Choledochal Cyst
Perceptor: Professor Pramod Garg
Speaker: Dr. Praneeth
Overview
• Epidemiology
• Classification
• Pathophysiology
• Clinical presentation
• Risk of malignancy
• Pathology
• Diagnosis
• Treatment
Typical case scenario in GE OPD
• A young female patient with vague abdominal
pain – found to have gallstones with dilated
CBD (=22 mm) on USG abdomen
• EUS: small stones in distal CBD
• After ERCP + CBD clearance + CBD stenting, on
follow-up ERCP, persistently dilated CBD but
no stones
Introduction
• Choledochal cysts (CC) are a rare congenital
cystic dilation of the biliary tract
• Improved imaging modalities have facilitated
the diagnosis at any time from antenatal to
adult life.
Epidemiology
•
80% of CC are diagnosed in infants & young children within
the first decade of life1
• Incidence: 1 in 100,000-150,000 individuals in West2 to
1:13,000 in Japan3
• Incidence in India: ??
• Frequency in females : males = 3-4:14
1.
2.
3.
4.
Wiseman K et al. Am J Surg 2005
Lee HK et al. Korean J Radiol 2009
Sato M et al. Abdom Imaging 2001
Huang CS et al. J Gastrointest Surg 2010
PATHOGENESIS
• CC may be either be congenital or
acquired
• Most cysts are congenital
• If it is acquired,
• what is the evidence and
• what is the pathogenesis?
Babbitt’s theory
Choledochal cysts may be the result of an
abnormal pancreaticobiliary junction
(APBJ)/APBDU1
• APBJ is a rare congenital anomaly, with a
prevalence of < 2% in general population2, in
80-96% of paediatric CC & 30-70% of patients
with CC3
1.
2.
3.
Cha SW. J Comput Assist Tomogr 2008
Nagi B. Abdom Imaging 2003
Huang CS et al. J Gastrointest Surg 2010
APBDU - definition
• APBDU/Long (most commonly ≥ 1.5 cm) common
channels are arbitrarily defined in terms of length
(from 1 to 4.5 cm), with wide variation based on
imaging modality and angles.1
• Okada et al recommend defining a long common
channel as any pancreaticobiliary junction that
lies outside of the duodenal wall and thus could
result in pancreobiliary reflux and mixing.2
1.
2.
Davenport M et al. J Pediatr Surg. 1995
Okada A et al. J Hepatobiliary Pancreat Surg. 2002
APBDU without and with CCs (AIIMS
archive)
APBDU – BP & PB types
• Patients with CC were more likely to have BP type, whereas
biliary pancreatitis, gallbladder cancer and adenomyomatosis of
GB were more likely to have PB alternate1
1.
Wang HP et al. Gastrointest Endosc. 1998
Komi’s classification of APBJ
Evidences supporting Babbitt’s
• Iatrogenic APBDU in murine models demonstrated cystic
dilation of CBD1
• Evidence for reflux of pancreatic juice into the biliary
system:
– Amylase levels in the fluid in GB and CC are typically elevated in
patients with APBDU2
– High trypsinogen and PLA2 in CC bile3
– Administration of secretin, which increases pancreatic
secretion, has been shown to dilate the CBD and gallbladder in
patients with CC, whereas controls showed duodenal filling
only.4
1.
2.
3.
4.
Yamashiro Y et al. J Pediatr Gastroenterol Nutr 1984
Iwai N et al. Ann Surg 1992
Okada A et al. J Hepatobiliary Pancreat Surg 2002
Oguchi Y et al. Surgery 1988
Evidences against Babbitt’s
• APBDU is observed in only 30-80% of CCs
• CCs detected antenatally don’t have
pancreatic juice reflux and neonatal acini
don’t secrete sufficient pancreatic enzymes1
1.
Imazu et al. Eur J Pediatr Surg 2001
Other hypotheses
• Unequal proliferation of embryologic biliary epithelial
cells (before bile duct cannulation is complete) (eg: due
to fetal viral infection)1
• Distal obstruction of CBD2
• Weak bile duct wall
• Sustained increased intrabiliary pressure
• Inadequate autonomic innervation
• Abnormally few ganglion cells in distal CBD resulting in
proximal dilation3
• Sphincter of Oddi dysfunction (may result in pancreatic
juice reflux)4
1.
2.
3.
4.
Yotuyangi S. Gann (Tokyo) 1936.
Spitz L et al. J Pediatr Surg 1977
Kusunoki M et al. Arch Surg 1988
Ponce J et al. Dig Dis Sci 1989
CC may be acquired
• 20% of CC present for first time in adults
• But only a few case reports have documented
previously normal bile ducts and CC later
Polido WT et al. WMC002920/Jan 2012
• Some speculated that all adult cysts are
acquired due to distal obstruction (eg: SOD or
scarring & stone formation from APBDJ), with
longer, narrower stenosis leading to round
lesions and shorter wider stenosis leading to
fusiform lesions
Singham et al. Can J Surg 2009
CC & Age
• Does CC increase in size with age ?
• Yes in intrauterine life (unlike CBA)
• Probably not after birth– Neither studies
nor case reports
• Is the mean diameter of CC larger in infants
than in adults ? Probably yes (as evidenced by
presentation as abdominal mass in infants)needs prospective studies – may suggest
acquired origin & a milder variant ??
Choledochocele/Type-III CC
• More evenly distributed between sexes1
• Much lower incidence of malignant
transformation (2.5%)2
• APBDU is less common1
• H/o previous cholecystectomy – more likely 1
• Pancreatitis is common1
• Biliary tract symptoms – less common1
• More likely to be diagnosed during ERCP and
managed enodscopically1
1.
2.
Ziegler KM et al. Ann Surg 2010
Ziegler KM et al. Adv Surg 2011
• Distinction of types-I and IVA CCs is arbitrary
as there is some intrahepatic involvement in
both types1
• Clinical courses, complications and
management of 5 types of CCs are different1
• Visser et al: Diverticula, choledochoceles, and
Caroli’s disease are completely unrelated to
CC ---- propose abandoning Todani
classification1
1. Visser et al. Arch Surg 2004
CC-types-I & IV (AIIMS archive)
Associated congenital anomalies
• Double CBD, Multiseptate gallbladder
• Biliary, duodenal & colonic atresias, Imperforate anus,
FAP
• Congenital hepatic fibrosis
• Pancreatic cysts, AVMs, Annular pancreas, Heterotopic
pancreas1
• Hemifacial microsomia with extracraniofacial anomalies
• Congenital absence of portal vein
• ARPKD & ADPKD
• Congenital cardiac anomalies (VSD, Aortic hypoplasia) in
30% of paediatric CCs – manifest during infancy2
1.
2.
Xie XY et al. Hum Pathol 2003
Murphy AJ et al. J Surg Res 2012
CLINICAL MANIFESTATIONS
• 75% of patients present at <10 years of age
• In more recent reports from the West, upto
74% of newly diagnosed CCs are in adults (due
to improved imaging)1
• Triad: Abdominal mass + jaundice + abdominal
pain
• 82 % of children present with ≥ 2 symptoms,
whereas symptoms are found in only 23% of
adult patients2
1.
2.
K Soreide et al. British Journal of Surgery 2004
Lipsett PA et al. Annals of Surgery 1994
Infant group: CC - presentation
•
•
•
•
Abdominal mass (82%)
Jaundice (64%)
Abdominal pain is usually not evident
Typical triad - found in 85% (only 17% in more
recent series) of infants
o Neonates detected antenatally are usually
asymptomatic at birth but it has to be
intervened early before the onset of
complications
Tadokoro H et al. Open journal of Gastroenterology 2012
Classical paediatric/adult group: CC presentation
• Chronic abdominal pain (70-90 %)
• Symptomatic gallstones (45-70%) or Acute
cholecystitis
• Recurrent cholangitis (20-50 %)
• Hepatomegaly (20%)
• Pancreatitis (10-20%)
• Abdominal mass (3-20 %)
Tadokoro H et al. Open journal of Gastroenterology 2012
Biliary calculi
• In a retrospective analysis of 57 adult CCs
managed surgically from 1988-2003, 35 (61.4%)
of patients had cystolithiasis and among them,
57% had GB stones (- APBDU was seen only in
14%)
• 7 patients had hepatolithiasis, 6 of them had
type-IVA CC
• Both gallstones, cystolithiasis, choledocholithiasis
and cholangitis in: Adult CCs > Paediatric CCs
Jesudason SRB et al. HPB 2006
Cholangitis & AP – How in CCs ?
• Dilated cysts & distal stricture (due to chronic inflammation) →
bile stasis → stone formation & infected bile → cholangitis &
further obstruction
• Bile stasis, sludge and stones →Bacterial colonization of dilated
IHBRs → Recurrent cholangitis seen in few cases of type IVA and
Caroli’s disease
• [Chronic inflammation + formation of albumin-rich exudates or
hypersecretion of mucin (from dysplastic epithelium)] → [protein
plugs in PD] [± distal CBD stone] → pancreatitis
Bhavsar MS et al. The Saudi Journal of Gastroenterology 2012
CC & Cirrhosis
• Secondary Biliary cirrhosis (SBC) may develop
due to chronic obstruction ± recurrent
cholangitis.
• SBC is the presenting symptom in 10% of
children1
• 40-50% of patients of CCs had cirrhosis in
biopsies during surgery2
• SBC affects surgical outcome emphasizing the
prompt early treatment of CCs
1.
2.
Samuel M et al. Eur J Pediatr Surg 1996
Nambirajan L et al. Trop Gastroenterol 2000
Rarer presentations of CCs
• Spontaneous intraperitoneal rupture often at
the junction of cystic duct and CBD (typically
only in infants)
• Portal hypertension due to obstruction of
portal vein by CCs
• GOO (in type-III CCs) ← obstruction of
duodenal lumen or intussusception.
• Bleeding due to erosion into adjacent vessels
Clinical features due to APBDU
Risk of malignancy in CCs
• Site of cancer: extrahepatic duct in 50–62%, GB in 38–46%, IHBs
in 2.5%, and in liver & pancreas in about 0.7% cases1
• CC-biliary malignancy is associated with unfavorable outcomes,
with a reported median survival of 6 to 21 months.2
• APBDU may be a significant risk factor for malignancy with the
cyst.3
• In addition, patients with APBJ without biliary cysts appear to
be at a markedly increased risk for gallbladder cancer4
1.
2.
3.
4.
Bhavsar MS et al. The Saudi Journal of Gastroenterology 2012
Lee SE et al. Arch Surg 2011
Cha SW. J Comput Assist Tomogr 2008
Okamura K et al. J Gastroenterol. 2000
Choledochal cyst & associated cancers in
adults: a multicenter survey in South Korea
• Retrospective study of 15 tertiary hospitals
• 808 adults with CCs underwent surgery from 1990-2007
• Type I was most common (499 [68.2%]) followed by type
IVa (208 [28.4%]).
• Of 654 patients, APBDU was identified in 467 patients
(71.4%)
• Biliary tract cancer was associated in 80 patients (9.9%); 40
had bile duct cancer (50.0%), 35 had gallbladder cancer
(43.8%), 3 had periampullary cancer, and 2 had
synchronous gallbladder and bile duct cancer.
• 22 patients (26.3%) had a recurrence, with a median
follow-up duration of 51.8 months.
Lee SE et al. Arch Surg 2011
Choledochal cyst-cancer
CC with cholangiocarcinoma
• More patients with gallbladder cancer
underwent curative resection than patients
with bile duct cancer (P = .004)
Author
Journa Year
l
n
Gong et
al
Am
surg
2012
221 24
(10.9%)
Retrospective
Akaravip J Med
uth et al. Assoc
Thai
2005
17
1 (6%)
Retrospective
(of operated
CCs)
Diagnosed simultaneously
Lee et al
2005
25
5 (20%)
Retrospective
Simultaneous (3-cyst wall, 1IHBR, 1-GB)
Wiseman Am J
Surg
2005
51
4 (8%)
Retrospective
2-H/o previous
cystenterostomy, 2simultaneous
Jordan
Am J
surg
2004
16
0
Prospective
(of operated
patients)
Zheng
J
2004
Korean
Med Sci
72
5 (7%)
Retrospective
(from 19852002)
Asian J
surg
Cancer Type of
study
Cancer detected – how ?
4/37 who did not undergo
surgery (10) or underwent
non-cyst excision (eg:
cystojejunostomy) (27) had
cancers metachronously
Malignancy in choledochal cysts
• 80 adults with CCs treated from Jan 1979 to
Dec 1995 were reviewed retrospectively
• 4 patients had synchronous and 4 had
metachronous carcinomas (Incidence: 10%)
arising in CC
• Cholangitis in 5 patients, GOO in 2 and RUQ
pain + weight loss in 1
• Postoperative survival time ranged from 4-13
months with a mean of 6.2 months
Jan YY et al. Hepatogastroenterology 2000
Bile duct cancer can develop even
after excision of CC
• In the Japanese patients with CC and/or APBDU, the incidence
of cancer was 16.2% (219/1353).
• The incidence of cancer development after cyst excision in
this population, of whom 1291/1353 underwent surgery, was
assumed to be 0. 7%.
• In the 23 patients of biliary tract cancers developing after
excision of CC, age at cyst excision: 1-55 years (mean, 23.0 +/13.7 years), and cancers were detected at 18-60 years (mean,
32.1 +/- 12.2 years), with intervals between cyst excision and
cancer detection of 1-19 years (mean, 9.0 +/- 5.5 years).
• Sites of cancer development were: intrahepatic, six;
anastomotic, eight; hepatic side residual cyst, three; and the
intrapancreatic duct, six.
Watanabe et al. J Hepatobiliary Pancreat Surg 1999
CC & cancer-is the link convincing ?
• Long-term prospective studies on patients of
unoperated CC with aim to study natural
history/development of cancers during follow-up
are lacking in literature
• The majority of tumors and CCs are diagnosed
simultaneously
• Such studies- difficult to do because CCs are
uncommon and anyway the majority with newly
diagnosed CC are getting operated soon after the
diagnosis
1. Soreide K et al. Annals of Surgical Oncology 2007
• H/o Cholangitis, drainage procedures (eg:
Cystenterostomy) and incomplete resection of
cysts increase risk of malignancy1
• Liu et al. observed 33.3% malignancy in
patients with incomplete cyst resection vs 6%
in complete cyst resection patients2
• Patients who had undergone cystenterostomy
in childhood should be advised reoperation
1.
2.
Bhavsar MS et al. The Saudi Journal of Gastroenterology 2012
Liu YB et al. Chin Med J 2007
Carcinogenesis
• Carcinogenesis occurs via multistep genetic
events where early K-ras and p53 mutations are
seen in > 60% of CC-related carcinomas followed
by a late occurring DPC-4 gene inactivation1
• Cancer occurs as a result of chronic inflammation,
cell regeneration and DNA breaks, leading to
dysplasia.2
• The inflammation can be from either recurrent
cholangitis or pancreaticobiliary reflux.
1.
2.
Shimotake T et al. J Pediatr Surg 2003
Bhavsar MS et al. The Saudi Journal of Gastroenterology 2012
CC-carcinogenesis (contd..)
• ↑ Biliary amylase in CC patients is associated with higher
expression of iNOS - ↑ carcinogenesis1
• Chronic postobstructive infection by gram-negative
bacteria such as Escherichia coli metabolizes bile acids
into carcinogens2
• The fraction of cholic acid tended to be lower, and that of
deoxycholic acid slightly higher in iatrogenic APBDJ-dogs,
while UDCA in APBDJ-dogs was significantly decreased
(compared with controls)3
1.
2.
3.
Zhan JH et al. Hepatobiliary Pancreat Dis Int. 2004
Bismuth H et al. Ann Oncol. 1999
Katsuhiro Masamune et al. J. Med. Invest 1997
Unanswered questions
• Is size of CC linked to risk of malignancy ?? – no data
• Is it possible that CC and bile duct cancer have a common
causative agent and we are assuming CC to be the cause
of the tumor but on the contrary, it is only a bystander ?
• Is the risk similar in pediatric and adult CC?
• Is the prognosis of CC-linked tumors more dismal than
biliary tract cancers without CC ?
• Is there a genetic mutation commoner in CC-associated
cancer compared to those with CC alone ?
• Are we getting CCs operated at a higher rate than
required, especially in adults ?
Important differential diagnosis
• Cystic biliary atresia (CBA) – obstructive jaundice at < 3 months,
1/3 develop liver failure or require LT
• CBA cysts appear smaller with less IHBRD and are associated
with atretic/elongated narrow GB
• USG in CBA: Triangular cord sign (Thick echogenic anterior wall
of RPV just proximal to RPV bifurcation), Presence of biliary
sludge
• CD56-positive hepatocytes & increased hepatic fibrosis in liver
biopsy
Soares KC et al. J Am Coll Surg 2014
Pathology
• No diagnostic/pathognomonic features
• The cyst wall is thin, fibrous, and frequently
devoid of a true epithelial surface
• Fibrous cyst wall lined with columnar
epithelium and lymphocytic infiltration is
typical in pediatric CC
• Adult CC may show evidence of inflammation
& hyperplasia
Soares KC et al. J Am Coll Surg 2014
Pathology – types of CC
• Type I (and sometimes type IV) CC lack biliary
mucosa
• Type II CC closely resemble gallbladder
duplication
• Type III cysts are lined by duodenal mucosa, while
type V cysts can have extensive hepatic fibrosis
• IHC demonstrates an increasing rate of epithelial
metaplasia and biliary intraepithelial neoplasia in
walls of CC with advancing age.
Soares KC et al. J Am Coll Surg 2014
Investigations
Transabdominal ultrasound
•
•
•
•
First imaging modality used for the evaluation
Not detect type III cysts
sensitivity of 71 to 97 %
Can not detect APBDU
MRI + MRCP
• Highly sensitive (73 - 100 %) and specific (90100%) in CC diagnosis, classification1
• Reliably identifies APBDU (especially with
Secretin), may identify associated CCA, CBD
calculi2
• Limited in ability to identify minor ductal
abnormalities or small choledochoceles1
• less sensitive than direct cholangiography for
excluding obstruction
1.
2.
Park DH et al. Gastrointest Endosc 2005
Matsufuji H et al. J Pediatr Surg 2006
Endoscopic ultrasound(EUS)
• Used mainly to rule out distal
obstructing lesion
• Can detect APBDU and
choledochoceles accurately
• Can differentiate pancreatic
cysts from type-II CC accurately
in cases of dilemma1
• Can exclude malignancy in CC
by demonstrating smooth walls
1. Oduyebo I et al. Surg Endosc. 2014
Cholangiography
• Direct cholangiography (whether intraoperative,
percutaneous, or endoscopic) has a sensitivity of up to 100%
for diagnosing biliary cysts and previously was a commonly
obtained test.
• In cases with filling defects, persistent dilation despite
stenting suggests CC
• Due to APBDU: increases the risk of post-ERCP pancreatitis
Imaging-pitfalls in CC-linked CCA
• Except the size and shape of CBD, preoperative
imaging only occasionally can be useful to
differentiate (Type-I CC + Cholangiocarcinoma)
presenting for first time from CCA without CC
• Thick walled & grossly dilated CBD may suggest
CCA in CC
• CBD stone + significantly dilated bile duct:
Confusion
• How to resolve?
• ERCP+stenting - if dilatation persists, likely CC
CT (± cholangiography)
 has high sensitivities for visualizing the biliary tree (93%), biliary
cysts (90%)
 However, its sensitivity is lower for imaging the pancreatic duct (64
%)
Intraductal ultrasound (IDUS)
• May be more sensitive than direct
cholangiography for detecting early
malignancy in the cyst wall.
Management
• In the past, some patients were treated with
internal drainage via cystenterostomy (+
cholecystectomy)
• This resulted in high rates of infection,
pancreatitis, cholangitis, cholangiocarcinoma
and recurrent stenosis
Current treatment strategies
Type
Typical procedure
Extra Procedures
Type I
Complete excision +
Roux-en-Y HJ + Cholecystectomy
Type II
Diverticular excision with ductoplasty T-tube placement
Type III
< 3mm: Endoscopic Sphincterotomy
> 3mm: Excision (Transduodenal
approach)
Reimplantation of pancreatic
duct
Type IV
Complete excision of extrahepatic
component + Roux-en-Y HJ +
Cholecystectomy
Intrahepatic components left
untouched
Lobar excision for intrahepatic
components if with stone,
strictures, or hepatic abscess
or coalescing in one lobe
Type V
Medical management
Liver transplant if two lobes
are affected.
Hepaticojejunostomy Roux-en-Y
When to operate in infants ?
• Fetal and newborn diagnosis is associated
with early progression to liver fibrosis,
especially in type-IV CC
• Diao et al demonstrated that early (< 1 month
old) CC excision in prenatally diagnosed
asymptomatic CC resulted in significantly less
fibrosis and improved the rate of LFT
normalisation1
1.
Diao M et al. J Pediatr Surg 2012
HD vs HJ
• Hepaticoduodenostomy has been associated
with increased rates of gastric cancer (due to
bile reflux) and biliary cancer.1
• A recent meta-analysis comparing RYHJ with
hepaticoduodenostomy reported significantly
more postoperative reflux and gastritis with
hepaticoduodenostomy.2
1.
2.
Shimotakahara A et al. Pediatr Surg Int 2005
Narayanan SK et al. J Pediatr Surg 2013
Complicated CC
• Resection of complicated CC is associated with
worse outcomes
• In CC-associated chronic pancreatitis and
atrophic pancreatic head due to APBDU,
pancreaticoduodenectomy may be indicated
• Severely ill CC patients may benefit from
staged procedures consisting of external
drainage followed by complete cyst excision
and hepaticoenterostomy.
Soares KC et al. J Am Coll Surg 2014
Treatment of CC-Type-V
• Localized/unilobar cystic disease is best managed
with hepatic resection
• Asymptomatic bilobar disease is typically
managed nonoperatively, with aggressive
surveillance for malignant transformation
• Although prophylactic OLT is not indicated,
complicated bilobar Caroli’s disease with
cholangitis, portal hypertension, or suspicion of
early malignant transformation is definitively best
managed with OLT
Soares KC et al. J Am Coll Surg 2014
Outcomes of surgery
• Postoperative complications in: Adults >>
children
• Late complications (> 30 days postoperatively)
occur in 40% of adult patients and include
anastomotic stricture, cancer, cholangitis, and
cirrhosis
• Type IVA cysts are most commonly associated
with complications after surgery including
intrahepatic stones and anastomotic stricture
Shah OJ et al. World J Surg 2009
Prognosis
• Overall, CC resection has an excellent
prognosis, with an 89% event-free rate and 5year overall survival rates well over 90%
• The risk of biliary malignancy remains
elevated even > 15 years after CC excision
• Long-term surveillance (with which modality
and how often ??) for biliary malignancy is
warranted postoperatively, particularly in
instances with persistent IHBRD
Lee SE et al. Arch Surg 2011
Alternatives to surgery
• In patients who refuse surgical resection or who are
poor surgical candidates, lesser interventions (such
as LC or ERCP) may treat symptoms caused by
gallstones or sludge.
• No proven effective method of screening biliary cysts
for dysplasia or intramucosal cancer.
• If screening is attempted, an intraductal ultrasound is
probably the most sensitive test for detecting early
malignancy in the cyst wall.
Conclusion
• CC: Either Congential or acquired
• Presentation: Abdominal mass, Jaundice, Abdominal
pain
• Malignant degeneration is the main concern
• More studies are warranted on natural history of CCs
• Diagnosis: MRCP best modality,
• D/D may be difficult if – (i) cancer at lower third of CBD
(ii) Stone + with significant dilatation
• Surgery is the standard of care
• Long-term postoperative surveillance is recommended
Thank you
APBDU & gallbladder carcinoma
• In a retrospective study of 680 cholangiograms,
APBDU was identified in 59 (8.7%) while 5/8
(62.5%) gallbladder carcinomas, 9/27 (33%) CBD
cancers and 6/12 Adenomyomatoses coexisted
with APBDU1
• In a retrospective study, gallbladder cancer was
identified in 5 out of 14 patients with APBDU2
• Gallbladder cancer was found in 12-39% of ‘form
fruste’ CCs (= Abnormal APBDU- present with
abdominal pain + jaundice but without dilated
bile duct)3
1.
2.
3.
LY Chang et al. Hepatogastroenterology 1998
Jung et al. Hepatogastroenterology. 2004
Bhavsar MS et al. The Saudi Journal of Gastroenterology 2012
• Patients with APBDU presented with GB
cancer at a younger median age, often
without GB stones
• In (APBDU + dorsal PD prominence); the
concentration of amylase in bile is significantly
less and rates of GB carcinoma are lower
Kang JK et al. Korean J Gastroenterol. 1998
CC diagnosed de novo in elderly
Radiology
MRCP
Intraductal ultrasound (IDUS)
Hepatobiliary scintigraphy
• using radio-labeled dyes : technetium-99m-labeled hepatic
iminodiacetic acid (HIDA), which is selectively taken-up by
hepatocytes and excreted into the bile.
• HIDA scanning is useful for extrahepatic cysts, with a
sensitivity up to 100% for type I cysts. However, it is
inadequate at visualizing the intrahepatic bile ducts
• HIDA scanning may also be useful in cases of cyst rupture
HIDA SCAN