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162 H. J. Bonenkamp
Treatment of the Leakage Site
Although abscess drainage may be sufficient
treatment in cases where communication with
the gastrointestinal tract is minimal, in most patients, this creates an enterocutaneous fistula and
the leakage of enteric fluid should be stopped as
well. After gastric surgery, leakage of saliva and
gastric juice can usually be prevented by nasogastric or nasoesophageal drainage. Only in rare
cases cervical esophageal diversion is needed.
Attempts to repair the leakage site during
surgery are usually ineffective and may actually
increase the risk of postoperative complications.
Small leaks do not require repair, and large leaks
are often caused by ischemia. In these patients,
complete resection of the anastomosis and creation of a new conduit should be postponed until
later.
There is increasing expertise with endoscopic
treatment of upper gastrointestinal (GI) leakage. Endoscopic clips, fibrin glues, and stents
are used frequently, and often successfully [13,
14]. There are, however, no comparative studies
of conservative or endoscopic management of
esophagojejunal leakage, and there are no clear
recommendations for either treatment [15]. Stent
placement in a hemodynamically unstable patient
may be difficult, although there seems to be no
additional perforation risk [16]. Smaller leaks are
usually covered easily, but these leaks probably
heal with conservative measures as well. In case
of a large leak, the stent may not cover all leakage, although additional stent-in-stent procedures
have been described. There seems to be no difference between self-expanding wall stents and
plastic stents, and the choice for these depends
on local availability and expertise [15]. Stent dislocation is a rare but threatening event, and stents
need to be removed after 4–6 weeks in order to
prevent ischemia and necrosis.
In cases where leakage is confirmed by CT,
we will always evaluate the endoscopic options.
Small leaks (arbitrarily less than 2 cm) are usually treated conservatively with nasogastric suction, but for larger leaks without signs of ischemia
stent placement is first choice. Fibrin glue and
endoscopic clips are only used in patients where
conservative management was unsuccessful.
Duodenal Stump Leakage
Blowout of the duodenal stump after total gastrectomy is a serious complication. Bile leakage
into the peritoneum causes ascites because of a
chemical peritonitis. If bacterial contamination is
present, this will soon develop into an infectious
peritonitis with severe sepsis. Furthermore, bile
will activate pancreatic trypsin, which is even
more irritating to the peritoneum. Apart from
leukocytosis, elevated bilirubin with mildly elevated alkaline phosphotase is a prominent laboratory finding. Ascites and the infiltration of the
duodenal stump will be recognized on CT, and
as soon as duodenal stump leakage is diagnosed,
general treatment of peritonitis with broad spectrum antibiotics and fluid replacement would be
started. Because of the irritation of the peritoneum, percutaneous drainage alone is often not
sufficient to treat the peritonitis. Furthermore,
drainage of the leakage site alone will result in
a long-lasting enterocutaneous fistula. Surgical
irrigation and drainage should be considered in
all patients that fail to improve after initial percutaneous drainage. During surgery, the aboral
jejunojejunal anastomosis can be checked for
stenosis, since that might be the reason for the
blowout of the duodenal stump. Decompression
of the duodenum can be achieved by a retrogade
drain from the jejunum into the duodenal stump,
fixed with Witzel’s sutures for easy removal after
4–6 weeks. Together with a drain at the failed
stump, this will result in a much quicker healing
process.
Summary
Treatment of an anastomotic leakage after gastrectomy requires swift action with antibiotics
and hemodynamic support. Detection of the leakage site by multislice CT is reliable, and it guides
immediate percutaneous drainage. Surgical
drainage is only needed if radiological drainage
16316 Postoperative Complications After Surgery for Gastric Cancer: Anastomotic Leakage
Fig.16 .1 Treatment algorithm
is declined due to interposition of other organs.
Small leaks may be managed with nasogastric
drainage. For larger leaks, temporary endoscopic
stent placement is a viable option. A treatment algorithm is shown in Fig. 16.1.
164 H. J. Bonenkamp
Five Key Points to Avoid Anastomotic Leakage
• Optimize pre- and postoperative calorie intake.
• Correct co-morbidities.
• Make a tension-free anastomosis with vital
tissue.
• If the anastomosis is not perfect, redo.
• Avoid postoperative NSAIDs.
Five Key Points to Diagnose and Manage Leakage
• If signs of abdominal infection are seen post-
operatively, start general treatment with anti-
biotics and hemodynamic support and order
CT scan with the possibility to drain any leak-
age or abscess.
• Percutaneous drainage is preferable if techni-
cally feasible.
• Duodenal stump leakage requires surgical
drainage, abdominal irrigation, and decom-
pression of the duodenum.
• Small anastomotic leaks can be managed with
percutaneous drainage and nasoesophageal
decompression.
• Large anastomotic leaks may require endo-
scopic stent placement.
References
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Terashima M. Poor survival rate in patients with post-
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16516 Postoperative Complications After Surgery for Gastric Cancer: Anastomotic Leakage
Part III
Hepatobiliary and Pancreatic Surgery
Postoperative Hepatic
Insuciency
Junichi Shindoh and Jean-Nicolas Vauthey
17
Introduction
With advances in hepatobiliary surgery and perioperative care, the number of patients undergoing major or extended hepatectomy is increasing.
In patients for whom these procedures are being
considered, the risk of postoperative hepatic insufficiency (PHI) should be carefully assessed.
PHI is closely associated with a small future liver
remnant (FLR) and the quality of the underlying liver. Consequences of PHI include nonobstructive jaundice, ascites, coagulopathy, and increased susceptibility to complications. Patients
with PHI are at high risk of death from liver failure and require prolonged hospitalization. Therefore, assessment of the risk of PHI and prevention of PHI are critical for safe performance of
major or extended hepatic resection.
J.-N. Vauthey ()
Department of Surgical Oncology, Anderson Cancer
Center, 1515 Holcombe, Unit 1484, HoustonTX 77030,
USA
e-mail: jvauthey@mdanderson.org
J. Shindoh
Hepatobiliary-Pancreatic Surgery Division,
Toranomon Hospital, 2-2-2 Toranomon,
Minato-ku, 105-8470 Tokyo, Japan
e-mail: shindou-tky@umin.ac.jp
Definition of PHI
At present, there is no standardized definition
of postoperative severe liver dysfunction. The
International Study Group of Liver Surgery defined posthepatectomy liver failure as “a postoperative acquired deterioration in the ability of
the liver to maintain its synthetic, excretory and
detoxifying functions, which are characterized
by an increased international normalized ratio
and concomitant hyperbilirubinemia on or after
postoperative day 5” (Table 17.1) [1]. However,
these criteria are complex, partly subjective, and
difficult to quantify.
In addition, PHI should sensitively predict
postoperative mortality from liver failure. Therefore, the definition of PHI should not include
clinical outcomes or ongoing treatment. Among
the various definitions of PHI reported in the
previous studies, the so-called 50–50 criteria [2]
(prothrombin time < 50 % and serum bilirubin
level > 50 μmol/L on postoperative day 5) and
our definition of PHI [3] (peak postoperative
total bilirubin level > 7 mg/dL) are simple and
promising objective criteria based on studies including large numbers of patients.
In a multiinstitutional study of 1059 patients
without cirrhosis, receiver operating characteristics curve analyses revealed that a peak total
bilirubin level of greater than 7 mg/dL was the
most sensitive predictor of death from liver failure, with an area under the curve of 0.982 (95 %
CI, 0.964–0.999) and a cutoff value of 7.0 mg/dL
(sensitivity, 93.3 %; specificity, 94.3 %; accuracy,
T. M. Pawlik et al. (eds.), Gastrointestinal Surgery, DOI 10.1007/978-1-4939-2223-9_17,
© Springer Science+Business Media New York 2015
169
170 J. Shindoh and J.-N. Vauthey
Table 17.1 International Study Group of Liver Surgery grading criteria for posthepatectomy liver failure. (Reprinted
with permission from [1] Elsevier 2010)
Grade A Grade B Grade C
Specific treatment Not required Fresh frozen plasma Transfer to intensive care unit
Albumin Circulatory support (vasoac-
Daily diuretics Hemodialysis
Noninvasive ventilation Intubation and mechanical
Transfer to intermediate care
unit or intensive care unit
Hepatic function Adequate coagulation (INR
Renal function Adequate urine output
Pulmonary function Arterial oxygen satura
Additional evaluation Not required Abdominal ultrasonogra-
BUN blood urea nitrogen, CT computed tomography, INR international normalized ratio
<
1.5)
No neurological symptoms Beginning of neurologic
(≥ 0.5 mL/kg/h), BUN
< 150 mg/dL, no symptoms
of uremia
tion
> 90 %. May
gen supply via nasal cannula
or oxygen mask
-
have oxy-
Inadequate coagulation (INR
≥ 1.5, < 2.0)
symptoms (i.e., somnolence,
confusion)
Inadequate urine out-
0.5 mL/kg/h),
put (≤
BUN < 150 mg/dL, no symptoms of uremia
Arterial oxygen saturation
< 90 % despite oxygen
supply via nasal cannula or
oxygen mask
phy/CT, chest radiography,
sputum, blood, urine culture,
brain CT
tive drugs)
ventilation
Extracorporeal liver support
Rescue hepatectomy/liver
transplantation
Inadequate coagulation (INR
≥ 2.0)
Severe neurologic symptoms/hepatic encephalopathy
Renal dysfunction not manageable with diuretics, BUN
≥
150 mg/dL, symptoms of
uremia
Severe refractory hypoxemia
(arterial oxygen saturation
≤ 85 % with high fraction of
inspired oxygen
Abdominal ultrasonogra-
phy/CT, chest radiography,
sputum, blood, urine culture,
brain CT, intracranial pressure monitoring device
94.3 %) (Table 17.2) [3]. In this study, peak total
bilirubin level predicted postoperative morbidity
(both any morbidity and major morbidity), liverrelated mortality, and death from any cause, independent of transfusion status.
Risk Factors for PHI
Reported risk factors for PHI or liver failure are
summarized in Table 17.3.
Among the surgery-related factors, small FLR
volume is the most important and modifiable factor for patients undergoing extended resection.
A strong correlation between small FLR volume
and increased risk of PHI is widely recognized,
and various FLR volume criteria have been used
to select patients who are at high risk of PHI. The
poorer the quality of the underlying hepatic parenchyma, the larger the FLR required; therefore,
the minimum FLR volume required should be
determined according to the status of the underlying liver.
At The University of Texas MD Anderson
Cancer Center, we calculate the estimated total
liver volume (TLV) using a formula that relies
on the linear correlation between the TLV and
body surface area (BSA): TLV (cm3) = − 794.41
+ 1267.28 × BSA (m2) [4]. The standardized FLR
(sFLR) is then calculated as the ratio of the FLR
volume to the estimated TLV. In a large cohort
study seeking optimal cutoff values for minimum sFLR required, it was estimated that for
patients with normal underlying liver, sFLR of at
least 20 % is needed to avoid PHI or death from
liver failure [5], while for patients who received
17117 Postoperative Hepatic Insufficiency
Table17.2 Diagnostic characteristics of various criteria for predicting liver failure-related death. (Reprinted with
permission [3] © Elsevier 2007)
Characteristic Postoperative peak
Sensitivity
Specificity, n (%)
Positive predic-
tive value ( n)
Negative predic-
tive value ( n)
Positive likeli-
hood ratio
Negative likeli-
hood ratio
INR international normalized ratio
Table 17.3 Risk factors for postoperative hepatic insufficiency. (Reprinted with permission from [31] © John Wiley
and Sons)
Surgery related
Small future liver remnant volume
Excessive intraoperative blood loss
Prolonged operating time
Patient related
Preexisting liver disease
Cirrhosis
Steatosis
Cholestasis
Chemotherapy-associated liver damage
Male gender
Advanced age (65 years or older)
Comorbid conditions
Malnutrition
Others
Hepatic parenchymal congestion
Ischemia–reperfusion injury
Infection
, n (%)
serum bilirubin level
7.0 mg/dL
>
28/30 (93.3) 23/30 (76.7) 22/30 (73.3) 14/28 (50.0)
963/1021 (94.3) 828/1010 (82.0) 982/1005 (97.7) 964/997 (96.6)
0.326 (28/86) 0.112 (23/205) 0.489 (22/45) 0.292 (14/48)
0.998 (963/965) 0.992 (828/835) 0.992 (982/990) 0.986 (964/978)
17.2 4.34 32.6 15.3
0.07 0.28 0.27 0.498
Postoperative peak
INR >
2.0
Postoperative peak
serum bilirubin level
7.0 mg/dL and postop-
>
erative peak INR >
Prothrombin time
<
50 % and serum bili-
rubin level >
on postoperative day 5
2.0
(“50–50 criteria”)
50 μmol/L
extensive chemotherapy (≥ 3 months) before
surgery, sFLR should be at least 30 % [6]. For
patients with liver cirrhosis, it was reported that
sFLR should be 40 % or more [7]. Current clinical evidence regarding the sFLR required is summarized in Fig. 17.1.
Another risk factor for PHI is chemotherapyassociated liver damage. Currently, the most
common indication for hepatectomy is colorectal liver metastases. Because of advances in
effective chemotherapy, the vast majority of patients with colorectal liver metastases are treated
with perioperative systemic therapy in combination with surgery. Specific associations between
chemotherapy regimens and types of liver injury
have been reported. Sinusoidal injury has been
associated with oxaliplatin [8, 9], and steatohepatitis has been linked to irinotecan, particularly in
patients with high body mass index [10]. In particular, steatohepatitis after major hepatectomy
172 J. Shindoh and J.-N. Vauthey
Fig. 17.1 Minimal standardized future liver remnant
(sFLR) required to prevent postoperative hepatic insufficiency. (With permission from: a [5]©Wolters Kluwer
has been correlated with high mortality rates
[10]. Chemotherapy-associated liver injuries
cannot be accurately predicted, but two factors
are known to correlate with increased likelihood
of chemotherapy-associated complications: longer duration of preoperative chemotherapy and
shorter time interval between the cessation of
chemotherapy and surgery. In patients who received chemotherapy for more than 3 months
[6], the possibility of hepatic injury should be
entertained, and in-depth histopathologic review
of the nontumorous liver, volumetry, and laparoscopy should all be considered.
Prevention of PHI
Systematic Volumetry of the “Fully Functioning” Part of the Liver
Volumetry of the liver is essential to assess the
risk of PHI. A previous anatomic study revealed
that the left lateral bisegments account for only
16 % of the total liver volume (Fig. 17.2) [11].
Thus, routine volumetry using an adequate
2009; b [29] ©Springer Science and Business Media; c
[32] ©Wolters Kluwer; d [7] ©John Wiley and Sons 1997)
method is recommended, especially in patients
undergoing extended right hepatectomy. FLR
volume should be defined as the absolute volume of the “fully functioning” part of the liver,
in other words, the part of the liver that will have
adequate inflow and outflow after hepatectomy.
When a hepatic vein draining a specific part of
the liver is deprived, the corresponding part of
the liver will be congested and will atrophy because of loss of its normal function [12, 13]. A
recent study using indocyanine fluorescent technique revealed that portal uptake function in the
venoocclusive part of the liver is approximately
40 % of that in the nonocclusive part of the liver
[14]. However, precise estimation of the volume
of the area to be congested is difficult without
the use of three-dimensional liver simulation
techniques (Fig. 17.3) [15, 16]. Therefore, on
volumetry for patients undergoing extended right
hepatectomy in which the middle hepatic vein
will be deprived, segment IV should not be included in the FLR volume because most of segment IV will be congested and lose its normal
function after deprivation of the middle hepatic
vein even when part of segment IV is preserved.
17317 Postoperative Hepatic Insufficiency
Frequency %
Frequency %
Frequency %
40
30
20
10
0
<10<15 <20<25 <30<35 <40<45 <50<55 <60<65 <70<75 <80
Right Liver % of TLV
40
30
20
10
0
<10<15 <20<25 <30<35 <40<45 <50<55 <60<65 <70<75 <80
Left Liver % of TLV
50
40
30
20
10
0
<10<15 <20<25 <30<35 <40<45 <50<55 <60<65 <70<75 <80
Segment II+III % of TLV
Fig. 17.2 Proportion of total liver volume ( TLV) con-
tributed by right liver, left liver, and segments II and III.
10% in Right Hemihepatectomy
sFLR (Le Hemiliver) ≤ 20%
75% in Extended Right Hepatectomy
sFLR (Segments 2+3) ≤ 20%
(Adapted with permission from [11] ©Elsevier 2004)
Fig. 17.3 Venous congestion after deprivation of drain-
age vein during hepatectomy. After extended left hepatectomy including the middle hepatic vein, a large part
of the right hemiliver is congested (a) as predicted on a
preoperative three-dimensional simulation (b). Normal
of the liver. Venous reconstruction should be considered
when the volume of remaining full-functioning liver is insufficient. MHV drainage area of the middle hepatic vein,
RHV drainage area of the right hepatic vein, V8 drainage
area of the intermediate vein for segment VIII
liver function cannot be expected in the congested part