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10/13/2015 Gallstones (Cholelithiasis) Clinical Presentation: History, Physical Examination http://emedicine.medscape.com/article/175667clinical 1/5 Gallstones (Cholelithiasis) Clinical Presentation Author: Douglas M Heuman, MD, FACP, FACG, AGAF; Chief Editor: Julian Katz, MD more... Updated: Jan 20, 2015 History Gallstone disease may be thought of as having the following 4 stages: 1. The lithogenic state, in which conditions favor gallstone formation 2. Asymptomatic gallstones 3. Symptomatic gallstones, characterized by episodes of biliary colic 4. Complicated cholelithiasis Symptoms and complications of gallstone disease result from effects occurring within the gallbladder or from stones that escape the gallbladder to lodge in the common bile duct. Asymptomatic gallstones Gallstones may be present in the gallbladder for decades without causing symptoms or complications. In patients with asymptomatic gallstones discovered incidentally, the likelihood of developing symptoms or complications is 12% per year. In most cases, asymptomatic gallstones do not require any treatment. Because they are common, gallstones often coexist with other gastrointestinal conditions. There is little evidence to support a causal association between gallstones and chronic abdominal pain, heartburn, postprandial distress, bloating, flatulence, constipation, or diarrhea. Dyspepsia that occurs reproducibly following ingestion of fatty foods is often wrongly attributed to gallstones, when irritable bowel syndrome or gastroesophageal reflux is the true culprit. Gallstones discovered during an evaluation for nonspecific symptoms are usually innocent bystanders, and treatment directed at the gallstones is unlikely to relieve these symptoms. Biliary colic Pain termed biliary colic occurs when gallstones or sludge fortuitously impact in the cystic duct during a gallbladder contraction, increasing gallbladder wall tension. In most cases, the pain resolves over 30 to 90 minutes as the gallbladder relaxes and the obstruction is relieved. Episodes of biliary colic are sporadic and unpredictable. The patient localizes the pain to the epigastrium or right upper quadrant and may describe radiation to the right scapular tip (Collins sign [8] ). The pain begins postprandially (usually within an hour after a fatty meal), is often described as intense and dull, and may last from 1 5 hours. From onset, the pain increases steadily over about 10 to 20 minutes and then gradually wanes when the gallbladder stops contracting and the stone falls back into the gallbladder. The pain is constant in nature and is not relieved by emesis, antacids, defecation, flatus, or positional changes. It may be accompanied by diaphoresis, nausea, and vomiting. Other symptoms, often associated with cholelithiasis, include indigestion, dyspepsia, belching, bloating, and fat intolerance. However, these are very nonspecific and occur in similar frequencies in individuals with and without gallstones; cholecystectomy has not been shown to improve these symptoms. Most patients develop symptoms prior to complications. Once symptoms of biliary colic occur, severe symptoms develop in 39% of patients, with complications in 1 3% per year and a cholecystectomy rate of 38% per year. Therefore, in people with mild symptoms, 50% have complications after 20 years. Zollinger performed studies in the 1930s in which the gallbladder wall or common bile duct was distended with a balloon; pain was elicited in the epigastric region. Only if the distended gallbladder touched the peritoneum did the patient experience right upper quadrant pain. Associated symptoms of nausea, vomiting, or referred pain were present in distention of the common bile duct (CBD) but not of the gallbladder. Physical Examination Patients with the lithogenic state or asymptomatic gallstones have no abnormal findings on physical examination. Distinguishing uncomplicated biliary colic from acute cholecystitis or other complications is important. Both often present with the same constellation of symptoms, and physical examination may help to differentiate the two. Since the gallbladder is not inflamed in uncomplicated biliary colic, the pain is poorly localized and visceral in origin; the patient has an essentially benign abdominal examination without rebound or guarding. Fever is absent. In acute cholecystitis, inflammation of the gallbladder with resultant peritoneal irritation leads to welllocalized pain in the right upper quadrant, usually with rebound and guarding. Although nonspecific, a positive Murphy sign (inspiratory arrest on deep palpation of the right upper quadrant during deep inspiration) is highly suggestive of cholecystitis. Fever is often present, but it may lag behind other

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Page 1: Gallstones (Cholelithiasis) Clinical Presentation_ History, Physical Examination

10/13/2015 Gallstones (Cholelithiasis) Clinical Presentation: History, Physical Examination

http://emedicine.medscape.com/article/175667clinical 1/5

Gallstones (Cholelithiasis) Clinical PresentationAuthor: Douglas M Heuman, MD, FACP, FACG, AGAF; Chief Editor: Julian Katz, MD more...

Updated: Jan 20, 2015

HistoryGallstone disease may be thought of as having the following 4 stages:

1. The lithogenic state, in which conditions favor gallstone formation2. Asymptomatic gallstones3. Symptomatic gallstones, characterized by episodes of biliary colic4. Complicated cholelithiasis

Symptoms and complications of gallstone disease result from effects occurringwithin the gallbladder or from stones that escape the gallbladder to lodge in thecommon bile duct.

Asymptomatic gallstones

Gallstones may be present in the gallbladder for decades without causing symptomsor complications. In patients with asymptomatic gallstones discovered incidentally,the likelihood of developing symptoms or complications is 12% per year. In mostcases, asymptomatic gallstones do not require any treatment.

Because they are common, gallstones often coexist with other gastrointestinalconditions. There is little evidence to support a causal association betweengallstones and chronic abdominal pain, heartburn, postprandial distress, bloating,flatulence, constipation, or diarrhea.

Dyspepsia that occurs reproducibly following ingestion of fatty foods is often wronglyattributed to gallstones, when irritable bowel syndrome or gastroesophageal reflux isthe true culprit. Gallstones discovered during an evaluation for nonspecificsymptoms are usually innocent bystanders, and treatment directed at the gallstonesis unlikely to relieve these symptoms.

Biliary colic

Pain termed biliary colic occurs when gallstones or sludge fortuitously impact in thecystic duct during a gallbladder contraction, increasing gallbladder wall tension. Inmost cases, the pain resolves over 30 to 90 minutes as the gallbladder relaxes andthe obstruction is relieved.

Episodes of biliary colic are sporadic and unpredictable. The patient localizes thepain to the epigastrium or right upper quadrant and may describe radiation to theright scapular tip (Collins sign[8] ). The pain begins postprandially (usually within anhour after a fatty meal), is often described as intense and dull, and may last from 15 hours. From onset, the pain increases steadily over about 10 to 20 minutes andthen gradually wanes when the gallbladder stops contracting and the stone fallsback into the gallbladder. The pain is constant in nature and is not relieved byemesis, antacids, defecation, flatus, or positional changes. It may be accompaniedby diaphoresis, nausea, and vomiting.

Other symptoms, often associated with cholelithiasis, include indigestion,dyspepsia, belching, bloating, and fat intolerance. However, these are verynonspecific and occur in similar frequencies in individuals with and withoutgallstones; cholecystectomy has not been shown to improve these symptoms.

Most patients develop symptoms prior to complications. Once symptoms of biliarycolic occur, severe symptoms develop in 39% of patients, with complications in 13% per year and a cholecystectomy rate of 38% per year. Therefore, in people withmild symptoms, 50% have complications after 20 years.

Zollinger performed studies in the 1930s in which the gallbladder wall or commonbile duct was distended with a balloon; pain was elicited in the epigastric region.Only if the distended gallbladder touched the peritoneum did the patient experienceright upper quadrant pain. Associated symptoms of nausea, vomiting, or referredpain were present in distention of the common bile duct (CBD) but not of thegallbladder.

Physical ExaminationPatients with the lithogenic state or asymptomatic gallstones have no abnormalfindings on physical examination.

Distinguishing uncomplicated biliary colic from acute cholecystitis or othercomplications is important. Both often present with the same constellation ofsymptoms, and physical examination may help to differentiate the two.

Since the gallbladder is not inflamed in uncomplicated biliary colic, the pain ispoorly localized and visceral in origin; the patient has an essentially benignabdominal examination without rebound or guarding. Fever is absent.

In acute cholecystitis, inflammation of the gallbladder with resultant peritonealirritation leads to welllocalized pain in the right upper quadrant, usually withrebound and guarding. Although nonspecific, a positive Murphy sign (inspiratoryarrest on deep palpation of the right upper quadrant during deep inspiration) ishighly suggestive of cholecystitis. Fever is often present, but it may lag behind other

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signs or symptoms.

Although voluntary guarding may be present, no peritoneal signs are present.Tachycardia and diaphoresis may be present as a consequence of pain. Theseshould resolve with appropriate pain management.

The presence of fever, persistent tachycardia, hypotension, or jaundice necessitatea search for complications of cholelithiasis, including cholecystitis, cholangitis,pancreatitis, or other systemic causes.

In severe cases of acute cholecystitis, ascending cholangitis, or acute pancreatitis,bowel sounds are often absent or hypoactive.

Choledocholithiasis with obstruction of the common bile duct produces cutaneousand scleral icterus that evolves over hours to days as bilirubin accumulates.

The Charcot triad of severe right upper quadrant tenderness with jaundice and feveris characteristic of ascending cholangitis.

Acute gallstone pancreatitis is often characterized by epigastric tenderness. Insevere cases, retroperitoneal hemorrhage may produce ecchymoses of the flanksand periumbilical ecchymoses (Cullen sign and GreyTurner sign).

Complications of gallbladder stones

Acute cholecystitis occurs when persistent stone impaction in the cystic duct causesthe gallbladder to become distended and progressively inflamed. Patientsexperience the pain of biliary colic, but, instead of resolving spontaneously, the painpersists and worsens.

Overgrowth of colonizing bacteria in the gallbladder often occurs, and, in severecases, accumulation of pus in the gallbladder, termed gallbladder empyema, occurs.The gallbladder wall may become necrotic, resulting in perforation andpericholecystic abscess. Acute cholecystitis is considered a surgical emergency,although pain and inflammation may subside with conservative measures, such ashydration and antibiotics.

Chronically, gallstones may cause progressive fibrosis of the gallbladder wall andloss of gallbladder function, termed chronic cholecystitis. The pathogenesis of thiscomplication is not completely understood. Repeated attacks of acute cholecystitismay play a role, as may localized ischemia produced by pressure of stones againstthe gallbladder wall. The chronically fibrotic gallbladder may become shrunken andadherent to adjacent viscera.

Gallbladder adenocarcinoma is an uncommon cancer that usually develops in thesetting of gallstones and chronic cholecystitis. Gallbladder cancers commonly invadethe adjacent liver and common bile duct, producing jaundice. The prognosis is poorunless the cancer is localized to the gallbladder, in which case cholecystectomy maybe curative.

Occasionally, a large stone may erode through the wall of the gallbladder into anadjacent viscus (typically the duodenum), producing a cholecystoenteric fistula. Thestone, if sufficiently large, may obstruct the small intestine, usually at the level ofthe ileum, a phenomenon termed gallstone ileus.

Complications of stones in the common bile duct

Gallstones are initially retained in the gallbladder by the spiral valves of the cysticduct. Following episodes of gallstone impaction in the cystic duct, these valves maybecome obliterated and stones may pass into the common bile duct. Patients whohave passed one stone tend to pass more stones over the subsequent months.

Stones in the common bile duct may be asymptomatic, but, more commonly, theyimpact distally in the ampulla of Vater. This may produce biliary colicindistinguishable from that caused by cystic duct stones. Because impaction ofcommon bile duct stones occludes the flow of bile from the liver to the intestine,pressure rises in the intrahepatic bile ducts, leading to increased liver enzymes andjaundice.

Bacterial overgrowth in stagnant bile above an obstructing common duct stoneproduces purulent inflammation of the liver and biliary tree, termed ascendingcholangitis. Characteristic features include the Charcot triad of fever, jaundice, andright upper quadrant pain. Patients may rapidly develop septic shock unless ductalobstruction is relieved.

A stone impacted in the ampulla of Vater may transiently obstruct the pancreaticduct, leading to in situ activation of pancreatic proteases and triggering an attack ofacute pancreatitis. Pancreatic pain is different from biliary pain. The pain is locatedin the epigastric and midabdominal areas and is sharp, severe, continuous, andradiates to the back. Nausea and vomiting are frequently present, and a similarprevious episode is reported by approximately 15% patients.

Stone impaction in the distal common bile duct is often relieved spontaneouslywithin hours to days by passage of the stone into the intestine.

Other complications

Inflammation from chronic cholelithiasis may result in fusion of the gallbladder tothe extrahepatic biliary tree, causing Mirizzi syndrome. Alternatively, a fistula intothe intestinal tract may form, causing gallstone ileus.[9]

Differential Diagnoses

Contributor Information and DisclosuresAuthorDouglas M Heuman, MD, FACP, FACG, AGAF Chief of Hepatology, Hunter Holmes McGuire Department ofVeterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Gastroenterology,

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Virginia Commonwealth University School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: AmericanAssociation for the Study of Liver Diseases, American College of Physicians, American GastroenterologicalAssociation

Disclosure: Received grant/research funds from Novartis for other; Received grant/research funds from Bayer forother; Received grant/research funds from Otsuka for none; Received grant/research funds from Bristol MyersSquibb for other; Received none from Scynexis for none; Received grant/research funds from Salix for other;Received grant/research funds from MannKind for other.

Coauthor(s)Jeff Allen, MD Assistant Professor, Department of Surgery, University of Louisville

Disclosure: Nothing to disclose.

Anastasios A Mihas, MD, DMSc, FACP, FACG Professor, Department of Medicine, Division ofGastroenterology, Virginia Commonwealth University School of Medicine; Consulting Staff, VirginiaCommonwealth University Hospitals and Clinics; Chief of GI Clinical Research, Director of GI Outpatient Service,Associate Director of Hepatology, Hunter Holmes McGuire Veterans Affairs Medical Center

Anastasios A Mihas, MD, DMSc, FACP, FACG is a member of the following medical societies: AmericanAssociation for the Study of Liver Diseases, American College of Gastroenterology, American College ofPhysicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, SigmaXi, Southern Society for Clinical Investigation, American Federation for Clinical Research, GastroenterologyResearch Group

Disclosure: Nothing to disclose.

Chief EditorJulian Katz, MD Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology,American College of Physicians, American Gastroenterological Association, American Geriatrics Society,American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law,Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, Physicians for SocialResponsibility

Disclosure: Nothing to disclose.

AcknowledgementsFirass Abiad, MD Head of Division, General and Laparoscopic Surgery, Specialized Medical Center Hospital,Saudi Arabia

Disclosure: Nothing to disclose.

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College ofMedicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of LiverDiseases, American College of Gastroenterology, American Gastroenterological Association, and AmericanSociety for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

David Eric Bernstein, MD Director of Hepatology, North Shore University Hospital; Professor of ClinicalMedicine, Albert Einstein College of Medicine

David Eric Bernstein, MD is a member of the following medical societies: American Association for the Study ofLiver Diseases, American College of Gastroenterology, American College of Physicians, AmericanGastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine,Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western ReserveUniversity School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha,American Academy of Emergency Medicine, American College of Chest Physicians, American College ofEmergency Physicians, American College of Physicians, American Heart Association, American ThoracicSociety, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, andSociety for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; ViceChair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of EmergencyPhysicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

William K Chiang, MD Associate Professor, Department of Emergency Medicine, New York University Schoolof Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center

William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology,American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Alfred Cuschieri, MD, ChM, FRSE, FRCS, Head, Professor, Department of Surgery and Molecular Oncology,University of Dundee, UK

Disclosure: Nothing to disclose.

Imad S Dandan, MD Consulting Surgeon, Department of Surgery, Trauma Section, Scripps Memorial Hospital

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Imad S Dandan, MD is a member of the following medical societies: American Association for the Surgery ofTrauma, American College of Surgeons, American Medical Association, American Trauma Society, CaliforniaMedical Association, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

David Greenwald, MD Associate Professor of Clinical Medicine, Fellowship Program Director, Department ofMedicine, Division of Gastroenterology, Montefiore Medical Center, Albert Einstein College of Medicine

David Greenwald, MD is a member of the following medical societies: Alpha Omega Alpha, American College ofGastroenterology, American College of Physicians, American Gastroenterological Association, American Societyfor Gastrointestinal Endoscopy, and New York Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Eugene Hardin, MD, FAAEM, FACEP Former Chair and Associate Professor, Department of EmergencyMedicine, Charles Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine,Martin Luther King Jr/Drew Medical Center

Disclosure: Nothing to disclose.

Faye Maryann Lee, MD Staff Physician, Department of Emergency Medicine, New York University/BellevueHospital Center

Faye Maryann Lee, MD is a member of the following medical societies: Phi Beta Kappa

Disclosure: Nothing to disclose.

Sally Santen, MD Program Director, Assistant Professor, Department of Emergency Medicine, VanderbiltUniversity

Sally Santen, MD is a member of the following medical societies: American College of Emergency Physiciansand Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Assaad M Soweid, MD, FASGE, FACG Associate Professor of Clinical Medicine, Endosonography andAdvanced Therapeutic Endoscopy, Director, EndoscopyBronchoscopy Unit, Division of Gastroenterology,Department of Internal Medicine, American University of Beirut Medical Center, Lebanon

Assaad M Soweid, MD, FASGE, FACG is a member of the following medical societies: American College ofGastroenterology, American College of Physicians, American College of PhysiciansAmerican Society of InternalMedicine, American Gynecological and Obstetrical Society, and American Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center Collegeof Pharmacy; EditorinChief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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