We use cookies to help you navigate efficiently and perform certain functions. You will find detailed information about all cookies under each consent category below.
The cookies that are categorized as "Necessary" are stored on your browser as they are essential for enabling the basic functionalities of the site. ...
Necessary cookies are required to enable the basic features of this site, such as providing secure log-in or adjusting your consent preferences. These cookies do not store any personally identifiable data.
Functional cookies help perform certain functionalities like sharing the content of the website on social media platforms, collecting feedback, and other third-party features.
Analytical cookies are used to understand how visitors interact with the website. These cookies help provide information on metrics such as the number of visitors, bounce rate, traffic source, etc.
Performance cookies are used to understand and analyze the key performance indexes of the website which helps in delivering a better user experience for the visitors.
Advertisement cookies are used to provide visitors with customized advertisements based on the pages you visited previously and to analyze the effectiveness of the ad campaigns.
A 4-year-old neutered male Yorkshire terrier dog, that had recently been adopted, was presented for evaluation of PU/PD. Urinalysis showed inappropriate SG (1.019). Physical examination, CBC, serum biochemistry, urine culture, abdominal radiographs, and ACTH stimulation test were normal. However, pre-and post-prandial bile acids were elevated at 31.4 and 99.7, respectively
It is likely that the elevated bile acids are due to portal vein hypoplasia in this case, which is a congenital hepatic parenchymal issue and necessitates medical treatment. No further surgical intervention is recommended given that the “double aorta” is not visible. The extrahepatic shunt appears to be completely resolved; the surgical intervention was successful. The minor residual dilation of the shunt is likely not a clinical issue. Portal vein to vena cava and aortic ratios appeared to be normal. The portal vein at the portal hilus prior to the branching appears to be of adequate width. There was no evidence of portal hypertension noted. Repeat liver biopsy could be considered in this case. However, given the prior biopsy, it is likely that primary parenchymal disease is the cause of elevated bile acids. Recommend strict medical treatment and strict diet for this patient.
This ultrasound was performed four months after the initial presentation. Surgical correction of the shunt, and a cystotomy had been performed. No pre-surgical images were provided. The portal vein at the portal hilus prior to branching measured 0.43 cm. The shunt attenuation entry into the portal vein measured 0.3 cm. The portal vein prior to the portal hilus and at the level of the pancreaticoduodenal vein measured 0.6 cm and appeared to be adequate in size. The liver presented adequate size. The right and left liver lobes appeared to be adequate. The medial lobes appeared to be slightly atrophied. Structural changes were insignificant at this time. A residual looping anomalous vessel was noted; however, there was no “double aorta” as noted on the prior sonogram. Therefore, attenuation of the shunt appears to be adequate with residual, minor dilation of the gastroazygos shunt. Given that the “double aorta” has resolved, extrahepatic shunting does not appear to be an issue, even though some minor congestion of the residual portion of the shunt appears to be present. The portal vein to vena cava ratio is approximately 0.85, which is normal.
None
Porto-caval shunt, primary portal vein hypoplasia, congenital fibrosis.
None
