The British Journal of Radiology, 76 (2003), 137–143 E 2003 The British Institute of Radiology
DOI: 10.1259/bjr/63382740
Pictorial review
CT of a thickened-wall gall bladder
1
R ZISSIN, MD, 1A OSADCHY, MD, 1M SHAPIRO-FEINBERG, MD and 2G GAYER, MD
1
Department of Diagnostic Imaging, Sapir Medical Center, Kfar Saba 44281 and 2Department of Diagnostic Imaging,
Assaf Harofe Medical Center, Zrifin, affiliated to the Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel
Abstract. This pictorial article reviews the various clinical entities that may cause mural thickening of the
gall bladder encountered on contrast enhanced CT.
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.
CT signs
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 thicken-
ing (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 sono-
graphy. On CT, however, the ‘‘halo’’ of oedema can be
distinguished from pericholecystic fluid by demonstrating
small enhancing punctate structures within the oedema-
tous 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].
Received 5 April 2002 and in revised form 6 August 2002, accepted 23
September 2002.
The British Journal of Radiology, February 2003
Acute cholecystitis
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 find-
ings suggestive of acute cholecystitis including:
(1) Transient focal hyperattenuation in the hepatic
parenchyma adjacent to the inflamed GB probably
related to hepatic arterial hyperaemia (Figure 5) [9].
(2) Indistinct interface of the GB wall and the juxtaposed
liver (Figure 3a), regarded as highly suggestive of
acute cholecystitis [3].
(3) Pericholecystic stranding, which represents inflam-
matory 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, dis-
continuous (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].
The presence of gas in the GB wall (Figure 7) represents
another variant of acute cholecystitis known as emphyse-
matous 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 calcifica-
tions or cholesterol deposits on ultrasound.
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
137

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].
Extracholecystic inflammatory processes
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 con-
gestion including small bilateral pleural effusions, thick-
ened 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].
Systemic diseases
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).
Acquired immunodeficiency syndrome
Hepatobiliary diseases are frequently encountered
among patients infected with human immunodeficiency
virus. Acalculous cholecystitis is the most common mani-
festation 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 pre-
sentation (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.
138
R Zissin, A Osadchy, M Shapiro-Feinberg and G Gayer
Trauma
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].
Neoplasms
Diffuse GB wall thickening secondary to tumour
infiltration and inflammatory change is a common mani-
festation 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 differentiat-
ing it from chronic cholecystitis (Figure 15).
Miscellaneous
GB wall thickening may be secondary to chronic cholecys-
titis, 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 diverti-
cula 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].
Summary
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.
The British Journal of Radiology, February 2003
Pictorial review: CT of a thickened-wall gall bladder
Figure 1. A 75-year-old woman with acute cholecystitis. Con-
trast 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).
(a)
(c)
The British Journal of Radiology, February 2003
Figure 2. An 81-year-old with acute cholecystitis. Contrast
enhanced CT shows a ‘‘sandwich-like’’ thickening of the gall-
bladder wall, representing hypodense submucosal oedema sur-
rounded by an inner layer of enhancing mucosa (arrow) and
an outer layer of enhancing serosa (arrowhead).
(b)
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 strand-
ing 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 juxta-
posed hepatic flexure (C) is demonstrated.
139

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 (arrow-
head) surrounded by subserosal oedema.
Figure 6. A 85-year-old woman with acute gangrenous chole-
cystitis. 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.
140
R Zissin, A Osadchy, M Shapiro-Feinberg and G Gayer
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 par-
enchyma (arrowheads) representing reactive hepatic arterial
hyperaemia.
Figure 7. A 74-year-old man with acute emphysematous chole-
cystitis. CT shows gas within a thickened gallbladder wall (arrows)
containing a large gallstone (arrowhead). Note the pericholecystic
dissection of the gas (G).
The British Journal of Radiology, February 2003
Pictorial review: CT of a thickened-wall gall bladder
Figure 8. A 93-year-old woman 10 days after surgery for per-
forated 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), compa-
tible with leak and cutaneous fistula. Reactive ‘‘sandwich-like’’
thickening of the gallbladder wall is seen.
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).
The British Journal of Radiology, February 2003
Figure 9. A 36-year-old woman with acute pancreatitis. Contrast
enhanced CT shows a thickened gallbladder wall with enhan-
cing, thickened mucosa (arrowhead) and subserosal oedema.
Note enlargement of the pancreatic head and the peripancreatic
fluid (arrow).
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.
141
 R Zissin, A Osadchy, M Shapiro-Feinberg and G Gayer

(a) (b)

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.

Figure 14. A 25-year-old woman presented with fever and

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 posi-
tive immunoperoxidase stain for Cytomegalovirus.
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.

142 The British Journal of Radiology, February 2003

Pictorial review: CT of a thickened-wall gall bladder
Figure 15. A 67-year-old woman with gallbladder (GB) carci-
noma. Contrast enhanced CT shows multiple metastatses
(black arrows) within the liver and a thick-walled GB with irre-
gular mucosal (white arrows) thickening and polypoid masses
(arrowhead) of soft-tissue density within the subserosal oedema
(asterisk).
References
1. Herbener TE. The gallbladder and biliary tract. In: Haaga
JR, Lanzieri CF, Sartoris DJ, Zerhouni EA, editors.
Computed Tomography and Magnetic Resonance Imaging
of Whole Body, Edn 3, Vol. 2. St Louis, MO: Mosby,
1994:978–1036.
2. Fidler J, Paulson EK, Layfield L. CT evaluation of acute
cholecystitis: findings and usefulness in diagnosis. AJR
1996;166:1085–8.
3. Paulson EK. Acute cholecystitis: CT findings. Seminars in
US, CT, and MRI. 2000;21:56–63.
4. Mirvis SE, Vainright JR, Nelson AW, Johnson GS, Shorr R,
Rodriguez A, et al. The diagnosis of acute acalculous
cholecystitis: a comparison of sonography, scintigraphy and
CT. AJR 1986;147:1171–5.
The British Journal of Radiology, February 2003
5. Zissin R, Kots E, Rachmani R, Hadari R, Shapiro-Feinberg
M. Hepatic periportal tracking associated with severe acute
pyelonephritis. Abdom Imaging 2000;25:251–4.
6. Goldstein RB, Wing VW, Laing FC, Jeffrey RB. Computed
Tomography of thick-walled gallbladder mimicking peri-
cholecystic fluid. JCAT 1986;10:55–6.
7. Somer K, Kivisaari L, Standertskjold-Nordenstam CG,
Kalima TV. Contrast-enhanced computed tomography of
the gallbladder in acute pancreatitis. Gastrointest Radiol
1984;9:31–4.
8. Wibbenmeyer LA, Sharafuddin MJA, Wolverson MK,
Heiberg EV, Wade TP, Shields JB. Sonographic diagnosis
of unsuspected gallbladder cancer: imaging findings in
comparison with benign gallbladder conditions. AJR 1995;
165:1169–74.
9. Yamashita K, Jin MJ, Hirose Y, Morikawa M, Sumioka H,
Itoh K, et al. CT findings of transient focal increased
attenuation of the liver adjacent to the gallbladder in acute
cholecystitis. AJR 1995;164:343–6.
10. Bennett GL, Rusinek H, Lisi V, Israel GM, Krinsky GA,
Slywotzky CM, et al. CT findings in acute gangrenous
cholecystitis. AJR 2002;178:275–81.
11. Gill KS, Chapman AH, Weston MJ. The changing face of
emphysematous cholecystitis. Br J Radiol 1997;70:986–91.
12. Jacobs JE, Birnbaum BA. Abdominal computed tomography
in intensive care unit patients. Semin Roentgenol 1997;
32:128–41.
13. Wicox CM, Monkemuller KE. Hepatobiliary disease in
patients with AIDS: focus on AIDS cholangiopathy and
gallbladder disease. Dig Dis 1998;16:205–13.
14. Sabetai MM, Velmahos GC, Schreier DZ. Preoperative
diagnosis of isolated penetrating gallbladder injury in an
asymptomatic patient: the role of hepato-iminodiacetic acid
scan as the definitive diagnostic test. Am Surg 1998;64:772–4.
15. Lublin M, Danforth DN. Iatrogenic gallbladder perforation:
conservative management by percutaneous drainage and
cholecystostomy. Am Surg 2001;67:760–3.
16. Rooholamini SA, Tehrani NS, Razavi MK, Au AH, Hansen
GC, Ostrzega N, Verma RC. Imaging of gallbladder
carcinoma. Radiographics 1994;14:291–306.
17. Furukawa H, Takayasu K, Mukai K, Inoue K, Kyokane T,
Shimada K, et al. CT evaluation of small polypoid lesion of
the gallbladder. Hepatogastroenterology 1995;42:800–10.
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