The CBC findings may include microcytic, normochromic erythrocytes and/or a mild nonregenerative anemia. Serum chemistry profiles
may reveal mild increases in the serum activity of ALT, AST and ALP. In most animals with congenital PSS, the total bilirubin
values are normal.
Albumin values may be mildly decreased. Coagulation profiles including prothrombin time, activated partial thromboplastin
time and fibrinogen are usually normal. Serum glucose values may be normal, mildly reduced or markedly hypoglycemic. The BUN
concentration may be low or in the low normal range in any young animal with hepatic dysfunction. The most reliable and consistent
blood test for the detection of liver dysfunction in puppies with congenital portosystemic shunt is the 12- to 24-hour fasted
and two-hour postprandial serum bile acid concentrations.
Diagnostic imaging of a puppy with abnormal serum bile acid values is to determine if a suspected congenital portosystemic
shunt is present. Animals with congenital portosystemic shunt frequently have reduced hepatic size, i.e., rounded contour
of the caudal edge of the liver and cranial displacement of the stomach radiographically.
In addition, these animals may have opaque ammonium biurate calculi. Ultrasonographic findings in puppies with congenital
portosystemic shunt include small liver, reduced visibility of intrahepatic portal vasculature, and anomalous blood vessel
draining into the caudal vena cava or sometimes into the azygos vein.
Two-dimensional, gray-scale ultrasonography is used to image through a ventral abdominal wall; however, in most large puppies
the optimal approach to the portal vein is through a lateral abdominal wall using the right intercostal spaces.
The portal vein is normally visible by ultrasound imaging as ultrasound waves enter the liver at the porta hepatis, ventral
to the caudal vena cava. Lobar branches of the portal vein have echogenic walls.
Congenital intrahepatic portocaval shunts are identified on the basis of their ultrasonographic appearance as left-divisional,
central-divisional or right-divisional intrahepatic shunts. Left-divisional intrahepatic shunts have a relatively consistent
bent tubular shape and drain into the left hepatic vein. Central-divisional intrahepatic shunts take the form of a foramen
between dilated portions of the intrahepatic portal vein and caudal vena cava. Right-divisional intrahepatic shunts appear
as large, tortuous vessels that extend far to the right of midline. The morphology of the left-divisional shunts is compatible
with patent ductus venosus.
Results of laboratory tests
The Irish Wolfhound and Deerhound are predisposed to left-divisional intrahepatic shunts; the Old English Sheepdog and Australian
Cattle Dog are predisposed to central-divisional intrahepatic shunts; Labrador and Golden Retrievers are affected by both
left- and central-divisional intrahepatic shunts.
Animals with extrahepatic congenital portosystemic shunt typically have an anomalous vessel that drains into the caudal vena
cava between the right renal vein and the hepatic veins; because of the dorsal location, this anomalous vessel may be visible
only through the right dorsal intercostal spaces.
Congenital portoazygos shunts may also be visualized using the right dorsal intercostal approach, looking for the shunting
vessel at the point where it drains into the caudal vena cava is more accurate than trying to examine the various tributaries
of the portal vein.
Extrahepatic shunts may be difficult to identify ultrasonographically if access to the relevant structures is hindered by
the skill level of the person doing the ultrasonographic study, animal's large body size, lack of acoustic windows as a result
of reduced hepatic size, or presents with excessive intestinal gas and ascites.
Ancillary serum bile acids results.
Further details about congenital portosystemic shunts and their management in puppies are found in my textbook - Hoskins JD:
The liver and pancreas. In Hoskins JD (ed): Veterinary Pediatrics: Dogs and Cats from Birth to Six Months, Third Edition.
Philadelphia, WB Saunders Co., 2001, pp 200-224.