16 Contrast-Enhanced Ultrasound (CEUS) in Biliary Diseases

The contrast dose for CEUS of the gallbladder wall is equal to that of the liver. The major and minor arteries of the gallbladder enhance with the hepatic arteries. In case a linear high frequency probe is being used, the dose has to be much higher, and doubled in most cases. After bolus injection in a peripheral vein, an arterial phase (< 30 s) can be differentiated from the late phase (> 31 s). The CEUS study of the gallbladder wall should aim at the evaluation of its perfusion, contrast kinetics, branching intramural vessels, and the intactness of the gallbladder wall.^{1 – 5} After completing the gallbladder study, the liver should be assessed in the late phase, exploiting the same contrast injection, searching for focal liver lesions.

16.3 Pathologic Findings

16.3.1 Cholecystitis and Cholangitis

Acute cholecystitis is associated with cholelithiasis in a vast majority of patients. Acalculous cholecystitis accounts for about 5% to 10% of cases.^{6 ,​ 7} It is associated with a higher incidence of gangrene and perforation compared to a calculous disease. In acute cholecystitis, the inflammatory process may involve the adjacent liver tissue (“reactive hepatitis”)^{8 – 10} causing a hepatic hyperenhancement on CEUS during the early hepatic arterial phase ( Fig. 16.1a,b). This sign might be helpful in cases of acute cholecystitis without thickening of the gallbladder wall. Acute cholecystitis may cause complications such as gangrenous, perforated, or emphysematous cholecystitis (Fig. 16.1c–e). Symptoms and clinical signs can be indistinguishable from those of uncomplicated acute cholecystitis that does not require CEUS.^{11 – 13} A gangrenous cholecystitis is defined as a transmural necrosis of the gallbladder wall, accounting for approximately one-third of all cases of acute cholecystitis.^{14 ,​ 15} This causes a discontinuous or irregular gallbladder wall on CEUS.^{16 ,​ 17} With transmural necrosis, the afferent nerves die and although the inflammation spreads to the adjacent parietal peritoneum, local symptoms will diminish (Fig. 16.1a–e, Fig. 16.2a–c). Detection of a transmural necrosis is of utmost importance as it precedes perforation and can be detected by using US contrast agent (CA). Despite conventional US, most gangrenous or perforated cholecystitis are rarely diagnosed preoperatively but are still detected during surgery.^{10 ,​ 18 ,​ 19} CEUS should therefore be considered in patients regarded to be at risk for complicated acute cholecystitis.^{2 ,​ 20 – 23}

The risk of gallbladder cancer is increased in case of gallbladder wall thickening in older patients with chronic cholecystitis and gallbladder stones, mostly in females. Superficial or infiltrating gallbladder carcinoma is mostly present with a diffuse thickening of the gallbladder wall, making it hard to visualize the tumor on baseline US. A gallbladder filled with stones or sludge may obscure a malignant tumor as well.^{5 ,​ 24 ,​ 25} As a result, CEUS may help to detect silent carcinoma earlier (for criteria, see 16.3.2: Fig. 16.3, 16.4, 16.6, 16.7, 16.8). Cholangitis also results in thickening of the gallbladder wall, and inflammation causes hyperperfusion of the gallbladder wall (Fig. 16.3a,b; Fig. 16.4a,b).

Polypoid lesions of the gallbladder are commonly seen on ultrasonography (2.6% to 12.1% of cholecystectomy specimens²⁶). It has been proposed that all preinvasive adenomas and papillary neoplasms > 10 mm should be described as “intracholecystic papillary-tubular neoplasms” (ICPTNs) regardless of the phenotype of tumor cells.³⁴ Gallbladder resection is recommended in patients with polyps > 10 mm³¹ and in patients with imaging evidence of vascular stalks. While polyps have a small, unrecognizable stalk, often on B-mode, adenomas have a wider vascular stalk, best seen on contrast study.^{27 ,​ 35} Adenomas originating from the glandular epithelium of the gallbladder represent 0.5% of cholecystectomy specimens.^{24 ,​ 36} Due to the small number of cases it remains unclear if CEUS can substantially contribute to the differentiation of ICPTNs, especially the differentiation between polyps, adenomas, and noninvasive gallbladder carcinoma.^{30 ,​ 33} Adenomas of size > 10 mm with a wide stalk and hyperenhancement during the arterial phase was described. Tumor enhancement was homogeneous with a “fast in–fast out” between 35 and 50 s. In contrast, polyps > 10 mm show iso- and inhomogeneous enhancement patterns that may be a criterion to differentiate adenomas from cholesterol polyps. However, the number of published cases to date is too small to give a valid recommendation^{1 ,​ 3 ,​ 29 ,​ 37} ( Fig. 16.5 ).

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