DOI:10.1111/j.1477-2574.2009.00046.

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REVIEW ARTICLE

Surgical management of hepatolithiasis

Sujit Vijay Sakpal1, Nitin Babel1 & Ronald Scott Chamberlain2
1
Department of Surgery, Saint Barnabas Medical Center, Livingston, NJ, USA and 2Department of Surgery, University of Medicine and
Dentistry of New Jersey, Newark, NJ, USA

Abstract
Background: Globalization and intercontinental migration have not just changed the socioeconomic
status of regions, but have also altered disease dynamics across the globe. Hepatolithiasis, although still
rare, is becoming increasingly evident in the West because of immigration from the Asia-Pacific region,
where the disease prevails in endemic proportions. Such rare but emerging diseases pose a therapeutic
challenge to doctors.
Methods: Here, we briefly introduce the topic of hepatolithiasis and describe features of intrahepatic
stones, the aetiology of hepatolithiasis and the symptoms and sequelae of the condition. We then provide
a comprehensive review of the various management modalities currently in use to treat hepatolithiasis.
Conclusions: In our opinion, and as is evident from the literature, surgery remains the definitive
treatment for hepatolithiasis. However, non-surgical procedures such as cholangiography, although
limited in their therapeutic capabilities, play a vital role in diagnosis and preoperative evaluation.

Keywords
hepatectomy, hepatolithiasis, percutaneous transhepatic cholangiography

Received 4 October 2008; accepted 5 February 2009

Correspondence
Ronald Scott Chamberlain, 94 Old Short Hills Road, Livingston, NJ 07039, USA. Tel: +1 973 322 5195.
Fax: +1 973 322 2471. E-mail: rchamberlain@sbhcs.com

Introduction Features of intrahepatic stones

Hepatolithiasis is endemic in the Asia-Pacific region, where its
prevalence can be as high as 30–50%.1 The disease is rare in the
West, with a prevalence of 0.6–1.3%.2 However, increased rates of
immigration from endemic areas are causing an ongoing rise in
the incidence of hepatolithiasis in the West.3–6
Hepatolithiasis is defined as the presence of gallstones in the
bile ducts proximal to the confluence of the right and left hepatic
ducts, irrespective of the co-existence of gallstones in the common
bile duct (CBD) and/or gallbladder. The aetiology of hepatolithi-
asis is not fully understood, but genetic, dietary and environmen-
tal factors are thought to be contributory. Malnutrition and low
socioeconomic conditions are associated with a high incidence of
intrahepatic stones. Hence, economic advancement and the West-
ernization of lifestyle are associated with an apparent decline in
the incidence of the disease in some East Asian countries.7 Intra-
hepatic stones occur more commonly in the 5th and 6th decades of
life and do not demonstrate a gender preference.3,7 However, con-
comitant intrahepatic and extrahepatic stones occur commonly in
older age groups (7th and 8th decades)4 and are found in approxi-
mately 70% of all hepatolithiasis cases.7
Gallstones in hepatolithiasis are typically of two types: calcium
bilirubinate stones (brown pigment stones), and cholesterol
stones. Cholesterol stones comprise only 5.8–13.1% of all intra-
hepatic stones; the majority are calcium bilirubinate stones, which
contain more cholesterol than similar stones in the extrahepatic
ducts.4 This suggests that the pathogenesis of intrahepatic stones
involves not only the precipitation of calcium bilirubinate, but
also an altered cholesterol metabolism. Bile duct stricture and
infection with b-glucuronidase-producing bacteria are speculated
to play a key role in bilirubin precipitation and formation of
calcium bilirubinate stones,4 which are primary intrahepatic
stones and are seen mostly in East Asian countries.7,8 By contrast,
hepatolithiasis in Western societies occurs from secondary stones
that are predominantly composed of cholesterol and have little
association with biliary strictures, stasis and bacterial infection.
Metabolic factors, acquired and/or congenital, act synergistically
in the development of cholesterol hepatolithiasis.7–9 Notably,
hepatolithiasis is more frequent in the left lobe because the left
hepatic duct coalesces with the CBD at an acute angle which tends
to induce bile stasis when associated with biliary strictures.7

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Table 1 Severity of hepatolithiasis graded according to the Tsunoda classification
Tsunoda class
I No marked dilatation or strictures of intrahepatic ducts
II Diffuse dilatation of intrahepatic ducts without strictures
III Unilateral
IV Bilateral
Aetiology of hepatolithiasis
Intrahepatic stone formation is most commonly associated with
bile stasis caused by postoperative strictures, sclerosing cholangi-
tis, Caroli’s disease or neoplasms that result in biliary stenosis and
stasis.2,10 Although hepatolithiasis is often thought to be associated
with parasitic infections in Far Eastern populations, their
co-existence appears to be incidental rather than causative.4–6
Infections with Clonorchis sinensis and Ascaris lumbricoides are
now rarely seen in countries such as Taiwan and Japan, where
hepatolithiasis persists.5 Some have proposed that leptin, the
product of the ob gene, which has a role in modulating lipid
metabolism, may be involved in biliary cholesterol secretion and
gallstone formation. However, in a study of 465 patients (382 with
cholelithiasis, 83 with hepatolithiasis), Lei et al. reported signifi-
cantly lower levels of serum leptin, cholecystokinin (CCK), lipids
and lipoproteins in patients with hepatolithiasis compared with
those with cholelithiasis.11 This implies that although leptin and
lipid metabolism may play a role in gallstone formation, their role
in intrahepatic stone formation is less obvious.
In normal biliary tract, the cystic fibrosis transmembrane
receptor (CFTR) is expressed on biliary canalicular cells and is
vital in the alkalinization and solubilization of bile. It has been
postulated that biliary strictures from cystic fibrosis (CF) liver
disease combined with altered expression of CFTR may set the
stage for intrahepatic stone formation.12 Interestingly, biliary
strictures from parenchymal ischaemic changes, varices within
bile ducts, and cavernous transformation of the portal vein in
anti-phospholipid syndromes may cause mechanical obstruction
of the bile duct with resultant hepatolithiasis.13 Finally, haemolytic
diseases which result in bilirubin overproduction are associated
with the formation of pigment stones, the retrograde migration of
which may be a causative mechanism of hepatolithiasis in this
group of patients.7
Symptoms and sequelae of hepatolithiasis
Asymptomatic patients exist in whom hepatolithiasis is an inci-
dental finding on abdominal imaging. Symptoms of hepatolithi-
asis may include epigastric or right upper quadrant (RUQ)
abdominal pain, jaundice and fever, thus representing Charcot’s
triad of symptoms typical of cholangitis. Pyogenic cholangitis
may occur and may progress to either hepatic abscess formation
or biliary sepsis in severe cases. Although rare, patients with hepa-
tolithiasis may develop thrombocytopenia and enhanced platelet
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Findings
Solitary or multiple cystic dilatation of intrahepatic ducts with strictures
Table 2 Severity of hepatolithiasis graded as proposed by the Hepa-
tolithiasis Research Group, Japan
Grade Symptoms
I No symptoms
II Abdominal pain
III Transient jaundice or cholangitis
IV Continuous jaundice, sepsis or cholangiocarcinoma
activation, resulting in coagulation and fibrinolysis disorder.14
Morbidity is primarily related to recurrent episodes of bacterial
cholangitis and the development of secondary sclerosing cholan-
gitis, biliary strictures, parenchymal atrophy, liver abscesses and
sepsis. Propagation of intrahepatic stones into the extrahepatic
biliary tree may cause gallstone pancreatitis, which may be the
initial presentation of hepatolithiasis in some patients.
The association of cholangiocarcinoma with hepatolithiasis is
well recognized and its prevalence in patients with hepatolithiasis
is 2.4–10.0%.2 Alternatively, the percentage of cholangiocarci-
noma patients with concomitant hepatolithiasis has been reported
to be in the range of 17–27%.3 In studies analysing hepatolithiasis
in Western populations, concurrent cholangiocarcinoma has been
identified in as many as 8.6–12.0% of patients with hepatolithi-
asis.1,6,8 It is suggested that chronic bacterial infection, bile stasis
and mechanical irritation of hepatolithiasis lead to mucosal
adenomatous hyperplasia and chronic proliferative cholangitis,
which may be a causative process for the development of cholan-
giocarcinoma.15 The occurrence and risk of cancer is higher in
calcium bilirubinate than in cholesterol hepatolithiasis,9 and mor-
tality in co-existent cholangiocarcinoma is high (60%).6 Given the
dismal prognosis of cholangiocarcinoma patients, in whom the
average 5-year survival rate is 5–10%,3 caution must be observed
with respect to its concurrent development when treating hepa-
tolithiasis. Both the Tsunoda classification system based on
intrahepatic anatomical findings (Table 1) and a symptom-based
system proposed by the Hepatolithiasis Research Group in Japan
(Table 2) can be used to grade the severity of hepatolithiasis.
Diagnosis of hepatolithiasis
Efforts at diagnosing hepatolithiasis should be aimed at accura-
tely locating stones, biliary strictures and segments of the liver
involved, and excluding concomitant cholangiocarcinoma. Ultra-
sound (US) is the simplest initial diagnostic modality and can
demonstrate intrahepatic stones and bile duct dilatation. Intrahe-
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Figure 1 Computed tomography scan of the abdomen showing mul-
tiple dilated bile ducts in the lateral segment (segment II) of the left
hepatic lobe
patic stones appear as echogenic spots with an acoustic shadow
behind them. A high echo rim on the anterior surface of stones
indicates high calcium content. In calcium bilirubinate stones,
marked biliary dilatation peripheral to the stones is usually
observed, whereas ductal dilatation in cholesterol stones is usually
limited to the stone location.4 However, US is an operator-
dependent study and is unable to differentiate pneumobilia from
intrahepatic stones.
Triple-phase, contrast-enhanced computed tomography (CT)
of the abdomen can detect ductal dilatation and stones, precisely
define liver anatomy and identify biliary strictures (Fig. 1). Cho-
langiography by CT using a slow i.v. infusion of meglumine
iotroxate demonstrates a contrast-filled biliary system and has a
higher sensitivity for intraductal stones (92%) than plain CT.4
However, the inadequate excretion of the contrast material by a
functionally impaired liver segment may limit precise visualiza-
tion. In 30 patients with hepatolithiasis, Park et al. were able to
precisely diagnose concomitant cholangiocarcinoma (14/30)
based on the analysis of specific CT findings such as periductal
soft tissue density, ductal wall thickening or enhancement, portal
vein involvement or obstruction, and lymph node enlargement.3
When more than two of the five aforementioned findings were
present, cholangiocarcinoma was correctly diagnosed with a
specificity of 87.5–100%. In obstructive jaundice, magnetic reso-
nance cholangiopancreatography (MRCP) (Fig. 2) has accuracies
of 96–100% and 90% for the level and cause of obstruction,
respectively, as well as sensitivity, specificity and accuracy of 97%,
99% and 98%, respectively, in detecting and locating intrahepatic
stones.4 Recently, two main classes of liver-specific contrast agents
for MR imaging (MRI) have been developed. These are the super-
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Figure 2 Magnetic resonance imaging of the abdomen revealing
dilated intrahepatic ducts with filling defects in segment II of the liver,
highly suggestive of stones or debris
paramagnetic iron oxide (SPIO) agents, uptake of which occurs
via the reticuloendothelial (RES) system mainly into the liver and
spleen, and hepatobiliary agents, with uptake into hepatocytes
followed by biliary excretion.16 The hepatobiliary agents, all of
which are paramagnetic (namely, mangafodipir trisodium, gado-
benate dimeglumine and gadolinium-ethoxybenzyl-diethylene-
triamine-pentaacetic acid [Gd-EOB-DTPA]), have shown
superior abilities in enhancement of the hepatobiliary ductal
anatomy and detection of liver lesions on MRI.16,17 Although both
CT and MRI can visualize hepatic abscess, detection of cholang-
iocarcinoma in association with hepatolithiasis can be difficult
using these modalities, or even intraoperatively, because the
affected liver segments may be fibrosed. A study by Kim et al.
suggested preoperative measurement of serum carcinoembryonic
antigen (CEA) may be useful in the detection of cholangiocarci-
noma in patients with hepatolithiasis.18
Direct cholangiography – endoscopic retrograde cholangio-
pancreatography (ERCP) or percutaneous transhepatic cholan-
giography (PTC) – is the gold standard diagnostic test in
hepatolithiasis, with a sensitivity of almost 100%.4 Although both
ERCP and PTC are invasive modalities which carry morbidity
rates of 1–7% and 3–5%, respectively, their therapeutic advantage
with regard to stone extraction, biopsy of intraductal lesions and
stent insertion for cholangitis makes them essential in the treat-
ment of most patients with hepatolithiasis (Figs 3–5).
Management of hepatolithiasis
The primary treatment goal in hepatolithiasis is to resolve
ongoing infections, prevent recurrent cholangitis and subsequent
hepatic fibrosis, decrease the need for recurrent instrumentation,
and prevent progression to cholangiocarcinoma.
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Figure 3 Endoscopic retrograde cholangiopancreatography demonstrating (A) extrabiliary opacification in the left liver, dilated common bile
duct (CBD) and left intrahepatic ducts with multiple lucencies of various sizes, and (B) markedly dilated CBD and left intrahepatic ducts with
ductal branch irregularity indicative of stones or tumours

Non-surgical therapy Percutaneous transhepatic cholangioscopic lithotomy or lithot-

Non-surgical approaches to hepatolithiasis consist of the extrac-
tion of stones under radiological (PTC with or without lithotripsy
or access through a T-tube) or endoscopic (ERCP with or without
lithotripsy) guidance. Extracorporeal shock wave lithotripsy
(ESWL) is particularly useful for cholesterol stones, and the use of
holmium (Ho): YAG laser for calcium bilirubinate hepatolithiasis
has shown favourable results.19 Although an ERCP is less invasive
and easier in most cases, access is limited by the location of the
strictures, ductal angulation and the degree of stone impaction.
ripsy (PTCSL) is a widely used procedure for stone removal and
dilation of strictures, particularly in right-sided, bilateral or recur-
rent disease.19 Note, however, that almost 40% of cases of hepa-
tolithiasis have intrahepatic bile duct strictures which make stone
extraction difficult, and the inability of non-surgical techniques to
resolve strictures results in disease recurrence. Hence, non-
surgical therapy is most useful in bilobar hepatolithiasis without
strictures, or in patients who pose high surgical risk or have short
life expectancies.

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Figure 4 (A) Preoperative percutaneous transhepatic cholangiography revealing filling defects in significantly dilated common bile duct and
left intrahepatic ducts indicative of stones. (B) Postoperative T-tube cholangiogram revealing no obstruction with free flow of contrast into
the duodenum

Figure 5 (A–C) Preoperative percutaneous transhepatic cholangiography images demonstrating dilated common bile duct and left intrahe-
patic ducts with numerous filling defects compatible with stones or debris

Surgical therapy
The surgical approach to hepatolithiasis typically involves the
removal of the affected segment(s). Hepatectomy removes stones,
eliminates strictures and the consequent bile stasis which is
responsible for stone formation, and eradicates the risk of cho-
langiocarcinoma; in rare cases it removes a known intraductal
tumour. Indications for hepatectomy in hepatolithiasis are: (i)
unilobar hepatolithiasis, particularly left-sided; (ii) atrophy,
fibrosis and multiple abscesses secondary to cholangitis; (iii) sus-
picion of concomitant intrahepatic cholangiocarcinoma, and (iv)
multiple intrahepatic stones with biliary strictures that cannot be
treated percutaneously or endoscopically. Complete removal of
the diseased lobe or segment is crucial to prevent recurrence and
progressive liver disease. Otani et al. retrospectively reviewed 54
patients treated for hepatolithiasis.20 At 10 years follow-up,
patients who had undergone hepatectomy had a lower bile duct
stricture rate (18.2% vs. 58.3%), longer survival (77.0% vs.
50.0%) and lower disease recurrence rate (16.0% vs. 54.3%) than
those who had undergone PTCSL. Cheung and Kwok published
their series of 174 patients and demonstrated a higher rate of
stone removal by hepatic resection compared with PTCSL
(98.0% vs. 70.5%).21 They also noted a lower incidence of cho-
langitis or biliary sepsis at 5 years follow-up in the hepatectomy
group (13.3% vs. 29.3%). Lee et al. reported 123 patients with
hepatolithiasis and noted a stone clearance rate of 92.7% (114/
123) at initial surgery, which increased to 95.9% (118/123) when
combined with postoperative choledochoscopic lithotripsy or
ERCP.15 The overall survival rate was 91.7% (111/121) at a
median follow-up of 40.3 months. In additional reports com-
paring surgical with non-surgical management of hepatolithiasis,
Uchiyama et al. demonstrated a similar reduction in disease
recurrence with hepatectomy, and were able to further decrease

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the rate of residual stones when hepatectomy was combined with
intraoperative and/or postoperative cholangioscopy.19,22 In addi-
tion, Al-Sukhni et al. reported stone clearance in 85.2% (23/27)
of patients treated with surgery.6 In this series, patients under-
went CBD exploration with stone extraction (10/27) or concomi-
tant liver resection (17/27), with or without construction of a
side-to-side choledochojejunostomy and Hutson access loop
(subcutaneous loop of jejunum for interventional access). The
Hutson access loop carried no additional operative morbidity
and offered an additional approach to residual or recurrent
stones. Finally, a very recent report published by Nuzzo et al.
revealed good longterm outcomes with partial hepatectomy for
primary hepatolithiasis in 26 patients.8 In this study, 76.9% of
patients (20/26) had no recurrent episodes of cholangitis, and
another 15.4% (4/26) experienced no more than two cholangitic
attacks per year when followed postoperatively over an average
period of 63 months. The authors reported no postoperative
mortality and 20% morbidity secondary to bile leak injuries,
which they admitted could have been avoided with better surgi-
cal technique.8 Catena et al. demonstrated that, in experienced
hands, operative morbidity and mortality rates in patients who
undergo liver resection for hepatolithiasis and hepatic masses are
similar.1
Despite numerous reports of successful surgical outcomes in
the treatment of hepatolithiasis (Table 3), Vetrone et al. have
outlined several limitations to surgical therapy.23 Right-sided
stones requiring right hepatectomy were associated with a higher
morbidity. If a CBD stricture is present or a combination of
both extra- and intrahepatolithiasis exists, these authors
promote resection of atrophic hepatic segments in bilobar
disease with hepaticojejunoanastomosis. By contrast, Li et al.
recommend selective use of hepaticojejunoanastomosis in hepa-
tolithiasis, and conclude that hepatectomy with CBD exploration
and T-tube drainage has the best longterm outcome.24 Unlike in
bilio-intestinal anastomosis, Li et al. recommend subcutaneous
tunnel and hepatocholangioplasty with utilization of the gall
bladder (STHG) in the treatment of localized hepatolithiasis if
no distal CBD stricture is present and a normal gall bladder
exists.25 They demonstrated a successful outcome without recur-
rent reflux cholangitis in 95.6% (44/46) of patients treated using
this technique.
Laparoscopic hepatectomy, although technically difficult, has
proved beneficial in hepatolithiasis in rare cases and may offer
postoperative advantages, including a shorter hospital stay, higher
serum albumin and lower serum aminotransferases, compared
with open procedures.26 Note that if liver parenchyma is diffusely
affected by disease, cirrhosis, portal hypertension and/or hepatic
failure could develop and liver transplantation may be the only
alternative.27
Novel alternatives to surgery
Alternatives to surgical therapy for hepatolithiasis include endo-
scopic resection of peripheral (away from the hepatic hilum)
biliary stenoses to ease evacuation of intrahepatic stones, and
chemical bile duct embolization (CBDE) using ethanol and
N-butyl-cyanoacrylate.10,28 These therapies may have a limited
role in patients at high risk for conventional hepatectomy. Li et al.
demonstrated successful chemical ‘resection’ of the diseased
hepatic lobe and no calculous recurrence with CBDE in two
patients with multiple biliary stones in the inferior branch of the
left lateral bile duct complicated with biliary strictures.28 However,
these procedures must be applied in larger series to determine
their efficacy and longterm outcomes.

Table 3 Major series (ⱖ25 patients in the hepatectomy group) depicting short- and longterm outcomes of hepatectomy, compared in some
cases with outcomes of percutaneous transhepatic cholangioscopic lithotomy or lithotripsy
Series Years Primary Number of Immediate stone Stone recurrence Recurrence rate of
therapy patients extraction rate rate within 5 years cholangitis or biliary
sepsis within 5 years
Uchiyama et al. 200722 1971–2006 Hepatectomy 38 NR 13.9% NR
PTCSL 10 NR 50.0% NR
Otani et al. 199920 1980–1996 Hepatectomy 26 96.2% 5.6% NR
PTCSL 28 96.4% 31.5% NR
Cheung & Kwok 200521 1989–2003 Hepatectomy 52 98.0% NR 13.3%
PTCSL 149 70.5% NR 29.3%
Li et al. 200629 1992–2002 Hepatectomy 161 80.1% NR 15.0%
Nuzzo et al. 20088 1992–2005 Hepatectomy 34 NR NR 15.4%
Cheung et al. 200331 1993–2001 PTCSL 79 76.8% NR 33.3%
25
Li et al. 2005 1994–2003 Hepatectomy 46 NR NR 4.0%
Kim et al. 200632 1994–2004 Hepatectomy 128 94.6% 4.2% 8.4%
Lee et al. 200715 2000–2005 Hepatectomy 123 96.0% NR NR

NR, not reported; PTCSL, percutaneous transhepatic cholangioscopic lithotomy or lithotripsy

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Figure 6 Management algorithm for hepatolithiasis. US, ultrasound; CT, computed tomography; MRI, magnetic resonance imaging; ESWL,
extracorporeal shock wave lithotripsy; PTC, percutaneous transhepatic cholangiography; PTCSL, percutaneous transhepatic cholangio-
scopic lithotomy or lithotripsy, CBD, common bile duct

Complications of hepatolithiasis treatment stricture removal. Complication rates for hepatectomies have con-
sistently ranged from 30% to 40 ⫾ 5% in several studies, which are
Recurrent biliary sepsis, hepatic fibrosis and cirrhosis are long- comparable with or less than those for non-surgical techniques.
term adverse outcomes usually resulting from inadequate stone or Wound infection is the most common post-hepatectomy compli-

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cation and occurs at a rate of 17%.15,29 Bile leakage is another
major complication, for which Li et al. reported an incidence of
7.4% in a series of 312 patients who underwent hepatectomy for
hepatolithiasis.29 In the majority of these patients (20/23), the bile
leak was successfully treated with US-guided percutaneous drain-
age; one patient required additional endoscopic nasobiliary drain-
age (ENBD) and the other two needed systemic administration
of antibiotics for septic complications. A multivariate analysis
showed that left hepatectomy and a period of >1 month between
operation and latest attack of acute cholangitis were independent
risk factors for the development of bile leakage in these patients.
Caudate lobe bile ducts and aberrant ducts draining the right
posterior or anterior sections into the left hepatic ducts are rela-
tively common and are another source of leak as they are at risk of
injury during left hepatectomy.29 As we noted earlier, hepatolithi-
asis mostly affects the left hepatobiliary system and the left lateral
segment of the liver (segments II and III) is the most common site
involved. Therefore, left lateral segmentectomy or left hepatec-
tomy are most routinely performed and precise understanding of
the existing biliary intrahepatic anatomy is essential to avoid bile
duct injuries.30
Conclusions
Hepatolithiasis, a highly prevalent disease in East Asian coun-
tries, is becoming increasingly common in Western populations.
Both ERCP and PTC are invaluable tools in the diagnosis and
treatment of hepatolithiasis and have the therapeutic ability to
allow for the extraction of stones, biopsy of intraductal lesions
and implantation of stents. However, although these modalities
may prove to be effective in temporarily resolving cholestasis
and stone clearance, they do not allow the definite removal of
sclerotic intrahepatic biliary ducts. Thus, such non-surgical
techniques may predispose to subsequent recurrence of cho-
langitis and septic complications and the need for repetitive
interventions.
Biliary strictures and dilatations cause bile stasis, cholangitis
and stone formation, and if the diseased ducts are not removed
the possibility of stone recurrence is very high because the predis-
posing factors remain unaltered. Thus, surgical resection remains
the definitive treatment of hepatolithiasis because its goals include
the complete removal of intrahepatic stones and the simultaneous
resolution of accompanying strictured bile ducts. Surgery may
also reduce the risk of recurrent stone formation, cholangitis and
the development of cholangiocarcinoma. However, PTCSL should
be attempted before other procedures in order to ascertain the
condition of the intrahepatic biliary tract and the location of
stones and biliary strictures or dilatations. A multidisciplinary
algorithmic approach (Fig. 6) integrating interventional radiol-
ogy, endoscopy and surgery is a vital component in the complete
therapeutic strategy for symptomatic hepatolithiasis. Of note, in
asymptomatic patients in whom hepatolithiasis is an incidental
finding, the goal should be to exclude the possibility of a concomi-
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tant cholangiocarcinoma, and if there is high suspicion of an
intrahepatic malignancy, hepatectomy should be performed.
Acknowledgements
We thank Margaret Eng and Amanda Porter (Saint Barnabas Medical Center
[SBMC] Library, Livingston, NJ) and Nicole Goode (Department of Radiology,
SBMC) for their assistance.
Conflicts of interest
None declared.
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