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Chapter 23 / Gallbladder Disease 281
FIGURE 23.1 (Continued) C. Black pigment stones. D. Brown pigment stones.
in gallbladder motility increase the residence time of bile in the gallbladder,
thereby playing a role in stone formation. Gallstone formation occurs in
clinical states with gallbladder stasis, as seen with prolonged fasting, the
use of long-term parenteral nutrition, after vagotomy, in diabetic patients,
and in patients with somatostatin-producing tumors or in those receiving
long-term somatostatin therapy.
e gallbladder is a very eective absorptive organ, and a normal func-
tion of the gallbladder is to concentrate and acidify bile. For many years,
three factors have been thought to be key in cholesterol gallstone patho-
genesis: cholesterol supersaturation, cholesterol crystallization, and biliary
Section III / Biliary282
motility. However, a fourth factor, gallbladder absorption/secretion, also is
key to gallstone formation. Alterations in sodium, chloride, bicarbonate,
and water absorption/secretion alter the milieu for both cholesterol crystal
formation and for calcium precipitation with various anions (Fig. 23.1B).
Pigment Gallstones
Precipitation of calcium with bilirubin, carbonate, phosphate, or palmitate
as insoluble calcium salts serves as a nidus for cholesterol stone formation.
Furthermore, calcium bilirubinate and calcium palmitate also form major
components of pigment gallstones. Pigment gallstones are classied as
either black or brown pigment stones. Black pigment stones are typically
tarry and frequently are associated with hemolytic conditions or cirrhosis
(Fig. 23.1C). In hemolytic states, the bilirubin load and concentration of
unconjugated bilirubin increases. ese stones usually are not associated
with infected bile and are located almost exclusively in the gallbladder.
In contrast to black pigment stones, brown pigment stones are earthy
in texture and are typically found in the bile ducts, especially in Asian
populations (Fig. 23.1D). Brown stones often contain more cholesterol and
calcium palmitate than black stones and occur as primary common duct
stones in Western patients with disorders of biliary motility and associated
bacterial infection. In these settings, bacteria producing slime and bacte-
ria containing the enzyme glucuronidase cause enzymatic hydrolysis of
soluble conjugated bilirubin glucuronide to form free bilirubin, which then
precipitates with calcium.
Prevalence
Gallstones are uncommon in patients younger than age 20 years, but
a sharp increase is noted, especially in women, with each decade to
approximately 70 years. Approximately 20% of women and 10% of Western
men have stones by age 60 years. In certain populations, such as Native
Americans, the incidence is extremely high, especially in women. In
Chileans and Bolivians of Indian ancestry, gallstones also are very com-
mon, and they are associated with a high incidence of gallbladder can-
cer. In the United States, the prevalence of stones is highest in Mexican
American women (26%), and the prevalence in white women (17%) is
higher than in black women (14%).
Risk Factors
Gallstones are more common in women, especially those who are obese,
have had multiple pregnancies, are taking birth control pills, are undergo-
ing rapid weight loss, or have elevated serum triglyceride levels. Diet plays
an important role in cholesterol supersaturation, and these gallstones do
not form in vegetarians. Cholesterol gallstones are common in populations
consuming a Western diet, which is relatively high in overall calories as well
as animal fats and carbohydrates. Diabetic patients also have an increased
incidence of gallstones, which may be caused, in part, by alterations in gall-
bladder motor function and/or absorption/secretion. Gallstones also are
known to occur more frequently in certain families. Current theory suggests
that approximately 30% of the risk for gallstone formation is hereditary,
whereas 70% is environmental, with diet being the primary environmen-
tal factor. As mentioned previously, prolonged fasting, TPN, ileal resection,
vagotomy, hemolytic states, and cirrhosis are additional risk factors, and
many of these factors lead to black pigment stone formation. Finally, bile
duct stasis, as occurs with biliary strictures, congenital cysts, chronic pan-
creatitis, sclerosing cholangitis, and perivaterian duodenal diverticula, is
the primary risk factor for brown pigment stone formation.
Chapter 23 / Gallbladder Disease 283
Natural History
An understanding of the natural history of gallstone disease is necessary
for the appropriate management of patients with cholelithiasis. e pres-
ence or absence of symptoms remains the most important factor in the
determination of the natural history of gallstones. Gallstone disease can be
considered as a spectrum of clinical entities that includes asymptomatic
gallstones, symptomatic gallstones, and complicated gallstone disease. e
complications of gallstone disease include (a) acute cholecystitis, (b) cho-
ledocholithiasis with or without cholangitis, (c) gallstone pancreatitis, (d)
gallstone ileus, and (e) gallbladder carcinoma.
Asymptomatic gallstones often are discovered at the time of laparot-
omy or during abdominal imaging for nonbiliary disease. e vast majority
of patients with gallstones are asymptomatic. ese stones remain in the
gallbladder and do not obstruct the cystic duct. As a result, the gallbladder
lls and empties normally, and the gallstones remain silent. However, asymp-
tomatic gallstones can progress to symptomatic disease. Symptomatic gall-
stones usually present with what is termed biliary colic, right upper quadrant
or epigastric abdominal pain that typically develops postprandially and may
be associated with nausea and vomiting. e pain results from the impaction
of a gallstone at the neck of the gallbladder or cystic duct.
Studies that have followed asymptomatic patients have shown that 20%
to 30% of patients become symptomatic within 20 years. Approximately 1%
to 2% of asymptomatic individuals with gallstones per year develop serious
symptoms or complications related to their gallstones (Table 23.1). e lon-
ger stones remain silent, the less likely symptoms are to develop. In addition,
almost all patients will develop symptomatic disease before developing one
of the complications of gallstones. erefore, prophylactic cholecystectomy
generally is not indicated in patients with asymptomatic gallstones.
In select groups of patients, however, prophylactic cholecystectomy
should be considered (Table 23.2). Children with gallstones almost always
Degree of Symptoms
Symptoms Requiring
Cholecystectomy
Complications
ofGallstones
Asymptomatic 1%–2%/y 1%–2%/y
Mild symptoms 6%–8%/y 1%–3%/y
Symptomatic 5%–30%/y 7%/y
Natural History of Gallstones
TABLE
23.1
Pediatric gallstones
Congenital hemolytic anemia
Gallstones >2.5cm in diameter
Calcied (porcelain) gallbladder
Long common channel
Bariatric surgery
Incidental gallstones found during intra-abdominal surgery
Solid organ transplantation
No access to medical care
Indications for Prophylactic Cholecystectomy
TABLE
23.2
Section III / Biliary284
develop symptoms and should be considered for early cholecystectomy. In
patients with sickle cell disease, cholecystitis can precipitate a crisis with sub-
stantial operative risks. erefore, these patients are best treated with elective
cholecystectomy. A nonfunctioning gallbladder usually
indicates advanced
disease with more than 25% of these patients developing symptoms that
require cholecystectomy. Large gallstones (>2.5cm) are more frequently asso-
ciated with acute cholecystitis and gallbladder carcinoma, and prophylactic
cholecystectomy also may be indicated in these patients. e presence of a
porcelain gallbladder (calcied gallbladder wall) is associated with a 5% to 10%
risk of malignant transformation, and prophylactic cholecystectomy has been
recommended for these patients. A long common channel between the bile
and pancreatic ducts also is a signicant risk for gallbladder cancer, and these
patients should undergo prophylactic cholecystectomy. In obese patients in
whom gallstones have already developed and who undergo bariatric surgery,
cholecystectomy may be indicated because symptoms are likely to develop
and may be dicult to distinguish from those caused by complications of the
operation. Prophylactic cholecystectomy adds minimal morbidity and mortal-
ity risks to most bariatric operations and is clearly indicated in patients with
gallstones. Finally, acute cholecystitis is a potentially life-threatening c ondition
in immunosuppressed patients. For this reason, prophylactic cholecystectomy
has been recommended prior to solid organ transplantation.
Patients with mild symptoms (intermittent biliary colic) are at higher
risk for developing gallstone-related complications than asymptomatic
patients who have gallstones (Table 23.1). Approximately 1% to 3% of mildly
symptomatic patients per year will develop gallstone-related complica-
tions, and at least 6% to 8% per year will require a cholecystectomy to man-
age their gallbladder symptoms. e diagnosis of symptomatic gallstones
requires the presence of characteristic symptoms and the documentation
of gallstones on diagnostic imaging.
Cholecystitis
Chronic Cholecystitis
e term chronic cholecystitis implies an ongoing or recurrent inam-
matory process involving the gallbladder. In more than 90% of patients,
gallstones are the causative factor and lead to recurrent episodes of
cystic duct obstruction manifest as biliary pain or colic. Over time, these
r
ecurrent attacks can result in scarring and a nonfunctioning gallbladder.
Histopathologically, chronic cholecystitis is characterized by an increase in
subepithelial and subserosal brosis and a mononuclear cell inltrate. e
primary symptom associated with chronic cholecystitis or symptomatic
cholelithiasis is pain, often labeled biliary colic. e pain is usually located
in the right upper quadrant and/or epigastrium and frequently radiates to
the right upper back, right scapula, or between the scapulae. Other symp-
toms such as nausea and vomiting often accompany each episode. e
physical examination is usually completely normal in patients with chronic
cholecystitis, particularly if they are pain-free. During an episode of biliary
colic, mild right upper quadrant tenderness may be present. Laboratory
values such as serum bilirubin, transaminases, and alkaline phosphatase
usually are normal in patients with uncomplicated gallstones.
Acute Cholecystitis
Acute cholecystitis is the most common complication of gallstones occurring
in 15% to 20% of patients with symptomatic disease. As in biliary colic, acute
cholecystitis results from a stone impaction at the gallbladder–cystic duct
junction (Fig. 23.2A). e extent of inammation and the progression of acute
Chapter 23 / Gallbladder Disease 285
cholecystitis are related to the duration and degree of obstruction. In the most
severe cases (5% to 18%), this process can lead to ischemia and necrosis of the
gallbladder wall (Fig. 23.2B). More frequently, the gallstone is dislodged, and the
inammation gradually subsides. Acute cholecystitis is primarily an inamma-
tion and not an infectious process with bacterial infection appearing as a sec-
ondary event. Approximately 50% of patients with acute cholecystitis will have
positive bile cultures, with Escherichia coli being the most common organism.
Patients with acute cholecystitis typically present with right upper
quadrant pain that is similar to that of biliary colic. In acute cholecysti-
tis, however, the pain is usually unremitting, may last several days, and is
FIGURE 23.2 A. Acutely inamed, edematous gallbladder with solitary pigment stone
obstructing the cystic duct. B. Gangrenous cholecystitis with solitary black pigment stone.
Section III / Biliary286
often associated with nausea, emesis, anorexia, and fever. On physical
e
xamination, patients with acute cholecystitis usually have a low-grade
fever and exhibit localized right upper quadrant tenderness and guarding.
e presence of Murphy sign, an inspiratory arrest during deep palpation
of the right upper quadrant, is the classic physical nding of acute chole-
cystitis. A palpable right upper quadrant mass is appreciated in one-third
of patients and usually represents omentum that has migrated to the area
around the gallbladder in response to the inammation. Severe jaundice is
rare, but mild jaundice may be present in up to 30% of patients. Severe jaun-
dice suggests the presence of CBD stones, cholangitis, or Mirizzi syndrome,
obstruction of the common hepatic duct by severe pericholecystic inam-
mation resulting from impaction of a large stone in the Hartmann pouch.
Laboratory evaluation can show a mild leukocytosis (white blood cell
[WBC] count 12,000 to 15,000 cells/mm
3
). However, many patients have a
normal WBC. A white cell count greater than 20,000 should suggest further
complications of cholecystitis, such as gangrene, perforation, or cholangitis.
Biliary Dyskinesia
A subgroup of patients presenting with typical symptoms of biliary colic
(postprandial right upper quadrant pain, fatty food intolerance, and nau-
sea) will not have any evidence of gallstones on ultrasound examination.
e vast majority of these patients are women who frequently are over-
weight or obese. Experimental work suggests that excess fat and cytokines
in the gallbladder wall (steatocholecystitis) may be the underlying cause
for this phenomenon. Many of these gallbladders are enlarged at rest sug-
gesting that a defect in absorption/secretion may be a contributing factor.
Further investigations usually are performed in these patients to
exclude any other pathology. is workup often includes an abdominal
computed tomography (CT) scan, an esophagogastroduodenoscopy, or
even an endoscopic retrograde cholangiogram. In these patients, the diag-
nosis of biliary dyskinesia or chronic acalculous cholecystitis should be
considered. e cholecystokinin-Tc-HIDA scan has been useful in identify-
ing patients with this disorder. Cholecystokinin (CCK) is infused intrave-
nously, and the gallbladder ejection fraction (EF) is calculated. An EF of less
than 35% at 20 minutes is considered abnormal.
DIAGNOSTIC IMAGING
Abdominal X-Rays
In general, plain abdominal x-rays have a low yield in diagnosing biliary tract
problems. Plain lms are most useful in diagnosing other causes of acute
abdominal pain such as a perforated viscus or a bowel obstruction. Only
approximately 15% of gallstones contain sucient calcium to appear radi-
opaque on a plain x-ray. Rarely, abdominal lms may show a calcied gall-
bladder wall or pneumobilia that may aid in the diagnosis of biliary disease.
Ultrasound
Transabdominal ultrasound is the radiologic procedure of choice for identify-
ing gallstones and bile duct dilation. Ultrasound is noninvasive, inexpensive,
and widely available. Patients should receive nothing by mouth for several
hours prior to performing an ultrasound examination so that the gallblad-
der is fully distended. Gallstones create echoes that are reected back to the
ultrasound probe. e ultrasound waves cannot penetrate the stones, and
therefore, acoustic shadowing is seen posterior to the stones (Fig. 23.3). In
addition, gallstones that are free oating in the gallbladder will move to a
dependent position when the patient is repositioned during scanning. When
Chapter 23 / Gallbladder Disease 287
these two features are present, the accuracy of ultrasound at diagnosing
gallstones approaches 100%. Echoes without shadows may be caused by gall-
bladder polyps. However, the majority of “polyps” are really small gallstones
that are attached to the mucus gel.
Several features lower the diagnostic accuracy of ultrasound in detect-
ing gallstones. Small gallstones may not demonstrate an acoustic shadow.
A lack of uid (bile) around the gallstones (stone impacted in the cystic
duct, gallbladder lled with gallstones) also impairs their detection. In
addition, an ileus with increased abdominal gas, as occurs with acute cho-
lecystitis, will hamper gallbladder visualization. Overall, the false-negative
rate for ultrasound in detecting gallstones is approximately 5% but may
increase to 15% with acute cholecystitis.
Cholescintigraphy
Cholescintigraphy provides a noninvasive evaluation of the liver, gallblad-
der, bile duct, and duodenum with both anatomic and functional infor-
mation.
99m
Technetium-labeled iminodiacetic acid derivatives (hepatic
2, 6-dimethyl-iminodiacetic acid [HIDA], diisopropylacetanilidoiminodi-
acetic acid, or p-isopropylacetanilido imidodiacetic acid) are injected intra-
venously, rapidly extracted from the blood, and excreted into the bile. ese
radionuclide scans provide functional information about the liver’s ability to
excrete radiolabeled substances into a nonobstructed biliary tree. Uptake by
the liver, gallbladder, common bile duct (CBD), and duodenum should all be
present after 1 hour. Slow uptake of the tracer by the liver suggests hepatic
parenchymal disease. Filling of the gallbladder and CBD with delayed or
absent lling of the intestine suggests an obstruction at the ampulla.
e primary use of cholescintigraphy is in the diagnosis of acute cho-
lecystitis. Although used less frequently for this indication because of the
FIGURE 23.3 Gallbladder ultrasound with solitary stone with acoustic shadowing.
Section III / Biliary288
availability and accuracy of ultrasound, cholescintigraphy demonstrates the
presence of cystic duct obstruction, which is invariably present in acute cho-
lecystitis. Nonvisualization of the gallbladder 1 hour after the injection of the
radioisotope with lling of the CBD and duodenum is consistent with total or
partial cystic duct obstruction and acute cholecystitis (Fig. 23.4). e sensitiv-
ity and specicity of cholescintigraphy for diagnosing acute cholecystitis are
each about 95%. False-positive results are increased in the setting of gallblad-
der stasis as in critically ill patients or in those receiving parenteral nutrition.
Computerized Tomography/Magnetic Resonance Imaging
Abdominal CT is less sensitive in diagnosing gallstones than ultrasound.
Calcied gallstones are visualized in approximately 50% of patients. e role
of CT scanning is primarily limited to the diagnosis of complications of gall-
stone disease such as acute cholecystitis (gallbladder wall thickening, peri-
cholecystic uid), gallbladder perforations, choledocholithiasis (intrahepatic
and extrahepatic bile duct dilation), pancreatitis (pancreatic edema and
inammation), and gallbladder cancer (Fig. 23.5). Magnetic resonance imag-
ing (MRI) also has been shown to be highly sensitive in the diagnosis of both
gallstones and common duct stones when T2-weighted images are obtained.
Both MRI and CT are much more expensive than ultrasound and, therefore,
are not cost-eective for the initial evaluation of gallbladder disease.
MANAGEMENT
Chronic Cholecystitis
e operative management of gallstones has been the standard of
care over the past 140 years. Cholecystectomy is the most common
FIGURE 23.4 HIDA scan demonstrating good hepatic uptake, a patent CBD
(CD), and visualization of the duodenum (D). This scan is “positive” for acute
cholecystitis because the gallbladder is not visualized.
Chapter 23 / Gallbladder Disease 289
gastrointestinal operation performed in the United States. Since the
introduction of
laparoscopic cholecystectomy in the late 1980s, the num-
ber of cholecystectomies performed in the United States has increased
from approximately 500,000 to 750,000 per year. Symptomatic choleli-
thiasis is the main indication for laparoscopic cholecystectomy. Relative
contraindications to laparoscopic cholecystectomy include the inability
FIGURE 23.5 A. CT scan demonstrating a thickened gallbladder wall
secondary to cancer. Note the low-density area in the adjacent liver due to
metastatic disease. B. Laparoscopic appearance of the gallbladder in the
same patient. Note that the gallbladder wall is white with neovascularization.
Section III / Biliary290
of the patient to withstand a general anesthetic, severe bleeding disor-
ders, and end-stage liver disease. In addition, patients with severe chronic
obstructive pulmonary disease or congestive heart failure may not tol-
erate the pneumoperitoneum required for performing laparoscopic sur-
gery. Morbid obesity, once thought to be a relative contraindication to the
laparoscopic approach, is not associated with a higher conversion rate.
Longer trocars and instruments and an increase in intra-abdominal pres-
sure may be helpful in these patients. Prior upper abdominal surgery may
increase the diculty but rarely precludes laparoscopic cholecystectomy.
Elective laparoscopic cholecystectomy also has been completed safely in
patients with well-compensated cirrhosis (Child class A and B), although
diculty retracting the rm liver and increased bleeding from collaterals
have been noted.
Conversion to an open cholecystectomy is required in less than 3%
of patients undergoing laparoscopic cholecystectomy for chronic cholecys-
titis. Conversion rates are increased in male and elderly patients. Elective
laparoscopic cholecystectomy can be safely performed as an outpatient
procedure (Fig. 23.6). Among patients selected for outpatient management,
75% to 95% of patients can be successfully discharged the same day. Factors
contributing to overnight admission include uncontrolled pain, nausea and
vomiting, urinary retention, and cases completed late in the day.
Acute Cholecystitis
Once the diagnosis of acute cholecystitis is made, the patient should be
given nothing by mouth, and intravenous hydration should begin. A naso-
gastric tube is placed if persistent nausea and vomiting or abdominal
FIGURE 23.6 Laparoscopic appearance of a minimally invasive diseased gallbladder, which
contained symptomatic gallstones.