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221
INTRODUCTION
Until the most recent two decades, hepatectomies were considered high-
risk operations with frequent hemorrhagic events and high rates of morbid-
ity and mortality that would be unacceptable by current standards. Even
as surgeons have become more aggressive with the extent and radicality of
hepatectomies, the overall mortality rate has decreased dramatically from
historical rates of 10% to 20% to around 2.5%. is mortality improvement
is due to better patient risk stratication and selection, optimization of the
future liver remnant (FLR), using portal vein embolization (PVE), limiting
preoperative chemotherapy toxicity, more advanced surgical techniques,
more experienced perioperative care, novel multidisciplinary sequenc-
ing strategies, and improved capabilities to rescue patients who develop
complications.
Although the hepatectomy mortality rate has decreased dramati-
cally, the rates of any morbidity (30% to 45% by retrospective analyses) and
of major morbidity (20% by the American College of Surgeons National
Surgical Quality Improvement Program, ACS NSQIP, analysis) still remain
clinically signicant. Major posthepatectomy complications include those
typical for major general surgery operations, such as bleeding, infected uid
collections, bile leaks, wound infections, cardiopulmonary events, organ
system failure, sepsis, and venous thromboembolism (VTE). Complication
rates often correlate with the extent of hepatectomy, making reports of
overall complication rates uninformative without specication of the types
of hepatectomy examined in these studies (Table 18.1).
ree complications specic to liver surgery are bleeding (intraopera-
tive and early postoperative), bile leak (and associated organ space infec-
tion), and postoperative hepatic insuciency (PHI, or liver failure) with
liver-related mortality. Generally, PHI can be split into “early” and “late”
phases, in which the late phase often leads to an irreversible cascade toward
liver-related mortality that can happen well past 30 p ostoperative days. Late
PHI mandates that surgeons look beyond the typical postoperative interval
of 30 days to completely capture all liver-related morbidity and mortality. In
fact, up to one-third of posthepatectomy deaths occur between 30 and 90
postoperative days.
Predictors of major complications can be divided into three catego-
ries—patient comorbidities, biochemical abnormalities, and perioperative
risk factors (including magnitude of operation). ese factors generally
include the American Society of Anesthesiologists (ASA) class, smoking,
elevated alkaline phosphatase, low albumin, elevated partial thrombo-
plastin time (PTT), extent of hepatectomy, intraoperative or postoperative
transfusions, and prolonged operative time. e last three factors are closely
related, and thus surgeons should be cautious about pairing major simulta-
neous operations with major hepatectomies. While not all risk factors are
Complications of Liver Surgery
Including Postoperative
Hepatic Insufciency
Ching-Wei D. Tzeng and Thomas A. Aloia
18
Section II / Liver222
completely reversible, certainly many are potentially modiable through
preoperative optimization of comorbidities and choosing operations of
lesser extent when oncologically feasible.
Besides the typically reported surgical quality outcomes of postopera-
tive complications and death, surgeons should also understand and further
study the secondary implications of major morbidity—failure to return to
preoperative performance status and failure to achieve intended oncologic
therapy. e long-term benets of the most extraordinary and aggressive
hepatectomy may be completely negated if the patient loses his or her inde-
pendence and becomes bound to a nursing home, is unable to return to his
or her previous functional state, or is unable to complete his or her planned
adjuvant cancer therapy.
e goal of this chapter is to describe the diagnosis, management, and
risk factors for three major liver-related complications specically associ-
ated with hepatic resection.
INTRAOPERATIVE AND POSTOPERATIVE HEMORRHAGE
Denition
Historically, hemorrhage has been the most feared complication of hepatec-
tomy. “Bleeding” broadly encompasses a range of complications including
catastrophic intraoperative hemorrhage, intraoperative bleeding requiring
intraoperative and recovery room transfusions, postoperative hemorrhage
requiring transfusions or even return to the operating room, symptomatic
anemia requiring postoperative transfusions, or small drops in hemoglobin
with no clinical sequelae.
Based on retrospective institutional reports, the posthepatectomy hem-
orrhage (PHH) rate ranges from 1% to 8%. Because of its broad denition,
the International Study Group of Liver Surgery (ISGLS) attempted to dene
PHH based on transfusion requirement and clinical severity. e proposed
denition is a hemoglobin drop greater than 3g/dL after completion of sur-
gery and/or transfusion for any postoperative hemoglobin drop and/or inva-
sive intervention (interventional radiology [IR] or surgery) to stop bleeding
(Table 18.2). Detection of hemorrhage can be via frank blood loss apparent in
perihepatic drains (drain uid hemoglobin >3g/dL), examination consistent
All Partial Left Right Extended
Organ space infection
a
6.0% 4.5% 5.2% 7.8% 10.9%
Pneumonia
a
4.0% 3.1% 3.5% 5.5% 7.0%
Ventilator >48h
a
4.4% 3.2% 3.0% 6.7% 7.4%
Acute renal failure 1.5% 1.0% 0.4% 3.1% 2.2%
DVT
a
2.0% 1.3% 1.7% 2.7% 5.2%
PE
a
1.6% 1.2% 0.4% 2.5% 3.5%
Sepsis
a
6.7% 5.7% 5.2% 8.4% 9.6%
Cardiac arrest 1.1% 0.7% 0.4% 2.0% 1.7%
Myocardial infarction 0.3% 0.4% 0% 0.4% 0.4%
Return to OR 4.8% 3.4% 4.8% 7.3% 7.9%
Death 2.5% 1.8% 0.9% 3.7% 5.2%
a
Complication rates increased with the extent of hepatectomy (p<0.05)
Columns divided by magnitude of hepatectomy; DVT, deep venous thrombosis; PE, pulmonary
embolus; OR, operating room.
Common 30-Day Posthepatectomy Complications
TABLE
18.1
Chapter 18 / Complications of Liver Surgery Including Postoperative Hepatic Insufciency 223
Denition Grade A Grade B Grade C
Post-hepatectomy
hemorrhage (PHH)
>3g/dL fall in hemoglobin or any
postoperative transfusion for bleeding or
reintervention for bleeding
≤2 units PRBC >2 units PRBC Requires intervention
(IR or surgery)
Posthepatectomy bile leak Drain bilirubin 3× serum bilirubin on or after
POD3 or biloma requiring radiologic or
operative intervention or bile peritonitis
No change from routine
care plan
Requires nonoperative
invasive intervention
Requires surgical
intervention
Posthepatectomy liver
failure or Postoperative
hepatic insufciency (PHI)
Impairment of liver synthetic, excretory, and
detoxifying abilities on or after POD5 or
elevation in INR or bilirubin
No change from routine
care plan
Clinical care deviates
from routine course
Requires intervention
(IR or surgery)
PRBC, packed red blood cells; IR, interventional radiology; POD, postoperative day; INR, international normalized ratio.
International Study Group on Liver Surgery Denitions of Posthepatectomy Complications
TABLE
18.2
Section II / Liver224
with intra-abdominal hematoma, or active bleeding with any radiographic
diagnosis. e ISGLS denition of PHH is specic to the postoperative period
and does not include patients who receive up to 2 units packed red blood
cells (PRBC) immediately after surgery in the recovery room. Functionally,
PHH is split into three grades, A to C. Grade A PHH is dened as transfusion
of ≤2 units PRBC with no signicant change in clinical management. Grade
B PHH corresponds to transfusion of greater than 2 units PRBC, often with
changes in management including further radiographic evaluation. Bleeding
that requires any invasive intervention is categorized as grade C. Import antly,
grades B and C PHH can be associated with mortality rates as high as 17%
and 50%, respectively.
e ACS NSQIP denes major postoperative transfusion as admin-
istration of greater than 4 units PRBC after leaving the operating room.
Currently, the national rates of any intraoperative transfusion, greater than
4 units intraoperative PRBC transfusion, and major postoperative transfu-
sion greater than 4 units PRBC are 26.4%, 9.0%, and 0.8%, respectively. is
nationwide sample suggests that a signicant intraoperative use of blood
products exists, but the major PHH seems to be rare.
Diagnosis and Management
e diagnosis of bleeding or hemorrhage involves clinical evaluation sup-
plemented by laboratory data, drain output (if available), and radiographic
imaging when indicated. Clinically, the patient may rst develop tachycar-
dia (unless beta-blocked) and/or oliguria, with hypotension and diapho-
resis only coming later as worsening hypovolemic shock ensues. As it is
atypical for a postoperative liver surgery patient to need a large volume of
intravenous uid, if a patient has required several uid boluses in the early
postoperative period, a necessary workup into reasons for hypotension
or low urine output is required. While ruling out extrinsic causes (exces-
sive narcotics or epidural anesthesia) and cardiovascular events, bleeding
should be high in the dierential. As bleeding becomes more likely, the
question turns to clinical signicance.
e abdominal examination may not be helpful as most patients will
have incisional tenderness. e exception is with massive hemoperito-
neum that should be readily apparent and warrants urgent measures. A
change in the character of the abdominal drain uid to a more sanguin-
eous consistency may be a sign of bleeding that can be conrmed with
serum and drain hemoglobin measurement. While the ISGLS PHH de-
nition includes drain hemoglobin of greater than 3g/dL, in many cases
when active bleeding is apparent, no uid sample is needed to secure the
diagnosis. e criteria for transfusion depend on the severity of anemia
(serum hemoglobin <7 g/dL or relative drop that is hemodynamically
relevant), the degree of coagulopathy, and the patient’s overall condi-
tion. Given the evidence that transfusions may be associated with post-
operative complications, which may in turn be detrimental to oncologic
outcome, routine transfusions should be discouraged unless warranted
by hemodynamic compromise with end-organ dysfunction. A contained
hematoma does not require immediate intervention if tamponade stops
further bleeding. In a stable patient with clinical evidence of bleeding,
radiographic imaging with angiography (either by IR angiogram or by
computed tomography [CT], angiogram) may allow for diagnosis and
therapeutic intervention. However, if the patient is unstable or if IR can-
not arrest the bleeding, then a return to the operating room is necessary.
Laboratory values including platelet count, prothrombin time (PT), PTT,
and brinogen help guide the resuscitation and replacement of decient
coagulation factors.
Chapter 18 / Complications of Liver Surgery Including Postoperative Hepatic Insufciency 225
Preoperative and Intraoperative Considerations
Preoperative risk factors for major postoperative transfusion needs
(dened by ACS NSQIP as >4 units PRBC) include preoperative bleeding
disorder, ASA class ≥3, low albumin, and preoperative anemia. Right and
extended hepatectomies are also at greater risk for PHH. One of the key
reasons mortality from hemorrhage is now less common is better under-
standing of hepatic vascular anatomy and more advanced parenchymal
transection techniques, either with or without inow control. e numer-
ous methods of parenchymal dissection and transection are discussed in
Chapter 13. A few salient technical issues are reviewed here. Although the
general use of stapling devices for parenchymal transection may be associ-
ated with higher bleeding rates, the targeted use of endovascular staplers to
control vascular pedicles may increase the speed and safety of liver surgery.
Newer tissue dissectors, including ultrasonic and water-jet devices, facili-
tate precise parenchymal dissection to identify vascular and biliary struc-
tures, which can be clipped or tied precisely rather than blindly transected
without ligation. Tissue-sealing devices, borrowed from minimally invasive
surgery, also aid in coagulation of the parenchymal before division.
Good planning and communication with the anesthesia team before
and during surgery facilitate the safety of hepatectomy. During the time-
out process, a discussion among the surgeon, nursing sta, and anesthe-
sia team, of the extent of hepatectomy, plan for inow clamping (Pringle
maneuver), predicted blood loss, and blood product availability and anti-
body status, can decrease intraoperative surprises.
e concept of “low central venous pressure (CVP) anesthesia” is rec-
ommended for liver resections. is concept is critical to reducing intra-
operative hemorrhagic events. However, accurate monitoring of CVP does
not require a central venous catheter. Regardless of the method of intra-
vascular volume monitoring, intravenous uid administration should
remain low (the surgeon can aid in monitoring this by examining the infe-
rior vena cava) until the transection is completed. Keeping the CVP low
signicantly reduces venous bleeding during the parenchymal transection.
Laparoscopic liver surgery has been associated with decreased blood loss
because the required pneumoperitoneum decreases venous oozing from
the parenchymal surface. e use of stay stitches to elevate the liver out
of the abdominal cavity (with laparotomy pads behind the mobilized liver)
may elongate and compress hepatic veins, decreasing venous bleeding dur-
ing transection.
Regardless of the parenchymal dissection and transection technique,
after the resection, the liver edge should be carefully inspected for vessels or
bile ducts that were not adequately ligated. A gentle Valsalva maneuver by
the anesthesia team can expose hepatic vein tributary bleeding, which may
require suture ligation. e role of topical hemostasis to the liver transection
bed with cautery, coagulant sheets, or brin glue is frequently debated. With
no overt bleeding sites, some surgeons leave the surface alone, arguing that
a viable liver edge may help decrease postoperative bile leak. Others cauter-
ize the entire cut surface with or without placement of a hemostatic agent
( brin glue or cellulose netting/gauze) applied to the surface. Others take
the time to develop and place an omental ap to cover the raw liver surface.
Although the elements that contribute to major bleeding events in
liver surgery are complex, an operative strategy that identies and controls
major hepatic vein tributaries and portal triad branches before and during
the parenchymal dissection is the best way to avert major bleeding (and
not coincidentally bile leak as well). Such a strategy is facilitated by care-
ful preoperative planning that includes a thorough understanding of the
patient’s liver anatomy including the relationship of the liver vasculature
Section II / Liver226
to the target lesion(s). High-quality three-phase liver protocol CT scan or
high-resolution magnetic resonance imaging (MRI) is important. General
abdominal CT scans (such as those ordered during emergency room evalu-
ation for abdominal pain) are inadequate and may be dangerous if used as
a guide. Intraoperative ultrasound is also essential to permit exact dissec-
tion along the correct planes. is precise dissection balances adequate
oncologic margins with maximal parenchymal sparing when possible,
dividing only the necessary vessels and biliary pedicles. While bleeding risk
cannot be fully eliminated, with adequate understanding of the patient’s
liver anatomy, good communication with the entire operating room team,
and proper use of available intraoperative surgical technology, the risk of
intraoperative and postoperative hemorrhage can be purposefully reduced
to minimal rates.
BILE LEAK AND ORGAN SPACE INFECTIONS
Denition
Despite an overall decrease in posthepatectomy complications during
the past two decades, the problem of bile leak still remains unsolved. In
modern series, the incidence of postoperative bile leak ranges from 2% to
33%, depending on the reported series, denition, and extent of hepatec-
tomy. Like high-grade PHH, high-grade bile leak remains a major cause
of associated morbidity, often leading to longer hospitalization, increased
health care costs, prolonged disability with abdominal drains, and the need
for additional procedures. e mortality associated with bile leak can be
as high as 39%. Data on rates of bile leak are varied because like PHH, a
variety of bile leak denitions have been used. Some perihepatic uid col-
lections remain undrained and are treated with antibiotics only, further
limiting the ability to accurately label them as “bilomas” in retrospective
series. However, after liver resection, most organ space infections can be
presumed to be bilomas or bile leaks.
e ISGLS convened an expert panel to dene three grades of bile
leak after hepatectomy. Mirroring the trend to grading surgical complica-
tions based on clinical sequelae rather than arbitrary laboratory values of
bilirubin or international normalized ratio (INR), the ISGLS divided bile
leaks into three categories. Bile leak was globally dened as a drain biliru-
bin at least three times the serum bilirubin on or after postoperative day
3, a biloma requiring radiologic or operative intervention, or clinically evi-
dent bile peritonitis. Grade A bile leak does not aect clinical management.
Grade B requires a deviation in typical postoperative management such as
a percutaneous drainage, but does not require surgery. Grade C bile leaks
require a return to the operating room and are associated with extremely
high mortality rates.
Diagnosis and Management
e management of a bile leak can be summarized by the singular impor-
tance of timely diagnosis and drainage if needed. Delays in diagnosis and
drainage only feed the inammatory cascade by allowing sepsis to trigger a
systemic inammatory response syndrome. In general, with proper external
drainage and control of infection with antibiotics, bile leaks will heal with
time as the surgical bed recovers from operative trauma. When left unat-
tended and discovered late, bile leaks can be highly morbid requiring longer
hospitalizations, more interventions, and transfers to higher-acuity beds.
Bile leaks with high mortality rates are typically from associated complica-
tions. As an example of its signicant downstream eects, organ space infec-
tion is the risk factor most strongly associated with posthepatectomy VTE.
Chapter 18 / Complications of Liver Surgery Including Postoperative Hepatic Insufciency 227
Bile leak, also known as biloma or biliary stula, can be diagnosed
by several methods depending on the timing, severity, and presence or
absence of an intraoperatively placed surgical drain. In the presence of a
drain, the character of the uid, which, if necessary, can be tested for bili-
rubin, can readily diagnose bile leak. By the ISGLS denition, a uid bili-
rubin three times the serum bilirubin constitutes a bile leak. If the drain
works well and there is no evidence of sepsis from an undrained biloma,
then no further imaging is necessary. e drain is simply left in place when
the patient is discharged from the hospital until the uid output drops to a
minimum. Antibiotics are not necessary in the absence of sepsis, abdomi-
nal wall infection, or undrained organ space infection. If the drain output
does not decrease with short-term outpatient management, then either an
endoscopic retrograde cholangiopancreatogram (ERCP) or percutaneous
transhepatic cholangiogram (PTC) is warranted to study where the leak is
coming from (central vs. peripheral bile ducts) and to place a biliary stent
to increase preferential bile drainage toward its natural outow tract (duo-
denum or enteric anastomosis). Neither ERCP nor PTC needs be reexively
ordered when bile leak is rst diagnosed and drain output has not yet been
dened, because both ERCP and PTC have their associated risks.
If no surgical drain is present or if the bile leak is diagnosed after the
drain has been removed, then CT is warranted to identify the location of the
uid collection. Because these bile leaks have been undrained for several
days, the patients will often present with pain, fever, leukocytosis, nausea,
ileus, and/or abdominal discomfort. Associated right pleural eusions may
also occur. With systemic symptoms and leukocytosis, antibiotics are usually
necessary. Antibiotics may be quickly tailored based on culture data. e CT
allows the surgeon to determine if IR can access the presumed biloma and
place a percutaneous drain. CT is important because it can help dierenti-
ate infected uid collections with a rind or air bubbles versus benign uid
collections that are likely seromas not requiring drainage. In some cases,
liver compression by a perihepatic uid collection can be appreciated and
helps to identify an ongoing bile leak “under pressure” (Fig. 18.1). Because of
their later diagnosis, these patients usually require a short inpatient admis-
sion for CT, percutaneous drainage, and antibiotics. After the sepsis is con-
trolled, they can be discharged and managed in a similar fashion as patients
who had a bile leak diagnosed by a surgically placed drain. Treatment of bile
leak includes timely diagnosis, control of sepsis through adequate drainage,
and conrmation (clinically or radiologically) of preferential anatomic ow
of bile toward the duodenum or through an enteric anastomosis.
Preoperative and Intraoperative Considerations
Perioperative risk factors for bile leak include bile duct resection/recon-
struction, extended hepatectomy, repeat hepatectomy, need for en bloc
diaphragm resection, and intraoperative transfusion. e surgeon should
utilize a preoperative high-quality CT or MRI to dene the planned extent
of resection. Part of the resection plan should include the strategy for
extrahepatic versus intrahepatic bile duct division. Using hilar cholangio-
carcinoma as an example, the extent of biliary resection, the level of recon-
struction, and the type of anastomosis should be anticipated. Preoperative
planning can help prevent both unplanned division of the contralateral
hepatic duct and accidental injury of hepatic duct tributaries, which can
lead to catastrophic postoperative bile leaks.
After the resection, the transected liver surface and the hepatic duct
division line are visually inspected for any bile staining. e liver itself
should also be inspected for areas where the capsule has been sheared o
or for areas with lacerations from retraction injury, as these can be the sites
Section II / Liver228
of subsequent bile leaks. A number of posttransection cholangiogram tech-
niques have been described in the literature. ese methods include intra-
ductal injections of uoroscopic contrast (conventional cholangiography),
saline, methylene blue, “white” fat emulsion, indocyanine green (ICG), or
air (at our institution) for the intraoperative detection and repair of poten-
tial postoperative bile leaks. As with PHH prevention, some surgeons use
various forms of hemostatic agents to “seal” the transection surface, and
omental aps can be used, although little evidence exists to support either
practice in the prevention of bile leaks. ere is also no consensus on the
role of surgical drain placement. Some surgeons routinely place drains,
even for partial hepatectomies. Others reserve drains for higher-risk opera-
tions such as major/extended hepatectomies or those with biliary–enteric
anastomoses, while others do not routinely drain any hepatectomies.
When drains are placed, they should be removed at the earliest possible
time when they no longer function as a reliable indicator of bleeding or bile
leak (usually 2 to 4 days). In summary, because bile leak remains a major
source of potentially preventable morbidity, mortality, cost, and disability,
surgeons should strive to develop a systematic preventative approach to the
intraoperative identication of bile leaks and to be vigilant about the early
detection of bile leaks in the postoperative setting.
POSTOPERATIVE HEPATIC INSUFFICIENCY AND
LIVER-RELATED MORTALITY
Denition
After liver resection, the least reversible complication in the recovery
period is PHI, or posthepatectomy liver failure. Its clinical consequences
range from mild biochemical derangements with no change in routine
postoperative course to irreversible liver failure with death. Ultimately,
PHI is related to inability of the FLR to perform the functions of protein
FIGURE 18.1 Posthepatectomy biloma. Liver compression by a posthepatectomy uid col-
lection can be appreciated and helps to identify an ongoing bile leak “under pressure.”
Chapter 18 / Complications of Liver Surgery Including Postoperative Hepatic Insufciency 229
synthesis, biliary drainage, and ltration. But, PHI can be divided into early
and late postoperative manifestations, each with its own risk factors. Early
PHI is from insucient FLR volume or acute liver injury that prevents the
FLR from tolerating the immediate surgical and postoperative stress. is
injury can include intraoperative liver ischemia from long inow occlusion
intervals without adequate reperfusion, perioperative major blood loss,
and/or perioperative systemic hypotension, which combined with mar-
ginal FLR volume can lead to early liver failure. Beyond the acute phase of
recovery, late failure is associated with insucient FLR regeneration. Most
commonly, this phenomenon is related to intrinsic parenchymal injury
from preoperatively underrecognized cirrhosis, steatohepatitis, and/or
extended-duration chemotherapy.
In general, PHI is dened by the ISGLS as the impairment of the liv-
er’s synthetic (INR), excretory (bilirubin), and detoxifying functions. e
ISGLS avoided the use of arbitrary serum laboratory values in their deni-
tion, focusing instead on three grades of clinical sequelae. Grade A causes
no change in routine postoperative care. ese patients might have mild
cholestasis, which does not aect their activities of daily living or their dis-
charge planning. Grade B PHI requires some deviation from the routine
clinical course. Grade C PHI requires invasive intervention.
A more clinically relevant denition of PHI was proposed in a retro-
spective international study of over 1,000 patients from three institutions
undergoing hepatectomy of ≥3 segments. PHI was dened as a peak
total bilirubin greater than 7mg/dL, which had a sensitivity and speci-
city of greater than 93% and an odds ratio of 10.8 for predicting 90-day
mortality. e authors found this cuto to be a better predictor of liver-
related mortality than previous combinations of hyperbilirubinemia
with elevated PT.
Diagnosis and Management
ere are a limited number of eective therapies to rescue patients from
severe liver failure after hepatectomy. If PHI is suspected, the management
includes ruling out biliary obstruction and biloma as reasons for increased
serum bilirubin. If the serum bilirubin remains high despite a patent bile
duct or biliary anastomosis, then cholestasis from PHI is the diagnosis. In
this state, patients are especially tenuous and unlikely to tolerate further
physiologic insults such as sepsis. As liver regeneration is dependent on
nutrition and a lack of sepsis, nutritional support and timely treatment of
any infections are especially important for recovery. Burdened by ascites,
many patients will need diuresis to control their abdominal symptoms and
to facilitate their ability to participate in activities of daily living. If there
is no sepsis and no further need for inpatient management, these patients
can be followed as outpatients. Labs every few days to weekly are sucient
to measure the trends, but it may take weeks to months for the late PHI to
resolve. If the liver function tests and bilirubin do not eventually plateau,
then death from liver failure is inevitable.
Preoperative and Intraoperative Considerations
Given the limited ability to reverse PHI, the best management of this com-
plication is prevention. To avoid this complication, the surgeon must focus
on preoperative planning and intraoperative considerations in choosing
the extent of hepatectomy based on the FLR size and functional capac-
ity. e FLR is the predicted volume of liver after resection, and adequate
size, synthetic function, biliary drainage, and regenerative capacity are
the keys to avoiding both early and late PHI. Based on a patient’s calcu-
lated total liver volume (TLV) standardized to body surface area (BSA)
Section II / Liver230
(TLV cm
3
=−794.41+1,267.28×BSA m
2
), the predicted FLR is compared as
a ratio to this standardized TLV calculation to yield the standardized FLR.
Generally, the required minimum standardized FLR is greater than 20% for
normal livers, greater than 30% for livers with limited parenchymal injury
such as from chemotherapy, and greater than 40% for permanently dam-
aged livers such as those with cirrhosis. A number of modiable risk factors
may decrease PHI from inadequate FLR.
Arguably, the greatest advance in preventing early and late PHI in the
past decade has been greater utilization of PVE before a major/extended
hepatectomy. With increased availability of CT volumetry, the FLR volume
can be accurately calculated down to the decimal point, and “eyeballing”
a CT scan to estimate FLR is now discouraged. Up to 10% of patients at
initial presentation have insucient FLR for a right hepatectomy, and as
many as 75% will have an inadequate FLR for an extended right hepatec-
tomy. In practice, the real number is higher for both, because these calcu-
lations were based on patients with normal liver parenchyma and normal
FLR volume requirements.
One may think of PVE as a functional test of the FLR that allows
assessment of regenerative capacity prior to committing to hepatic resec-
tion. During the time between PVE and hepatectomy, surgeons can study
both the degree of hypertrophy (DH, needs to be >5% points) and the kinetic
growth rate (KGR=DH divided by time in weeks) of the FLR. Importantly,
the technical aspects of PVE should be carefully considered to achieve max-
imum hypertrophy. With complete PVE of the right portal vein and segment
IV branches with spherical microparticles and coils, an FLR hypertrophy of
up to 69% can be expected.
In some cases with bilateral and/or multifocal disease, safe hepatec-
tomy cannot be accomplished with a single operation. In this setting, the
two-stage approach, with rst-stage partial left hepatectomy, followed by
percutaneous PVE, and second-stage extended right hepatectomy, has
achieved excellent oncologic outcomes. As it facilitates extensive liver
resection while limiting PHI, it is important to add the two-stage approach
to the surgeon’s armamentarium.
A major modiable risk factor for late PHI is the duration of preop-
erative chemotherapy given to patients with liver tumor. e goal of pre-
operative chemotherapy should not be “optimal response” with complete
disappearance of the liver lesions because extended-duration chemo-
therapy (>8 cycles) can increase the risk of chemotherapy-associated liver
injury (CALI) and postoperative complications. Steatohepatitis from irino-
tecan (usually in patients with metabolic syndrome phenotype) is particu-
larly important as it is the only CALI associated with increased mortality
from PHI. is may be a key consideration when choosing neoadjuvant
treatment with between FOLFOX and FOLFIRI. All of the aforementioned
modiable factors require preoperative planning by the surgeon in the con-
text of a multidisciplinary discussion with medical oncologists, patholo-
gists, hepatologists, and radiologists.
OUTCOMES/FOLLOW-UP
Posthepatectomy complications have signicant short-term and long-
term consequences. Certainly, the most impactful short-term complica-
tion is death, but fortunately, mortality from hepatectomy is infrequent.
Early mortality from PHH is rare because of improved knowledge of liver
anatomy, better preoperative imaging, intraoperative ultrasound, and bet-
ter parenchymal dissection/transection tools. Late PHI-related mortality
is better understood, and the necessary preoperative preventative steps