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ScintigraphicDetectionof SegmentalBile-DuctObstruction
Shiv Gupta, David Owshalimpur, George Cohen, Richard Margules, and Nib Herrera


In a patientwith acute obstructiveJaundice,cholescintigraphywith technetium

99m-iabelediminodiaceticacid (HiDA) showeduniformlyreduceduptake in the
left lobe of the liver. Endoscoplcretrograde cholangiopancreatography(ERCP)
demonstratedcholeifthiaslsandobstructionofthe distalhepaticduct.Surgery,and
later a T-tube cholangiogram,confirmedthe presence of numerousstonesin the
left intrahepatlcandcommonhepaticducts.The liver was free of tumor.Intrahe
patlc segmentalductalobstructionmay producea spectrumof patternsonhepato
biliary imagingrangingfrom reduceduptake to intrahepatlcpooling.

J Nucl Med 23: 890—891,1982

Segmental obstruction of one or more parts of the biliary tree seen in the intrahepatic biliary radicles or in the common bile duct.
has been reported with primary or metastatic tumors of the liver The gallbladder was not visualized. At 24 hr there was still no
(1), and intrahepatic calculi (2). Such stones may be present with activityseenin the left lobe,bileducts,or gallbladder,ancfnotracer
or without stones in the gallbladder. The common scintigraphic passed down into the bowel, suggesting complete biliary obstruc
patterns described with intrahepatic lithiasis are intrahepatic tion.
pooling and partial stasis of radiotracer (2). We encountered a On digital gray-scale ultrasonography the gallbladder lumen
pattern of uniformly reduced hepatic lobar uptake of Tc-99 imi could not be identified, but because of a sharply defined zone of
nodiacetic acid (HIDA), in a patient with documented intrahepatic echogenicity with strong posterior acoustic shadowing in the region
stones, producing a “mass effect.―A brief report of the case is ofthe gallbladder, a contracted gallbladder containing calculi was
presented and the literature reviewed. inferred. Both intrahepatic ducts and common duct were report
edly undilated. Endoscopic retrograde cholangiopancreatography
(ERCP) showed an obstructing calculus in the common hepatic
CASE REPORT duct, with cholelithiasis (Fig. 1). At surgery, two days after scm
tigraphy, a cholangiogram demonstrated a 15-mm calculus ob
A 72-year-old white male was admitted with a history of in
structing the distal common hepatic duct. The gallbladder was
termittent upper abdominal pain, mild jaundice, and low-grade
chronically inflamed and contained several stones. The patient
fever. Total serum bilirubin was 4.9 mg/dl (normal <1.1 mg/dl),
underwent cholecystectoniy and common-duct exploration. The
serum alkaline phosphatase 279 IU/L (normal 20-1 10), and
SGOT 149lU/L (normal8-36). Radionuclidecholescintigraphy liver was edematous and discolored but there was no evidenceof
tumor. A week later, T-tube cholangiogram demonstrated dila
was performed with Tc-99 HIDA, [N-(2,6-dimethylphenylcar
bamoylmethyljiminodiacetic acid.* Following administration of
tation of the common hepatic and intrahepatic ducts, with several
small filling defects in some of the inferior peripheral right intra
5 mCi intravenously, images were obtained with a gamma camera
hepatic bile ducts. The left hepatic duct was distended, with
(general-purpose collimator) at 5-mm intervals to 45 mm, at
multiple filling defects; its diameter measured 1 cm, and no con
15-mm intervals to 3 hr, and a further delayed image at 24 hr.
trast went beyond the filling defects, indicating complete oh
Throughout the study there was normal radiotracer uptake in the
struction (Fig. I). The patient made an uneventful recovery and
right lobe of the liver, whereas uptake in all of the left lobe was
was discharged with T-tube in place and plans to try medical dis
uniformly reduced, producing a lobar photopenic “mass effect―
solution of the calculi in the near future.
(90-mm image at upper left, Fig. 1). There was no suggestion of
dilated intrahepatic bile ducts or intrahepatic pooling of ra
diotracer in either lobe during the entire study. No activity was DISCUSSION

Segmental intrahepatic biliary-duct obstruction secondary to

Received Mar. 8, 1982; revision accepted May 12, 1982. calculi is rarely seen in Western countries and is usually associated
For reprints contact: Shiv M. Gupta, MD, Dept. of Nuclear Mcd with common-duct and gallbladder calculi. The incidence of in
icine, Danbury Hospital, Danbury, CT 06810. trahepatic biliary calculi is relatively high in the Far East, probably



branching bile ducts. The common bile duct and gallbladder were
In the absence of tumor, the mechanism of uniformly reduced
hepatocyte uptake ofradiotracer is not clear. One possible expla
nation might be that almostcompletefailure of bile transport
across the hepatocytes occurs in the affected lobe secondary to
biliary obstruction, this being analogous to renal shutdown sec
ondary to acute obstruction of the renal outflow tract. Long
standing complete obstruction, with associated recurrent chol
angitis, may also contribute to biliary destruction and segmental
lobar fibrosis, resulting in poor hepatic uptake. Recently it has been

—i—p--- f)&
shown experimentally that bile flow becomes undetectable, and
significant secondary hepatocyte damage occurs, as early as two
days after complete biliary obstruction (5).
It is likely that more frequent use of radionuclide cholescintig
raphy with Tc-99m-labeled HIDA and its analogs will reveal
similar cases with either partial or complete duct obstruction
secondary to intrahepatic calculi or neoplasm. Such findings as
intrahepatic pooling or segmental lobar defects associated with
cholelithiasis, with or without evidence of common-duct obstruc
tion, in both jaundiced and nonjaundiced patients should alert the
,i±@ nuclear medicine physician to the possibilityofsegmental biliary
FIG.1. Largelobarphotopenlc
uptake in left lobe of liver at 90 mm (upper left). Endoscopicretro
grade choiangio-pancreatography shows numerous gallstones
(upperright)andobstructing calculusInthehepaticduct(lowerright).
PostoperativeT-tube cholangiogram(lower left) demonstrates
multipleintrahepaticfilling defectswith completeobstructionof C Union Carbide, NY.
distended left main hepatic duct.
related to nutritional factors or parasitic infestation with Clo
norchis sinensis or Ascaris lumbricoides (2). Intrahepatic lithiasis 1. ZEMAN RK, GOLD JA, GLUCK L, et al: Tc-99m HIDA
occurs in about 5% ofcases with cholelithiasis. Without gallbladder scintigraphy in segmental biliary obstruction. J Nuci Med
or duct stones, its occurrence is much less frequent (3). Any stones 22:456—458,1981
are mostly of pigment material with low calcium content, and 2. YEHSH, Liu OK, HUANGMJ:Sequential
therefore are not visualized on plain abdominal radiographs with Technetium-99m Pyindoxylidene glutamate in the de
(4). tectionofintrahepaticlithiasis:Concisecommunication.
J Nucl
The presenceof photon-deficientareas with intrahepatic pooling Med 21:17—21,
has been reported as the most common pattern produced by in 3. GLENN F, MOODY FG: Intrahepatic calculi: Ann Surg 153:
trahepatic lithiasis, followed by partial stasis, with or without vi 711—724,
sualization of the common bile duct and gallbladder (3). In con 4. WENCC, LEEHC: Intrahepatic
A clinicalstudy.Ann
trast, photon-deficient branching bile ducts on hepatobiliary Surg 175:166—177, 1972
scanning has been reported with unilateral segmental biliary oh 5. KLINGENSMITH WC III, WHITNEY WP, SPITZER VM, ci
struction secondary to neoplasm (1 ). In our case, however, there al: Effect ofcomplete biliary-tract obstruction on serial hepa
was a uniform photon-deficient area involving the entire left lobe tobiliaryimagingin an experimentalmodel.J Nuci Med 22:
of the liver without intrahepatic pooling, stasis, or evidence of 866—868,

Societyof NuclearMedicine
April10-15,1983 WaiohaiHotel(Kauai) Kauai and Oahu, Hawaii
Howard Parker, M.D., Program Chairman, announces plans for a Western Regional Hawaii Spring Conference to
take place April 10-14, 1983 atthe Waiohai Hotel on Kauai and April 14-15, 1983atthe Hawaiian Regent in Honolulu.
The program will feature invited speakers covering topics of current interest, including cardiology, instrumentation,
computers, NMR, and interesting clinical case studies. The meeting is sponsored by the Pacific Northwest, Southern
California, Northern California, and Hawaii Chapters ofthe Society of Nuclear Medicine.
For further information. contact: Jean Parker. P.O. Box 40279. San Francisco. CA 94140. Tel: (415)647-0722.

Volume 23, Number 10 891