British Journal of Radiology (2003) 76, 137-143
© 2003 British Institute of Radiology
doi: 10.1259/bjr/63382740
CT of a thickened-wall gall bladder
R Zissin, MD1,
A Osadchy, MD1,
M Shapiro-Feinberg, MD1 and
G Gayer, MD2
1 Department of Diagnostic Imaging, Sapir Medical Center, Kfar Saba 44281 and 2 Department of Diagnostic Imaging, Assaf Harofe Medical Center, Zrifin, affiliated to the Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel
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Abstract
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This pictorial article reviews the various clinical entities that may cause mural thickening of the gall bladder encountered on contrast enhanced CT.
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Introduction
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The current widespread use of abdominal CT has resulted in the detection of various pathological processes, that cause thickening of the gall bladder (GB) wall.
On contrast enhanced CT, the normal GB wall is usually perceptible as a thin enhancing rim of soft tissue density. Although its thickness depends upon the degree of GB distention, 3 mm is regarded as the upper limit of normal and mural thickening is defined as a transverse wall measurement of 4 mm or greater [1]. GB wall thickening is the most common finding in either acute calculus or acalculous cholecystitis [2, 3]. It is a non-specific finding that may be seen in GB cancer and in a variety of extracholecystic benign conditions such as hepatitis, heart failure, hypoalbuminaemia and acute severe pyelonephritis [1, 3, 5–7]. This review illustrates the CT features of a spectrum of pathological conditions affecting the GB.
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CT signs
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The thickened GB wall may be of soft tissue density (Figure 1
) due to mural hypervascularity associated with the inflammatory process analogous to the hyperaemic inflamed GB found pathologically in acute cholecystitis [3], or because of diffuse tumoural infiltration. Alternatively, it may present as a layered, "sandwich-like", mural thickening (Figures 2, 3a) of an inner enhancing layer of mucosa and an outer enhancing layer of serosa with a hypodense layer of subserosal oedema in between, or as a "halo" of low-attenuation subserosal oedema surrounding the enhancing mucosa (Figure 4). Occassionally the enhanced mucosa of the thickened GB wall may mimic a large rim-calcified stone or a GB wall surrounded by pericholecystic fluid. These simulations can readily be excluded by sonography. On CT, however, the "halo" of oedema can be distinguished from pericholecystic fluid by demonstrating small enhancing punctate structures within the oedematous wall, which is typically global compared with the pericystic fluid, which is usually focal [6]. We assume that, as on ultrasound, both appearances of "sandwich" or "halo" types of GB wall thickening favour a relative benign aetiology [8].
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Figure 1. A 75-year-old woman with acute cholecystitis. Contrast enhanced CT shows a distended gallbladder with mural thickening of soft tissue density, pericholecystic stranding (arrowhead) and reactive thickening of the adjacent colonic wall at the hepatic flexure (arrow).
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Figure 2. An 81-year-old with acute cholecystitis. Contrast enhanced CT shows a "sandwich-like" thickening of the gallbladder wall, representing hypodense submucosal oedema surrounded by an inner layer of enhancing mucosa (arrow) and an outer layer of enhancing serosa (arrowhead).
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Figure 3. A 76-year-old woman with acute cholecystitis. (a) Contrast enhanced CT shows a distended gallbladder (GB) with "sandwich-like" mural thickening, pericholecystic stranding of inflammatory changes and indistinct interface between the GB and the adjacent liver (arrows). (b) 2 cm caudally to (a), marked pericholecystic inflammatory changes (arrowheads) are seen with reactive thickening of the adjacent duodenum (D). (c) 2 cm caudally to (b), reactive mural thickening of the juxtaposed hepatic flexure (C) is demonstrated.
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Figure 4. A 28-year-old man with drug-induced hepatitis. Contrast-enhanced CT shows a "halo-like" thickening of the gallbladder wall, representing the enhancing mucosa (arrowhead) surrounded by subserosal oedema.
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Acute cholecystitis
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CT may be used for the evaluation of patients with acute right upper quadrant (RUQ) complaints with inconclusive ultrasound findings or with a perplexing clinical presentation when acute cholecystitis is not the first diagnostic choice, but may be the first modality to detect it.
Thickening of the GB wall is the most common finding of acute cholecystitis (Figures 1, 2, 3a
) while gallstones may or may not be seen [2, 3]. In fact, 95% of patients with acute cholecystitis have gallstones, but only approximately 75% of these are detected on CT [3]. Conversely, the presence of gallstones alone is not a reliable sign of acute cholecystitis [1].
A thick-walled GB is, however, a non-specific finding that may occur in a variety of extrabiliary conditions. The radiologist should therefore look for associated CT findings suggestive of acute cholecystitis including:
- Transient focal hyperattenuation in the hepatic parenchyma adjacent to the inflamed GB probably related to hepatic arterial hyperaemia (Figure 5) [9].
- Indistinct interface of the GB wall and the juxtaposed liver (Figure 3a), regarded as highly suggestive of acute cholecystitis [3].
- Pericholecystic stranding, which represents inflammatory changes within the fat surrounding the GB (Figure 3b). Extensive changes may cause reactive mural thickening and oedema in the adjacent colon (Figure 3c) or duodenum (Figure 3b). Irregular, discontinuous (Figure 6) or absence of GB wall enhancement on contrast-enhanced CT as well as pericholecystic abscess are specific signs of mural necrosis indicating gangrenous cholecystitis, a severe form of acute cholecystitis [10].
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Figure 5. A 71-year-old man with acute cholecystitis. Contrast-enhanced CT shows a distended thickened-wall gallbladder with a fluid–fluid level of high-attenuation bile (arrow). Note the focal increased attenuation within the adjacent liver parenchyma (arrowheads) representing reactive hepatic arterial hyperaemia.
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Figure 6. A 85-year-old woman with acute gangrenous cholecystitis. Contrast enhanced CT shows a distended gallbladder with gas-containing gallstones. Halo-like mural thickening with interrupted mucosa (curved arrow) is seen, compatible with necrotizing, gangrenous cholecystitis.
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The presence of gas in the GB wall (Figure 7) represents another variant of acute cholecystitis known as emphysematous cholecystitis, which is more common in men and in diabetic patients. Gas may also appear within the GB lumen and in the pericholecystic tissue [11]. CT has a significant role in detecting the gas as it mimics calcifications or cholesterol deposits on ultrasound.
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Figure 7. A 74-year-old man with acute emphysematous cholecystitis. CT shows gas within a thickened gallbladder wall (arrows) containing a large gallstone (arrowhead). Note the pericholecystic dissection of the gas (G).
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Acute acalculous cholecystitis is an infrequent but potentially fatal form of acute cholecystitis that usually occurs in critically ill patients [12]. The CT diagnosis is based on either two major criteria, which include GB mural thickening, necrosis or gas and pericholecystic stranding, or on one major and two minor criteria, including distended GB and hyperdense bile (Figure 6) [4, 12].
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Extracholecystic inflammatory processes
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Acute hepatitis (Figure 4), peritonitis (Figure 8), acute pancreatitis (Figure 9) [7] and acute pyelonephritis (Figure 10) [5] may cause GB wall thickening. Somer et al reported increased GB wall thickness in 64% of patients with acute pancreatitis in addition to intense contrast enhancement and pericholecystic oedematous changes [7]. Zissin et al reported signs of venous congestion including small bilateral pleural effusions, thickened interlobular septa in the lungs, congestion of the hepatic veins and of the inferior vena cava (IVC) and hepatic periportal tracking, a hypodense thickened GB wall and ascites in addition to hypodense lesions within enlarged kidneys compatible with acute pyelonephritis [5].
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Figure 8. A 93-year-old woman 10 days after surgery for perforated duodenal ulcer presented with fever and pus discharge through operative sutures. Contrast enhanced CT shows gas bubbles and extravasation of the orally ingested contrast medium (black arrow) reaching the skin (white arrow), compatible with leak and cutaneous fistula. Reactive "sandwich-like" thickening of the gallbladder wall is seen.
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Figure 9. A 36-year-old woman with acute pancreatitis. Contrast enhanced CT shows a thickened gallbladder wall with enhancing, thickened mucosa (arrowhead) and subserosal oedema. Note enlargement of the pancreatic head and the peripancreatic fluid (arrow).
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Figure 10. A 57-year-old woman with acute pyelonephritis. Contrast enhanced CT at the mid-abdomen shows a halo-like thickening of the gallbladder wall, ascitic fluid and hypodense lesions within the enlarged right kidney (arrowheads).
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Systemic diseases
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Hypoalbuminaemic states (Figure 11) and congestive right heart failure (Figure 12) may cause thickening of the GB wall [1, 3]. Additional findings of extravascular volume overload may be seen, such as pleural or pericardial effusions, ascites, dependent subcutaneous oedema and distended IVC. Pulmonary congestion in the lung bases may be demonstrated in patients with congestive heart failure as well. Hypoalbuminaemia in patients on intensive care units may cause GB wall thickening and can cause confusion with acute acalculous cholecystitis, which occurs most commonly in these patients. CT findings of the above-mentioned major or minor criteria of this diagnosis may be helpful for distinguishing these conditions (see Acalculous cholecystitis).
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Figure 11. A 73-year-old man with liver cirrhosis. Contrast enhanced CT shows thickening of the gallbladder wall of soft-tissue density (arrowhead), ascites, splenomegaly and atrophic liver with lobular borders.
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Figure 12. A 79-year-old woman with right-sided heart failure. (a) Contrast enhanced CT at the level of the upper abdomen shows "geographic" appearance of the congested liver and bilateral pleural effusions. (b) At a lower level, a thickened-wall gallbladder with enhancing mucosa (arrows) subserosal oedema is seen as well as ascitic fluid.
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Acquired immunodeficiency syndrome
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Hepatobiliary diseases are frequently encountered among patients infected with human immunodeficiency virus. Acalculous cholecystitis is the most common manifestation of GB disease of acquired immunodeficiency syndrome cholangiopathy, being primarily infectious in nature. Whilst it is related to various pathogens, Cryptosporidium is the most common cause of GB wall thickening in this situation followed by microsporidia such as Enterocytozoon bieneusi [13]. The thickened GB wall is typically more severe than expected from clinical presentation (Figure 13). Other causes of GB wall thickening in these patients include neoplastic infiltration of the GB wall by Kaposi's sarcoma and primary lymphoma.
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Figure 13. A 31-year-old HIV positive man presented with jaundice and abnormal liver function tests. Contrast enhanced CT shows splenomegaly a distended, thick-walled gallbladder (asterisk), which was further confirmed at surgery. Histology revealed acute and chronic inflammatory changes with a positive immunoperoxidase stain for Cytomegalovirus.
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Trauma
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Isolated penetrating trauma involving the GB is a rare injury. Clinical symptoms may be minimal initially with gradual clinical deterioration related to spillage of bile into the peritoneal cavity. A high clinical index of suspicion is needed to avoid a diagnostic delay. As abdominal CT is often performed it may elicit findings of mural thickening and high-density fluid content within the GB representing haemobilia as well as pericholecystic stranding along the tract of the invasion (Figure 14) [14]. Iatrogenic GB penetration due to hepatic percutaneous biopsy or needle aspiration and more rarely, following percutaneous nephrostomy or nephrolithotomy is another uncommon cause of GB perforation [15].
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Figure 14. A 25-year-old woman presented with fever and abdominal tenderness 2 days following penetrating trauma in the right upper quadrant (RUQ). Contrast-enhanced CT shows gallbladder (GB) wall thickening (asterisk) with intraluminal bile-blood level (arrowhead), infiltration within the posterior pericholecystic tissue (black arrow) and the RUQ subcutaneous defect (white arrow) indicating the stab wound. At surgery two lacerations were found within the anterior and posterior aspect of the GB with mild biliary peritonitis.
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Neoplasms
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Diffuse GB wall thickening secondary to tumour infiltration and inflammatory change is a common manifestation of advanced GB carcinoma, which is often detected at a late stage due to lack of early clinical signs [8, 16]. Associated findings such as biliary dilatation, invasion of adjacent structures and liver and nodal metastases, may help in establishing the correct diagnosis and differentiating it from chronic cholecystitis (Figure 15).
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Figure 15. A 67-year-old woman with gallbladder (GB) carcinoma. Contrast enhanced CT shows multiple metastatses (black arrows) within the liver and a thick-walled GB with irregular mucosal (white arrows) thickening and polypoid masses (arrowhead) of soft-tissue density within the subserosal oedema (asterisk).
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Miscellaneous
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GB wall thickening may be secondary to chronic cholecystitis, adenomyomatosis and polyps [1, 17]. Chronic cholecystitis may appear on CT with soft-tissue density wall thickening of, usually, a contracted GB, often around gallstones. A "porcelain" GB is an uncommon form of chronic cholecystitis with coarse mural calcification. Thickening of the GB wall, either focal or diffuse, on CT is the common finding of adenomyomatosis. Proliferation of the subserosal fat and intramural diverticula containing small calculi have also been reported [1]. Polypoid lesions of the GB, most commonly cholesterol polyp, appear on CT as focal mural thickening, usually of less than 10 mm, classified into pedunculated, sessile or mass-forming type [17].
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Summary
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GB wall thickening may result from a broad spectrum of pathological conditions, intrinsic as well as extrinsic to the biliary tract, and may have different appearances. A correct diagnosis is usually established after a correlation of imaging findings, laboratory data and clinical history.
Received for publication April 5, 2002.
Revision received August 6, 2002.
Accepted for publication September 23, 2002.
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Abstract
Introduction
