tumors, as it can define the anatomy of the biliary tree proximal
to the affected segment. As with any invasive procedure, there
Figure 32-11. A view from the choledochoscope showing
cholangiocarcinoma.
been described.20 Further refinement of this technology will
likely enhance ERCP as a diagnostic and therapeutic tool.
Endoscopic Ultrasound
Endoscopic ultrasound (EUS) has improved significantly
in recent years and offers additional diagnostic utility to the
workup of biliary disease. It requires a specialized 30° endo-
scope with either a radial or linear ultrasound transducer at its
tip. The results are operator dependent and require a skilled
endoscopist but offer noninvasive imaging of the bile ducts and
adjacent structures. Endoscopic ultrasound can also be used to
identify choledocholithiasis. It is useful for evaluation of the
retroduodenal potion of the bile duct, which is difficult to visu-
alize with transabdominal ultrasonography. Although EUS is
less sensitive than ERCP for biliary stones, the technique is less
invasive as it does not require cannulation of the sphincter of
Oddi. EUS is also of particular value in the evaluation of tumors
near or behind the duodenum and their resectability. Using a
linear EUS scope that has a biopsy channel, fine-needle aspira-
tion (FNA) of tumors or lymph nodes, therapeutic injections,
or drainage procedures under direct ultrasonic guidance can be
performed.21
Percutaneous Transhepatic Cholangiography
In settings in which the biliary tree cannot be accessed endo-
scopically, antegrade cholangiography can be performed by
accessing the intrahepatic bile ducts percutaneously with a small
needle under fluoroscopic guidance. Once the position in a bile
duct has been confirmed, a guidewire is inserted and a catheter
is passed over the wire (Fig. 32-12). Through the catheter, an
antegrade cholangiogram can be obtained and therapeutic inter-
ventions such as tissue sampling, biliary drain insertions, or stent
placements performed. Percutaneous transhepatic cholangiog-
raphy (PTC) can also be performed through previously placed
percutaneous biliary drainage tubes, if present. PTC has little
role in the management of patients with uncomplicated gallstone
disease but can be useful in patients with bile duct strictures or
1401
are potential risks. For PTC, these are mainly bleeding, cholan-
gitis, bile leak, and other catheter-related problems.12
GALLSTONE DISEASE
Prevalence and Incidence
Gallstone disease (cholelithiasis) is one of the most common
afflictions of the digestive tract. Autopsy reports show that
CHAPTER 32 GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEM
gallstones are present in between 10% and 15% of adults.22 The
prevalence of gallstones is related to many factors, including
diet, age, gender, BMI, and ethnic background with increased
prevalence in patients of Native American and Latin American
descent. Certain conditions also predispose to the development
of gallstones including pregnancy, non-HDL hyperlipidemia,
Crohn’s disease, and certain blood disorders such as heredi-
tary spherocytosis, sickle cell disease, and thalassemia. Sur-
geries that alter the normal neural or hormonal regulation of
the biliary tree including terminal ileal resection and gastric
or duodenal surgery increase the risk of cholelithiasis. Rapid
weight loss following bariatric surgery or lifestyle changes
can also precipitate gallstone formation by creating an imbal-
ance in bile composition. Medications such as somatostatin
analogues and estrogen-containing oral contraceptives are also
associated with an increased risk of developing gallstones.22
Women are three times more likely to develop gallstones than
men, and first-degree relatives of patients with gallstones have
a twofold greater prevalence, possibly indicating a genetic
predisposition.23
Natural History
Despite the high prevalence of cholelithiasis, most patients will
remain asymptomatic from their gallstones throughout life.
For unknown reasons, some patients progress to a symptom-
atic stage, with typical symptoms of postprandial right upper
quadrant pain (biliary colic) caused by a stone obstructing the
cystic duct. In addition to pain, gallstones may progress to cause
complications such as acute cholecystitis, choledocholithiasis,
cholangitis, gallstone pancreatitis, gallstone ileus, and gallblad-
der cancer. Rarely, one of these complications of gallstones may
be the initial presenting picture.
Gallstones in patients without biliary symptoms are com-
monly diagnosed incidentally during unrelated abdominal imag-
ing or at the time of surgery for an unrelated diagnosis. Several
studies have examined the likelihood of developing biliary colic
or developing significant complications of gallstone disease
after incidental diagnosis in the asymptomatic patient. About
80% of these patients will remain symptom free.24 However, 2%
to 3% will become symptomatic per year (i.e., develop biliary
colic). Once symptomatic, patients tend to have recurring bouts
of biliary colic. Complicated gallstone disease (cholecystitis,
choledocholithiasis, gallstone pancreatitis, etc.) develops in 3%
to 5% of symptomatic patients per year.25
Because few patients develop complications without previ-
ous biliary symptoms, prophylactic cholecystectomy in asymp-
tomatic persons with gallstones is rarely indicated.24 Exceptions
exist for individuals who will be isolated from medical care for
extended periods of time, or in populations with increased risk
of gallbladder cancer, in which case a prophylactic cholecys-
tectomy may be advisable. The presence of porcelain gallblad-
der, marked by significant calcifications thought to be related to
1402

Bile Safety
duct wire
21-guage tumor inserted
needle
B
PART II

External
SPECIFIC CONSIDERATIONS

drainage
catheter

C
D

Drainage
catheter

Guidewire inserted
through introducer

E F

Figure 32-12. Schematic diagram of percutaneous transhepatic cholangiogram and drainage for obstructing proximal cholangiocarcinoma.
A. Dilated intrahepatic bile duct is entered percutaneously with a fine needle. B. Small guidewire is passed through the needle into the duct.
C. A plastic catheter has been passed over the wire, and the wire is subsequently removed. A cholangiogram can be performed through the
catheter. D. An external drainage catheter in place. E. Long wire placed via the catheter and advanced past the tumor and into the duodenum.
F. Internal stent has been placed through the tumor.

gallstones, is a rare premalignant condition and is an absolute
indication for cholecystectomy, even when asymptomatic.
Gallstone Formation
Gallstones form as a result of solids settling out of solution. The
major organic solutes in bile are bilirubin, bile salts, phospho-
lipids, and cholesterol. Gallstones are classified by their choles-
terol content as either cholesterol stones or pigment stones.
Pigment stones can be further classified as either black or brown.
In Western countries, about 80% of gallstones are cholesterol
stones and about 15% to 20% are black pigment stones.22 Brown
pigment stones account for only a small percentage. Both
2 types of pigment stones are more common in Asia.
Cholesterol Stones. Pure cholesterol stones are uncommon
and account for <10% of all stones. They usually occur as a sin-
gle large stone with a smooth surface. The majority of choles-
terol stones are mixed but are at least 70% cholesterol by weight
in addition to variable amounts of bile pigments and calcium.
These stones are usually multiple, of variable size, and may be
hard and faceted or irregular, multilobed, and soft (Fig. 32-13).
Colors range from whitish yellow to green or black. Most cho-
lesterol stones (>90%) are radiolucent, though some have a high
calcium carbonate component and become radioopaque.
The primary event in the formation of cholesterol stones
is supersaturation of bile with cholesterol. Cholesterol is highly
nonpolar and its solubility in water and bile depends on the
relative concentration of cholesterol, bile salts, and lecithin (the
main phospholipid in bile). Cholesterol is secreted into bile and
is surrounded by bile salts and phospholipids to form a soluble
vesicle complex. When cholesterol hypersecretion is present,
either through increased intake or dysfunctional processing,
A the ability of the bile salts and phospholipid to maintain solu-
B disorders like hereditary spherocytosis and sickle cell disease
C that enzymatically cleaves conjugated bilirubin to produce the
Figure 32-13. Gallbladder with cholesterol stones. A. Stones
of multiple shapes and sizes. B. Solitary large stone. C. Multiple
stones of varying composition. (Reproduced with permission from
Slesinger MH, Fordtran JS: Gastrointestinal Diseases. Philadelphia,
PA: Elsevier/Saunders; 1989.)
Metastable 1403
supersaturated
100 0 zone
Mo
80 20
les
rol
ste
%
60 40
ole
Lec
2 or more
Ch
ithi
phases
s%
n
40 60
le
Mo
20 80
CHAPTER 32 GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEM
Micellar
liquid
0 100
100 80 60 40 20 0
Moles % Bile salts
Figure 32-14. The three major components of bile plotted on
triangular coordinates, cholesterol, bile salts and phospholipids
(lecithin). A given point represents the relative molar ratios
of each. The area labeled “micellar liquid” shows the range of
concentrations in which cholesterol is fully solubilized. The shaded
area directly above this region corresponds to a metastable zone,
supersaturated with cholesterol. Above the shaded area, bile has
exceeded the solubilization capacity of cholesterol and precipitation of
cholesterol crystals and stones occurs.
supersaturation occurs. When cholesterol concentrations exceed
bility, the cholesterol precipitates out of solution into a solid,
forming a cholesterol stone (Fig. 32-14).26 Cholesterol hyperse-
cretion is almost always the cause of supersaturation rather than
reduced secretion of phospholipid or bile salts.2
Pigmented Stones. Pigmented stones contain <20% choles-
terol and are dark because of the presence of calcium bilirubi-
nate. Black and brown pigment stones have little in common
and should be considered as separate entities.
Black pigment stones are usually small, brittle, dark, and
sometimes spiculated. They are formed by supersaturation of
unconjugated bilirubin within the bile. Deconjugation of bili-
rubin occurs normally in bile at a slow rate. Thus, excessive
levels of conjugated bilirubin excretion, as occurs in hemolytic
will lead to an increased rate of production of unconjugated
bilirubin. Cirrhosis and hepatic dysfunction may also lead to
increased secretion of unconjugated bilirubin directly from the
liver. The insoluble unconjugated bilirubin will then precipitate
with calcium as insoluble calcium bilirubinate, forming a pig-
ment stone. Due to their high calcium content, pigment stones
are often radiopaque. Like cholesterol stones, they almost
always form in the gallbladder. In Asian countries such as
Japan, black stones account for a much higher percentage of
gallstones than in the Western hemisphere.
Brown stones are usually <1 cm in diameter, brownish-yel-
low, soft, and often mushy. They may form either in the gallblad-
der or in the bile ducts secondary to bacterial infection and bile
stasis. Bacteria such as Escherichia coli secrete β-glucuronidase
insoluble unconjugated bilirubin. This unconjugated bilirubin
then precipitates with calcium, and along with dead bacterial cell
bodies, forms soft brown stones in the biliary tree. Brown stones
are typically found in Asian populations and are associated with
stasis secondary to parasite infection with Ascaris lumbricoides
1404 (roundworm) or Clonorchis sinensis (liver fluke). In Western
populations, brown stones most often occur as primary bile duct
stones in patients with biliary strictures or other common bile
duct stones that cause stasis and bacterial contamination.2,27
Symptomatic Gallstones
Symptomatic Cholelithiasis. Patients with symptomatic gall-
stone disease typically present with recurrent attacks of pain. The
pain develops when a stone obstructs the cystic duct, resulting
in a progressive increase of tension in the gallbladder wall as it
contracts in response to a meal. This postprandial right upper
PART II
quadrant or epigastric pain is often referred to as biliary colic. If
untreated, about two-thirds of these patients will develop chronic
noninfectious inflammation of the gallbladder wall, termed
chronic cholecystitis. The pathologic changes, which often do
not correlate well with symptoms, vary from an apparently nor-
SPECIFIC CONSIDERATIONS
mal gallbladder with minor chronic inflammation in the mucosa,
to a shrunken, nonfunctioning gallbladder with transmural fibro-
sis and adhesions to nearby structures. The mucosa is initially
normal or hypertrophied but later becomes atrophied, with the
epithelium protruding into the muscle coat, leading to the forma-
tion of the so-called Aschoff-Rokitansky sinuses.
Clinical Manifestations The chief symptom associated with
symptomatic cholelithiasis is pain (biliary colic). The pain is con-
stant and increases in severity over the first half hour or so after
a meal and can last 1 to 5 hours. It is located in the epigastrium
or right upper quadrant and frequently radiates to the right upper
back or between the scapulae (Fig. 32-15). The pain is severe and
comes on abruptly, typically during the night or after a fatty meal.
It often is associated with nausea and sometimes vomiting. Patients
generally suffer discrete, recurrent attacks of pain, between which
they feel well. Physical examination may reveal mild right upper
quadrant tenderness during an episode of pain. If the patient is pain
free, the physical examination is usually unremarkable. Labora-
tory values, such as WBC count and liver function tests, are usu-
ally normal in patients with uncomplicated gallstones.
Atypical presentations of gallstone disease are common
and a high index of suspicion for biliary disease must be main-
tained when evaluating patients with abdominal complaints.
Association with meals is present in only about 50% of patients.
Some patients report milder attacks of pain but relate it to meals.
The pain may be located primarily in the back or the left upper
or right lower quadrant. Bloating and belching may be present
and associated with the attacks of pain. In patients with atypi-
cal presentations, other conditions that may be causing upper
abdominal pain should be ruled out, even in the presence of
gallstones. These include but are not limited to peptic ulcer dis-
ease, gastroesophageal reflux disease, herpes zoster, abdominal
wall hernias, inflammatory bowel disease, diverticular disease,
pancreatitis, liver disease, renal calculi, pleuritic pain, and car-
diac pain.
When the pain lasts >24 hours without resolving, an
impacted stone in the cystic duct or acute cholecystitis (see
later “Acute Cholecystitis” section) should be suspected. An
impacted stone without cholecystitis will result in what is called
hydrops of the gallbladder. Bile will be unable to enter the gall-
bladder due to the obstructed cystic duct, but the gallbladder
epithelium will continue to secrete mucus, and the gallbladder
will become distended with clear-white mucinous material. The
gallbladder may be palpable but usually is not tender. Hydrops
of the gallbladder may result in edema of the gallbladder wall,
inflammation, infection, and perforation. Although hydrops
2
2
2 9 6
14 15 7
64
50 24 1 4
13 5 4
4 1
A
3
9 6
11 35 33
2 3 2
15
2 11 2 3
19
5 3
2
B
Figure 32-15. A. Sites of the most severe pain during an episode
of biliary colic in 107 patients with gallstones (% values add up to
>100% because of multiple responses). The subxiphoid and right
subcostal areas were the most common sites; note that the left sub-
costal area was not an unusual site of pain. B. Sites of pain radiation
(%) during an episode of biliary colic in the same group of patients.
may persist with few consequences, early cholecystectomy is
generally indicated to avoid complications.
Diagnosis The diagnosis of symptomatic cholelithiasis or
chronic cholecystitis depends on the presence of typical symp-
toms and the demonstration of stones on diagnostic imaging.
An abdominal ultrasound is the standard diagnostic test for
gallstones as it is noninvasive and highly sensitive (see earlier
“Ultrasonography” section).28 Gallstones are occasionally iden-
tified on abdominal CT scans that were obtained as part of a
broader workup of abdominal pain. In these cases, if the patient
has typical symptoms, it is reasonable to proceed with interven-
tion. Stones diagnosed incidentally on CT or plain radiographs
in patients without symptoms should be left in place. Occasion-
ally, patients with typical attacks of biliary pain have no evi-
dence of stones on ultrasound but have evidence of sludge in the
gallbladder. If a patient has attacks of typical biliary pain and
sludge is detected, cholecystectomy is warranted.
In addition to sludge and stones, cholesterolosis and adeno-
myomatosis of the gallbladder may cause typical biliary symp-
toms and may be detected on ultrasound or CT. Cholesterolosis is
caused by the accumulation of cholesterol in macrophages in the
gallbladder lamina propria, either locally or as polyps. It produces
the classic studded macroscopic appearance of a “strawberry
gallbladder.” Adenomyomatosis (cholecystitis glandularis prolif-
erans) is characterized on microscopy by hypertrophic smooth
muscle bundles and by the ingrowths of mucosal glands into the
muscle layer (epithelial sinus formation). Granulomatous polyps
develop in the lumen at the fundus, and the gallbladder wall is
thickened. Septae or strictures may be seen within the gallblad-
der. In symptomatic patients, cholecystectomy is the treatment of
choice for patients with these conditions.29
Treatment Nonsurgical management of gallstone disease
using medications or lithotripsy has had disappointing long-
term results. These modalities are not considered to be part of
the primary treatment algorithm for gallstone disease.30 Surgi-
cal cholecystectomy offers the best long-term results for
patients with symptomatic gallstones. About 90% of patients
with typical biliary symptoms and stones are rendered symp-
tom free after cholecystectomy. For patients with atypical
symptoms such as dyspepsia, flatulence, belching, bloating,
and dietary fat intolerance, the results are not as favorable. The
laparoscopic approach has been proven to be safe and effective
and has become the standard of care for symptomatic gallstone
disease, replacing open cholecystectomy in routine cases.29,31
3 toDuegallstone
to the possibility of developing complications related
disease, patients with symptomatic choleli-
thiasis should be offered elective cholecystectomy. While wait-
ing for surgery, or if surgery has to be postponed, the patient
should be advised to avoid dietary fats and large meals. Dia-
betic patients with symptomatic gallstones should be encour-
aged to have a cholecystectomy promptly, as they are more
prone to developing severe acute cholecystitis. Pregnant
women with symptomatic gallstones who cannot be managed
expectantly with diet modifications can safely undergo laparo-
scopic cholecystectomy. The operation should be performed
during the second trimester if possible.
Acute Cholecystitis. Acute cholecystitis, or infection of the
gallbladder, is associated with gallstones in 90% to 95% of cases.
Rarely, acalculous cholecystitis can occur, usually in patients
with other acute systemic diseases (see later “Acalculous Chole-
cystitis” section). Obstruction of the cystic duct by a gall-
stone is the initiating event that leads to gallbladder distention,
inflammation, and edema of the gallbladder wall. In <1% of acute
cholecystitis, the cause is a tumor obstructing the cystic duct.
Why inflammation develops only occasionally with cystic duct
obstruction is unknown, but it is probably related to the duration
of obstruction. Initially, acute cholecystitis is an inflammatory
process, probably mediated by the mucosal toxin lysolecithin,
a product of lecithin, as well as bile salts and platelet-activat-
ing factor. An increase in prostaglandin synthesis amplifies the
inflammatory response. In acute cholecystitis, the gallbladder
wall becomes grossly thickened and reddish with subserosal
hemorrhages. Pericholecystic fluid often is present. The mucosa
may show hyperemia and patchy necrosis. In severe cases, about
5% to 10%, the inflammatory process progresses and leads to
ischemia and necrosis of the gallbladder wall. More frequently,
the gallstone is dislodged and the inflammation resolves.
Not all episodes of uncomplicated acute cholecystitis
involve infection. Secondary bacterial contamination is thought
to occur in only 15% to 30% of patients. With some severe
infections, gangrenous cholecystitis can develop, and an abscess
or perforation may occur. When they happen, perforations are
usually contained in the subhepatic space by the omentum and
adjacent organs. However, free perforation with peritonitis, 1405
intrahepatic perforation with intrahepatic abscesses, and per-
foration into adjacent organs (duodenum or colon) with cho-
lecystoenteric fistula have been described. When gas-forming
organisms are part of the secondary bacterial infection, gas may
be seen in the gallbladder lumen and in the wall of the gallblad-
der on abdominal radiographs and CT scans, an entity called
emphysematous cholecystitis.
Clinical Manifestations About 80% of patients with acute
cholecystitis give a history compatible with chronic cholecysti-
CHAPTER 32 GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEM
tis. Acute cholecystitis often begins as an attack of biliary colic
with relapsing and remitting pain in the right upper quadrant or
epigastrium that may radiate to the right back or interscapular
area. In contrast to biliary colic, the pain of acute cholecystitis
does not subside. It is unremitting, may persist for several days,
and is usually more severe than the pain associated with uncom-
plicated gallstone disease. The patient is often febrile, complains
of anorexia, nausea, and vomiting, and may be reluctant to move
as the inflammatory process creates focal peritonitis. On physi-
cal examination, tenderness and guarding are usually present in
the right upper quadrant. A mass, the gallbladder and adherent
omentum, is occasionally palpable; however, guarding may pre-
vent identification of this. Murphy’s sign, an inspiratory arrest
with deep palpation in the right subcostal area, is characteristic
of acute cholecystitis.
Laboratory evaluation commonly reveals a mild to mod-
erate leukocytosis (12,000–15,000 cells/mm3). However, a
normal WBC does not rule out the diagnosis. An unusually
high WBC count (>20,000 cells/mm3) suggests a complicated
form of cholecystitis such as gangrenous cholecystitis, perfo-
ration, or associated cholangitis. In uncomplicated acute cho-
lecystitis, serum liver chemistries are usually normal, but a
mild elevation of serum bilirubin (<4 mg/mL) may be present
along with mild elevation of alkaline phosphatase, transami-
nases, and amylase.28 Severe jaundice is suggestive of obstruc-
tion of the bile ducts. This can be a result of common bile
duct stones or severe pericholecystic inflammation secondary
to impaction of a stone in the infundibulum of the gallblad-
der that mechanically obstructs the bile duct, known as Mir-
izzi’s syndrome (Fig. 32-16). In elderly patients and in those
with diabetes mellitus, acute cholecystitis may have a subtle
Figure 32-16. Mirizzi’s syndrome. Impaction of a large stone in
the neck of the gallbladder causing obstruction at the level of the
confluence of the cystic duct and common hepatic duct.
1406
PART II
SPECIFIC CONSIDERATIONS
Figure 32-17. Ultrasonography from a patient with acute cholecystitis. The white arrowheads indicate the thickened gallbladder wall. There
are several stones in the gallbladder (white arrows) throwing acoustic shadows (black arrowheads). Trace pericholecystic fluid can be seen
surrounding the gallbladder (black arrows).
presentation resulting in a delay in diagnosis. These patients
may also have higher rates of treatment related morbidity com-
pared to younger and healthier patients.
The differential diagnosis for acute cholecystitis includes
but is not limited to peptic ulcer disease, pancreatitis, appen-
dicitis, hepatitis, perihepatitis (Fitz-Hugh–Curtis syndrome),
myocardial ischemia, pneumonia, pleuritis, and herpes zoster
involving the intercostal nerve.
Diagnosis Ultrasonography is considered the most useful ini-
tial radiologic test for diagnosing acute cholecystitis, with a sen-
sitivity and specificity of 70% to 90%. Ultrasound is effective at
documenting the presence or absence of stones, and it can show
gallbladder wall thickening and pericholecystic fluid, both of
which are highly suggestive of acute cholecystitis (Fig. 32-17).
Focal tenderness over the gallbladder when compressed by the
sonographic probe (sonographic Murphy’s sign) also supports
the diagnosis of acute cholecystitis. Biliary scintigraphy (HIDA
scanning) may be of help in atypical cases if the diagnosis
remains in question after initial workup. Lack of filling of the
gallbladder after 4 hours indicates an obstructed cystic duct and,
in the clinical setting of suspected acute cholecystitis, confirms
the diagnosis with a reported sensitivity above 90%.32 Con-
versely, a normal HIDA scan with clear filling of the gallblad-
der rules out the diagnosis of acute cholecystitis. CT scans are
frequently performed on patients with acute abdominal pain of
unknown etiology, as they can evaluate for a number of poten-
tial pathologic processes at once. In patients with acute chole-
cystitis, a CT scan can demonstrate thickening of the gallbladder
wall, pericholecystic fluid, and the presence of gallstones, but it
is somewhat less sensitive than ultrasonography.
Treatment Patients who present with acute cholecystitis
should receive IV fluids, broad-spectrum antibiotics, and anal-
gesia. The antibiotics should cover gram-negative enteric organ-
isms as well as anaerobes. Although the inflammation in acute
cholecystitis may be sterile in some patients, it is difficult to
know who is secondarily infected. Therefore, antibiotics have
become a standard part of the initial management of acute cho-
lecystitis in most centers.
Cholecystectomy is the definitive treatment for acute cho-
lecystitis. In the past, the timing of cholecystectomy has been
a matter of debate. Early cholecystectomy performed within
72 hours of the onset of the illness is preferred over delayed
cholecystectomy that is performed 6 to 10 weeks after initial
medical treatment and recuperation. Several studies have shown
that unless the patient is unfit for surgery, early cholecystectomy
should be recommended as soon as possible, as it offers the
patient a definitive solution in one hospital admission, quicker
recovery times, similar complication rates, and an earlier return
to work.33,34
Laparoscopic cholecystectomy is the procedure of choice
for acute cholecystitis. The conversion rate to an open cholecys-
tectomy has fallen in recent years to less than 5% as laparoscopic
equipment and experience has improved.35 While laparoscopic
cholecystectomy for acute cholecystitis may be more tedious
and take longer than an elective cholecystectomy for symp-
tomatic cholelithiasis, the laparoscopic approach remains safe
and effective, even in the setting of acute and sometimes severe
inflammation. Open cholecystectomy must remain an option in
particularly difficult cases, or in patients suspected of having
prohibitive intraabdominal adhesions, but it is rarely the primary
treatment choice.
When patients are medically unfit for surgery due to the
severity of their illness or medical comorbidities, they can be
treated with antibiotics and biliary decompression with cho-
lecystostomy tube placement, which is usually effective in
stabilizing the patient.36 For those who do recover after chole-
cystostomy, the tube can be removed once the track is mature
(approximately 4 weeks) and cholangiography through it shows
a patent cystic duct. Elective laparoscopic cholecystectomy
can be scheduled within approximately 6 to 8 weeks, assum-
ing their medical fitness recovers.37 Failure to improve after
cholecystostomy may be due to gangrene of the gallbladder
or perforation, in which case, damage control surgery may be
unavoidable.
Choledocholithiasis. Common bile duct (CBD) stones may be
small or large, single or multiple, and are found in 6% to 12% of
patients with stones in the gallbladder. The incidence increases
with age. About 20% to 25% of patients above the age of 60 with
symptomatic gallstones have stones in the common bile duct as
well as in the gallbladder.38 The vast majority of ductal stones in
Western countries are formed within the gallbladder and migrate
down the cystic duct into the common bile duct. These are clas-
sified as secondary CBD stones, in contrast to the primary CBD
stones that form in the bile duct itself. Secondary stones are usu-
ally cholesterol stones, whereas primary stones are usually of
the brown pigment type. The primary stones are associated with
biliary stasis and infection, and they are more commonly seen in
Asian populations. Biliary stasis leading to the development of
primary CBD stones can be caused by biliary strictures, papillary
stenosis, tumors, or other (secondary) stones.
Clinical Manifestations Choledochal stones may be silent and
often are discovered incidentally. They may cause complete or
incomplete obstruction, or they may manifest with cholangitis
or gallstone pancreatitis. The typical pain caused by a stone in
the bile duct is very similar to that of biliary colic caused by
impaction of a stone in the cystic duct. Nausea and vomiting are
common. Physical examination may be normal, but mild epigas-
tric or right upper quadrant tenderness as well as mild icterus
are common. The symptoms may also be intermittent, such as
pain and transient jaundice caused by a stone that temporar-
ily impacts the ampulla but subsequently moves away, acting
as a ball valve. A small stone may pass through the ampulla
spontaneously with resolution of symptoms. Finally, the stones
may become completely impacted, causing severe progressive
jaundice. Elevation of serum bilirubin, alkaline phosphatase,
and transaminases are commonly seen in patients with bile duct
stones. However, in about one-third of patients with common
bile duct stones, the liver chemistries are normal, particularly if
the obstruction is incomplete or intermittent.
Diagnosis Ultrasonography is useful for documenting stones
in the gallbladder (if still present), as well as determining the
size of the common bile duct. As stones in the bile ducts tend
to move down to the distal part of the common duct behind the
duodenum, bowel gas can preclude their detection on ultraso-
nography. A dilated common bile duct (>8 mm in diameter) on
ultrasonography in a patient with gallstones, jaundice, and bili-
ary pain is highly suggestive of common bile duct stones. If the
presence of bile duct stones is in question, magnetic resonance
cholangiopancreatography (MRCP) provides excellent anatomic
detail and has a sensitivity and specificity of 95% and 89%,
respectively, for detecting choledocholithiasis.14 Endoscopic
A B
retrograde cholangiopancreatography (ERCP) is highly effec- 1407
tive at diagnosing choledocholithiasis and in experienced hands,
cannulation of the ampulla of Vater and diagnostic cholangiog-
raphy are achieved in >90% of cases. However, due to the risks
associated with the procedure, it is rarely used as a purely diag-
nostic modality, rather being reserved for cases in which a thera-
peutic intervention such as stone extraction or sphincterotomy is
planned. Endoscopic ultrasound has been demonstrated to be as
good as ERCP for detecting common bile duct stones (sensitivity
of 95% and specificity of 97%). However, EUS has fewer thera-
CHAPTER 32 GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEM
peutic capabilities and requires endoscopic expertise, making it
less desirable except in specific clinical senarios.39 Percutaneous
transhepatic cholangiography (PTC) is rarely needed in patients
with common bile duct stones but can be performed for both
diagnostic and therapeutic reasons in patients with contraindica-
tions to endoscopic or surgical approaches.
Treatment For patients with symptomatic gallstones and sus-
pected common bile duct stones, bile duct clearance and cho-
lecystectomy are indicated. This may be safely achieved either
with preoperative ERCP followed by surgery or by going directly
to surgery with intraoperative cholangiogram and common bile
duct exploration to address retained stones. Both approaches are
considered safe and effective, and no formal recommendation
exists to definitively support one over the other.40,41
If upfront laparoscopic cholecystectomy is pursued, the
surgery should include an intraoperative cholangiogram to doc-
ument the presence or absence of bile duct stones. If stones are
identified, laparoscopic common bile duct exploration via the
cystic duct or with formal choledochotomy allows the stones
to be retrieved in the same setting (see “Choledochal Explora-
tion” section). If the expertise and/or instrumentation for lapa-
roscopic common bile duct exploration are not available, the
patient can be awoken and scheduled for ERCP with sphincter-
otomy the following day. An open common bile duct explora-
tion is an option if the endoscopic and laparoscopic methods are
not feasible. If a choledochotomy is performed, primary repair
can be considered in large ducts, while smaller ducts should be
repaired over a T-tube. To do this, a standard T-tube should be
modified by cutting the ends short enough to allow placement
within the duct and dividing the T longitudinally to facilitate
easy removal from the duct later on (Fig. 32-18). If a common
Figure 32-18. T-tube placement. A. A standard
T-tube that has been cut and modified for use in
the biliary tract. B. The T-tube is placed through a
ductotomy in the common bile duct with the defect
closed over the tube. The opposite end is brought out
through the abdominal wall for decompression of the
bile ducts.
1408 bile duct exploration was performed and a T tube left in place,
a T-tube cholangiogram should be obtained before its removal,
at least several weeks after its placement.
In very severe cases, stones impacted in the ampulla may
be unable to be cleared by endoscopic approaches or common
bile duct exploration (open or laparoscopic). In these cases,
transduodenal sphincterotomy can be considered. If one is
entirely unable to disimpact the duct, choledochoduodenostomy
or Roux-en-Y choledochojejunostomy may be the only option
to restore biliary continuity.42
If the stones were left in place at the time of surgery or
diagnosed shortly after the cholecystectomy, they are classified
PART II
as retained. Those diagnosed months or years later are termed
recurrent (Fig. 32-19). Retained or recurrent stones following
cholecystectomy are best treated endoscopically. A generous
sphincterotomy will allow for stone retrieval as well as spon-
taneous passage of stones. Alternately, retained stones can be
SPECIFIC CONSIDERATIONS
A life-threatening septicemia. Patients with gallstone-induced
B nography is helpful, as it will document the presence of gall-
Figure 32-19. Retained common bile duct stones. The patient pre-
sented 3 weeks after laparoscopic cholecystectomy. A. An ultra-
sound shows a normal or mildly dilated common bile duct with a
stone. Note the location of the right hepatic artery anterior to the
common hepatic duct (an anatomic variation). B. An endoscopic
retrograde cholangiography from the same patient shows multiple
stones in the common bile duct. Only the top one showed on ultra-
sound as the other stones lie in the distal common bile duct behind
the duodenum.
cleared via a mature T-tube tract (4 weeks) if one was placed
at the time of surgery. To do this, the T-tube is removed and
a catheter passed through the tract into the common bile duct.
Under fluoroscopic guidance, the stones can be retrieved with
baskets or balloons. A similar approach will allow for stone
clearance by percutaneous transhepatic cholecystostomy (PTC)
if there is no other way to reach the duct. Repeat surgery should
be a last resort if other interventions have failed.
Cholangitis. Cholangitis is one of the main complications
of choledochal stones. Acute cholangitis is an ascending bac-
terial infection associated with partial or complete obstruc-
tion of the bile ducts.43 Hepatic bile is sterile, and bile in the
bile ducts is kept sterile by continuous antegrade bile flow
and by the presence of antibacterial substances in bile, such as
immunoglobulin. Mechanical hindrance to bile flow facilitates
ascending bacterial contamination from the bowel. Positive
bile cultures are common in the presence of bile duct stones
as well as with other causes of obstruction. Biliary bacterial
contamination alone does not lead to clinical cholangitis; the
combination of both significant bacterial contamination and
biliary obstruction is required for its development. Gallstones
are the most common cause of obstruction in cholangitis.
Other causes include primary sclerosing cholangitis, benign
and malignant strictures, parasites, instrumentation of the
ducts, and indwelling stents, as well as partially obstructed
biliary-enteric anastomoses. The most common organisms
cultured from bile in patients with cholangitis include E coli,
Klebsiella pneumoniae, Streptococcus faecalis, Enterobacter,
and Bacteroides fragilis.43
Clinical Manifestations Cholangitis may present as anything
from a mild, self-limited episode to a fulminant, potentially
cholangitis are most commonly older and female. The most
common presentation is fever, epigastric or right upper quad-
rant pain, and jaundice. These classic symptoms, known as
Charcot’s triad, are present in about two-thirds of patients.
The illness can progress rapidly with the development of shock
and altered mental status, known as Reynolds’ pentad (e.g.,
fever, jaundice, right upper quadrant pain, septic shock, and
mental status changes). However, the presentation may be
atypical, with little if any fever, jaundice, or pain. This occurs
most commonly in the elderly, who may have unremarkable
symptoms until the process is already quite advanced. Patients
with indwelling stents are at particularly high risk for cholan-
gitis, though rarely become jaundiced as a patent stent will
prevent the obstruction of bile flow. On abdominal examina-
tion, the findings are indistinguishable from those of acute
cholecystitis.44
Diagnosis Leukocytosis, hyperbilirubinemia, and elevation of
alkaline phosphatase and transaminases are common and, when
present, support the clinical diagnosis of cholangitis. Ultraso-
bladder stones, demonstrate dilated ducts, and possibly pinpoint
a site of obstruction. CT scanning and MRI can show pancreatic
and periampullary masses, if present, in addition to the ductal
dilatation. However, abdominal imaging will rarely elucidate
the exact cause of cholangitis, and the initial diagnosis is gener-
ally made clinically.
Treatment The initial treatment of patients with cholangi-
tis includes broad-spectrum IV antibiotics to cover enteric
organisms and anaerobes, fluid resuscitation, and rapid biliary
decompression. This is most often accomplished through ERCP
and sphincterotomy. ERCP will show the level and the reason
for the obstruction, allow for culture of the bile, permit the
removal of stones if present, and accomplish drainage of the
bile ducts. Placement of drainage catheters or stents can
also be performed if needed. In cases in which ERCP is not
available, PTC, EUS, or surgical drainage can be utilized. The
selection of the appropriate approach will depend on the type
and location of the suspected obstruction as well as the avail-
ability of local resources and expertise. Cholecystostomy tubes
are not indicated in the acute management of cholangitis as the
primary source of the infection is extrinsic to the gallbladder.
Patients with cholangitis can deteriorate rapidly and may
require intensive care unit monitoring and vasopressor support.
However, most patients will respond to biliary decompression
and supportive measures. In the current era, acute cholangitis
is associated with an overall mortality rate of approximately
5%. When associated with renal failure, cardiac impairment,
hepatic abscesses, and malignancies, the morbidity and mortal-
ity rates are much higher. Patients who have suffered an episode
of acute cholangitis related to gallstone disease should be rec-
ommended to undergo elective cholecystectomy approximately
6 weeks after the resolution of their cholangitis.45 Those whose
cholangitis was related to another cause of biliary obstruction
should be followed and treated for the specific etiology of their
obstruction but do not necessarily require cholecystectomy if
gallstones were not the causative etiology of their cholangitis.
Patients with indwelling stents and cholangitis usually require
repeated imaging and stent exchange to mitigate the risk of
recurrent infections.
Gallstone Pancreatitis. Gallstones in the common bile duct
can provoke attacks of acute pancreatitis through transient or
persistent obstruction of the pancreatic duct by a stone passing
through or impacted in the ampulla. The exact mechanism by
which obstruction of the pancreatic duct leads to pancreatitis
is unclear, but it may be related to increased ductal pressures
causing leakage of pancreatic enzymes into the glandular tissue.
The initial management of gallstone pancreatitis is supportive,
A B
Figure 32-20. Gallstone Ileus. A. A choledochoenteric fistula has formed between the gallbladder and the duodenum, allowing a gallstone
to pass into the intestinal tract. B. Intraoperative photo showing a longitudinal enterotomy and extraction of an impacted stone from the distal
small bowel.
including admission for bowel rest, IV hydration, and pain 1409
control. Antibiotics are not indicated in the absence of signs
of infected pancreatic necrosis. Imaging of the biliary tree with
ultrasound, CT, or MRCP is essential to confirm the diagnosis.
When gallstones are present and the pancreatitis is mild and
self-limited, the stone has probably passed. For these patients,
a cholecystectomy with intraoperative cholangiogram is indi-
cated as soon as the pancreatitis has clinically resolved. It is
strongly recommended that cholecystectomy be performed dur-
ing the same admission whenever possible due to the high rate
CHAPTER 32 GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEM
of recurrence and increased morbidity of subsequent attacks of
pancreatitis.46 If gallstones are present obstructing the duct and
the pancreatitis is severe, an ERCP with sphincterotomy and
stone extraction may be necessary. This must be balanced with
the risk of ERCP-induced pancreatitis and thus is usually only
employed if supportive measures are failing.
Gallstone Ileus. Gallstone ileus can occur when a large gall-
stone erodes through the wall of the gallbladder directly into
the intestine via a choledochoenteric fistula (Fig. 32-20A).
These stones can then pass through the intestinal tract until they
reach an area of fixed obstruction. Proximal stones can become
impacted in the pylorus or proximal duodenum causing gastric
outlet obstruction (Bouveret syndrome). Those that travel dis-
tally may become lodged at surgical anastomoses or the ileoce-
cal valve, where they can become impacted and cause small
bowel obstruction. Gallstone ileus is responsible for less than
1% of all intestinal obstructions.47 These patients present with
symptoms of obstipation, nausea, and abdominal pain. Plain
films may show an obstructive bowel gas pattern but may fail to
identify a radiolucent stone. Ultrasound evaluation may be lim-
ited by extensive bowel gas. CT is highly sensitive and specific
for gallstone ileus and will help to determine the location of the
obstruction. Management of gallstone ileus focuses on relieving
the intestinal obstruction and removing the stone. In cases of
very proximal obstructions in the stomach or duodenum, endo-
scopic retrieval can be effective. For more distal stones, surgical
enterolithotomy can be accomplished either laparoscopically or
open. This procedure entails the removal of the stone through
1410 an enterotomy that is then either repaired or resected depend-
ing on its size (Fig. 32-20B). Stones that have successfully
traversed the ileocecal valve are likely to pass without further
intervention. The role of pursuing cholecystectomy and/or cho-
ledochoenteric fistula closure at the time of enterolithotomy or
addressing it at a later time remains a topic of debate, but it
should be considered to reduce the risk of recurrence.47
Cholangiohepatitis
Cholangiohepatitis, also known as recurrent pyogenic cholan-
gitis, is endemic to the Orient. It also has been encountered in
Asian population in the United States, Europe, and Australia.
PART II

It affects both sexes equally and occurs most frequently in the

third and fourth decades of life. Cholangiohepatitis is caused
by bacterial contamination (commonly E coli, Klebsiella spe-
cies, Bacteroides species, or Enterococcus faecalis) of the bili-
ary tree, and often it is associated with biliary parasites such Figure 32-21. Percutaneous cholecystostomy. A pigtail catheter
SPECIFIC CONSIDERATIONS

as Clonorchis sinensis, Opisthorchis viverrini, and A lumbri-
coides. Bacterial enzymes cause deconjugation of bilirubin,
which precipitates as bile sludge. The sludge and dead bacterial
cell bodies form brown pigment stones, the nucleus of which
may contain an adult Clonorchis worm, an ovum, or an ascarid.
These stones can form throughout the biliary tree and cause par-
tial obstructions that contribute to repeated bouts of cholangi-
tis, biliary strictures, further stone formation, infection, hepatic
abscesses, or liver failure (secondary biliary cirrhosis).48
Patients with cholangiohepatitis usually present with pain
in the right upper quadrant or epigastrium, fever, and jaundice.
Relapsing symptoms are one of the most characteristic features
of the disease. The episodes may vary in severity but, without
intervention, will gradually lead to malnutrition and hepatic
insufficiency. An ultrasound may detect stones in the biliary
tree, pneumobilia from infection by gas-forming organisms,
liver abscesses, and, occasionally, strictures. The gallbladder
may be thickened and inflamed in about 20% of patients but
rarely contains gallstones. ERCP or MRCP can be utilized for
biliary imaging for cholangiohepatitis. They can detect obstruc-
tions and define strictures and stones. ERCP (or PTC if nec-
essary) has the additional benefit of allowing for emergent
decompression of the biliary tree in the septic patient. Hepatic
abscesses may be drained percutaneously. The long-term goal
of therapy is to extract stones and debris and relieve strictures.
It may take several procedures, and in severe, refractory cases
in which stones and strictures cannot be relieved, it may require
a hepaticojejunostomy to reestablish biliary–enteric continuity.
Occasionally, resection of involved areas of the liver may offer
the best form of treatment. Recurrences are common, and the
prognosis is poor once hepatic insufficiency has developed.49
PROCEDURAL INTERVENTIONS FOR
GALLSTONE DISEASE
Percutaneous Transhepatic
Cholecystostomy Tubes
In cases in which a patient with cholecystitis is deemed to be too
ill to safely undergo cholecystectomy, a cholecystostomy tube
may be placed into the gallbladder to decompress and drain a
distended, inflamed, hydropic, or purulent gallbladder.36 Surgi-
cal cholecystostomy with a large catheter placed under local
anesthesia is rarely required today. Rather, percutaneous tran-
shepatic cholecystostomy (PTC) tubes are most often pigtail
catheters inserted percutaneously under ultrasound guidance.50
has been placed through the abdominal wall, the right lobe of the
liver, and into the gallbladder.
The catheter is inserted over a guidewire that has been passed
through the abdominal wall, the liver, and into the gallblad-
der (Fig. 32-21). By passing the catheter through the liver, the
risk of uncontrolled bile leak around the catheter and into the
peritoneal cavity is minimized. The catheter can be removed
when the inflammation has resolved and the patient’s condition
has improved. A patent cystic duct should be confirmed by a
tube cholangiogram prior to its removal. Interval cholecystec-
tomy should be considered if the patient’s fitness has improved,
particularly in individuals whose etiology of cholecystitis was
gallstones.
Endoscopic Interventions
Endoscopic advances in the last few decades have made endos-
copy and ERCP a valuable therapeutic tool in the management
of gallstone disease, particularly in the setting of common bile
duct stones or abnormalities. Using a 90-degree side-viewing
endoscope, the duodenum can be entered and the ampulla of
Vater on the medial wall of the second portion of the duode-
num visualized. This can then be cannulated to allow wire and
catheter access to the biliary tree, facilitating retrograde chol-
angiogram, diagnostic brushings, stenting, dilations, or fluoro-
scopically guided basket or balloon retrieval of common bile
duct stones. When CBD stones are present, endoscopic sphinc-
terotomy should be performed, which will allow for passage
of larger stones both at the time of bile duct clearance and in
the case of any ongoing choledocholithiasis (Fig. 32-22). In the
hands of experts, ERCP has high rates of successful cannulation
and bile duct clearance, and it is a safe and tolerable procedure.
Debate remains when comparing ERCP to surgical common bile
duct exploration in terms of timing and outcomes for choledo-
cholithiasis, but both are considered acceptable treatments.41 In
special cases, such as the presence of Roux-en-Y anatomy or
a previous hepaticojejunostomy, ERCP can be difficult. How-
ever, such anatomy does not preclude the option for endoscopic
intervention. Laparoscopic-assisted ERCP (in which the rem-
nant stomach is accessed surgically and the endoscope passed
into the duodenum) or double-balloon ERCP can be utilized to
reach the biliary tree.
Cholecystectomy
Cholecystectomy is one of the most common abdominal sur-
geries performed in Western countries, with over 750,000

A
B C
Figure 32-22. An endoscopic sphincterotomy. A. The sphincterotome in place. B. Completed sphincterotomy. C. Endoscopic picture of
ampulla before and after sphincterotomy.
being performed each year in the United States alone.51 Carl
Langenbuch performed the first successful open cholecystectomy
in 1882, and for >100 years, it was the standard treatment for
symptomatic gallbladder stones. In 1987, laparoscopic chole-
cystectomy was introduced by Philippe Mouret in France and
quickly revolutionized the treatment of gallstone disease. It not
only supplanted open cholecystectomy, but it also more or less
ended attempts for noninvasive management of gallstones (such
as extracorporeal shock wave or cholangioscopic lithotripsy) or
medical therapies (such as bile salts). Laparoscopic cholecystec-
tomy offers a cure for gallstones with a minimally invasive pro-
cedure, minor pain and scarring, and early return to full activity.
Today, laparoscopic cholecystectomy is the treatment of choice
for symptomatic gallstones and the complications of gallstone
disease.
Few absolute contraindications exist to laparoscopic
cholecystectomy, but they include hemodynamic instability,
uncontrolled coagulopathy, or frank peritonitis. In addition,
patients with severe obstructive pulmonary disease (COPD) or
congestive heart failure (e.g., cardiac ejection fraction <20%)
might not tolerate the increased intraabdominal pressures of
pneumoperitoneum with carbon dioxide and may require open
cholecystectomy. Conditions formerly believed to be relative
contraindications such as acute cholecystitis, gangrene and
empyema of the gallbladder, biliary-enteric fistulae, obesity,
pregnancy, ventriculoperitoneal shunts, cirrhosis, and previous
upper abdominal procedures are now considered risk factors for
a potentially difficult cholecystectomy, but they do not preclude
1411
CHAPTER 32 GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEM
an attempt at laparoscopy. While laparoscopic outcomes have
steadily improved and laparoscopic cholecystectomy has been
shown multiple times to be safe and feasible, conversion to an
open operation should always remain an option, and it is not
a failure. Conversion to open may be necessary if the patient
is unable to tolerate pneumoperitoneum, a complication occurs
that cannot be fixed laparoscopically, important anatomic struc-
tures cannot be clearly identified, or when no progress is made
over a set period of time. In the elective setting, conversion to
an open procedure is needed in about 5% of patients.51 Emer-
gent procedures or patients with complicated gallstone disease
can be more challenging, and the incidence of conversion has
been reported to be between 10% and 30%. The possibility of
conversion to open should always be discussed with the patient
preoperatively.
Serious complications of cholecystectomy are rare. The
mortality rate for laparoscopic cholecystectomy is about 0.1%.
Wound infection and cardiopulmonary complication rates are
considerably lower following laparoscopic cholecystectomy
than are those for an open procedure.52 While laparoscopic cho-
lecystectomy has historically been associated with a higher rate
of injury to the bile ducts than the open approach, modern data
appears to show this trend disappearing as familiarity with lapa-
roscopic techniques and technologies have improved.53
Patients undergoing cholecystectomy should have a
complete blood count and liver function tests preoperatively.
Prophylaxis against deep venous thrombosis with either low
molecular weight heparin or compression stockings is indicated.
1412 The patient should be instructed to empty their bladder before
coming to the operating room to avoid the need for urinary cath-
eterization. An orogastric tube can be placed if the stomach is
distended with gas, but it is generally removed at the end of the
operation.
Laparoscopic Cholecystectomy. The patient is typically
positioned supine with the operating surgeon standing at the
patient’s left side. Split-leg positioning with the surgeon stand-
ing between the patient’s legs can also provide ergonomic
access to the right upper quadrant. Tucking one arm can be
helpful if a cholangiogram is planned to allow easier maneu-
PART II
closed-needle technique (Veress). Typical access is at the supra-
umbilical region, though in the case of previous surgery or scars,
alternate access sites should be considered. Once an adequate
pneumoperitoneum is established, a 5- or 10-mm trocar is
inserted through the supraumbilical incision, through which a
5- or 10-mm 30° laparoscope is introduced. Traditionally, three
additional ports are then placed with a 10- or 12-mm port in the
epigastrium, a 5-mm port in the right midclavicular line, and a
5-mm port in the right flank (Fig. 32-23). Additional ports may
be placed as needed to aid with retraction in difficult cases.
Through the lateral-most port, the assistant uses a locking
instrument to grasp the gallbladder fundus and retract it over

vering of the fluoroscopy machine around the patient. Pneu- the liver edge and upward towards the patient’s right shoulder.
moperitoneum is established with carbon dioxide gas, either This will help visualize the body of the gallbladder and the
with an open technique (Hasson), optical viewing trocar, or hilar area. Exposure may be facilitated by placing the patient
SPECIFIC CONSIDERATIONS

B D
A

C
F

Figure 32-23. Laparoscopic cholecystectomy. A. The trocar placement. B. The fundus has been grasped and retracted cephalad to expose
the proximal gallbladder and the hepatoduodenal ligament. Another grasper retracts the gallbladder infundibulum posterolaterally to better
expose the triangle of Calot (hepatocystic triangle bound by the common hepatic duct, cystic duct, and liver margin). C. Intraoperative photo
of the critical view of safety. The hepatocystic triangle has been cleared of fat and fibrous tissue, the lower one-third of the gallbladder is
separated from the liver to expose the cystic plate, and two and only two structures are seen entering the gallbladder. D. A clip is being placed
on the cystic duct–gallbladder junction. E. A small opening has been made in the cystic duct, and a cholangiogram catheter is being inserted.
F. Additional clips have been placed, the cystic duct has been divided, and the cystic artery is being divided.
in reverse Trendelenburg position with slight tilting of the table
to bring the right side up. Through the midclavicular port, the
surgeon uses a grasper in the left hand to retract the gallbladder
infundibulum laterally and expose the neck of the gallbladder
and hepatoduodenal ligament. It may be necessary to take down
any adhesions between the omentum, duodenum, or colon to the
gallbladder in order to reach the infundibulum. The majority of
the dissection can then be performed with the right hand through
the epigastric port, utilizing a combination of electrocautery and
sharp and blunt dissection.
Dissection starts at the infundibulum of the gallbladder,
just above the takeoff of the cystic duct. The peritoneum, fat,
and loose areolar tissue around the gallbladder and the cystic
duct–gallbladder junction is dissected off and reflected inferi-
orly toward the bile duct. This is continued until the gallbladder
neck and the proximal cystic duct are clearly identified. The
next step is the identification of the cystic artery, which usually
runs parallel to and somewhat behind the cystic duct, and often
lies behind a prominent lymph node (Lund’s node, often called
Calot’s node). At this point, a critical view of safety should be
obtained. This requires that the hepatocystic triangle is cleared
of fat and fibrous tissue, the lower third of the gallbladder is
separated from the liver to expose the cystic plate, and two and
only two structures (cystic duct and cystic artery) are going into
the gallbladder (see Fig. 32-19).54 At this point, an intraopera-
tive cholangiogram can be performed if indicated (see “Intraop-
erative Cholangiogram” section).
With a critical view of safety obtained, the cystic duct and
artery are clipped with two clips at the base and one clip on the
gallbladder side. They can then be safely divided. Sometimes,
a very dilated cystic duct may be too large for clips. Such ducts
can be successfully managed by ligation with an endoloop, lapa-
roscopic stapler, or suture closure. Finally, the gallbladder is
dissected off the liver bed using electrocautery while watching
for potential abnormal posterior branches of ducts or arteries.
Before the gallbladder is completely removed from the liver
edge, it can be used as a retractor for a final evaluation of the
operative field. The surgeon should be sure to evaluate for bleed-
ing points or bile staining, and confirm placement of the clips on
the cystic duct and artery. The gallbladder is then divided from
its final attachments and removed either through the epigastric
or umbilical incision, often with the aid of a retrieval bag. The
fascial defect and skin incision may need to be enlarged in order
to remove the specimen, particularly if the stones are large or
the gallbladder is very inflamed. Any bile or blood that has
accumulated during the procedure should be cleaned away, and
if stones were spilled, they should be retrieved and removed. If
the gallbladder was severely inflamed or gangrenous, or if any
bile or blood is expected to accumulate, a closed-suction drain
can be placed through one of the 5-mm ports and left underneath
the right liver lobe close to the gallbladder fossa, though this is
not routinely required.
Open Cholecystectomy. The same surgical principles apply
for laparoscopic and open cholecystectomies. Open cholecystec-
tomy has become an uncommon procedure, usually performed
either as a conversion from laparoscopic cholecystectomy or
as a second procedure in patients who require laparotomy for
another reason. The approach can either be through a midline
laparotomy, or more commonly through a right subcostal inci-
sion. The gallbladder is dissected free from the liver bed, usu-
ally starting at the fundus and working proximally toward the
hepatocystic triangle. Once the cystic artery and cystic duct 1413
have been dissected and clearly identified, they are ligated and
divided, and the gallbladder is removed. In particularly difficult
cases, in which the gallbladder is partially obliterated or ductal
or arterial anatomy cannot be identified, a partial cholecystec-
tomy may be performed. This includes removal of as much gall-
bladder mucosa as possible and attempted closure of the cystic
duct stump with wide drainage of the area.
Intraoperative Cholangiogram. Intraoperative cholangio-
gram is an optional but valuable tool for evaluating the extra-
CHAPTER 32 GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEM
hepatic bile ducts, identifying common bile duct stones, or
clarifying aberrant ductal anatomy. The use of routine versus
selective cholangiography remains a topic of debate with a lack
of definitive evidence on either side.55-57 However, routine intra-
operative cholangiography will detect stones in approximately
7% of patients, and it assists with outlining anatomy and detect-
ing injury.58 Selective intraoperative cholangiogram should be
performed when the patient has a history of abnormal liver func-
tion tests, pancreatitis, jaundice, a large duct and small stones, a
dilated duct on preoperative ultrasonography, or if preoperative
endoscopic cholangiography for the aforementioned reasons
was unsuccessful. Although there is no consensus recommenda-
tion on the use of routine versus selective cholangiography, all
surgeons performing cholecystectomy should be familiar with
the procedure. If a cholangiogram is to be performed, a clip is
placed on the proximal cystic duct, and a small incision is made
on its anterior surface, just inferior to the clip. A cholangiogram
catheter is passed into the cystic duct and secured with a clamp
or clip. The fluoroscopy machine is then positioned over the
patient and a cholangiogram performed by injection of contrast
through the cholangiocatheter during live fluoroscopic dynamic
imaging. An ideal cholangiogram includes filling of the right
and left hepatic ducts, emptying into the duodenum, and no
visualized filling defects (Fig. 32-24). Care must be taken not
to introduce air bubbles into the system during contrast injec-
tion as these will appear as filling defects on the cholangiogram
images. If no contrast is visualized in the duodenum, a dose
of glucagon can be utilized to relax the sphincter of Oddi and
facilitate contrast flow. Once the cholangiogram is completed,
the catheter is removed. Laparoscopic ultrasonography is as
accurate as intraoperative cholangiography in detecting com-
mon bile duct stones, and it is less invasive. However, it requires
more skill to perform and interpret and is not always readily
available.59
Common Bile Duct Exploration
Common bile duct stones that are detected pre- or intraopera-
tively may be managed with common bile duct exploration
(CBDE) at the time of the cholecystectomy. While preopera-
tive ERCP is also an appropriate option for known bile duct
stones, laparoscopic CBDE can be used as a primary approach
to choledocholithiasis safely and with good outcomes, even in
higher risk populations such as the elderly.60 If stones in the duct
are small, they may sometimes be simply flushed into the duo-
denum with saline irrigation via the cholangiography catheter.
This can be facilitated by the administration of IV glucagon to
relax the sphincter of Oddi. If irrigation is unsuccessful, several
options exist to clear the duct, including fluoroscopic or endo-
scopic approaches.
With access to the cystic duct by a small ductotomy, a bal-
loon catheter is used to dilate the cystic duct, and a wire basket
can be passed down the common bile duct under fluoroscopic
1414
PART II
SPECIFIC CONSIDERATIONS
A B
Figure 32-24. A. An intraoperative cholangiogram. The bile ducts are of normal size, with no intraluminal filling defects. The left and the
right hepatic ducts are visualized, the distal common bile duct tapers down, and the contrast empties into the duodenum. Cholangiography
grasper that holds the catheter and the cystic duct stump partly projects over the common hepatic duct. B. An intraoperative cholangiogram
showing a common bile duct stone (arrow) with very little contrast passing into the duodenum.
guidance to catch and remove the stones (Fig. 32-25). Alter-
nately, endoscopic evaluation with a flexible choledocho-
scope will allow for direct visualization and retrieval of the
stones within the common duct. To do this, reliable catheter
access must be obtained with an introducer sheath placed either
through one of the laparoscopic ports or a new stab incision
in the anterior abdominal wall. The cystic duct should first be
dilated with a small balloon catheter to allow for passage of the
introducer and scope and for effective retrieval of larger stones.
Once the scope is within the common bile duct, irrigation is
used to distend the lumen. Stones may then be caught in a wire
basket under direct visualization or simply pushed into the duo-
denum. Once the common bile duct has been cleared of stones,
the cystic duct is ligated below the level of the ductotomy and
divided, and the cholecystectomy is completed.
While the cystic duct is the preferred route of access for
common bile duct exploration, occasionally an incision into the
common bile duct itself (choledochotomy) is necessary. The
flexible choledochoscope is then passed into the duct for visu-
alization and clearance of stones. The choledochotomy can be
closed primarily of the duct is very large, or over a T-tube. If
available, common bile duct exploration can be highly advan-
tageous as it provides the opportunity to treat the entirety of
the disease in a single event, rather that subjecting patients to
multiple procedures. However, the procedure can be techni-
cally challenging to perform and requires the availability of the
proper equipment and surgical expertise.61
Common Bile Duct Drainage Procedures
In very rare cases in which stones or obstructions cannot be
cleared by either ERCP with sphincterotomy or CBDE, and
the patient is suffering clinical effects from their common
duct stones, an additional choledochal drainage procedure
may become necessary. In the case of an open operation,
transduodenal sphincterotomy can be attempted by incising the
duodenum transversely and cutting the sphincter of Oddi at the
11 o’clock position, taking care to avoid injury to the pancreatic
duct. The impacted stones can then be manually removed or
simply allowed to pass through the sphincterotomy.
Bypass procedures can also be used to restore continu-
ity of bile flow in the setting of irretrievable impacted stones.
For short distance bypasses, a Choledochoduodenostomy is
performed by mobilizing the second part of the duodenum
(a Kocher maneuver) and anastomosing it side to side with the
common bile duct (Fig. 32-26A-C). If the distance is too great
to safely complete a choledochoduodenostomy without ten-
sion, a choledochojejunostomy can be done by bringing up a
roughly 45-cm limb of jejunum and anastomosing it end to side
to the common bile duct (Fig. 32-26D-E). If the entirety of the
extrahepatic biliary tree must be bypassed, hepaticojejunostomy
allows for drainage of the hepatic ducts directly a loop of jeju-
num (Fig. 32-26F-G). These choledochal drainage procedures
can also be used to manage common bile duct strictures or as a
palliative procedure for malignant obstruction in the periampul-
lary region.
OTHER BENIGN DISEASES AND LESIONS
Biliary Dyskinesia and Sphincter of Oddi
Dysfunction
Biliary dyskinesia is an umbrella term that refers to disorders
affecting the normal motility and function of the gallbladder
and sphincter of Oddi. These disorders are becoming increas-
ingly recognized as improvements in imaging allow for more
detailed evaluations of biliary tract function. Patients with bili-
ary dyskinesia may present with typical biliary type symptoms,
but without evidence of stones or sludge on abdominal imaging.
 I II 1415

CHAPTER 32 GALLBLADDER AND THE EXTRAHEPATIC BILIARY SYSTEM

A B C D

III

E F G

Figure 32-25. Laparoscopic common bile duct exploration. I. Transcystic basket retrieval using fluoroscopy. A. The basket has been
advanced past the stone and opened. B. The stone has been entrapped in the basket, and together, they are removed from the cystic duct.
II. Transcystic choledochoscopy and stone removal. C. The basket has been passed through the working channel of the scope, and the stone is
entrapped under direct vision. D. Entrapped stone. E. A view from the choledochoscope with stone captured in basket. III. Choledochotomy
and stone removal. F. A small incision is made in the common bile duct. G. The common bile duct is cleared of stones.

A decreased gallbladder ejection fraction on HIDA scanning Acalculous Cholecystitis

(EF <35%) is considered diagnostic of biliary dyskinesia. In
these patients, studies suggest that symptoms will be improved
or resolved by cholecystectomy in up to 90% of cases.62
Sphincter of Oddi dysfunction can occur as a primary pre-
sentation of episodic biliary type pain with abnormal liver func-
tion tests or as recurrent biliary type pain after cholecystectomy.
More severe cases may present with recurrent jaundice or pan-
creatitis. If other causes are ruled out, such as retained stones,
strictures or periampullary tumors, a stenotic or dyskinetic
sphincter of Oddi should be suspected. A benign stenosis of the
outlet of the common bile duct is usually associated with inflam-
mation, fibrosis, or muscular hypertrophy. The pathogenesis is
unclear, but trauma from the passage of stones, sphincter motil-
ity disorders, and congenital anomalies have been suggested. A
dilated common bile duct that is difficult to cannulate during
ERCP or delayed emptying of contrast from the biliary tree after
ERCP are useful diagnostic features. Ampullary manometry and
specific provocation tests are available in specialized units to
aid in the diagnosis. Once identified, sphincterotomy will typi-
cally yield good results.63
Acalculous cholecystitis is an acute inflammation of the gall-
bladder that occurs in the absence of gallstones. It is a rare entity
that typically develops in critically ill patients in the intensive
care unit.64 Patients on parenteral nutrition, with extensive burns,
sepsis, major operations, multiple trauma, or prolonged illness
with multiple organ system failure are at risk for developing
acalculous cholecystitis. The cause is unknown, but gallblad-
der distention, bile stasis, and ischemia have been implicated
as causative factors. After resection, pathologic examination of
the gallbladder wall after an episode of acalculous cholecystitis
reveals edema of the serosa and muscular layers, with patchy
thrombosis of arterioles and venules.65
The ability to recognize the symptoms and signs of
acalculous cholecystitis can depend on the condition and
mental status of the patient, but acalculous cholecystitis can
be similar to acute calculous cholecystitis, with right upper
quadrant pain and tenderness, fever, and leukocytosis. In the
sedated or unconscious patient, the clinical features are often
masked, but fever and elevated WBC count, as well as eleva-
tion of alkaline phosphatase and bilirubin, are indications for