Thirteen year old FS Beagle presented for vomiting and anorexia of 5 days duration. Six months ago, ALT was mid 200’s. At that time, bile acids were mildly elevated (pre 8.9, post 15.2) and an abdominal ultrasound showed micro hepatica. Today, ALT was too elevated for rDVM analyst to read (diluting sample now), ALP 1800, T bili 6.6, GGT83. Normal albumin (2.7) and BUN. Cholesterol 550 (fasted). Normal CBC.
Thirteen year old FS Beagle presented for vomiting and anorexia of 5 days duration. Six months ago, ALT was mid 200’s. At that time, bile acids were mildly elevated (pre 8.9, post 15.2) and an abdominal ultrasound showed micro hepatica. Today, ALT was too elevated for rDVM analyst to read (diluting sample now), ALP 1800, T bili 6.6, GGT83. Normal albumin (2.7) and BUN. Cholesterol 550 (fasted). Normal CBC. Did not take home any ultrasound images to post, but the liver was small, no parenchymal abnormalities, no obvious vascular abnormalities, no ascites, and mild gravity dependent, non-shadowing gall bladder debris with no evidence of biliary obstruction.
Has not been vaccinated for Lepto and in an endemic area, so testing. My other differentials include toxin, storage disease, chronic hepatitis and cirrhosis, but shouldn’t I see some parenchymal changes with the latter two? Regarding shunts, wouldn’t microvascular dysplasia be the primary possibility at this age and ultrasound findings not distinctive? A congenital intraheptic or extrahepatic shunt doesn’t make sense to me at her age with previously only mild elevations in biles acids, but just want to be sure I am not missunderstanding something.
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The usuals that do this at
The usuals that do this at this age are CAH in which diffuse hepatic parenhcymal changes will occur… “raisin liver” or at least diffuse firbotic changes and increased portal markings. If there is acute disease like lepto or toxin then the liver can look like anything … or what it looked like prior to the insult. The oldest primary shunt dog I have seen was 9 years but always a potential like splenoazygos shunts can go nearly a lifetime without a clinical issue. If microhepatica is present wihtout diffuse degenerative parenchymal changes then portal hypoplasia/mv dysplasia may be underlying and brought to clinical status by an acute or acute on chronic phase disease. Sounds like core bx is the way to go. Re copper storage in my experience this is usually a younger to mid-age lumped up liver disease if primary… then secondary copper as they get older and chornic insults coccur and you get some copper on core bx.
want to find out quiclkly what presentes with elevated bilirubin? Just put in key word hyperbilirubinemia in the search engine.
http://sonopath.com/members/case-studies/search?text=hyperbilirubinemia&species=All
What insults the liver?
just insert “liver cytology”
http://sonopath.com/members/case-studies/search?text=liver+cytology&species=All
or shunt hunt it
http://sonopath.com/members/case-studies/search?text=liver+shunt&species=All