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Chapter 10 / Liver Anatomy, Physiology, and Preoperative Evaluation
121
complete radiographic response in small tumors. However, this does not
mean there is complete pathologic response. Approximately 60% of “disap-
peared metastases” will recur if left unresected. One preoperative consid-
eration when treating multiple metastases of dierent sizes is the need for
ducial marker placement by interventional radiology for tiny lesions so
that if they disappear, the surgeon will know the original site to resect.
FIGURE 10.6 Preoperative portal vein embolization (PVE). Figure (A) shows preembolization
ow to right portal vein branches. Figure (B) shows stasis of portal vein ow after emboliza-
tion of the right portal vein and segment IV portal vein branches with microspheres and coils.
(Continued)
Section II / Liver122
Timing of Surgery and Treatment Sequencing Strategy
A key modiable risk factor for po sthepatectomy complications is the duration
of preoperative chemotherapy, most often used for CLM. Extended-duration
(4 months) chemotherapy only increases the risk of CALI and associated post-
operative complications without improving the pathologic response. us,
every patient with CLM who might be a candidate for surgery (including
patients with “initially unresectable” CLM who have bilateral disease, small
livers, or resectable extrahepatic disease) should be evaluated at diagnosis by a
multidisciplinary team that includes a liver surgeon. e goal of chemotherapy
for resectable lesions is not and should not be complete disappearance of the
CLM. Further chemotherapy can be given after recovery from hepatectomy.
FIGURE 10.6 (Continued) Figures (C) and (D) show the resultant hypertrophy from pre- to
postembolization.
Chapter 10 / Liver Anatomy, Physiology, and Preoperative Evaluation
123
A second method of decreasing morbidity is treatment sequencing
for synchronous CLM with intact primary colorectal cancer. e liver-rst,
or reverse, approach allows the cleaner operation to be done before resec-
tion of the primary tumor while removing the patient’s metastatic disease.
Used for patients with nonobstructing primary tumors, this is usually cho-
sen for patients requiring preoperative chemotherapy and larger hepatic
resections for CLM, which are the real life-limiting process (rather than
the primary lesion) for the patient. Concerns about the morbidity of major
colorectal operations, even proctectomies, staged after major hepatecto-
mies should not preclude reverse approach sequencing.
Frequently, patients with extensive bilateral liver disease require two-
stage hepatectomy. e rst stage involves clearing the left liver of small-
volume disease. e time in between stages is used for interval percutan eous
PVE to grow the FLR (Fig. 10.6). If there will be a signicant break in ther-
apy, one or two rounds of chemotherapy can be given without any negative
consequence on FLR hypertrophy. e second stage is often an extended
right hepatectomy to clear the remaining tumor burden. While this staged
sequencing is more time and resource consuming compared to single-stage
extended hepatectomy with contralateral ablation or wedge resections, it
provides a greater margin of safety for avoidance of PHI-related mortality.
Figure 10.6 demonstrates the right portal venography before and after PVE
with CT images before and after PVE-induced hypertrophy. With periopera-
tive chemotherapy, two-stage hepatectomy ± PVE can result in prolonged
5-year overall survival of 51% (Fig. 10.7).
FIGURE 10.7 Overall 65% survival in patients with advanced bilateral colorectal liver
metastases (median 6 metastases per patient) treated with chemotherapy and two-stage
hepatectomy. This survival was achieved in a subset of patients with advanced metastatic
disease by selecting patient candidate for surgery based a combination of response to
chemotherapy and adequate regeneration from portal vein embolization. (Reproduced from
Brouquet A, Abdalla EK, et al. High survival rate after two-stage resection of advanced
colorectal liver metastases: response-based selection and complete resection dene out-
come. J Clin Oncol 2011;29(8):1083–1090.)
Section II / Liver124
CONCLUSIONS
Over the past two decades, hepatectomy has evo lved into a safe and eective
therapy for a wide range of benign and malignant diseases. Postoperative
complications may be related to patient factors, anatomic factors associ-
ated with resection extent, or technical factors that result in major intra-
operative bleeding. Some patient-related factors (e.g., age, Child-Pugh
class, and body mass index) cannot be modied preoperatively. Others can
be reversed with prehabilitation and aggressive medical optimization to
increase the rescue rate of expected complications. e FLR volume and
the degree of hypertrophy after preoperative PVE are important predictors
of outcome and can help select appropriate patients for major hepatecto-
mies. Bleeding can be minimized with preoperative anatomic evaluation,
image-guided resection, low central venous pressure uid management,
and judicious use of modern surgical instruments. Proper preoperative
evaluation and surgical planning before hepatectomy can minimize surgi-
cal complications, PHI, and mortality.
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126
ETIOLOGY
Cirrhosis is a chronic liver disease that results in hepatic failure. Etiologies
of cirrhosis range from alcohol abuse to immune disorders to toxin expo-
sure. Regardless of its various causes, cirrhosis is caused by the destruction
of hepatic parenchyma with replacement by brosis and regenerative nod-
ules. Usually, the damage is done by multiple insults of various etiologies
that occur repeatedly over time. In addition to hepatic failure, cirrhosis can
lead to hepatocellular carcinoma (HCC). e complications of cirrhosis are
devastating and potentially life threatening. Unfortunately, once cirrhosis
occurs, the only cure is liver transplantation (LT).
Pathophysiology
Figure 11.1 details the evolution of cirrhosis. Hepatocytes are damaged by
an insult or disease, leading to destruction of hepatic parenchyma. Initially,
the liver’s ability for regeneration can lead to restoration of normal archi-
tecture; however, this capacity is nite. e exact mechanism leading to
impaired regeneration is poorly understood and remains a key question
in current clinical investigation. Impaired regeneration results in disrup-
tion of architecture, disturbance to blood supply, poor nutrient supply to
hepatocytes, and eventual inhibition of hepatocyte proliferation. Attempts
at healing this damage lead to brosis and eventual regenerative nodule
formation.
Stellate cells play an important role in the development of cirrhosis.
ey are found at the interface between the basolateral membranes of
hepatocytes and sinusoidal endothelial cells, in the space of Disse. eir
normal function is paracrine in nature, regulating hepatocyte and endothe-
lial cells as well as the storage of vitamin A. When hepatocytes are injured,
cytokine release results in hypertrophy and proliferation of stellate cells.
Eventually, the space of Disse becomes thickened with collagen deposits,
and the normal architecture of the fenestrated sinusoidal endothelium is
distorted. is leads to vascular distortion and portal hypertension.
Under normal circumstances, portal vein pressure ranges from 5 to
8mm Hg. Any pressure greater than 8mm Hg or a hepatic portal venous
gradient (HPVG) greater 5 mm Hg is dened as portal hypertension.
Practically, this measurement is taken via hepatic vein wedge pressure,
similar to a measurement of pulmonary arterial pressure using a Swan-
Ganz catheter. e normal venous drainage of the gastrointestinal tract is
through the portal vein, into the liver, out of the hepatic veins, into the infe-
rior vena cava (IVC), and then back to the heart. e portal vein is formed
by the splenic vein and superior mesenteric vein (SMV). Usually, the inferior
mesenteric vein (IMV) joins the splenic vein prior to its junction with the
SMV; however, this anatomy varies widely. With obstruction of ow at the
presinusoidal, sinusoidal, or postsinusoidal level, portal venous
p
ressure
Cirrhosis and Portal
Hypertension
Rachelle N. Damle and Shimul A. Shah
11
Chapter 11 / Cirrhosis and Portal Hypertension 127
increases and decompression occurs with ow back to the heart via col-
laterals. ese collaterals are generally thin walled and fragile and, with
increased ow, become varicosities. Given their fragility, varicosities rup-
ture easily and can cause life-threatening bleeding. Figure 11.2 depicts the
collaterals that can form with portal hypertension.
Causes
Table 11.1 lists the causes of cirrhosis. e most common cause of cirrhosis
in the world is viral hepatitis, but alcohol abuse is the most common cause
in the United States. Nonalcoholic fatty liver disease (with progression to
nonalcoholic steatohepatitis or NASH) is increasing in prevalence in the
United States and is linked with hyperlipidemia, non–insulin-dependent
diabetes, and obesity. Immune or inammatory cirrhosis due to cholesta-
sis is caused by primary biliary cirrhosis and primary sclerosing cholan-
gitis. Hemochromatosis, an inborn error in metabolism, leads to cirrhosis
secondary to lipid peroxidation of iron deposits in periportal regions of the
liver. Wilson disease is an inherited deciency in hepatocyte transport of
FIGURE 11.1 Evolution of cirrhosis. Fibrosis develops in nonregenerative necrotic areas,
producing scars. The pattern of nodularity and scars reects the type of response to injury
(e.g., uniform vs. nonuniform necrosis) and the extent of injury. (From Mulholland MW,
Lillemoe KD, Doherty GM, et al. Greeneld’s surgery: scientic principles & practice, 5thed.
Philadelphia, PA: Lippincott Williams & Wilkins, 2010.)
Section II / Liver128
FIGURE 11.2 Potential venous collaterals that develop with portal hypertension. The veins
of Sappey drain portal blood through the bare areas of the diaphragm and through paraum-
bilical vein collaterals to the umbilicus. The veins of Retzius form in the retroperitoneum
and shunt portal blood from the bowel and other organs to the vena cava. (From Mulholland
MW, Lillemoe KD, Doherty GM, et al. Greeneld’s surgery: scientic principles & practice,
5th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2010.)
Causes of Cirrhosis
TABLE
11.1
Viral
Alcoholic
Nonalcoholic steatohepatitis
Cholestasis
Extrahepatic
Stones
Extrinsic mass
Strictures
Primary sclerosing cholangitis
Intrahepatic
Primary biliary cirrhosis
Primary sclerosing cholangitis
Cystic brosis
Vanishing bile duct syndrome
Genetic disorders
Hemochromatosis
Wilson disease
Cystic brosis
α-Antitrypsin deciency
Glycogen storage disease
Venous outow occlusion
Budd-Chiari syndrome
Idiopathic
Chapter 11 / Cirrhosis and Portal Hypertension 129
copper into biliary tract, resulting in copper accumulation in the liver, once
again causing periportal inammation and eventual cirrhosis. Obstruction
of hepatic venous outow (Budd-Chiari syndrome) causes sinusoidal con-
gestion and hepatocyte necrosis and, eventually, cirrhosis. Hepatic venous
outow obstruction is associated with “nutmeg” appearance of the liver sec-
ondary to multiple small areas of hemorrhage.
DIAGNOSIS
As with any disease, a history and physical examination yield most of the
information needed to diagnose a patient with cirrhosis. Clues in the his-
tory include acknowledged alcohol abuse, hepatitis, toxin exposure, previ-
ous upper gastrointestinal bleeding, hemorrhoids, infections, and increased
abdominal girth. Classic physical exam ndings in a cirrhotic patient are
found in Table 11.2. Fetor hepaticus, bruising, decreased body hair, and pur-
pura are also physical signs associated with cirrhosis.
Diagnostic tests are indicated if the history and physical exam raise sus-
picion for liver disease. Laboratory evaluation includes hepatic panel, com-
plete blood count, chemistry panel, and coagulation prole. As mentioned
in earlier sections of this handbook, functional capacity of the liver is evalu-
ated by coagulation studies, platelet count, and bilirubin. Inability of the liver
to produce coagulation factors, thrombopoietin, and bilirubin will lead to
abnormal values of these labs. Markers of hepatocyte or cholangiocyte dam-
age are AST, ALT, and alkaline phosphatase. e term liver “function” panel
traditionally includes AST, ALT, alkaline phosphatase, bilirubin, and lactate
dehydrogenase. It is important to understand this misnomer of “function”
as these values do not all indicate the liver’s functional capacity. Importantly,
abnormal values are not specic for liver dysfunction and may even be normal
in the setting of hepatic disease.
In addition to laboratory values, imaging studies are commonly used
to further investigate a suspicion of liver dysfunction. Ultrasonography,
computed tomography, and magnetic resonance imaging (MRI) can detect
cirrhosis. Generally, these studies will reveal a nodular, atrophic liver and
splenomegaly. Ultrasound is nearly 90% sensitive and specic for diagnos-
ing cirrhosis. Cirrhotic livers demonstrate multiple nodular
irregularities
Physical Findings Incidence (%)
Palpable liver 96
Jaundice 68
Ascites 66
Spider angiomas 49
Dilated abdominal wall veins 47
Palpable spleen 46
Testicular atrophy 45
Palmar erythema 24
Noninfectious fever 22
Hepatic coma 18
Gynecomastia 15
Dupuytren contractures 5
From Mulholland MW, Lillemoe KD, Doherty GM, et al. Greeneld’s surgery: scientic principles &
practice. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2010.
Physical Findings in Cirrhosis
TABLE
11.2
Section II / Liver130
on the anterior surface of the liver distinct from the abdominal wall.
Fibrosis can be seen with disruption in parenchyma, though this is often
dicult to detect. Computed tomography and MRI are more expensive
modalities and do not yield any more information than ultrasound; how-
ever, they may reveal an atrophic liver, evidence of venous thrombosis, and/
or splenomegaly.
Invasive diagnostic methods (biopsy) denitively establish the diag-
nosis of cirrhosis; however, in the presence of strong clinical, laboratory,
and radiographic evidence, they are not necessary. Direct visualization
of the liver during an abdominal surgical procedure can reveal a nodular,
atrophic liver. Percutaneous, laparoscopic, or transjugular biopsy, as well as
image-guided ne needle aspiration, can be used. Histology will reveal fatty
inltration, balloon-cell degeneration, Mallory bodies, hepatocyte necrosis,
brosis, or features of cirrhosis.
Two methods of classifying liver disease severity are the Child-
Turcotte-Pugh (CTP) score and the Model for End-Stage Liver Disease
(MELD) score. ese prognostic models of disease severity are important
in operative planning and liver transplant allocation. e CTP score is the
best predictive score for most patients with cirrhosis and is used to deter-
mine risk of morbidity and mortality for surgical procedures (Table11.3).
Originally, the MELD score was developed to determine survival follow-
ing transjugular intrahepatic portosystemic shunt (TIPS) procedure. It
was then adopted as a prognostic indication of a patient’s 90-day sur-
vival with optimized medical management. Bilirubin, international nor-
malized ratio, and creatinine are the only values used in calculating the
MELD score, so it is a more objective system than CTP score. Because of
its objectivity, the MELD score is used as the main determinant of liver
transplant allocation in the UnitedStates.
CLINICAL MANIFESTATIONS
Renal
Complications of impaired renal function in the setting of cirrhosis are
caused by dysregulation of vascular tone. is results in sodium retention,
water retention, and ultimately hepatorenal syndrome (HRS) and renal fail-
ure. When ascites develops, there is an inability to excrete sodium. Water
retention follows sodium retention and is due to the inability of patients
with ascites to process free water. Excess water leads to dilutional hypona-
tremia, which may cause nausea, vomiting, lethargy, and seizures.
HRS is a complex complication of cirrhosis, characterized by renal
failure in the absence of intrinsic renal disease. Up to 10% of patients with
cirrhosis and ascites develop HRS. Signs of HRS include oliguria, increasing
serum creatinine level, rising cardiac output, proteinuria, and decreased
arterial pressure. e renin–angiotensin–aldosterone system is overactive,
and the renal cortex is markedly vasoconstricted. Prerenal azotemia is dif-
cult to distinguish from HRS, and laboratory values are similar in the two
Estimated Mortality Rates for Surgical Intervention by CTP
Score
TABLE
11.3
Child-Turcotte-Pugh (CTP) Score Mortality
A 10%–15%
B 30%–40%
C 75%–90%