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The gallbladder is an ovoid cystic organ along the undersurface of the liver at the interlobar fissure, between the right and the left lobes of the liver. Although the size and shape of the gallbladder vary with the fasting state, it is approximately 10 cm long and 3 to 5 cm in diameter. The normal capacity of the gallbladder is approximately 50 mL. The normal gallbladder wall is 2 to 3 mm in thickness and composed of columnar epithelium. The gallbladder connects with the biliary tree via the cystic duct, measuring 2 to 4 cm in length and 1 to 5 mm in caliber, characterized by prominent concentric folds, known as the spiral valves of Heister . The cystic duct usually joins the extrahepatic bile duct halfway between the porta hepatis and the ampulla of Vater. Variant anatomy, such as low medial cystic duct insertion, occurs approximately 20% of the time.
The function of the gallbladder is to store and concentrate bile. As such, the T1-weighted appearance of the gallbladder lumen varies with the concentration of the bile. In general, bile salts are of increased signal intensity on T1-weighted imaging in the fasting state; however, the bile salt and protein concentration affects the degree of the T1-weighted signal intensity. The gallbladder contents demonstrate increased signal on T2-weighted imaging as a result of the static fluid content of bile.
MRI of the gallbladder should be performed in a manner similar to other abdominal imaging protocols. When possible, the patient should fast for at least 4 hours to promote adequate gallbladder distention. In addition, the use of newer contrast agents with increased hepatobiliary excretion can provide limited information regarding gallbladder and biliary function.
When there is aberrant branching of the foregut during development, gallbladder anomalies potentially arise. Frequently these anomalies are a part of a larger picture of heterotaxy syndrome with more significant anomalies (ie, cardiac and pulmonary). Congenital and developmental anomalies of the gallbladder are often incidentally noted at autopsy; their only clinical relevance is for presurgical planning ( Fig. 4.1 ).
Cholelithiasis (or gallstones) is the most common gallbladder disorder by a wide margin, afflicting 10% of the population. Risk factors include obesity, pregnancy, rapid weight loss, and estrogens, with women being affected twice as often as men. Although most often asymptomatic, pain (or biliary colic) occasionally ensues. Cholelithiasis is also the usual culprit in acute and chronic cholecystitis.
Gallstones appear as filling defects within the gallbladder lumen. The rigid internal structure of gallstones facilitates relaxation resulting in signal voids—best visualized against the bright background of fluid in T2-weighted images ( Fig. 4.2 ). The two dominant forms of gallstones feature slightly different imaging findings. Cholesterol stones—the more common variety (80%)—are decreased in signal intensity on all pulse sequences. Pigmented stones are hypointense in T2-weighted images, but exhibit variable T1 signal depending on the degree of hydration. Regardless of the composition, the sensitivity of MRI for detecting gallstones approaches 100%.
Acute inflammation of the gallbladder is caused by cystic duct obstruction in the majority of cases. At imaging, gallstones are identified in the gallbladder and/or cystic duct as signal voids best visualized in T2-weighted images. Associated findings include mural thickening (>3 mm), mural hyperemia (as evidenced by hyperenhancement on postgadolinium images), and occasionally, transient adjacent hepatic hyperemia in immediate postgadolinium images ( Fig. 4.3 ). Pericholecystic inflammatory changes and fluid are best appreciated in T2-weighted and postcontrast images ( Fig. 4.4 ). Occasionally abscesses may form within or outside the gallbladder wall ( Fig. 4.5 ). Acute acalculous cholecystitis accounts for the remainder of the cases of acute cholecystitis and is often related to decreased gallbladder motility, decreased blood flow, or bacterial infection.
In chronic cholecystitis, mural enhancement is mild and most prominent in delayed postgadolinium images, related to fibrosis within the gallbladder wall ( Fig. 4.6 ). In addition, the gallbladder is often small and/or contracted with no adjacent hepatic hyperemia. The gallbladder wall may calcify, resulting in a porcelain gallbladder.
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