Several hepatobiliary disorders have recently come under increased awareness in dogs. Understanding theses specific conditions
is essential in the diagnosis and management of canine liver disease. Conditions presented below include vacuolar hepatopathies,
biliary mucoceles, hepatocutaneous syndrome, and portal vein hypoplasia.
Several recent studies report this condition as an enlarged gallbladder with immobile stellate or finely striated patterns
within the gallbladder on ultrasound. Changes often result in biliary obstruction or perforation. Smaller breeds and older
dogs were overrepresented, with Cocker Spaniels being most commonly affected. Most dogs are presented for nonspecific clinical
signs such as vomiting, anorexia and lethargy. Abdominal pain, icterus and hyperthermia are common findings on physical examination.
Most have serum elevations of total bilirubin, ALP, GGT and variable ALT. Ultrasonographically, mucoceles are characterized
by the appearance of stellate or finely striated bile patterns (wagon wheel or kiwi fruit appearance) and differ from biliary
sludge by the absence of gravity dependent bile movement. The gallbladder wall thickness and wall appearance are variable
and nonspecific. The cystic, hepatic or common bile duct may be normal size or dilated suggesting biliary obstruction. In
one series, loss of gallbladder wall integrity and gallbladder rupture was present in 50% of the dogs and positive aerobic
bacterial culture was obtained from bile in a majority of these dogs. Gallbladder wall discontinuity on ultrasound indicated
rupture whereas neither of the bile patterns predicted the likelihood of gallbladder rupture. Cholecystectomy is the treatment
Mucosal hyperplasia is present in all gallbladders examined histologically but infection is not present with all cases, suggesting
biliary stasis and mucosal hyperplasia as the primary factors involved in mucocele formation. Based on information to date,
the recommended course of action with an immobile ultrasonographic stellate or finely striated bile gallbladder with clinical
or biochemical signs of hepatobiliary disease a cholecystectomy should be performed.
Portal Vein Hypoplasia
Portal vein hypoplasia also referred to as microvascular dysplasia (MVD) is a confusing syndrome associated with abnormal
microscopic hepatic portal circulation. The condition has been initially referred to as hepatic microvascular dysplasia. Hepatic
portal vein hypoplasia has been suggested as a better terminology by the WSAVA Liver Standardization Group that may better
reflect the etiology of this condition. It is believed that the primary defect in affected dogs is the result of hypoplastic
small intrahepatic portal veins. This condition is thought to be a defect in embryologic development of the portal veins.
With a paucity in size or presence of portal veins there is a resultant increased arterial blood flow in attempt to maintain
hepatic sinusoidal blood flow. The hepatic arteries become torturous and abundant in the triad. Sinusoidal hypertension occurs
under this high pressure system. Lymphatic and venous dilation results with opening up of embryologic sinusoidal vessels and
thus acquired shunts develop to transport some of the blood to the central vein thus by-passing the sinusoidal hepatocytes.
This results in abnormal hepatic parenchymal perfusion and lack of normal trophic factors bathing the sinusoids causing hepatic
atrophy. With portal shunting of blood increased iron uptake also occurs that results in hepatic iron granuloma formation.
Ascites or portal hypertension generally do not occur in this condition.
Because similar histological changes occur in dogs having congenital macroscopic portosystemic shunts the diagnosis can be
confusing. If an intrahepatic or extrahepatic macroscopic shunt is not observed then portal vein hypoplasia (MVD) becomes
the probable diagnosis. Angiography or transcolonic portal scintigraphy fail to demonstrate macroscopic shunting in this condition.
Often a needle biopsy is not sufficient to provide enough portal areas to make the diagnosis, and consequently a wedge or
laparoscopic biopsy may be necessary.
The condition that was first described in Cairn terriers and now is felt to occur in other breeds of dogs. Yorkshire Terriers
and Maltese may be over represented. Two presentations are observed; either subclinical animals with no signs or those with
signs typical of portal systemic shunts and hepatic encephalopathy. All patients have abnormal serum bile acid concentrations
(usually moderate elevations) and variable liver enzymes. Therapy is symptomatic and includes management of hepatic encephalopathy.
Evidence of oxidative damage to livers of shunt dogs provides evidence for antioxidant supplementation. The long-term prognosis
is uncertain because of lack of experience with this relative new disease.