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SMALL ANIMALS

Blackwell Publishing Asia

CASE REPORT

SMALL ANIMALS
Gallbladder mucocoele and concurrent hepatic
lipidosis in a cat
BENNETT SL, MILNE M, SLOCOMBE RF and LANDON BP
University of Melbourne Veterinary Clinic and Hospital, Werribee VIC 3030
slbenn@unimelb.edu.au

not move with changes in patient position, nor on ballottement

A 3-year-old Domestic Shorthair cat was presented with weight
loss, anorexia and icterus. Feline hepatic lipidosis and gallbladder
mucocoele were diagnosed; this is the first report of gallbladder
mucocoele in the cat. The case was managed successfully
with cholecystojejunostomy, gastrostomy tube placement and
tube feeding for 3 months. The cat has survived over the long
term with minimal complications.
Key words: gallbladder mucocoele, feline hepatic lipidosis,
cholecystojejunostomy, cat
Aust Vet J 2007;85:397–400 doi: 10.1111/j.1751-0813.2007.00182.x
of the cranial abdomen. Gallbladder enlargement and alteration
in wall thickness are variably present and not specific for the disease.
Characteristic stellate, ‘kiwi-fruit’, to finely striated patterns of
the inspissated bile have been described. It has been postulated
that such patterns represent stages in maturation of the mucocoele.
This case report describes gallbladder mucocoele and discusses
the possible causal relationship between this disease and concurrent
feline hepatic lipidosis (FHL) in one cat.

ALP Alkaline phosphatase Case report

ALT Alanine aminotransferase A 3-year-old, male, neutered Domestic Shorthair cat was
APTT Activated partial thromboplastin time presented to the referring veterinary practitioner with loss of
AST Aspartate aminotransferase approximately 50% of its body mass, icterus, and anorexia over
BMBT Bucchal mucosal bleeding time a 6-week period. The onset of clinical signs coincided with a 3-
CBD Common bile duct
week absence of the main carers. Abnormalities found on routine
FHL Feline hepatic lipidosis
GGT Gamma-glutamyl transpeptidase haematological and serum biochemical analyses were: ALT 149
PIVKA Proteins induced by vitamin K U/L (reference values 20 to 100 U/L), ALP 422 U/L (10 to 90 U/L)
absence or antagonism and total bilirubin 139 μmol/L (2 to 10 μmol/L). The cat was
PT Prothrombin time treated with IV crystalloid fluids, amoxicillin-clavulanic acid
TS Total solids 12.5 mg/kg orally twice daily and metronidazole 50 mg/kg
orally once daily in the 5 days prior to referral. At the initial
referral examination, the cat was found to be alert but icteric,

G allbladder mucocoele has been described in dogs1,2

but has not been reported in the cat. Diagnostic criteria
in dogs include typical ultrasonographic appearance,
demonstration of inspissated mucus within the gallbladder
lumen and mucosal mucus-secreting gland hyperplasia upon
histological examination of the gallbladder wall.2,3 Pressure necrosis
and rupture of the gallbladder may occur.1 If the common bile
duct (CBD) is not involved in the disease process, the clinical
signs of abdominal pain, inappetance and jaundice are usually
resolved by cholecystectomy.1 Cholecystojejunostomy may be an
effective therapy if the gallbladder wall is not necrotic.1
The ultrasonographic appearance of canine gallbladder muco-
coele has been described.3 The defining feature is the presence of
echogenic immobile bile that is not gravity dependent and does
with a body condition score of 1.5/6 and body weight of 3.6 kg
(down from 7 kg). Faeces were not acholic. The cat’s posture and
behaviour was not consistent with severe pain, but the level of
abdominal pain could not be determined because the cat responded
aggressively to palpation. Rectal temperature was not measured
due to the cat’s behaviour.
The cat was premedicated with butorphanol 0.1 mg/kg and
acepromazine 0.05 mg/kg, then anaesthetised with alfaxalone
2 mg/kg and isofluorane 2% with nitrous oxide for abdominal
ultrasonography (Ausonics Aspen Advanced) and placement of a
14 French oesophagostomy tube (Nelaton Catheter, Unomedical).
Ultrasonographic findings (Figure 1) consisted of a moderate
volume of hypoechoic free abdominal fluid, an enlarged hyper-
echoic liver with rounded margins, and a moderately distended

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Figure 1. Ultrasonographic image of the cranial abdomen of a 3-year-old
male-neuter DSH cat using a 7 MHz probe. The gallbladder (open headed
arrow) contains a layer of immobile hyperechoic bile (small arrow heads)
measuring 3 to 4 mm thickness. Fluid (closed arrows) surrounds the gall-
bladder and liver (large arrow heads).
gall bladder. The gall bladder had a hyperechoic outer wall
1.6 mm thick, surrounding an inner layer of immobile hyperechoic
bile measuring 3 to 4 mm in width, encircling a central hypoechoic
portion. The hepatic ducts and CBD were not distended and the
pancreas appeared normal. Abdominocentesis via an 18 gauge
needle yielded a tiny volume of jelly-like yellow liquid. Cytological
examination of a smear of this liquid was non-diagnostic. Liver
biopsies were collected using an 18 gauge percutaneous core
biopsy needle (Tru-Cut, Alliegance) and findings on histopatho-
logical examination were consistent with feline hepatic lipidosis
(FHL). Post-hepatic biliary disease, possible peritoneal disease
and FHL were suspected. The owners were unwilling to allow
exploratory coeliotomy and the cat was discharged on pureed
Prescription Diet Feline l/d (Hills Pet Nutrition Inc.) and
continued administration of amoxicillin-clavulanic acid via
the oesophagostomy tube. The cat became depressed and began
vomiting and was presented 2 days later to the weekend after hours
service. Vitamin K1 3 mg/kg once daily SC and metaclopramide
0.5 mg/kg every 6 h SC was commenced. Oesophagostomy tube
feeding was continued.
The cat was anaesthetised again for an exploratory coeliotomy.
After induction, haematocrit and TS were 0.34 L/L (reference
range 0.30 to 0.45 L/L) and 67 g/L (reference range 6 to 80 g/L)
respectively. Grossly, the liver was enlarged and pale. The gall-
bladder was moderately distended and firm. The CBD appeared
normal but its patency and integrity were not confirmed. There
was no ascites. The rest of the abdominal contents, including the
pancreas, appeared normal. The gallbladder and small intestine
were isolated from the peritoneal cavity using saline-moistened
laparotomy sponges. Stay sutures of 4-0 polydioxanone were
398 Australian Veterinary Journal Volume 85, No 10, October 2007
Figure 2. The submucosa of the gallbladder lies to the left. The mucosa is
greatly thickened by papillary and adenomatous hyperplasia of the
mucosal epithelium. Few inflammatory cells are present. Haematoxylin
and eosin stain, microscope magnification × 200.
placed in the fundus of the gallbladder to assist in its manipula-
tion. The gallbladder was dissected from the hepatic fossa by a
combination of sharp and blunt dissection. The serosa of the
jejunum was approximated to the serosa of the gallbladder using
a Lembert pattern of 4-0 polydioxanone suture. Doyen bowel
forceps were placed on the jejunum oral and aboral to the site of
the enterotomy to limit intestinal spillage. A 5 cm incision in the
fundus of the gallbladder was made and a portion of the wall was
excised for histological assessment. The gallbladder and cystic
duct were lavaged with saline using an 18 gauge IV catheter to
remove inspissated bile. A 5 cm incision in the anti-mesenteric
border of the mid-jejunum was made close to the serosal suture
line. Corresponding edges of the gallbladder and jejunal mucosa
and submucosa were sutured using a single layer closure of
simple interrupted full thickness 4-0 polydioxanone sutures.
The remaining serosal layer was approximated with a continuous
Lembert pattern of 4 -0 polydioxanone, completing the chole-
cystojejunostomy. An 18 French gastrostomy tube was placed
(Urological Catheter, Bard), followed by routine saline lavage
and closure of the abdomen. Gallbladder contents consisted of firm,
elastic, grey-green mucus, encasing inspissated, pigmented bile.
Aerobic and anaerobic cultures of bile were negative. Subsequent
histological examination of the gallbladder wall showed mucus
gland hyperplasia of the gallbladder epithelium (Figure 2).
Histological examination of a wedge biopsy of the liver showed
similar changes to those seen in the percutaneous biopsy sample;
there was severe diffuse lipid vacuolation and hydropic change,
predominantly affecting peri-portal to midzonal hepatocytes, and
mild accumulation of pigment, consistent with bilirubin, within
Kupffer cells. Ito cells were prominent, and inflammatory cells
were not seen.
© 2007 The Authors
Journal compilation © 2007 Australian Veterinary Association
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Immediate postoperative care included IV crystalloid fluids,
continuous rate infusion of metaclopramide at 0.05 mg/kg/h IV,
ranitidine 1.5 mg/kg twice daily IV, ursodeoxycholic acid
(Ursofalk Suspension, Provalis) at 15 mg/kg once daily via the
gastrostomy tube and continued Vitamin K1 and amoxicillin-
clavulanic acid. The cat developed signs consistent with hepatic
encephalopathy (salivation, depression and head pressing) when
fed, so lactulose was administered at 1 mL three times daily via
the gastrostomy tube. The haematocrit and TS dropped gradu-
ally to 0.13 L/L and 47 g/L respectively over 24 hours following
surgery, while red cell morphology, platelet count and PT were
within normal limits, findings consistent with bleeding from the
surgical site. Fifty mL of type-matched, fresh, whole blood was
administered. This raised the haematocrit/TS to 19/50 and it
continued to rise to 24/56 over the next 3 days. Serum bilirubin
concentration decreased to 21 μmol/L 2 days after surgery.
By day 4 the cat’s mental status was normal, and all non-nutritional
therapies had been discontinued. Maintenance caloric require-
ments were tolerated and the cat was discharged to the owners
for continued feeding of Feline l/d via the gastrostomy tube.
Three months after discharge, the cat reached normal condition
score of 3/6 and body weight of 5.2 kg. It ate its daily ration
voluntarily and the gastrostomy tube was removed. The cat is
obese but well 2.5 years after surgery. Over this period, there has
been one episode of acute vomiting and mild elevation of ALT
and AST, suspected to be due to ascending cholangitis. This
resolved quickly with IV crystalloid fluid and SC, then oral,
amoxicillin-clavulanic acid therapy.
Discussion
The pre-operative use of ancilliary clinicopathological diagnostic
tests was limited in this case. Tests such as GGT, AST, pre- and
postprandial bile acid estimation, and urine urobilinogen may
have provided some information as to the nature of the lesion,
however some of these results would have been inconclusive4, 5 and
a coeliotomy would still have been required. The anaemia that
developed in the immediate postoperative period was deemed
to be the result of postoperative blood loss. PT, PTT, PIVKA,
d-dimer and BMBT may have been useful to assess the cat’s
coagulation status prior to surgery, but were not performed in
this case. The postoperative bleeding resolved after transfusion
with fresh, whole blood, possibly due to provision of coagulation
factors. Due to the hepatopathy and risk of vitamin K1 deficiency,
the haematocrit was monitored and prophylactic parenteral
vitamin K1 was administered in the perioperative period.
The ultrasonographic appearance of the gallbladder in this cat
did not match the classic stellate or striated patterns described in
dogs.3 The appearance of peripheral immobile echogenic bile in the
absence of a striated pattern, surrounding the hypoechoic central
region, may represent an early stage of the disease. Alternatively,
recent leakage of a hydrated outer layer of mucoid bile into the
abdominal cavity could explain the findings. Increased thickness
of the gallbladder wall to ≥ 1.0 mm is reported to be an accurate
predictor of gall bladder disease in cats.6 In this cat, the gallbladder
© 2007 The Authors
Journal compilation © 2007 Australian Veterinary Association
SMALL ANIMALS
wall measured 1.6 mm, and was deemed indicative of gallbladder
disease. In dogs, gallbladder wall thickening is described as a variable
and non-specific finding in cases of gallbladder mucocoele.3
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Self-limiting gallbladder rupture was suspected due to the
temporary occurrence of mucoid bile free within the abdominal
cavity, however an obvious site of rupture was not identified
at subsequent surgery. The gallbladder may rupture in cases of
canine gallbladder mucocoele, either at the fundus (usually) or neck
(occasionally).2,3 The gallbladder has an excellent regenerative
capacity, with canine biliary epithelium demonstrating an
extraordinary mitotic activity. If a strip of the wall of the biliary
tract remains intact, it will regenerate to almost normal function
and anatomy.7 It is presumed that the feline biliary tract has similar
regenerative capabilities and so it could be expected to heal follow-
ing rupture in the absence of infection in a tension-free wound.
The mucocoele appeared to have developed as a sterile process.
Although amoxicillin-clavulanic acid was administered for 5
days prior to collection of bile for culture, it is unlikely that the
drug would have penetrated to the central core of inspissated bile
obtained. When all reported cases of canine gallbladder muco-
coele in which aerobic and/or anaerobic bacterial culture of bile was
performed are considered together, culture is mostly negative.1– 3
In spite of the temporary presence of mucoid bile within the
peritoneal cavity of this cat, peritonitis did not occur, and may be
explained by the absence of bacteria in this bile.
The patency and integrity of this cat’s post-hepatic biliary system
prior to cholecytojejunostomy was never established. Gallblad-
der expression could not be used as a test of patency due to the
nature of the contents of the gallbladder. Retrograde catheterisa-
tion of the CBD at the duodenal papilla via a duodenotomy8 was
not performed, as the cat was considered at increased risk of
haemorrhage and dehiscence due to cachexia and hepatobiliary
disease. Since cholecystojejunostomy was used to achieve biliary
tract patency, thorough assessment of the patency of the CBD
was not essential.
Cholecystectomy is considered the treatment of choice in dogs.2
Cholecystojejunostomy may be followed by chronic intermittent
cholangitis, causing ongoing morbidity.9,10 Lack of acholic
faeces and normal CBD diameter at surgery suggested patency
of the CBD. While the prognosis is better for cats undergoing
cholecystectomy than cholecystojejunostomy,9–11 cholecystectomy
precludes the possibility of biliary diversion should CBD
obstruction occur in the future.
To the authors’ knowledge, gallbladder mucocoele has not
been previously described in the cat. In this case, the gallbladder
mucocoele occurred concurrently with FHL. FHL occurs
commonly after severe weight loss in previously overweight cats
and may therefore occur secondarily to any disease, including
gallbladder mucocoele, or environmental stress that leads to
anorexia.12 Absence of the main carers at the onset of signs may
have been a causal event of FHL in this cat, with the gallbladder
mucocoele being a concurrent problem or incidental finding.
Although the aetiopathogenesis of gallbladder mucocoele is
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unknown, it is unlikely that the gallbladder mucocoele occurred
secondarily to FHL. Jaundice may have been caused by FHL,
gallbladder mucocoele, or both. There was no histopathological
SMALL ANIMALS
evidence of cholangitis. Bilirubin concentration decreased mark-
edly within 2 days of surgery, suggesting jaundice was caused by
the gallbladder mucocoele, however feeding was also introduced
around this time and reversal of FHL may have commenced.
The prognosis for post-hepatic biliary obstruction in cats is
guarded and partially dependent on the underlying aetiology,8,9,11
but in this cat the disease was managed successfully. Gallbladder
mucocoele is an uncommon diagnosis but it should be considered
when investigating feline post-hepatic biliary disease.
References
1. Worley DR, Hottinger HA, Lawrence HJ. Surgical management of gallbladder
mucoceles in dogs: 22 cases (1999–2003). J Am Vet Med Assoc. 2004;225:
1418 –1422.
2. Pike FS, Berg J, King NW, Penninck DG, Webster CR. Gallbladder mucocele
in dogs: 30 cases (2000–2002). J Am Vet Med Assoc. 2004;224:1615–1622.
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3. Besso JG, Wrigley RH, Gliatto JM, Webster CR. Ultrasonographic appearance
and clinical findings in 14 dogs with gallbladder mucocele. Vet Radiol Ultrasound
2000;41:261–271.
4. Leveille-Webster CR. Laboratory diagnosis of hepatobiliary disease. In:
Ettinger SJ, Feldman EC, editors. Textbook of Veterinary Internal Medicine. 5th
edn. Saunders, Philadelphia, 2000:1277–1293.
5. Scherk MA, Center SA. Toxic, Metabolic, Infectious and Neoplastic Liver Diseases.
In: Ettinger SJ, Feldman EC, editors. Textbook of Veterinary Internal Medicine.
6th edn. Elselvier Saunders, St Louis, 2005:1464 –1478.
6. Hittmair KM, Vielgrader HD, Loupal G. Ultrasonographic evaluation of gallbladder
wall thickness in cats. Vet Radiol Ultrasound 2001;42:149 –155.
7. Peacock EE. Healing and repair of peritoneum and viscera. In: Peacock EE,
editor. Wound Repair. 3rd edn. Saunders, Philadelphia,1984:438 – 484.
8. Fossum TW. Surgery of the extrahepatic biliary system. In: Duncan L, editor.
Small Animal Surgery. 1st edn. Mosby-Year Book, St Louis, 1997:389 –399.
9. Mayhew PD, Holt DE, McLear RC, Washabau RJ. Pathogenesis and outcome
of extrahepatic biliary obstruction in cats. J Small Anim Pract 2002;43:247– 253.
10. Bacon NJ, White RA. Extrahepatic biliary tract surgery in the cat: a case
series and review. J Small Anim Pract. 2003;44:231– 235.
11. Eich CS, Ludwig LL. The surgical treatment of cholelithiasis in cats: a study
of nine cases. J Am Anim Hosp Assoc 2002;38:290 –296.
12. Center SA. Feline Hepatic Lipidosis. Vet Clin N Am Small Anim Pract.
2005;35:225–269.
(Accepted for publication 24 April 2007)
© 2007 The Authors
Journal compilation © 2007 Australian Veterinary Association