Introduction

Background

Cholecystitis, which has long been considered an adult disease, is quickly gaining
recognition in pediatric practice because of the significant documented increase in
nonhemolytic cases over the last 20 years. Gallbladder disease is common throughout the
adult population, affecting as many as 25 million Americans and resulting in 500,000-
700,000 cholecystectomies per year.

Although gallbladder disease is much rarer in children, with 1.3 pediatric cases occurring
per every 1000 adult cases, pediatric patients undergo 4% of all cholecystectomies. In
addition, acalculous cholecystitis, uncommon in adults, is not that unusual in children
with cholecystitis. Because of the increasing incidence of gallstones and the
disproportionate need for surgery in the pediatric population, consider cholecystitis and
other gallbladder diseases in the differential diagnosis in any pediatric patient with
jaundice or abdominal pain in the right upper quadrant, particularly if the child has a
history of hemolysis.

Pathophysiology

Cholecystitis is defined as inflammation of the gallbladder and is traditionally divided

into acute and chronic subtypes. These subtypes are considered to be 2 separate disease
states; however, evidence suggests that the 2 conditions are closely related, especially in
the pediatric population. Most gallbladders that are removed for acute cholecystitis show
evidence of chronic inflammation, supporting the concept that acute cholecystitis may
actually be an exacerbation of chronic distension and tissue damage. Cholecystitis may
also be considered calculous or acalculous, but the inflammatory process remains the
same.

Chronic cholecystitis is most often related to gallstone disease but has been documented
without gallstones. Its course may be insidious or involve several acute episodes of
obstruction. The initiating factor is thought to be the supersaturation of bile, often with
cholesterol crystals and/or calcium bilirubinate, which contributes to stone formation and
inflammation. These processes lead to chronic obstruction, decreased contractile
function, and biliary stasis, which contribute to further inflammation of the gallbladder
wall. Biliary stasis also permits the increased growth of bacteria, usually Escherichia coli
and enterococci, which may irritate the mucosa and increase inflammatory response.
Chronic acalculous cholecystitis is less understood, but it may result from a functional
deficiency of the gallbladder, which leads to spasm and an inability to appropriately
empty its contents, causing chronic bile stasis.

Acute calculous cholecystitis results from a more sudden obstruction of the cystic duct by
gallstones, which results in distension of the sac, edema, and bile stasis with bacterial
overgrowth. These events lead to inflammation and a local release of lysolecithins, which
further exacerbates the inflammatory process. In addition, edema of the wall and duct
reinforces obstruction and may cause ischemia of the local tissue, releasing still more
inflammatory mediators. Local lymph node hypertrophy and duct torsion or congenital
anomalies may further complicate the obstructive process. As obstruction and
inflammatory tissue damage progress, bacteria may proliferate. Bile cultures are positive
in 75% of cases, usually with E coli, enterococci, or Klebsiella species. Bacterial
infection most likely follows tissue damage, but after colonization, the severity of the
disease can dramatically worsen. This cascade of events quickly leads pain and, possibly,
a toxic appearance.

Acute acalculous cholecystitis develops in a similar manner but from different etiologic
factors than acute calculous cholecystitis. Acute acalculous cholecystitis is most often
associated with systemic illness, whether chronic or critical and acute. Increased mucous
production, dehydration, and increased pigment load all are factors that increase
cholesterol saturation and biliary stasis, whereas hyperalimentation, assisted ventilation,
intravenous narcotics, ileus, and prolonged fasting contribute to cholestatic hypofunction.

These conditions allow the formation of biliary sludge and may lead to obstruction. The
resulting inflammation and edema lead to compromised blood flow and bacterial
infection, as in acute calculous cholecystitis; however, the compromised blood flow
appears more central in acute acalculous cholecystitis because acute acalculous
cholecystitis can occur in vasculitides (eg, Kawasaki disease, periarteritis nodosa)
presumably because of direct vascular compromise.

Frequency

United States

The exact frequency of acute and chronic cholecystitis in children is not known. The
overall incidence appears to have increased in the last 3 decades because of the high
consumption of fatty foods by young children (ie, Western diet). In children with chronic
hemolysis (eg, hemolytic anemias), the incidence of cholecystitis is much more prevalent
than in the general population. Biliary sludge and/or gallstones are likely to form in 1 in 5
children with hemolytic anemia before their adolescent years.

Mortality/Morbidity

Most information related to morbidity and mortality in gallstone disease is related to the
adult population, although some trends can be extracted and applied to the pediatric
population. In general, the mortality rate of cholecystectomy in acute cholecystitis has
dropped from 6.6% in 1930 to 1.8% in 1950 to nearly 0% in recent studies. In one study,
the overall mortality rate in 42,000 patients receiving open cholecystectomy (OC) was
0.17%; the mortality rate in patients younger than 65 years was 0.03%. Children can be
expected to do well, although comorbid conditions are common and may cause
complications. Risk factors for morbidity and mortality in the pediatric population
include associated conditions, such as cystic fibrosis (CF), obesity, hepatic disease,
diabetes mellitus, sickle cell disease, and immunocompromise.
General complications, such as pulmonary, cardiac, thromboembolic, hepatic, and renal
insufficiency, account for most deaths. Procedure-related complications mainly contribute
to morbidity and occur with higher frequency in acute cholecystitis in which symptoms
of gallstone disease have been present longer than 1 year. The most common procedure-
related complications are wound infections, abscess, cholangitis or pancreatitis, ileus,
hemorrhage, and bile duct complications.

Although OC is still commonly performed, the laparoscopic approach has become much
more common and is now the new criterion standard. In 1994, approximately 80% of all
cholecystectomies were performed laparoscopically. This approach reduces the morbidity
associated with length of recovery. Patients report less pain, a shortened hospital stay, and
a faster return to productivity. In addition, cosmetic results are improved. Lugo-Vicente
found that the length of stay, days that pain medication is taken, and time before a regular
diet can be resumed were all reduced by one half.1

Laparoscopic cholecystectomy (LC) is associated with risks as well. Major complications

include bleeding, pancreatitis, leakage from the duct stump, and major bile duct injury.
The risk of ductal injury increases from 0.1-0.2% in OC to 0.5-1% in LC; however,
Holcomb et al reported no iatrogenic injuries with LC in their first 100 patients.2 They
believe that with conscientious surgical care, morbidity related to the laparoscopic
approach can be minimized.

Acalculous cholecystitis has its own statistics for mortality and morbidity. Mortality in
the adult population has been reported to be as high as 10% and, in patients with critical
illness, up to 50%. The mortality rate in patients with critical illness is most likely related
to the close association with severe systemic illness. Surrounding illness and risk factors
should be considered when predicting morbidity and mortality in children.

Other procedures used in cholecystitis carry risks. Choledochotomy and endoscopic

papillotomy may be performed independently or in conjunction with cholecystectomy to
aid in the treatment of choledocholithiasis. The overall mortality rate from
choledochotomy (also applied to papillotomy) was determined to be 2.1%; however, by
excluding patients with preexisting cholangitis or pancreatitis, the mortality rate
decreased to 1.2%. The morbidity rate with these exclusions rests at 6-8%. The most
serious complications resulting from these procedures have been hemorrhage,
cholangitis, and pancreatitis.

Although controversy still surrounds the use of cholecystectomy versus medical

management, the morbidity and mortality rates have been the same in patients receiving
early surgery as in those in whom surgery was delayed more than 48 hours for
stabilization of inflammation. However, because symptoms continued in 24% of patients
in whom surgery was delayed, if surgery is the goal of treatment, no advantage to
delaying surgery is noted. In general, the complication rates of cholecystitis and
cholecystectomy are low in the absence of critical illness. The ability to tolerate general
anesthesia and operative conditions for cholecystectomy has become the most significant
indicator of outcome in cholecystitis. As a rule, children recover well once appropriate
operative treatment has been established.

Race

Racial and genetic influences in the adolescent age group are similar to those of adults.
African Americans (without hemolytic disease) and the African Masai are less prone to
cholelithiasis, whereas Chilean women, Pimas, and whites are more predisposed to this
disease. Two contributing diseases in particular have a genetic component and racial
distribution. Hemolytic diseases, including sickle cell disease and hemoglobin C disease,
occur almost exclusively in the black population, although thalassemia also has a
Mediterranean distribution. CF, which occurs mainly in whites, may also contribute to the
formation of biliary sludge and, possibly, acalculous cholecystitis.

Sex

No sex predilection is observed in children. In adult patients, the disease is more

prevalent in females than in males.

Age

The incidence of cholecystitis in the pediatric population varies mostly according to age,
with some racial and cultural influences. In a review of 693 cases of cholelithiasis, 10%
of gallstones were found in children younger than 6 months, 21% were found in children
aged 6 months to 10 years, and 69% were found in persons aged 11-21 years.3 In general,
the infants who had cholelithiasis tended to be patients who were ill, were receiving
hyperalimentation, and had prematurity, congenital anomalies, and necrotizing
enterocolitis as compounding risk factors. Children aged 1-5 years most frequently had
hemolysis as the underlying condition. Adolescent risk factors included menarche,
pregnancy, and use of birth control pills; sex, race, and genetic influences also
contributed to risk.

Cholelithiasis in infancy is most often related to acute and chronic illness and
hyperalimentation. Risk factors include abdominal surgery, sepsis, bronchopulmonary
dysplasia, hemolytic disease, malabsorption, necrotizing enterocolitis, and hepatobiliary
disease. Other factors implicated include CF, polycythemia, phototherapy, and distal ileal
resection. The immature hepatobiliary system of infants may predispose them to stone
formation. Decreased hepatobiliary flow and immature bilirubin conjugation both
contribute to stasis and sludge formation. Interestingly, as much as one half of infantile
gallstones, especially those associated with hyperalimentation, may spontaneously
resolve.

Risk factors in children include hepatobiliary disease, abdominal surgery, artificial heart
valves, and malabsorption. Gallstones usually contain a mixture of calcium bilirubinate
and cholesterol. Hemolysis and prolonged hyperalimentation are significant influences in
this age group. In adolescents, the epidemiology more closely resembles that of adults.
Major risk factors include pregnancy, hemolytic disease, obesity, abdominal surgery,
hepatobiliary disease, hyperalimentation, and malabsorption. In addition, differences
based on race, genetics, and sex become more evident. Adolescent girls are much more at
risk than boys. The female-to-male ratio in white adults is 4:1; in adolescents, the ratio is
estimated to be 14-22:1.

Pregnancy, birth control pills, dehydration, and obesity have contributory roles. Early
menarche has been shown to significantly increase incidence, perhaps because of the
lithogenic effect of estrogen on bile. Racial and genetic influences in the adolescent age
group are similar to those in adults (see Race).

Clinical
History

Symptoms of cholelithiasis often precede those of cholecystitis, although patients may

have acute cholecystitis on initial presentation. Cholelithiasis causes biliary colic.
Patients may complain of intermittent abdominal pain of inconsistent severity in the right
upper quadrant, with possible radiation to the scapular region of the back, or pain may be
diffuse or localized to the epigastrium. Discomfort is more likely to be nonspecific in
infants and younger children. Patients of this age group often present with irritability,
jaundice, and acholic stools. The classic history of patients with gallstones is postprandial
right upper quadrant pain associated with nausea and vomiting, but this is usually
observed only in older children. Jaundice in pediatric cholelithiasis is much more
frequent than in adults and can occur in the absence of gallstone obstruction of the
common bile duct. Most likely, the stone causes inflammation of the ductal tissue,
creating an edematous obstruction to bile flow.

• Patients with chronic cholecystitis usually present similarly to patients with

biliary colic, with an intermittent and indolent history of pain. Therefore,
differentiation must be made on the basis of findings from the physical
examination and diagnostic tests.
• Acute cholecystitis pain resembles biliary colic but is usually more severe and
constant, lasting for several days. The pain may begin as a vague discomfort;
however, as inflammation spreads and affects the surrounding peritoneum, the
pain localizes to the right upper quadrant. Patients often report a recent history of
nausea, vomiting, anorexia, and a low-grade fever. Onset of symptoms usually
occurs approximately 1 week prior to presentation, although the patient may
report years of the less severe symptoms of biliary colic and chronic cholecystitis.

Physical

The physical examination in acute cholecystitis usually reveals right upper quadrant
tenderness. The classic triad is right upper quadrant pain, fever, and leukocytosis. The
patient may have abdominal guarding and a positive Murphy sign (ie, arrest of inspiration
on deep palpation of the gallbladder in the right upper quadrant of the abdomen).
Omental adherence to the inflamed gallbladder combined with distension may create a
palpable mass between the 9th and 10th costal cartilages. The ductal system may become
inflamed, causing cholangitis. In 50% of these cases, the examiner may find a Charcot
triad.

• Charcot triad: This combination of right upper quadrant pain, fever, and jaundice
is indicative of obstruction to the common bile duct and the presence of acute
cholangitis. The Charcot triad is considered a medical emergency, and patients
require immediate intervention.
• Biliary colic versus chronic cholecystitis: Performing a physical examination may
be the only way to distinguish biliary colic from chronic cholecystitis. In chronic
cholecystitis, the patient usually complains of tenderness to palpation in the right
upper quadrant; however, the differentiation may be trivial given the high
likelihood of chronic cholecystitis in the presence of recurring biliary colic.

Causes

Cholelithiasis is the most common cause of acute or chronic cholecystitis in adults and
children. Three major types of gallstones may form, although most gallstones have
components of more than one type. Cholesterol gallstones are radiolucent and are
composed of cholesterol (>50%), calcium salts, and glycoproteins. They form within the
gallbladder and migrate to the bile duct. Pigment gallstones are black, often radiopaque,
and usually associated with hemolytic diseases. Radiopacity and color are related to an
increased concentration of calcium bilirubinate, which interacts with mucin glycoproteins
to form gallstones. These gallstones also form within the gallbladder and migrate to the
ductal system. Brown gallstones, in contrast, form within the ductal system and are
orange, soft, and greasy. They are composed of calcium salts of bilirubin, stearic acid,
lecithin, and palmitic acid. These gallstones are more often associated with infection.

In rural Asia, infections with Opisthorchis sinensis or Ascaris lumbricoides are

predisposing conditions. In the United States, these gallstones are more rare, although
they have been found after cholecystectomy in which the bile was infected (most often by
E coli) and in infants and children infected with Staphylococcus, Enterobacter,
Citrobacter, and Salmonella species. In addition, chronic urinary tract infections may
predispose individuals to the formation of these gallstones, and isolated gallstones
associated with Ascaris have been recorded in the United States.

All gallstones require similar conditions to form. First, the bile must be supersaturated
either by cholesterol or bilirubin. Second, chemical kinetics must favor nucleation of
cholesterol. This occurs when cholesterol is no longer soluble in bile. Finally, stasis of the
gallbladder allows cholesterol or calcium bilirubinate crystals to remain long enough to
aggregate to form gallstones.

Many disease processes can precipitate or foster these events. Infection induces the
deconjugation of bilirubin glucuronide, thereby increasing the concentration of
unconjugated bilirubin in the bile. Hemolysis overwhelms the conjugation abilities of the
liver, increasing the amount of unconjugated bilirubin in the bile. Hemolytic diseases
include hereditary spherocytosis, sickle cell disease, thalassemia major, hemoglobin C
disease, and possible uncontrolled glucose-6-phosphate dehydrogenase (G-6-PD)
deficiency. Multiple blood transfusions also increase the pigment load, which predisposes
the bile to the formation of biliary sludge.

Dehydration concentrates the bile, thereby increasing viscosity and stone formation.
Cystic fibrosis (CF) is associated with increased mucous production and may cause a
similar scenario. Gallstones remain the most common cause of cholecystitis. Although
acalculous cases significantly contribute to incidence of cholecystitis, most acalculous
cases are related to systemic illness and risk factors rather than epidemiologic
determinants. Therefore, the discussion of epidemiology focuses on the development of
cholelithiasis.

• Acalculous cholecystitis
o The aforementioned diseases may also contribute to the development of
acalculous cholecystitis because the formation of gallstones is not
necessary for the obstruction of the bile duct. In addition, acalculous
cholecystitis has been heavily associated with local inflammation,
endocarditis, vasculitides, and systemic infection. Implicated infections
include those occurring in typhoid fever, scarlet fever, measles, and
acquired immunodeficiency syndrome (AIDS) and those caused by
mycoplasma, Streptococcus (groups A and B), and gram-negative
organisms, such as Shigella and E coli.
o Acalculous cholecystitis may also occur postoperatively. Tsakayannis et al
observed acute cholecystitis occurring after open-heart surgery in 4 of
their patients, although it is more commonly observed in other nonbiliary
surgeries and trauma.4 Shock, sepsis, hyperalimentation, prolonged fasting,
intravenous narcotics, and multiple transfusions were the most common
risk factors for the development of acute acalculous cholecystitis. The
presence of 4 or more of these risk factors is highly predisposing.
• Other unusual causes
o Gallstones may also be caused by medications. Furosemide,5 octreotide,
ceftriaxone,6,7 and cyclosporine8 have all been associated with gallstone
disease. Ceftriaxone causes a reversible pseudolithiasis through several
mechanisms. Ceftriaxone displaces bilirubin on albumin, thereby
increasing the blood concentration of unconjugated bilirubin. Ceftriaxone
is also secreted in bile, and calcium salts of ceftriaxone have been found in
biliary sludge.
o Risk factors associated with gallstone formation include prolonged fasting
and age older than 24 months. Lasix has also been implicated in
gallbladder disease, but it usually is only a compounding factor in the
presence of prematurity, sepsis, or small-bowel disease. Cyclosporine may
be lithogenic, but it seems to require high drug levels and hepatotoxicity.
Finally, ileal disease or resection has been correlated with cholelithiasis in
adults and children, although the risks associated with resection seem to be
 highest after puberty. These patients have an increased cholesterol
secretion and a lowered bile acid secretion, which leads to cholesterol
supersaturation.

Differential Diagnoses
Appendicitis Hepatitis B
Biliary Atresia Hepatitis C
Colitis Irritable Bowel Syndrome
Constipation Pancreatitis and Pancreatic Pseudocyst
Gastroesophageal Reflux Pneumonia
Hepatitis A Small-Bowel Obstruction

Other Problems to Be Considered

The differential diagnosis of cholecystitis is based on the presenting symptoms of

abdominal pain in the right upper quadrant (patients with any of the diseases listed above
may present with right upper quadrant pain). In the pediatric population, consider the
following conditions in addition to the ones listed above:

• Biliary colic
• Cholangitis
• Rupture of the gallbladder
• Peptic ulcer disease
• Renal colic
• Gastritis
• Pleurisy
• Fitz-Hugh and Curtis syndrome (gonococcal perihepatitis)
• Hepatic abscess
• Abdominal tumor
• Pyelonephritis

Workup
Laboratory Studies

• In assessing for cholecystitis, appropriate laboratory studies include a CBC count,

gamma-glutamyltransferase (GGT) assessment, amylase measurement, urinalysis,
direct and indirect bilirubin tests, alkaline phosphatase measurement, and
transaminase levels.
• In acute cholecystitis, the WBC count is elevated, with a predominance of
polymorphonuclear cells and bands. Bilirubin, alkaline phosphatase and GGT
levels rise secondary to a blocked biliary system.
• The traditional cholestatic picture involves direct hyperbilirubinemia, with a
direct-to-indirect ratio approaching 1:1. Amylase may be elevated even in the
 absence of obstructive pancreatitis. In addition, transaminases may show mild
elevation but not a significant increase, unless obstruction has been severe enough
to cause hepatocyte damage.
• Transaminase levels are more likely to rise early in patients with obstruction of
the common bile duct.

Imaging Studies

• Plain abdominal radiography may be used for initial screening in abdominal pain.
Calcifications representing radiopaque gallstones may be observed in the
gallbladder or ductal system. Radiopaque gallstones contain more calcium
bilirubinate and are more common in the pediatric population, especially in
infants and children. In addition, complications such as porcelain gallbladder and
emphysematous cholecystitis may be visible on radiographs, although these
complications are rare in children.
• Abdominal ultrasonography has become the diagnostic tool of choice in
evaluating cholelithiasis. The accuracy of abdominal ultrasonography in depicting
gallstones is estimated to be more than 95%, but its reliability in the accurate
diagnosis of acute cholecystitis is more limited. Ultrasonographic findings in
acute cholecystitis include a discrete echodensity representing the gallstone, the
presence of sludge, and, possibly, ductal anomalies or dilation. The gallbladder
may be dilated with thickened walls. Imhof et al found gallbladder wall thickness
of more than 3.5 mm to be a reliable independent diagnostic indicator of
cholecystitis.9 Gallstones are often in a dependent position in the gallbladder and
may move as the patient changes position. The reliability of ultrasonography is
well established with both opaque and lucent gallstones. Results are immediate,
and accessibility is usually excellent.
• Oral cystography has been used in the past, but is now largely ignored because of
the refinement of ultrasonography. Oral cystography involves the ingestion of
contrast material that is secreted in the bile. Lack of visualization of the
gallbladder indicates cholelithiasis. This procedure is limited by liver dysfunction
and malabsorption. In addition, the contrast tablets have been associated with
emesis and diarrhea, further complicating effectiveness.
• The most accurate tool in the diagnosis of acute cholecystitis is biliary
scintography, otherwise known as the hepatic 2,6-dimethyliminodiacetic acid or
hepatoiminodiacetic acid (HIDA) scanning. This procedure involves the
intravenous injection of substances labeled with technetium 99m, taken into the
hepatocytes, and excreted into the biliary system. Normal hepatic uptake without
gallbladder visualization is diagnostic, but false positive results occur with
decreased biliary function secondary to prolonged fasting and the use of
hyperalimentation. Morphine augmentation of this test has been shown to
decrease false positive results. Induced spasm of the sphincter of Oddi increases
biliary pressure and enhances gallbladder filling. This test may be unnecessary,
however, because the clinical diagnosis and treatment are determined by the
symptoms and presence of gallstones or sludge. Ultrasonography has proved its
 usefulness in depicting gallstones, does not rely on contrast, and, therefore, maybe
safer.
• Other imaging techniques that can be used in the diagnosis of cholecystitis
include MRI and CT, especially in cases in which ultrasonography is not helpful.
Ultrasonographic results may be compromised by ileus, surgical incisions, and
coexisting diseases, especially those found in patients who are critically ill. MRI
and CT may be more sensitive than ultrasonography in detecting inflammation
within and around the gallbladder. In addition, the presence of other sources of
abdominal sepsis are more easily discovered and treated by means of MRI and
CT.

Other Tests

• Other tests associated with the diagnosis and treatment of cholecystitis include
cholecystokinin (CCK) stimulation, intraoperative cholangiography, and
endoscopic retrograde cholangiopancreatography (ERCP). CCK stimulation may
be used during other imaging studies, such as cholescintigraphy. Gallbladder
dyskinesia after CCK administration is diagnostic of gallbladder hypofunction
and may be useful in discerning acalculous or chronic cholecystitis and acute
inflammation.
• Intraoperative cholangiography, whether intravenous or percutaneous, is widely
used for the visualization of the gallbladder and ductal system. However,
cholangiography can be time-consuming and an added expense to the patient,
although some data show no statistical difference in operative time with and
without its use. Consider cholangiography for any risk of obstruction of the
common bile duct. Indications are a history of jaundice, pancreatitis, dilated
common bile duct, and the presence of small gallstones. The benefits of using
cholangiography have not been proven for routine cholecystectomy, routine
screening for congenital anomalies, or assessment of the common bile duct for
obstruction in the absence of clinical suspicion.
• If the patient displays signs and symptoms of choledocholithiasis, ERCP may also
be used preoperatively for exploration of the common bile duct. This procedure is
both diagnostic and therapeutic because it may be used for stent placement, basket
retrieval, or papillotomy to allow passage of gallstones; however, available
choledochoscopes may be too large for small patients.

Procedures

• One alternative to cholecystectomy is percutaneous transhepatic cholecystostomy.

In this approach, thread a catheter directly into the gallbladder and place it to
allow gravity drainage. Cholecystostomy is especially useful in acalculous
cholecystitis and in seriously ill patients with simple gallstones in whom
obstruction of the common bile duct is ruled out. Because cholecystectomy is the
standard of care for cholecystitis, cholecystostomy is usually reserved for
seriously ill patients who may not tolerate surgery.
 • Choledocholithiasis complicates the picture of cholecystitis and usually requires
adjunctive procedures to cholecystectomy. If obstruction of the common bile duct
is suspected preoperatively, perform ERCP before surgery with papillotomy, stent
placement, or basket retrieval. If gallstones are found intraoperatively, several
techniques can be used. The common bile duct can be flushed with saline or
opened and explored. Additionally, an endoscope or nephroureteroscope may be
used intraoperatively for basket retrieval.

Histologic Findings

• The histology of the inflamed gallbladder is fairly straightforward. Acute

cholecystitis shows changes similar to that of any acute inflammation. Edema,
leukocytic infiltration, and vascular congestion are prominent. Inflammation may
progress to abscess formation, gangrenous necrosis, and perforation, especially in
acalculous cholecystitis. Chronic cholecystitis shows long-term inflammatory
changes, with lymphocytes, plasma cells, and macrophages scattered throughout
the mucosa. Subserosal fibrous tissue forms and may extend into the subepithelial
layer with increasing disease severity. As the mucosa proliferates, epithelium may
become buried in crypts known as Rokitansky-Aschoff sinuses.
• Over time, chronic obstruction and inflammation may lead to the deposit of
calcium within the gallbladder wall, causing the porcelain gallbladder, which is
visible on flat plate imaging of the abdomen. Another variation is
xanthogranulomatous cholecystitis in which chronic inflammation leads to a
shrunken nodular gallbladder with many foci of necrosis and hemorrhage. This
condition may be confused with malignancy but is actually benign. Hydrops of
the gallbladder may also develop with chronic obstruction. This is characterized
by a distended lumen and atrophic walls. Obstruction of the common bile duct
may cause histologic change in nearby organs. Ductal hyperplasia ensues from
obstruction and distension, and periportal fibrosis in the liver may occur with
hepatic bile flow obstruction. Gallstones may also cause transient acute
pancreatitis, resulting in characteristic histologic changes in the pancreas.

Treatment
Medical Care

Medical care of the patient with acute cholecystitis centers around stabilization of the
patient and preparation for surgery if the patient is a candidate. Administer intravenous
(IV) fluids to correct any dehydration and continue as maintenance therapy. Standard
regimens include 5% dextrose in 0.2% sodium chloride solution or 5% dextrose in 0.45%
sodium chloride solution with 20 mEq of potassium chloride (KCl) per liter at a rate
determined by standard pediatric calculations.

Patients who are at risk for vaso-occlusion, including those with sickle
hemoglobinopathies, should receive hydration at 1.5 times maintenance dose. The patient
should receive nothing by mouth (NPO), and a nasogastric tube should be placed to low-
intermittent wall suction for evacuation of gastric contents. This step minimizes
stimulation to the inflamed gallbladder and prepares the patient for general anesthesia.
Administer pain medications; however, avoid morphine because of its spasmodic effects
on the sphincter of Oddi.

Antibiotics with biliary excretion covering enteric pathogens may be administered to

control infection. The combination of ampicillin, gentamicin, and clindamycin is a
common and well-accepted regimen. In addition, cefoperazone has a broad spectrum of
coverage and good biliary excretion. The use of antibiotics remains controversial. Some
authors assert that antibiotics are not necessary in simple cases and should be reserved for
persistent fever or worsening condition; however, Agrawal et al found a significant
reduction in postoperative infection with the use of prophylactic preoperative antibiotic
administration in elective cholecystectomy.10 Because of the high percentage of cases of
acute cholecystitis that are complicated by bacterial colonization, clinicians should
maintain a low threshold for the use of antibiotic therapy.

Removal of the gallbladder is the standard of care in patients with symptomatic gallstone
disease, although some exceptions are noted. Critically ill children with acute acalculous
cholecystitis may not tolerate anesthesia and operative conditions. These children should
receive antibiotic therapy, hyperalimentation, and gastric decompression until their
conditions improve. These patients may then undergo surgery if symptoms persist;
however, many cases resolve with medical therapy alone. One author reported a 75%
resolution of acute acalculous cholecystitis with the use of antibiotics, nasogastric
suction, and hyperalimentation. Therefore, antibiotics may be sufficient in critically ill
patients who do not tolerate anesthesia and who may be assisted by other procedures,
such as cholecystotomy, if gallbladder drainage is necessary.

Observation is also recommended in infants with gallstone disease, especially those with
hyperalimentation-associated gallstones. These gallstones often dissolve with maturation
of the hepatobiliary system. The gallbladder should be removed with any sign of common
duct obstruction, pancreatitis, or cholecystitis. Cholecystectomy should also be performed
if gallstones persist longer than 1 year or if long-term hyperalimentation is anticipated, as
in Crohn disease, pseudo-obstruction, or short-bowel syndrome. Medical care in chronic
cholecystitis or other gallbladder disease is also supportive. Cholecystectomy is
recommended in most patients with gallstone disease. Treatment should be aimed at
control of any underlying conditions and preparation for surgery.

Children with sickle cell disease present a unique challenge because their
hemoglobinopathy may cause perioperative and postoperative complications. These
patients are susceptible to vaso-occlusive crises, pneumonia, sepsis, and pulmonary
infarct, most likely secondary to hypoxia, dehydration, and acidosis in response to
anesthesia.

Ware et al observed no complications when preoperative transfusion of packed RBCs

were performed to obtain a hemoglobin A (Hgb A) ratio greater than 2:1 while the
hematocrit level was maintained at 35-45%.11 This required 2 transfusions 2 weeks apart
in most patients with partial volume exchange used for those with hemoglobin sickle cell
(Hgb SC) or sickle beta-thalassemia (SB thalassemia) disease. The preparation involved
with such improved outcomes suggests that planned elective surgery is beneficial to
patients with sickle hemoglobinopathies.

Other medical management strategies include contact dissolution and biliary lithotripsy.
Percutaneous transhepatic cholecystolitholysis involves the injection of a cholesterol
solubilizer, such as methyl-tert -butyl ether, directly into the gallbladder.

The time between instillation and aspiration must be conscientiously limited to avoid
leakage into the bile duct, causing abdominal pain and duodenitis. This method has been
successful in a few children. Biliary lithotripsy has also been used with limited success.
Similar to lithotripsy for nephrolithiasis, biliary lithotripsy uses shock waves to pulverize
gallstones. Biliary lithotripsy causes fragmentation in most patients but rarely causes
complete dissolution. Because fragments may still cause biliary colic and cholecystitis,
additional oral therapy may be necessary. All management techniques that involve
leaving the gallbladder in situ have 1-year recurrence rates of approximately 10% and 5-
year recurrence rates of approximately 50%.

Biliary dyskinesia is increasingly diagnosed in children, and these patients respond

favorably to cholecystectomy. As opposed to the adult population, the incidence of
complicated gallstone disease appears less common in children because most present
with symptomatic cholelithiasis without active inflammation, accounting for the very low
rate of ductal complications. For that reason, surgical treatment of gallbladder disease
(laparoscopic cholecystectomy) is now considered the most acceptable treatment
modality in pediatric patients.

Surgical Care

The surgical options available are open cholecystectomy (OC) and laparoscopic
cholecystectomy (LC). Although OC was considered the criterion standard 20 years ago,
the laparoscopic approach is now accepted as the criterion standard and preferred
procedure in almost all cases. Advantages of the laparoscopic approach include reduced
pain and hospital stay and improved cosmetic results and patient satisfaction. Some
concern remains regarding the previously reported higher risk of bile duct injury. Acute
inflammation of the gallbladder was a concern, but many authors now agree that acute
cholecystitis is not a contraindication; however, the surgeon must be experienced and
well skilled with laparoscopic techniques. In addition, conversion to OC can always be
performed in difficult cases.

Some authors assert that LC is ideal in infants and children and should be the procedure
of choice. In this case, surgical experience with laparoscopy and with infants is a must.
Wide spacing of cannulas is helpful in small children to allow for visualization and
adequate working distance. Also, with conscientious surgical technique, some authors
believe that bile duct injury can be minimized. In general, OC is reserved for conversion
and cases of prior major abdominal surgery. OC is accomplished through a right
subcostal incision or a transverse abdominal incision if a splenectomy is also indicated.
Laparoscopic entry involves 4 ports: 2 subcostal, 1 subxiphoid, and 1 umbilical.

The surgical course is usually routine. Patients can be admitted to the hospital the day of
surgery and discharged within 48-72 hours. The average postsurgical hospital stay after
LC is 36 hours, whereas patients undergoing OC typically need to stay in the hospital for
3 days. Continue hydration until the patient can tolerate a regular diet, usually the
morning after LC. In either procedure, it is recommended to observe the patient
postoperatively for complications, including fever, jaundice, ileus, pancreatitis, bile leak,
or urinary retention. Jaundice or continued right upper quadrant pain may signify a
retained common duct stone or biliary injury and should be investigated using endoscopic
retrograde cholangiopancreatography (ERCP) or hepatoiminodiacetic acid (HIDA)
scanning as soon as possible.

Technique for laparoscopic cholecystectomy in children

The technique for laparoscopic cholecystectomy in pediatric patients is very similar to the
one described in adult patients; however, a few variables must be considered.12,13,14

First, the trocar placement is determined by patient size and position of the gallbladder
and the liver. The authors usually start by placing a 12-mm trocar in the umbilical
position. A small incision is made from the center of the umbilicus inferiorly, in order to
expose the midline fascia at the umbilicus. Local anesthetic is infiltrated at that site.

The authors' preferred approach is to place a STEP trocar (Covidien Surgical; Mansfield,
MA) through that site using a Verees needle technique. Starting with a 5-mmSTEP trocar
is recommended and, once the peritoneal cavity is insufflated with CO 2 , the trocar is
upgraded to a 12-mm STEP placed through the same sleeve as the 5-mm trocar.

Typically the peritoneal cavity is insufflated with CO 2 using the following pressure
limits:

• Teenaged patients who are obese - 16 mm Hg

• Normal-sized, healthy teenaged patients - 14 mm Hg
• Patients aged 8-12 years - 12 mm Hg
• Patients younger than 7 years - 10 mm Hg

If the patient had any previous abdominal surgery or is significantly obese, the authors
prefer to use an open technique for the initial trocar placement. In such cases, creating an
opening on the inferior aspect of the umbilicus until the muscle fascia and the linea Alba
can be visualized is important. Stay sutures of 2-0 Vicryl are placed on each side of the
muscle fascia, which is than opened under direct visualization. Additional Vicryl sutures
may be needed in order to elevate the fascia until the peritoneal membrane can be
visualized and entered.

Once the peritoneum is open, a 12-mm trocar can be inserted under direct visualization,
and the peritoneal cavity is insufflated with CO 2 . The authors perform most LCs with a
5-mm, 30 º- angled laparoscope. However, in patients who are significantly obese, a 10-
mm trocar should be used to perform the cystic duct dissection. This is primarily due to
the fact that the small 5-mm laparoscope does not generate enough light inside the large
abdominal cavity of a patient who is obese and may compromise the surgeon's ability to
clearly visualize all vital structures surrounding the cystic duct. Considering that most
complications related to laparoscopic gallbladder surgery occur during the dissection and
exposure of the cystic duct, one should never work under poor light and inadequate
visualization at that point of the operation. Beginning the procedure with the 10-mm
laparoscope in place via the 12-mm trocar is fairly easy, as is changing to a 5-mm
laparoscope once the dissection and exposure of the cystic duct and artery are completed.

Second, subsequent trocar placement in children must be determined individually once

the gallbladder fundus is visualized with the laparoscope. A 5-mm trocar is typically
placed in the subxyphoid region. Another 5-mm trocar should be placed in the mid-right
upper quadrant of the abdomen (at the level of the mid-clavicular line) in such a way to
allow the introduction of a laparoscopic instrument used to manipulate the neck of the
gallbladder. This trocar is usually placed about 2 cm below the costal margin. However,
in small children, it must be placed closer to the costal margin.

The last trocar should be a 5-mm trocar placed laterally in the right upper quadrant. This
trocar is used for placement of a grasping instrument, such as a McKernan grasping-
locking forceps, that is placed on the fundus of the gallbladder for retraction. For that
reason, the trocar should not be placed too far from the costal margin. Once the
gallbladder fundus is grasped, it must be displaced towards the patient's right shoulder,
above the right lobe of the liver. This maneuver allows for exposure of the neck of the
gallbladder. One assistant should keep the fundus of the gallbladder pushed towards the
patient's shoulder region at all times. This elevates the neck of the gallbladder together
with the cystic duct and artery, facilitating dissection and exposure.

The third important step is the exposure and dissection of the neck of the gallbladder. If
significant inflammatory changes are identified, the authors prefer to perform an
intraoperative cholangiography to help define the anatomy of the cystic duct and its
relationship to the gallbladder and common bile duct. The authors prefer to perform a
cholangiography through the gallbladder. This can be easily performed by placing a
percutaneous catheter in the gallbladder under laparoscopic visualization. The gallbladder
is filled with water soluble dye, and radiographic images are obtained with live-
fluoroscopy. This allows the surgeon to determine any points of biliary obstruction and
if any evidence of common bile duct stones is present. In addition, it provides
information about the length and relative location of the cystic duct, facilitating
dissection and minimizing the risk of injury to the ducts.

The dissection for exposure of the cystic duct and artery is started at the neck of the
gallbladder. Initially mobilizing the visceral peritoneum and any inflammatory adhesions
away from the neck of the gallbladder is important. This can be easily performed using a
hook with electrocautery. The authors usually have the surgeon manipulate the
laparoscopic camera, with a hook or Maryland dissector in the right hand placed via the
subxyphoid trocar. The assistant should be retracting the fundus of the gallbladder
towards the right shoulder at all times and should also have a blunt grasper on the right
hand to manipulate the neck of the gallbladder. This manipulation involves moving the
neck towards the patient's right and left side, providing dynamic exposure for the
surgeon. The assistant should never keep the neck of the gallbladder on a fixed and
locked position.

Using careful dissection, the surgeon must achieve the so-called "critical view." This
refers to the visualization of the cystic duct and artery as they enter the gallbladder.
Dissecting towards the common bile duct and exposing the duct is not necessary. Once
the point of entry of the cystic duct is clearly visualized on the gallbladder, the duct can
be clipped and divided. The authors prefer to place one 5-mm clip on the cystic duct next
to the gallbladder and two clips towards the common bile duct. Again, the dissection and
exposure of the cystic duct is kept very close to the gallbladder, which should minimize
the risk of injury to the common bile duct. The cystic artery can be simultaneously
clipped with the cystic duct or can be separately clipped, depending on how close it is
located next to the duct.

Completely dissecting the artery and fully exposing it is not necessary because this may
lead to bleeding from small branches. In young children, cauterizing the artery
is possible. Controlling the artery with a LigaSure or Harmonic scalpel is also possible.
However, such devices are rarely necessary during LC. Once the cystic duct is divided
with laparoscopic scissors, its lumen should be inspected to make sure that no evidence
of any abnormalities suggests the presence of an injury to the common bile duct. At this
point of the operation, the surgeon should use an electrocautery hook to divide the
visceral peritoneum at the plane between the gallbladder and the liver. Again, the
assistant moves the gallbladder back and forth, providing continuous exposure of that
plane until the gallbladder is completely free.

If a hole is accidentally made in the gallbladder wall, the leakage of bile and gallstones
can be controlled by placing the grasping instrument over the hole. Any stones that
leaked should be removed using a suction irrigation device. Occasionally, a gallbladder is
partially intrahepatic. In such cases, removing a wedge of liver tissue with the gallbladder
is necessary. Electrocautery dissection at high settings should be enough for hemostasis.
Once the gallbladder is completely disconnected from the liver, the authors move the
laparoscope to the subxyphoid port and insert a 10-mm endopouch through the umbilical
port. The gallbladder is placed inside the bag and brought into the trocar. In most cases,
the gallbladder is too big to be removed through the 12-mm port. The authors prefer to
enlarge the umbilical incision and expose the muscle fascia, which is than divided with
electrocautery. This allows extraction of the pouch that contains the gallbladder. The
fascia can than be reapproximated with Vicryl sutures. After the gallbladder is removed,
the authors prefer to reinspect the liver bed to make sure that no evidence of bleeding or
bile leaking is present. Any residual bile is suctioned. At this point, all trocars are
removed under direct laparoscopic visualization, and the operation is completed. The
fascia at the 5-mm trocar sites does not need to be closed, unless the patient is younger
than 5 years.

Recent experience has demonstrated the feasibility of a mini-laparoscopic technique for

removal of the gallbladder in pediatric patients. The laparoscopic operation can be
achieved using 3-mm instruments and minimal use of ports. A 3-port mini-approach has
been reported. However, remember that patient selection is essential when performing
this operation with mini-instruments. One should not sacrifice good visualization and
optimal exposure of the vital structures. The risk of iatrogenic injury to the common bile
duct outweighs any benefit that can be achieved with mini-scopes and mini-instruments.
Inflammation and adhesions, frequently seen in symptomatic patients, may limit the use
of the mini-laparoscopic approach.

Consultations

Use a team approach to achieve proper care of the patient with cholecystitis. Consult a
pediatric gastroenterologist and surgeon early in the treatment of the patient. The
assistance of a dietitian may be very useful if observation without surgery is to be used.
In addition, consulting a radiologist is helpful if percutaneous cholecystotomy is
considered.

Diet

Dietary recommendations in gallbladder disease differ according to the stage of disease.

The 2 available strategies include acute management and preventative measures. The
patient with acute cholecystitis should receive NPO and undergo nasogastric evacuation
of gastric contents. The goal in this stage of disease is to eliminate unnecessary
stimulation to the biliary system and to reduce infectious exposure. Additionally,
preparations can be more readily made for surgery.

No widely accepted dietary therapy exists for the prevention of cholecystitis; however,
the contemporary Western diet and obesity have been implicated as predisposing factors
in the development of gallstone disease. Certainly, diet and exercise are influential, and
the West is infamous for poor dietary and exercising habits. In the Jamaican cohort study,
Walker examined a population of patients with sickle cell disease similar to that
examined by Winter et al in the United States. The progression of biliary sludge to
cholecystitis and the need for cholecystectomy was significantly decreased in the
Jamaican population. Walker theorized that dietary differences in the 2 countries were
causal. These cultural influences affect the adolescent and adult populations.

Presumably, a decrease in cholesterol and fatty food consumption would lower risk of
disease, but no specific data supporting this have been collected. Dietary restriction to
achieve weight reduction may minimize risk in children with obesity. Weight loss should
be controlled and gradual because rapid reduction may increase bile cholesterol
saturation and gallbladder stasis, actually promoting stone formation. Dietary
management of chronic gallbladder disease in the absence of surgery also follows this
preventative approach with the added goal of preventing symptoms. Although biliary
colic in children is less likely to directly correspond with fatty food consumption than in
adults, still advise the patient to avoid high-fat meals. Finally, in patients with
hyperalimentation-associated gallstones, administer low-dose enteral feedings, which
may prevent stone formation by stimulating contraction of the gallbladder and reduction
bile stasis.

Activity

Cholecystitis does not directly affect activity. Children should remain as active as their
condition, comfort, and development allow. Postoperatively, activity recommendations
correspond with the general precautions recommended abdominal surgery. Ambulation,
as soon as tolerable, improves outcomes, although patients should restrict lifting to less
than 5 pounds for several weeks.

Medication
Medical treatment of cholecystitis remains inadequate, especially in the pediatric
population. The only treatments approved for use in children are open cholecystectomy
(OC), laparoscopic cholecystectomy (LC), cholecystotomy, and endoscopic retrograde
cholangiopancreatography (ERCP). The 2 oral medications that have been used with
some success are chenodiol (chenodeoxycholic acid) and ursodiol (ursodeoxycholic
acid). Both medications selectively inhibit hydroxymethylglutaryl-coenzyme A reductase
(HMG-CoA reductase), thereby decreasing bile cholesterol supersaturation and
lithogenicity. Chenodiol was shown to achieve complete dissolution of pure cholesterol
gallstones in 15% of adult patients and partial dissolution in 28% of adult patients.
However, the medications are expensive and cause adverse effects, including diarrhea
and hepatotoxicity.

Combination treatment may be more effective and allow lower doses of each medication,
causing fewer adverse effects. Although ursodiol was found to be unsuccessful in
dissolving radiolucent gallstones in 10 children with cystic fibrosis (CF), it has been
shown to increase hepatobiliary excretion and may be useful in a cytoprotective and
preventative role.

Bile acids

Bile acids are used for the medical dissolution of cholesterol gallstones. Ursodiol and
chenodiol both are orphan drugs and have been approved by the US Food and Drug
Administration (FDA) for the dissolution of gallstones.

Ursodiol (Actigall, Urso)

Suppresses hepatic synthesis and secretion and intestinal absorption of cholesterol. Does
not seem to significantly inhibit synthesis and secretion of endogenous bile acids or affect
secretion of phospholipids into bile. Overall, increases concentration at which cholesterol
saturation occurs and allows cholesterol to solubilize in an aqueous medium. Preferred
over chenodiol because of its relative safety.

• Dosing
• Interactions
• Contraindications
• Precautions

Adult

300 mg PO bid pc

Pediatric

30 mg/kg/d PO divided tid pc; not to exceed 600 mg/d

Adolescents: Administer as in adults

• Dosing
• Interactions
• Contraindications
• Precautions

Bile acid sequestrants (eg, cholestyramine, colestipol) decrease absorption of bile acids;
aluminum-based antacids may decrease absorption in a similar mechanism; estrogens, PO
contraceptives, and clofibrate increase hepatic synthesis of cholesterol and can counteract
effects

• Dosing
• Interactions
• Contraindications
• Precautions

Documented hypersensitivity; calcified cholesterol gallstones, radiopaque gallstones, and

radiolucent bile pigment stones (because of ineffectiveness)

• Dosing
• Interactions
• Contraindications
• Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in
animals

Precautions
Hepatotoxicity not associated with ursodiol but has been related to other bile acids;
monitor liver enzymes before use and during therapy; obtain ultrasonograms q6mo
during therapy to monitor progress; adverse effects are rare; diarrhea is most commonly,
noted in <1% of patients

Chenodiol (Chenix)

Acts in a similar fashion to ursodiol; however, its metabolite lithocholic acid is

hepatotoxic and may cause hepatobiliary damage itself. Low-dose (<10 mg/kg/d) may
actually increase the rate of cholecystectomy. Because of these effects, ursodiol is
preferred.

• Dosing
• Interactions
• Contraindications
• Precautions

Adult

Optimal dosage range: 13-16 mg/kg/d PO divided bid

250 mg PO bid for 2 wk initially; increase by 250 mg/d qwk until therapeutic doses
achieved

Pediatric

Not recommended

Deterrence/Prevention

• The focus of prevention of cholecystitis is the minimization of controllable risk

factors. Because most of these factors for pediatric cholecystitis are related to
underlying disease processes, options are limited, but conscientious treatment by
the primary provider, knowledge of risks, and close observation for symptoms are
helpful.
• Certain risks can be decreased. Weight control in the child with obesity may
decrease the risk of cholelithiasis and many other long-term sequelae. The use of
pancreatic enzymes and bile acid supplements in patients with CF decreases the
saturation and lithogenicity of bile. Limited enteral feedings in children who
require long-term hyperalimentation decrease the biliary hypofunction observed
in prolonged fasting. The addition of ursodeoxycholic acid (Actigall) in settings
of chronic biliary stasis may mitigate the potential for cholelithiasis to develop.
Finally, seriously consider the risks associated with medications, (eg, oral
contraception, Lasix, Rocephin, octreotide, cyclosporine) before using them in
patients who are at risk.
Complications

• Distinct complications can occur at any point in the course or treatment of

gallbladder disease. They can be divided into complications of gallstones,
inflammation, and treatment. At any of the 3 stages, disease may exacerbate
preexisting medical conditions leading to cardiac, hepatic, pulmonary, or renal
demise.
• Gallstones may cause obstruction of the common bile duct, acute or chronic
cholecystitis, cholangitis, gallbladder perforation, or pancreatitis.
Choledocholithiasis occurs less often in children. Risk increases with age.
Obstruction of the common bile duct may still accompany pediatric cholelithiasis,
especially in the presence of congenital ductal narrowing or stenosis, and it may
cause hepatocyte damage. Rule out common bile duct stones in the presence of
any jaundice. Stones may also perforate the gallbladder, allowing bile leakage into
the peritoneum, or create a cystoenteric fistula, possibly leading to a gallstone
ileus. However, the most common complication of gallstones in children is
pancreatitis, reported to occur in 8% of cases. The course is usually mild and
resolves spontaneously with passage of the stone, which occurs in several days.
• More danger occurs in the presence of inflammation. Acute infection and
inflammation of the gallbladder or ductal system may lead to sepsis or local
spread of disease. Perforation, abscess, empyema, infarction, or gangrene may
develop in acute cholecystitis, causing peritonitis and threatening the patient's life.
Chronic cholecystitis may lead to acute hydrops, acute cholecystitis, or, more
insidiously, porcelain gallbladder. The well-known radiographic finding of
porcelain gallbladder is caused by chronic calcium deposition in the wall of the
gallbladder as a result of inflammation; it ominously leads to cancer in 50% of
adults in whom it is found.
• Procedure-related complications are predictable and include hemorrhage, bile
duct injury, ileus, pancreatitis, and leakage from the newly created stump. Risks
from anesthesia are also noted. In addition, wound infections, abscess, or
cholangitis may complicate the postoperative course.

Prognosis

• Isolated cholecystitis generally has an excellent prognosis if diagnosed and treated

appropriately. Children can be expected to return to presurgical functioning soon
after cholecystectomy, especially after a laparoscopic procedure. The greatest
indicator for poor prognosis is the underlying disease process itself. Cholecystitis
that is treated is usually well tolerated. Acute acalculous cholecystitis has higher
morbidity and mortality rates; however, because it often occurs in patients who
are critically ill, these statistics are also most likely related to the underlying
disease process.

Patient Education
• Patient education can be focused on prevention, observation, timely treatment,
and information about the intraoperative procedure. Preventative measures
include diet and weight management. In addition, educate patients with cystic
fibrosis (CF) about compliance with pancreatic enzyme and bile acid
supplementation. At-risk patients, whether because of chronic disease of cultural
and/or genetic risk factors, should be aware of signs and symptoms of
cholecystitis and gallstone disease. This enables them to seek timely medical
attention and avoid complications of acute cholecystitis. Finally, educate all
patients undergoing operative procedures about preoperative and postoperative
care and the expectations and risks of surgery.
• For excellent patient education resources, see eMedicine's Liver, Gallbladder, and
Pancreas Center and Cholesterol Center. Also, visit eMedicine's patient education
article, Gallstones.