151. Toumpanakis C, Meyer T, Caplin ME. Cytotoxic treatment including

embolization/chemoembolization for neuroendocrine tumours. Best Pract Res Clin Endocrinol Metab

127. Norton JA, Doppman JL, Jensen RT. Curative resection in Zollinger-Ellison syndrome. Results of a

10-year prospective study. Ann Surg 1992; 215(1):8–18.

128. Fraker DL, Norton JA, Alexander HR, et al. Surgery in Zollinger-Ellison syndrome alters the natural

history of gastrinoma. Ann Surg 1994;220(3):320–328; discussion 328–330.

129. Delcore R, Friesen SR. The place for curative surgical procedures in the treatment of sporadic and

familial Zollinger-Ellison syndrome. Curr Opin Gen Surg 1994:69–76.

130. Zogakis TG, Gibril F, Libutti SK, et al. Management and outcome of patients with sporadic

gastrinoma arising in the duodenum. Ann Surg 2003; 238(1):42–48.

131. von Schrenck T, Howard JM, Doppman JL, et al. Prospective study of chemotherapy in patients

with metastatic gastrinoma. Gastroenterology 1988;94(6):1326–1334.

132. Mozell E, Woltering EA, O’Dorisio TM, et al. Effect of somatostatin analog on peptide release and

tumor growth in the Zollinger-Ellison syndrome. Surg Gynecol Obstet 1990;170(6):476–484.

133. Mozell EJ, Cramer AJ, O’Dorisio TM, et al. Long-term efficacy of octreotide in the treatment of

Zollinger-Ellison syndrome. Arch Surg 1992;127(9):1019–1024; discussion 1024–1026.

134. Elias D, Lasser P, Ducreux M, et al. Liver resection (and associated extrahepatic resections) for

metastatic well-differentiated endocrine tumors: a 15-year single center prospective study. Surgery

2003;133(4):375–382.

135. Sarmiento JM, Heywood G, Rubin J, et al. Surgical treatment of neuroendocrine metastases to the

liver: a plea for resection to increase survival. J Am Coll Surg 2003;197(1):29–37.

136. Sarmiento JM, Que FG, Grant CS, et al. Concurrent resections of pancreatic islet cell cancers with

synchronous hepatic metastases: outcomes of an aggressive approach. Surgery 2002;132(6):976–

982; discussion 982–983.

137. Norton JA, Kivlen M, Li M, et al. Morbidity and mortality of aggressive resection in patients with

advanced neuroendocrine tumors. Arch Surg 2003;138(8):859–866.

138. Florman S, Toure B, Kim L, et al. Liver transplantation for neuroendocrine tumors. J Gastrointest

Surg 2004;8(2):208–212.

139. Verner JV, Morrison AB. Islet cell tumor and a syndrome of refractory watery diarrhea and

hypokalemia. Am J Med 1958;25(3):374–380.

140. Schiller LR. Chronic diarrhea. Gastroenterology 2004;127(1):287–293.

141. Chu QD, Al-kasspooles MF, Smith JL, et al. Is glucagonoma of the pancreas a curable disease? Int J

Pancreatol 2001;29(3):155–162.

142. House MG, Yeo CJ, Schulick RD. Periampullary pancreatic somatostatinoma. Ann Surg Oncol

2002;9(9):869–874.

143. Mutch MG, Frisella MM, DeBenedetti MK, et al. Pancreatic polypeptide is a useful plasma marker

for radiographically evident pancreatic islet cell tumors in patients with multiple endocrine

neoplasia type 1. Surgery 1997;122(6):1012–1019; discussion 1019–1020.

144. Phan GQ, Yeo CJ, Hruban RH, et al. Surgical experience with pancreatic and peripancreatic

neuroendocrine tumors: review of 125 patients. J Gastrointest Surg 1998;2(5):473–482.

145. Solorzano CC, Lee JE, Pisters PW, et al. Nonfunctioning islet cell carcinoma of the pancreas:

survival results in a contemporary series of 163 patients. Surgery 2001;130(6):1078–1085.

146. House MG, Cameron JL, Lillemoe KD, et al. Differences in survival for patients with resectable

versus unresectable metastases from pancreatic islet cell cancer. J Gastrointest Surg 2006;10(1):138–

145.

147. Thompson GB, van Heerden JA, Grant CS, et al. Islet cell carcinomas of the pancreas: a twenty-year

experience. Surgery 1988;104(6):1011–1017.

148. Chen H, Hardacre JM, Uzar A, et al. Isolated liver metastases from neuroendocrine tumors: does

resection prolong survival? J Am Coll Surg 1998;187(1):88–92; discussion 92–93.

149. Chamberlain RS, Canes D, Brown KT, et al. Hepatic neuroendocrine metastases: does intervention

alter outcomes? J Am Coll Surg 2000;190(4):432–445.

150. Touzios JG, Kiely JM, Pitt SC, et al. Neuroendocrine hepatic metastases: does aggressive

management improve survival? Ann Surg 2005;241(5):776–783; discussion 783–785.

151. Toumpanakis C, Meyer T, Caplin ME. Cytotoxic treatment including

embolization/chemoembolization for neuroendocrine tumours. Best Pract Res Clin Endocrinol Metab

1449

2007;21(1):131–144.

152. Cheng PN, Saltz LB. Failure to confirm major objective antitumor activity for streptozocin and

doxorubicin in the treatment of patients with advanced islet cell carcinoma. Cancer

1999;86(6):944–948.

153. Gorden P, Comi RJ, Maton PN, et al. NIH conference. Somatostatin and somatostatin analogue

(SMS 201–995) in treatment of hormone-secreting tumors of the pituitary and gastrointestinal tract

and non-neoplastic diseases of the gut. Ann Intern Med 1989;110(1):35–50.

154. Arnold R, Trautmann ME, Creutzfeldt W, et al. Somatostatin analogue octreotide and inhibition of

tumour growth in metastatic endocrine gastroenteropancreatic tumours. Gut 1996;38(3):430–438.

155. Oberg K. Chemotherapy and biotherapy in the treatment of neuroendocrine tumours. Ann Oncol

2001;12(Suppl 2):S111–S114.

156. Kvols L, Wiedenmann K, Oberg K, et al. Safety and efficacy of pasireotide (SOM230) in patients

with metastatic carcinoid tumors refractory or resistant to octreotide LAR: Results of a phase 2

study. J Clin Oncol 2006;24(18):4082.

157. Raymond E, Dahan L, Raoul JL, et al. Sunitinib malate for the treatment of pancreatic

neuroendocrine tumors. N Engl J Med 2011;364(6):501–513.

158. Yao JC, Shah MH, Ito T, et al. Everolimus for advanced pancreatic neuroendocrine tumors. N Engl J

Med 2011;364(6):514–523.

1450

SECTION H: HEPATOBILIARY AND PORTAL VENOUS SYSTEM

1451

Chapter 57

Hepatobiliary Anatomy

Trevor L. Nydam and Richard D. Schulick

Key Points

1 The most widely accepted nomenclature for liver anatomy is based on Couinaud’s description of

eight anatomic segments of the liver.

2 There are three major hepatic veins, with most patients having a right hepatic vein that joins the

right anterior wall of the inferior vena cava (IVC) and middle and left hepatic veins that converge

into a common trunk before joining the IVC.

3 Classic hepatic arterial anatomy exists in only approximately 50% of patients, with a replaced or

accessory right hepatic artery arising from the superior mesenteric artery and a replaced or

accessory left hepatic artery arising from the left gastric artery being the most common variants.

4 Callot triangle is bounded by the common hepatic duct on the left, the cystic duct inferiorly, and the

cystic artery superiorly.

5 The blood supply of the common bile duct is segmental in nature and consists of branches from the

cystic, hepatic, and gastroduodenal arteries, which meet to form collateral vessels that run in the 3

and 9 o’clock positions.

6 Multiphase computed tomography (CT) and magnetic resonance imaging (MRI) with intravenous

contrast are commonly used to characterize hepatic lesions.

7 Magnetic resonance cholangiopancreatography (MRCP) is often used to view biliary anatomy as it

involves no contrast agent and optimally can provide images that rival formal cholangiography.

8 Intraoperative ultrasonography is used routinely to assess the anatomy of the hepatic pedicles

(portal vein, hepatic artery, and bile duct) and hepatic veins and to identify and characterize hepatic

lesions within the parenchyma and their relationships within the eight anatomic segments.

9 The portal pedicles are invested with the Glisson capsule and have a very echogenic covering to

them on ultrasound in contrast to hepatic vein branches.

10 The steps involved in major hepatectomy include optimal exposure, vascular inflow control, vascular

outflow control, and parenchymal transection.

A precise knowledge of the anatomy of the liver and biliary tract and their relationship to associated

blood vessels is essential for the performance of hepatobiliary surgery. Every surgeon caring for a

patient with a hepatobiliary problem should have a thorough understanding of the general anatomy and

an absolute understanding of each individual patient’s anatomy, because variations are common.

TOPOGRAPHIC ANATOMY

The normal adult liver is a large, wedge-shaped organ that occupies much of the right upper quadrant of

the abdomen. Most of the liver bulk lays to the right of the midline where it molds to the undersurface

of the right diaphragm, and where the lower border coincides with the right costal margin. The liver

extends as a wedge to the left of the midline between the anterior surface of the stomach and the left

dome of the diaphragm. The anterior surface of the liver is invested by visceral peritoneum that extends

to the anterior abdominal wall in the midline from the ligamentum teres, or round ligament (the

obliterated umbilical vessels), and by an obliquely oriented fusion of peritoneum known as the falciform

ligament. Posteriorly, the investing peritoneum is contiguous with the peritoneum of the diaphragm and

covers the liver, except for a bare area bounded by the right and left triangular ligaments (Fig. 57-1). The

Glisson capsule is a thin, fibrous covering that envelops the liver deep to the peritoneum, sending

fibrous septa into the hepatic parenchyma investing the portal structures.

Ordinarily, the liver can be separated from adjacent organs and structures by simply moving it or

1452