NMT » Case Studies » Current Case


CCK EVALUATION OF CHOLECYSTITIS


Jennifer Fry, Student NMT
Corey Jones, CNMT, RT(N)
Athens Regional Medical Center


Mary Anne Owen, M.H.E., RT(N),
Program Director, NMT
Medical College of Georgia

 

 

NM Technologists Concerns (click to view)
ORGAN/
PATHOLOGY
RPH AND DOSE
METHOD OF
LOCALIZATION
METHOD OF ADMINISTRATION
ROUTE OF EXCRETION
BIODISTRIBUITON
PITFALLS
 
Gallbladder
Acute
Cholecystitis
 
 
 
 
 
 
 
 
 
 
 
Choletec
(mebrofenin)
6.5 mCi
Other imaging options?
(Disofenin, Lidofenin?)
 
CCK
1.0 ug
 
 
Active
Transport via bile excretory pathways
 
IV
 
Bowel / Renal
 
5min-liver brighter
          than blood
          pool
10min-no vascular
           pool
15min-biliary
30min-gallbladder
60-bowel
90-normal visualize
     GB and bowel
 
Narcotics
High bilirubin levels

Use IDA agent appropriate for bili level

Pt. not NPO at least 4 hours demonstrate 70% false positive
COLLIMATOR
MODE
(D or PL)
COUNTS OR
TIME
VIEWS
ENERGY
WINDOWS
PATIENT
PREP
DRUG INTERVENTIONS
AND FINDINGS
 
 
Low energy-
All purpose
 
 
 
 
 
 
 
 
 
 
Dynamic
 
Flow Acquisition Parameters?
Frame Time?
 
N/A
 
Counts or Time of any statics?
 
Anterior 10 degree LAO -- To separate the bowel from the GB
 
Computer Processing:
Anything special about maintaining a good ROI?
 
 keV?
Window Percentage?
 
NPO 4-6 hours
 
CCK:  rate varies according to clinical setting general range,: .01-.03 ug/kg reconstituted with 5ml of sterile water, injected over 2-4 minutes or via pump drip in 250 ml over 1 hour.
 
For non-visualization of GB by 1 hour, can administer Morphine at 0.04 mg/kg (Max. 2-3mg) given over a 3 minute infusion
 
EF < 35% is abnormal
 
Non visualization of GB by 4-12 hours is considered Acute Cholecystitis
Acute Cholecystitis

 

 

Detailed Discussion (click to view)

The gallbladder is an approximately 2.5 cm x 7 cm sac, which is capable of holding 50 ml of bile. The majority of bile secreted by the liver enters the gallbladder where it is concentrated and stored. The rhythmic contractions of the gallbladder occur at a rate of 2 to 6 minutes. When the gallbladder is stimulated it has tonic contractions that last from 5 to 30 minutes. The primary hormone that causes gallbladder contraction is called cholecystokinin (CCK).

 

A patient with acute cholecystitis usually presents right upper quadrant pain accompanied by tenderness. Nausea and vomiting are also common symptoms. Although ninety five percent of these patients have gallstones with obstruction of the cystic duct, in this case no gallstones were present. Less than five percent of patients with acute cholecystitis do not have gallstones (Early & Sodee , 1995).

 

The radiopharmaceuticals used for cholecystography are mebrofenin (Choletec), disofenin (DISIDA / Hepatolite), and Lidofenin (HIDA). All of these are labeled with technetium-99m. The method of localization is active transport via the hepatocytes and bile excretory pathways. The numerous receptor binding sites on the hepatocytes are responsible for hepatic uptake. In patients with high bilirubin levels, the Tc-99m IDA uptake is compromised due to the fact that bilirubin competes with IDA derivatives. With Choletec the hepatic duct and gallbladder may be seen at 10-15 minutes. Intestinal activity is seen at 30-60 minutes. Gallbladder studies using the Tc-99m IDA deriviatives is useful in determining the difference between acute and chronic cholecystitis. In acute cholecystitis, the gallbladder is not visualized for as long as four hours after administration of the tracer. With chronic cholecystitis, the gallbladder nay not be seen in the first hour, but is visualized in delayed images.

 

Normal biodistribution:
5 min- liver brighter than blood pool

10 min- no vascular pool

15 min- biliary activity

30 min- gall bladder

60 min- bowel

90 min- all normals visualize gallbladder and bowel

 

The hormone cholecystokinin (CCK) causes the gallbladder to contractand increases gastro-intestinal motility and the secretion of bile. CCK may be given with the Tc-99m IDA scan. In the case of acute cholecystitis, the gallbladder does not clear upon stimulation with CCK because CCK does not have any effect on cystic duct obstruction. In chronic cholecystitis, the gallbladder does clear with CCK stimulation.

 


Patient History

A 42 year -old female entered the emergency department suffering from severe right side abdominal pain, nausea, vomiting and dehydration. The patient was admitted into the hospital. An ultrasound of the abdomen was performed. No gallstones were found, however, prominent gallbladder wall thickening was present. No biliary ductal dilation or liver lesions were found. Acute cholecystitis was of concern and a nuclear medicine HIDA scan was ordered for further evaluation.



Radiopharmacy

6.5 mCi Choletec ( mebrofenin), followed by subsequent reinjection with 1.0 ug of Cholecystokinin (cck). These injections were made by intravenous method.

* T1/2 of Tc99m MEBROFENIN CHOLETEC = 6 hour
* Method of Localization : Active Transport, binds to change pathways of bilirubin. It is taken up by the hepatocytes
* Method of Excretion: Primary route of excretion is through the hepatobiliary system (80%-90%) and the secondary route is the urinary tract (10%-20%)
* Method of calculating CCK dose:

Patient weight converted to kg (lb/2.2) then multiply by.02. This equals the ug CCK dose to be put into a 250 ml bag of saline for one hour infusion.



Procedure


Patient Prep: NPO 4-6 hours



Instrumentation

 

Low energy, all purpose collimator
128 x 128 matrix
140 kev energy window

Instructor's Comments:
Q: Dynamic or static?
Q: Counts, Time per frame?



Positioning

Patient supine, 10 degree LAO , anterior images obtained for approximately one hour.

The patient was given 6.5 mCi Tc 99m CHOLETEC by intravenous administration. A one hour delay was observed. The patient was then given 1.0 ug of CCK in 250 ml of saline. This was infused through the existing IV line.

Instructor's Comments:
Q: Is this done by injection pump? If so, set at what rate?

Uptake of activity by the gallbladder as well as the small bowel was observed. A markedly abnormal negative ejection fraction was identified. It was elected to proceed with another attempt at CCK administration due to questionable infiltration and amount of CCK previously administered. Repeat imaging was performed following administration of a second CCK dose. The ejection fraction was then found to be an abnormal 1.87%. Normal is approximately 35%. The cystic duct and distal common bile duct remained patent.



Followup


The patient did have her gallbladder surgically removed.



References (click to view)

Early, Paul J. & Sodee, Bruce D. (1995). Principles and Practice of Nuclear Medicine. Second edition. St. Louis: Mosby.


Saha, Gopal B. (1998). Fundamentals of Nuclear Pharmacy. Fourth edition. New York: Springer.


Williams, S. (2001). Nuclear Medicine on the Internet. Available Online: URL http://www.auntminnie.com/ScottWilliamsMD2/nucmed/Gastrointestinal/GI%20table%20of%20contents.htm