Completed left hepatic lobectomy (left hepatec-tomy) resecting segments II, III, and IV.Brunicardi_Ch31_p1345-p1392.indd 138420/02/19 2:37 PM 1385LIVERCHAPTER 3125% of the time, either the right posterior or right anterior duct would be transected. After the LHD is divided as described ear-lier (Step 17), the liver parenchyma is scored and divided hori-zontally approximately 1 cm above the left hilum; the surgeon thus assumes that an aberrant right anterior or posterior duct is coming off the LHD in the hilum and preserves it. Then as the parenchymal transection reaches the left side of the gallblad-der fossa, the transection plane turns vertical to run parallel to Cantlie’s line (or the left edge of the gallbladder bed). The left lobe of the liver will be well demarcated at this point (after the vascular
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Surgery_Schwartz. hepatic artery, and right bile duct ligated and divided. The right hepatic vein is ligated and divided. Middle hepatic vein branches inside the liver are divided.Figure 31-23. Completed left hepatic lobectomy (left hepatec-tomy) resecting segments II, III, and IV.Brunicardi_Ch31_p1345-p1392.indd 138420/02/19 2:37 PM 1385LIVERCHAPTER 3125% of the time, either the right posterior or right anterior duct would be transected. After the LHD is divided as described ear-lier (Step 17), the liver parenchyma is scored and divided hori-zontally approximately 1 cm above the left hilum; the surgeon thus assumes that an aberrant right anterior or posterior duct is coming off the LHD in the hilum and preserves it. Then as the parenchymal transection reaches the left side of the gallblad-der fossa, the transection plane turns vertical to run parallel to Cantlie’s line (or the left edge of the gallbladder bed). The left lobe of the liver will be well demarcated at this point (after the vascular
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the transection plane turns vertical to run parallel to Cantlie’s line (or the left edge of the gallbladder bed). The left lobe of the liver will be well demarcated at this point (after the vascular inflow has been divided), which guides the transection plane on the anterior surface. In general, the transection plane should be close to the demarcation line to minimize the amount of devascularized liver remaining. When dividing the LHV and MHV, the surgeon should keep in mind that they have a com-mon trunk approximately 90% of the time. If it is not easy to open the window deep to the MHV and LHV, then division of the MHV and LHV can be accomplished after the parenchymal transection.Left Lateral Segmentectomy (Left Lateral Sectionectomy) 8. Widely open the gastrohepatic ligament flush with the undersurface of the left lateral section and the caudate lobe. 9. Doubly ligate and divide a replaced or accessory LHA if present.10. Clamp the round ligament and pull it anteriorly as a handle
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Surgery_Schwartz. the transection plane turns vertical to run parallel to Cantlie’s line (or the left edge of the gallbladder bed). The left lobe of the liver will be well demarcated at this point (after the vascular inflow has been divided), which guides the transection plane on the anterior surface. In general, the transection plane should be close to the demarcation line to minimize the amount of devascularized liver remaining. When dividing the LHV and MHV, the surgeon should keep in mind that they have a com-mon trunk approximately 90% of the time. If it is not easy to open the window deep to the MHV and LHV, then division of the MHV and LHV can be accomplished after the parenchymal transection.Left Lateral Segmentectomy (Left Lateral Sectionectomy) 8. Widely open the gastrohepatic ligament flush with the undersurface of the left lateral section and the caudate lobe. 9. Doubly ligate and divide a replaced or accessory LHA if present.10. Clamp the round ligament and pull it anteriorly as a handle
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the undersurface of the left lateral section and the caudate lobe. 9. Doubly ligate and divide a replaced or accessory LHA if present.10. Clamp the round ligament and pull it anteriorly as a handle to expose the left hilum.11. Divide any existing parenchymal bridge between segments III and IVB.12. Carry the dissection down from the end of the round liga-ment, and the segment III pedicle will be encountered.13. Incise the peritoneal reflection on the left side of the round ligament as it inserts into the umbilical fissure. This will facilitate encircling the segment III and II pedicles, which can be divided separately. When encircling the segment II pedicle, take care to avoid injury to the caudate inflow ves-sels coming off the LPV.14. Divide the liver parenchyma, staying flush on the left side of the falciform ligament using Bovie electrocautery.15. Divide the LHV as the parenchymal transection is complete.16. A Pringle maneuver usually is not required for a left lateral
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Surgery_Schwartz. the undersurface of the left lateral section and the caudate lobe. 9. Doubly ligate and divide a replaced or accessory LHA if present.10. Clamp the round ligament and pull it anteriorly as a handle to expose the left hilum.11. Divide any existing parenchymal bridge between segments III and IVB.12. Carry the dissection down from the end of the round liga-ment, and the segment III pedicle will be encountered.13. Incise the peritoneal reflection on the left side of the round ligament as it inserts into the umbilical fissure. This will facilitate encircling the segment III and II pedicles, which can be divided separately. When encircling the segment II pedicle, take care to avoid injury to the caudate inflow ves-sels coming off the LPV.14. Divide the liver parenchyma, staying flush on the left side of the falciform ligament using Bovie electrocautery.15. Divide the LHV as the parenchymal transection is complete.16. A Pringle maneuver usually is not required for a left lateral
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on the left side of the falciform ligament using Bovie electrocautery.15. Divide the LHV as the parenchymal transection is complete.16. A Pringle maneuver usually is not required for a left lateral sectionectomy because complete devascularization occurs before transection and little back bleeding is encountered.Comments If the segment III and II LHA branches are large, they can be individually ligated in the left hilum before the pedicles (with portal vein and hepatic duct branches) are taken. If the tumor is more peripheral in the left lateral segment, then the segment III and II pedicles can be divided with a vascular stapler inside the liver during the parenchymal transection.Pringle and Ischemic PreconditioningPringle described clamping of the portal triad a century ago in the landmark paper “Notes on the Arrest of Hepatic Hemorrhage Due to Trauma.”4 Although the Pringle maneuver was initially described for controlling bleeding due to traumatic liver injury, it is commonly used
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Surgery_Schwartz. on the left side of the falciform ligament using Bovie electrocautery.15. Divide the LHV as the parenchymal transection is complete.16. A Pringle maneuver usually is not required for a left lateral sectionectomy because complete devascularization occurs before transection and little back bleeding is encountered.Comments If the segment III and II LHA branches are large, they can be individually ligated in the left hilum before the pedicles (with portal vein and hepatic duct branches) are taken. If the tumor is more peripheral in the left lateral segment, then the segment III and II pedicles can be divided with a vascular stapler inside the liver during the parenchymal transection.Pringle and Ischemic PreconditioningPringle described clamping of the portal triad a century ago in the landmark paper “Notes on the Arrest of Hepatic Hemorrhage Due to Trauma.”4 Although the Pringle maneuver was initially described for controlling bleeding due to traumatic liver injury, it is commonly used
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paper “Notes on the Arrest of Hepatic Hemorrhage Due to Trauma.”4 Although the Pringle maneuver was initially described for controlling bleeding due to traumatic liver injury, it is commonly used during elective hepatic resections.173,174 The goal is to minimize blood loss and hypotension, which add sig-nificant morbidity to the operation. Furthermore, intraoperative blood transfusion has been shown to be an independent risk fac-tor for increased postoperative infection as well as worse patient survival in some studies. Therefore, all efforts should be made to minimize blood loss during hepatic resection.Although the liver has been shown to tolerate up to 1 hour of warm ischemia, some technical variations of the Pringle maneuver include intermittent vascular occlusion with cycles of approximately 15 minutes on and 5 minutes off. Experimental and clinical studies have demonstrated the efficacy of intermit-tent vascular occlusion in decreasing ischemia/reperfusion injury compared with
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Surgery_Schwartz. paper “Notes on the Arrest of Hepatic Hemorrhage Due to Trauma.”4 Although the Pringle maneuver was initially described for controlling bleeding due to traumatic liver injury, it is commonly used during elective hepatic resections.173,174 The goal is to minimize blood loss and hypotension, which add sig-nificant morbidity to the operation. Furthermore, intraoperative blood transfusion has been shown to be an independent risk fac-tor for increased postoperative infection as well as worse patient survival in some studies. Therefore, all efforts should be made to minimize blood loss during hepatic resection.Although the liver has been shown to tolerate up to 1 hour of warm ischemia, some technical variations of the Pringle maneuver include intermittent vascular occlusion with cycles of approximately 15 minutes on and 5 minutes off. Experimental and clinical studies have demonstrated the efficacy of intermit-tent vascular occlusion in decreasing ischemia/reperfusion injury compared with
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15 minutes on and 5 minutes off. Experimental and clinical studies have demonstrated the efficacy of intermit-tent vascular occlusion in decreasing ischemia/reperfusion injury compared with continuous vascular occlusion, with less eleva-tion of postoperative liver enzyme levels.175 Another variation is selective hemihepatic vascular occlusion, which can reduce the severity of visceral congestion and total liver ischemia. In one prospective trial of total versus selective portal triad clamping, both techniques of inflow clamping were found to be equally effective for patients with normal livers, but greater liver dam-age was observed with total inflow occlusion in patients with cirrhotic livers.176In an attempt to decrease the ischemic damage associated with inflow occlusion, some hepatic surgeons have advocated the use of ischemic preconditioning.177 Ischemic precondition-ing refers to the brief interruption of blood flow to an organ, fol-lowed by a short reperfusion period, and then
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Surgery_Schwartz. 15 minutes on and 5 minutes off. Experimental and clinical studies have demonstrated the efficacy of intermit-tent vascular occlusion in decreasing ischemia/reperfusion injury compared with continuous vascular occlusion, with less eleva-tion of postoperative liver enzyme levels.175 Another variation is selective hemihepatic vascular occlusion, which can reduce the severity of visceral congestion and total liver ischemia. In one prospective trial of total versus selective portal triad clamping, both techniques of inflow clamping were found to be equally effective for patients with normal livers, but greater liver dam-age was observed with total inflow occlusion in patients with cirrhotic livers.176In an attempt to decrease the ischemic damage associated with inflow occlusion, some hepatic surgeons have advocated the use of ischemic preconditioning.177 Ischemic precondition-ing refers to the brief interruption of blood flow to an organ, fol-lowed by a short reperfusion period, and then
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surgeons have advocated the use of ischemic preconditioning.177 Ischemic precondition-ing refers to the brief interruption of blood flow to an organ, fol-lowed by a short reperfusion period, and then a more prolonged period of ischemia. In a randomized clinical trial involving 100 patients undergoing major hepatic resection, Clavien and col-leagues reported significantly less liver injury in the group who received ischemic preconditioning with a 10-minute clamp, a 10-minute reperfusion, and then a 30-minute clamp than in those who received a 30-minute clamp alone.178 Patients with steatosis also were especially protected by ischemic preconditioning, and the mechanism was shown to be related in part to preservation of the adenosine triphosphate content of liver tissue.Preoperative Portal Vein EmbolizationThe observation that tumor thrombosis of a major portal vein branch induced ipsilateral lobar atrophy and contralateral lobe hypertrophy led to the concept of intentional preoperative
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Surgery_Schwartz. surgeons have advocated the use of ischemic preconditioning.177 Ischemic precondition-ing refers to the brief interruption of blood flow to an organ, fol-lowed by a short reperfusion period, and then a more prolonged period of ischemia. In a randomized clinical trial involving 100 patients undergoing major hepatic resection, Clavien and col-leagues reported significantly less liver injury in the group who received ischemic preconditioning with a 10-minute clamp, a 10-minute reperfusion, and then a 30-minute clamp than in those who received a 30-minute clamp alone.178 Patients with steatosis also were especially protected by ischemic preconditioning, and the mechanism was shown to be related in part to preservation of the adenosine triphosphate content of liver tissue.Preoperative Portal Vein EmbolizationThe observation that tumor thrombosis of a major portal vein branch induced ipsilateral lobar atrophy and contralateral lobe hypertrophy led to the concept of intentional preoperative
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EmbolizationThe observation that tumor thrombosis of a major portal vein branch induced ipsilateral lobar atrophy and contralateral lobe hypertrophy led to the concept of intentional preoperative portal vein embolization (PVE) to induce compensatory hypertrophy of the remnant liver. This procedure was first described in the 1980s and is accomplished via a percutaneous, transhepatic route.160,161 Numerous studies have subsequently confirmed that PVE is effective in inducing hypertrophy of nonembolized hepatic segments.86,181 PVE usually is performed in the setting of a planned right trisectionectomy or extended left hepatec-tomy (also referred to as a left trisectionectomy; resection of Couinaud’s segments II, III, IV, V, and VIII of the liver) or extended hepatic lobectomy when it is thought that the patient’s remnant liver will be too small to support liver function. The future liver remnant volume (e.g., the volume of segments II, III, and I) in a patient undergoing a planned right
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Surgery_Schwartz. EmbolizationThe observation that tumor thrombosis of a major portal vein branch induced ipsilateral lobar atrophy and contralateral lobe hypertrophy led to the concept of intentional preoperative portal vein embolization (PVE) to induce compensatory hypertrophy of the remnant liver. This procedure was first described in the 1980s and is accomplished via a percutaneous, transhepatic route.160,161 Numerous studies have subsequently confirmed that PVE is effective in inducing hypertrophy of nonembolized hepatic segments.86,181 PVE usually is performed in the setting of a planned right trisectionectomy or extended left hepatec-tomy (also referred to as a left trisectionectomy; resection of Couinaud’s segments II, III, IV, V, and VIII of the liver) or extended hepatic lobectomy when it is thought that the patient’s remnant liver will be too small to support liver function. The future liver remnant volume (e.g., the volume of segments II, III, and I) in a patient undergoing a planned right
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that the patient’s remnant liver will be too small to support liver function. The future liver remnant volume (e.g., the volume of segments II, III, and I) in a patient undergoing a planned right trisectionec-tomy can be directly measured by helical CT and then divided by the total estimated liver volume to calculate the percentage of the future liver remnant. If the future liver remnant is thought to be too small, then PVE should be considered to increase the size of the future liver remnant.182 In general, surgery is planned approximately 4 weeks after PVE to allow adequate time for hypertrophy.There is no universal agreement on what constitutes a future liver remnant adequate to avoid postoperative liver fail-ure. It is thought that 25% to 30% of the total liver volume is ade-quate in patients with a normal liver.183 Vauthey and associates reported that major postoperative complications were increased when the estimated future liver remnant was <25%.184 Farges and colleagues
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Surgery_Schwartz. that the patient’s remnant liver will be too small to support liver function. The future liver remnant volume (e.g., the volume of segments II, III, and I) in a patient undergoing a planned right trisectionec-tomy can be directly measured by helical CT and then divided by the total estimated liver volume to calculate the percentage of the future liver remnant. If the future liver remnant is thought to be too small, then PVE should be considered to increase the size of the future liver remnant.182 In general, surgery is planned approximately 4 weeks after PVE to allow adequate time for hypertrophy.There is no universal agreement on what constitutes a future liver remnant adequate to avoid postoperative liver fail-ure. It is thought that 25% to 30% of the total liver volume is ade-quate in patients with a normal liver.183 Vauthey and associates reported that major postoperative complications were increased when the estimated future liver remnant was <25%.184 Farges and colleagues
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in patients with a normal liver.183 Vauthey and associates reported that major postoperative complications were increased when the estimated future liver remnant was <25%.184 Farges and colleagues conducted a prospective study to assess the benefits of PVE before right hepatectomy. They demonstrated Brunicardi_Ch31_p1345-p1392.indd 138520/02/19 2:37 PM 1386SPECIFIC CONSIDERATIONSPART IIthat PVE had no beneficial effect on the postoperative course in patients with normal livers but significantly reduced postop-erative complications in patients with chronic liver diseases.185 A larger remnant may be necessary even in patients with nor-mal livers when a complex hepatectomy is planned or when the background liver is steatotic.186 This is especially relevant with the increased incidence of fatty liver disease. A larger remnant may also be needed when patients have received pre-operative chemotherapy. Some have suggested that 40% of the total hepatic volume should remain to minimize
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Surgery_Schwartz. in patients with a normal liver.183 Vauthey and associates reported that major postoperative complications were increased when the estimated future liver remnant was <25%.184 Farges and colleagues conducted a prospective study to assess the benefits of PVE before right hepatectomy. They demonstrated Brunicardi_Ch31_p1345-p1392.indd 138520/02/19 2:37 PM 1386SPECIFIC CONSIDERATIONSPART IIthat PVE had no beneficial effect on the postoperative course in patients with normal livers but significantly reduced postop-erative complications in patients with chronic liver diseases.185 A larger remnant may be necessary even in patients with nor-mal livers when a complex hepatectomy is planned or when the background liver is steatotic.186 This is especially relevant with the increased incidence of fatty liver disease. A larger remnant may also be needed when patients have received pre-operative chemotherapy. Some have suggested that 40% of the total hepatic volume should remain to minimize
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of fatty liver disease. A larger remnant may also be needed when patients have received pre-operative chemotherapy. Some have suggested that 40% of the total hepatic volume should remain to minimize postoperative complications in patients who have underlying liver disease or who have received preoperative chemotherapy for colorectal cancer metastases.187,188 In a recent study encompassing 112 patients who underwent PVE, major complications, hepatic insufficiency, length of hospital stay, and 90-day mortality rate were significantly greater in patients with a standardized future liver remnant of ≤20% or a degree of hypertrophy of <5% than in patients with higher values.189 In another study, the authors performed PVE during neoadjuvant chemotherapy for colorec-tal cancer metastases. After a median wait of 30 days after PVE, patients receiving neoadjuvant chemotherapy showed median liver growth of 22% in the contralateral (nonembolized) lobe compared with 26% for those not receiving
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Surgery_Schwartz. of fatty liver disease. A larger remnant may also be needed when patients have received pre-operative chemotherapy. Some have suggested that 40% of the total hepatic volume should remain to minimize postoperative complications in patients who have underlying liver disease or who have received preoperative chemotherapy for colorectal cancer metastases.187,188 In a recent study encompassing 112 patients who underwent PVE, major complications, hepatic insufficiency, length of hospital stay, and 90-day mortality rate were significantly greater in patients with a standardized future liver remnant of ≤20% or a degree of hypertrophy of <5% than in patients with higher values.189 In another study, the authors performed PVE during neoadjuvant chemotherapy for colorec-tal cancer metastases. After a median wait of 30 days after PVE, patients receiving neoadjuvant chemotherapy showed median liver growth of 22% in the contralateral (nonembolized) lobe compared with 26% for those not receiving
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a median wait of 30 days after PVE, patients receiving neoadjuvant chemotherapy showed median liver growth of 22% in the contralateral (nonembolized) lobe compared with 26% for those not receiving chemotherapy (not a statistically significant difference), which indicated that liver growth occurs after PVE even when cytotoxic chemotherapy is administered.190 PVE-related complications occur at a relatively low rate and include bleeding, hemobilia, liver abscess, incom-plete embolization, and small bowel obstruction. To augment the ability to increase liver function reserve in patients who have undergone PVE, some groups have added ipsilateral hepatic artery embolization and ipsilateral hepatic vein embolization.191Staged Hepatectomy, ALPPS, and Repeat Hepatic Resection for Recurrent Liver CancerA two-stage hepatectomy is a sequential resection strategy to remove all metastatic liver tumors when it is impossible to resect all disease in a single operative procedure. The first-stage
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Surgery_Schwartz. a median wait of 30 days after PVE, patients receiving neoadjuvant chemotherapy showed median liver growth of 22% in the contralateral (nonembolized) lobe compared with 26% for those not receiving chemotherapy (not a statistically significant difference), which indicated that liver growth occurs after PVE even when cytotoxic chemotherapy is administered.190 PVE-related complications occur at a relatively low rate and include bleeding, hemobilia, liver abscess, incom-plete embolization, and small bowel obstruction. To augment the ability to increase liver function reserve in patients who have undergone PVE, some groups have added ipsilateral hepatic artery embolization and ipsilateral hepatic vein embolization.191Staged Hepatectomy, ALPPS, and Repeat Hepatic Resection for Recurrent Liver CancerA two-stage hepatectomy is a sequential resection strategy to remove all metastatic liver tumors when it is impossible to resect all disease in a single operative procedure. The first-stage
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CancerA two-stage hepatectomy is a sequential resection strategy to remove all metastatic liver tumors when it is impossible to resect all disease in a single operative procedure. The first-stage hepatectomy usually consists of clearance of the left hemiliver by nonanatomic resection, followed by right portal vein ligation or embolization to induce left lobe hypertrophy.192,193 This is fol-lowed by a second-stage major right hepatectomy or extended right hepatectomy to resect the right liver metastases. This approach is most commonly used in cases of initially unresect-able colorectal hepatic metastases and has yielded very good results.193Another technique to increase future liver remnant to avoid post-hepatectomy liver failure is known as “Associating Liver Partition and Portal Vein Ligation for Staged Hepatec-tomy (ALPPS)” and was described in 2012. This technique consists of operative portal vein ligation with in situ liver tran-section along the future line of resection leaving
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Surgery_Schwartz. CancerA two-stage hepatectomy is a sequential resection strategy to remove all metastatic liver tumors when it is impossible to resect all disease in a single operative procedure. The first-stage hepatectomy usually consists of clearance of the left hemiliver by nonanatomic resection, followed by right portal vein ligation or embolization to induce left lobe hypertrophy.192,193 This is fol-lowed by a second-stage major right hepatectomy or extended right hepatectomy to resect the right liver metastases. This approach is most commonly used in cases of initially unresect-able colorectal hepatic metastases and has yielded very good results.193Another technique to increase future liver remnant to avoid post-hepatectomy liver failure is known as “Associating Liver Partition and Portal Vein Ligation for Staged Hepatec-tomy (ALPPS)” and was described in 2012. This technique consists of operative portal vein ligation with in situ liver tran-section along the future line of resection leaving
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for Staged Hepatec-tomy (ALPPS)” and was described in 2012. This technique consists of operative portal vein ligation with in situ liver tran-section along the future line of resection leaving the arterial and hepatic vein branches intact.194 There have been several techni-cal modifications to the original description, and this remains a hot topic that is actively debated (ALPPS vs. PVE) at the current liver surgery meetings.The majority of patients undergoing hepatic resection for colorectal cancer metastases experience a recurrence. For those with limited disease recurrence confined to the liver, repeat hepatectomy is a reasonable option and can be performed with low morbidity and mortality in experienced hands.195 In one study, 126 patients who underwent a second liver resection for colorectal cancer metastases had 1-, 3-, and 5-year survival rates of 86%, 51%, and 34%, respectively. By multivariate analysis, the presence of more than one lesion and a tumor size of >5 cm were
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Surgery_Schwartz. for Staged Hepatec-tomy (ALPPS)” and was described in 2012. This technique consists of operative portal vein ligation with in situ liver tran-section along the future line of resection leaving the arterial and hepatic vein branches intact.194 There have been several techni-cal modifications to the original description, and this remains a hot topic that is actively debated (ALPPS vs. PVE) at the current liver surgery meetings.The majority of patients undergoing hepatic resection for colorectal cancer metastases experience a recurrence. For those with limited disease recurrence confined to the liver, repeat hepatectomy is a reasonable option and can be performed with low morbidity and mortality in experienced hands.195 In one study, 126 patients who underwent a second liver resection for colorectal cancer metastases had 1-, 3-, and 5-year survival rates of 86%, 51%, and 34%, respectively. By multivariate analysis, the presence of more than one lesion and a tumor size of >5 cm were
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colorectal cancer metastases had 1-, 3-, and 5-year survival rates of 86%, 51%, and 34%, respectively. By multivariate analysis, the presence of more than one lesion and a tumor size of >5 cm were independent prognostic indicators of reduced survival.196 In another study, 40 patients underwent a second hepatectomy for liver metastases from colorectal cancer and experienced a survival benefit similar to that from the first hepatectomy; how-ever, the results suggested that this approach should be limited to those patients who do not have extrahepatic disease and for whom >1 year has elapsed since the first operation.197 A meta-analysis of 21 studies examining clinical outcomes after first and second liver resections for colorectal cancer metastases showed that repeat hepatectomy was safe and provided a sur-vival benefit equal to that from the first liver resection.198Repeat hepatectomy also has been performed in patients with HCC. Nakajima and colleagues reported on follow-up of 94
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Surgery_Schwartz. colorectal cancer metastases had 1-, 3-, and 5-year survival rates of 86%, 51%, and 34%, respectively. By multivariate analysis, the presence of more than one lesion and a tumor size of >5 cm were independent prognostic indicators of reduced survival.196 In another study, 40 patients underwent a second hepatectomy for liver metastases from colorectal cancer and experienced a survival benefit similar to that from the first hepatectomy; how-ever, the results suggested that this approach should be limited to those patients who do not have extrahepatic disease and for whom >1 year has elapsed since the first operation.197 A meta-analysis of 21 studies examining clinical outcomes after first and second liver resections for colorectal cancer metastases showed that repeat hepatectomy was safe and provided a sur-vival benefit equal to that from the first liver resection.198Repeat hepatectomy also has been performed in patients with HCC. Nakajima and colleagues reported on follow-up of 94
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and provided a sur-vival benefit equal to that from the first liver resection.198Repeat hepatectomy also has been performed in patients with HCC. Nakajima and colleagues reported on follow-up of 94 patients who underwent curative liver resection for HCC from 1991 to 1996.199 Of these, 57 patients had isolated recur-rent disease in the liver. Twelve of these 57 patients underwent repeat hepatic resection, whereas the other 45 patients received ablation therapy. The overall survival rate in those undergoing a second hepatectomy was 90% at 2 years; however, the disease-free survival rate was only 31% at 2 years, significantly lower than the 62% rate after initial hepatectomy. Likewise, in another group of 84 patients who underwent second hepatectomy for recurrent HCC, the overall 5-year survival rate was 50%, but the recurrence-free survival rate was only 10%.200 In a report of 67 patients undergoing a second resection for HCC, over-all 1-, 3-, and 5-year survival rates were 93%, 70%,
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Surgery_Schwartz. and provided a sur-vival benefit equal to that from the first liver resection.198Repeat hepatectomy also has been performed in patients with HCC. Nakajima and colleagues reported on follow-up of 94 patients who underwent curative liver resection for HCC from 1991 to 1996.199 Of these, 57 patients had isolated recur-rent disease in the liver. Twelve of these 57 patients underwent repeat hepatic resection, whereas the other 45 patients received ablation therapy. The overall survival rate in those undergoing a second hepatectomy was 90% at 2 years; however, the disease-free survival rate was only 31% at 2 years, significantly lower than the 62% rate after initial hepatectomy. Likewise, in another group of 84 patients who underwent second hepatectomy for recurrent HCC, the overall 5-year survival rate was 50%, but the recurrence-free survival rate was only 10%.200 In a report of 67 patients undergoing a second resection for HCC, over-all 1-, 3-, and 5-year survival rates were 93%, 70%,
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rate was 50%, but the recurrence-free survival rate was only 10%.200 In a report of 67 patients undergoing a second resection for HCC, over-all 1-, 3-, and 5-year survival rates were 93%, 70%, and 56%, respectively.201 Multivariate analysis showed that absence of portal invasion at the second resection, single HCC at primary hepatectomy, and disease-free interval of ≥1 year after primary hepatectomy were independent prognostic factors after the sec-ond resection.LAPAROSCOPIC LIVER RESECTIONCherqui and colleagues first reported in 2000 that laparoscopic hepatic surgery was feasible.202 Since this initial report, laparo-scopic liver surgery has expanded from the simple unroofing of hepatic cysts to resection of peripheral benign lesions to formal anatomic lobectomies for malignancy and laparoscopic hepa-tectomy for living donor liver transplantation. While minimally invasive approaches have been widely adopted in other areas of abdominal surgery, there was initial apprehension regarding
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Surgery_Schwartz. rate was 50%, but the recurrence-free survival rate was only 10%.200 In a report of 67 patients undergoing a second resection for HCC, over-all 1-, 3-, and 5-year survival rates were 93%, 70%, and 56%, respectively.201 Multivariate analysis showed that absence of portal invasion at the second resection, single HCC at primary hepatectomy, and disease-free interval of ≥1 year after primary hepatectomy were independent prognostic factors after the sec-ond resection.LAPAROSCOPIC LIVER RESECTIONCherqui and colleagues first reported in 2000 that laparoscopic hepatic surgery was feasible.202 Since this initial report, laparo-scopic liver surgery has expanded from the simple unroofing of hepatic cysts to resection of peripheral benign lesions to formal anatomic lobectomies for malignancy and laparoscopic hepa-tectomy for living donor liver transplantation. While minimally invasive approaches have been widely adopted in other areas of abdominal surgery, there was initial apprehension regarding
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hepa-tectomy for living donor liver transplantation. While minimally invasive approaches have been widely adopted in other areas of abdominal surgery, there was initial apprehension regarding laparoscopic liver resection (LLR), hampering its widespread adoption.203 Great strides have been made in the past decade with techniques of laparoscopic liver resection,204,205 and two International Laparoscopic Liver Resection Consensus Confer-ences have been convened in Louisville (2008) and Morioko (2014).206,207 Indications for liver resection should not be altered by the availability of minimally invasive liver resection tech-niques. Currently, over 9500 cases of laparoscopic liver resec-tion have been reported worldwide, with over 50% of the cases being done for malignancy.208Pure laparoscopic and hand-assisted laparoscopic liver resection are the two most commonly used techniques for mini-mally invasive liver resection surgery,209,210 while robotic liver resection is being used by several
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Surgery_Schwartz. hepa-tectomy for living donor liver transplantation. While minimally invasive approaches have been widely adopted in other areas of abdominal surgery, there was initial apprehension regarding laparoscopic liver resection (LLR), hampering its widespread adoption.203 Great strides have been made in the past decade with techniques of laparoscopic liver resection,204,205 and two International Laparoscopic Liver Resection Consensus Confer-ences have been convened in Louisville (2008) and Morioko (2014).206,207 Indications for liver resection should not be altered by the availability of minimally invasive liver resection tech-niques. Currently, over 9500 cases of laparoscopic liver resec-tion have been reported worldwide, with over 50% of the cases being done for malignancy.208Pure laparoscopic and hand-assisted laparoscopic liver resection are the two most commonly used techniques for mini-mally invasive liver resection surgery,209,210 while robotic liver resection is being used by several
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and hand-assisted laparoscopic liver resection are the two most commonly used techniques for mini-mally invasive liver resection surgery,209,210 while robotic liver resection is being used by several groups.211 Advantages of the hand-port include tactile feedback, facilitation of liver mobiliza-tion, and ease of ability to control bleeding. Also, when doing a large parenchymal resection, the hand-port can be comparable in size to the extraction port utilized in the purely laparoscopic Brunicardi_Ch31_p1345-p1392.indd 138620/02/19 2:37 PM 1387LIVERCHAPTER 31approach. The hand-assisted approach can be ideal for surgeons beginning the transition to laparoscopic liver resection and for more experienced laparoscopic HPB surgeons doing laparo-scopic major hepatectomies or as an alternative to conversion to open surgery.Benefits of laparoscopic liver resection include less blood loss, decreased morbidity, decreased postoperative pain and narcotic requirements, faster return of bowel
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Surgery_Schwartz. and hand-assisted laparoscopic liver resection are the two most commonly used techniques for mini-mally invasive liver resection surgery,209,210 while robotic liver resection is being used by several groups.211 Advantages of the hand-port include tactile feedback, facilitation of liver mobiliza-tion, and ease of ability to control bleeding. Also, when doing a large parenchymal resection, the hand-port can be comparable in size to the extraction port utilized in the purely laparoscopic Brunicardi_Ch31_p1345-p1392.indd 138620/02/19 2:37 PM 1387LIVERCHAPTER 31approach. The hand-assisted approach can be ideal for surgeons beginning the transition to laparoscopic liver resection and for more experienced laparoscopic HPB surgeons doing laparo-scopic major hepatectomies or as an alternative to conversion to open surgery.Benefits of laparoscopic liver resection include less blood loss, decreased morbidity, decreased postoperative pain and narcotic requirements, faster return of bowel
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to conversion to open surgery.Benefits of laparoscopic liver resection include less blood loss, decreased morbidity, decreased postoperative pain and narcotic requirements, faster return of bowel function, and shorter length of hospital stay compared to open hepatic resection.212 Long-term oncologic outcomes for HCC and CLM have been shown to be comparable for laparoscopic vs. open liver resection using propensity score matching and meta-analysis studies.213-215 The learning curve for laparoscopic liver resection has been reported to be around 60 cases,216 although this may be greater for laparoscopic major hepatectomy.217-219 Cost analy-sis has shown that laparoscopic liver resection is cost effective compared to open liver resection, where the added cost of the operating room disposables are more than offset by the savings associated with ∼50% reduction in the hospital length of stay.221,222Initial experience with laparoscopic living-donor hepatec-tomy for transplantation was with
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Surgery_Schwartz. to conversion to open surgery.Benefits of laparoscopic liver resection include less blood loss, decreased morbidity, decreased postoperative pain and narcotic requirements, faster return of bowel function, and shorter length of hospital stay compared to open hepatic resection.212 Long-term oncologic outcomes for HCC and CLM have been shown to be comparable for laparoscopic vs. open liver resection using propensity score matching and meta-analysis studies.213-215 The learning curve for laparoscopic liver resection has been reported to be around 60 cases,216 although this may be greater for laparoscopic major hepatectomy.217-219 Cost analy-sis has shown that laparoscopic liver resection is cost effective compared to open liver resection, where the added cost of the operating room disposables are more than offset by the savings associated with ∼50% reduction in the hospital length of stay.221,222Initial experience with laparoscopic living-donor hepatec-tomy for transplantation was with
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are more than offset by the savings associated with ∼50% reduction in the hospital length of stay.221,222Initial experience with laparoscopic living-donor hepatec-tomy for transplantation was with left lateral segmentectomy during liver allograft procurement for pediatric transplants.222 With continued advances in laparoscopic liver surgery, LLR has been applied to adult-to-adult donor right hepatectomy,223,224 although this approach remains controversial.In summary, laparoscopic liver resection can now be per-formed safely by experienced surgeons in selected patients. Compared to open hepatic resection, the laparoscopic approach has benefits of less blood loss, reduced postoperative pain, and a shorter length of hospital stay, with similar oncologic out-comes for resection of HCC and limited colorectal liver metastases.REFERENCESEntries highlighted in bright blue are key references. 1. Wikipedia. Prometheus. Available at: http://en.wikipedia.org/wiki/Prometheus. Accessed July 26,
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Surgery_Schwartz. are more than offset by the savings associated with ∼50% reduction in the hospital length of stay.221,222Initial experience with laparoscopic living-donor hepatec-tomy for transplantation was with left lateral segmentectomy during liver allograft procurement for pediatric transplants.222 With continued advances in laparoscopic liver surgery, LLR has been applied to adult-to-adult donor right hepatectomy,223,224 although this approach remains controversial.In summary, laparoscopic liver resection can now be per-formed safely by experienced surgeons in selected patients. Compared to open hepatic resection, the laparoscopic approach has benefits of less blood loss, reduced postoperative pain, and a shorter length of hospital stay, with similar oncologic out-comes for resection of HCC and limited colorectal liver metastases.REFERENCESEntries highlighted in bright blue are key references. 1. Wikipedia. Prometheus. Available at: http://en.wikipedia.org/wiki/Prometheus. Accessed July 26,
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limited colorectal liver metastases.REFERENCESEntries highlighted in bright blue are key references. 1. Wikipedia. Prometheus. Available at: http://en.wikipedia.org/wiki/Prometheus. Accessed July 26, 2018. 2. Keen WW IV. Report of a case of resection of the liver for the removal of a neoplasm, with a table of seventy-six cases of resection of the liver for hepatic tumors. Ann Surg. 1899;30(3):267-283. 3. Fortner JG, Blumgart LH. A historic perspective of liver sur-gery for tumors at the end of the millennium. J Am Coll Surg. 2001;193(2):210-222. 4. Pringle JH V. Notes on the arrest of hepatic hemorrhage due to trauma. Ann Surg. 1908;48(4):541-549. 5. Cantlie J. On a new arrangement of the right and left lobes of the liver. Proc Anat Soc Great Britain Ireland. 1897;32:4-9. 6. Couinaud C. Lobes de segments hepatiques: notes sur l’architecture anatomique et chirurgical de foie. Presse Med. 1954;62(33):709-712. 7. Abdalla EK, Vauthey JN, Couinaud C. The caudate lobe of the liver:
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Surgery_Schwartz. limited colorectal liver metastases.REFERENCESEntries highlighted in bright blue are key references. 1. Wikipedia. Prometheus. Available at: http://en.wikipedia.org/wiki/Prometheus. Accessed July 26, 2018. 2. Keen WW IV. Report of a case of resection of the liver for the removal of a neoplasm, with a table of seventy-six cases of resection of the liver for hepatic tumors. Ann Surg. 1899;30(3):267-283. 3. Fortner JG, Blumgart LH. A historic perspective of liver sur-gery for tumors at the end of the millennium. J Am Coll Surg. 2001;193(2):210-222. 4. Pringle JH V. Notes on the arrest of hepatic hemorrhage due to trauma. Ann Surg. 1908;48(4):541-549. 5. Cantlie J. On a new arrangement of the right and left lobes of the liver. Proc Anat Soc Great Britain Ireland. 1897;32:4-9. 6. Couinaud C. Lobes de segments hepatiques: notes sur l’architecture anatomique et chirurgical de foie. Presse Med. 1954;62(33):709-712. 7. Abdalla EK, Vauthey JN, Couinaud C. The caudate lobe of the liver:
|
Surgery_Schwartz_9188
|
Surgery_Schwartz
|
C. Lobes de segments hepatiques: notes sur l’architecture anatomique et chirurgical de foie. Presse Med. 1954;62(33):709-712. 7. Abdalla EK, Vauthey JN, Couinaud C. The caudate lobe of the liver: implications of embryology and anatomy for surgery. Surg Oncol Clin N Am. 2002;11(4):835-848. 8. Bismuth H. Surgical anatomy and anatomical surgery of the liver. World J Surg. 1982;6(1):3-9. 9. Nordlie RC, Foster JD, Lange AJ. Regulation of glucose pro-duction by the liver. Annu Rev Nutr. 1999;19:379-406. 10. Merriman R. Approach to the patient with jaundice. In: Yamada T, ed. Textbook of Gastroenterology. 4th ed. Philadelphia: Lippincott Williams & Williams; 2003:911. 11. Ramadori G, Christ B. Cytokines and the hepatic acute-phase response. Semin Liver Dis 1999;19(2):141-155. 12. Tsung A, Geller DA. CD14 and Toll Receptor. In: Dufour JF, Clavien PA, eds. Signaling Pathways in Liver Diseases. Berlin: Springer; 2005:165-171. 13. Su GL. Lipopolysaccharides in liver injury: molecular
|
Surgery_Schwartz. C. Lobes de segments hepatiques: notes sur l’architecture anatomique et chirurgical de foie. Presse Med. 1954;62(33):709-712. 7. Abdalla EK, Vauthey JN, Couinaud C. The caudate lobe of the liver: implications of embryology and anatomy for surgery. Surg Oncol Clin N Am. 2002;11(4):835-848. 8. Bismuth H. Surgical anatomy and anatomical surgery of the liver. World J Surg. 1982;6(1):3-9. 9. Nordlie RC, Foster JD, Lange AJ. Regulation of glucose pro-duction by the liver. Annu Rev Nutr. 1999;19:379-406. 10. Merriman R. Approach to the patient with jaundice. In: Yamada T, ed. Textbook of Gastroenterology. 4th ed. Philadelphia: Lippincott Williams & Williams; 2003:911. 11. Ramadori G, Christ B. Cytokines and the hepatic acute-phase response. Semin Liver Dis 1999;19(2):141-155. 12. Tsung A, Geller DA. CD14 and Toll Receptor. In: Dufour JF, Clavien PA, eds. Signaling Pathways in Liver Diseases. Berlin: Springer; 2005:165-171. 13. Su GL. Lipopolysaccharides in liver injury: molecular
|
Surgery_Schwartz_9189
|
Surgery_Schwartz
|
A, Geller DA. CD14 and Toll Receptor. In: Dufour JF, Clavien PA, eds. Signaling Pathways in Liver Diseases. Berlin: Springer; 2005:165-171. 13. Su GL. Lipopolysaccharides in liver injury: molecular mecha-nisms of Kupffer cell activation. Am J Physiol Gastrointest Liver Physiol. 2002;283:G256-G265. 14. Geller DA, Billiar TR. Molecular biology of nitric oxide syn-thases. Cancer Metastasis Rev. 1998;17:7-23. 15. Prince JM, Billiar TR. Nitric Oxide. In: Dufour JF, Clavien PA, eds. Signaling Pathways in Liver Diseases. Berlin: Springer; 2005:299-310. 16. Tsuchihashi S, Busuttil RW, Kupiec-Weglinski JW. Heme Oxygenase System. In: Dufour JF, Clavien PA, eds. Sig-naling Pathways in Liver Diseases. Berlin: Springer; 2005: 291-298. 17. Zuckerbraun BS, Billiar TR. Heme oxygenase-1: a cellular Hercules. Hepatology. 2003;37:742-744. 18. Akira S, Takeda K. Toll-like receptor signalling. Nat Rev Immunol. 2004;4:499-511. 19. Mollen KP, Anand RJ, Tsung A, Prince JM, Levy RM, Billiar TR. Emerging
|
Surgery_Schwartz. A, Geller DA. CD14 and Toll Receptor. In: Dufour JF, Clavien PA, eds. Signaling Pathways in Liver Diseases. Berlin: Springer; 2005:165-171. 13. Su GL. Lipopolysaccharides in liver injury: molecular mecha-nisms of Kupffer cell activation. Am J Physiol Gastrointest Liver Physiol. 2002;283:G256-G265. 14. Geller DA, Billiar TR. Molecular biology of nitric oxide syn-thases. Cancer Metastasis Rev. 1998;17:7-23. 15. Prince JM, Billiar TR. Nitric Oxide. In: Dufour JF, Clavien PA, eds. Signaling Pathways in Liver Diseases. Berlin: Springer; 2005:299-310. 16. Tsuchihashi S, Busuttil RW, Kupiec-Weglinski JW. Heme Oxygenase System. In: Dufour JF, Clavien PA, eds. Sig-naling Pathways in Liver Diseases. Berlin: Springer; 2005: 291-298. 17. Zuckerbraun BS, Billiar TR. Heme oxygenase-1: a cellular Hercules. Hepatology. 2003;37:742-744. 18. Akira S, Takeda K. Toll-like receptor signalling. Nat Rev Immunol. 2004;4:499-511. 19. Mollen KP, Anand RJ, Tsung A, Prince JM, Levy RM, Billiar TR. Emerging
|
Surgery_Schwartz_9190
|
Surgery_Schwartz
|
Hepatology. 2003;37:742-744. 18. Akira S, Takeda K. Toll-like receptor signalling. Nat Rev Immunol. 2004;4:499-511. 19. Mollen KP, Anand RJ, Tsung A, Prince JM, Levy RM, Billiar TR. Emerging paradigm: toll-like receptor 4-sentinel for the detection of tissue damage. Shock 2006;26:430-437. 20. Farombi EO, Surh YJ. Heme oxygenase-1 as a potential therapeutic target for hepatoprotection. J Biochem Mol Biol 2006;39:479-491. 21. Kruskal JB, Kane RA. Intraoperative US of the liver: techniques and clinical applications. Radiographics. 2006;26(4):1067-1084. 22. Martinez SM, Crespo G, Navasa M, Forns X. Noninvasive assessment of liver fibrosis. Hepatology. 2011;53(1):325-335. 23. Federle MP, Blachar A. CT evaluation of the liver: principles and techniques. Semin Liver Dis. 2001;21(2):135-145. 24. Hyodo T, Kumano S, Kushihata F, et al. CT and MR cholan-giography: advantages and pitfalls in perioperative evaluation of biliary tree. Br J Radiol. 2012;85(1015):887-896. 25. Ros PR, Davis GL. The
|
Surgery_Schwartz. Hepatology. 2003;37:742-744. 18. Akira S, Takeda K. Toll-like receptor signalling. Nat Rev Immunol. 2004;4:499-511. 19. Mollen KP, Anand RJ, Tsung A, Prince JM, Levy RM, Billiar TR. Emerging paradigm: toll-like receptor 4-sentinel for the detection of tissue damage. Shock 2006;26:430-437. 20. Farombi EO, Surh YJ. Heme oxygenase-1 as a potential therapeutic target for hepatoprotection. J Biochem Mol Biol 2006;39:479-491. 21. Kruskal JB, Kane RA. Intraoperative US of the liver: techniques and clinical applications. Radiographics. 2006;26(4):1067-1084. 22. Martinez SM, Crespo G, Navasa M, Forns X. Noninvasive assessment of liver fibrosis. Hepatology. 2011;53(1):325-335. 23. Federle MP, Blachar A. CT evaluation of the liver: principles and techniques. Semin Liver Dis. 2001;21(2):135-145. 24. Hyodo T, Kumano S, Kushihata F, et al. CT and MR cholan-giography: advantages and pitfalls in perioperative evaluation of biliary tree. Br J Radiol. 2012;85(1015):887-896. 25. Ros PR, Davis GL. The
|
Surgery_Schwartz_9191
|
Surgery_Schwartz
|
T, Kumano S, Kushihata F, et al. CT and MR cholan-giography: advantages and pitfalls in perioperative evaluation of biliary tree. Br J Radiol. 2012;85(1015):887-896. 25. Ros PR, Davis GL. The incidental focal liver lesion: photon, proton, or needle? Hepatology. 1998;27(5):1183-1190. 26. Wald C, Scholz FJ, Pinkus E, Wise RE, Flacke S. An update on biliary imaging. Surg Clin North Am. 2008;88(6):1195-1220. 27. Wiering B, Krabbe PF, Jager GJ, Oyen WJ, Ruers TJ. The impact of fluor-18-deoxyglucose-positron emission tomogra-phy in the management of colorectal liver metastases. Cancer. 2005;104(12):2658-2670. 28. Sacks A, Peller PJ, Surasi DS, Chatburn L, Mercier G, Sub-ramaniam RM. Value of PET/CT in the management of liver metastases, part 1. AJR Am J Roentgenol. 2011;197(2): W256-W259. 29. Bernal W, Auzinger G, Dhawan A, Wendon J. Acute liver failure. Lancet. 2010;376(9736):190-201. An outstanding review of pathophysiology, treatment, and evidence based outcomes for patients with acute
|
Surgery_Schwartz. T, Kumano S, Kushihata F, et al. CT and MR cholan-giography: advantages and pitfalls in perioperative evaluation of biliary tree. Br J Radiol. 2012;85(1015):887-896. 25. Ros PR, Davis GL. The incidental focal liver lesion: photon, proton, or needle? Hepatology. 1998;27(5):1183-1190. 26. Wald C, Scholz FJ, Pinkus E, Wise RE, Flacke S. An update on biliary imaging. Surg Clin North Am. 2008;88(6):1195-1220. 27. Wiering B, Krabbe PF, Jager GJ, Oyen WJ, Ruers TJ. The impact of fluor-18-deoxyglucose-positron emission tomogra-phy in the management of colorectal liver metastases. Cancer. 2005;104(12):2658-2670. 28. Sacks A, Peller PJ, Surasi DS, Chatburn L, Mercier G, Sub-ramaniam RM. Value of PET/CT in the management of liver metastases, part 1. AJR Am J Roentgenol. 2011;197(2): W256-W259. 29. Bernal W, Auzinger G, Dhawan A, Wendon J. Acute liver failure. Lancet. 2010;376(9736):190-201. An outstanding review of pathophysiology, treatment, and evidence based outcomes for patients with acute
|
Surgery_Schwartz_9192
|
Surgery_Schwartz
|
W, Auzinger G, Dhawan A, Wendon J. Acute liver failure. Lancet. 2010;376(9736):190-201. An outstanding review of pathophysiology, treatment, and evidence based outcomes for patients with acute liver failure. 30. Polson J, Lee WM. Etiologies of acute liver failure: location, location, location! Liver Transpl. 2007;13(10):1362. 31. Agopian V, Petrowsky H, Kaldas FM, et al. The evolution of liver transplantation during three decades: analysis of 5347 consecutive liver transplants at a single center. Ann Surg. 2013;258(3):409-421. 32. Escorsell A, Mas A, de la Mata M, Spanish Group for the Study of Acute Liver F. Acute liver failure in Spain: analysis of 267 cases. Liver Transpl. 2007;13(10):1389-1395. 33. Larson AM, Polson J, Fontana RJ, et al. Acetaminophen-induced acute liver failure: results of a United States multi-center, prospective study. Hepatology. 2005;42(6):1364-1372. 34. Ostapowicz G, Fontana RJ, Schiodt FV, et al. Results of a pro-spective study of acute liver failure at 17
|
Surgery_Schwartz. W, Auzinger G, Dhawan A, Wendon J. Acute liver failure. Lancet. 2010;376(9736):190-201. An outstanding review of pathophysiology, treatment, and evidence based outcomes for patients with acute liver failure. 30. Polson J, Lee WM. Etiologies of acute liver failure: location, location, location! Liver Transpl. 2007;13(10):1362. 31. Agopian V, Petrowsky H, Kaldas FM, et al. The evolution of liver transplantation during three decades: analysis of 5347 consecutive liver transplants at a single center. Ann Surg. 2013;258(3):409-421. 32. Escorsell A, Mas A, de la Mata M, Spanish Group for the Study of Acute Liver F. Acute liver failure in Spain: analysis of 267 cases. Liver Transpl. 2007;13(10):1389-1395. 33. Larson AM, Polson J, Fontana RJ, et al. Acetaminophen-induced acute liver failure: results of a United States multi-center, prospective study. Hepatology. 2005;42(6):1364-1372. 34. Ostapowicz G, Fontana RJ, Schiodt FV, et al. Results of a pro-spective study of acute liver failure at 17
|
Surgery_Schwartz_9193
|
Surgery_Schwartz
|
of a United States multi-center, prospective study. Hepatology. 2005;42(6):1364-1372. 34. Ostapowicz G, Fontana RJ, Schiodt FV, et al. Results of a pro-spective study of acute liver failure at 17 tertiary care centers in the United States. Ann Intern Med. 2002;137(12):947-954. 35. Hodgman MJ, Garrard AR. A review of acetaminophen poi-soning. Crit Care Clin. 2012;28(4):499-516.10Brunicardi_Ch31_p1345-p1392.indd 138720/02/19 2:37 PM 1388SPECIFIC CONSIDERATIONSPART II 36. Kortsalioudaki C, Taylor RM, Cheeseman P, Bansal S, Mieli-Vergani G, Dhawan A. Safety and efficacy of N-acetylcysteine in children with non-acetaminophen-induced acute liver fail-ure. Liver Transpl. 2008;14(1):25-30. 37. O’Grady JG, Alexander GJ, Hayllar KM, Williams R. Early indicators of prognosis in fulminant hepatic failure. Gastroen-terology. 1989;97(2):439-445. 38. Bismuth H, Samuel D, Castaing D, et al. Orthotopic liver transplantation in fulminant and subfulminant hepatitis. The Paul Brousse experience. Ann
|
Surgery_Schwartz. of a United States multi-center, prospective study. Hepatology. 2005;42(6):1364-1372. 34. Ostapowicz G, Fontana RJ, Schiodt FV, et al. Results of a pro-spective study of acute liver failure at 17 tertiary care centers in the United States. Ann Intern Med. 2002;137(12):947-954. 35. Hodgman MJ, Garrard AR. A review of acetaminophen poi-soning. Crit Care Clin. 2012;28(4):499-516.10Brunicardi_Ch31_p1345-p1392.indd 138720/02/19 2:37 PM 1388SPECIFIC CONSIDERATIONSPART II 36. Kortsalioudaki C, Taylor RM, Cheeseman P, Bansal S, Mieli-Vergani G, Dhawan A. Safety and efficacy of N-acetylcysteine in children with non-acetaminophen-induced acute liver fail-ure. Liver Transpl. 2008;14(1):25-30. 37. O’Grady JG, Alexander GJ, Hayllar KM, Williams R. Early indicators of prognosis in fulminant hepatic failure. Gastroen-terology. 1989;97(2):439-445. 38. Bismuth H, Samuel D, Castaing D, et al. Orthotopic liver transplantation in fulminant and subfulminant hepatitis. The Paul Brousse experience. Ann
|
Surgery_Schwartz_9194
|
Surgery_Schwartz
|
failure. Gastroen-terology. 1989;97(2):439-445. 38. Bismuth H, Samuel D, Castaing D, et al. Orthotopic liver transplantation in fulminant and subfulminant hepatitis. The Paul Brousse experience. Ann Surg. 1995;222(2):109-119. 39. Antoniades CG, Berry PA, Bruce M, et al. Actin-free Gc globulin: a rapidly assessed biomarker of organ dysfunc-tion in acute liver failure and cirrhosis. Liver Transpl. 2007;13(9):1254-1261. 40. Renner EL. How to decide when to list a patient with acute liver failure for liver transplantation? Clichy or King’s College criteria, or something else? J Hepatol. 2007;46(4):554-557. 41. Faybik P, Krenn CG. Extracorporeal liver support. Curr Opin Crit Care. 2013;19(2):149-153. 42. Ekser B, Gridelli B, Tector AJ, Cooper DK. Pig liver xenotrans-plantation as a bridge to allotransplantation: which patients might benefit? Transplantation. 2009;88(9):1041-1049. 43. Yu Y, Fisher JE, Lillegard JB, Rodysill B, Amiot B, Nyberg SL. Cell therapies for liver diseases. Liver
|
Surgery_Schwartz. failure. Gastroen-terology. 1989;97(2):439-445. 38. Bismuth H, Samuel D, Castaing D, et al. Orthotopic liver transplantation in fulminant and subfulminant hepatitis. The Paul Brousse experience. Ann Surg. 1995;222(2):109-119. 39. Antoniades CG, Berry PA, Bruce M, et al. Actin-free Gc globulin: a rapidly assessed biomarker of organ dysfunc-tion in acute liver failure and cirrhosis. Liver Transpl. 2007;13(9):1254-1261. 40. Renner EL. How to decide when to list a patient with acute liver failure for liver transplantation? Clichy or King’s College criteria, or something else? J Hepatol. 2007;46(4):554-557. 41. Faybik P, Krenn CG. Extracorporeal liver support. Curr Opin Crit Care. 2013;19(2):149-153. 42. Ekser B, Gridelli B, Tector AJ, Cooper DK. Pig liver xenotrans-plantation as a bridge to allotransplantation: which patients might benefit? Transplantation. 2009;88(9):1041-1049. 43. Yu Y, Fisher JE, Lillegard JB, Rodysill B, Amiot B, Nyberg SL. Cell therapies for liver diseases. Liver
|
Surgery_Schwartz_9195
|
Surgery_Schwartz
|
allotransplantation: which patients might benefit? Transplantation. 2009;88(9):1041-1049. 43. Yu Y, Fisher JE, Lillegard JB, Rodysill B, Amiot B, Nyberg SL. Cell therapies for liver diseases. Liver Transpl. 2012;18(1):9-21. 44. Faraj W, Dar F, Bartlett A, et al. Auxiliary liver trans-plantation for acute liver failure in children. Ann Surg. 2010;251(2):351-356. 45. Wanless IR, Nakashima E, Sherman M. Regression of human cirrhosis. Morphologic features and the gen-esis of incomplete septal cirrhosis. Arch Pathol Lab Med. 2000;124(11):1599-1607. 46. Fattovich G, Giustina G, Degos F, et al. Morbidity and mortal-ity in compensated cirrhosis type C: a retrospective follow-up study of 384 patients. Gastroenterology. 1997;112(2):463-472. 47. Rinella ME, Sanyal AJ. Management of NAFLD: a stage-based approach. Nat Rev Gastroenterol Hepatol. 2016:13:196-205. 48. Loomba R, Sanyal AJ. The global NAFLD epidemic. Nat Rev Gastroenterol Hepatol. 2013;10:686-690. 49. Michelotti GA, Machado MV, Diehl
|
Surgery_Schwartz. allotransplantation: which patients might benefit? Transplantation. 2009;88(9):1041-1049. 43. Yu Y, Fisher JE, Lillegard JB, Rodysill B, Amiot B, Nyberg SL. Cell therapies for liver diseases. Liver Transpl. 2012;18(1):9-21. 44. Faraj W, Dar F, Bartlett A, et al. Auxiliary liver trans-plantation for acute liver failure in children. Ann Surg. 2010;251(2):351-356. 45. Wanless IR, Nakashima E, Sherman M. Regression of human cirrhosis. Morphologic features and the gen-esis of incomplete septal cirrhosis. Arch Pathol Lab Med. 2000;124(11):1599-1607. 46. Fattovich G, Giustina G, Degos F, et al. Morbidity and mortal-ity in compensated cirrhosis type C: a retrospective follow-up study of 384 patients. Gastroenterology. 1997;112(2):463-472. 47. Rinella ME, Sanyal AJ. Management of NAFLD: a stage-based approach. Nat Rev Gastroenterol Hepatol. 2016:13:196-205. 48. Loomba R, Sanyal AJ. The global NAFLD epidemic. Nat Rev Gastroenterol Hepatol. 2013;10:686-690. 49. Michelotti GA, Machado MV, Diehl
|
Surgery_Schwartz_9196
|
Surgery_Schwartz
|
approach. Nat Rev Gastroenterol Hepatol. 2016:13:196-205. 48. Loomba R, Sanyal AJ. The global NAFLD epidemic. Nat Rev Gastroenterol Hepatol. 2013;10:686-690. 49. Michelotti GA, Machado MV, Diehl AM. NAFLD, NASH and liver cancer. Nat Rev Gastroenterol Hepatol. 2013;10:656-665. 50. Schuppan D, Afdhal NH. Liver cirrhosis. Lancet. 2008;371:838-851. 51. Bhala N, Angulo P, van der Poorten D, et al. The natural his-tory of nonalcoholic fatty liver disease with advanced fibrosis or cirrhosis: an international collaborative study. Hepatology. 2011;54:1208-1216. 52. Sanyal AJ, Banas C, Sargeant C, et al. Similarities and differ-ences in outcomes of cirrhosis due to nonalcoholic steatohepa-titis and hepatitis C. Hepatology. 2006;43:682-689. 53. Lehmann K, Rickenbacher A, Weber A, et al. Chemotherapy before liver resection of colorectal metastases: friend or foe? Ann Surg. 2012;255:237-247. 54. Vetelainen R, van Vliet A, Gouma DJ, van Gulik TM. Steatosis as a risk factor in liver surgery. Ann
|
Surgery_Schwartz. approach. Nat Rev Gastroenterol Hepatol. 2016:13:196-205. 48. Loomba R, Sanyal AJ. The global NAFLD epidemic. Nat Rev Gastroenterol Hepatol. 2013;10:686-690. 49. Michelotti GA, Machado MV, Diehl AM. NAFLD, NASH and liver cancer. Nat Rev Gastroenterol Hepatol. 2013;10:656-665. 50. Schuppan D, Afdhal NH. Liver cirrhosis. Lancet. 2008;371:838-851. 51. Bhala N, Angulo P, van der Poorten D, et al. The natural his-tory of nonalcoholic fatty liver disease with advanced fibrosis or cirrhosis: an international collaborative study. Hepatology. 2011;54:1208-1216. 52. Sanyal AJ, Banas C, Sargeant C, et al. Similarities and differ-ences in outcomes of cirrhosis due to nonalcoholic steatohepa-titis and hepatitis C. Hepatology. 2006;43:682-689. 53. Lehmann K, Rickenbacher A, Weber A, et al. Chemotherapy before liver resection of colorectal metastases: friend or foe? Ann Surg. 2012;255:237-247. 54. Vetelainen R, van Vliet A, Gouma DJ, van Gulik TM. Steatosis as a risk factor in liver surgery. Ann
|
Surgery_Schwartz_9197
|
Surgery_Schwartz
|
before liver resection of colorectal metastases: friend or foe? Ann Surg. 2012;255:237-247. 54. Vetelainen R, van Vliet A, Gouma DJ, van Gulik TM. Steatosis as a risk factor in liver surgery. Ann Surg. 2007;245:20-30. 55. Reddy SK, Marsh JW, Varley PR, et al. Underlying steato-hepatitis, but not simple hepatic steatosis, increased morbid-ity after liver resection: a case-control study. Hepatology. 2012;56(6):221-230. 56. Doberneck RC, Sterling WA, Jr, Allison DC. Morbidity and mortality after operation in nonbleeding cirrhotic patients. Am J Surg. 1983;146(3):306-309. 57. Northup PG, Wanamaker RC, Lee VD, Adams RB, Berg CL. Model for End-Stage Liver Disease (MELD) predicts non-transplant surgical mortality in patients with cirrhosis. Ann Surg. 2005;242(2):244-251. 58. Farnsworth N, Fagan SP, Berger DH, Awad SS. ChildTurcotte-Pugh versus MELD score as a predictor of outcome after elective and emergent surgery in cirrhotic patients. Am J Surg. 2004;188(5):580-583. 59. Hanje AJ, Patel T.
|
Surgery_Schwartz. before liver resection of colorectal metastases: friend or foe? Ann Surg. 2012;255:237-247. 54. Vetelainen R, van Vliet A, Gouma DJ, van Gulik TM. Steatosis as a risk factor in liver surgery. Ann Surg. 2007;245:20-30. 55. Reddy SK, Marsh JW, Varley PR, et al. Underlying steato-hepatitis, but not simple hepatic steatosis, increased morbid-ity after liver resection: a case-control study. Hepatology. 2012;56(6):221-230. 56. Doberneck RC, Sterling WA, Jr, Allison DC. Morbidity and mortality after operation in nonbleeding cirrhotic patients. Am J Surg. 1983;146(3):306-309. 57. Northup PG, Wanamaker RC, Lee VD, Adams RB, Berg CL. Model for End-Stage Liver Disease (MELD) predicts non-transplant surgical mortality in patients with cirrhosis. Ann Surg. 2005;242(2):244-251. 58. Farnsworth N, Fagan SP, Berger DH, Awad SS. ChildTurcotte-Pugh versus MELD score as a predictor of outcome after elective and emergent surgery in cirrhotic patients. Am J Surg. 2004;188(5):580-583. 59. Hanje AJ, Patel T.
|
Surgery_Schwartz_9198
|
Surgery_Schwartz
|
Berger DH, Awad SS. ChildTurcotte-Pugh versus MELD score as a predictor of outcome after elective and emergent surgery in cirrhotic patients. Am J Surg. 2004;188(5):580-583. 59. Hanje AJ, Patel T. Preoperative evaluation of patients with liver disease. Nat Clin Pract Gastroenterol Hepatol. 2007;4(5):266-276. 60. Shah V. Cellular and molecular basis of portal hypertension. Clin Liver Dis. 2001;5(3):629-644. 61. Poynard T, Cales P, Pasta L, et al. Beta-adrenergic-antagonist drugs in the prevention of gastrointestinal bleeding in patients with cirrhosis and esophageal varices. An analysis of data and prognostic factors in 589 patients from four randomized clini-cal trials. Franco-Italian Multicenter Study Group. N Engl J Med. 1991;324(22):1532-1538. 62. Garcia-Pagan JC, Bosch J. Endoscopic band ligation in the treatment of portal hypertension. Nat Clin Pract Gastroenterol Hepatol. 2005;2(11):526-535. 63. Valla DC. The diagnosis and management of the Budd-Chiari syndrome: consensus and
|
Surgery_Schwartz. Berger DH, Awad SS. ChildTurcotte-Pugh versus MELD score as a predictor of outcome after elective and emergent surgery in cirrhotic patients. Am J Surg. 2004;188(5):580-583. 59. Hanje AJ, Patel T. Preoperative evaluation of patients with liver disease. Nat Clin Pract Gastroenterol Hepatol. 2007;4(5):266-276. 60. Shah V. Cellular and molecular basis of portal hypertension. Clin Liver Dis. 2001;5(3):629-644. 61. Poynard T, Cales P, Pasta L, et al. Beta-adrenergic-antagonist drugs in the prevention of gastrointestinal bleeding in patients with cirrhosis and esophageal varices. An analysis of data and prognostic factors in 589 patients from four randomized clini-cal trials. Franco-Italian Multicenter Study Group. N Engl J Med. 1991;324(22):1532-1538. 62. Garcia-Pagan JC, Bosch J. Endoscopic band ligation in the treatment of portal hypertension. Nat Clin Pract Gastroenterol Hepatol. 2005;2(11):526-535. 63. Valla DC. The diagnosis and management of the Budd-Chiari syndrome: consensus and
|
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|
Surgery_Schwartz
|
band ligation in the treatment of portal hypertension. Nat Clin Pract Gastroenterol Hepatol. 2005;2(11):526-535. 63. Valla DC. The diagnosis and management of the Budd-Chiari syndrome: consensus and controversies. Hepatology. 2003;38(4):793-803. 64. Henderson JM, Warren WD, Millikan WJ, Jr, et al. Surgical options, hematologic evaluation, and pathologic changes in Budd-Chiari syndrome. Am J Surg. 1990;159(1):41-50. 65. Barnes PF, De Cock KM, Reynolds TN, Ralls PW. A com-parison of amebic and pyogenic abscess of the liver. Medicine (Baltimore). 1987;66(6):472-483. 66. Pedrosa I, Saiz A, Arrazola J, Ferreiros J, Pedrosa CS. Hydatid disease: radiologic and pathologic features and complications. Radiographics. 2000;20(3):795-817. 67. Khuroo MS, Zargar SA, Mahajan R. Hepatobiliary and pan-creatic ascariasis in India. Lancet. 1990;335(8704):1503-1506. 68. Scaglione SJ, Lok AS. Effectiveness of hepatitis B treatment in clinical practice. Gastroenterology. 2012;142(6):1360-1368. 69. Corey KE,
|
Surgery_Schwartz. band ligation in the treatment of portal hypertension. Nat Clin Pract Gastroenterol Hepatol. 2005;2(11):526-535. 63. Valla DC. The diagnosis and management of the Budd-Chiari syndrome: consensus and controversies. Hepatology. 2003;38(4):793-803. 64. Henderson JM, Warren WD, Millikan WJ, Jr, et al. Surgical options, hematologic evaluation, and pathologic changes in Budd-Chiari syndrome. Am J Surg. 1990;159(1):41-50. 65. Barnes PF, De Cock KM, Reynolds TN, Ralls PW. A com-parison of amebic and pyogenic abscess of the liver. Medicine (Baltimore). 1987;66(6):472-483. 66. Pedrosa I, Saiz A, Arrazola J, Ferreiros J, Pedrosa CS. Hydatid disease: radiologic and pathologic features and complications. Radiographics. 2000;20(3):795-817. 67. Khuroo MS, Zargar SA, Mahajan R. Hepatobiliary and pan-creatic ascariasis in India. Lancet. 1990;335(8704):1503-1506. 68. Scaglione SJ, Lok AS. Effectiveness of hepatitis B treatment in clinical practice. Gastroenterology. 2012;142(6):1360-1368. 69. Corey KE,
|
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|
Surgery_Schwartz
|
ascariasis in India. Lancet. 1990;335(8704):1503-1506. 68. Scaglione SJ, Lok AS. Effectiveness of hepatitis B treatment in clinical practice. Gastroenterology. 2012;142(6):1360-1368. 69. Corey KE, Mendez-Navarro J, Gorospe EC, Zheng H, Chung RT. Early treatment improves outcomes in acute hepatitis C virus infection: a meta-analysis. J Viral Hepat. 2010;17(3):201-207. 70. Tsung A, Geller DA. Workup of the incidental liver lesion. Adv Surg. 2005;39:331-341. 71. Caremani M, Vincenti A, Benci A, Sassoli S, Tacconi D. Eco-graphic epidemiology of non-parasitic hepatic cysts. J Clin Ultrasound. 1993;21(2):115-118. 72. Tahvanainen P, Tahvanainen E, Reijonen H, Halme L, Kaari-ainen H, Hockerstedt K. Polycystic liver disease is genetically heterogeneous: clinical and linkage studies in eight Finnish families. J Hepatol. 2003;38(1):39-43. 73. Drenth JP, Chrispijn M, Nagorney DM, Kamath PS, Torres VE. Medical and surgical treatment options for polycystic liver disease. Hepatology.
|
Surgery_Schwartz. ascariasis in India. Lancet. 1990;335(8704):1503-1506. 68. Scaglione SJ, Lok AS. Effectiveness of hepatitis B treatment in clinical practice. Gastroenterology. 2012;142(6):1360-1368. 69. Corey KE, Mendez-Navarro J, Gorospe EC, Zheng H, Chung RT. Early treatment improves outcomes in acute hepatitis C virus infection: a meta-analysis. J Viral Hepat. 2010;17(3):201-207. 70. Tsung A, Geller DA. Workup of the incidental liver lesion. Adv Surg. 2005;39:331-341. 71. Caremani M, Vincenti A, Benci A, Sassoli S, Tacconi D. Eco-graphic epidemiology of non-parasitic hepatic cysts. J Clin Ultrasound. 1993;21(2):115-118. 72. Tahvanainen P, Tahvanainen E, Reijonen H, Halme L, Kaari-ainen H, Hockerstedt K. Polycystic liver disease is genetically heterogeneous: clinical and linkage studies in eight Finnish families. J Hepatol. 2003;38(1):39-43. 73. Drenth JP, Chrispijn M, Nagorney DM, Kamath PS, Torres VE. Medical and surgical treatment options for polycystic liver disease. Hepatology.
|
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in eight Finnish families. J Hepatol. 2003;38(1):39-43. 73. Drenth JP, Chrispijn M, Nagorney DM, Kamath PS, Torres VE. Medical and surgical treatment options for polycystic liver disease. Hepatology. 2010;52(6):2223-2230. 74. Robinson TN, Stiegmann GV, Everson GT. Laparo-scopic palliation of polycystic liver disease. Surg Endosc. 2005;19(1):130-132. 75. Caroli J. Disease of the intrahepatic biliary tree. Clin Gastro-enterol. 1972;2:147-161. 76. Yoon SS, Charny CK, Fong Y, et al. Diagnosis, management, and outcomes of 115 patients with hepatic hemangioma. J Am Coll Surg. 2003;197(3):392-402. 77. Geller DA, Tsung A, Marsh JW, Dvorchik I, Gamblin TC, Carr BI. Outcome of 1000 liver cancer patients evaluated at the UPMC Liver Cancer Center. J Gastrointest Surg. 2006;10(1):63-68. 78. International Agency for Research on Cancer. GLOBOCAN 2008. Available at: http://globocan.iarc.fr/. Accessed July 26, 2018. 79. Liaw YF, Tai DI, Chu CM, et al. Early detection of hepatocel-lular carcinoma in
|
Surgery_Schwartz. in eight Finnish families. J Hepatol. 2003;38(1):39-43. 73. Drenth JP, Chrispijn M, Nagorney DM, Kamath PS, Torres VE. Medical and surgical treatment options for polycystic liver disease. Hepatology. 2010;52(6):2223-2230. 74. Robinson TN, Stiegmann GV, Everson GT. Laparo-scopic palliation of polycystic liver disease. Surg Endosc. 2005;19(1):130-132. 75. Caroli J. Disease of the intrahepatic biliary tree. Clin Gastro-enterol. 1972;2:147-161. 76. Yoon SS, Charny CK, Fong Y, et al. Diagnosis, management, and outcomes of 115 patients with hepatic hemangioma. J Am Coll Surg. 2003;197(3):392-402. 77. Geller DA, Tsung A, Marsh JW, Dvorchik I, Gamblin TC, Carr BI. Outcome of 1000 liver cancer patients evaluated at the UPMC Liver Cancer Center. J Gastrointest Surg. 2006;10(1):63-68. 78. International Agency for Research on Cancer. GLOBOCAN 2008. Available at: http://globocan.iarc.fr/. Accessed July 26, 2018. 79. Liaw YF, Tai DI, Chu CM, et al. Early detection of hepatocel-lular carcinoma in
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