CHOLEDOCHOLITHIASIS IN A DOG
COLEDOCOLITIASI IN UN CANE
VeroniCa MARCHETTI, Mario MODENATO,
Simonetta CITI, Grazia GUIDI
A 14-year-old, intact male Siberian Husky was examined because of recurrence of
inappetence, weakness and vomiting. Results of a CBC showed mild normocytic normocromic
anaemia, hypereosinophilia with activated monocytes. Increase of ALT, AST, ALP, GGT,
cholesterol and bilirubin supported a diagnosis of hepatobiliary disease. Abdominal ultrasound
evaluation showed an incomplete extrahepatic biliary tract obstruction (EHBO), with suspected
cholelithiasis and cholecystitis. Any evidence of radiopaque stone was showed at abdominal
A cause to the incomplete response to medical treatment with amoxicilline and clavulanic
acid, ursodeoxycholic acid, vitamin E and silymarin, biliary surgery was performed, showing
a hugely dilated biliary tree and several stones in the common bile duct. The choleliths were
removed, using a combined approach through common bile duct, gallbladder and duodenum.
During surgery a biopsy sample was collected, and histologically a diagnosis of chronic
cholangitis with diffuse cholestasis and periportal fibrosis was formulated. The bacterbilia was
not demonstrate to cultural and cytologic exam. Any complication was revealed in postoperative
time; the clinical condition, CBC and serum biochemical profile were normal during the 8-
month follow-up period.
Stones usually form in the gallbladder, but sometimes they can form directly in the
common bile duct or move here from the biliary tree. Multiple small stones, causing incomplete
obstruction, with a major one of 1,5x7mm, were removed from the final tract of the common
bile duct in this dog.
Key words: cholelithiasis, dog, biliary surgery
Un Siberian Husky, maschio intero di 14 anni, è stato portato alla nostra attenzione per
episodi ricorrenti di disappetenza, abbattimento e vomito. L’emogramma rivelava la presenza
di una lieve anemia normocitica normocromica, accompagnata da eosinofilia e monociti
attivati. L’incremento di ALT, AST, ALP, GGT, colesterolo e bilirubina, evidenziabili nel
profilo biochimico, supportavano l’ipotesi diagnostica di una patologia epatobiliare. L’ecografia
addominale confermava la presenza di un’ostruzione incompleta delle vie biliari extraepatiche,
con sospette colelitiasi e colecistite. Il radiogramma addominale non evidenziava radiopacità
sospette nell’area epatica.
In seguito alla parziale risposta al trattamento medico a base di amoxicillina e acido
Dipartimento di Clinica Veterinaria, Direttore Prof. francesco Camillo.
ANNALI FAC. MED. VET., LIX (2006)210
clavulanico, acido ursodeossicolico, vitamina E e silimarina, il paziente veniva sottoposto a
terapia chirurgica. La laparotomia permetteva di confermare la dilatazione delle vie biliari e
metteva in evidenza la presenza di diversi coleliti nel coledoco. I coleliti venivano rimossi con
un approccio combinato attraverso il coledoco, la colecisti ed il duodeno. In sede chirurgica
venivano eseguiti campionamenti bioptici del fegato e della colecisti; l’esame istologico
formulava diagnosi di colangite cronica con colestasi diffusa e fibrosi periportale. La bile
risultava negativa per batteri sia all’esame citologico che colturale. Nel periodo postoperatorio
non sono comparse complicazioni e durante il follow up di 8 mesi si è assistito ad una
normalizzazione stabile dell’emogramma e del profilo biochimico.
I coleliti solitamente si formano nella colecisti, ma in alcuni casi si possono formare nel
coledoco o arrivare in questa sede dalle vie biliari superiori. In questo cane, nel tratto finale del
coledoco, sono stati rimossi alcuni piccoli coleliti ed un calcolo di 1,5x7 mm che causavano una
incompleta ostruzione delle vie biliari.
Parole chiave: colelitiasi, cane, chirurgia biliare
The incidence of disorders restricted to the gallbladder and the biliary tree is low,
if compared with the many parenchymal hepatic conditions that occur in dogs (Center,
The extrahepatic biliary tract obstruction (EHBO) in dog is caused most frequently
by pancreatic disease, biliary carcinoma, pancreatic carcinoma and intestinal
neoplasia, and the biliary or intestinal inflammations are less commonly recognized.
The cholelithiasis is considered an uncommon cause of EHBO, and canine bile has
a very low lithogenic index, because of the low concentration of cholesterol and free
Ca+ (Willard & Fossum, 2005; Center, 1996).
In a study (Kirpensteijn et al., 1993) about 29 cases of canine cholelithiasis, small
breed aged female were overrepresented, although one case in a puppy poodle is
reported (Rajaut & Diquélou, 2004).
Choleliths are often fortuitous ultrasonographic and, if radiopaque, radiographic
findings (Nyland et al., 2002). Usually they do not cause any problem; nevertheless
they may be associated with cholecistitis and rupture (Matthiesen & Lammerding,
1984; Duhautois, 2000). The cholelithiasis symptomatic cases generally show signs of
abdominal pain, nausea and vomiting because of larger bile ducts and gallbladder rich
autonomous innervation (Rothuizen, 2005; Ward, 2006). There is a limited number of
reported cases of obstructive cholelithiasis in the literature.
In this report, a case of a cholelithiasis in a dog with chronic biliary inflammation
A 14-year-old, intact male, vaccinated, Siberian Husky was examined because
of inappetence, weakness and vomiting arising five-days before referral. The dog
V. MARCHEttI, M. MODENAtO, S. CItI, G. GUIDI
was vomiting daily, sometimes with undigested food, sometimes with gastric mucus,
without any relationship with feeding. Fecal aspect was normal. The owner reported
that the same clinical signs were present 4 times in the last five months. These
alterations were successfully treated with amoxicilline and a supportive fluid therapy
for five days.
Physical examination revealed exclusively mild weakness and a body condition
score of 2/5 (19 kg). A CBC (Hemat 8, Seac Diagnostics, Florence, Italy) and a
serum biochemical profile (Slim, Seac Diagnostics, Florence, Italy) were performed
(Tab. I and II). Mild normocytic normocromic anaemia and hypereosinophilia
with activated monocytes were the sole alterations of CBC. The leakage enzymes
(alanine aminotransferase-ALT, aspartate aminotransferase-AST) and cholestasis
enzymes (alkaline phosphatase-ALP, gamma glutamyl transpeptidase-GGT) showed
a marked increase with a mild increase of total bilirubin. Hypoalbuminemia and
hyperglobulinemia were also present. Leishmania infantum, Ehrlichia canis,
Anaplasma phagocytophilum, Rickettsia Rickettsii and Rickettsia conorii serology
Tab. I. CBC results.
Analytesday 0 day 20day 40 day 100
Neutrophils seg (/μL)
Neutrophils bands (/μL)
ANNALI FAC. MED. VET., LIX (2006)212
were negative. Results of the urinalysis were within normal limits with exception of
a mild bilirubinuria.
Abdominal ultrasound showed (Figg. 1 and 2) a distended gallbladder, with
thickened, irregular and hyperechoic walls; its content was strongly corpuscular, with
acoustic shadowing. Intrahepatic biliary ducts were dilated and tortuous. The common
hepatic duct was dilated, with the latter presenting an intraluminal hyperechoic image
close to the duodenal papilla, measuring about 7 mm in diameter, with acoustic
A diagnosis of incomplete extrahepatic biliary tract obstruction (EHBO), with
suspected cholelithiasis, and cholecystitis was formulated. Abdominal radiography
did not show biliary mineralization. A therapy with amoxicilline and clavulanic acid
(14 mg/kg per os two times daily), ursodeoxycholic acid (15 mg/kg/day divided over
two doses), vitamin E (10 IU/kg/day) and silymarin (20 mg/kg/day) was begun.
On day 20, a general improvement was reported and the dog appeared vivacious
and with a good appetite; no more episodes of vomiting were referred. The patient
weight was 20.8 kg. The results of CBC and biochemical analysis showed a
general improvement (Tab. I and II), whereas on ultrasonography the findings were
Owing to the good response to medical treatment, the same therapy was continued;
the antibiotic therapy was discontinued.
Three weeks later, on day 40 after the initial presentation, the patient was re-
Tab. II. Biochemical profile results.
Tot Bilirubin (mg/dL)
Ionìzed calcium (mMol/L)
Total protein (g/dL)
*Alfa 1 globulin
*Alfa 2 globulin
* obtained by SPE
V. MARCHEttI, M. MODENAtO, S. CItI, G. GUIDI
Fig. 1. Dilated common hepatic duct, with anechoic and slightly corpusculated
content; in the most caudal portion a hemispheric structure, with a smooth surface,
can be seen; this structure is causing a posterior acoustic shadowing
Fig. 2. Left lateral hepatic lobe: the dilated bile ducts can be visualized as anechoic
structures, with hyperechic walls and sinuous pattern.
ANNALI FAC. MED. VET., LIX (2006) 21?
Fig. 3. Dilated biliary tree (head top); the common bile duct diameter is similar to
Fig. 4. The major choledochal stone.
V. MARCHEttI, M. MODENAtO, S. CItI, G. GUIDI
examined for poor appetite. The physical examination showed good conditions with
further weight gain (21.5 kg); moreover the dog was mildly depressed. On the basis of
CBC, biochemical profile (ALT, AST, ALP increased and hypercholesterolemia) and
imaging results (unchanged), a surgical treatment was proposed. Prothrombin time
and Partial Prothrombin time were done prior to surgery and were both within normal
The liver, the gallbladder and the biliary tree, and the descending duodenum were
exposed via a median laparotomy. The gallbladder and the liver appeared grossly
normal. A big cholelith, with several smaller other choleliths, were found in the distal
part of the common bile duct. The common bile duct and the cystic duct appear hugely
dilated (more than 1,5 cm) (Fig. 3). The big cholelith was mobile, but many attempts
to move it toward the gallbladder were unsuccessful. A combined approach to the
gallbladder, the common bile duct and the sphincter of Oddi was decided, to ensure
the possibility to remove all the choleliths and to control the bile duct patency. A bile
sample was collected by fine needle aspiration (22G) for bacteriologic and cytologic
After the choledochotomy and the major cholelith (a brownish and soft stone of
2,5x1cm, Fig. 4) removal, the gallbladder was incised to aspirate and flush all the
remaining bile and smaller choledocholiths. Then a small duodenotomy, made at the
level of the sphincter of Oddi, was performed and the sphincter and the common bile
duct cannulated with a soft 12F cathether, to verify the sphincter patency and irrigate
to guarantee the complete removal of the smaller choleliths from the distal common
bile duct tract. The duodenum, the common bile duct and the gallbladder were closed
with 4/0 polygliconate, in a simple layer interrupted pattern the duodenum and the
common bile duct, in a double layer continuous pattern the gallbladder. Two biopsy
forceps samples from the liver were collected. The abdomen was then copiously flushed
with warm saline solution and the abdominal wall closed in a routine manner.
At histology, the liver architecture was maintained; at low magnification, a
periportal fibrosis was revealed; in these areas chronic inflammation infiltrate,
constituted by non degenerate neutrophils, rare eosinophils and small lymphocytes
was present. Histopathological examination of the gallbladder was unremarkable.
A diagnosis of chronic cholangitis with diffuse cholestasis was formulated.
The bile was negative for bacteria at cytologic and cultural exam. The cholelith
analysis was not performed. No complications were reported in the postoperative
period, and therapy with the same antibiotic and hepato-protectors was continued, for
15 days and 30 days respectively.
Two months after surgery, the CBC and biochemical abnormalities were normalized
(Tab. I and II) and the dog showed good general condition. The last clinical evaluation
was performed 8 months from the date of surgery and the dog appeared to be sound.
The pathogenesis of cholelithiasis in dogs is unknown. Proposed cause for formation
of choleliths include trauma, biliary stasis, diet alterations, cholecystitis and parasitic
ANNALI FAC. MED. VET., LIX (2006) 21?
or bacterial biliary infection (Kirpensteijn et al., 1993). Cholelithiasis was found in
a dog with biliary neoplasia (Brömel et al., 1998), metastatic liver hemangiosarcoma
(Jacobs & O’Brien, 1997) and hyperadrenocorticism (Huang et al., 2002).
Choleliths in dogs, as in human, have been classified as cholesterol, pigment
or mixed. The stones appear usually dark brown or black, and soft, as described in
our case (Rothuizen, 2005). Mixed or cholesterol choleliths contain more than 70%
cholesterol monohydrate plus an admixture of calcium salts, bile acids and pigments,
proteins, fatty acids and phospholipids. Pigment stones contain <10% cholesterol and
are primarily composed of calcium bilirubinate, and appear radiopaque. In dog the
prevalence of radiopaque stones is higher (48%) than in human (15%) (Kirpenstenijn
et al., 1993). In this dog, the stone was not radiopaque and presumed to be composed
of cholesterol or mixed.
The presence of bacteria predisposes to calcium-bilirubinate stones. Some bacteria
produce ß-glucuronidase that deconjugates soluble bilirubin glucuronide to insoluble
unconjugated bilirubin and glucuronic acid. Unconjugated bilirubin may then form
insoluble calcium-bilirubinate (Kirpenstenijn et al., 1993). Moreover, recent sensitive
polymerase chain reaction techniques have shown the presence of bacterial DNA also
in pure or mixed cholesterol stones, suggesting that bacteria may be related to the
formation of any kind of gallstones (Lee et al., 1999).
In our case the bacterbilia was not demonstrate by cultural exam and the
mineralization was not identified. It is possible that bile was sterile at the moment, also
due to the antibiotic therapy (stopped 20 days before surgery), but stones formation
in aseptic biliary stasis is also possible. During the stasis within the biliary tree, the
bile becomes progressively thicker as water is absorbed, and secondary inflammation
induced by bile acids can provoke mucin secretion. Hypersecreted gallbladder mucin
is well known to be precursor in both cholesterol and pigment stone formation (Hong-
Ja et al., 2003). Also the impaired gallbladder motility can contribute to gallstone
precipitation (Center., 1996).
The chronic inflammation in our patient was present and supported by various
clinical-pathological data. Hypereosinophilia without leucocytosis, the activated
monocytes and the mild normocytic normochromic anemia related to chronic
gastroenteric inflammation (Schultze, 2000). Hyperglobulinemia suggests a
persistent inflammation and the moderate hypoalbuminemia is compatible with
hyperglobulinemia inducing down-regulation of synthesis and, improbably, also with
a lesser production by liver. The hyperbilirubinemia support the cholestasis alteration
with hyperphosphatasemia, the increase of GGT and hypercholesterolemia, because
the excretion of bilirubin into the canalicular lumen is against a high concentration
gradient and is the rate-limiting step in its elimination (Meyer & Harvey, 1998).
The ALT and AST increase supports the parenchymal involvement due to toxic
effects of bile acids, also if a exclusively degenerative pattern was evidenced at
histopathologic exam. The mild hepatocytes alteration agrees with the good output of
this case, whereas a fibrosis in the portal areas was present.
Ultrasonography resulted an indispensable and the most informative method to
examine the presence and the nature of this biliary disorder.
Gallbladder stones can easily be detected sonographically when they have both
V. MARCHEttI, M. MODENAtO, S. CItI, G. GUIDI
distinct echogenicity and discrete posterior acoustic shadowing, becoming more
evident as the size and calcium content of the calculus increase. In the gallbladder
the stones shift to the dipendent portion when the animal is repositioned. Calculi
in the extrahepatic ducts or common hepatic duct are difficult to detect because of
interference from bowel gas (Nyland et al., 2002). Their identification can be tempted
by detection of the twinkling artifact, which appears as a quickly fluctuating mixture
of Doppler signals with an associated characteristic spectrum of noise (Weichselbaum
et al., 2000; Louvet, 2006).
In the present case, we have not been able to detect the twinkling artifact,
because of the presence of gastric gas, which allowed only brief imaging of the
stone; furthermore, it has to be noted that there is a grade of correlation between the
biochemical composition of biliary stones and the grade of twinkling artefact.
In the absence of a definitive diagnosis, CT is considered necessary.
We suspected that the stone in the common hepatic duct was causing biliary
obstruction or sub-ostruction because we could visualize dilated intrahepatic bile
ducts; these can be differentiated from portal veins by their sudden changes in lumen
caliber, irregular walls, and absence of signal to Doppler evaluation. The gold standard
for biliary ducts obstruction is hepatobiliary scintigraphy, which allows a functional
study of the biliary system (Head & Daniel, 2005).
The poor calcified aspect of the cholelith and the signs of incomplete obstruction
induced to defer the surgery. Non-calcified stones may resolve in response to oral
medication with ursodeoxycholic acid (Rothuizen, 2005), that module the toxic bile
acid pool, shows choleretic effect, decrease the hepatic production and secretion of
cholesterol; the sylimarin and the vitamin E reduce the liver oxidant damage. The
antibiotic used is excreted in therapeutic concentration in the bile and is active against
gram-negative bacteria, since most of the bacteria isolated reported in literature were
enterococci (Kirpenstenijn et al., 1993). The absence of pure cholesterol choleliths
and the dimensions of this stone may explain the failure of medical treatment. In
humans, where gallstone dissolution has been intensely studied, stones dissolve no
faster than approximately 1 mm of diameter per month (Senior et al., 1990).
Surgical options for the cholelithiasis in dog are represented by cholecistotomy,
choledochotomy and, finally, by cholecistectomy and biliary diversion (Martin, 1993;
Fossum, 2002; Mehler & Bennet, 2006).
Although the gallbladder is the site of formation of most choledocholiths, stones
can form primarily in the duct, as in our case. In the choledocholithiasis, our preferred
method for cholelits removal is represented by cholecistotomy, after retrograde
dislocation of the choledocal stones into the gallbladder; this is usual accomplished
by digital retropulsion or by retrograde catheterization via the sphincter of Oddi,
approached with a small antimesenteric duodenotomy. We prefer this surgical option
every time retropulsion is possible, especially when the choledocal diameter is less
than 5mm, with possible postsurgical stenosis
Although the parietal healing of the gallbladder is sometimes critical, cholecistotomy
shows a reduced postoperative morbidity with respect with choledochotomy or biliary
diversion (Mehler & Bennet, 2006).
The choledochotomy is usually adopted when the choledocal diameter is more
ANNALI FAC. MED. VET., LIX (2006)21?
than 5mm, because the possibility of postsurgical stenosis is high, even when the
suture is made transversely on a longitudinal incision.
All the techniques of biliary diversion are associated with high postsurgical
morbidity, and are reserved to those cases where neoplastic involvement of the region,
fibrotic reaction around the sphincter, or severe bile tree ruptures make anatomic
restoration impossible (Fossum, 2002).
In our case, retropulsion was attempted without success, so choledochotomy
represented the unique choice. Since many small stones were present, we prefer to
perform a combination of the choledocothomy with cholecystotomy and duodenotomy
to ensure complete removal of all stones, and contemporarily to verify the sphincter
patency and to flush all the biliary tree. The big choledocal diameter (more than 1cm)
and the healthy appearance of the gallbladder made us comfortable with this approach,
with minimal postsurgical risks of strictures or bile leakage or suture dehiscence.
There are a limited number of reported cases of obstructive cholelithiasis in the
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