Open Access
CC BY 4.0 · Journal of Gastrointestinal and Abdominal Radiology
DOI: 10.1055/s-0046-1817151
Review Article

Gallstones and Choledocholithiasis: A Comprehensive Imaging Review

Authors

  • Aruna Raman Patil

    1   Department of Radiology, Apollo Hospitals, Bangalore, Karnataka, India
  • Shrivalli Nandikur

    1   Department of Radiology, Apollo Hospitals, Bangalore, Karnataka, India
  • Satyajit Godhi

    2   Department of Gastrosurgery, Aster Hospitals, Bangalore, Karnataka, India
  • Vijay Kumar H. J.

    3   Department of Gastroenterology and Interventional Endoscopy, Krishna Institute of Medical Sciences, Bangalore, Karnataka, India
 

Abstract

Gallstone disease is recognizably common and increasing in the current population, adding to significant morbidity and mortality and health care costs. Imaging plays a crucial role in the diagnosis, follow-up, and assessment of complications. Due to great advances in diagnostics and management options, it is important for clinicians and radiologists to be equipped with changing trends and atypical clinical presentations. This review article aims to provide a comprehensive coverage of pathogenesis, imaging options, and features of gallstone disease with teaching points on tackling pitfalls in interpretation.


Introduction

The incidence of gallstone disease is increasing in the current population, adding to significant morbidity and mortality and health care costs. Advances in minimal invasive treatment options require a credible radiology report encompassing details that provide the roadmap and help in decision-making and prognostication. The type, location, and complications of gallstones can be readily assessed by multiple imaging modalities.[1] [2] Knowledge of imaging modality choices and their limitations is essential for clinicians and radiologists. This review article aims to provide a comprehensive coverage of pathogenesis, imaging options, and features of gallstone disease with teaching points on tackling pitfalls in interpretation.


Pathogenesis and Predisposing Factors

Gallstone formation is secondary to an interplay between cholesterol crystals, pigment polymers, calcium salts, and mucin stimulated by bile stasis, supersaturation, or infection.[3] Genetic causes include mutations in hepatic and intestinal cholesterol transporters, and others that result in low phosphatidylcholine concentrations in bile.[4] [Table 1] summarizes the predisposing factors for gallstone formation.

Table 1

Factors predisposing gallstone formation

• Female gender

• Middle age

• Obesity

• Western, Caucasian, Asian races

• On oral contraceptives and estrogen replacement treatments

• Diabetes mellitus

• Altered lipid profile

• Hemolysis

• Drugs such as cephalosporins

Gallstones are classified into three major types[1] based on their composition ([Fig. 1]).

  • Cholesterol stones: pure cholesterol stones constitute 10% of the total and appear as round, white/yellow in color with a lobulated contour. They are variable in size and number and contain cholesterol as the main component (>50%).

  • Pigment stones: they constitute 10% of the total and are composed of bile pigments (in the form of calcium bilirubinate or calcium carbonate), rendering them black or brown. The cholesterol content is <20%. The stones can be smooth or rugged on the outside and can be variable in size and number. Black stones are primarily the result of hemolysis, whereas brown stones are secondary to an underlying infective process.

  • Mixed stones: the most common type (80%) and contain 20 to 50% cholesterol. They are yellowish-brown in color.

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Fig. 1 Post-cholecystectomy specimens of (A) cholesterol stones, (B) pigment stones (black), and (C) mixed stones.

Some stones contain central gas (nitrogen/carbon dioxide) containing fissure resembling a tri/multiradiate pattern referred to as “Mercedes Benz” sign ([Fig. 2]). Presence of gas within the calculus helps is easy diagnosis of an otherwise radiolucent stone. These stones are formed rapidly with coexisting inflammation and are known to auto-fragment and spontaneously pass out.[5] Gas-containing stones should not be mistaken for emphysematous cholecystitis.

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Fig. 2 Gas-containing gallstones on CT coronal (A) and axial (B) sections (arrows) with cholecystitis changes. Note the tri/multiradiate pattern referred to as “Mercedes Benz” sign. CT, computed tomography.

Imaging Modalities

The incidence of gallstones is on the rise, especially in females. While the majority of gallstones remain asymptomatic, 10 to 15% become symptomatic eventually.[1] Imaging plays a vital role in the diagnosis of gallstones and their complications. There has been tremendous evolution of diagnostic methods over the years for gallstones, with certain investigations like oral cholecystography becoming obsolete.[2]

Radiography: pigmented gallstones and mixed gallstones can be visualized on abdominal radiograph as radio-dense foci in the right upper quadrant (RUQ). Overall, only 10 to 15% of gallstones can be confidently picked up on radiography. The visibility is based on the concentration of iron or calcium. Cholesterol stones are not visualized. Differentials for radiodensity in RUQ include renal calculus, calcified liver lesions, enteroliths including a subhepatic appendicolith, foreign body, and porcelain gallbladder. They can be differentiated with the help of lateral radiographs and the morphology of the radiodensity ([Fig. 3]). Small intestinal obstruction secondary to gallstone, pneumobilia, and emphysematous cholecystitis are some conditions that can be diagnosed on radiographs.

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Fig. 3 Multimodality appearances of gallstones: (A) chest radiograph with a gallstone appearing as a rounded radiodensity in the right hypochondrium. (B) US appearance of gallstones—echogenic with posterior acoustic shadowing. (C) Coronal CECT section of the abdomen showing multiple small radio-dense gallstones with cholecystitis. (D) T2 axial section MR showing gallstones as small hypointense foci within the lumen. CECT, contrast-enhanced computed tomography; MR, magnetic resonance; US, ultrasound.

Ultrasonography (US): US is the preferred modality for suspected gallstones. A gallstone, irrespective of the composition, appears echogenic with posterior acoustic shadowing ([Figs. 3] and [4]). Mobility on change of posture can help in differentiating from polyps. Comet tail artifacts and twinkling artifacts can be seen in both gallstones and intramural cholesterol deposits. Among the gallstones, the effect is pronounced with cholesterol stones, and pigmented stones tend to show less artifact.[6] Wall echo shadow refers to a US finding that is seen when the gallbladder is replaced with numerous stones, in contracted states and in chronic cholecystitis ([Fig. 4]). Nonmobile, iso or hypoechoic intraluminal lesions with absent posterior acoustic shadowing and demonstrable vascularity should raise a possibility of neoplastic polyps ([Fig. 5]).

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Fig. 4 Typical Ultrasound appearances of gallstones: (A) dependent echogenic round focus (solid arrow) with posterior acoustic shadowing (dashed arrow). (B, C) Echogenic round focus with “twinkling” artifact on color. (D) “Wall–Echo–Shadow” complex in chronic calculus cholecystitis/contracted gallbladder.
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Fig. 5 Mimics of gallstones on US. (A) Cholesterolosis/adenomyomatosis showing echogenic nondependent foci with “comet tail” artifacts. (B) Gallbladder sludge (solid arrow). Also note the coexisting calculus (dashed arrow). (C) Benign pedunculated gallbladder polyp—iso/hypoechoic with no post-acoustic shadowing. Vascular polypoidal mass on US (D), T2 coronal MR (E), eventually turned out as adenoma (F). MR, magnetic resonance; US, ultrasound.

Computed tomography (CT): CT is the preferred modality for the evaluation of gallstone-related complications presenting as an acute abdomen, along with magnetic resonance cholangiopancreatography (MRCP). Pure cholesterol stones are radiolucent and not easily seen on CT. Instances where they can be picked up occur when the bile is hyperdense (supersaturated or vicarious excretion of intravenous contrast) and stones seen as filling defects. Radiolucent calculi can be suspected on CT when subtle heterogeneity is seen within the lumen, soft rim, or central calcifications, or a gas-containing center ([Fig. 6]). Pigment stones appear variably hyperdense on CT ([Fig. 7]). Unlike renal calculi, lithotripsy for gallstones is not very commonly practiced due to incomplete clearance and high recurrence. In centers where lithotripsy is done for gallstones,[7] details of gallstone burden, largest size, numbers, whether the stone is radiolucent or minimally calcified are worth mentioning in the report for a successful outcome.[8]

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Fig. 6 (A, B) Plain CT axial and sagittal sections showing a radiolucent calculus at the neck, made conspicuous by a calcified rim and hyperdense bile. (C) US of the same confirming neck calculus. CT, computed tomography; US, ultrasound.
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Fig. 7 Pigment stones in a patient with sickle cell anemia. (A) T2 axial section showing multiple tiny hypointense gallbladder calculi. Coronal CT showing the calculi as radio-dense. Note the shrunken hyperdense spleen (dotted arrow). (C) CT bone window sagittal section showing sclerotic bones with central infarcts. CT, computed tomography.

Dual-energy CT (DECT): DECT has better sensitivity for gallstone detection. Isodense stones on normal CT become more apparent on low or high monochromatic images.[3] Suspected gallstone disease or complications, for which CT is done, should always be complemented by US or magnetic resonance (MR) to document calculi.

Magnetic resonance imaging (MRI): On T2-weighted MRI sequences, gallstones (all types) are seen as hypointense foci against the background hyperintense bile. T1-weighted 3D fast spoiled gradient echo sequence (T1FSGRE) can be used for differentiating pigment from cholesterol stones. Pigment stones appear hyperintense on T1FSGRE, whereas cholesterol stones remain hypointense ([Fig. 8]). The metal ions within the pigment stones act as paramagnetic ions, shortening the T1 relaxation time, thus appearing hyperintense on T1-weighted images.[9] This sequence can be used in difficult diagnoses encountered in cases of ampullary calculus, differentiating from pneumobilia, clot, and tumor.

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Fig. 8 Pigment stones in a patient with sickle cell anemia. (A) T2 axial section showing multiple tiny hypointense gallbladder calculi. (B) T1 axial section showing the calculi as hyperintense. (C) T2 coronal section showing paravertebral extramedullary hematopoiesis (dotted arrow) and exaggerated renal corticomedullary differentiation. (D) T2 axial section showing shrunken hypointense spleen (dotted arrow).

Nuclear medicine techniques using technetium-labelled mebrofenin can assess the gallbladder dynamics and complications such as cholecystitis or obstruction and are not primarily used for gallstone detection.[1]

Cholelithiasis in children: gallstone formation in the pediatric population follows a bimodal distribution peaking at infancy and at adolescence. The overall incidence is 0.1 to 2%.[10] The latter peak has a female predominance similar to adult presentation. Gallstones in children are increasingly diagnosed in recent years, likely due to the wide use of US as an investigation in the evaluation of pediatric abdominal symptoms. Causes include hemolytic (20–30%), nonhemolytic (40–50%), and idiopathic (30–40%).[11] Nonhemolytic causes include total parenteral nutrition, drug-induced, post-bowel resection, congenital biliary malformations, etc. Management is based on symptoms. Asymptomatic children can be safely followed up ([Fig. 9]). Pigment stones in hemolytic anemia may warrant prophylactic cholecystectomy based on the standard guidelines. Sludge and calculi can rarely be seen in fetal gallbladders on antenatal scans. Most of them resolve spontaneously.[12] [13] The hypothesized etiology is maternal estrogen influence and cholestasis.

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Fig. 9 Incidentally detected gallbladder calculus (solid arrow) in a 1-year-old boy seen as hyperintense on T1-weighted image (A) and hypointense on T2-weighted image (B). The dashed arrow refers to the calculus in the distal bile duct.

Complications of Gallstones

Up to 15% of gallstones are symptomatic. Presentation depends on the type and site of complication. Biliary colic is the most common sequelae of gallstone and occurs due to obstruction of bile flow by the calculus, resulting in increased lumen pressure, which is intermittent and relieved by change of posture or spontaneously.[3] [Table 2] summarizes various gallstone complications.

Table 2

Gallstone complications

• Biliary colic

• Cholecystitis

• Choledocholithiasis

• Pancreatitis

• Mirizzi syndrome

• Bouveret syndrome

• Gallstone ileus, coleus

• Carcinoma gallbladder

Cholecystitis: occurs in 10 to 15% of cases and is dealt with in detail in a separate review article.


Choledocholithiasis

Choledocholithiasis refers to a stone or stones within the common bile duct and occurs in up to 20% cases of cholelithiasis. Bile duct stones are most commonly symptomatic, unlike gallstones, and present with RUQ pain, vomiting, fever, or jaundice.[14] Bile duct stones can be primary (formed within the ducts) or secondary (slipped from the gallbladder). Secondary stones are more common.[15] Strong predictors for a clinical diagnosis of choledocholithiasis include the presence of a common bile duct stone on transabdominal US, acute cholangitis, and serum bilirubin greater than 4 mg/dL.[16] Serum alanine aminotransferase and aspartate aminotransferase concentrations are initially elevated, followed by a delayed and consistent rise in alkaline phosphatase, serum bilirubin, and gamma-glutamyl transpeptidase.[17]

Initial diagnostic workup for suspected choledocholithiasis includes abdominal US, which can detect ductal calculus as an echogenic focus with posterior acoustic shadowing and dilated extra- and intrahepatic bile ducts ([Fig. 10]). US has approximately 72% sensitivity for assessment of the distal duct; ampullary tip calculus may be difficult due to bowel gases. CT is not a definitive test for radiolucent calculi as they remain isodense to the surrounding bile.

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Fig. 10 (A, B) Ultrasound, color doppler of the portal region in a patient with biliary coli showing a dilated common bile duct (solid arrow) secondary to a distal duct calculus (dashed arrow). (C) T2 coronal section showing a hypointense calculus in the distal common bile duct with upstream biliary dilatation.

Definitive diagnosis can be obtained by noninvasive methods like MRCP and endoscopic ultrasound (EUS). Both MRCP and EUS have similar sensitivity and specificity for the diagnosis of choledocholithiasis.[18] However, EUS supersedes MRCP in calculi less than 5 mm in size ([Fig. 11]). Use of modalities depends on availability and individual practice guidelines.

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Fig. 11 (A–D) Endoscopic US appearance of common bile duct stones (arrows). US, ultrasound.

MRCP provides a larger field of view in assessing the entire biliary tree, burden of the disease, and associated complications like cholangitis and pancreatitis. Studies report 93 to 95%[14] sensitivity for the diagnosis of choledocholithiasis for stones bigger than 5 mm. For small stones, the sensitivity drops to 70% secondary to flow artifacts, air bubbles, vascular compressions, and breathing misregistration. On MRCP, a bile duct calculus is seen as a T2 hypointense focus lined by T2 hyperintense bile or a thickened, edematous biliary wall with upstream biliary dilatation ([Fig. 10]). Air within the bile duct is generally nondependent. Flow voids are central and span a longer length of the bile duct and can be confirmed on coronal sequences. Vessels are seen outside the biliary wall, appear as eccentric voids rather than central, and can be traced in both directions ([Fig. 12]).

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Fig. 12 MRCP pitfalls: (A, B) extrinsic compression by crossing artery mimicking stone on MIP and coronal T2 sequences. (C) Pneumobilia (solid arrow) and calculus (dashed arrow) on the axial T2 sequence. MRCP, magnetic resonance cholangiopancreatography.

Confident identification of distal bile duct calculus on MRCP can be made by the following:

  • Familiarity with pitfalls related to technique, artifacts, and variant anatomy.

  • Use of T1 gradient echo sequences—pigment stones appear hyperintense, providing adequate contrast at the distal end and ampulla ([Fig. 9]).

  • Matching the size and morphology of gallstones and bile duct stones.

  • Assessing the duodenal lumen for projecting ampullary calculus.

  • Correlation between clinical symptoms and liver function tests.

Endoscopic retrograde cholangiopancreatography is both a diagnostic and therapeutic procedure for confirmation and retrieval of stones and sphincterotomy ([Fig. 13]). Other invasive procedures for the diagnosis of ductal stones include intraoperative cholangiography and percutaneous transhepatic cholangiography.

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Fig. 13 ERCP image showing a common bile duct calculus as a filling defect (arrow) within the contrast opacified duct. ERCP, endoscopic retrograde cholangiopancreatography.

Mucocele: Mucocele or hydrops is due to sudden overdistension of the gallbladder secondary to obstruction by a gallstone at the neck or cystic duct without inflammation.[3] The size cutoff for mucocele is 10 cm by 4 cm. Imaging plays a key role in the diagnosis ([Figs. 14] and [15]). A “Tense gallbladder sign” refers to a bulging gallbladder against the parietal wall with fundal flattening due to increased intraluminal pressure.

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Fig. 14 (A) US right upper quadrant showing an overdistended gallbladder (*). (B) T2 axial section showing an impacted hypointense calculus at the neck. (C) MIP MRCP images showing an overdistended gallbladder. Note the absence of wall thickening or inflammatory changes. (D) Post-op specimen of a “baggy” gallbladder with a large pigment stone. MIP MRCP, maximum intensity projection magnetic resonance cholangiopancreatography; US, ultrasound.
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Fig. 15 (A, B) Mucocele secondary to cystic duct calculus (arrow) on T2 coronal and MIP MRCP images. The gallbladder measured 15 cm in length. MIP MRCP, maximum intensity projection magnetic resonance cholangiopancreatography.

Mirizzi spectrum: It is seen in up to 2% of cholecystectomies,[19] Mirizzi syndrome refers to extrinsic compression of the bile duct by an impacted calculus in the neck or cystic duct of the gallbladder. The obstruction is at the level of the proximal bile duct with intrahepatic biliary dilatation and normal caliber distal duct ([Figs. 16] and [17]). There are various types and subtypes of Mirizzi syndrome and most classifications[20] include cholecystobiliary and cholecystoenteric fistulas in them. Prolonged impaction and compression of gallstones on the adjacent bile duct and bowel can cause inflammation, pressure erosion, and eventually enteric communication. Diagnosis of Mirizzi syndrome is important as the management is complex and challenging. Variants such as long or low inserting cystic duct predispose to Mirizzi syndrome. Both CT and MR are reliable modalities for the diagnosis. Oral positive contrast may be required to demonstrate the fistulous communication on CT. The most common site of enteric communication is the duodenum and if the stone lodges within the duodenal lumen, it can cause gastric outlet obstruction, the condition referred to as Bouveret syndrome.[21] [22] [23] Presence of pneumobilia, air in the gallbladder, ectopic location of the stone surrounded by bowel, and positive contrast on CT suggest the diagnosis. A distended stomach and wall thickening at the site of stone impaction are other findings ([Fig. 18]).

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Fig. 16 Mirizzi syndrome: (A) T2 coronal section showing an impacted calculus at the gallbladder neck (solid arrow) compressing the common hepatic duct, causing upstream dilatation. (B) MIP image demonstrates the same. Note the normal caliber distal common bile duct (dashed arrow). MIP, maximum intensity projection.
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Fig. 17 Mirizzi syndrome: (A) coronal CECT showing radiolucent calculus impacted at the neck with cholecystitis changes. (B, C) T2 coronal and MIP MRCP showing smooth extrinsic compression of the common hepatic duct, causing mild intrahepatic biliary dilatation. (D) ERCP confirms the same. Inset shows post-stenting. CECT, contrast-enhanced computed tomography; ERCP, endoscopic retrograde cholangiopancreatography; MIP MRCP, maximum intensity projection magnetic resonance cholangiopancreatography.
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Fig. 18 Bouveret syndrome: axial plain CT (A), coronal CECT (B), and sagittal CT with oral positive contrast (C) images showing evidence of a radio-dense calculus lodged in the duodenum with distended stomach (*), pneumobilia, and contrast lined fistula between the gallbladder and the duodenum. T2 axial (D), coronal (E), and volume rendered image (F) demonstrate a duodenal calculus with a fistulous track. CECT, contrast-enhanced computed tomography; CT, computed tomography.

Migrated gallstones within the small bowel commonly lodge in the ileum or ileocecal valve due to anatomical narrowing in 60% cases. This condition is the gallstone ileus that presents with symptoms and signs of small bowel obstruction. The most common way of entry is via a cholecystoduodenal fistula. Other types of fistulas include cholecystogastric, cholecystojejunal, hepatoduodenal, choledochoduodenal, and cholecystocolonic.

Unusual sites of gallstone impaction include within diverticula, prior stenosis, and the colon (gallstone coleus). The classic imaging triad[24] [25] of gallstone ileus on abdominal radiograph, described by Rigler and seen in 14 to 50% cases, comprises pneumobilia, small bowel dilatation, and an ectopic radio-dense gallstone ([Fig. 19]). On CT, the presence of pneumobilia and small bowel dilation must prompt careful review of the small bowel transition, where the stone is commonly found. Radiolucent stones may still have faint central or rim calcification that can aid in the diagnosis ([Fig. 20]). DECT has shown promise in identifying ectopic gallstones in suspected cases.[26]

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Fig. 19 Gallstone ileus: (A) abdominal radiograph showing pneumobilia (dashed arrow) and small bowel obstruction (solid arrows). (B–D) CT in coronal and axial sections confirms air in the common hepatic duct (dashed arrow) with fistulization with the duodenum first part and an ectopic gallstone (solid arrow) causing small bowel obstruction. CT, computed tomography.
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Fig. 20 Gallstone ileus: (A) CT scanogram showing small bowel obstruction (solid arrow) with a linear lucent area in the right hypochondrium (dashed arrow). (B, C) CT in the coronal plane (inset in axial) showing dilated small bowel with a dense filling defect (with faint fat and calcium) in the distal jejunum (solid arrow) and cholecystoduodenal fistula (dashed arrow). (D–F) Intraoperative images showing the site of obstruction. Enterotomy and stone removal were done. CT, computed tomography.

Gallstone pancreatitis: 40 to 60% of acute pancreatitis is secondary to gallstones and is due to obstruction of the common bile duct. While most of the gallstones spontaneously pass out, 3 to 7% can result in persistent obstruction, causing pancreatitis.[27] Pancreatitis is a clinical and biochemical diagnosis. Imaging is done for assessing complications ([Fig. 21]). Both CT and MRCP help in the confirmation of diagnosis and complications.

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Fig. 21 (A, B) T2 axial sections showing cholelithiasis (solid white arrow) and choledocholithiasis (dashed arrow). The pancreas is diffusely bulky, edematous with surrounding inflammation (black arrows)—gallstone-induced acute interstitial pancreatitis.

Malignancy: gallstones and associated chronic cholecystitis are the most common risk factors for the development of gallbladder carcinoma. Up to 95% of gallbladder carcinomas are associated with gallstones ([Fig. 22]). Stones larger than 2 to 3 cm and cholesterol stones have the strongest association.[28]

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Fig. 22 CECT in axial (A) and coronal (B) sections showing an irregular enhancing mass replacing the gall bladder—carcinoma with contiguous liver extension. Note the gallstone (dashed arrow). CECT, contrast-enhanced computed tomography.

Conclusion

Gallstones are an increasing cause of hospital admissions and morbidity. It is crucial for radiologists to understand the pathogenesis, imaging correlates of its presentation, and complications to guide appropriate management.



Conflict of Interest

None declared.


Address for correspondence

Aruna Raman Patil, MD, DNB, FRCR, FICR
Department of Radiology, Apollo Hospitals
Bangalore 560076, Karnataka
India   

Publication History

Article published online:
27 February 2026

© 2026. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

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Fig. 1 Post-cholecystectomy specimens of (A) cholesterol stones, (B) pigment stones (black), and (C) mixed stones.
Zoom
Fig. 2 Gas-containing gallstones on CT coronal (A) and axial (B) sections (arrows) with cholecystitis changes. Note the tri/multiradiate pattern referred to as “Mercedes Benz” sign. CT, computed tomography.
Zoom
Fig. 3 Multimodality appearances of gallstones: (A) chest radiograph with a gallstone appearing as a rounded radiodensity in the right hypochondrium. (B) US appearance of gallstones—echogenic with posterior acoustic shadowing. (C) Coronal CECT section of the abdomen showing multiple small radio-dense gallstones with cholecystitis. (D) T2 axial section MR showing gallstones as small hypointense foci within the lumen. CECT, contrast-enhanced computed tomography; MR, magnetic resonance; US, ultrasound.
Zoom
Fig. 4 Typical Ultrasound appearances of gallstones: (A) dependent echogenic round focus (solid arrow) with posterior acoustic shadowing (dashed arrow). (B, C) Echogenic round focus with “twinkling” artifact on color. (D) “Wall–Echo–Shadow” complex in chronic calculus cholecystitis/contracted gallbladder.
Zoom
Fig. 5 Mimics of gallstones on US. (A) Cholesterolosis/adenomyomatosis showing echogenic nondependent foci with “comet tail” artifacts. (B) Gallbladder sludge (solid arrow). Also note the coexisting calculus (dashed arrow). (C) Benign pedunculated gallbladder polyp—iso/hypoechoic with no post-acoustic shadowing. Vascular polypoidal mass on US (D), T2 coronal MR (E), eventually turned out as adenoma (F). MR, magnetic resonance; US, ultrasound.
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Fig. 6 (A, B) Plain CT axial and sagittal sections showing a radiolucent calculus at the neck, made conspicuous by a calcified rim and hyperdense bile. (C) US of the same confirming neck calculus. CT, computed tomography; US, ultrasound.
Zoom
Fig. 7 Pigment stones in a patient with sickle cell anemia. (A) T2 axial section showing multiple tiny hypointense gallbladder calculi. Coronal CT showing the calculi as radio-dense. Note the shrunken hyperdense spleen (dotted arrow). (C) CT bone window sagittal section showing sclerotic bones with central infarcts. CT, computed tomography.
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Fig. 8 Pigment stones in a patient with sickle cell anemia. (A) T2 axial section showing multiple tiny hypointense gallbladder calculi. (B) T1 axial section showing the calculi as hyperintense. (C) T2 coronal section showing paravertebral extramedullary hematopoiesis (dotted arrow) and exaggerated renal corticomedullary differentiation. (D) T2 axial section showing shrunken hypointense spleen (dotted arrow).
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Fig. 9 Incidentally detected gallbladder calculus (solid arrow) in a 1-year-old boy seen as hyperintense on T1-weighted image (A) and hypointense on T2-weighted image (B). The dashed arrow refers to the calculus in the distal bile duct.
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Fig. 10 (A, B) Ultrasound, color doppler of the portal region in a patient with biliary coli showing a dilated common bile duct (solid arrow) secondary to a distal duct calculus (dashed arrow). (C) T2 coronal section showing a hypointense calculus in the distal common bile duct with upstream biliary dilatation.
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Fig. 11 (A–D) Endoscopic US appearance of common bile duct stones (arrows). US, ultrasound.
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Fig. 12 MRCP pitfalls: (A, B) extrinsic compression by crossing artery mimicking stone on MIP and coronal T2 sequences. (C) Pneumobilia (solid arrow) and calculus (dashed arrow) on the axial T2 sequence. MRCP, magnetic resonance cholangiopancreatography.
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Fig. 13 ERCP image showing a common bile duct calculus as a filling defect (arrow) within the contrast opacified duct. ERCP, endoscopic retrograde cholangiopancreatography.
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Fig. 14 (A) US right upper quadrant showing an overdistended gallbladder (*). (B) T2 axial section showing an impacted hypointense calculus at the neck. (C) MIP MRCP images showing an overdistended gallbladder. Note the absence of wall thickening or inflammatory changes. (D) Post-op specimen of a “baggy” gallbladder with a large pigment stone. MIP MRCP, maximum intensity projection magnetic resonance cholangiopancreatography; US, ultrasound.
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Fig. 15 (A, B) Mucocele secondary to cystic duct calculus (arrow) on T2 coronal and MIP MRCP images. The gallbladder measured 15 cm in length. MIP MRCP, maximum intensity projection magnetic resonance cholangiopancreatography.
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Fig. 16 Mirizzi syndrome: (A) T2 coronal section showing an impacted calculus at the gallbladder neck (solid arrow) compressing the common hepatic duct, causing upstream dilatation. (B) MIP image demonstrates the same. Note the normal caliber distal common bile duct (dashed arrow). MIP, maximum intensity projection.
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Fig. 17 Mirizzi syndrome: (A) coronal CECT showing radiolucent calculus impacted at the neck with cholecystitis changes. (B, C) T2 coronal and MIP MRCP showing smooth extrinsic compression of the common hepatic duct, causing mild intrahepatic biliary dilatation. (D) ERCP confirms the same. Inset shows post-stenting. CECT, contrast-enhanced computed tomography; ERCP, endoscopic retrograde cholangiopancreatography; MIP MRCP, maximum intensity projection magnetic resonance cholangiopancreatography.
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Fig. 18 Bouveret syndrome: axial plain CT (A), coronal CECT (B), and sagittal CT with oral positive contrast (C) images showing evidence of a radio-dense calculus lodged in the duodenum with distended stomach (*), pneumobilia, and contrast lined fistula between the gallbladder and the duodenum. T2 axial (D), coronal (E), and volume rendered image (F) demonstrate a duodenal calculus with a fistulous track. CECT, contrast-enhanced computed tomography; CT, computed tomography.
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Fig. 19 Gallstone ileus: (A) abdominal radiograph showing pneumobilia (dashed arrow) and small bowel obstruction (solid arrows). (B–D) CT in coronal and axial sections confirms air in the common hepatic duct (dashed arrow) with fistulization with the duodenum first part and an ectopic gallstone (solid arrow) causing small bowel obstruction. CT, computed tomography.
Zoom
Fig. 20 Gallstone ileus: (A) CT scanogram showing small bowel obstruction (solid arrow) with a linear lucent area in the right hypochondrium (dashed arrow). (B, C) CT in the coronal plane (inset in axial) showing dilated small bowel with a dense filling defect (with faint fat and calcium) in the distal jejunum (solid arrow) and cholecystoduodenal fistula (dashed arrow). (D–F) Intraoperative images showing the site of obstruction. Enterotomy and stone removal were done. CT, computed tomography.
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Fig. 21 (A, B) T2 axial sections showing cholelithiasis (solid white arrow) and choledocholithiasis (dashed arrow). The pancreas is diffusely bulky, edematous with surrounding inflammation (black arrows)—gallstone-induced acute interstitial pancreatitis.
Zoom
Fig. 22 CECT in axial (A) and coronal (B) sections showing an irregular enhancing mass replacing the gall bladder—carcinoma with contiguous liver extension. Note the gallstone (dashed arrow). CECT, contrast-enhanced computed tomography.