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Cholecystokinin (CCK) Hepatobiliary Scan in Acalculous Disorder of the Gall Bladder
Written by Tatiana Kain, M.D.
September 22, 2000

Persistent recurrent right upper quadrant pain and biliary colic are common symptoms in the general population. Most patients who present with these symptoms undergo routine right upper quadrant ultrasound and /or nuclear medicine hepatobiliary scan. These studies are frequently normal. A large number of patients with normal results, however, may suffer from chronic cholecystitis caused by inflammation of the gallbladder wall, gallbladder dyskinesia or cystic duct syndrome. Gallbladder dyskinesia is believed to be a result of an abnormal distribution of cholecystokinin (CCK) receptors within the gallbladder wall. Cystic duct syndrome is caused by partial, noncalculous obstruction of the cystic duct and is frequently associated with fibrosis, adhesion, or kinking. These conditions are greatly relieved by cholecystectomy.

Nuclear medicine plays a major role in detecting patients with the above conditions. Today we are able to study the motor function of the gallbladder by performing hepatobiliary imaging in conjunction with CCK stimulation. This physiologic test provides information concerning the gallbladder's response to CCK, which is measured by the gallbladder ejection fraction (GB EF). Cholecystokinin ( CCK: Karolyski Institute, Stockholm, Sweden) is a 33–amino acid polypeptide hormone. In vivo, CCK is released into the circulation from the duodenal mucosa in response to food containing fat, amino acids, and lipolytic products. Subsequently, CCK binds with CCK receptors in the gallbladder wall causing contraction of the gallbladder. Other functions of CCK include relaxation of the sphincter of Oddi.

PROCEDURE PROTOCOL
Fasting patient receive an intravenous injection of 5 mCi of Tc– 99m DISIDA. One hour later, and only after the gallbladder has filled, imaging is performed with a large field of view gamma camera using a low energy collimator, 20% window, and stored in a 64x64x16 matrix. The patient should be placed supine in approximately 10 degree LAO position. The technologist should obtain best separation of the gallbladder from the overlying structures. When this task is achieved, computer acquisition of the images should be started. Only if the gallbladder has filled, the patient should receive intravenous injection of CCK (CCK–8, or sincalide, commercially named Kinevac, Squibb). The CCK dose is calculated to 0.02 mcg/kg i.v. The injection should be performed slowly and continuously over a 3 minute period. During the injection and up to 10 minutes following it, the patient should be monitored by qualified medical personnel (nurse or physician). Please note that adverse reactions of CCK include nausea, abdominal pain, and/or discomfort. These symptoms may be reduced or avoided if the injection is performed slowly.

Gallbladder ejection fraction ( GB EF ) is next calculated (See Figures 1a and 1b).

GB EF=( Pre CCK GB counts–Post CCK GB counts)
Pre CCK GB counts

The normal gallbladder ejection fraction is 35% or higher. The sensitivity and specificity for this test are 82–100% and 87–100%, respectively, when maximum gallbladder EF in response to CCK challenge is calculated as shown above. The positive predictive value for this test in identifying patients with acalculous GB disease is 90–100% (see references below). The correspondingly high negative predictive value of the test should assure the clinician that, if the test is negative, the patient's symptoms are not related to acalculous gallbladder disease.

References

  1. Bobba VR, Krishnamurthy GT, Kingston E, Turner FE, Brown PH, Langrell K. Gallbladder dynamics induced by fatty meal in normal subjects and in patients with gallstones. J Nucl Med 1984;25:21–24.
  2. Fink–Bennett D, DeRidder P, Kolozsi WZ, Gordon R, Jaros R. Cholecystokinin cholescintigraphy : Detection of abnormal gallbladder motor function on patients with chronic acalculous gallbladder disease. J Nucl Med 1991;32:1695–9.
  3. Fink–Bennett D. Augmented Cholescintigraphy: Its role in detecting acute and chronic disorders of the hepatobiliary tree. Seminars in Nuclear Medicine 1991;21:128–139.
  4. Krishnamurthy S, Krishnamurthy GT. Cholecystokinin and morphine pharmacological intervention during Tc–99m– HIDA cholescintigraphy: A rational approach. Seminars in Nuclear Medicine 1996;26:16–24.

 
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