Benign Hepatic or Biliary Cysts
These single cysts are often limited to one liver lobe, usually cause no substantial compressive injury, and are occasionally discovered serendipitously during ultrasonographic examinations for other disorders, at surgery, or at necropsy. They do not expand to damage adjacent tissues, are not associated with increased liver enzyme activity, and are considered inconsequential. However, they may be problematic if they enlarge or interfere with bile flow through the common bile duct.
Hepatic Fibropolycystic Disorders
These diseases have been identified in most companion animals and reflect embryologic malformations involving ductal plate development of biliary structures and renal tubules. Disorders have been divided into 6 groups in humans, and this divisional classification also appears relevant to animals: congenital hepatic fibrosis, Caroli's syndrome, von Meyenburg complexes, simple hepatic cysts, polycystic liver disease, and choledochal cysts. These disorders are complex. The diversity of manifestations can predispose to cholangitis, cause portal hypertension, or evolve into space-occupying lesions (cystic structures). A single genetic mutation has been identified in cats (autosomal onset dominant polycystic kidney disease), most of which demonstrate renal rather than biliary malformations. In some cats, however, many large hepatic cysts cause profound hepatomegaly and require repeated drainage, fenestration, marsupialization, or surgical resection. Uncommonly, cystic structures may become mineralized. Severely affected cats have little normal hepatic parenchyma. Extensive connective tissue causes intrahepatic portal hypertension, a firm large liver, development of APSS, signs of HE, and ascites.
Biliary dysplastic syndromes rarely occur in dogs concurrent with renal cystic malformations. Affected dogs develop increased AP activity and high TSBA concentrations. As in cats, extensive connective tissue can cause intrahepatic portal hypertension, APSS, HE, and ascites.
The only treatment for these disorders is to palliate HE with protein-restricted diets and efforts to alter the enteric microbial flora and pH (lactulose, milk, or low-dose metronidazole). Diuretics and dietary sodium restriction are used to control ascites.
This congenital cystic dilation associated with the distal segment of the common bile duct is recognized in cats. Clinical signs include fever, abdominal pain, and jaundice, associated with cyst infection. Surgical exploration is usually required for definitive diagnosis. Extirpation of the cystic structure or marsupialization into the common bile duct has been successful.
These lesions, also termed cystadenomas, bile-duct adenomas, cholangiocellular adenomas, cystic cholangiomas, and hepatobiliary cystadenomas, are relatively uncommon, benign tumors of elderly cats. The well-demarcated, single tumors can invade adjacent hepatic parenchyma causing compressive atrophy. Cyst contents range from clear, watery fluid to viscous or solid material. Cyst sizes vary, ranging from 1 mm to 8 cm, with tumor mass ranging from 5 mm to 12.5 cm. Imaging studies (ultrasonography or CT) are key to diagnosis.
Surgical excision is the treatment of choice but may not be possible if the structure integrates into the porta hepatis. Prognosis after complete excision is good. If complete excision is not possible, partial resection may delay complications from mechanical invasion of normal tissue. Repeated aspiration, catheter drainage, marsupialization, and partial excision have been used for palliative management but impose risk of infections and neoplastic transformation to a malignant process.
Last full review/revision March 2012 by Sharon A. Center, DVM, DACVIM