Lindquist on portal hypoplasia/microvascular dysplasia and concurrent inflammatory liver disease:

Sonopath Forum

Lindquist on portal hypoplasia/microvascular dysplasia and concurrent inflammatory liver disease:

 
 

A client recently had a case of this in her own dog so I cut and pasted the discussion:

 
 

A client recently had a case of this in her own dog so I cut and pasted the discussion:

 

Remember re LEs and where they come from: ALT is from cytosol and membrane leakage (i.e.Hole in a wall), SAP brush border congestion (Backed up plumbing), AST deep insult from the mitochondrion so thats a bad one (Like a truck running into your house and ending up in the living room), BA is a function of the urea cycle and can be liver but also form GI disease and other non hepatic factors or spurious during growth phase (Sz shunts and end stage liver disease usually spikes BAs > 80 umol/L)

These portal hypoplasia or even shunt cases (yorkies and others) smolder with 30-50%(roughly) less metabolic capacity than normal to start then throw smoldering inflammatory disease on top and an acute phase disease somewhere along the line such as G-itis or pancreatitis, cholecystitis and the rest of the liver gets lumped up… portal pressures increase and ascites forms and the liver becomes a raisin instead of a grape. The problem is the patients don’t get clinical til this point of end stage liver disease (ascites, hyporhexia, low albumin, bun, cholesterol or any combination of the same) and LEs jump up and down so catching them early at the point where the ALT is 1000 in a fast burn is a crap shoot… Then the LEs drop toward the fibrotic/cirrhotic phase because there is less hepatocyte population burn to occur… like throwing wood on a fire and then it dies down over time. This back end low grade burn of LEs with ALT 200 or normal and SAP gradually climbing or staying the same is because the liver parenchyma is just not there…then we have to watch the albumin, cholesterol and bun drop and BAs rise and control portal hypertension/ascites and support he liver all we can. Its so very important to keep the albumin above 2.0 g/dl because when oncotic pressure drops bad things happen. Plasma, plasma expanders, quality protein is key here. Bx can be problematic but a talented needle wielding sonographer a small needle may get a decent sample if there is a window but these small livers don;t offer that easily. Its a case by case judgement call. Laparoscopy best to be minimally invasive and get a decent chunk and surgery of course but these guys don;t handle any acute phase issue including surgery. Center & Twedt discussed copper storage in some of these guys as well being an issue but need Bx for than… dirty way on US-guided FNA cytology (easier and safer to get) is Rhodanine stain that may suggest copper accumulation on FNA but Sharon Center said its theoretical and I don’t know anyone attacking that approach but maybe a solid cytologist out of the box may take a look at it.

This is the hepatic support diet I recommend based on the latest info as of ECVIM 2013 and before:

Hepatic Support

Royal Canin Hepatic Support diet, Metronidazole (25 mg/kg PO bid) over the next 14 days, Lactulose (Oral: 3.1-3.7 g/5 ml lactulose in a syrup base) long term, with a high quality protein supplement of minor amount of yogurt or cheddar cheese. Monitor bile acids, with attention paid to dropping albumin, BUN or cholesterol. SAMe and neutraceuticals as needed.

Refs:
David Twedt:
http://www.dcavm.org/01june.htm

http://www.wsava.org/guidelines/liver-disease-guidelines

 
 
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