eMedicine Specialties > Gastroenterology > Biliary

Biliary Disease: Follow-up

Author: Annie T Chemmanur, MD, Attending Physician, Metrowest Medical Center and University of Massachusetts Memorial Hospital, Marlborough Campus
Coauthor(s): Jeanette G Smith, MD, Fellow, Department of Gastroenterology-Hepatology, University of Connecticut School of Medicine; George Y Wu, MD, PhD, Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine
Contributor Information and Disclosures

Updated: Aug 29, 2009

Follow-up

Complications

  • The complications common to all of the chronic cholestatic liver diseases, such as PSC and PBC, include fatigue, pruritus, steatorrhea, fat-soluble vitamin deficiencies (A, D, E, and K), metabolic bone disease, hypercholesterolemia xanthomas, hypothyroidism, and anemia. There is a reported association of PBC with Sjögren syndrome, Raynaud phenomenon, and sicca symptoms.
  • Approximately 20% of patients with PSC develop a dominant stricture in the intrahepatic or extrahepatic biliary tree. Medical therapy to treat biliary strictures has been ineffective. Nonsurgical modalities to relieve biliary obstruction, such as endoscopically- or radiologically–guided balloon dilation of strictures or placement of prosthetic stents across strictures, should be attempted initially.
  • Choledocholithiasis and cholelithiasis due to cholesterol and/or pigment stones may be present in up to one third of patients with PSC. Bacterial cholangitis can occur in patients with PSC.
  • Cholangiocarcinoma eventually develops in about 20% of patients with PSC, principally late in the course of long-standing ulcerative colitis and the cirrhotic stage of biliary disease. This complication is difficult to detect, as evidenced by the finding of cholangiocarcinoma in 10% of patients undergoing liver transplantation for PSC.12
  • The incidence of hepatocellular carcinoma is increased in patients with PBC who have had stage IV disease for many years.13
  • Patients with both PSC and ulcerative colitis have an increased risk of colon cancer and progression of neoplastic transformation.

Prognosis

  • In PSC, several factors suggest a high risk of death. These include advancing age, serum bilirubin, blood hemoglobin, presence or absence of inflammatory bowel disease, and histologic stage on liver biopsy.

Patient Education

Miscellaneous

Medicolegal Pitfalls

  • Choose the procedure that is appropriate for the patient. Know the limitations of the procedure. The presence of dense adhesions, advanced liver disease, unexpected cancer, or a severely inflamed gallbladder or encountering troublesome bleeding should prompt assessment of the need to convert to an open procedure.

Special Concerns

  • Postcholecystectomy syndrome: The persistence, recurrence, or development of pain following removal of the gallbladder is referred to as the postcholecystectomy syndrome. It occurs in 10-15% of the 600,000 cholecystectomies performed annually in the United States.
    • A retained common duct stone can be identified in 0.3-18% of cases. A history of recurrent biliary-type pain associated with nausea, vomiting, fever, and chills is suggestive of a retained common duct stone, and sonographic evidence of ductal dilation is supportive of this diagnosis. An intraoperative cholangiogram is better to do during surgery to exclude a retained common duct stone.
    • Biliary leaks or fistula occur following 0.1-0.4% of all gallbladder operations. Leakage from the cystic duct stump is most common, but it may (1) emanate from accessory ducts along the gallbladder fossa, (2) be the result from injury to a major extrahepatic duct, or (3) follow T-tube removal after open cholecystectomy and common bile duct exploration. In the past, these were associated with a mortality rate of about 30%.
    • Benign biliary strictures occur with a frequency of 0.1-0.8% of all gallbladder operations. This usually is the result of an operative injury to the bile duct. The first type results from a surgical misadventure such as inadvertent duct ligation or placing clips on the bile duct. Only 10% of patients present with pain and jaundice in the first week, and another 60% present within 3 months of the surgery. The second type results either from ischemic injury or from crush injury from clamps. Many months or years may pass before mild cholestasis or symptoms develop when biliary sludge or stones form proximal to a stricture.
    • Cystic duct remnants are a rare and controversial cause of postcholecystectomy pain. The long cystic duct stump promotes bile stasis within which microlithiasis or stones may form. The passage of this material through the papilla is believed to cause intermittent biliary-type pain. In extremely rare instances, a neuroma or granuloma of the cystic duct stump can cause pain.
  • Sphincter of Oddi dysfunction is an uncommon, probably overdiagnosed, cause of biliary-type pain. The 2 subtypes are papillary stenosis and sphincter of Oddi dyskinesia (SOD). The former is a mechanical problem, and the latter is a functional problem.
    • Papillary stenosis: This is a mechanical problem involving an inflammatory stenosis of the duodenal papilla of Vater. It may be caused by choledocholithiasis, ascariasis, sclerosing cholangitis, pancreatitis, iatrogenic instrumentation of the duodenal papilla, peptic duodenitis, and Crohn disease involving the duodenum and cholesterolosis of the papilla. It is diagnosed manometrically when the sphincter of Oddi manometry reveals a basal sphincter pressure greater than 40 mm Hg that does not decrease in response to CCK or amyl nitrate. It also may be diagnosed surgically via the inability to pass a #3 Bakes dilator through the sphincter or during ERCP via an inability to advance a 5F cannula retrograde over a wire placed into the bile duct.
    • The term sphincter of Oddi dysfunction (SOD) has been used to describe a clinical syndrome of biliary or pancreatic obstruction related to mechanical or functional abnormalities of the sphincter of Oddi.
    • SOD is diagnosed by a sphincter manometry revealing a basal pressure greater than 40 mm Hg that is responsive to CCK or amyl nitrate. Other supportive features may include phasic wave contractions with a peak amplitude greater than 220 mm Hg, contraction duration greater than 8 seconds, and frequency of greater than 10 per minute. An increased percentage of retrograde contractions have also been cited. Abnormal sphincter motility is uncommon, identified in 1% of 454 patients following cholecystectomy; 14% of those were diagnosed with a postcholecystectomy syndrome.
  • HIV-associated cholangiopathy: Several biliary tract abnormalities are associated with HIV infection, but the CD4+ lymphocytes usually fall below 100 cells per microliter before these problems develop. These include acalculous cholecystitis, papillary stenosis, and a sclerosing cholangitis–like picture.
    • The causes include opportunistic infections, such as infection with cytomegalovirus, Cryptosporidium species, Enterocytozoon bieneusi, and Mycobacterium species, or neoplasms, such as Kaposi sarcoma and non-Hodgkin lymphoma. Liver-associated enzymes usually show a cholestatic picture, without significant hyperbilirubinemia, unless a neoplasm obstructs the bile duct. Medical therapy to date has been ineffective in treating opportunistic infections.
    • UDCA has been used in the treatment of primary sclerosing cholangitis, a disorder with similar intrahepatic changes to AIDS cholangiopathy. This observation has led to its experimental use in patients with AIDS cholangiopathy; results in a small number of patients have found an improvement in symptoms and a fall in levels of serum alkaline phosphatase and gamma-glutamyl transpeptidase. The authors recommend giving UDCA in a dose 300 mg 3 times daily, primarily in patients who have intrahepatic ductal disease and markedly elevated liver function test results.
  • Endoscopic sphincterotomy alleviates biliary-type pain in most, but not all, patients with papillary stenosis.
  • Vanishing bile duct syndrome
    • This is a rare syndrome affecting the intrahepatic bile ducts. Most patients are asymptomatic, but some may present with pruritus and, rarely, jaundice. The alkaline phosphatase level usually is elevated, along with GGT, which may exceed 600 IU/L. Obtaining a wedge liver biopsy often is necessary to make the diagnosis. The cause of ductopenia may be related to developmental abnormalities of the intrahepatic biliary system, as in Alagille syndrome. On physical examination, frontal bossing and triangular facies may be noted, and tests that are more specific can reveal butterfly vertebrae and posterior embryotoxon of the eye. Progressive familial intrahepatic cholestasis is another type, caused by a genetic mutation of the membrane transporter for phospholipids (MDR3).
    • Other types are acquired and are associated with cystic fibrosis, systemic mastocytosis, histiocytosis-X, Hodgkin disease, and drug-induced hepatotoxicity. Patients without a clear association are diagnosed with idiopathic adult ductopenia.
 
Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Paul Yakshe, MD, to the development and writing of this article.



More on Biliary Disease

Overview: Biliary Disease
Differential Diagnoses & Workup: Biliary Disease
Treatment & Medication: Biliary Disease
Follow-up: Biliary Disease
Multimedia: Biliary Disease
References
Further Reading
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Further Reading

Related eMedicine Topics

Clinical Trials
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Keywords

biliary disease, abnormal bile composition, abnormal biliary anatomy, abnormal biliary function, gallstones, gall stones, gallbladder disease, cirrhosis, primary biliary cirrhosis, PBC, liver disease, primary sclerosing cholangitis, PSC, acute cholecystitis, cholecystectomy, cholestasis, steatorrhea, cholelithiasis, papillary stenosis, pancreatitis, cholangiocarcinoma, postcholecystectomy syndrome, sphincter of Oddi dyskinesia, vanishing bile duct syndrome

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Contributor Information and Disclosures

Author

Annie T Chemmanur, MD, Attending Physician, Metrowest Medical Center and University of Massachusetts Memorial Hospital, Marlborough Campus
Annie T Chemmanur, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Medical Association, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

Jeanette G Smith, MD, Fellow, Department of Gastroenterology-Hepatology, University of Connecticut School of Medicine
Jeanette G Smith, MD is a member of the following medical societies: American College of Physicians, American Gastroenterological Association, and American Public Health Association
Disclosure: Nothing to disclose.

George Y Wu, MD, PhD, Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine
George Y Wu, MD, PhD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, American Medical Association, American Society for Clinical Investigation, and Association of American Physicians
Disclosure: Humana Press Consulting fee Consulting; Novartis Consulting fee Review panel membership

Medical Editor

Ronnie Fass, MD, Director of GI Motility Laboratory, Tucson VA Medical Center, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, University of Arizona School of Medicine
Ronnie Fass, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Motility Society, American Society for Gastrointestinal Endoscopy, and Israel Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

James L Achord, MD, Professor Emeritus, Department of Medicine, Division of Digestive Diseases, University of Mississippi School of Medicine
James L Achord, 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, American Medical Association, American Society for Gastrointestinal Endoscopy, Mississippi State Medical Association, New York Academy of Sciences, Sigma Xi, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
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 and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
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