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Hida scan and imaging

1. HIDA SCAN
OSR
Dr. Yash Kumar Achantani

2. Definition
HIDA scan also known as Hepatobiliary scintigraphy is a radionuclide
diagnostic imaging study that evaluates hepatocellular function and
patency of the biliary system by tracing the production and flow of bile
from the liver through the biliary system into the small intestine.
Sequential images of the liver, biliary tree and gut are obtained.
The term HIDA came from the
Application of the study i.e. H-hepatic function
And pharmaceutical agent used for this i.e. IDA-2 lidocaine analogs
bichelatedto 99mTc by iminodiaceticacid (IDA).

3. Hepatobiliary physiology

6. Common Indications
A.Functional assessment of the hepatobiliary system
B. Integrity of the hepatobiliary tree
These broad categories include, for example:
• Evaluation of suspected acute cholecystitis.
• Evaluation of suspected chronic biliary tract disorders.
• Evaluation of common bile duct obstruction.
• Detection of bile extravasation.
• Evaluation of congenital abnormalities of the biliary tree.

7. Procedure

8. Patient Preparation
To permit gallbladder visualization, the patient must have fasted for a
minimum of two, and preferably four hours prior to administration of
the radiopharmaceutical.
If the patient has fasted for longer than 24 hr or is on total parenteral
nutrition the gallbladder may not fill with tracer. In these cases the
patient may be pretreatedwith Sincalide.

9. History
1. History of previous surgeries, especially biliary and gastrointestinal.
2. Time of most recent meal.
3. Current medications, including the time of their most recent
administration (with particular attention to opioid compounds).
4. Results of bilirubin and liver enzyme levels.
5. Results of gallbladder or abdominal ultrasound.

10. Precautions
The test should be performed fasting to avoid a false-positive result.
Interference by opioids can be minimized by delaying the study for 4
hours after the last dose.

11. Radiopharmaceutical
The discovery of 99mTc-hepatobiliary (HIDA) radiopharmaceuticals was by
chance. During investigation for a cardiac imaging radiopharmaceutical, it
was found that 99mTc-labeled lidocaine was not a good cardiac imaging
agent but cleared through the hepatobiliary system.
With chemical modification, 99mTc-HIDA imaging agents were born.
Its structure is simply that of 2 lidocaine analogsbichelatedto 99mTc by
iminodiaceticacid (IDA).

13. Other modifications
99mTc disofenin(diisopropyl-IDA). It provided images of diagnostic quality
with bilirubin levels of as high as 25–30 mg/dL.
99mTc-mebrofenin(bromotriethyl-IDA) was approved. It had higher liver
extraction (98% vs. 89%) and more rapid biliary clearance than 99mTc
disofenin(half-life of 19 min vs. 17 min).
After intravenous injection, 99mTc-HIDA radiopharmaceuticals
are transported in the blood bound to serum albumin. They dissociate
from albumin in the hepatic perisinusoidalspace and are extracted by
hepatocytes by receptor-mediated endocytosis, similar to bile salts, free
fatty acids, and bilirubin. They then follow the same metabolic pathway as
bilirubin, except that they are secreted into biliary caliculiunchanged,
without undergoing conjugation.

14. Image Acquisition
A large field of view gamma camera equipped with a low energy all-
purpose or high-resolution collimator is usually used.
For a smaller field of view gamma camera a diverging collimator may be
needed.
Continuous computer acquisition (usually in the anterior view) should
be performed (1 frame/min for 30–60 min).
Imaging should start at injection and continue serially for 60 min or until
activity is seen in both the gallbladder (which confirms patency of the
cystic duct) and the small bowel (which confirms patency of the
common bile duct).

15. Additional views (e.g., right lateral, left or right anterior oblique) may
be obtained as needed to clarify anatomy.
When acute cholecystitis is suspected and the gallbladder is not seen
within 40–60 min, 3–4 hr delayed images should be obtained, or
morphine augmentation may be employed instead of delayed
imaging.
Delayed imaging at 18–24 hr may be necessary in some cases (e.g.,
severely ill patient, severe hepatocellular dysfunction, suspected
common bile duct obstruction, suspected biliary atresia).
If the patient is being studied for a biliary leak, 2–4 hr delayed
imaging and patient-positioning maneuvers(e.g., decubitus views)
may be helpful.

16. Interventions
A variety of pharmacologic or physiologic interventions may
enhance the diagnostic value of the examination.
Sincalidepretreatment: Sincalide, a synthetic octapeptideof
cholecystokinin (CCK), in doses of 0.01–0.02 μg/kg, may be given
intravenously, 30–60 min prior to the hepatobiliary tracer
injection to minimize the potential for a false-positive study (e.g.,
in patients who have fasted longer than 24 hr, or NPO).
Sincalideshould be administered slowly (over a 3–5 min
duration) to prevent biliary spasm and abdominal cramps. A
slower infusion (30–45 min) may also be used.

17. Morphine Sulfate: When acute cholecystitis is suspected and the
gallbladder is not seen by 40-60 min, morphine sulfate, 0.04–0.1 mg/kg,
may be administered intravenously over 2-3 min.
If the cystic duct is patent, flow of bile into the gallbladder will be
facilitated by morphine induced temporary spasm of the sphincter of oddi.
The intrahepatic biliary tree and common bile duct (CBD) must contain
radioactive bile, and tracer activity should be present in the small bowel at
the time of morphine injection.
Imaging is usually continued for another 30 min following morphine
administration but may be extended if desired.
Contraindications to the use of morphine include respiratory depression in
non-ventilated patients (absolute), morphine allergy (absolute) and acute
pancreatitis (relative).

18. Sincalidestimulation: Gallbladder contractility may be evaluated by
determining the gallbladder ejection fraction (GBEF) response to
sincalide.
The study involves an intravenous injection over a minimum of 3 min
or a 30-45 min infusion of 0.01-0.02 μg/kg sincalideafter the
gallbladder is maximally filled with radiopharmaceutical (usually 60
min after the injection) and there is minimal activity in the liver.
Computer acquisition (1-2 frames/min) thencontinues for 30 min.
Phenobarbital: In jaundiced infants in whom biliary atresia is
suspected, pretreatmentwith phenobarbital, 5 mg/kg/day, may be
given orally in two divided doses daily for a minimum of 3–5 days prior
to the hepatobiliary imaging study to enhance the biliary excretion
of the radiotracer and increase the specificity of the test.

19. Processing
Gallbladder ejection fraction (GBEF): Using the immediate pre-sincalide
and the post-sincalidedata, regions of interest (ROI) are drawn around the
gallbladder (taking into account patient motion) and adjacent liver
(background) using any standard nuclear medicine software package.
The liver background ROI is selected taking care to exclude ductal activity.
GBEF is calculated from the gallbladder time-activity curve as:

20. Interpretation Criteria
Normal:
A normal hepatobiliary scan is characterized by immediate
demonstration of hepatic parenchyma, followed sequentially by
activity in the intra-and extrahepatic biliary ductal system, gallbladder
and upper small bowel.
All these structures should be seen within one hour. Gallbladder filling
implies a patent cystic duct and excludes acute cholecystitis with a
high degree of certainty.

21. Uniform radiotracer activity throughout the liver
Prompt excretion into the bile ducts
Radioactivity tracer activity seen in the gallbladder after 10 min
Ongoing accumulation of radiotracer over the 30 min study

22. Normal HIDA scan
taken at
4min/frame

23. (Left) Anterior Tc-99m HIDA hepatobiliary scan in a patient post cholecystectomy
shows normal hepatic uptake and biliary-to-bowel transit without a bile leak.
(Right) Anterior Tc-99m HIDA hepatobiliary scan in a patient with right upper
quadrant pain shows normal gallbladder and bowel activity.

24. (Left) Normal hepatobiliary scintigraphy study shows. GB , cystic duct and CBD
Note faint radiotracer in the liver and bowel.
(Right) MRCP 3D reconstruction of the biliary system in patient post
cholecystectomy is shown. Left and right intrahepatic ducts , CBD , second
portion of duodenum, gallstone in the distal CBD.

25. Acute cholecystitis
Acute calculous cholecystitis (ACC): No GB visualization on hepatobiliary
scintigraphy due to cystic duct obstruction secondary to gallstone
impaction
Acute acalculouscholecystitis (AAC): No GB visualization on hepatobiliary
scintigraphy secondary to cystic duct obstruction not related to gallstones.
•Absence of GB filling in 1st hr of imaging
•No GB visualization despite IV morphine sulfateadministration or
delayed 4 hr images
•Partial GB filling in 15% of AAC cases

26. Low-grade common bile duct (CBD) obstruction
Delayed biliary-to-bowel transit > 1 hr but < 24 hrs
High-grade CBD obstruction
Delayed biliary-to-bowel transit on hepatobiliary scintigraphy > 24 hrs
Persistent hepatogram
Angiographic phase
Hyperemicblush in GB fossa represents GB inflammation.
Abscess or gangrene in 36% of patients with hyperemia.
Rim sign
Hepatic retention of tracer due to adjacent inflammation around GB fossa
with no GB filling Seen within 1st hr of imaging
Although radiotracer clears from liver, rim sign persists on delayed images.
Seen in 20% of acute cholecystitis cases
Almost 50% of cases with rim sign have complicated cholecystitis
GB ulceration/necrosis, Fibrinous exudate/empyema, Gangrene Perforation

27. Imaging acquisition
–Patient supine
–Image over abdomen
–Large field-of-view camera equipped with low-energy all-purpose or
high-resolution collimator
–Matrix: 128 x 128
–Angiographic phase x 1 min (4 sec/frame)
–Dynamic acquisition (1 frame/min) for 60 min
Delayed images as necessary
-If small bowel is present but no GB within 60 min
-Morphine sulfate0.04 mg/kg or standard 2 mg dose IV over 2-3 min and
additional imaging up to 60 min to evaluate for GB uptake.
-If morphine contraindicated, 4 hr delayed images to evaluate for GB
uptake

28. If GB is present but no small bowel within 60 min
•Continue delayed imaging up to 24 hr to evaluate for biliary-to-
bowel transit.
•Oral fatty meal or IV CCK infusion to contract GB if no
contraindication.
Dosimetry
GB wall receives highest dose

29. (Left) Hepatobiliary scan in a patient with acute cholecystitis shows no activity
in the GB on post-morphine images . A rim sign is evident on delayed images, signifying
hyperemia.
(Right) The duodenal bulb mimics GB filling on early hepatobiliary scintigraphy
images. Over time, the radiotracer moves from the bulb. At 45 min, the GB is
identified and radiotracer has washed out of the duodenal bulb .

30. (Left) Hepatobiliary scintigraphy shows GB fossa blush on angiographic
phase and a rim sign . The GB was not visualized in this patient with acute
acalculouscholecystitis.
(Right) Axial CECT in the same patient shows marked GB and cystic duct wall
enhancement. Note the lack of enhancement in the posterior GB wall
consistent with necrosis, increasing risk of perforation

31. (Left) Hepatobiliary scintigraphy shows abnormal blood flow with poor hepatic
uptake of radiotracer. At 1 hr and 24 hr, blood pool activity remains high. These
findings suggest severe hepatic dysfunction and limit the evaluation of acute
cholecystitis.
(Right) Hepatobiliary scintigraphy shows persistent hepatogramwith no GB or small bowel
activity on 24 hr images, consistent with high-grade CBD obstruction.

32. (Left) Axial CECT in a patient post cholecystectomy shows enhancement of the
cystic stump and pericysticfat stranding suggestive of cholangitis. No stones are
identified.
(Right) Hepatobiliary scintigraphy in the same patient shows activity in the CBD .
On 24 hr delayed images, the entire CBD is evident, but lack of bowel activity
suggests highgradeCBD obstruction. MRCP confirmed distal choledocholithiasis.

33. (Left) Hepatobiliary scintigraphy shows photopenicdefect in the liver parenchyma.
On later images, activity is evident in this region suggestive of intrahepatic GB.
(Right) Coronal CECT in the same patient shows the intrahepatic GB.

34. (Left) Hepatobiliary scintigraphy in a patient post cholecystectomy with
hyperbilirubinemia shows no biliary-to-bowel transit to 24 hrs of imaging.
Retained gallstones in the CBD are suspected.
(Right) Cholangiogram in the same patient shows a CBD clip and no gallstones.

35. (Left) Hepatobiliary scintigraphy shows heterogeneous filling of the GB with
central photopenia. Enterogastricreflux of bile is also evident.
(Right) Axial CT shows a fundal GB mass with pericholecysticstranding,
consistent with primary neoplasm.

36. (Left) Hepatobiliary scintigraphy shows abnormal pattern of GB filling, possibly a
congenital anomaly or choledochalcyst.
(Right) Coronal CT in the same patient confirms a partially septated, bilobedGB.

37. (Left) Hepatobiliary scintigraphy shows progressive accumulation of activity
inferior to the left hepatic lobe and normal biliary-to-bowel transit.
(Right) Axial CECT in the same patient correlates with GB. Note the malrotated
kidney as well.

38. (Left) Hepatobiliary scintigraphy shows normal angiogram and persistent
hepatogramwith no GB or bowel activity on images to 12 hrs, suggestive of high-
grade CBD obstruction in a patient with marked jaundice.
(Right) Coronal CECT in the same patient shows a pancreatic head mass
obstructing the distal CBD.

39. (Left) Hepatobiliary scintigraphy in a patient with a pancreatic mass shows central
photopenicdefect , a large liver metastasis. Note left intrahepatic biliary drain.
Small bowel is identified on delayed images confirming patency of the CBD stent.
PhotopenicGB fossa on delayed images suggests either acute cholecystitis or
tumorinvolvement of the cystic duct.
(Right) Coronal CT in the same patient shows CBD stent and distended GB without
tumorinvolvement .

40. (Left) Hepatobiliary scintigraphy in a patient post laparoscopic cholecystectomy
is shown. No small bowel is visualized on 24 hr delayed static image. High-grade
CBD obstruction is suspected.
(Right) MRCP reconstruction in the same patient shows choledocholithiasis.

41. Mimics of acute cholecystitis on hepatobiliary scan
○Bowel loop simulating GB (especially duodenal bulb)
○15% of AAC has visualization of GB (false negative)
○Bile leak due to GB perforation
○Congenital anomaly simulating GB
○Renal excretion of radiotracer
Mimics of high-grade CBD obstruction on hepatobiliary scan
○Low-grade, partial, or intermittent CBD obstruction
–Poor clearance from biliary ducts and delayed transit into small
bowel > 60 min
–Small or transient stones in CBD
–Normal lab values

42. Biliary Leak
Focal collection or free flow of bile into abdomen
○Usually postsurgical complication
Tc-99m IDA hepatobiliary scintigraphy: Radiotracer found outside
normal biliary system or small bowel
–Abnormal activity usually starts in gallbladder (GB) fossa, porta
hepatis, near cystic stump as biloma
–Reappearing liver sign: As radiotracer decreases in liver parenchyma
over time, focal leak projecting over liver increases over time
–Radiotracer can track inferior to right hepatic lobe → right paracolic
gutter/Morison pouch, over liver dome, or freely into peritoneum
–Near biliary enteric anastomosis after liver transplant
–Bile may flow through surgical drainage tubes
–Bile may spread to retroperitoneum
–Bile may spread to dependent portions of pelvis

43. Imaging acquisition
–Patient supine
–Large field-of-view camera with low-energy all purpose collimator
–Matrix: 128 x 128
–Image over abdomen
□Angiographic phase x 1 min (4 sec/frame)
□Dynamic acquisition (1 frame/min) for 60 min
□Static images at 2-4 hr, 24 hr for slow leak
–Image over pelvis on delayed static images
–SPECT/CT for anatomic correlation if prior enterobiliaryanastomosis, complex
surgical procedures, or multiple fluid collections.
Dosimetry
–Biliary system receives highest radiation dose

44. (Left) In a patient post cholecystectomy, progressive accumulation of radiotracer
in the gallbladder (GB) fossa suggests biloma. On delayed images, this activity
traverses the left upper abdomen.
(Right) In a patient post cholecystectomy, bile leakage starts in the GB fossa and
moves to the bilateral paracolicgutters and the pelvis.

45. (Left) A patient post cholecystectomy underwent hepatobiliary scintigraphy.
Activity near the GB fossa could represent a bile leak or duodenal activity. On
SPECT, accumulation of radiotracer in the left upper quadrant suggests
enterogastricreflux.
(Right) Axial fused SPECT/CT in the same patient shows air fluid collection without
radiotracer, confirming no bile leak. The activity on the scintigraphy represents the
duodenum and enterogastricreflux.

46. (Left) Hepatobiliary scintigraphy confirms prompt radiotracer activity in a
percutaneous GB fossa drain and receptacle bag post cholecystectomy. Note the
normal activity in the small bowel .
(Right) In a patient post cholecystectomy with percutaneous GB fossa drain,
normal radiotracer progression through the biliary system and the small bowel is
evident. Subtle activity in GB fossa could represent the cystic duct stump. On a 2-
hour image, radiotracer in the drain signifies bile leak.

47. (Left) A patient with right upper quadrant pain underwent hepatobiliary
scintigraphy. Activity accumulates in the GB fossa and spreads to the right
paracolicregion. However, the radiotracer moves to the left upper quadrant in
a pattern that suggests intraluminal transit of tracer through the colon.
(Right) A delayed static image in the same patient shows activity within the
colon, confirming a cholecystocolonicfistula.

48. (Left) Activity in the GB fossa is evident with foci of activity in the left upper
quadrant and the left paracolicgutter in a patient post cholecystectomy with
suspected bile leak.
(Right) A delayed static image of the lower abdomen and pelvis in the same
patient shows activity in the bilateral paracolicgutters and the pelvis , signifying
a bile leak.

49. (Left) A patient with blunt abdominal trauma had free fluid in the abdomen on
CT. On hepatobiliary scintigraphy, radiotracer accumulates inferior to the left
hepatic lobe and the left paracolicgutter, confirming bile leak.
(Right) Reappearing liver sign is shown in a patient with bile leak . Activity
appears in GB fossa and spreads superiorly, accumulating into the perihepatic
spaces. Note that hepatic activity clears over time, and then seems to reappear.

50. (Left) In a patient post liver transplant, radiotracer accumulates in the mid
abdomen.
(Right) Axial fused SPECT/CT in the same patient shows a biliary
enterocutaneousfistula.
Radiotracer tracked from the porta hepatisthrough the abdominal cavity and
saturated the laparotomy bandages.

51. Chronic Cholecystitis
Chronic calculous cholecystitis
○Decreased gallbladder ejection fraction (GBEF) in presence of cholelithiasis
Chronic acalculouscholecystitis/GB dyskinesia
○Decreased GBEF in absence of cholelithiasis
Sphincter of Oddidysfunction (SOD)
○Delayed biliary-to-bowel radiotracer transit

52. Best diagnostic clue
○Chronic cholecystitis
–Delayed GB filling > 60 min
–Delayed biliary-to-bowel transit > 60 min
–Calculated GBEF < 38%
○Sphincter of Oddidysfunction (SOD)
–Delayed biliary-to-bowel transit > 30 min
–Time of biliary visualization > 15 min
–Prominent biliary tree
–Sensitivity 49%, specificity 78%

53. Imaging acquisition to investigate chronic cholecystitis
–Patient supine
–Large field-of-view camera with low-energy all purpose collimator
–Matrix: 128 x 128
–Image over abdomen
–Angiographic phase x 1 min (4 sec/frame)
–Dynamic acquisition (1 frame/min) for 60 min
CCK protocol
–If GB filling and bowel activity is seen by 45-60 min, GBEF can be
calculated
–Best-validated reference database, which resulted in least variability of
reference values, recommends
□Infusion of IV CCK at 0.02 μg/kg for 60 min with normal GBEF > 38%
□Infusion of IV CCK at 0.015 μg/kg for 45 min with images at 60 min with
normal GBEF > 40%

54. –Using immediate pre-CCK image and last post-CCK images, regions of
interest (ROIs) are drawn around GB and adjacent liver (background)
–GBEF (%) = [(net GBmax) -(net GBmin) / GBmax] x 100
–Motion correction should be applied if needed
–Fatty meal often used as alternative to CCK; however, it is not reproducible
and normal gastric emptying is needed

55. (Left) Hepatobiliary scan shows common bile duct (CBD) at 20 min. The CBD
remains visible without passage of radiotracer into the small bowel for 120 min.
Finally, after CCK infusion, small bowel is seen .
(Right) Normal GBEF with 30 minute protocol CCK infusion is shown. Abnormal
retention of radiotracer in the CBD is concerning for sphincter of Oddidysfunction
(SOD) vs. partial CBD obstruction.

56. (Left) There is a qualitative impression of normal GBEF. Small bowel is seen by 15
min, and GB filling is seen by 10 min.
(Right) GBEF with 30 minute CCK infusion protocol in the same patient is
abnormally low at 24%. This may be a false-positive and could be normal with a
longer infusion time of 1 hr.

57. (Left) 30 minute CCK infusion protocol shows markedly abnormal GBEF (< 35%).
(Right) Axial CECT in the same patient shows cholelithiasisfavouring the diagnosis
of chronic calculous cholecystitis.

58. (Left) Patient with suspected SOD shows normal biliary-to bowel transit in < 5 min
and marked enterogastricreflux extending superiorly to an outpouching, likely a
hiatal hernia.
(Right) Patient with right upper quadrant pain shows a large defect on flow images
during entire examination. The patient had normal GBEF and biliary-to-bowel
transit. Hepatic masses consistent with metastases were evident on US.

59. Biliary atresia
Biliary atresia (BA) is a congenital biliary disorder, which is characterised
by an absence or severe deficiency of the extrahepatic biliary tree. It is
one of the most common causes of neonatal cholestasis, often causing
cirrhosis immediately and leading to death and accounts for over half of
children who undergo liver transplantation.
Cases of biliary atresia typically demonstrate
oRelatively good hepatic uptake with no evidence of excretion into the
bowel at 24 hours.
oPretreatmentwith phenobarbital (5 mg/kg/day for 5 days) to increase
biliary secretion by stimulating hepatic enzymes is frequently helpful to
minimize the possibility of a false-positive study in a patient with a
patent biliary system but poor excretion.

60. The patient presented for evaluation of
suspected biliary atresia at 3 months of
age. The exam demonstrated delayed, but
homogeneous uptake of tracer on early
images .No bowel activity can be seen.
Delayed images at 24 hours demonstrated
persistent hepatic activity, no bowel activity,
and bladder activity secondary urinary
excretion of the tracer. A shielded image
was also obtained to enhance detection of
any subtle GI activity. The patient was
confirmed to have biliary atresia.

61. Benign Solid Liver Lesions
FNH-Fibro Nodular Hyperplasia
Tc-99m IDA scintigraphy
–Typical findings (~ 90% of FNH lesions): Focal activity > liver parenchyma,
better seen with lesions > 2 cm
–Early visualization with persistent tracer/delayed washout
Imaging acquisition
□Patient supine
□Large FOV camera with low-energy all-purpose (LEAP) collimator
□128 x 128 matrix
□Image over abdomen
□Angiographic phase x 1 min (4 sec/min)
□Static anterior and posterior images at 15, 30, and 60 min if needed
□SPECT/CT if needed for better localization, multiple lesions, &/or size 1-2 cm

62. (Left) Axial Tc-99m IDA SPECT in a patient with right upper quadrant pain shows
focal increased uptake above the liver background, likely focal nodular
hyperplasia.
(Right) Axial T1 FS MR in the same patient shows an enhancing lesion in the
posterior right hepatic lobe with a central scar that is consistent with focal
nodular hyperplasia.

63. Choledochalcyst
Choledochalcysts represent congenital cystic dilatations of the biliary
tree.

64. This neonate presented for
evaluation of suspected
biliary atresia. The early
images demonstrated
heterogeneous tracer
uptake by the liver. There
was no evidence of bowel
activity at one hour.
Delayed 24 hour images
revealed a change in the
distribution of tracer
activity. Marked increased
activity was now noted in a
previously central
photopenicregion.

65. Ultrasound exam revealed a large choledochalcyst.