topics

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resection between the right and left liver. Greater exposure of the superior aspect of the hepatic hilum

and exposure of a high or intraparenchymal bifurcation of a portal triad structure may be aided by

exposing the hilar plate (Fig. 57-22) and dividing the Glisson capsule at the most inferior border of

segment IV. Inflow control to the liver can also be obtained by pedicle ligations in which small

hepatotomies are made around the main right pedicle, main left pedicle, right anterior pedicle, or right

posterior pedicle after identification with ultrasound (Fig. 57-23).10 The pedicle of interest can be

dissected out bluntly with a right angle or by palpation. The pedicle can then be clamped to confirm

that it does indeed supply the area of liver of interest (i.e., right half, left half, right anterior section, or

right posterior section). Once confirmed, the pedicle can be divided. Alternatively, the inflow pedicles

can be divided as they are encountered while transecting hepatic parenchyma. With this technique,

hemorrhage can be minimized by intermittent portal inflow occlusion, which is accomplished by gently

clamping the main portal triad within the hepatoduodenal ligament (“Pringle maneuver”).

Outflow control of the hepatic veins can be obtained before or after hepatic transection and should be

decided on a case-by-case basis. When there is a significant extraparenchymal component to the hepatic

vein(s), often it is easier to divide the hepatic vein(s) early and before parenchymal transection (but

after inflow control) (Fig. 57-24). When the extraparenchymal component to the hepatic vein(s) is very

short or absent and when the tumor margin is not near the junction of the hepatic vein(s) and IVC, it

may be easier and safer to divide the hepatic vein(s) within the hepatic parenchyma after most of the

parenchymal transection has been performed. The use of endoscopic vascular stapling devices has made

the ligation of hepatic veins, whether extra- or intraparenchymally, much quicker and safer (Fig. 57-

25).10 It is often useful to keep the central venous pressure (CVP) of the patient low (<5 mm Hg) until

after parenchymal transection as this will decrease bleeding from the IVC and hepatic vein branches.11

Figure 57-23. Hepatotomies to access pedicles for ligation: right hepatectomy, 1 and 2; left hepatectomy, 3 and 5; right anterior

sectorectomy, 2 and 4; and right posterior sectorectomy, 1 and 4.

During live donor hepatectomy, a meticulous dissection of the portal triad is done isolating the main

bifurcations of the hepatic artery, bile duct, and portal vein on the side that will be recovered. A

cholecystectomy and trans-cystic intraoperative cholangiogram is performed to confirm the biliary

anatomy. Outflow control is obtained by dissection of the extrahepatic portion of the hepatic veins as

previously described. After the graft hemiliver has been dissected off the IVC, the parenchyma is

transected while ensuring continued inflow and outflow to both sides limiting any ischemia to the graft

and remnant liver. The portal triad structures and the hepatic vein are divided and the graft is removed

in coordination with the recipient operation.

Over the last decade there has been significant advances in minimally invasive liver resection. In

large volume hepatobiliary centers with advanced laparoscopic skills both benign and malignant tumors

in the peripheral segments (II to VI) are safely resected with good results. With more experience,

formal hemihepatectomies are becoming more common. As with other laparoscopic operations,

advantages include decreased postoperative pain, decreased length of stay, and earlier return to normal

activity. A minimally invasive liver resection should proceed with the same indications and

intraoperative steps employed in an open resection. The indications to resect benign tumors should not

be broadened because an operation with potentially less associated morbidity can be offered to the

patient. As with open resections, major minimally invasive liver resections include optimal exposure,

vascular inflow and outflow control prior to parenchymal transection. Options for minimally invasive

liver resection include a purely laparoscopic approach that does not employ the planned use of a hand

port or mini-laparotomy incision. The specimen is removed through an extension of one of the

laparoscopic port incisions or a small Pfannenstiel incision. The planned use of a hand port is an option

for resections that require more manual control. Hybrid procedures that utilize the laparoscope to

mobilize the liver and then proceed with a mini-laparotomy for the portal triad dissection and

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parenchymal are use by many for major resections. As centers gain more experience the trend is to

perform more resections with the purely laparoscopic approach. Minimally invasive liver resection will

progressively be used for more complex cases including live donor hepatectomies.

Figure 57-24. Caudal retraction of the left hepatic lobe with division of middle and left hepatic veins during left hepatic

lobectomy. Often, the division of the middle and left hepatic veins is intraparenchymal.

Figure 57-25. A vascular endoscopic stapling device is used to divide the right hepatic vein after the right side of the liver has been

mobilized.

MAJOR HEPATECTOMIES

To develop a uniform nomenclature understood by all, the American and International HepatoPancreato-Biliary Associations (AHPBA and IHPBA) have adopted the Brisbane 2000 terminology of

hepatic anatomy and resections. Right hepatectomy or right hemihepatectomy involves the resection of

segments V through VIII. Left hepatectomy or hemihepatectomy involves the resection of segments II

through IV. Either of these resections may or may not include resection of segment I, which should be

stated. Extended right hepatectomy involves the resection of segments IV through VIII. Extended left

hepatectomy involves the resection of segments II through V plus VIII. Again, either of these extended

resections may or may not include resection of segment I, which should be stipulated.

Right anterior sectorectomy includes segments V and VIII. Right posterior sectorectomy includes

segments VI and VII. Left medial sectionectomy removes segment IV. Left lateral sectionectomy

includes segments II and III. A segmentectomy involves the resection of a single segment and a

bisegmentectomy involves the resection of two contiguous segments.

The steps involved in each of these major hepatectomies include optimal exposure of the liver,

vascular inflow control, vascular outflow control, and parenchymal transection. Vascular inflow control

can be obtained by directly ligating the main right or left branches of the hepatic artery and portal vein

in the hilum or by intermittent 10- to 20-minute intervals of a Pringle maneuver with 3 minutes in

between to reestablish blood flow (or both). It is the authors’ preference to encircle the hepatoduodenal

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ligament twice with a quarter-inch Penrose drain that is tightened and clamped for a Pringle maneuver.

Pedicle ligation can also be performed, as described previously, or the pedicles can be controlled as they

are encountered during parenchymal transection. It is the authors’ preference to obtain vascular inflow

by ligating the appropriate vessels in the hilum or by pedicle ligations and to supplement this with

intermittent Pringle maneuvers, as necessary, during parenchymal transection. Often the Pringle

maneuver is not required, but if bleeding from inflow vessels becomes significant, then it should be

performed. Vascular outflow to the right or left liver can be obtained by exposing and ligating the

hepatic veins, as previously described, or by ligating the vessels intraparenchymally during transection

of the liver tissue. Parenchymal transection can be performed using a multitude of techniques including

finger fracture, using a Kelly clamp to fracture, Cavitron Ultrasonic Surgical Aspirator (CUSA),

harmonic scalpel, stapling devices, electrocautery devices with or without saline perfusion, highpressure water jets, and radiofrequency planar arrays. The superiority of any one of these techniques

has not been established, and all are used. With these techniques, individual blood vessels and bile ducts

are cauterized, clipped, or sutured in rapid succession as they are encountered. Constant reevaluation of

the direction of transection is important both to not injure vital structures to the remnant liver and to

maintain a negative margin. After parenchymal transection and removal of the specimen, the raw

surface of the liver is carefully inspected for bleeding and bile leakage, which can then be controlled by

suture ligation and the use of argon beam coagulation. The authors’ preferences are to selectively use

closed suction drains near resected liver surfaces to monitor and drain unrecognized postoperative bile

leaks. Some centers have decreased the use of closed suction drains in favor of radiologic intervention

when necessary, because they often clog or do not actually drain the fluid collections that form.

SEGMENTAL RESECTIONS

To maximize functional reserve, (multi)segmental or subsegmental (or nonanatomic) hepatectomies can

be performed. For example, left lateral sectionectomy (segments II and III), central hepatectomy to

remove the right anterior section (segments V and VIII) and left medial section (segment IV), right

posterior sectionectomy (segments VI and VII), or caudate resection (segment I) are examples in which

one, two, or three contiguous segments are removed to eradicate tumors within those regions of the

liver. These resections are often done with intermittent Pringle maneuvers until the specific pedicles

supplying these areas are controlled.

References

1. McIndoe AH, Counseller VX. A report on the bilaterality of the liver. Arch Surg 1927;15:589.

2. Hjörtsjö CH. The topography of the intrahepatic duct systems. Acta Anat (Basel) 1931;11:599–615.

3. Tung TT. La vascularixation veineuse du foie et ses applications aux resections hepatiques. Thèse

Hanoi 1939.

4. Healy JE, Schroy PC. Anatomy of the biliary ducts within the human liver. Analysis of the

prevailing pattern of branchings and the major variations of the biliary ducts. AMA Arch Surg

1953;66:599–616.

5. Goldsmith NA, Woodvurne RT. Surgical anatomy pertaining to liver resection. Surg Gynecol Obstet

1957;195:310–318.

6. Couinaud C. Le Foi: Etudes anatomogiques et chirurgicales. Paris: Masson; 1957.

7. Bismuth J, Houssin D, Castaing D. Major and minor segmentectomies–réglées–in liver surgery.

World J Surg 1982;6:10–24.

8. Blumgart LH, Hann LE. Surgical and radiologic anatomy of the liver and biliary tract. In: Blumgart

LH, Fong Y, eds. Surgery of the Liver and Biliary Tract, 3rd ed. New York, NY: WB Saunders; 2000.

9. Michels NA. Newer anatomy of the liver and its variant blood supply and collateral circulation. Am

J Surg 1966;112:337.

10. Fong Y, Blumgart LH. Useful stapling techniques in liver surgery. J Am Coll Surg 1997;185:93–100.

11. Melendez JA, Arslan V, Fischer ME, et al. Perioperative outcomes of major hepatic resections under

low central venous pressure anesthesia: blood loss, blood transfusion, and the risk of postoperative

renal dysfunction. J Am Coll Surg 1998;187:620–625.

1471

Chapter 58

Hepatic Infection and Acute Liver Failure

Andrew M. Cameron and Christine Durand

Key Points

1 Pyogenic abscess is increasing due to the rise of invasive procedures involving the liver, biliary tree,

and pancreas.

2 The treatment for hydatid cysts is surgical resection after the introduction of antiparasitic

medication.

3 Viral hepatitis due to hepatitis B and C represents a principal cause of chronic liver disease in the

United States and worldwide, newer antiviral agents have made these diseases treatable or curable.

4 Liver transplant is the treatment of choice for decompensated cirrhosis or early hepatocellular cancer

in a cirrhotic liver.

5 One-third of acute liver failure patients will die without a liver transplant. Results after liver

transplant show greatly improved survival, though still inferior to that seen with transplantation for

chronic disease.

PYOGENIC LIVER ABSCESS

Abscess in the liver due to bacteria is known as pyogenic abscess. Pyogenic liver abscess occurs

relatively infrequently (incidence of 2.3 cases per 100,000 population) but still represents around 13%

of abdominal abscesses. It most frequently occurs in the setting of bowel compromise in which spread to

the liver is via the portal circulation or in the setting of direct spread from the biliary tree. Pyogenic

abscess may also occur as a result of seeding in the setting of systemic infection.1 Lastly, hepatic abscess

is seen in liver transplant recipients and when observed suggests hepatic artery compromise (Fig. 58-1).

1 Over the past 20 years the increase in invasive procedures involving the liver, biliary tree, and

pancreas has resulted in an increase in the rate of pyogenic abscess. Most pyogenic abscesses are

solitary and polymicrobial and involve the right lobe of the liver. Individuals over 50 years of age,

diabetics, liver transplant recipients, and those with malignancy are at the highest risk for pyogenic

abscess.

Fever is the most frequent presenting symptom of pyogenic liver abscess, sometimes without other

localizing signs. Right upper quadrant pain, chills, anorexia, weight loss, malaise, weakness, and

jaundice are frequently present. Laboratory studies show elevated white blood cell count in most cases,

though not always. Abnormal liver function tests, including elevated bilirubin or transaminases are seen

in about half of the cases.2,3

Though a chest x-ray may reveal a right pleural effusion or elevated hemidiaphragm in 50% of cases,

the radiographic test of choice is ultrasound (US) or CT scan. US will reveal abscess in 90% of cases and

can guide drainage. CT is even more sensitive and will reveal small abscesses and differentiate these

lesions from other pathology.4

Causative agents in hepatic abscess are gram-negative aerobes in two-thirds of patients, most

commonly Escherichia coli, Klebsiella pneumonia, and Proteus species. Enterococci may also be present if

the cause of the abscess is biliary; anaerobes may be isolated if the source is colonic. Streptococci

species are frequently found as well. These microbes will be isolated from the lesion and the blood in

most patients and it is helpful to draw blood cultures prior to the administration of antibiotics.

Coverage should be broad and its duration is based on clinical response. A typical course is 14 days of

IV antibiotics followed by oral medication for a total of 6 weeks.5–7

Percutaneous drainage is standard at this time and is almost always easily accomplished. A drainage

catheter should be left in place until output is minimal, often around 7 days. If attempt at percutaneous

drainage is complicated by ascites, multiple abscesses, transpleural approach, large size, or other

consideration, an open approach may be required. Adequate drainage and prompt initiation of

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Figure 57-18. A,B: Intraoperative ultrasound images of liver demonstrating right hepatic pedicle (RHP), right anterior sector

pedicle (RASP), right posterior sector pedicle (RPSP), left hepatic pedicle (LHP), segment II pedicle (SIIP), segment IV pedicle

(SIVP), segment I (SI), and inferior vena cava (IVC). C,D: Intraoperative ultrasound images of liver demonstrating inferior vena

cava (IVC), right hepatic vein (RHV), middle hepatic vein (MHV), left hepatic vein (LHV), segment I (SI), and a metastatic

gastrointestinal stromal tumor lesion straddling segments IV and V of the liver.

Figure 57-19. Positron emission tomography and computed tomography (PET-CT) scan images of patient in Figure 57-18B and C

with solitary gastrointestinal stromal tumor metastasis straddling segments IV and V. Noncontrast CT images (left). PET images

(center). Fusion images (right).

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Figure 57-20. Computed tomography scan demonstrating segmental anatomy of the liver with cuts through the dome (A), just

above the portal bifurcation (B), and below the portal bifurcation (C).

Table 57-1 Strategies to Predict Hepatic Reserve

ONCOLOGIC CONSIDERATIONS IN HEPATIC RESECTION

The decision of when and whether to operate is often just as important as the technical details of

successfully removing a liver lesion(s) identified in a patient. It is very important to consider the likely

diagnosis in making the decision of whether to operate. For example, a solitary liver lesion presenting

in an elderly patient with a rising carcinoembryonic antigen (CEA) and a recent history of a resected

colon cancer should be treated differently from a young woman with a solitary lesion with radiologic

characteristics of a focal nodular hyperplasia lesion. It is important to consider the biology of the tumor

within the patient. For example, a patient who represents with a solitary hepatic colorectal cancer

metastasis 4 years after resection of the primary tumor will more likely benefit from hepatic resection

than another patient who presents with eight synchronous lesions in the liver at the time of diagnosis of

the primary tumor. It is important to consider whether the goal of resection is curative or palliative. For

example, patients with neuroendocrine tumor metastases of the liver may be debulked of hepatic

metastases, but they are rarely totally eradicated of disease. If the tumor is functional and difficult to

control medically, then there may be a benefit to debulking. Even if the tumor is not functional, some

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evidence indicates that surgical debulking of liver metastases in carefully selected patients may benefit

long-term survival. It is important to exclude other distant extrahepatic disease with a reasonable

number of preoperative tests. For example, before performing hepatic resection for colorectal cancer

metastases, it is often helpful to obtain a PET scan to exclude extrahepatic metastases. This will allow

better selection of patients most likely to benefit from hepatic resection and will allow patients with

previously unsuspected systemic disease to get systemic therapy sooner.

Table 57-2 Child–Pugh Classification

Table 57-3 MELD Score

The comorbid status of the patient is also important. Extended hepatic resections with or without

biliary reconstruction can exert a toll on even very fit patients. It is important to identify patients who

may have difficulties with hepatic regeneration (e.g., those with a history of hepatitis, cirrhosis, or

metabolic disorders). Patients with suspected cardiopulmonary disease should undergo appropriate

preoperative evaluation and treatment before hepatic resection. Finally, other effective treatments and

the optimal sequence of treatments should be considered. For example, in the treatment of

hepatocellular carcinoma the possibilities include liver transplantation, liver resection, radiofrequency

or microwave ablation, transarterial chemoembolization, and systemic chemotherapies. A patient with

limited hepatocellular carcinoma and poor hepatic reserve due to chronic liver disease, cirrhosis, and

portal hypertension is best treated with liver transplant, whereas a patient with normal liver

parenchyma, minimal portal hypertension, and a resectable lesion may be best treated with liver

resection. Additionally, some patients may best be treated with ablative techniques, especially if they

have very small lesions that are easily approached percutaneously. Many patients are treated with a

combination of these modalities. For example, most transplant centers will first treat hepatocellular

carcinoma patients with chemoembolization to provide locoregional control while the patient is

upgraded on the waiting list. Whether the patient is a candidate for liver transplantation or resection,

this combination can give insight into the biology of the disease prior to definitive treatment.

INTRAOPERATIVE ASSESSMENT

Incisions for open hepatic resections usually involve a right subcostal incision. Significant exposure can

be obtained with a trifurcated incision as shown in Figure 57-21. In the majority of cases, however, all

that is needed is an extended right subcostal incision with a vertical extension to the base of the xiphoid.

The xiphoid can be resected for better exposure. For bulky lesions on the left or if the left half of the

liver extends significantly to the left upper quadrant, a left subcostal component can be added. In rare

circumstances, especially for lesions high on the dome, an intercostal extension or even median

sternotomy may improve exposure. This is especially true for lesions involving the hepatic vein and IVC

confluences.

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Several versions of self-retaining costal margin retractors or ringed retractors are available that

provide good access to the subdiaphragmatic surface. For complete intraoperative ultrasonography and

for major resections, complete mobilization of the involved side of the liver is required. The round

ligament is divided and the falciform ligament divided. The right and/or left triangular ligaments are

then divided to expose the bare areas of the liver. During exposure of the bare areas of the liver, care

should be taken to avoid entering the right or left chest through the ligamentous portions of the

diaphragm because this will cause excessive bellowing of the diaphragm and poor exposure until a chest

tube is placed on that side or the hemithorax is “bubbled out” to remove the air and the diaphragm

repaired. Additionally, the right and left phrenic veins are very superficial on the hemidiaphragm and

can be injured. The right colon can be mobilized out of the field by dividing Gerota fascia over the right

kidney and pulling the hepatic flexure inferiorly. To completely assess the caudate lobe, the overlying

lesser omentum should be divided. Care should be taken to avoid inadvertently dividing a replaced or

accessory left hepatic artery running in this space. After mobilization, a thorough bimanual examination

should be performed and intraoperative ultrasonography used as previously described.

Figure 57-21. Incisions used for open hepatic resection.

Figure 57-22. Lowering the hilar plate. A: The inferior border of segment IV overlies the hepatic duct confluence. B: Division of

the connective tissue investment allows elevation of segment IV, which results in a “lower” hilar plate and surgical exposure to the

hepatic duct confluence.

10 The porta hepatis is often dissected to identify the main bifurcations of the hepatic artery and

portal vein and the confluence of the bile ducts. This allows individual ligation of the branches of these

structures supplying one side of the liver while preserving the branches to the other side. Ligation of the

hepatic artery and portal vein to one side also allows the liver parenchyma to demarcate a line of

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to help further characterize hepatic lesions. Resolution of some lesions may be slightly better with MRI.

Additionally, certain lesions, such as hemangiomas and cysts, can easily be identified based on MRI

characteristics when the CT characteristics are indeterminate (Fig. 57-16). The disadvantages of MRI are

its increased cost, increased amount of time to perform, inability to quickly screen other organs and

body cavities within the same session, and wide variability in quality from one imaging center to

another.

7 Magnetic resonance cholangiopancreatography (MRCP) is becoming more widely used to

noninvasively view biliary anatomy (Fig. 57-17). The scans are heavily T2 weighted, which maximizes

the signal from the biliary tree. No injection of contrast agent is needed, and under optimal conditions

the resulting imaging can rival that of formal cholangiography. Three-dimensional reconstructions can

be performed to view the biliary tree from multiple angles and can be helpful in distinguishing between

stones, strictures, and neoplasms. Again, these reconstructions are vital to donor selection in live donor

liver transplantation. Rarely is it necessary to proceed with endoscopic retrograde

cholangiopancreatography (ERCP) to define the distal intrahepatic ductal anatomy.

Figure 57-15. Three-dimensional reconstruction of the hepatic vasculature.

Ultrasonography

8 Hepatic ultrasonography can be applied transcutaneously or intraoperatively via open or laparoscopic

surgery. It can be useful in identifying lesions within the hepatic parenchyma, to describe the

consistency (i.e., fatty or cirrhotic) and identify dilation of the biliary tree and any abnormalities or

stones within the gallbladder. In hepatobiliary surgical centers, intra operative ultrasonography is used

routinely to assess the anatomy of the pedicles (portal vein, hepatic artery, and bile duct), the hepatic

veins, and the hepatic parenchyma. It is useful both to further identify and characterize lesions within

the hepatic parenchyma and to delineate their relationships within the eight anatomic segments of the

liver. Additionally, it is often helpful to delineate proximity of lesions to major vascular structures and

to survey for abnormal anatomy in planning a resection.

With ablation therapies more commonly employed, ultrasound has become indispensable in directing

the use of radiofrequency ablation. This ablation therapy can be performed percutaneously,

laparoscopically, and during open surgery.

9 Typically, intraoperative assessment of the liver involves examining the portal pedicles. The main

portal pedicle is identified within the hepatoduodenal ligament. It is followed superiorly to the portal

bifurcation into the main right and left pedicles. The portal pedicles are invested with the Glisson

capsule and have a very echogenic covering to them in contrast to hepatic vein branches. The main right

portal pedicle is followed toward the right where it gives off an anterior branch and a posterior branch

(Fig. 57-18A). The right anterior branch gives off separate pedicles to segment V (caudad) and to

segment VIII (cephalad). The right posterior branch gives off separate pedicles to segment VI (caudad)

and to segment VII (cephalad). The main left pedicle is usually much longer and courses intact to the

base of the umbilical fissure before branching into various segmental pedicles (Fig. 57-18B). At the base

of the umbilical fissure, the main left pedicle courses anteriorly toward the round ligament and gives off

a pedicle to segment IV medially and pedicles to segments II and III laterally. Next, if the falciform

ligament has been divided, the hepatic veins can easily be visualized using intraoperative

ultrasonography (Fig. 57-18C). As described previously, usually a larger right hepatic vein can be

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delineated and smaller left and middle hepatic veins joining into a common trunk before emptying into

the IVC are seen. Commonly, an umbilical hepatic vein branch can be identified coursing between the

middle and left hepatic veins and running under the falciform ligament. Not uncommonly, significant

accessory right hepatic veins can be seen emptying from the posterior surface of the right liver directly

into the IVC as it courses posterior to the liver. The identification of these accessory right hepatic veins

is potentially important for both vascular control and preservation of outflow from the liver (in

occasional cases where outflow of the remnant right liver can be supported by a very large accessory

vein). Finally, the hepatic parenchyma is systematically scanned to identify lesions within the liver (Fig.

57-18). It is sometimes useful to adjust the ultrasound settings on a known lesion defined preoperatively

to maximize the echogenicity in the hopes of identifying other occult lesions not identified

preoperatively.

Figure 57-16. A,B: T1-weighted magnetic resonance imaging (MRI) with gadolinium from the same patient as in Figure 57-14

with history of colorectal cancer and three lesions in the liver. Lesion 1 in segment VIII is irregular and rim enhancing and was a

colorectal cancer metastasis. Lesion 2 straddling segments IV and VIII has smooth borders, is not rim enhancing, and was found to

be a cyst. Lesion 3 straddling segments IV and III across the umbilical fissure is irregular, rim enhancing, and was a colorectal

cancer metastasis. C,D: T2-weighted MRI from the same patient with history of colorectal cancer and three lesions in liver. Lesion

1 in segment VIII is irregular and mildly bright and was a colorectal cancer metastasis. Lesion 2 straddling segments IV and VIII

has smooth borders, is very bright, and was found to be a cyst. Lesion 3 straddling segments IV and III across the umbilical fissure

is mildly bright and was a colorectal cancer metastasis. Colorectal metastases and many tumors are mildly bright on T2-weighted

MRI, whereas cysts and hemangiomas are typically very bright.

Positron Emission Tomography

Positron emission tomography (PET), especially when combined with CT (PET-CT), has become a

valuable tool in helping to select patients who will most benefit from aggressive liver resection. This

technique is based on the increased metabolism of glucose in neoplastic tissues. A glucose analog,

fluorodeoxyglucose, that is tagged with fluorine-18 is injected intravenously before scanning and is

retained preferentially in metabolically active tumors over normal tissue. Sometimes PET scans will

identify areas of occult disease within the liver, but more importantly, they can identify areas of

extrahepatic occult disease previously unsuspected. When combined with a CT scanner within the same

machine and the ability to fuse images, the areas of increased activity can be more precisely

anatomically identified (Fig. 57-19).

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Figure 57-17. Magnetic resonance cholangiopancreatography (MRCP) of a patient after cholecystectomy with mild dilation of

common hepatic duct (CHD). The pancreatic duct (PD) is also visible.

Correlation of Computed Tomographic Images with Segmental Anatomy

Preoperative CT remains the primary imaging modality used by most surgeons before hepatic resection.

Figure 57-14 is provided to help correlate CT images to the segmental anatomy defined previously. The

segments of the liver are defined using identifiable structures on the CT (Fig. 57-20).

PREOPERATIVE EVALUATION OF HEPATIC RESERVE

Whenever a surgical resection is planned, an important consideration is whether the remnant liver will

be sufficient to regenerate and sustain the patient long term. In patients with relatively normal hepatic

parenchyma (without active hepatitis, cirrhosis, or metabolic defects), up to 75% of the hepatic volume

can be resected with good recovery as long as the remnant liver has adequate portal venous and hepatic

arterial inflow, adequate hepatic venous outflow, and adequate biliary drainage. Many groups around

the world have used various strategies to predict hepatic reserve (Tables 57-1 to 57-3). None of these

tests or strategies has been demonstrated to clearly better predict outcome than another. Many centers

in the United States rely simply on the Child–Pugh or MELD score and the prediction of adequate liver

remnant volume after resection. In select circumstances, it may be of benefit to perform portal vein

embolization to the right or left half (rare) of the liver in the hopes of obtaining compensatory

hypertrophy of the other side before resection. This is especially useful when the predicted liver

remnant after resection is small or if the patient has an underlying hepatic dysfunction that may not

allow the remnant to fully regenerate and sustain the patient long term. To gain maximal growth of the

left lateral section of the liver, some centers will also embolize the portal vein branches to segment IV

in addition to the main right portal vein. The disadvantages of portal vein embolization include the need

to wait 3 to 4 weeks before resection to allow the compensatory hypertrophy to occur and, for more

central lesions, the need to commit to taking out one or the other side with an extended hepatectomy

without the benefit of intraoperative evaluation.

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Figure 57-8. Variations in hepatic arterial anatomy.

Hepatic Arteries

3 There is much variability in the hepatic arterial supply to the liver. The most common anatomy is a

common hepatic artery that arises from the celiac trunk and courses near the superior border of the

neck of the pancreas. After the origins of the gastroduodenal, supraduodenal, and right gastric arteries,

the proper hepatic artery courses in the left anterior aspect of the hepatoduodenal ligament in front of

the portal vein and to the left of the common hepatic duct. The proper hepatic artery usually bifurcates

into right and left hepatic arteries outside the liver. The anatomy of the hepatic artery is variable and

should be familiar to surgeons operating in this area (Fig. 57-8). Approximately 45% of people have

variant hepatic arterial anatomy.9 The right hepatic artery usually courses posterior to the common

hepatic duct but anterior to the right portal vein to supply the right liver. The left hepatic artery usually

remains extrahepatic until near the base of the umbilical fissure, where it enters the liver to give off

branches to segments II, III, and IV. Small branches from near the bifurcation of the proper hepatic

artery also supply segment I. A middle hepatic artery branch may arise from either the right or left

hepatic arteries after bifurcation. Although this anatomy is described as normal, it is found only in

approximately 50% to 60% of patients. A replaced or accessory right hepatic artery may arise off of the

superior mesenteric artery near its origin and course posteriorly or through the head of the pancreas to

lie along the right posterior border of the hepatoduodenal ligament. A replaced or accessory left hepatic

artery may arise off of the left gastric artery and course transversely toward the base of the umbilical

fissure in the lesser omentum. In general, within the hepatic parenchyma, the hepatic arterial branches

course closely with bile duct branches and fairly closely with portal venous branches, but not always,

and anatomic variations should be suspected. The descriptions and frequency of hepatic arterial variants

have been well characterized by Michels.9

Intrahepatic Biliary Tree

The right and left livers are respectively drained by the right and left hepatic ducts, whereas the caudate

(segment I) is drained by several small ducts joining the confluence and the first several centimeters of

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both hepatic ducts. The intrahepatic ducts are tributaries of the corresponding hepatic ducts, which

penetrate the liver invaginating the Glisson capsule at the hilus. Bile ducts are usually located above the

corresponding portal branches, whereas hepatic arterial branches run inferiorly to the veins. The left

hepatic duct directly drains the bile ducts to segments II, III, and IV, which constitute the left liver. The

right hepatic duct drains the bile ducts from segments V, VI, VII, and VIII, which constitute the right

liver. Usually, the bile ducts from segments V and VIII join to first form the anterior sectoral duct and

the bile ducts from segments VI and VII join to first form the posterior sectoral duct prior to forming

the right hepatic duct (Fig. 57-9).

Figure 57-9. Intrahepatic divisions of the bile ducts and hepatic arteries.

Gallbladder

4 The gallbladder is a reservoir for bile located on the undersurface of the liver at the confluence of the

right and left halves of the liver. It is separated from the hepatic parenchyma by a cystic plate, which is

constituted of connective tissue applied to the Glisson capsule. The gallbladder may be deeply imbedded

into the liver or occasionally presents on a mesenteric attachment, but usually lays in a gallbladder

fossa. The gallbladder varies in size and consists of a fundus, a body, and an infundibulum. The tip of

the fundus usually reaches the free edge of the liver and is closely applied to the cystic plate. The

infundibulum of the gallbladder makes an angle with the body and may obscure the common hepatic

duct, constituting a danger point during cholecystectomy. The cystic duct arises from the infundibulum

of the gallbladder and extends to join the common hepatic duct. The lumen measures between 1 and 3

mm in diameter, and its length varies depending on the type of union with the common hepatic duct

(Fig. 57-10). Callot triangle is bounded by the common hepatic duct on the left, the cystic duct

inferiorly, and the cystic artery superiorly. Arterial blood reaches the gallbladder via the cystic artery,

which usually originates from the right hepatic artery. Several known variations in the origin and

course of the cystic artery are illustrated in Figure 57-11. The venous drainage of the gallbladder is

directly into the liver parenchyma or into the common bile duct plexus.

1458

Figure 57-10. Variations in the junction of the cystic duct and common hepatic duct.

Figure 57-11. Variations of the cystic artery.

Common Bile Duct

The cystic and common hepatic ducts join to form the common bile duct. The common bile duct is

approximately 8 to 10 cm in length and 0.4 to 0.8 cm in diameter. The common bile duct can be divided

into three anatomic segments: supraduodenal, retroduodenal, and intrapancreatic (Fig. 57-12). The

supraduodenal segment resides in the hepatoduodenal ligament lateral to the hepatic artery and anterior

1459

to the portal vein (Fig. 57-13). The course of the retroduodenal segment is posterior to the first portion

of the duodenum, anterior to the IVC, and lateral to the portal vein. The pancreatic portion of the duct

lies within a tunnel or groove on the posterior aspect of the pancreas. The common bile duct then enters

the medial wall of the duodenum, courses tangentially through the submucosal layer for 1 to 2 cm, and

terminates in the major papilla in the second portion of the duodenum (Fig. 57-12). The distal portion

of the duct is encircled by smooth muscle that forms the sphincter of Oddi. The common bile duct

usually joins the pancreatic duct to form a common channel before entering the duodenum at the

ampulla of Vater. Some patients will have an accessory pancreatic duct emptying into the duodenum.

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

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

9 o’clock positions. The venous drainage forms a plexus on the anterior surface of the common bile duct

that enters the portal system. The lymphatic drainage follows the course of the hepatic artery to the

celiac nodes.

LIVER IMAGING

Computed Tomography

Computed tomography (CT) is widely available and quick and has become the main modality to initiate

the assessment of hepatic processes. It also has the advantage of being able to quickly assess other

organs within the abdominal cavity and chest. With the introduction of multidetector spiral CT, the

resolution of hepatic lesions is quite good. This scanning technique allows total hepatic imaging in

arterial, portal venous, and delayed phases after a rapid intravenous contrast bolus during a single

breath hold by the patient (Fig. 57-14). In addition, three-dimensional reconstructions can be created to

construct high-quality hepatic artery angiograms, portal venograms, and hepatic venograms. These

reconstructions play a vital role in the selection of appropriate donors for live donor liver

transplantation (Fig. 57-15). Drip infusion cholangiography with CT can provide distal intrahepatic duct

cholangiograms that with the three-dimensional arteriograms and venograms are vital in planning donor

hepatectomies and avoiding serious complications.

Figure 57-12. Anatomy of the extrahepatic biliary tree and pancreatic duct.

1460

Figure 57-13. Relationship of structures within the hepatoduodenal ligament.

Figure 57-14. Portal venous phase of computed tomography (CT) scan from a patient with a history of colorectal cancer and three

lesions in the liver. Lesion 1 in segment VIII is irregular and rim enhancing and was a colorectal cancer metastasis. Lesion 2

straddling segments IV and VIII has smooth borders, is not rim enhancing, and was found to be a cyst. Lesion 3 straddling segments

IV and III across the umbilical fissure is irregular and rim enhancing and was a colorectal cancer metastasis.

Magnetic Resonance Imaging

6 Magnetic resonance imaging (MRI) of the liver with gadolinium as a contrast agent is commonly used

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dividing loose areolar tissue (Fig. 57-2). Neoplastic or inflammatory conditions may obliterate these

planes. Superiorly and anteriorly, the diaphragm or abdominal wall and liver may jointly be involved in

a pathologic process. Posteriorly, the right adrenal gland or upper pole of the right kidney may involve

or be involved by the liver. Inferiorly, the gallbladder, colon, duodenum, or periportal lymphatics may

be involved. Cancers of the stomach or gastroesophageal junction may involve the left liver or vice

versa.

MORPHOLOGIC AND FUNCTIONAL ANATOMY

The description and definition of the anatomic divisions of the liver have been revised and written

about numerous times in the past 100 years.1–8 At present, there is still confusion between the various

hepatic anatomic nomenclatures in the English and French literature. Based only on morphologic criteria

and surface anatomy, the liver can be divided into right and left halves by forming a plane through the

gallbladder fossa (Cantlie line) and inferior vena cava (IVC) (Fig. 57-3). As will be shown later, this

plane approximates the true division between the right and left halves using the more strict definition of

a plane through the middle hepatic vein and IVC, but the middle hepatic vein is not obvious based

solely on morphology and without ultrasound. Further subdivisions of the right half of the liver into a

right anterior sector and a right posterior sector are not possible based only on surface anatomy. The

left half of the liver can be further subdivided into a left medial section and left lateral section based on

the umbilical fissure and falciform ligament. The caudate (tail-shaped) process of the liver is identified

as lying posterior to the gastrohepatic ligament and emanating from a process of liver situated posterior

to the main portal pedicle and anterior to the IVC.

Figure 57-1. Posterior view of the liver, showing the level of peritoneal reflections.

Figure 57-2. Posterior view of the liver, showing organs that produce impressions on its inferior surface.

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Figure 57-3. Anatomic division of the liver into right and left halves by a plane extending from the gallbladder fossa posteriorly to

the inferior vena cava.

Figure 57-4. Functional divisions of the liver and liver segments according to Couinaud nomenclature with the liver in the natural

position (A) and after it is mobilized (B).

1 The most widely accepted nomenclature is based on Couinaud’s description of the discrete anatomic

segments of the liver (Fig. 57-4).6 The eight segments of a liver can be determined using surface

anatomy and location of the three main hepatic veins, the portal pedicle bifurcation into right and left,

and the umbilical fissure and falciform ligament. As described, the right and left halves of the liver are

delineated by a plane through the middle hepatic vein and IVC. Segments II, III, and IV lie to the left of

this plane and form the left half of the liver. Segments V, VI, VII, and VIII lie to the right of this plane

and form the right half of the liver. Segment I, or the caudate process, is morphologically distinct from

the two halves of the liver and emanates from a process of liver lying posterior to the portal pedicle and

anterior to the IVC. Whereas the right and left halves of the liver derive blood supply from the

corresponding right and left portal veins and hepatic arteries, segment I derives blood supply from both.

Additionally, the right half of the liver has venous drainage primarily through the right and middle

hepatic veins, and the left half of the liver primarily through the left and middle hepatic veins. Segment

I, however, drains directly via small branches into the IVC. The left liver and especially the right liver

usually have small accessory hepatic venous branches draining directly into the IVC. Occasionally on the

right, the accessory branch is significant in size.

The right half of the liver can be further subdivided using a plane through the right hepatic vein and

the IVC. Liver anterior to this plane forms the right anterior sector, and liver posterior to this plane

forms the right posterior sector. The right anterior sector of the liver is composed of segment V

(inferior to the portal bifurcation) and segment VIII (superior to the portal bifurcation). The right

posterior sector of the liver is composed of segment VI (inferior to the portal bifurcation) and segment

VII (superior to the portal bifurcation).

The left half of the liver can be further subdivided using a plane through the umbilical fissure and

falciform ligament. Liver medial to this plane forms the left medial section of the liver or segment IV,

and liver lateral to this plane forms the left lateral section of the liver. The left medial section of the

liver is sometimes divided into two halves, with IVa closer to the IVC and IVb farther. The left lateral

section of the liver is further subdivided into segment II (which is superior) and segment III (which is

inferior).

Hepatic Veins

2 Three major hepatic veins carry blood from the liver to the IVC. Most patients have a right hepatic

1454

vein that joins the right anterior wall of the IVC and middle and left hepatic veins that converge into a

common trunk about 1 cm from the IVC that enters the left anterior wall of the IVC (Fig. 57-5). In some

patients, the three main hepatic veins join the IVC via three distinct trunks. These hepatic veins usually

lie within the hepatic parenchyma. Usually, a definable extraparenchymal segment of the hepatic veins,

especially the right, can be dissected out before it empties into the IVC, which makes outflow control

safer and easier. Usually, multiple accessory right hepatic veins empty from the right half of the liver

directly into the IVC as it courses posterior to the liver (Fig. 57-6). On occasion, these accessory right

hepatic veins are sizable and may even support venous outflow should the native right hepatic vein

need to be taken. Additionally, sometimes an umbilical vein can be appreciated running to the falciform

ligament between the middle and left hepatic veins and emptying into the terminal portion of the left

hepatic vein.

Portal Veins

The superior mesenteric and splenic veins join posterior to the neck of the pancreas to form the main

portal vein. It receives pyloric and coronary vein branches as it courses cephalad and obliquely to the

right to form the most posterior structure within the hepatoduodenal ligament (portal triad). In the

hilus of the liver, the main portal vein bifurcates into a short oblique right portal vein and a longer,

more transverse, and more superficial left portal vein (Fig. 57-7). These branches then enter the

parenchyma and become invested along with the other components of the portal triad by extensions of

the Glisson capsule. Both the right and left portal veins give off small branches to dually supply segment

I. The right portal vein usually enters the hepatic parenchyma immediately and is quick to divide into a

right anterior portal vein supplying segments V and VIII and a right posterior portal vein supplying

segments VI and VII. The left portal vein may remain near the surface of the left half of the liver in the

hilar plate for a significant distance as it courses to the umbilical fissure to give off medial branches to

segment IV and lateral branches to segments II and III.

Figure 57-5. Three major hepatic veins drain the liver. The caudate segment of the liver usually drains directly into the inferior

vena cava.

1455

Figure 57-6. Retraction of right liver medially exposes small venous tributaries that drain the right liver directly into the

retrohepatic vena cava. Several branches are ligated.

Figure 57-7. Intrahepatic divisions of the portal vein.

1456

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

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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.

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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

localization of gastrinoma in the Zollinger-Ellison syndrome. Ann Surg 1987;205(3):230–239.

79. Rosato FE, Bonn J, Shapiro M, et al. Selective arterial stimulation of secretin in localization of

gastrinomas. Surg Gynecol Obstet 1990;171(3):196–200.

80. Gower WR Jr, Buzogany JA Jr, Ellison EC, et al. Control of gastrin release in cultured gastrinomaderived G cells. Surgery 1988;104(2):424–430.

81. Chiba T, Yamatani T, Yamaguchi A, et al. Mechanism for increase of gastrin release by secretin in

Zollinger-Ellison syndrome. Gastroenterology 1989;96(6):1439–1444.

82. Brown CK, Bartlett DL, Doppman JL, et al. Intraarterial calcium stimulation and intraoperative

ultrasonography in the localization and resection of insulinomas. Surgery 1997;122(6):1189–1193;

discussion 1193–1194.

83. Pereira PL, Roche AJ, Maier GW, et al. Insulinoma and islet cell hyperplasia: value of the calcium

intraarterial stimulation test when findings of other preoperative studies are negative. Radiology

1998;206(3):703–709.

84. Whipple AO, Frantz VK. Adenoma of islet cells with hyperinsulinism: a review. Ann Surg

1935;101(6):1299–1335.

85. Howard TJ, Stabile BE, Zinner MJ, et al. Anatomic distribution of pancreatic endocrine tumors. Am

J Surg 1990;159(2):258–264.

86. Ectors N. Pancreatic endocrine tumors: diagnostic pitfalls. Hepatogastroenterology 1999;46(26):679–

690.

87. Richards ML, Gauger PG, Thompson NW, et al. Pitfalls in the surgical treatment of insulinoma.

Surgery 2002;132(6):1040–1049; discussion 1049.

88. Menegaux F, Schmitt G, Mercadier M, et al. Pancreatic insulinomas. Am J Surg 1993;165(2):243–

248.

89. Sauvanet A, Partensky C, Sastre B, et al. Medial pancreatectomy: a multi-institutional retrospective

study of 53 patients by the French pancreas club. Surgery 2002;132(5):836–843.

90. Efron DT, Lillemoe KD, Cameron JL, et al. Central pancreatectomy with pancreaticogastrostomy

for benign pancreatic pathology. J Gastrointest Surg 2004;8(5):532–538.

91. Goldstein MJ, Toman J, Chabot JA. Pancreaticogastrostomy: a novel application after central

pancreatectomy. J Am Coll Surg 2004;198(6):871–876.

92. Udelsman R, Yeo CJ, Hruban RH, et al. Pancreaticoduodenectomy for selected pancreatic endocrine

tumors. Surg Gynecol Obstet 1993;177(3):269–278.

93. Phan GQ, Yeo CJ, Cameron JL, et al. Pancreaticoduodenectomy for selected periampullary

neuroendocrine tumors: fifty patients. Surgery 1997;122(6):989–996; discussion, 996–997.

94. Fernandez-Cruz L, Blanco L, Cosa R, et al. Is laparoscopic resection adequate in patients with

neuroendocrine pancreatic tumors? World J Surg 2008;32(5):904–917.

95. Jaroszewski DE, Schlinkert RT, Thompson GB, et al. Laparoscopic localization and resection of

insulinomas. Arch Surg 2004;139(3):270–274.

96. Iihara M, Kanbe M, Okamoto T, et al. Laparoscopic ultrasonography for resection of insulinomas.

Surgery 2001;130(6):1086–1091.

97. Ayav A, Bresler L, Brunaud L, et al.; SFCL (Societe Francaise de Chirurgie Laparoscopique), AFCE

(Association Francophone de Chirurgie Endocrinienne). Laparoscopic approach for solitary

insulinoma: a multicentre study. Langenbecks Arch Surg 2005;390(2):134–140.

98. Sweet MP, Izumisato Y, Way LW, et al. Laparoscopic enucleation of insulinomas. Arch Surg

2007;142(12):1202–1204; discussion 1205.

99. Thompson GB, Service FJ, van Heerden JA, et al. Reoperative insulinomas, 1927 to 1992: an

institutional experience. Surgery 1993;114(6):1196–1204;discussion 1205–1206.

100. Carty SE, Jensen RT, Norton JA. Prospective study of aggressive resection of metastatic pancreatic

endocrine tumors. Surgery 1992;112(6):1024–1031;discussion 1031–1032.

101. Modlin IM, Lewis JJ, Ahlman H, et al. Management of unresectable malignant endocrine tumors of

the pancreas. Surg Gynecol Obstet 1993; 176(5):507–518.

102. McEntee GP, Nagorney DM, Kvols LK, et al. Cytoreductive hepatic surgery for neuroendocrine

tumors. Surgery 1990;108(6):1091–1096.

103. Kulke MH, Bergsland EK, Yao JC. Glycemic control in patients with insulinoma treated with

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everolimus. N Engl J Med 2009;360(2):195–197.

104. Moertel CG, Lefkopoulo M, Lipsitz S, et al. Streptozocin-doxorubicin, streptozocin-fluorouracil or

chlorozotocin in the treatment of advanced islet-cell carcinoma. N Engl J Med 1992;326(8):519–523.

105. Moertel CG, Hanley JA, Johnson LA. Streptozocin alone compared with streptozocin plus

fluorouracil in the treatment of advanced islet-cell carcinoma. N Engl J Med 1980;303(21):1189–

1194.

106. Altimari AF, Badrinath K, Reisel HJ, et al. DTIC therapy in patients with malignant intra-abdominal

neuroendocrine tumors. Surgery 1987;102(6):1009–1017.

107. Zollinger RM, Ellison EH. Primary peptic ulcerations of the jejunum associated with islet cell

tumors of the pancreas. Ann Surg 1955;142(4):709–723;discussion, 724–728.

108. Zollinger RM, Ellison EC, Fabri PJ, et al. Primary peptic ulcerations of the jejunum associated with

islet cell tumors. Twenty-five-year appraisal. Ann Surg 1980;192(3):422–430.

109. Ellison EC, Johnson JA. The Zollinger-Ellison syndrome: a comprehensive review of historical,

scientific, and clinical considerations. Curr Probl Surg 2009;46(1):13–106.

110. Wolfe MM, Jensen RT. Zollinger-Ellison syndrome. Current concepts in diagnosis and management.

N Engl J Med 1987;317(19):1200–1209.

111. Andersen DK. Current diagnosis and management of Zollinger-Ellison syndrome. Ann Surg

1989;210(6):685–703.

112. Maton PN, Vinayek R, Frucht H, et al. Long-term efficacy and safety of omeprazole in patients with

Zollinger-Ellison syndrome: a prospective study. Gastroenterology 1989;97(4):827–836.

113. Metz DC, Pisegna JR, Fishbeyn VA, et al. Currently used doses of omeprazole in Zollinger-Ellison

syndrome are too high. Gastroenterology 1992; 103(5):1498–1508.

114. Stabile BE, Morrow DJ, Passaro E Jr. The gastrinoma triangle: operative implications. Am J Surg

1984;147(1):25–31.

115. Sugg SL, Norton JA, Fraker DL, et al. A prospective study of intraoperative methods to diagnose

and resect duodenal gastrinomas. Ann Surg 1993; 218(2):138–144.

116. Frucht H, Norton JA, London JF, et al. Detection of duodenal gastrinomas by operative endoscopic

transillumination. A prospective study. Gastroenterology 1990;99(6):1622–1627.

117. Farley DR, van Heerden JA, Grant CS, et al. Extrapancreatic gastrinomas. Surgical experience. Arch

Surg 1994;129(5):506–511; discussion 511–512.

118. Chiarugi M, Pucciarelli M, Goletti O, et al. Outcome of surgical treatment for extrapancreatic

gastrinomas. Surg Gynecol Obstet 1993;177(2):153–157.

119. Norton JA, Alexander HR, Fraker DL, et al. Does the use of routine duodenotomy (DUODX) affect

rate of cure, development of liver metastases, or survival in patients with Zollinger-Ellison

syndrome? Ann Surg 2004; 239(5):617–625; discussion 626.

120. Arnold WS, Fraker DL, Alexander HR, et al. Apparent lymph node primary gastrinoma. Surgery

1994;116(6):1123–1129; discussion 1129–1130.

121. Norton JA, Alexander HR, Fraker DL, et al. Possible primary lymph node gastrinoma: occurrence,

natural history, and predictive factors: a prospective study. Ann Surg 2003;237(5):650–657;

discussion 657–659.

122. Richardson CT, Peters MN, Feldman M, et al. Treatment of Zollinger-Ellison syndrome with

exploratory laparotomy, proximal gastric vagotomy, and H2-receptor antagonists. A prospective

study. Gastroenterology 1985; 89(2):357–367.

123. Norton JA, Fraker DL, Alexander HR, et al. Surgery to cure the Zollinger-Ellison syndrome. N Engl J

Med 1999;341(9):635–644.

124. Norton JA, Jensen RT. Role of surgery in Zollinger-Ellison syndrome. J Am Coll Surg 2007;205(4

Suppl 1):S34–S37.

125. Cadiot G, Vuagnat A, Doukhan I, et al. Prognostic factors in patients with Zollinger-Ellison

syndrome and multiple endocrine neoplasia type 1. Groupe d’etude des neoplasies endocriniennes

multiples (GENEM and groupe de recherche et d’etude du syndrome de zollinger-ellison (GRESZE).

Gastroenterology 1999;116(2):286–293.

126. Lowney JK, Frisella MM, Lairmore TC, et al. Pancreatic islet cell tumor metastasis in multiple

endocrine neoplasia type 1: correlation with primary tumor size. Surgery 1998;124(6):1043–1048;

discussion 1048–1049.

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