Nuclear scintigraphic studies are useful in confirming cholecystitis and for differ-
entiating between acute and chronic cases, in selected patients. 99m-Tc iminodiacetic acid
derivates (i.e., HIDA and its derivates) are injected intravenously, are taken up by hepatocytes,
and are then transported into the biliary system in a fashion similar to bilirubin. Nonvisualization
of the gallbladder at four hours has 99% specificity for diagnosing cholecystitis. Intravenous
morphine may be administered if initial images do not demonstrate the gallbladder, to cause
sphincter of Oddi spasm, increasing biliary pressure and forcing radiotracer into a chronically
inflamed gallbladder, but not in acute gallbladder inflammation (3).
MRI findings of acute cholecystitis include a distended gallbladder with stones, gallbladder
wall thickening and edema, and increased signal in the pericholecystic fat on T2-weighted
images. MR cholangiopancreatography (MRCP, i.e., multi-planar heavily T2-weighted images)
can be used to visualize obstructing stones within the biliary tree with a high degree of accuracy
in patients with suspected cholecystitis and/or cholangitis, which are seen as filling defects and/
or a cutoff of the common duct (3).
Mimic of Calculous Cholecystitis
Approximately 90% of cases of cholecystitis are associated with stones, but 10% occur without
them, i.e., acalculous cholecystitis (AC). The precise etiology of AC is still not fully understood.
Existing theories propose the noxious effect of superconcentrated bile due to prolonged fasting
and the lack of cholecystokinin-stimulated emptying of the gallbladder. Gallbladder wall
ischemia from low-flow states in patients with fever, dehydration, or heart failure has also
been proposed. The disease occurs in very ill patients, such as those on mechanical ventilation
or those having experienced severe trauma or burns. Mortality is much higher with AC, as the
entity is much more prone to gangrene and perforation (20,22,23).
AC has proven to be an elusive diagnosis to make, both clinically and radiologically. In
the appropriate clinical context, in any patient with presumed cholecystitis without
demonstration of stones on either ultrasound, CT, or MR, AC should be the leading diagnosis.
Prior studies have shown decreased sensitivity for both ultrasound and nuclear medicine
studies in the detection of AC. Sonographic findings include an enlarged gallbladder, diffuse
or focal wall thickening with focal hypoechoic regions, pericholecystic fluid, and diffuse
homogeneous echogenicity (possibly from debris) in the gallbladder lumen without identi-
fiable calculi. Visualization of the gallbladder on HIDA scans is possible in some cases of AC
due to a patent cystic duct, leading to false negatives. False positives on HIDA scans may also
occur since parenteral alimentation, prolonged fasting, and hepatocellular dysfunction, all seen
in the critically ill, are the same factors that cause nonvisualization of the gallbladder despite
lack of acute or chronic inflammatory gallbladder disease (23,24).
Figure 9 (A) Ultrasound examination demonstrates a thickened gallbladder wall, pericholecystic fluid, and
gallstones (arrow). Correlating with a positive sonographic Murphy’s sign, these findings were diagnostic of acute
cholecystitis in this patient. (B) Contrast-enhanced CT scan of the abdomen in the same patient demonstrates
increased enhancement of the gallbladder wall and pericholecystic fluid, but the gallstones are not identifiable.
Radiology of Infectious Diseases and Their Mimics in Critical Care 83