Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Biliary Disease Workup

  • Author: Annie T Chemmanur, MD; Chief Editor: BS Anand, MD  more...
 
Updated: Jun 03, 2016
 

Laboratory Studies

Alkaline phosphatase

Alkaline phosphatase is a marker of cholestasis (ie, elevation of alkaline phosphatase occurs in more than 90% of patients with cholestasis) and suggests a reduction in bile flow. It also is elevated in infiltrative disorders or fungal infections of the liver, often quite strikingly, with levels above 1000 U/L.

Because isozymes are found in the liver, bone, placenta, leukocytes, and small intestine, an elevated alkaline phosphatase is not specific for the biliary tract. Although the source can be determined by measuring isozyme subtypes, these electrophoretic tests seldom are available clinically. A biliary source is inferred when the alkaline phosphatase is associated with an elevated gamma-glutamyl transpeptidase (GGT), 5'-nucleotidase, or leucine aminopeptidase.

An elevation of the hepatic alkaline phosphatase level involves an enzyme-induced secretory process, ie, it represents enzyme induction and accelerated de novo synthesis of alkaline phosphatase and backup into the circulation, not just a simple mechanical obstruction to flow. For this reason, an elevation of alkaline phosphatase may be delayed in the setting of acute obstruction.

Bilirubin

Bilirubin is a breakdown product of heme, with 80% coming from senescent red blood cells and 20% coming from cytochromes and myoglobin. Unconjugated bilirubin is hydrophobic and transported in the blood reversibly bound to albumen. It is taken up by the hepatocyte, converted to conjugated bilirubin by glucuronyl transferase, and actively secreted into the biliary canaliculi.

Aminotransferases

In addition to the liver, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are found in cardiac and skeletal muscle and renal and cerebral nerve cells. The ALT is found predominantly in the cytosol of the hepatocyte, and an elevated ALT is more likely to suggest liver injury. The AST has both cytosolic and mitochondrial forms. Elevated aminotransferase levels are observed with hepatocellular injury (eg, viral hepatitis), usually sustained over weeks. A rapid rise and fall may be observed in acute posthepatic biliary obstruction or transient hepatic ischemia.

Antimitochondrial antibodies

More than 95% of cases of primary biliary cholangitis are associated with positive test results for antimitochondrial antibodies (AMA). The antigen that reacts with AMA is part of the 2-oxo-acid dehydrogenase multienzyme complex in the mitochondria, especially the E2 subunit of pyruvate dehydrogenase, located on the inner mitochondrial membrane.

Miscellaneous immunologic markers

An emerging role for immune markers in inflammatory bowel disease may have implications in the diagnostic evaluation of cholestatic liver disease. Just as AMA is an immunologic marker of PBC, 2 markers are used in the evaluation of patients with suspected inflammatory bowel disease and PSC. These are antineutrophil cytoplasmic antibody (ANCA) and anti-Saccharomyces cerevisiae antibody (ASCA). ANCA is strongly associated with ulcerative colitis (79%) and PSC (82%). Although ASCA is associated with Crohn disease, currently, no association with PSC exists.

Next

Imaging Studies

Ultrasonography

Ultrasonography uses technology similar to sonar. A 2-dimensional image of echoes is created. Fluid appears black, solid organs appear hypoechoic, and structures with high amounts of fat or minimal water are hyperechoic.

Right upper quadrant ultrasound

This is the principal study used to evaluate biliary-type pain and detect gallbladder disease and biliary dilatation. Gallstones appear as a highly echogenic focus with acoustic shadows and move to a dependent portion of the gallbladder. Right upper quadrant ultrasound can detect stones as small as 1-2 mm and has a sensitivity of 95% and a specificity of 97%. The presence of a thickened gallbladder wall, pericholecystic fluid, and a sonographic Murphy sign supports the diagnosis of cholecystitis. Because of interference by bowel gas, ultrasound does not reveal the common bile duct well, and ultrasound may miss 25-40% of bile duct stones.

Endoscopic ultrasonography (EUS)

By placing a higher-frequency transducer into the gut adjacent to the hepatobiliary tract, endoscopic ultrasound provides more detailed images than a transcutaneous approach. Although no major advantage to examining the gallbladder exists, EUS can be used to detect intraductal stones with a sensitivity of 88-97% and specificity of 97%. It also can be used to assess adjacent structures, such as porta hepatis nodes; malignancy is suggested by the presence of large (>1 cm), round, sharply demarcated hypoechoic nodes. By better defining the local anatomy of ampullary tumors in relation to neighboring structures, information obtained with EUS can help guide the physician's selection of appropriate intervention.

Computed abdominal tomography (CAT) scanning

This imaging study usually is not very helpful in evaluating the biliary system. It may demonstrate dilated bile ducts and reveal the cause of a biliary obstruction. Recent technologic advances, such as thin-section helical CT scan, have increased the sensitivity for detection of bile duct stones from 60% to 90%.

Cholangiography

Both endoscopic retrograde cholangiopancreatography (ERCP) and magnetic resonance cholangiopancreatography (MRCP) provide images of the biliary ductal system, which has an appearance similar to a deciduous tree in the wintertime. ERCP is an invasive endoscopic procedure in which radiopaque contrast is injected into the biliary ductal system under fluoroscopic guidance. MRCP is a noninvasive procedure that relies on heavily T2-weighted images to create an image of the fluid within the biliary and pancreatic ductal system.

Choledocholithiasis

On a cholangiogram, stones within the bile ducts appear as filling defects within the trunk or branches of the biliary tree. Depending on the type of stone and duration of the illness, they may be single or multiple, round or faceted, free-floating or adherent.

Primary sclerosing cholangitis

In PSC, the bile ducts are characterized by strictures and ectatic areas in an irregular, diffuse pattern. In some cases, the duct may resemble a string of beads due to alternating annular bandlike strictures separating areas of cholangiectasia. Diverticular outpouchings occur in 10% of cases and are observed exclusively in PSC, not cholangiocarcinoma. Specific radiologic patterns (ie, diffuse involvement versus intrahepatic versus extrahepatic) are not associated with differences in median survival.

Hepatobiliary scintigraphy

This test should be ordered when acute cholecystitis is suspected. Nonvisualization of the gallbladder supports the diagnosis of acute calculous cholecystitis with a sensitivity of 92-98% and a specificity of 95-98%. It also is used to confirm the presence of a biliary leak.

Although controversial, hepatobiliary scintigraphy occasionally is helpful in diagnosing chronic cholecystitis or gallbladder dyskinesia in patients with biliary-type pain and normal findings on right upper quadrant ultrasound. The test employs a 45-minute infusion of cholecystokinin (CCK) octapeptide to measure the gallbladder ejection fraction; values lower than 35% are considered abnormal. In some patients, an abnormal gallbladder ejection fraction may be associated with sphincter of Oddi dysfunction.

Previous
Next

Staging

Hepatobiliary histology has emerged as an objective reference for staging PBC and PSC. In both, 4 stages are identified.

Primary sclerosing cholangitis

In PSC, stage 1 is characterized by portal tracts that are enlarged by edema, increased connective tissue, and proliferation of interlobular bile ducts. Periductal inflammation and fibrosis characterize stage 2. Connective tissue begins to encroach into the periportal parenchyma, and a fibrous-obliterative cholangitis is present. Stage 3 is defined by a discernible loss of interlobular bile ducts, and stage 4 is reached when cirrhosis is present.

Primary biliary cholangitis

In PBC, stage 1 is characterized by dramatic evidence of asymmetric destruction of septal and interlobular bile ducts by a mononuclear infiltrate (the typical appearance is referred to as a florid duct lesion). Occasionally, hepatic granulomas are observed. Diffuse periportal inflammation characterizes stage 2 and is accompanied by portal fibrosis, periportal liver cell necrosis, patchy ductopenia, and ductular proliferation. Stage 3 is defined by the presence of bridging fibrosis, and stage 4 is reached when cirrhosis is present.

Previous
 
 
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, Massachusetts Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

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, Association of American Physicians

Disclosure: Received consulting fee from Springer for consulting; Received consulting fee from Gilead for review panel membership; Received honoraria from Vertex for speaking and teaching; Received honoraria from Bristol-Myers Squibb for speaking and teaching; Received royalty from Springer for review panel membership; Received honoraria from Merck for speaking and teaching.

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, American Public Health Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

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

Ronnie Fass, MD, FACP, FACG Chief of Gastroenterology, Head of Neuroenteric Clinical Research Group, Southern Arizona Veterans Affairs Health Care System; Professor of Medicine, Division of Gastroenterology, University of Arizona School of Medicine

Ronnie Fass, MD, FACP, FACG 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 Neurogastroenterology and Motility Society, American Society for Gastrointestinal Endoscopy, Israeli Medical Association

Disclosure: Received grant/research funds from Takeda Pharmaceuticals for conducting research; Received consulting fee from Takeda Pharmaceuticals for consulting; Received honoraria from Takeda Pharmaceuticals for speaking and teaching; Received consulting fee from Vecta for consulting; Received consulting fee from XenoPort for consulting; Received honoraria from Eisai for speaking and teaching; Received grant/research funds from Wyeth Pharmaceuticals for conducting research; Received grant/research funds f.

Acknowledgements

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

References
  1. Yun EJ, Choi CS, Yoon DY, et al. Combination of magnetic resonance cholangiopancreatography and computed tomography for preoperative diagnosis of the Mirizzi syndrome. J Comput Assist Tomogr. 2009 Jul-Aug. 33(4):636-40. [Medline].

  2. Reynolds BM, Dargan EL. Acute obstructive cholangitis; a distinct clinical syndrome. Ann Surg. 1959 Aug. 150 (2):299-303. [Medline]. [Full Text].

  3. American Liver Foundation. Primary biliary cholangitis (PBC, primary biliary cirrhosis). Available at http://www.liverfoundation.org/abouttheliver/info/pbc/. Updated March 29, 2016; Accessed: June 3, 2016.

  4. Solis Herruzo JA, Solis Munoz P, Munoz Yague T. The pathogenesis of primary biliary cirrhosis. Rev Esp Enferm Dig. 2009 Jun. 101(6):413-423. [Medline].

  5. Uibo R, Kisand K, Yang CY, Gershwin ME. Primary biliary cirrhosis: a multi-faced interactive disease involving genetics, environment and the immune response. APMIS. 2012 Nov. 120(11):857-71. [Medline].

  6. Berg CP, Kannan TR, Klein R, et al. Mycoplasma antigens as a possible trigger for the induction of antimitochondrial antibodies in primary biliary cirrhosis. Liver Int. 2009 Jul. 29(6):797-809. [Medline].

  7. Cavallaro A, Cavallaro V, Di Vita M, Cappellani A. Main bile duct carcinoma management. Our experience on 38 cases. Ann Ital Chir. 2009 Mar-Apr. 80(2):107-11. [Medline].

  8. Allison RR, Zervos E, Sibata CH. Cholangiocarcinoma: an emerging indication for photodynamic therapy. Photodiagnosis Photodyn Ther. 2009 Jun. 6(2):84-92. [Medline].

  9. Belli G, Limongelli P, Fantini C, et al. Laparoscopic and open treatment of hepatocellular carcinoma in patients with cirrhosis. Br J Surg. 2009 Sep. 96(9):1041-8. [Medline].

  10. Drebber U, Mueller JJ, Klein E, et al. Liver biopsy in primary biliary cirrhosis: clinicopathological data and stage. Pathol Int. 2009 Aug. 59(8):546-54. [Medline].

  11. US Food and Drug Administration. FDA approves Ocaliva for rare, chronic liver disease [press release]. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm503964.htm. May 31, 2016; Accessed: June 1, 2016.

  12. Edwards JE, LaCerte C, Pheng LH, et al. Sa1576 Exposure-response relationship of obeticholic acid for alkaline phosphatase and total bilirubin in patients with primary biliary cirrhosis (PBC). Poster presented at Digestive Disease Week; San Diego, California; May 21, 2016.

  13. Kageoka M, Watanabe F, Maruyama Y, et al. Long-term prognosis of patients after endoscopic sphincterotomy for choledocholithiasis. Dig Endosc. 2009 Jul. 21(3):170-5. [Medline].

  14. Ohashi A, Tamada K, Wada S, et al. Risk factors for recurrent bile duct stones after endoscopic papillary balloon dilation: long-term follow-up study. Dig Endosc. 2009 Apr. 21(2):73-7. [Medline].

  15. Gurusamy K, Sahay SJ, Burroughs AK, Davidson BR. Systematic review and meta-analysis of intraoperative versus preoperative endoscopic sphincterotomy in patients with gallbladder and suspected common bile duct stones. Br J Surg. 2011 Jul. 98(7):908-16. [Medline].

  16. Castaing D, Vibert E, Bhangui P, et al. Results of percutaneous manoeuvres in biliary disease: The Paul Brousse experience. Surg Endosc. 2011 Jun. 25(6):1858-65. [Medline].

  17. Catena F, Ansaloni L, Di Saverio S, et al. Prospective analysis of 101 consecutive cases of laparoscopic cholecystectomy for acute cholecystitis operated with harmonic scalpel. Surg Laparosc Endosc Percutan Tech. 2009 Aug. 19(4):312-6. [Medline].

  18. Murphy MM, Shah SA, Simons JP, et al. Predicting major complications after laparoscopic cholecystectomy: a simple risk score. J Gastrointest Surg. 2009 Aug 12. epub ahead of print. [Medline].

  19. Sultan AM, El Nakeeb A, Elshehawy T, Elhemmaly M, Elhanafy E, Atef E. Risk Factors for Conversion during Laparoscopic Cholecystectomy: Retrospective Analysis of Ten Years' Experience at a Single Tertiary Referral Centre. Dig Surg. 2013 Apr 26. 30(1):51-55. [Medline].

  20. Moody FG, Vecchio R, Calabuig R. Transduodenal sphincteroplasty with transampullary septectomy for stenosing papillitis. Am J Surg. 1991 Feb. 161(2):213-8. [Medline].

  21. Acosta JM, Civantos F, Nardi GL. Fibrosis of the papilla of Vater. Surg Gynecol Obstet. 1967 Apr. 124(4):787-94. [Medline].

  22. Afdhal NH, Smith BF. Cholesterol crystal nucleation: a decade-long search for the missing link in gallstone pathogenesis. Hepatology. 1990 Apr. 11(4):699-702. [Medline].

  23. Bennion LJ, Grundy SM. Risk factors for the development of cholelithiasis in man (second of two parts). N Engl J Med. 1978 Nov 30. 299(22):1221-7. [Medline].

  24. Boey JH, Way LW. Acute cholangitis. Ann Surg. 1980 Mar. 191(3):264-70. [Medline].

  25. Bohacek L, Pace DE. Advanced laparoscopic training and outcomes in laparoscopic cholecystectomy. Can J Surg. 2009 Aug. 52(4):291-294. [Medline]. [Full Text].

  26. Bolondi L, Gaiani S, Testa S. Gall bladder sludge formation during prolonged fasting after gastrointestinal tract surgery. Gut. 1985 Jul. 26(7):734-8. [Medline].

  27. Broome U, Olsson R, Loof L, et al. Natural history and prognostic factors in 305 Swedish patients with primary sclerosing cholangitis. Gut. 1996 Apr. 38 (4):610-5. [Medline].

  28. Burnstein MJ, Ilson RG, Petrunka CN. Evidence for a potent nucleating factor in the gallbladder bile of patients with cholesterol gallstones. Gastroenterology. 1983 Oct. 85(4):801-7. [Medline].

  29. Carey MC, Small DM. The physical chemistry of cholesterol solubility in bile. Relationship to gallstone formation and dissolution in man. J Clin Invest. 1978 Apr. 61(4):998-1026. [Medline].

  30. Castiella A, Iribarren JA, Lopez P. Ursodeoxycholic acid in the treatment of AIDS-associated cholangiopathy. Am J Med. 1997 Aug. 103(2):170-1.

  31. Csendes A, Burdiles P, Maluenda F. Simultaneous bacteriologic assessment of bile from gallbladder and common bile duct in control subjects and patients with gallstones and common duct stones. Arch Surg. 1996 Apr. 131(4):389-94.

  32. Denman ST. A review of pruritus. J Am Acad Dermatol. 1986 Mar. 14(3):375-92. [Medline].

  33. Everhart JE, Khare M, Hill M. Prevalence and ethnic differences in gallbladder disease in the United States. Gastroenterology. 1999 Sep. 117(3):632-9.

  34. Gallinger S, Taylor RD, Harvey PR. Effect of mucous glycoprotein on nucleation time of human bile. Gastroenterology. 1985 Sep. 89(3):648-58. [Medline].

  35. Gerecht WB, Henry NK, Hoffman WW, et al. Prospective randomized comparison of mezlocillin therapy alone with combined ampicillin and gentamicin therapy for patients with cholangitis. Arch Intern Med. 1989 Jun. 149 (6):1279-84. [Medline].

  36. Graziadei IW, Wiesner RH, Batts KP. Recurrence of primary sclerosing cholangitis following liver transplantation. Hepatology. 1999 Apr. 29(4):1050-6. [Medline].

  37. Harnois DM, Angulo P, Jorgensen RA, Larusso NF, Lindor KD. High-dose ursodeoxycholic acid as a therapy for patients with primary sclerosing cholangitis. Am J Gastroenterol. 2001 May. 96 (5):1558-62. [Medline].

  38. Harnois DM, Lindor KD. Primary sclerosing cholangitis: evolving concepts in diagnosis and treatment. Dig Dis. 1997 Jan-Apr. 15 (1-2):23-41. [Medline].

  39. Heathcote EJ. Management of primary biliary cirrhosis. The American Association for the Study of Liver Diseases practice guidelines. Hepatology. 2000 Apr. 31 (4):1005-13. [Medline].

  40. Hendrickse MT, Rigney E, Giaffer MH, et al. Low-dose methotrexate is ineffective in primary biliary cirrhosis: long-term results of a placebo-controlled trial. Gastroenterology. 1999 Aug. 117 (2):400-7. [Medline].

  41. Holzbach RT. Recent progress in understanding cholesterol crystal nucleation as a precursor to human gallstone formation. Hepatology. 1986 Nov-Dec. 6(6):1403-6. [Medline].

  42. Izumi Y, Teramoto K, Ohshima M. Endoscopic resection of duodenal ampulla with a transparent plastic cap. Surgery. 1998 Jan. 123(1):109-10. [Medline].

  43. Jones DE, Gray JC, Newton J. Perceived fatigue is comparable between different disease groups. QJM. 2009 Sep. 102(9):617-24. [Medline].

  44. Kaplan MM. Primary biliary cirrhosis. N Engl J Med. 1996 Nov 21. 335 (21):1570-80. [Medline].

  45. Krishnamurthy GT, Turner FE. Pharmacokinetics and clinical application of technetium 99m-labeled hepatobiliary agents. Semin Nucl Med. 1990 Apr. 20(2):130-49. [Medline].

  46. Lam SK, Wong KP, Chan PK. Recurrent pyogenic cholangitis: a study by endoscopic retrograde cholangiography. Gastroenterology. 1978 Jun. 74(6):1196-1203. [Medline].

  47. Levy PF, Smith BF, LaMont JT. Human gallbladder mucin accelerates nucleation of cholesterol in artificial bile. Gastroenterology. 1984 Aug. 87(2):270-5. [Medline].

  48. Liermann Garcia RF, Evangelista Garcia C, McMaster P. Transplantation for primary biliary cirrhosis: retrospective analysis of 400 patients in a single center. Hepatology. 2001 Jan. 33(1):22-7. [Medline].

  49. Lim JH. Oriental cholangiohepatitis: pathologic, clinical, and radiologic features. Am J Roentgenol. 1991 Jul. 157(1):1-8. [Medline].

  50. Mazer NA, Carey MC. Quasi-elastic light-scattering studies of aqueous biliary lipid systems. Cholesterol solubilization and precipitation in model bile solutions. Biochemistry. 1983 Jan 18. 22(2):426-42. [Medline].

  51. Moody FG. Pathogenesis and treatment of inflammatory lesions of the papilla of Vater. Jpn J Surg. 1985 Sep. 15(5):341-7. [Medline].

  52. Nijhawan PK, Therneau TM, Dickson ER, Boynton J, Lindor KD. Incidence of cancer in primary biliary cirrhosis: the Mayo experience. Hepatology. 1999 May. 29 (5):1396-8. [Medline].

  53. O'Connor MJ, Schwartz ML, McQuarrie DG, Sumer HW. Acute bacterial cholangitis: an analysis of clinical manifestation. Arch Surg. 1982 Apr. 117(4):437-41. [Medline].

  54. O'Connor MJ, Sumner HW, Schwartz ML. The clinical and pathologic correlations in mechanical biliary obstruction and acute cholangitis. Ann Surg. 1982 Apr. 195(4):419-23. [Medline].

  55. Palazzo L, Girollet PP, Salmeron M. Value of endoscopic ultrasonography in the diagnosis of common bile duct stones: comparison with surgical exploration and ERCP. Gastrointest Endosc. 1995 Sep. 42(3):225-31. [Medline].

  56. Pomeranz IS, Shaffer EA. Abnormal gallbladder emptying in a subgroup of patients with gallstones. Gastroenterology. 1985. 88:801. [Medline].

  57. Quirk DM, Rattner DW, Fernandez-del Castillo C. The use of endoscopic ultrasonography to reduce the cost of treating ampullary tumors. Gastrointest Endosc. 1997 Oct. 46(4):334-7. [Medline].

  58. Ransohoff DF, Gracie WA, Wolfenson LB. Prophylactic cholecystectomy or expectant management for silent gallstones. A decision analysis to assess survival. Ann Intern Med. 1983 Aug. 99(2):199-204. [Medline].

  59. Ros E, Zambon D. Postcholecystectomy symptoms. A prospective study of gall stone patients before and two years after surgery. Gut. 1987 Nov. 28(11):1500-4. [Medline].

  60. Ruffolo TA, Sherman S, Lehman GA. Gallbladder ejection fraction and its relationship to sphincter of Oddi dysfunction. Dig Dis Sci. 1994 Feb. 39(2):289-92. [Medline].

  61. Sampliner RE, Bennett PH, Comess LJ. Gallbladder disease in Pima Indians. Demonstration of high prevalence and early onset by cholecystography. N Engl J Med. 1970 Dec 17. 283(25):1358-64. [Medline].

  62. Schoenfield LJ, Carey MC, Marks JW. Gallstones: an update. Am J Gastroenterol. 1989 Sep. 84(9):999-1007. [Medline].

  63. Sievers MS, Marquis JR. The Southwest American Indian's burden: biliary disease. JAMA. 1962. 182:570-2.

  64. Strauch GO. Primary carcinoma of the gall bladder: presentation of seventy cases from the Rhode Island Hospital and a cumulative review of the last ten years of the American literature. Surgery. 1960 Mar. 47:368-83. [Medline].

  65. Strom BL, Soloway RD, Rios-Dalenz JL, et al. Risk factors for gallbladder cancer. An international collaborative case-control study. Cancer. 1995 Nov 15. 76 (10):1747-56. [Medline].

  66. Thistle JL, Cleary PA, Lachin JM, Tyor MP, Hersh T. The natural history of cholelithiasis: the National Cooperative Gallstone Study. Ann Intern Med. 1984 Aug. 101 (2):171-5. [Medline].

  67. Wienser RH, Porayko MK, LaRusso NF, et al. In: Schiff L, Schiff ER, eds. Diseases of the Liver. 7th ed. Philadelphia, Pa: JB Lippincott; 1993: 411-26.

  68. Wolfhagen FH, Sternieri E, Hop WC. Oral naltrexone treatment for cholestatic pruritus: a double-blind, placebo-controlled study. Gastroenterology. 1997 Oct. 113(4):1264-9. [Medline].

  69. Yap L, Wycherley AG, Morphett AD. Acalculous biliary pain: cholecystectomy alleviates symptoms in patients with abnormal cholescintigraphy. Gastroenterology. 1991 Sep. 101(3):786-93. [Medline].

  70. Yoshida J, Chijuwa K. Practical classification of the branching types of the biliary tree: an analysis of 1094 consecutive direct cholangiograms. J Am Coll Surg. 1997. 185:274-82. [Medline].

  71. Zeman RK. Cholelithiasis and cholecystitis. In: Gore RM, Levine MS, Laufer I, eds. Text of Gastrointestinal Radiology. Philadelphia, Pa: WB Saunders.; WB Saunders. 1994: 1654-5.

 
Previous
Next
 
A normal postcholecystectomy cholangiogram.
Biliary disease. In this patient with persistent elevation of liver-associated enzymes, the contrast entering the biliary ductal system preferentially enters the cystic duct.
Biliary disease. Even when the catheter is advanced to the proximal common hepatic duct, contrast dye preferentially fills the cystic duct and gallbladder rather than allowing visualization of the intrahepatic ductal system.
Biliary disease. In this image, the common bile duct is occluded with a balloon-tipped catheter. Contrast fills the intrahepatic ductal system to reveal diffuse intrahepatic sclerosing cholangitis.
Biliary disease. Common bile duct stones are among the most common problems occurring in the biliary system. In this cholangiogram, the stones line up like peas in a pod.
Biliary disease. After a biliary sphincterotomy, a balloon-tipped catheter is used to remove the stones one by one.
Biliary disease. This clearing cholangiogram shows a common bile duct free of filling defects and good flow into the duodenum. The stones are visible as filling defects in the duodenal bulb.
Biliary disease. This patient with pancreatic cancer has developed jaundice during his treatment. The cholangiogram shows a stricture in the distal common bile duct.
Biliary disease. A patient with pancreatic cancer has developed jaundice during his treatment. To palliate the jaundice, the biliary stricture is dilated and stented with a 10F plastic stent. Note the contrast flowing down the stent.
Biliary disease. The CT scan of the abdomen shows a large tumor mass in the head of the pancreas. The brightly colored object within the mass is the biliary stent placed by endoscopic retrograde cholangiopancreatography (ERCP).
Biliary disease. This abdominal CT scan shows mild intrahepatic biliary ductal dilation.
Biliary disease. This patient with jaundice has polycystic liver disease on abdominal CT scan.
Biliary disease. Findings on an endoscopic retrograde cholangiopancreatography (ERCP) exclude extrahepatic biliary obstruction but demonstrate that the intrahepatic biliary ductal system is splayed by multiple hepatic cysts.
Biliary disease. This cholangiogram shows a choledochal cyst. Fusiform dilation of the entire extrahepatic bile duct is present.
This 92-year-old woman had recurrent abdominal pain and jaundice. A right upper quadrant ultrasound showed a dilated biliary duct with no stones. She had a previous Roux-en-Y surgery that made endoscopic retrograde cholangiopancreatography (ERCP) impossible. Critical aortic stenosis that increased the risk of most interventions. This percutaneous cholangiogram, performed under conscious sedation in the operating room, revealed a large stone missed by the ultrasound. It was removed successfully with percutaneous choledochoscopy and electrohydraulic lithotripsy.
Biliary disease. This cholangiogram shows a stone too large to deliver through a standard biliary sphincterotomy.
Biliary disease. Here, a mechanical lithotripter is used to grab a stone too large to deliver through a standard biliary sphincterotomy and crush it into small pieces. The smaller pieces then are removed with a balloon-tipped catheter.
Biliary disease. This patient had malignant strictures of the biliary system that were palliated with metal mesh stents. Unfortunately, the tumor has grown through the metal mesh to reobstruct the biliary system.
Biliary disease. This patient had malignant strictures of the biliary system that were palliated with metal mesh stents. Unfortunately, the tumor has grown through the metal mesh to reobstruct the biliary system. After a wire is passed through the lumen, a balloon-dilating catheter is passed into the metal mesh stents and inflated to enlarge the lumen.
Biliary disease. This patient had malignant strictures of the biliary system that were palliated with metal mesh stents. The tumor has grown through the metal mesh to reobstruct the biliary system. After a wire was passed through the lumen, a balloon-dilating catheter was passed into the metal mesh stents and inflated to enlarge the lumen. In this image, 2 plastic stents were passed into the intrahepatic ductal system to again palliate the obstruction.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.