1. Biliary colic
Further reading
http://emedicine.medscape.com/article/171256-overview
Cholelithiasis:
"Presence or formation of GALLSTONES in the BILIARY
TRACT, usually in the gallbladder (CHOLECYSTOLITHIASIS)
or the common bile duct (CHOLEDOCHOLITHIASIS)."
Source: Medical Subject Headings, 2010_2009_08_17
Cholelithiasis:
"presence or formation of gallstones in the gallbladder."
Source: CRISP Thesaurus, 2006
Biliary Colic:
"Painful sensation in the gallbladder region."
Source: NCI Thesaurus, 2009_04D
Biliary calculi:
"Solid crystalline precipitates in the BILIARY TRACT, usually
formed in the GALLBLADDER, resulting in the condition of
CHOLELITHIASIS. Gallstones, derived from the BILE, consist
mainly of calcium, cholesterol, or bilirubin."
Source: Medical Subject Headings, 2010_2009_08_17
Cholecystolithiasis:

2. "Presence or formation of GALLSTONES in the 4. Labs
GALLBLADDER."
1. Complete Blood Count usually normal
Source: Medical Subject Headings, 2010_2009_08_17
2. Mild elevation of Liver Function Tests
1. Bilirubin slightly elevated
2. Alkaline Phosphatase slightly
elevated
________________________
3. Pancreatic enzyme tests normal
1. Amylase normal
2. Lipase normal
Biliary Colic 4. Urinalysis normal
5. HCG NORMAL
1. Symptoms
1. Abdominal Pain characteristics
1. RUQ Abdominal Pain or Epigastric
Abdominal Pain
2. Dull visceral ache 5. Radiology
3. Poorly localized discomfort 1. XRay Abdomen
4. PAIN RADIATES TO RIGHT 1. Test Sensitivity: 10-20% for Gallstones
POSTERIOR SHOULDER OR 2. Chest XRay normal
SCAPULA 3. RUQ Ultrasound
1. Test Sensitivity: 95% for Gallstones
4. Oral Cholecystography
1. Indicated for normal or equivocal
Ultrasound
2. Abdominal Pain timing:
1. Occurs suddenly 30-60 minutes after
a meal
1. Normal meal 6. Management
2. Large meal after a fast 1. Laparoscopic Cholecystectomy
3. Fatty meal 1. Preferred option
2. Increasing frequency and intensity of
attacks
3. Pain lasts for 1-6 hours
4. Intermittent "colicky" exacerbations
of pain 2. Antispasmodic
5. Mild abdominal aching for 1-2 days 1. Glycopyrrolate (Robinul)
after attack 1. Parenteral: 0.1 to 0.2 mg IV
or IM
2. Oral: 1.0 to 2.0 mg PO bid-tid
3. Associated symptoms
1. Nausea and Vomiting
2. No Fever or chills (see differential 3. Analgesic
diagnosis) 1. Meperidine (Demerol)
1. Less sphincter of Oddi spasm
than morphine
2. Ketorlac (Toradol)
2. Signs 1. Relieves pain of gallbladder
1. RUQ abdominal tenderness distention
2. No signs of peritoneal irritation 2. Not as effective if infection
3. Dehydration from protracted Vomiting present
4. Antiemetics
3. Differential Diagnosis
1. Acute Cholecystitis 1. Promethazine (Phenergan)
2. Cholangitis 5. Nasogastric Suction
3. Pancreatitis 1. Indicated for protracted Vomiting
6. Alternatives in non-surgical candidates
1. BILE ACID ORAL DISSOLUTION
THERAPY

3. Differential Diagnoses
Abdominal Abscess Gallbladder Volvulus
Abdominal Angina Gastric Ulcers
Abdominal Aortic Gastritis, Acute
Aneurysm
Angina Pectoris Gastroesophageal Reflux
Disease
Appendicitis Irritable Bowel Syndrome
Cholangitis Liver Abscess
Cholecystitis Mesenteric Venous
Thrombosis
Colonic Obstruction Myocardial Infarction
Diverticulitis Opioid Abuse
Duodenal Ulcers Pancreatitis, Acute
Esophageal Spasm Pancreatitis, Chronic
Esophagitis Pericarditis, Acute
Other Problems to Be Considered
o Biliary dyskinesia
Sphincter of Oddi dysfunction
Spinal nerve root compression Pathophysiology
Myocardial ischemia
Nonulcer dyspepsia A gallstone produces visceral pain by obstructing the
Acute hepatitis cystic duct or ampulla of Vater, resulting in distention of
the gallbladder or biliary tree. Pain is relieved when the
gallstone migrates back into the gallbladder, passes
through the ampulla, or falls back into the common bile
duct (CBD). The pain of biliary colic may accompany
sphincter of Oddi spasm.

4. Meperidine (Demerol) Ibuprofen (Motrin, Advil, Ibuprin)
Analgesic with multiple actions similar to those of morphine; Indicated for patients with mild to moderate pain. Inhibits
may produce less constipation, smooth-muscle spasm, and inflammatory reactions and pain by decreasing prostaglandin
depression of cough reflex than equal analgesic doses of synthesis.
morphine.
Adult
Adult
Mild to moderate pain: 400 mg PO q4-6h prn; not to exceed 3.2
50-150 mg PO/IV/IM/SC q3-4h prn g/d; IM dosing for those with concurrent nausea
Pediatric Precautions
Not established; problem rare <20 y Pregnancy category D in third trimester; caution in patients
with congestive heart failure, hypertension, and decreased
Increased respiratory and CNS depression with renal and hepatic function; caution in patients with coagulation
coadministration of cimetidine; hydantoins may decrease abnormalities or during anticoagulant therapy
effects; protease inhibitors (eg, ritonavir) may increase
normeperidine levels, enhancing risk of CNS toxicity
Precautions Ketorolac (Toradol)
Pregnancy category D with prolonged use or high doses at Inhibits prostaglandin synthesis by decreasing activity of
term; caution in patients with head injuries, may increase cyclooxygenase, which results in decreased formation of
respiratory depression and CSF pressure; caution prostaglandin precursors.
postoperatively and in patients with history of pulmonary
disease (suppresses cough reflex); increased doses due to Adult
tolerance may aggravate or cause seizures (even without prior
history); caution in patients with renal dysfunction (decrease 30-60 mg IM initially, followed by 15-30 mg q6h;
dose), do not use in patients with severe renal dysfunction, alternatively 15-30 mg IV initially, followed by 15-30 mg IV
normeperidine metabolite accumulation may induce CNS prn; not to exceed 120 mg/d (60 mg/d in renal failure, >65 y,
toxicity or <50 kg); not to exceed 5 d of treatment
Precautions
Hydromorphone (Dilaudid) Pregnancy category D in third trimester; may cause acute
renal insufficiency, hyperkalemia, hyponatremia, interstitial
nephritis, and renal papillary necrosis; increases risk of
Potent semisynthetic opiate agonist similar in structure to
acute renal failure in patients with preexisting renal disease
morphine. Approximately 7- to 8-times as potent as
or compromised renal perfusion; leukopenia (rare) usually
morphine on mg-to-mg basis, with shorter or similar duration
returns to normal during ongoing therapy; discontinue
of action (ie, 4-5 h).
therapy if persistent leukopenia, granulocytopenia, or
thrombocytopenia occur; decrease dose in renal failure, >65
Adult y, or <50 kg
1-2 mg IV/IM/SC q4h; adjust dose according to pain scale
assessment
Precautions
Pregnancy category D with prolonged use or high doses at
term; caution in patients with head injuries, may increase
respiratory depression and CSF pressure; caution
postoperatively and in patients with history of pulmonary
disease (suppresses cough reflex); caution in patients with
impaired hepatic function (decrease dose), hypothyroidism,
Crohn disease, ulcerative colitis, Addison disease, or
prostatic hypertrophy

5. Ondansetron (Zofran)
Antiemetic agents 5-HT-3 receptor antagonist used when other classes fail
or are contraindicated.
Adult
THE CNS VOMITING CENTER (VC) MAY BE STIMULATED DIRECTLY
BY GI IRRITATION. INCREASED ACTIVITY OF CENTRAL
NEUROTRANSMITTERS, DOPAMINE IN THE CHEMORECEPTOR
TRIGGER ZONE, OR ACETYLCHOLINE IN THE VC APPEARS TO BE A
MAJOR MEDIATOR FOR INDUCING VOMITING. ANTIDOPAMINERGIC
AGENTS (EG, METOCLOPRAMIDE, PHENOTHIAZINES) ARE 4 mg IV q6h prn; 8 mg PO tid prn
EFFECTIVE FOR NAUSEA DUE TO GI IRRITATION.
Metoclopramide (Reglan)
Dopamine antagonist that stimulates acetylcholine release in
the myenteric plexus. Acts centrally on chemoreceptor triggers
in the floor of the fourth ventricle, which provides important
antiemetic activity.
Adult
10 mg IV q6h prn
Precautions
Caution in breastfeeding women, patients with depression,
hypertension, Parkinson disease, and conditions aggravated by
anticholinergic or antidopaminergic effects; may cause tardive
dyskinesia
Prochlorperazine (Compazine)
May relieve nausea and vomiting by blocking postsynaptic
mesolimbic dopamine receptors through anticholinergic
effects and depressing reticular activating system.
Adult
5-10 mg PO/IM tid/qid; not to exceed 40 mg/d; alternatively,
2.5-10 mg IV q3-4h prn; not to exceed 10 mg/dose or 40
mg/d
25 mg PR bid
Precautions
Drug-induced Parkinson syndrome or pseudoparkinsonism
occurs frequently, akathisia is most common extrapyramidal
reaction in elderly persons; tardive dyskinesia may occur,
especially in elderly persons (up to 40%); extrapyramidal
effects most pronounced in children <5 y or elderly persons;
lowers seizure threshold, caution in patients with history of
seizures; caution in patients with prostatic hypertrophy,
peptic ulcer, dehydration, or history of neuroleptic malignant
syndrome

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Past Issues Management of Gallstones and Their
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Contact AFP The accurate differentiation of gallstone-induced biliary colic from other
Careers abdominal disease processes is the most crucial step in the successful
management of gallstone disease. Despite the availability of many imaging
techniques to demonstrate the presence of gallstones, clinical judgment
ultimately determines the association of symptoms with cholelithiasis and its
complications. Adult patients with silent or incidental gallstones should be
observed and managed expectantly, with few exceptions. In symptomatic
patients, the intervention varies with the type of gallstone-induced
complication. In this article, we review the salient clinical features, diagnostic
tests and therapeutic options employed in the management of gallstones and
their complications. (Am Fam Physician 2000;61:1673-80,1687-8.)
G allstones are a major cause of morbidity worldwide, and
cholecystectomy is the most commonly performed abdominal surgery
in medicine. Gallstone-induced complications have a limited and
overlapping pattern of clinical presentation. 1
Pathogenesis of Gallstones
Gallstones found in the gallbladder are classified as cholesterol, pigmented or mixed
stones, based on their chemical composition. Up to 90 percent of gallstones are
cholesterol (more than 50 percent cholesterol) or mixed (20 to 50 percent cholesterol)
gallstones. The remaining 10 percent of gallstones are pigmented stones, which have
less than 20 percent cholesterol.
The basic mechanism underlying the
formation of gallstones is supersaturation, TABLE 1
with constituents in bile exceeding their Risk Factors for Gallstone
maximum solubilities.2,3 Additional factors Formation
contributing to gallstone formation are
Age Increasing age*
nucleation factors, bile stasis within the
Body habitus Obesity, rapid
gallbladder and calcium in bile. Biliary
weight loss
cholesterol usually exists in a soluble single

7. Childbearing Pregnancy
phase as micellar cholesterol. As the
Drugs Fibric acid
cholesterol concentration increases, derivatives (or
cholesterol crystals begin to form. fibrates),
contraceptive
Mucin and a soluble glycoprotein are steroids,
potential nucleation factors. Prostaglandins postmenopausal
estrogens,
stimulate the synthesis and secretion of bile progesterone,
mucin. Inflammation and other stimuli, which octreotide
enhance prostaglandin secretion, increase the (Sandostatin),
risk for gallstone formation. Biliary sludge, ceftriaxone
(Rocephin)
also referred to as microlithiasis, is a viscous
Ethnicity Pima Indians,
gel composed of mucin, precipitates of Scandinavians
cholesterol and calcium bilirubinate. Family Maternal family
Gallstone formation is usually preceded by history of gallstones
the presence of biliary sludge.4 Therefore, Gender Females
sludge should be regarded as part of the Hyperalimentation Total parenteral
spectrum of gallstone disease. Retarded or nutrition,† fasting
incomplete emptying of bile from the Ileal and other Ileal disease
gallbladder can promote sludge formation. metabolic (Crohn's disease),
diseases resection or
The risk factors for gallstone formation are bypass,* high
summarized in Table 1. triglycerides,
diabetes mellitus,
People with diabetes have a propensity for chronic hemolysis,*
obesity, hypertriglyceridemia and gallbladder alcoholic cirrhosis,*
hypomotility. Therefore, it has been difficult biliary infection,*
primary biliary
to prove that diabetes is an independent risk cirrhosis, duodenal
factor for gallstone formation. However, some diverticula,* truncal
studies have shown an increased prevalence vagotomy,
(without statistical significance) of diabetes in hyperparathyroidism,
low level of high-
patients with gallstones.5 density lipoprotein
cholesterol
Common bile duct stones
*--Risk factors for pigment gallstone
(choledocholithiasis) may form de novo in
formation.
bile ducts (primary, 5 percent of common bile †--Risk factor for cholesterol and
duct stones) or migrate to the common bile pigment gallstone formation.
duct from the gallbladder (secondary, 95
percent of common bile duct stones). Composition of gallstones in the common bile
duct is usually the same as that of gallstones in the gallbladder, although some bile duct
stones are softer and more brownish because of deposition of calcium bilirubinate and
other calcium salts caused by the bacterial deconjugation of bilirubin and hydrolysis of
phospholipids. Primary common bile duct stones are more common in Asian
populations because of the increased prevalence of flukes and parasitic infections, such
as clonorchiasis, fascioliasis and ascariasis.
Clinical Presentations
The clinical presentation of gallstone-induced complications varies. Differentiating
features such as pain site and duration, presence or absence of a mass, fever and
laboratory parameters can assist in establishing the correct diagnosis (Table 2).
TABLE 2
Differentiating Features of Gallstone-Induced Complications*
Biliary Acute Chronic
Feature colic cholecystitis cholecystitis Cholangitis Pancreatitis
Pain site Epigastrium RUQ RUQ RUQ Epigastric
Pain duration <3 hours > 3 hours Variable Variable Variable
Mass No masses RUQ mass No masses ± ±
Fever ± ± ± ±
Increased WBC ± ± ± ±
Increased Normal ± ± +
amylase level
RUQ = right upper quadrant; WBC = white blood cell count; + = present; = absent; ± =
present or absent.
*--These characteristics may not always be present.
Biliary Colic
As many as one third of patients with gallstones will develop symptoms (Table 3). It is
thought that the pain of biliary colic is caused by the functional spasm of the cystic
duct when obstructed by stones, whereas pain in acute cholecystitis is caused by

8. inflammation of the gallbladder wall.6 Pain often develops without any precipitating
symptoms. Typically, the pain has a sudden onset and rapidly increases in intensity over
a 15-minute interval to a plateau that can last as long as three hours. The pain may
radiate to the interscapular region or to the right shoulder.
It is worthwhile to clarify some misconceptions
Biliary colic pain develops
about biliary pain. First, biliary colic is a suddenly, rapidly increases in
misnomer, because the pain is steady, not colicky. intensity over 15 minutes and can
Second, the pain site is primarily in the last as long as three hours.
epigastrium, and it is incorrect to interpret pain
located in the epigastrium as nonbiliary. Third, fat intolerance is not a feature of biliary
colic.
Acute Cholecystitis
The most common cause of acute cholecystitis is obstruction of the cystic duct by
gallstones, resulting in acute inflammation. Approximately 90 percent of cases of acute
cholecystitis are associated with cholelithiasis. The clinical features of acute
cholecystitis may include symptoms of local inflammation (e.g., right upper quadrant
mass, tenderness) and systemic toxicity (e.g., fever, leukocytosis). Most patients with
acute cholecystitis have had previous attacks of biliary pain. The pain of acute
cholecystitis typically lasts longer than three hours and, after three hours, shifts from
the epigastrium to the right upper quadrant. This sequence of clinical features includes
visceral pain from ductal impaction by stones, progressing to inflammation of the
gallbladder with parietal pain.
In elderly patients, localized tenderness may be the only presenting sign; pain and fever
may be absent. 7 In 30 to 40 percent of patients, the gallbladder and adherent omentum
can be perceived as a palpable mass. Jaundice is noted in approximately 15 percent of
patients with acute cholecystitis, even without choledocholithiasis. The pathogenesis
may involve edema and inflammation secondary to the impacted stone in the cystic
duct. This leads to the compression of the common hepatic duct or the common bile
duct (Mirizzi's syndrome).
In the event of delayed diagnosis in the setting
TABLE 3 of acute cholecystitis, the cystic duct remains
Complications of obstructed, and the lumen may become
Gallstones* distended with clear mucoid fluid (hydrops of
the gallbladder). Although rare, a large
Complication Percentage
gallstone in the gallbladder will sometimes
Biliary colic 70 to 80†
erode through the gallbladder wall into an
Acute cholecystitis 10
adjacent viscus, usually the duodenum.
Emphysematous <1‡
Subsequently, the stone may become impacted
cholecystitis
in the terminal ileum (small bowel
Mirizzi's syndrome <1‡
obstruction) or in the duodenal bulb/pylorus,
Hydrops of the <1‡
gallbladder causing gastric outlet obstruction (Bouveret's
Small bowel obstruction 1‡ syndrome). Patients with chronic cholecystitis
(gallstone ileus) usually have had repeated attacks of biliary
Gastric outlet obstruction <1‡ pain or acute cholecystitis. This results in a
(Bouveret's syndrome) thickened and fibrotic gallbladder that may
Perforation of gallbladder 12‡ not be palpable in these patients.
Acute biliary pancreatitis --
Acute -- Acute cholecystitis may present as an
suppurative/obstructive acalculous disorder in 5 to 10 percent of
cholangitis patients. Acalculous cholecystitis typically
*--One third of patients with gallstones affects critically ill, older men in the setting of
develop symptoms. major surgery, critical illness, total parenteral
†--Percentage incidence in patients
with symptomatic gallstones.
nutrition, extensive trauma or burn-related
‡--Percentage incidence in patients injury. The pathogenesis probably involves a
with acute cholecystitis. combination of biliary stasis, chemical
inflammation and ischemia. Complications
develop more frequently in acalculous cholecystitis than in calculous cholecystitis.
Rarely, infectious agents can cause acute cholecystitis. Cytomegalovirus and
cryptosporidia can result in cholecystitis and cholangitis in immunocompromised
persons. Salmonella can colonize the gallbladder epithelium without eliciting
inflammation, creating a carrier state.
Choledocholithiasis
Acute suppurative cholangitis is a common complication of choledocholithiasis. The
usual clinical presentation, occurring in 70 percent of the cases of choledocholithiasis,
consists of pain, jaundice and chills (i.e., Charcot's triad). Refractory sepsis

9. characterized by altered mentation, hypotension and Charcot's triad constitutes
Raynold's pentad. Depending on the progression of the illness, endotoxemia with shock
or multiple liver abscesses may be noted. On the other hand, cholangitis may be a short,
self-limited illness complicating choledocholithiasis. The most commonly found
organisms are Escherichia coli, Klebsiella, Pseudomonas and enterococci, with a 15
percent contribution by anaerobes.
Acute biliary pancreatitis is another potential complication of choledocholithiasis.8
Differentiating acute pancreatitis from cholecystitis can be difficult because both
conditions produce tenderness in an overlapping area. Although acute cholecystitis
alone can be associated with hyperamylasemia, pancreatitis often has higher enzyme
levels. Also, cholecystitis and pancreatitis may coexist.
Diagnostic Studies
A wide array of laboratory and radiologic studies is used for the evaluation of
gallstones located in the gallbladder and the common bile duct. There are strengths and
limitations to each diagnostic test.
Laboratory Tests
In uncomplicated biliary colic, there are usually no accompanying changes in
hematologic and biochemical tests. In acute cholecystitis, leukocytosis with a "left
shift" is usually observed. Serum aminotransferase, alkaline phosphatase, bilirubin and
amylase levels may also be elevated. The most reliable indicator of gallstones as the
cause of acute pancreatitis is an elevation of alanine aminotransferase levels greater
than 2.5 times above normal. 8
Ultrasonography
Gallbladder ultrasonography
Ultrasonography should be a routine examination should be a routine examination in
for the confirmation or exclusion of gallstone the evaluation of patients
disease. Ultrasonography provides more than 95 suspected of having gallstone
percent sensitivity and specificity for the diagnosis disease.
of gallstones greater than 2 mm in diameter.
Ultrasonography of the gallbladder should follow a fast of at least eight hours because
gallstones are visualized better in a distended, bile-filled gallbladder.
Ultrasonography is less sensitive for the diagnosis of choledocholithiasis and may
document only one half of common bile duct stones. 9 Ultrasound scans may indicate
dilatation of intrahepatic or extrahepatic bile ducts, which is highly suggestive of distal
obstruction, with a sensitivity of 76 percent. Ultrasonographic findings that are
suggestive of acute cholecystitis include the following: pericholecystic fluid (in the
absence of ascites); gallbladder wall thickening greater than 4 mm (in the absence of
hypoalbuminemia); and sonographic Murphy's sign (abrupt arrest of breathing during
the inspiration phase secondary to pain elicited by placing the ultrasound probe in the
right upper quadrant).
Endoscopic Retrograde Cholangiopancreatography
Endoscopic retrograde cholangiopancreatography (ERCP) is the best method for
determining a diagnosis of choledocholithiasis.10 ERCP provides diagnostic and
therapeutic options, and has a sensitivity and specificity of 95 percent for the detection
of common bile duct stones.
Bile Microscopy
It is essential that gallbladder bile (induced by cholecystokinin), rather than hepatic or
ductal bile, be obtained to maximize sensitivity for detecting sludge. A bile sample may
be obtained by aspiration through the catheter during ERCP. Bile must be centrifuged
and examined under polarizing or light microscopy for detection of precipitates.
Computed Tomography and Magnetic Resonance Imaging
The latest computer technology, processing computed tomographic (CT) and magnetic
resonance imaging (MRI) data into a three-dimensional image of the bile duct, is now
comparable to the ERCP in terms of diagnostic accuracy. 11,12 Although CT and MRI
provide the advantage of noninvasiveness, they offer no therapeutic options.
Hepatobiliary Scintigraphy
Hepatobiliary scintigraphy can confirm or exclude the diagnosis of acute cholecystitis
with a high degree of sensitivity and specificity. 13 After a two- to four-hour fast, the
patient is given an intravenous injection of a technetium-99mlabeled iminodiacetic acid
derivative (IDA agent) that is excreted into the bile ducts and sequentially imaged
under a gamma camera.
In a normal study, images of the gallbladder,

10. A normal hepatobiliary scintigram
common bile duct and small bowel appear within virtually rules out acute
30 to 45 minutes. 14 A normal Tc-99m-IDA scan cholecystitis in patients who
virtually rules out the diagnosis of acute present with abdominal pain.
cholecystitis in patients who present with
abdominal pain. An abnormal or "positive" Tc-99m-IDA scan can be defined as
nonvisualization of the gallbladder with preserved excretion into the common bile duct
and small bowel. Failure to image the gallbladder within 90 minutes despite adequate
views of the liver, common bile duct and small bowel strongly suggests acute
obstruction of the cystic duct. False-positive findings can result from nonfasting or
prolonged fasting states, 14 chronic alcoholism and chronic cholecystitis. Repeat scanning
after four or more hours decreases the false-positive rate.
In patients with acute acalculous cholecystitis, prolonged fasting may result in viscous
(concentrated) bile and a false-positive hepatobiliary scan. Alternatively, patients with
acalculous cholecystitis may not have an obstructed cystic duct, resulting in a false-
negative hepatobiliary scan. False-positive results occur more frequently than false-
negative results. The hepatobiliary scan has a sensitivity greater than 90 percent, but the
lack of specificity in fasting, critically ill patients limits the use of the hepatobiliary
scan to exclusion of acute acalculous cholecystitis rather than confirmation of the
diagnosis.
Management of Gallstones
*--Consider emergent therapeutic ERCP in patients with acute
gallstone/biliary pancreatitis or acute suppurative cholangitis.
†--Patients with suspected choledocholithiasis should undergo
ERCP (preoperative or postoperative) or intraoperative
cholangiography
‡--Consider percutaneous cholecystostomy or transpapillary
endoscopic cholecystostomy in patients with acute cholecystitis.
See Table 5.
FIGURE 1.Management of gallstones and its complications. (ERCP
= endoscopic retrograde cholangiopancreatography)
Management
Cholelithiasis can be diagnosed in a variety of clinical circumstances. A patient can be
asymptomatic, have a history of one or more uncomplicated biliary pain episodes or
have complications of acute cholecystitis, gangrene, jaundice or even gallbladder
cancer.
Asymptomatic Gallstones
It is estimated that 60 to 80 percent of all gallstones are asymptomatic at some point.15
Adult patients with silent or incidental gallstones should be observed and managed
expectantly, including patients with diabetes.16 In diabetic patients, the natural history of
gallstones is generally benign, and there is low risk of a major complication. 15 There is
no evidence to suggest that prophylactic cholecystectomy prolongs life expectancy.
However, prophylactic cholecystectomy should be performed in patients at high risk of
gallbladder carcinoma (Figure 1). The specific groups at high risk of gallbladder cancer
include patients with asymptomatic gallstones who are Pima Indians or who have a
calcified gallbladder, gallbladder polyps greater than 10 mm, gallstones greater than 2.5
cm or anomalous pancreaticobiliary ductal junction, and carriers of Salmonella typhosa.
TABLE 4
Nonoperative Therapies for Symptomatic Gallstones
Agent Advantages Disadvantages
Oral bile acid Stone 50 percent recurrence of stones; dissolves
dissolution: clearance: noncalcifiedcholesterol stones; optimal for stones <5
ursodeoxycholic 30 to 90 mm; symptom relief does not start for 3 to 6 weeks;
acid (Actigall), at percent with may take 6 to 24 months for results
8 to 10 mg per zero percent
kg per day mortality

11. Contact solvents: Stone 70 percent recurrence of stones; experimental, with
methyl tert-butyl clearance: insufficient data; duodenitis; hemolysis; nephrotoxicity;
ether/n-propyl 50 to 90 mild sedation
acetate percent
Extracorporeal Stone 70 percent recurrence; not approved by FDA; performed
shock-wave clearance: only at centers with expertise; selection criteria require
lithotripsy: 70 to 90 no more than one radiolucent stone (<20 mm in
electrohydraulic/ percent with diameter), patent cystic duct, functioning gallbladder in
electromagnetic <0.1 percent a patient with symptomatic gallstones without
mortality complications
FDA = U.S. Food and Drug Administration.
Symptomatic Gallstones
Once an episode of biliary colic has occurred, there is a high risk of repeated pain
attacks. Cohort studies with follow-up of patients with symptomatic gallstones indicate
a 38 to 50 percent incidence rate of recurrent biliary pain per year.17 Patients with
symptomatic gallstones are more likely to develop biliary complications.18 The risk of
developing biliary complications is estimated to be 1 to 2 percent per year.
As many as 30 percent of patients who are
Adult patients with silent or
observed for several years do not have further incidental gallstones should be
problems. Therefore, a management plan is observed and managed
dependent on the patient's decision and surgical expectantly.
candidacy. For patients who do not want to risk the
possibility of a future attack, a laparoscopic cholecystectomy is recommended.
In the 1980s, considerable interest was generated in the evaluation of nonsurgical
treatment strategies for gallstone disease. Nonoperative therapy is costly and time-
consuming, and should be reserved for use in the symptomatic patient who declines
surgery or has a high operative risk 19,20 (Table 4).
Acute Cholecystitis
Most physicians agree that early laparoscopic TABLE 5
cholecystectomy (within 24 to 48 hours) is Contraindications for
indicated once the diagnosis of acute Laparoscopic
cholecystitis is secure and the patient is
Cholecystectomy
hemodynamically stable. Use of this surgical
High risk for general anesthesia
technique is supported by large randomized
Morbid obesity
trials conclusively demonstrating its clinical Signs of gallbladder perforation such
21
superiority over open cholecystectomy. The as abscess, peritonitis or fistula
potential advantages of laparoscopic Giant gallstones
End-stage liver disease with portal
cholecystectomy include a marked reduction
hypertension and severe coagulopathy
in postoperative pain, a shorter hospital stay Suspected gallbladder malignancy
and a more rapid return to work and usual Last trimester of pregnancy
activities. A percutaneous cholecystostomy or
transpapillary endoscopic cholecystostomy should be considered in patients with acute
cholecystitis who are at excessive risk for surgery22,23 (Table 5).
Choledocholithiasis
When a patient with known gallbladder stones has concomitant choledocholithiasis, the
management varies with the severity of clinical features. 24,25 In general, the presence of
obstructive cholangitis or jaundice with a dilated common bile duct detected by
ultrasonography should lead promptly to a preoperative ERCP with possible
sphincterotomy and stone extraction. Once the bile duct has been cleared by ERCP, the
patient can undergo a routine laparoscopic cholecystectomy within one or two days.
However, if liver enzyme levels are only mildly elevated and there is a low suspicion
for common bile duct stones, many physicians proceed directly with laparoscopic
surgery. In this case, intraoperative cholangiography should be performed to rule out
choledocholithiasis. If common bile duct stones are present, they can be removed
intraoperatively or by a postoperative ERCP. 26
The Authors
AIJAZ AHMED, M.D.,
is a staff physician in gastroenterology at Stanford (Calif.) University School of
Medicine, where he completed a fellowship in gastroenterology. Dr. Ahmed graduated
from the University of Karachi, Dow Medical College, in Karachi, Pakistan, and
completed a residency in internal medicine at Brown University School of Medicine in
Providence, R.I.
RAMSEY C. CHEUNG, M.D.,

12. is assistant professor of medicine at Stanford University School of Medicine, where he
completed a fellowship in gastroenterology. He graduated from the University of
Chicago Pritzker School of Medicine and completed a residency in internal medicine at
the University of California, Irvine, College of Medicine.
EMMET B. KEEFFE, M.D.,
is professor of medicine at Stanford University School of Medicine and chief of clinical
gastroenterology and medical director of the Liver Transplant Program at Stanford
University Medical Center. After graduating from Creighton University School of
Medicine in Omaha, Neb., he completed a residency in internal medicine at the Oregon
Health Sciences University, and a fellowship in gastroenterology at the Oregon Health
Sciences University School of Medicine in Portland and the University of California,
San Francisco, School of Medicine.
Address correspondence to Emmet B. Keeffe, M.D., Stanford University
Medical Center, 750 Welch Rd., Ste. 210, Palo Alto, CA 94304-1509.
Reprints are not available from the authors.
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