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15 Digital Surgical Diagnosis andTreatment ofGallbladder Cancer
357
• Step 5 The Hepatic artery was dissected to the distal end,
peripheral lymphatic adipose tissue was removed. The
root of the right gastric artery originated from the proper
hepatic artery was ligated allowing dissociation of the
gastroduodenal artery by further distal separation
(Figs.15.20 and 15.21). The common bile duct was pulled
downward, and the hepatic artery pulled laterally,
exposing the portal vein, and the peripheral lymphatic
adipose tissue was separated (Fig.15.22).
Fig. 15.20 Showing the gastroduodenal artery (GDA)
• Step 6 PMOD was used to clean the adipose tissue around
the common hepatic artery in the arterial sheath along the
centripetal direction of the common hepatic artery, until
the lymphatic adipose tissue around the abdominal trunk
was removed.
• Step 7 The transverse colon was lifted to identify the
Treitz ligament on the left side of the mesenteric root,
allowing touch and identication of the superior mesenteric artery, and cutting of the mesenteric serosa along the
direction of the artery. The middle colon arteriovenous
could be identied on the inferior margin of the pancreas,
and the rst and second branches of the jejunal artery
could be ligated underneath, and the ascending and horizontal part of duodenum could be fully dissociated. At
approximately 15 cm distal to the Treitz ligament, the
jejunum was dissected by a cut-and-close device, and the
distal jejunum was anastomosed (Fig.15.23). Care should
be taken to avoid damage to the deep mesenteric vein
when dissociating the upper segment of jejunum.
• Step 8 Before pancreatic dissection, the upper and lower
edges of the left and right sides of the predetermined dissection line was sutured by a needle, respectively, and
ligated for traction thread, respectively, to block the transverse small blood vessels in the head and neck of the pancreas, to reduce intraoperative bleeding (Fig.15.24). The
Fig. 15.21 Disconnecting gastroduodenal artery
Fig. 15.22 Dissecting the hepatoduodenal ligament
Fig. 15.23 Transecting the jejunum
Fig. 15.24 Pancreas in suspension
358
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Y. Liu et al.
traction line was lifted to the left and right sides, respectively, and the pancreas was cut off by PMOD scraping
and suction method (Fig. 15.25). During the process of
pancreas dissection, attention should be paid to nding the
opening of the pancreatic duct and dissecting the pancreatic duct to prepare pancreaticojejunostomy (Fig.15.26).
• Step 9 The severed end of the pancreas head and duode-
num were turned up to the right, and the right and posterior
walls of the superior mesenteric vein were drawn to the
left by the vein retractor. The superior posterior pancreaticoduodenal vein, the inferior anterior vein, and the inferior
posterior vein were seen. Several small veins were injected
into the superior mesenteric vein. The vein was stripped
and exposed by PMOD curettage. About 4mm from the
superior mesenteric vein or portal vein, the blood vessels
were clamped, disconnected, and ligated, respectively. The
superior mesenteric vein was fully dissociated from the
uncinate part of the pancreas (Fig.15.27a).
• Step 10 The superior mesenteric vein was pulled farther
to the left to expose the left posterior superior mesenteric
artery and open the external sheath of the artery lengthwise along the anterior wall of the superior mesenteric
artery. The superior mesenteric artery and inferior pancreaticoduodenal artery or its branches could then be further
exposed by further separation to the right margin, and the
artery and branch could be clamped, severed, and ligated.
The arteries could also be pulled to the left, exposing the
uncinate process of the pancreas as far as was possible,
splicing the clamp, dissecting the vessel, removing the
uncinate process intact, and simultaneously sweeping the
lymphatic adipose tissue around the superior mesenteric
arteriovenous area (Fig.15.27b).
• Step 11 Disconnecting the hepatic duct above the entrance
of the cystic duct (Fig.15.28). The hepatic artery and portal vein, respectively, were blocked by noninvasive vascular forceps (Figs.15.29 and 15.30) to control the hepatic
blood ow. Hepatectomy was performed according to the
predetermined hepatectomy line. After the liver capsule
was cut open by electrotome, the two sections of the liver
were kept in proper reverse tension. The liver was cut off
on the liver resection line by PMOD curettage (Fig.15.30).
Meanwhile, liver debris, blood, and bile were sutured and
removed. Separate dissection and suture were needed
when the pipeline structure was encountered (Fig.15.31).
The Segment S4b+S5 was completely resected. After the
hepatic artery and portal vein occlusion were relieved,
electrocoagulation was performed on the hepatic transection (Fig.15.32).
Fig. 15.26 Look for the pancreatic ductFig. 15.25 Pancreas amputation
Fig. 15.27 (a, b) Uncinate process of the pancreas
15 Digital Surgical Diagnosis andTreatment ofGallbladder Cancer
359
Fig. 15.28 Transverse hepatic duct
Fig. 15.29 Hepatic artery occlusion
Fig. 15.32 Treatment of pipelines on the hepatic transection
Fig. 15.33 Surgical eld after removal of specimen
Fig. 15.30 Portal vein occlusion
Fig. 15.31 Liver resection
Fig. 15.34 A silicone tube was inserted at the broken end of the pan-
creatic duct
• Step 12 So far, the liver S4b+S5 segment, including the
gallbladder tumor, the lower common bile duct, the duodenum, the upper jejunum, and the pancreatic head, as
well as the distal end of the stomach have been completely
excised and removed (Fig.15.33).
• Step 13 The digestive tract was reconstructed using the
Child method in the order of pancreaticojejunostomy,
choledochojejunal anastomosis, and gastrointestinal
anastomosis. A silicone tube was inserted into the broken
end of the pancreatic duct (Fig. 15.34). End-to-side
anastomosis between the pancreatic duct and jejunum
mucosa was performed (Fig.15.35).
360
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Y. Liu et al.
Fig. 15.35 (a, b) End-to-side anastomosis between the pancreatic duct and jejunum mucosa
Fig. 15.36 (a, b) End-to-side anastomosis between the common hepatic duct and jejunum
• Step 14 The end-to-side anastomosis between the common hepatic duct and jejunum was performed about
10cm below the anastomotic stoma of pancreas and jejunum (Fig.15.36).
• Step 15 In front of the transverse colon, the posterior gas-
tric wall was anastomosed to the jejunum about 45 cm
below the anastomotic stoma of pancreas and jejunum
(Fig.15.37).
• Step 16 After reconstruction and anastomosis of the
digestive tract, the drainage tube was placed, and the
abdomen was closed layer by layer.
Fig. 15.37 Gastrointestinal anastomosis
15 Digital Surgical Diagnosis andTreatment ofGallbladder Cancer
361
15.4.4 Surgical Prognosis
In 2015, a meta-analysis of HPD included 397 cases of gallbladder cancer and cholangiocarcinoma. The results showed
that 71.3% of the patients achieved R0 resection, the incidence of postoperative complications was 78.9%, and the
perioperative mortality was 10.3%. The overall 5-year survival rate was 31%. For those who achieved R0 resection, the
5-year survival rate was 51.3%, and the 5-year survival rate
of gallbladder cancer was 10.4% (Zhou etal. 2016). Nimura
etal. (1991) performed HPD on 17 patients with advanced
gallbladder cancer, with a 5-year survival rate of 15.3%.
Nakamura etal. (1994) performed HPD on 7 patients with
stage IV gallbladder cancer, with 1-year and 2-year survival
rates of 57% and 28.6%, respectively, and the median survival time was 12months. The 2-year survival rate of the
corresponding nonsurgical group was 5.8%, and the median
survival time was only 2months. It can be seen that the surgical treatment of gallbladder cancer needs to be further
improved. Besides early diagnosis and early treatment,
patients with advanced gallbladder cancer should not be
given up easily. Active surgical treatment may still give them
a long-term tumor-free survival opportunity. Surgical treatment can improve the life quality of patients and extend their
survival time, at least until appropriate drugs are available.
During this period, 3D visualization technology plays an
essential role in the accurate evaluation of the disease and
delicate operation of surgery.
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Digital Diagnosis andManagement
ofCholangiocarcinoma
FengShen, KuiWang, QifeiZou, NingZeng,
XiangchengLi, andChihuaFang
16
16.1 Introduction
Cancer of biliary duct can be divided into intrahepatic cholangiocarcinoma (ICC) and extrahepatic cholangiocarcinoma
(ECC). ECC is further divided into hilar cholangiocarcinoma
and distal cholangiocarcinoma based on the junction point of
the cystic duct and common hepatic duct. The main risk factors of cholangiocarcinoma include bile duct stones, HBV,
and HCV infection, primary sclerosing cholangitis, liver
ukes, and chemical substances. The risk factors of ECC
also include biliary and pancreatic duct conuence abnormalities and common bile duct cystic dilatation. According
to the general appearance of the tumor, ICC is classied as
mass forming, perivascular inltration, and intravascular
growth, while ECC is classied as polyp, nodular, sclerosing, and diffusely inltrating. Adenocarcinoma is the most
common type in both ICC and ECC.Surgical resection is the
only radical treatment for cholangiocarcinoma. Radical
resection should be actively sought as long as the patient’s
systemic condition is tolerable to surgery, and there is no
distant metastasis. As digital medical technology has become
widely used in liver and gallbladder surgery in our country,
three-dimensional visualization technology has brought new
ideas for accurate diagnosis, preoperative assessment, choice
schemes, and treatment of cholangiocarcinoma. The mode of
diagnosis and treatment of hepatobiliary diseases is changing constantly, and the digitization of anatomy, the procedure
of diagnosis and the visualization of operation have been
realized in hepatobiliary surgery. Digitization has played an
active role in the accurate and efcient diagnosis of diseases,
F. Shen · K. Wang · Q. Zou
Eastern Hepatobiliary Surgery Hospital, Naval Medical University,
Shanghai, China
N. Zeng · C. Fang (
Zhujiang Hospital, Southern Medical University,
Guangzhou, China
X. Li
The First Afliated Hospital of Nanjing Medical University,
Nanjing, China
*)
the selection of reasonable treatment schemes, the improvement of surgical success rates, and the reduction of surgical
risk.
16.2 Digital Diagnosis andSurgical
Management ofIntrahepatic
Cholangiocarcinoma
16.2.1 Epidemiology ofIntrahepatic
Cholangiocarcinoma
ICC is a malignant tumor of the liver that originates from the
epithelial cells of the intrahepatic small bile duct or the intrahepatic bile duct (extending to the proximal end of the
hepatic duct bifurcation), and some ICC is even derived from
the hepatocytes (Fan etal. 2012). ICC accounts for 10–15%
of the primary malignant tumor of the liver (Shaib et al.
2005). The incidence of ICC is second only to that of hepa-
tocellular carcinoma, and the incidence rate has been increasing in recent years.
Many diseases may affect the biliary system, resulting in
chronic biliary inammation, cholestasis, and cirrhosis of
the liver, leading to the development of biliary malignancies,
such as ICC.Intrahepatic bile duct stones, primary sclerosing cholangitis (PSC), congenital bile duct malformations,
parasitic infections, and exposure to toxic substances may all
be associated with increased ICC risk (Khan et al. 2005;
Lipsett etal. 1994). Notably, chronic liver diseases such as
viral infection and cirrhosis, are considered risk factors for
cholangiocarcinoma, especially ICC (Palmer and Patel 2012)
(Fig.16.1). Recent studies have shown that metabolic abnormalities, such as type 2 diabetes and obesity, and chronic
pancreatitis, may increase the risk of ICC (Welzel et al.
2007).
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2021
C. Fang, W. Y. Lau (eds.), Biliary Tract Surgery, https://doi.org/10.1007/978-981-33-6769-2_16
363
364
Table 2 - Comparison of the prevalence of risk factors between ICC cases and controls.
Risk factors
Seropositive HBsAg
Cirrhosis
HBV-associated cirrhosis
Alcohol-associated cirrhosis
Cirrhosis from other causes
Total
Cholelithiasis
Hepatolithiasis
Choledocholithiasis
Cholecystolithiasis
Total
Liver schistosomiasis
ICC: intrahepatic cholangiocarcinoma; HBsAg: hepatitis B surface antigen; HBV: hepatitis B virus.
Fig. 16.1 Etiological factors for ICC
Controls (n = 634) ICC cases (n = 317)
n %
42
6
2
1
9
7
9
56
64
4 0.6
%
6.6 154
1
0.3
0.2
1.4
1.1
1.4
8.8
10.1
n
84
6
5
95
25
20
32
54
16 5.0
F. Shen et al.
Value
p
48.6 <0.001
26.5
1.9
1.6
30.0
7.8
6.3
10.1
17.0
<0.001
0.027
0.035
<0.001
<0.001
<0.001
0.572
<0.001
Fig. 16.2 B-ultrasound image of ICC
16.2.2 Diagnosis ofICC
16.2.2.1 General Clinical Manifestations
andLaboratory Diagnosis
There is no obvious symptom in the early stage of ICC, and
a small number of patients are treated for jaundice caused by
tumor thrombus obstructing the bile duct or metastatic lymph
nodes and tumor self-compression of the bile duct (Brown
etal. 2014). Patients with ICC often have elevated gammaglutamyl transpeptidase (GGT), 5′-nucleotidase (5′NT) and
tumor marker (CA19-9), but lack sensitivity and specicity
(Dodson etal. 2013).
16.2.2.2 Imaging Diagnosis
The ultrasonographic features of ICC are varied, mainly
manifesting as irregular shape and indistinct boundary of
hypoechoic masses. Under color Doppler ultrasound, the
images are mostly of hypovascular type, while the arterial
blood ow in the angiographic lesion is multipotent and
high-resistance (Fig.16.2).
CT scan is of great value in detecting intrahepatic tumors
and determining the degree of biliary obstruction, hepatic
atrophy, or hypertrophy. Multistage enhancement of MSCT
can also help to identify the causes of intrahepatic biliary
stricture and evaluate tumor staging and resectability (Valls
16 Digital Diagnosis andManagement ofCholangiocarcinoma
365
et al. 2000). Typical CT features include non-cystic lowdensity lesions and distal biliary dilatation. Cystic retraction
can be seen in individual patients with hepatic brosis. After
administration of contrast medium, peripheral enhancement
in arterial stage and the venous stage is observed, and thick
ring enhancement or incomplete thick ring enhancement in
portal phase is also observed, but with a relatively low den-
sity. The tumor boundary is more clearly displayed in this
phase than in the arterial phase, which aids observation of
the extent of the lesion (Fig.16.3). The pattern of contrast
enhancement in some ICC cases, especially in small tumors,
is similar to that of hepatocellular carcinoma (HCC) (Kim
etal. 2011a, b).
Fig. 16.3 CT ndings of ICC
366
F. Shen et al.
Fig. 16.4 MRI ndings of ICC
The MRI of ICC is characterized by T1-weighted lowsignal lesions and T2-weighted images when the tumor tissue exhibits a peripheral high signal and a central low-signal
heterogeneous mass (Ciresa etal. 2015). A lobulated lesion
with marginal weakening may occur after Gd-DTPA contrast medium enhancement. Because intrahepatic cholangiocarcinoma is usually a tumor with little blood supply
and rich in brous tissue, early enhancement is not obvious,
or partial marginal enhancement is slight. Delayed centripetal enhancement is the most common sign (Fig.16.4). CT
and MRI have a certain value in differentiating metastatic
tumors of lymph nodes, peritoneum, lung, and pleura. CT
enhanced scan combined with MRCP can help to exclude
intrahepatic metastatic lesions, accurately locate the lesion
site, conrm bile duct involvement, and then differentiate
ICC from HCC.Positron emission tomography (PET) can
play an important role in preoperative evaluation, especially in the detection of potential occult metastatic diseases and the exclusion of metastatic liver cancer (Ringe
and Wacker 2015).
16.2.2.3 Pathological Diagnosis
The general pathological types of ICC were classied as
mass forming (MF), periductal inltration (PI), intraductal
growth (IG), and mixed (Okabayashi etal. 2001). The most
common type is MF, accounting for 60%–80% of ICC.CT or
MRI ndings are mainly large masses, with enhanced periphery without obvious dilatation of ducts. Periductal inltration
type accounts for 15%–35%. It can diffuse inltration along
with the biliary and portal vein systems, leading to bile duct
stricture and peripheral bile duct dilatation. Imaging ndings
are mainly irregular masses around the bile duct, and larger
masses may cause bile duct stenosis. Intratubular growth
type accounts for 8%~29%, mostly papillary, polypoid, or
granular growth, along with the supercial spread of bile
duct surface. The dilated bile duct is visible on imaging, but
no mass is seen, which is typical on MRCP.Another type of
mixed type, also known as nodular inltration, is characterized by an intrahepatic mass with peripheral bile duct dilatation and sometimes dilated intraductal tumors (Chen and
Shang 2015) (Fig.16.5). The histopathological types of ICC