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Gallstones (Cholelithiasis) Clinical Presentation

  • Author: Douglas M Heuman, MD, FACP, FACG, AGAF; Chief Editor: BS Anand, MD  more...
 
Updated: Apr 14, 2016
 

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 1-2% 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[9] ). 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 3-9% of patients, with complications in 1-3% per year and a cholecystectomy rate of 3-8% 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 with distention of the common bile duct (CBD) but not of the gallbladder.

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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 a well-localized 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 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. These should resolve with appropriate pain management.

The presence of fever, persistent tachycardia, hypotension, or jaundice necessitate a 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 cutaneous and scleral icterus that evolves over hours to days as bilirubin accumulates.

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

Acute gallstone pancreatitis is often characterized by epigastric tenderness. In severe cases, retroperitoneal hemorrhage may produce ecchymoses of the flanks and periumbilical region (Cullen sign and Grey-Turner sign).

Complications of gallbladder stones

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

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

Chronically, gallstones may cause progressive fibrosis of the gallbladder wall and loss of gallbladder function, termed chronic cholecystitis. The pathogenesis of this complication is not completely understood. Repeated attacks of acute cholecystitis may play a role, as may localized ischemia produced by pressure of stones against the gallbladder wall. The chronically fibrotic gallbladder may become shrunken and adherent to the adjacent viscera.

Gallbladder adenocarcinoma is an uncommon cancer that usually develops in the setting of gallstones and chronic cholecystitis. Gallbladder cancers commonly invade the adjacent liver and common bile duct, producing jaundice. The prognosis is poor unless the cancer is localized to the gallbladder, in which case cholecystectomy may be curative.

Occasionally, a large stone may erode through the wall of the gallbladder into an adjacent viscus (typically the duodenum), producing a cholecystoenteric fistula. The stone, if sufficiently large, may obstruct the small intestine, usually at the level of the 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 cystic duct. Following episodes of gallstone impaction in the cystic duct, these valves may become obliterated and stones may pass into the common bile duct. Patients who have passed one stone tend to pass more stones over the subsequent months.

Stones in the common bile duct may be asymptomatic, but, more commonly, they impact distally in the ampulla of Vater. This may produce biliary colic indistinguishable from that caused by cystic duct stones. Because impaction of common bile duct stones occludes the flow of bile from the liver to the intestine, pressure rises in the intrahepatic bile ducts, leading to elevation of liver enzymes and jaundice.

Bacterial overgrowth in stagnant bile above an obstructing common duct stone produces purulent inflammation of the liver and biliary tree, termed ascending cholangitis. Characteristic features include the Charcot triad of fever, jaundice, and right upper quadrant pain. Patients may rapidly develop septic shock unless the ductal obstruction is relieved.

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

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

Other complications

Inflammation from chronic cholelithiasis may result in fusion of the gallbladder to the extrahepatic biliary tree, causing Mirizzi syndrome. Alternatively, a fistula into the intestinal tract may form, causing gallstone ileus.[10]

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Contributor Information and Disclosures
Author

Douglas M Heuman, MD, FACP, FACG, AGAF Chief of Hepatology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine

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

Disclosure: Received grant/research funds from Novartis for other; Received grant/research funds from Bayer for other; Received grant/research funds from Otsuka for none; Received grant/research funds from Bristol Myers Squibb 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 of Gastroenterology, Virginia Commonwealth University School of Medicine; Consulting Staff, Virginia Commonwealth 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: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, Sigma Xi, Southern Society for Clinical Investigation, American Federation for Clinical Research, Gastroenterology Research Group

Disclosure: Nothing to disclose.

Chief Editor

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

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

Julian 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 Social Responsibility

Disclosure: Nothing to disclose.

Acknowledgements

Firass 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 of Medicine

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

Disclosure: Nothing to disclose.

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

David Eric Bernstein, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological 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 Reserve University 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 of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

William K Chiang, MD Associate Professor, Department of Emergency Medicine, New York University School of 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

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

Disclosure: Nothing to disclose.

David Greenwald, MD Associate Professor of Clinical Medicine, Fellowship Program Director, Department of Medicine, 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 of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for 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 Emergency Medicine, 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/Bellevue Hospital 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, Vanderbilt University

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

Disclosure: Nothing to disclose.

Assaad M Soweid, MD, FASGE, FACG Associate Professor of Clinical Medicine, Endosonography and Advanced Therapeutic Endoscopy, Director, Endoscopy-Bronchoscopy 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 of Gastroenterology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, 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 College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Excised gall bladder opened to show 3 gallstones. Image from Science Source (http://www.sciencesource.com/).
Magnetic resonance cholangiopancreatography (MRCP) showing 5 gallstones in the common bile duct (arrows). In this image, bile in the duct appears white; stones appear as dark-filling defects. Similar images can be obtained by taking plain radiographs after injection of radiocontrast material in the common bile duct, either endoscopically (endoscopic retrograde cholangiography) or percutaneously under fluoroscopic guidance (percutaneous transhepatic cholangiography), but these approaches are more invasive.
Intraoperative cholangiogram demonstrating a distal common bile duct stone with dilatation.
Intraoperative cholangiogram demonstrating a distal common bile duct stone without dilatation.
Cholecystitis with small stones in the gallbladder neck. Classic acoustic shadowing is seen beneath the gallstones. The gallbladder wall is greater than 4 mm. Image courtesy of DT Schwartz.
The WES (wall echogenic shadow) sign, long axis of the gallbladder. The arrow head points to the gallbladder wall. The second hyperechoic line represents the edge of the congregated gallstones. Acoustic shadowing (AS) is readily seen. The common bile duct can be seen just above the portal vein (PV). Image courtesy of Stephen Menlove.
Wall echogenic shadow (WES sign), short axis view of the gallbladder. Image courtesy of Stephen Menlove.
Sludge in the gallbladder. Note the lack of shadowing. Image courtesy of DT Schwartz.
Common bile duct stone (choledocholithiasis). The sensitivity of transabdominal ultrasonography for choledocholithiasis is approximately 75% in the presence of dilated ducts and 50% for nondilated ducts. Image courtesy of DT Schwartz.
 
 
 
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