1.Biliary colic Further readinghttp://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_17Cholelithiasis: "presence or formation of gallstones in the gallbladder." Source: CRISP Thesaurus, 2006Biliary Colic: "Painful sensation in the gallbladder region." Source: NCI Thesaurus, 2009_04DBiliary 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_17Cholecystolithiasis:

2. "Presence or formation of GALLSTONES in the4. Labs GALLBLADDER."1. Complete Blood Count usually normal Source: Medical Subject Headings, 2010_2009_08_172. Mild elevation of Liver Function Tests 1. Bilirubin slightly elevated 2. Alkaline Phosphatase slightlyelevated________________________3. Pancreatic enzyme tests normal 1. Amylase normal 2. Lipase normal Biliary Colic4. Urinalysis normal5. HCG NORMAL 1. Symptoms 1. Abdominal Pain characteristics 1. RUQ Abdominal Pain or EpigastricAbdominal Pain 2. Dull visceral ache5. Radiology 3. Poorly localized discomfort 1. XRay Abdomen 4. PAIN RADIATES TO RIGHT 1. Test Sensitivity: 10-20% for GallstonesPOSTERIOR SHOULDER OR 2. Chest XRay normalSCAPULA 3. RUQ Ultrasound 1. Test Sensitivity: 95% for Gallstones4. 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 pain2. Antispasmodic 5. Mild abdominal aching for 1-2 days 1. Glycopyrrolate (Robinul) after attack 1. Parenteral: 0.1 to 0.2 mg IV or IM2. Oral: 1.0 to 2.0 mg PO bid-tid 3. Associated symptoms1. Nausea and Vomiting2. No Fever or chills (see differential 3. Analgesic diagnosis)1. Meperidine (Demerol) 1. Less sphincter of Oddi spasm than morphine 2. Ketorlac (Toradol) 2. Signs1. Relieves pain of gallbladder 1. RUQ abdominal tenderness distention 2. No signs of peritoneal irritation2. Not as effective if infection 3. Dehydration from protracted Vomiting present4. Antiemetics 3. Differential Diagnosis 1. Acute Cholecystitis1. Promethazine (Phenergan) 2. Cholangitis 5. Nasogastric Suction 3. Pancreatitis 1. Indicated for protracted Vomiting6. Alternatives in non-surgical candidates 1. BILE ACID ORAL DISSOLUTIONTHERAPY 3. Differential Diagnoses Abdominal Abscess Gallbladder Volvulus Abdominal AnginaGastric Ulcers Abdominal AorticGastritis, Acute Aneurysm Angina Pectoris Gastroesophageal Reflux Disease AppendicitisIrritable Bowel Syndrome Cholangitis Liver Abscess Cholecystitis Mesenteric Venous Thrombosis Colonic Obstruction Myocardial Infarction DiverticulitisOpioid Abuse Duodenal Ulcers Pancreatitis, Acute Esophageal SpasmPancreatitis, Chronic Esophagitis Pericarditis, AcuteOther Problems to Be Consideredo Biliary dyskinesia Sphincter of Oddi dysfunction Spinal nerve root compressionPathophysiology Myocardial ischemia Nonulcer dyspepsia A gallstone produces visceral pain by obstructing the Acute hepatitiscystic duct or ampulla of Vater, resulting in distention ofthe gallbladder or biliary tree. Pain is relieved when thegallstone migrates back into the gallbladder, passesthrough the ampulla, or falls back into the common bileduct (CBD). The pain of biliary colic may accompanysphincter 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, andinflammatory reactions and pain by decreasing prostaglandin depression of cough reflex than equal analgesic doses of synthesis. morphine.Adult AdultMild to moderate pain: 400 mg PO q4-6h prn; not to exceed 3.2 50-150 mg PO/IV/IM/SC q3-4h prng/d; IM dosing for those with concurrent nauseaPediatricPrecautions Not established; problem rare 65 y, toxicity or 65 Adulty, or Journals > American Family Physician ID Number Last Name/Password Remember Me Log-in Help Advanced SearchAdvertisement 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 QuizSEARCH AFPAFP Advanced SearchAFP AT A GLANCEPast Issues Management of Gallstones and Their Annual IndexesComplications 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 medicalStanford 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, andcholecystectomy is the most commonly performed abdominal surgeryin medicine. Gallstone-induced complications have a limited andoverlapping pattern of clinical presentation. 1Pathogenesis 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 theirRisk Factors for Gallstone maximum solubilities.2,3 Additional factorsFormation contributing to gallstone formation areAgeIncreasing age* nucleation factors, bile stasis within theBody 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 DrugsFibric acid cholesterol concentration increases, derivatives (or cholesterol crystals begin to form.fibrates),contraceptive Mucin and a soluble glycoprotein are steroids, potential nucleation factors. Prostaglandins postmenopausalestrogens, stimulate the synthesis and secretion of bileprogesterone, 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 EthnicityPima 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 theHyperalimentation Total parenteral spectrum of gallstone disease. Retarded ornutrition, fasting incomplete emptying of bile from theIleal and otherIleal 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 gallbladderalcoholic cirrhosis,* hypomotility. Therefore, it has been difficult biliary infection,*primary biliary to prove that diabetes is an independent riskcirrhosis, duodenal factor for gallstone formation. However, somediverticula,* truncal studies have shown an increased prevalence vagotomy, (without statistical significance) of diabetes inhyperparathyroidism,low level of high- patients with gallstones.5 density lipoproteincholesterol 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 bilepigment 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 2Differentiating Features of Gallstone-Induced Complications*BiliaryAcute Chronic Featurecoliccholecystitis cholecystitisCholangitis Pancreatitis Pain siteEpigastrium RUQRUQRUQ Epigastric Pain duration 3 hours Variable VariableVariable Mass No masses RUQ mass No masses Fever Increased WBC IncreasedNormal + amylase levelRUQ = 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 settingTABLE 3of acute cholecystitis, the cystic duct remainsComplications of obstructed, and the lumen may becomeGallstones*distended with clear mucoid fluid (hydrops of the gallbladder). Although rare, a large Complication Percentage gallstone in the gallbladder will sometimes Biliary colic70 to 80 erode through the gallbladder wall into an Acute cholecystitis10 adjacent viscus, usually the duodenum. Emphysematous