Biliary colic
Further reading

"Presence or formation of GALLSTONES in the                    4. Labs
Differential Diagnoses
Abdominal Abscess       Gallbladder Volvulus
Abdominal Angina        Gastric Ulcers
Abdominal Aorti...
Meperidine (Demerol)                                             Ibuprofen (Motrin, Advil, Ibuprin)

Analgesic with multip...
Ondansetron (Zofran)

Antiemetic agents                                                5-HT-3 receptor antagonist used whe...

                                                                                      Home Page > News &...
Childbearing       Pregnancy
phase as micellar cholesterol. As the
inflammation of the gallbladder wall.6 Pain often develops without any precipitating
symptoms. Typically, the pain has a s...
characterized by altered mentation, hypotension and Charcot's triad constitutes
Raynold's pentad. Depending on the progres...
A normal hepatobiliary scintigram
common bile duct and small bowel appear within         virtually rules out acute
30 to 4...
Contact solvents:   Stone          70 percent recurrence of stones; experimental, with
  methyl tert-butyl   clearance:   ...
is assistant professor of medicine at Stanford University School of Medicine, where he
  completed a fellowship in gastroe...
Copyright © 2000 by the American Academy of Family Physicians.
This content is owned by the AAFP. A person viewing it onli...
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30 Biliar Y Coli C

  1. 1. Biliary colic Further reading 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. 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. 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. 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. 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
  6. 6. Advertisement Home Page > News & Publications > Journals > American Family Physician® ID Number Last Name/Password Remember Me Log-in Help Advanced Search Advertisement ARTICLE TOOLS Please note: The American Family Physician Web archive extends from 1998 to the present. Enhanced features are Email this page available for content published after 2000. Share this page AFP CME Quiz SEARCH AFP AFP Advanced Search AFP AT A GLANCE Past Issues Management of Gallstones and Their Annual Indexes Complications CME Quiz Dept Collections A patient information AIJAZ AHMED, M.D., EBM Toolkit handout on gallstones and RAMSEY C. CHEUNG, M.D., and their treatment, written by About AFP EMMET B. KEEFFE, M.D. Joseph Cooney, a medical Stanford University School of Medicine, Stanford, Information for editing clerk at Georgetown California Advertisers University Medical Center, is provided on page 1687. Subscriptions 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. 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. 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. 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. 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. 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. 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. REFERENCES 1. Egbert AM. Gallstone symptoms. Myth and reality. Postgrad Med 1991;90:119-26. 2. Marks JW, Bonorris GG, Albers G, Schoenfield LJ. The sequence of biliary events preceding the formation of gallstones in humans. Gastroenterology 1992;103:566-70. 3. Donovan JM. Physical and metabolic factors in gallstone pathogenesis. Gastroenterol Clin North Am 1999;28:75-97. 4. Ko CW, Sekijima JH, Lee SP. Biliary sludge. Ann Intern Med 1999;130:301-11. 5. Jorgensen T. Gall stones in a Danish population. Relation to weight, physical activity, smoking, coffee consumption, and diabetes mellitus. Gut 1989; 30:528-34. 6. Traverso LW. Clinical manifestations and impact of gallstone disease. Am J Surg 1993;165:405-9. 7. Raine PA, Gunn AA. Acute cholecystitis. Br J Surg 1975;62:697-700. 8. Soetikno RM, Carr-Locke DL. Endoscopic management of acute gallstone pancreatitis. Gastrointest Endosc Clin N Am 1998;8:1-12. 9. Houdart R, Perniceni T, Darne B, Salmeron M, Simon JF. Predicting common bile duct lithiasis: determination and prospective validation of a model predicting low risk. Am J Surg 1995;170:38- 43. 10. Prat F, Amouyal G, Amouyal P, Pelletier G, Fritsch J, Choury AD, et al. Prospective controlled study of endoscopic ultrasonography and endoscopic retrograde cholangiography in patients with suspected common-bileduct lithiasis. Lancet 1996;347:75-9. 11. Neri E, Caramella D, Boraschi P, Braccini G, Lehmann ED, Perri G, et al. Magnetic resonance virtual endoscopy of the common bile duct stones. Surg Endosc 1999;13:632-3. 12. Coakley FV, Schwartz LH. Magnetic resonance cholangiopancreatography. J Magn Reson Imaging 1999;9:157-62. 13. Shea JA, Berlin JA, Escarce JJ, Clarke JR, Kinosian BP, Cabana MD, et al. Revised estimates of diagnostic test sensitivity and specificity in suspected biliary tract disease. Arch Intern Med 1994;154:2573-81. 14. Marton KI, Doubilet P. How to image the gallbladder in suspected cholecystitis. Ann Intern Med 1988;109:722-9. 15. Gracie WA, Ransohoff DF. The natural history of silent gallstones: the innocent gallstone is not a myth. N Engl J Med 1982;307:798-800. 16. Del Favero G, Caroli A, Meggiato T, Volpi A, Scalon P, Puglisi A, et al. Natural history of gallstones in non-insulin-dependent diabetes mellitus. a prospective 5-year follow-up. Dig Dis Sci 1994;39:1704-7. 17. Thistle JL, Cleary PA, Lachin JM, Tyor MP, Hersh T. The natural history of cholelithiasis: the National Cooperative Gallstone Study. Ann Intern Med 1984;101:171-5. 18. Newman HF, Northup JD, Rosenblum M, Abrams H. Complications of cholelithiasis. Am J Gastroenterol 1968;50:476-96. 19. Cesmeli E, Elewaut AE, Kerre T, De Buyzere M, Afschrift M, Elewaut A. Gallstone recurrence after successful shock wave therapy: the magnitude of the problem and the predictive factors. Am J Gastroenterol 1999;94:474-9. 20. Howard DE, Fromm H. Nonsurgical management of gallstone disease. Gastroenterol Clin North Am 1999;28:133-44. 21. Cuschieri A. Laparoscopic cholecystectomy. J R Coll Surg Edinb 1999;44:187-92. 22. Chevallier P, Hastier P, Buckley MJ, Oddo F, Diaine B, Padovani B. Removal of a common bile duct stone via percutaneous cholecystostomy. Endoscopy 1999;31:S17-8. 23. Johlin FC, Neil GA. Drainage of the gallbladder in patients with acute acalculous cholecystitis by transpapillary endoscopic cholecystostomy. Gastrointest Endosc 1993;39:645-51. 24. Snow LL, Weinstein LS, Hannon JK, Lane DR. Management of bile duct stones in 1572 patients undergoing laparoscopic cholecystectomy. Am Surg 1999;65:530-45. 25. Montori A, Miscusi G, Masoni L, Gasparrini M, Pietropaolo V, Montori J, et al. Endoscopic and surgical integration in the approach to biliary tract disease. J Clin Gastroenterol 1999;28:198-201. 26. Sahai AV, Mauldin PD, Marsi V, Hawes RH, Hoffman BJ. Bile duct stones and laparoscopic cholecystectomy: a decision analysis to assess the roles of intraoperative cholangiography, EUS, and ERCP. Gastrointest Endosc 1999;49:334-43.
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