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5 Surgical Approach to Pancreas, Liver, Biliary Physiologic Impairment
41
are rare (2% of CC) true biliary diverticula that project from
the common bile duct and are histologically consistent with
the gall bladder [108, 109]. Type III are rare (2–5% of CC)
intra-duodenal dilations of the common pancreaticobiliary
channel (choledochoceles) and are lined by duodenal mucosal cells [108, 109]. Type IV CC (15–25% of CC) are divided
into two subtypes both of which lack biliary mucosal cells:
Type IVA involves dilation of the common hepatic duct and
intrahepatic biliary tree while Type IVB involves multiple
areas of extrahepatic biliary dilation only (“string of beads”)
[108, 109]. Type V (20% of CC) involves diffuse dilation of
the entire intrahepatic biliary system (Caroli’s disease) and
can be associated with hepatic brosis (Caroli’s Syndrome)
[108, 109]. There are many theories regarding the origins of
CC, but most experts support the hypothesis that CC form
secondary to a congenitally abnormal union of the pancreatic
and biliary ducts (either extra-duodenally or>15mm distal
to the ampulla of Vater) [109]. Such an aberrant anatomy
allows for reux of caustic pancreatic juice into the biliary
system, predisposing to biliary cystic dilation [109]. While
this hypothesis is generally supported Type I and Type IV
CC, other pathogenic mechanisms may better explain the
differences in location, histology, and malignant potential
Types II, III, and V CC [109].
Malignant transformation occurs in 10–30% of Type I and
Type IV CC and is thought to occur secondary to a synergistic relationship between caustic pancreatic enzyme exposure,
bile stasis, and underlying K-Ras, p53, and DPC-4 mutations
[109]. Associated cancers are most commonly extrahepatic
cholangiocarcinoma (50–60% of associated cancers), gall
bladder cancer (38–46% of associated cancers), and rarely
intrahepatic cholangiocarcinoma (3% of associated cancers)
[110]. Cancer can occur in the choledochal cyst or at sites of
cyst-induced biliary stasis (i.e. the gall bladder) [110]. By
subtype of CC, 68% of cancers occur in Type I CC, 5% in
Type II, 2% in Type III, 21% in Type IV, and 6% in Type V
[110, 111].
Surgical or endoscopic resection is generally recommended for Types I-IV to mitigate the risk of malignant transformation, however, the extent of surgery depends on the
subtype. Management of Type I and IV CC require complete
extrahepatic bile duct cyst excision down to the level of the
pancreatic duct with cholecystectomy, followed by biliary
reconstruction (hepaticoduodenostomy or roux-en-Y hepaticojejunostomy). Type IVA may require hepatectomy, however, if the intrahepatic component is minimal. Type II CC are
typically treated with diverticulectomy. Large Type III CC are
treated with transduodenal excision while small Type III CC
can be treated with endoscopic sphincterotomy and drainage.
Due to the intrahepatic nature of Type V CC, liver resection or
orthotopic liver transplant is required for denitive manage-
ment. Importantly, if diseased duct is not removed with hepatectomy for Type V CC, the patient remains at risk for
continued biliary stasis and malignancy [109]. Patients who
undergo cyst excision remain, however, at risk of biliary
malignancy even after resection and therefore require routine
laboratory and imaging surveillance [109].
5.3.8 Primary Sclerosing Cholangitis
Primary Sclerosing Cholangitis (PSC) is thought to represent
an autoimmune process whereby repeated insult to the biliary tree results in inammation, biliary stasis, eventual
scarring, and predisposition to cancer. Additionally, this
inammatory cycle can lead to portal hypertension, cirrhosis, and liver failure. PSC is associated with inammatory
bowel disease (IBD) in 70% of cases but only 5% of people
with IBD develop PSC [112]. It has also been hypothesized
that PSC with colitis represents a disease process that is distinct from either isolated IBD or isolated PSC, as its patterns
of colonic inammation differ from those exhibited in IBD
[112]. Cholangiocarcinoma is the most common PSCassociated cancer, which occurs in 10–15% of patients with
PSC [113–115]. However, this may be an underestimation,
as 10% of patients undergoing liver transplantation for PSC
have clinically occult cholangiocarcinoma upon pathologic
examination of the explanted liver [116]. Gallbladder cancer
is also seen in 3–14% of patients with PSC and can occur
independently from strictured areas [115]. Patients with PSC
are also at increased risk of hepatocellular carcinoma [115].
Intervention to treat PSC-related biliary strictures depends
on the extent and location of disease. For isolated extrahepatic strictures, ERCP with stricture biopsy and balloon dilation can be employed. Randomized trials have demonstrated
that stenting across a dominant stricture has equivalent success and recurrence rates versus balloon dilation, but is associated with higher morbidity. Therefore stenting should not
be routinely employed [117]. In the event that endoscopic
approaches are unsuccessful or anatomically impossible,
biliary tract resection with reconstruction may be considered
in surgically-t patients [118]. Of note, biliary reconstruction may technically complicate future liver transplantation,
which is the standard of care treatment in advanced
PSC.Previous biliary surgery is also associated with reduced
survival in patients undergoing liver transplantation for PSC
[119]. Indications for liver transplant in PSC include intractable/untreatable jaundice, severe recurrent cholangitis, cirrhosis with reduced liver function, concomitant small HCC
or non-metastatic cholangiocarcinoma [119]. Unfortunately,
20–40% of patients who undergo liver transplantation for
PSC will have recurrent disease [119].
42
A. W. Acher et al.
5.3.9 Benign Biliary Stricture
Non-PSC benign biliary strictures may result from chronic
pancreaticobiliary inammation (recurrent pancreatitis,
recurrent cholangitis), iatrogenic etiology (operative bile
duct injury), postoperative scarring in biliary-biliary or
biliary- enteric anastomosis, or scarring after repeated endoscopic sphincterotomy. An endoscopic approach with balloon dilation (preceded by biopsy to rule out malignancy)
and sphincterotomy is the recommended initial treatment
approach [120]. Temporary plastic stents may also be placed,
but with risk of migration and necessity of replacement
[120].
5.4 Malignant Biliary Disease:
Pathophysiology andIndications
forSurgical Treatment
The most common extrahepatic malignant biliary tumors
include extrahepatic cholangiocarcinoma (ECC) and gall
bladder cancer (GBC). The treatment approach for extrahepatic biliary malignancies should be based in multidisciplinary collaboration between medical and radiation
oncologists, interventional radiologists, pathologists, and
surgeons.
5.4.1 Extrahepatic Cholangiocarcinoma
ECC arises from biliary epithelial cells lining the extrahepatic biliary tract. ECC is classied as either distal or hilar
(Fig.5.3). Hilar cholangiocarcinomas are further categorized
by their location relative to the conuence of the right and
left hepatic ducts [121]. In the Bismuth-Corlette classication (Fig.5.3), Type I tumors involve the common hepatic
duct just inferior to the conuence of the right and left
hepatic ducts and above the cystic duct origin. Type II tumors
involve the conuence of the right and left hepatic ducts but
do not extend superiorly. Type III tumors involve the hepatic
duct conuence with extension to either the proximal right
(Type IIIA) or left hepatic duct (Type IIIB). Type IV tumors
extend from the conuence to bilateral hepatic ducts and
may involve bilateral second-order biliary radical ducts.
ECC is most commonly seen in association with PSC; in
fact, 30% of cholangiocarcinomas are diagnosed in patients
with PSC.ECC also occurs in up to 30% of patients with
choledochal cysts [109]. Additionally, ECC is associated
with toxin exposure (i.e. Thorotrast), biliary stone disease,
and chronic pancreatitis [122, 123]. Although the exact
pathogenic mechanism is unclear, ECC is thought to form
secondary to biliary inammation and stasis. In contrast,
ICC is associated with chronic hepatitis B or C infection,
cirrhosis, fatty liver disease, toxin exposure (asbestos), parasitic infection, obesity, and diabetes, in addition to PSC and
CC [63].
Treatment of ECC should be approached from a multidisciplinary perspective. Long term survival is rare and only
possible when a negative resection margin (R0) is achieved
[124, 125]. Distal ECC can be approached with pancreaticoduodenectomy. Bismuth-Corlette Type I-III tumors require
biliary duct resection, formal hepatectomy and caudate
lobectomy, and biliary tract reconstrcution [124]. Historically,
Bismuth-Corlette Type IV tumors have been considered
unresectable due to their high perioperative morbidity (14–
66%), mortality (19% in some series), and recurrence rates
[125]. However, some centers have demonstrated improved
5year survival (30–41% vs 11% in historical controls) when
aggressive surgery (biliary resection with major hepatectomy, portal vein and hepatic artery reconstruction) is performed in select patients [126, 127]. General contraindications
to resection include involvement of the portal vein trunk or
bilobar involvement of portal vein branches, involvement of
unilateral hepatic artery with contralateral hepatic duct
involvement, or metastatic disease [124]. Portal vein embolization may be employed prior to surgery to increase FLR
volume [124, 125]. Even with curative intent surgery and an
R0 surgical margin, disease recurs in 65% of patients with a
median time to recurrence of 12 to 43 months [125]. Because
of these factors, orthotopic liver transplant has surfaced as a
treatment option for patients with locally advanced hilar
cholangiocarcinoma. Initial studies demonstrated prohibitively high recurrence and low 5year survival (50% and 28%
respectively) in patients who underwent liver transplantation
for hilar cholangiocarcinoma [128]. However, the very stringently selected patients with early stage perihilar cholangiocarcinoma neoadjuvant radiation, brachytherapy, and
chemotherapy (5-FU and oral capecitabine) have demonstrated a 5year survival of 82% after transplant. The results
of this study, however, may be heavily inuenced by selection bias inherent in their stringent enrollment criteria [129].
Ultimately, despite a diversity of surgical approaches, prognosis associated with ECC remains poor.
5.4.2 Gall Bladder Cancer
Gall bladder cancer is the most common extrahepatic biliary
tract cancer and is most commonly adenocarcinoma (80%)
histologically. Gall bladder cancer results from chronic gallbladder inammation that triggers malignant transformation
of cholangiocytes [127]. Unfortunately, most gallbladder
cancer is clinically occult until advanced stages that are not
amenable to surgical resection [127].
Surgical approach depends on the T category of the tumor.
Tumors that invade the inner most layer of the gallbladder,
5 Surgical Approach to Pancreas, Liver, Biliary Physiologic Impairment
43
the lamina propria (T1a), are treated with cholecystectomy.
Tumors that invade the muscularis propria (T1b) or perimuscular connective tissue (T2) are treated with radical cholecystectomy (cholecystectomy with segments 4b and 5
resection). T3 tumor stage (invasion to liver or other peritoneal organs) necessitates radical cholecystectomy and if the
positive cystic duct margin is positive, bile duct resection
with reconstruction is necessary [130]. Portal lymphadenectomy should always be performed during radical cholecystectomy. The all-stage post-resection 5year survival is 40%
and by T stage is 92% for T1a tumors, 87% for T1b tumors,
64% for T2 tumors, 19–27% for T3 tumors and<10% for T4
tumors [131]. Unfortunately, rst line systemic therapy
offers only a small survival benet (1year) and is not associated with tumor response in all patients [127].
5.5 Benign Pancreas Disease:
Pathophysiology andIndications
forSurgical Treatment
Acute and chronic pancreatitis are common benign pathophysiologic derangements with potential for severe systemic
implications. Pancreas neoplasms can be distinguished based
on involvement of endocrine or exocrine function of the pancreas with varying degrees of malignant potential.
5.5.1 Acute Pancreatitis
Acute pancreatitis is an inammatory process that occurs
when injury or hyper-stimulation of the pancreas incites
intra-acinar protease activation leading to auto-digestion of
normal pancreas parenchyma. Pro-inammatory cytokines
(TNF-alpha, IL-1, IL-2, IL-6) are subsequently released and
increase basolateral membrane permeability that further
propagates this inammatory cascade [132]. In western
countries, gallstones and alcohol are the two most common
causes of acute pancreatitis (80–90% of cases). However, <
7% of people with gallstones and<10% of chronic alcohol
users develop acute pancreatitis [132]. Less common causes
include hypertriglyceridemia (both genetic and acquired),
endoscopic retrograde cholangiography, trauma, medications, sphincter of Oddi dysfunction, congenital anomalies
(pancreas divisum, annular pancreas), and hereditary predisposition [132].
The Atlanta Criteria can be used to diagnose acute pancreatitis, grade the severity of presentation, and guide treatment options (Table5.2) [133]. Most sequelae from acute
pancreatitis (sepsis, peripancreatic uid collections, peripancreatic and pancreatic necrosis, pseudocyst, walled off
necrosis) are treated medically and may involve percutaneous or endoscopic drainage procedures [134]. Historically,
Table 5.2 Revised Atlanta Criteria for the classication of acute
pancreatitis
Mild acute pancreatitis
No organ failure
No local or systemic complications
Moderately severe acute pancreatitis
Organ failure that resolves within 48hours
Local or systemic complications without persistent organ failure
Severe acute pancreatitis
Persistent organ failure >48hours
Multiple organ failure
surgical necrosectomy was reserved for patients with
infected necrotizing pancreatitis; however, endoscopic
transgastric necrosectomy and retroperitoneal drainage is a
more recent promising treatment strategy. Randomized trials comparing open necrosectomy with endoscopic transgastric necrosectomy and drainage for patients with
infected necrotizing pancreatitis demonstrated faster normalization of IL-6 and lower rates of organ failure, bleeding, enterocutaneous stula, and pancreatic stula in the
endoscopic arm [135].
5.5.2 Chronic Pancreatitis
Chronic pancreatitis occurs secondary to the cumulative
impact of recurrent episodes of acute pancreatitis and is
dened by permanent morphologic change, parenchymal
atrophy, and reduced exocrine and endocrine function [136].
Chronic alcohol use, smoking, and hypertriglyceridemia are
common etiologies associated with chronic pancreatitis.
Additionally, chronic pancreatitis can result from a hereditary predisposition or autoimmune pancreatitis. Repeated
episodes of acute pancreatitis predisposes to pancreatic duct
strictures that unfortunately increase the likelihood of pancreatic duct obstruction and recurrent acute pancreatitis.
Congenital anomalies (pancreas divisum, annular pancreas)
usually manifest with recurrent pancreatitis during childhood [136].
Management of chronic pancreatitis is challenging and
requires collaboration by gastroenterologists, hepatopancreatobiliary surgeons, interventional radiologists, and nutritionists. Surgical management is mainly reserved for patients
who have failed medical and endoscopic management.
Surgical management may involve pancreatic duct decompression (Puestow procedure), parenchymal resection with
either biliary decompression or reconstruction (pancreaticoduodenectomy, distal pancreatectomy, Beger procedure,
Frey procedure), or total pancreatectomy with islet cell autotransplantation in highly selected patients. The optimal
approach is dictated by duct size, location and extent of pancreatic duct obstruction, degree of gland atrophy, and the
patient’s goals and comorbidities [137].
44
A. W. Acher et al.
5.5.3 Pancreas Neuroendocrine Tumors
Pancreatic neuroendocrine tumors (PNETs) arise from endocrine cells within the pancreas, with varying degrees of malignant potential. These tumors likely arise from altered pluripotent
stem cell differentiation resulting in hyper- proliferation of
mature pancreatic endocrine cells (i.e. alpha, beta, delta, enterochromafn, G, and pancreatic polypeptide cells) [138]. PNETs
can manifest as specic clinical syndromes according to the
type of cells that are involved. Although most PNETs occur
sporadically, they are sometimes associated with other genetic
disorders; PNETS occur in 80–100% of patients with multiple
endocrine neoplasia Type I (MEN1), 10–20% of patients with
von Hippel-Lindau syndrome, and 10% of patients with neurobromatosis-1 [138]. Interestingly, Kras and p53 oncogene
mutations are uncommon in PNETs [138]. About 10–30% of
PNETS are functional tumors, while the majority are considered as non- functional tumors (60–90%) [138, 139]. The most
common functional PNET syndromes is Insulinoma, followed
by gastrinoma (Zollinger-Ellison syndrome) [138, 139]. Rare
functional PNETs are associated with secretion of vasoactive
intestinal peptide, glucagon, somatostatin, growth hormone,
ACTH, and serotonin [139]. Even more rare functional PNETs
are associated with secretion of renin, luteinizing hormone,
erythropoietin, insulin-like growth factor, cholecystokinin, and
glucagon-like peptide [139]. Tumor type, grade, Ki-67 index,
and mitotic count are critical to staging and prognosis. The
PNETs with the most malignant potential are gastrinomas (60–
90%), VIPoma (40–70%), glucagonoma (50–80%), stomatostinoma (>70%), growth hormone secreting PNET (> 60%),
ACTH secreting PNET (> 95%) [139]. In contrast, insulinomas
have a relatively low malignant potential (<10%) [139].
Management of PNETs is complex and requires collaboration within a multidisciplinary team, individualized to
patient comorbidities, symptoms, tumor location, grade and
malignant potential, and patient goals. Small (< 2cm) low
grade non-functional PNETs are usually indolent and can be
routinely surveyed [139]. Management of larger or clinically
apparent PNETs should include medical management and
curative intent resection when possible. Metastatic disease
does not preclude curative intent surgery [139]. Resection of
metastatic hepatic metastases is appropriate in select cases
[138, 139]. Liver transplantation for unresectable hepatic
metastases can be considered in very select patients after
resection of primary disease, however, recurrent disease is
likely [140].
5.5.4 Pancreas Cystic Neoplasms
Pancreatic cystic neoplasms (PCN) derive from pancreatic exocrine cells and are classied as either epithelial or nonepithelial, and neoplastic or non-neoplastic [141]. Common
PCNs without malignant potential include serous cystadenoma
(<3% incidence of invasive cancer, SCN), pseudocyst (sequela
from pancreatitis), lymphoepithelial cysts, and epidermoid
cysts. Common PCNs with malignant potential include mucinous cystic neoplasm (MCN), intraductal mucinous papillary
neoplasm (IPMN), solid pseudopapillary tumor [142].
The management of PCNs with malignant potential is
complex and despite the publication of many society-based
guidelines, a formal consensus on best management practices
is still lacking [143]. Management should be approached
from a collaborative multidisciplinary team of radiologists,
pathologists, surgeons, and gastroenterologists catered to
PCN type, the presence or absence of features concerning for
invasive cancer, patient symptoms, comorbidities, and goals.
Given the complexity of both pathogenesis and management
of PCNs, the following is a brief summary of dening features of the most common PCNs whose management may
include surgery.
5.5.4.1 Intraductal Papillary Mucinous Neoplasm
IPMNs are mucin producing neoplasms that have the greatest malignant potential (30–68% incidence of progression)
and are categorized as intestinal, oncocytic, pancreaticobiliary, or gastric histologic subtypes. The intestinal type is the
most common, while the rare pancreaticobiliary subtype has
the highest recurrence rate (32–71%) and lowest 5year survival (36–52%) due to its association with invasive cancer
(present in 63% of cases) [142]. IPMNs may be associated
with the main pancreatic duct or a side branch duct, and may
occur in isolation or involve the entire duct. IPMN features
that are concerning for malignant transformation and may
serve as indications for surgical resection include jaundice,
enhancing mural nodule or associated solid mass, dysplasia
or malignant cells on cytology, dilated main pancreatic duct
>5–10 mm, however, society-specic guidelines vary and
are more nuanced (Fig. 5.5) [141–143]. Invasive IPMN
(intraductal papillary mucinous cystadenocarcinoma) has a
better prognosis than patients with pancreatic ductal adenocarcinoma (5year overall survival of 28–68% versus approximately <10% in pancreatic ductal adenocarcinoma) [142].
5.5.4.2 Mucinous Cystic Neoplasm
MCNs derive from ductal epithelial mucin-producing cells
and can be distinguished from IPMNs by lack of communication with a pancreatic duct and a predominance in the pancreatic tail. Invasive cancer is found in approximately 17%
of MCNs and is associated with larger size (≥ 3cm) and the
presence of mural nodules [142, 144, 145]. Indications for
surgery include associated symptoms, mural nodules, or
tumor size >3–4 cm but vary by guideline [141–143].
Prognosis for invasive MCN (mucinous cystadenocarcinoma) is similar to that of invasive IPMN and 5year survival
ranges from 26–57% [144, 145].
5 Surgical Approach to Pancreas, Liver, Biliary Physiologic Impairment
45
Fig. 5.5 Fukuoko guidelines for the management of IPMN of the pan-
creas. (a) Pancreatitis may be an indication for surgery for relief of
symptoms. (b) Differential diagnosis includesmucin. Mucin can move
with change in patient position, may be dislodged on cystlavageand
does not have Doppler ow. Features of true tumor nodule include lack
of mobility, presence of Doppler ow and FNA of nodule showing
5.5.4.3 Solid Pseudopapillary Neoplasm
Solid pseudopapillary neoplasms lack glandular cells, are
dened by degenerative pseudopapillary structures, have a
relatively good prognosis with low malignant potential
(8–20% incidence of solid pseudopapillary carcinoma at
resection and a 5year overall survival of >95%) [141]. Given
the excellent prognosis, surgery is the standard of care and
may even be recommended for highly-selected patients with
locally advanced, metastatic, or recurrent disease [141, 142].
5.6 Malignant Pancreas Disease:
Pathophysiology andIndications
forSurgical Treatment
The most common primary pancreas cancer is pancreatic
ductal adenocarcinoma, but other types of pancreas cancer
can develop from cystic neoplasms (intraductal papillary
tumor tissue. (c) Presence of any one of thickened walls, intraductal
mucin or mural nodules is suggestive of main duct involvement. In their
absence main duct involvement is inconclusive. Abbreviations:
BD-IPMN branch duct intraductal papillary mucinous neoplasm,
FNAne needle aspiration
mucinous cystadenocarcinoma, mucinous cystadenocarcinoma, solid pseudopapillary carcinoma, and even serous
cystadenocarcinoma, although this is exceedingly rare), and
neuroendocrine neoplasms (discussed previously).
5.6.1 Pancreas Adenocarcinoma
Pancreatic ductal adenocarcinoma (PDAC) arises from
malignant transformation of ductal epithelial cells in association with PCN or pancreatic intraepithelial neoplasia
(PanIN). Kras mutations are thought to promote dysplastic
transformation of ductal epithelial cells to form PanIN-1
lesions which propagate to PanIN-2 and PanIN-3 lesions
before progressing to invasive ductal adenocarcinoma. This
propagation may be further promoted by other genetic aberrancies (i.e. CDKN2A, TP53, SMAD4, BRCA2, PRSS1)
and synergistic environmental exposure (i.e. smoking, alco-
46
A. W. Acher et al.
hol, obesity, chronic pancreatitis) [146]. PDAC is also associated with hereditary breast and ovarian cancer syndrome
(BRCA1/2 genes), hereditary breast cancer (PALB2 gene),
familial atypical multiple mole melanoma (p16/CDKN2A
gene), familial pancreatitis (PRSS1 gene), lynch syndrome/
HNPCC (MLH1/MLH2 genes), and Peutz-Jeghers syndrome (STK11 gene). Prognosis is stage dependent: 5year
survival is 37% for localized disease, 12% for regional disease, and 3% for metastatic disease [147]. Unfortunately,
most patients present with either regional or distant disease
[147].
Management should be approached from a multidisciplinary perspective of radiologists, pathologists, medical and
radiation oncologists, and pancreas surgeons. Given the
advanced stage at time of diagnosis in majority of patients, in
addition to a poor prognosis, it is critical that the care team
and patient communicate effectively about patient goals.
While resection with a negative margin (R0) remains the
only hope for longtime survival, systemic therapy is essential
to any surgical approach and should be planned in conjunction [148–152]. Surgery based on the location of the tumor
might include pancreaticoduodenectomy or distal pancreatectomy with regional lymphadenectomy. Biliary and
enteric reconstruction are required for pancreas head cancers. Vascular resection and reconstruction may be required
to achieve negative resection margins [153–155].
Unfortunately, despite aggressive surgery and advances in
systemic therapy, the median post-treatment survival remains
15–18 months [149, 150, 153–157].
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Biliary Tract Functions andImpairment
HideoOhtsuka andMichiakiUnno
6
Abstract
The biliary tract includes the entire biliary excretion
route from the liver to the duodenum. Bile is secreted
from hepatocytes into the bile canaliculi. It is eventually
excreted into the duodenum after passing through the
biliary tract. The main components of bile include bile
acids, phospholipids, cholesterols, and bilirubin. Some
of these substances are reabsorbed in the intestine and
returned to the liver via the portal vein, a cycle termed
enterohepatic circulation. Enterohepatic circulation
involves physiologically active substances and ensures
its effective use. The function of the biliary tract is controlled by the autonomic nervous system. Branches from
the hepatic plexus, which is formed by the sympathetic
nerves and the vagus nerve, are distributed across the
biliary tract. The sphincter of Oddi at the papilla and
gallbladder play important roles in the control of the bile
efux, and dysfunctions can occur when their motility is
inhibited. The gallbladder dysfunction is a motility disorder and causes pain similar to chronic cholecystitis. The
sphincter of Oddi regulates the excretion of bile and prevents the regurgitation of duodenal juice. In papillary
dysfunction, the sphincter of Oddi is excessively contracted, which inhibits the excretion of bile and pancreatic juice. Pancreaticobiliary maljunction is a congenital
malformation in which the pancreatic duct and the bile
duct join outside the duodenal wall. In this condition, the
sphincter of Oddi does not regulate the conuence of the
pancreatic duct and bile duct, resulting in bidirectional
regurgitation of bile and pancreatic juice and various
complications in the bile duct and the pancreas.
6.1 The Structure oftheBiliary Tract
The biliary tract collectively refers to the bile ducts and the
gallbladder. It includes the entire biliary excretion route from
the liver to the duodenum. Bile is secreted into the bile canaliculi, which are located between hepatocytes. Bile passes
through the terminal cholangioles (canals of Haring ductules, diameter < 15 μm) and interlobular ductules (15–
100μm) before entering the intrahepatic bile ducts and then
passes through the left and right hepatic ducts and the common hepatic duct to the duodenum [1, 2] (Fig. 6.1). The
intrahepatic bile ducts course parallel to a branch of the portal vein and with one or two branches of the hepatic artery,
forming Glisson’s triads, which are also referred to as portal
triads. The cystic duct joins the gallbladder to the common
hepatic duct. The cystic duct is approximately 2–3cm long
and 2–3mm in diameter. The conuence of the cystic duct
and the common hepatic duct forms the common bile duct,
which opens into the duodenal cavity through the pancreatic
parenchyma after coursing through the posterior side of the
rst part of the duodenum. The opening of the common bile
Classification of Bile ducts
Intrahepatic bile ducts
Small bile ducts (peribiliary grands(-))
terminal cholangioles (canals of Haring ductules)
Interlobular bile duct
Septal duct
Large bile ducts (peribiliary grands(+))
Area duct
Segmental duct
Extrahepatic bile ducts
Left and Right hepatic duct
Common hepatic duct
m >
15
15 –100
100 –300
300 –400
400 –800
m <
800
m
m
m
m
H. Ohtsuka · M. Unno (*)
Department of Surgery, Tohoku University, Sendai, Miyagi, Japan
e-mail: m_unno@surg.med.tohoku.ac.jp
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2022
M. Makuuchi et al. (eds.), The IASGO Textbook of Multi-Disciplinary Management of Hepato-Pancreato-Biliary Diseases,
https://doi.org/10.1007/978-981-19-0063-1_6
Fig. 6.1 Classication of the bile ducts according to the ductal
diameter
51