Abstract
An 8-year-old male neutered Persian cat was presented for investigation of progressive abdominal distention over the preceding 4 weeks. The cat had a reduced appetite and had lost muscle mass.
At presentation the cat was bright and alert, and had a grossly distended abdomen. Abdominal palpation revealed a marked fluid thrill but was otherwise unrewarding. The rest of the clinical examination was unremarkable.
Questions
What differential diagnoses would you consider for abdominal distention in this cat? Routine haematology, serum biochemistry and urinalysis were performed; these results were unremarkable. FIV/FeLV serology (ELISA) was negative and systolic blood pressure was within normal limits. The cat was sedated and a lateral abdominal radiograph taken (Fig 1). Abdominal ultrasound was also performed (Figs 2a, b & 3).
Right lateral abdominal radiograph.
(A) Ultrasound image of the right kidney; (B) ultrasound image of the left kidney.
Ultrasound image of the cranial abdomen and liver. Describe the findings on the abdominal radiograph Describe the ultrasound findings What is the most likely diagnosis in this case? What would you do next?
Answers on page 361
Answers to What is Your Diagnosis? on page 359 Progressive abdominal distention
Differential diagnoses for abdominal distention in this cat would include an abdominal mass, fluid (ascites), organomegaly (eg, hepatomegaly, distended urinary bladder) and fat. In this case a fluid thrill was palpable leading to the initial suspicion of ascites. Differential diagnoses for ascites depend on the origin of the fluid, eg,
Transudate, eg, hypoproteinaemia Modified transudate, eg, congestive heart failure, abdominal neoplasia Exudate, eg, feline infectious peritonitis, bacterial peritonitis Bile, eg, traumatic biliary tract rupture, cholangiohepatitis Blood, eg, trauma, neoplasia, coagulopathy Chyle, eg, right sided heart failure, idiopathic Urine, eg, trauma, secondary to urethral obstruction
There is increased soft tissue density in the cranial and mid abdomen obscuring the cranial abdominal viscera. The ground glass like appearance is consistent with free abdominal fluid. However not all of the abdominal contents are obscured as the colon and bladder can clearly be seen in the caudal abdomen. These radiographic findings are suggestive of a cranial abdominal mass or fluid filled cavity (eg, a cyst or abscess) which is causing caudal and dorsal displacement of the colon and bladder. There is also significant vertebral spondylosis between vertebrae L5/6, L6/7 and at the lumbosacral junction. The L6/7 joint space is also slightly narrowed.
Ultrasound examination demonstrated the fluid to be within a cyst, with clear internal lobulations, which appeared to be adjacent to and possibly arising from the edge of the liver. Differential diagnoses for a cranial abdominal cyst include: hepatic cysts, biliary cysts or hepatic or pancreatic cysts associated with polycystic kidney disease (PKD). Multiple small renal cysts are also seen in both kidneys.
In this case given the renal cysts (Fig 2a, b), hepatic cysts (Fig 3) and the cat's breed (Persian), polycystic disease was considered the most likely diagnosis.
In order to obtain a diagnostic sample of the fluid and relieve abdominal pressure abdominocentesis was performed. So whilst the cat was sedated, the cyst was drained yielding 800 ml of clear straw coloured fluid (Fig 4). This was acellular, but had a moderate protein content, 52 g/l.
Straw coloured fluid aspirated from the cyst. The cat's mobility and demeanour improved dramatically at this point, however over the next 7 days the abdominal distention returned. A midline exploratory laparotomy was performed and the cyst exposed (Fig 5). Further exploration revealed the cyst to arise from the liver parenchyma, just adjacent to the biliary tract (Fig 6). The cyst was removed and the hepatic margin omentalised. Histopathology revealed the cyst lining to contain sheets of collagenous material, with small cuboidal and columnar epithelial cells; some areas also contained acinar glands thought to represent biliary epithelium. These findings are consistent with hepatobiliary cysts seen with PKD. The cat recovered uneventfully and was discharged 2 days later.
Large thin walled cyst.
Cyst lining arising from the hepatic parenchyma, just adjacent to the biliary tract. At follow-up examination 9 months later the cat was bright and well, abdominal ultrasound revealed there was no recurrence of the hepatic cyst and the renal cysts had not changed. Serum biochemistry and urinalysis remained unremarkable.
Discussion
PKD is common genetic disorder of Persian cats with renal cysts being found in between 35% and 57% of the Persian population (DiBartola 2005). Cannon et al (2001) reported a prevalence of 49.2% in the UK. Young cats are often asymptomatic although the cysts often increase in both number and size over time, and can eventually lead to chronic renal failure (Eaton et al 1997).
PKD in Persians is very similar to autosomal dominant PKD (ADPKD) seen in man. In both man and cats cysts are present from birth but do not usually become clinically significant until middle age. Disease may manifest as renomegaly, irregular kidneys on clinical examination or as a slow progression to renal failure. There is variable disease penetration and no sex predilection. Both PKD and ADPKD are also associated with non-renal lesions. In man the cysts are reported in many anatomical locations including liver, spleen, ovary, pancreas and central nervous system. In man the incidence of hepatic cysts associated with ADPKD increases with age. In one study only 10% of patients aged 20–29 years had liver cysts, whereas they were present in 75% of patients older than 60 years (Gabow 1993). These cysts rarely cause clinical signs, although occasionally have been reported to grow to a large size, interestingly this is much more common in female patients.
Hepatic cysts have been reported in association with PKD in Persian cats (Stebbins 1989, Bosje et al 1998, Eaton et al 1997). These are rarely clinically significant and appear to be fairly uncommon. The reported incidence of hepatic cysts was less than 10% in the study by Eaton et al (1997), however in man cysts increase in incidence with age and the cats in this study were reasonably young. Although this cat had renal cysts, these were not causing renal compromise at the time of surgery. This cat's clinical signs of reduced appetite probably relate to increased pressure on abdominal organs due to the space-occupying effect of the hepatic cyst. Surgery to remove the cyst and cyst lining may offer a good prognosis, as seen in this case.
The genetic mutation that gives rise to feline PKD has recently been characterised (Lyons et al 2004). This has allowed the development of a PCR assay which can identify the defective gene; this can either be performed on a buccal cheek swab (not pre-weaned kittens, due to the interference of maternal DNA) or from a blood sample. Prior to the development of the PCR, screening for the disease was reliant on renal ultrasound in kittens over 10 months of age. The PCR based test allows PKD affected individuals to be identified at a younger age using a much more convenient test. It is hoped that this will increase the number of cats screened for PKD leading to a reduction in prevalence of this disease through careful breeding programmes.
Further information
The PKD PCR test is available in the USA at the University of California (http://www.felinepkd.com) and at the Animal Health Trust (www.aht.org.uk) and at Langford Veterinary Diagnostics (www.bristol.ac.uk/vetpath/lvd) in the UK.
Footnotes
Acknowledgments
The authors would like to thank Professor Peter Holt, Professor Geoff Pearson and the Imaging Department, University of Bristol for their help with this case.