Hi there. We recently purchased an American Eskimo puppy from a breeder with the intent to breed the puppy in the future. One month later the breeder informed us that two of the three pups in the litter had developed a liver shunt, had seizures and were put down as a result. We are having our pup tested for liver shunt. She has frequent urination but no other symptoms. My question is if we were to get genetic testing done on the pup would it show any genetic predisposition to having a liver shunt or passing on the gene to any future pups if we were to breed her? Thank you so much!

I have a 4 month old yorkshire terrier puppy who was just diagnosed using ultrasound with a single vessel extrahepatic liver shunt. She is currently 2.3 lbs and has been on the liver diet for 2 weeks along with lactulose and kepra. She presented with a seizure which is how we found the problem and thus the kepra. We are planning on doing the banding but the surgeon would like her to be a bit bigger. Weight gain is slow and was wondering what the best age/size is typically for this surgery and other items we can safely use to help with weight gain.

I have a 10 month old pup with a liver shunt. Is it possible it came from the stud, and Should I stop using the stud? He has fathered several other litters, with no other problems.

We are not sure what to do next after these reports...we were told the next steps would be a CT scan and a biopsy that could cost up to $4500. She is now not really eating anything and throwing up when she does eat. All of the information is overwhelming and the options are all expensive so we want to make the best decision possible. This is the report from the vet so far: "young dog, anorexia, weight loss low BUN, low Potassium, low Albumin, elevated ALT, AST, & ALKP and bilirubin, low cholesterol, urine SG is 1.004, Bile Acids 262 & 252 pre&post." After this, we had an ultrasound done with these reports: "The liver was small, hyperechoic and irregularly marginated. The gallbladder was within normal limits. The abdominal fat was diffusely hyperechoic, more severely so in the cranial abdomen. A small volume of anechoic abdominal effusion was detected. Insufficient portal vasculature was visible to reliably assess for portosystemic shunting. The adrenal glands were slightly small. The spleen, kidneys, urinary bladder, GI tract, pancreas and abdominal lymph nodes were within normal limits. Conclusions: Evaluation for portal vascular anomalies was not possible due to the patient's body conformation, the hyperechoic abdominal fat graft interposed GI gas. Intrahepatic and extrahepatic portosystemic shunting remain possible. CT would be necessary to further evaluate. A small liver would be compatible with a shunt, although the hyperechoic parenchyma and irregular contours are not characteristic of a simple portosystemic shunt, and chronic acquired liver parenchymal disease should also be ruled out. Histopathology is recommended to further evaluate this possibility. Unfortunately, due to the small size of the liver and the patient's body conformation, ultrasound guided sampling would not be possible. The hyperechoic abdominal fat and abdominal effusion may be due to the reported hypoalbuminemia, portal hypertension or combination of processes. The slightly small adrenal glands may be a normal variant in this young patient, although Addison's disease is also possible. Adrenal function testing may prove useful in further evaluating this possibility."