Gallbladder Mucocele
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The term gallbladder mucocele refers to an overdistended gallbladder filled with mucoid or clear and watery content. Usually noninflammatory, it results from outlet obstruction of the gallbladder and is commonly caused by an impacted stone in the neck of the gallbladder or in the cystic duct. (See the image below.)
Symptoms of a gallbladder mucocele include the following:
The following suggest other conditions:
Physical findings include the following:
See Presentation for more detail.
Laboratory studies that may be helpful include the following:
Imaging modalities that may be considered include the following:
See Workup for more detail.
Surgery is definitive treatment for gallbladder obstruction, and no absolute contraindication to such treatment exists. However, the following factors may be considered:
Surgical options include the following:
See Treatment for more detail.
Mucocele (hydrops) of the gallbladder is a term denoting an overdistended gallbladder filled with mucoid or clear and watery content. The condition can result from gallstone disease, the most common affliction of the biliary system. Gallstone disease affects 15-20% of the US population, with nearly 1 million new cases reported annually. [1, 2, 3]
The gallbladder mucocele distention, which is usually noninflammatory, results from an outlet obstruction of the gallbladder and is commonly caused by an impacted stone in the neck of the gallbladder or in the cystic duct. [1, 2, 4, 5]
No single laboratory test is diagnostic of a gallbladder mucocele. However, laboratory workup should include all tests performed for acute cholecystitis. Ultrasonography is extremely sensitive in detecting stones in the gallbladder; other imaging modalities may be helpful in certain circumstances (see Workup).
Cholecystectomy is the definitive treatment for an obstructed gallbladder. Medical approaches may be considered in specific circumstances (see Treatment).
For patient education resources, see the Digestive Disorders Center and the Cholesterol Center, as well as Gallstones.
Long-standing obstruction to the gallbladder’s outflow results in overdistention of the gallbladder; occasionally, the gallbladder assumes massive proportions, and its volume may reach 1.5 L. The bile or bile pigment is slowly resorbed, and continuing secretion from the mucosa of the gallbladder results in clear and watery or mucoid content (white bile).
The gallbladder wall may be of normal thickness, though in long-standing cases, the mucosa atrophies and the wall becomes thin, sometimes even transparent. Wall thickening can occur with recurrent attacks of cholecystitis (see the image below). The contents are usually sterile, and any bacterial contamination ends in empyema of the gallbladder.
Gross overdistention may result in gangrene or perforation of the gallbladder, with ensuing pericholecystic collection or peritonitis. The severity of the inflammatory episode dictates the clinical presentation.
Microscopic examination reveals a flattened mucosa lined by low columnar or cuboidal cells; the increased intraluminal pressure results in plentiful Rokitansky-Aschoff sinuses. Inflammatory cells may be present, either in small numbers or in abundance. [1, 2, 4]
Causes of gallbladder mucoceles include the following:
In infants and children, acute, acalculous, noninflammatory hydrops of the gallbladder may be associated with the following:
About 3% of all pathologic gallbladders in adults are mucoceles. Because different authors use varying criteria to define the condition, the true prevalence of gallbladder mucocele may be higher. [1, 2, 7] Some reports indicate that an association could exist between mucoceles and solitary stones of the gallbladder. [8]
The prognosis is excellent if the diagnosis is correct and no complications have ensued.
Complications may develop when progressive inflammation leads to acute cholecystitis and all its attendant manifestations.
In addition, bacterial contamination of the bile can lead to empyema of the gallbladder, in which case the patient will usually have a toxic and ill appearance. Gas-producing organisms may lead to an emphysematous gallbladder; air bubbles in the wall of the gallbladder can be visualized by means of plain radiography, ultrasonography, or computed tomography (CT).
Another potential complication is perforation of the gallbladder (see the first image below) with ensuing pericholecystic abscess or fluid collection and peritonitis (see the second image below); the diagnosis is usually strongly suspected on clinical grounds. Pseudomyxoma peritonei may result from the rupture of a true mucocele of the gallbladder.
Perforation of the gallbladder into the intestinal tract results in a cholecystenteric fistula. This occurs when the stone erodes into adjacent bowel, usually the duodenum. Gas in the biliary tree may be evident on plain radiographs of the abdomen or on ultrasonograms. If the stone is large, this may result in obstruction of the distal small bowel, leading to gallstone ileus.
Large gallbladders may compress the pylorus or duodenum, causing gastric outlet obstruction. [1, 9]
Agrawal S, Jonnalagadda S. Gallstones, from gallbladder to gut. Management options for diverse complications. Postgrad Med. 2000 Sep 1. 108(3):143-6, 149-53. [Medline].
Wang DQH, Afdhal NH. Gallstone disease. Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 10th ed. Philadelphia: Elsevier Saunders; 2016. Vol 1: 1100-33.
Haines EJ, Oyama LC. Disorders of the liver and biliary tract. Walls RM, Hockberger RS, Gausche-Hill M, et al, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th ed. Philadelphia: Elsevier; 2018. Vol 1: 1083-103.
Diseases of the digestive system: gallbladder and extrahepatic ducts. Damjanov I, Linder J, eds. Anderson’s Pathology. 10th ed. St Louis: Mosby-Year Book; 1996. Vol 2:
Wight DGD, Symmers WS, eds. Liver, Biliary Tract and Exocrine Pancreas. 3rd ed. Philadelphia: Churchill Livingstone; 1994. Vol 11:
Maurer K, Unsinn KM, Waltner-Romen M, et al. Segmental bowel-wall thickening on abdominal ultrasonography: an additional diagnostic sign in Kawasaki disease. Pediatr Radiol. 2008 Sep. 38(9):1013-6. [Medline].
Lamps LW. Gallbladder and extrahepatic bile ducts. Goldblum JR, Lamps LW, McKenney JK, Myers JL, eds. Rosai and Ackerman’s Surgical Pathology. 11th ed. Phialdelphia: Elsevier; 2018. Vol 1: 844-85.
Mofti AB, Al-Momen A, Suleiman SI, et al. The single gallbladder stone – is it innocent?. Ann Saudi Med. 1994 Nov. 14(6):471-3. [Medline].
Vijayaraghavan R, Belagavi CS. Double gallbladder with different disease entities: a case report. J Min Access Surg. 2006. 2:23-6. [Full Text].
Majeed AW, Reed MW, Stephenson TJ, Johnson AG. Chemical ablation of the gallbladder. Br J Surg. 1997 May. 84(5):638-41. [Medline].
Georgiades CP, Mavromatis TN, Kourlaba GC, et al. Is inflammation a significant predictor of bile duct injury during laparoscopic cholecystectomy?. Surg Endosc. 2008 Sep. 22(9):1959-64. [Medline].
Popkharitov AI. Laparoscopic cholecystectomy for acute cholecystitis. Langenbecks Arch Surg. 2008 Nov. 393(6):935-41. [Medline].
Gurusamy KS, Samraj K, Fusai G, Davidson BR. Robot assistant for laparoscopic cholecystectomy. Cochrane Database Syst Rev. 2009 Jan 21. CD006578. [Medline].
Mahid SS, Jafri NS, Brangers BC, et al. Meta-analysis of cholecystectomy in symptomatic patients with positive hepatobiliary iminodiacetic acid scan results without gallstones. Arch Surg. 2009 Feb. 144(2):180-7. [Medline].
Widmer J, Singhal S, Gaidhane M, Kahaleh M. Endoscopic ultrasound-guided endoluminal drainage of the gallbladder. Dig Endosc. 2014 Jul. 26 (4):525-31. [Medline].
R Vijayaraghavan, MBBS, MS, FRCS(Edin) Consultant General and Laparoscopic Surgeon, Department of Surgery, RMV Hospital, India
R Vijayaraghavan, MBBS, MS, FRCS(Edin) is a member of the following medical societies: International College of Surgeons, Royal College of Surgeons of Edinburgh
Disclosure: Nothing to disclose.
John Geibel, MD, DSc, MSc, AGAF Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, Professor, Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital; American Gastroenterological Association Fellow
John Geibel, MD, DSc, MSc, AGAF is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, Society for Surgery of the Alimentary Tract
Disclosure: Nothing to disclose.
Oscar Joe Hines, MD Assistant Professor, Department of Surgery, University of California at Los Angeles School of Medicine
Oscar Joe Hines, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Endocrine Surgeons, American College of Surgeons, Association for Academic Surgery, Society for Surgery of the Alimentary Tract, and Society of American Gastrointestinal and Endoscopic Surgeons
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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