Portosystemic shunts (PSS) are the result of reduced total hepatic blood flow and the inability of the liver to extract noxious
substances from the portal circulation. Many different patterns of portovascular anomaly have been described in dogs. The
most common are single extrahepatic communications between the portal vein or one of the mesenteric veins and the caudal vena
cava or the azygos vein in small-breed dogs and the patent ductus venosus in large-breed dogs. Hypoplasia or aplasia of intrahepatic
portal vasculature could complicate any of these anomalies, but it is rare. In addition, intrahepatic arteriovenous fistulas
which cause marked volume overload of the porta circulation system result in portal hypertension and acquired PSSs.
Congenital shunts occur more commonly in purebred dogs than in mixed breeds; miniature schnauzers, Yorkshire Terriers, and
Irish Wolfhounds appear to be at increased risk. The prevalence of portosystemic shunts in certain breeds suggests an inherited
predisposition. This has been proven only in Irish Wolfhounds, where a number of previously unknown genes appear to be involved.
Extrahepatic shunts are most common, accounting for 61% to 94% of congenital shunts, and are typically seen in small breeds
of dogs, such as the Miniature Schnauzer and Yorkshire Terrier. Intrahepatic shunts represent between 6% and 40% of congenital
shunts and are more common in large and giant breeds of dogs such as Irish Wolfhounds and Golden Retrievers. The majority
of intrahepatic shunts are a result of the embryonic connection between the umbilical vein and the caudal vena cava remaining
open; in most dogs this connection closes 3 days after birth but, for unknown reasons, remains open in dogs with intrahepatic
Hepatic microvascular dysplasia is an unusual form of intrahepatic portosystemic shunting in which no gross vascular abnormality
can be identified. This rare condition is associated with somewhat milder clinical signs and appears to be the consequence
of a developmental abnormality; it has a higher prevalence in Cairn Terriers, suggesting a hereditary basis.
Acquired shunts arise secondary to diffuse liver disease where excessive and sustained pressure at some point within the portal
vein causes embryonic, nonfunctional vascular communications to open. These are generally seen in older dogs with cirrhosis,
hepatitis, or neoplasia of the liver. In contrast to congenital portosystemic shunts, a number of vessels are usually affected.
As veterinary technicians we have a significant role in triaging, diagnosing and especially nursing these patients back to
a healthy state. Our training, knowledge and care can and, does often times, make all the difference in the outcome of these
Pathogenesis and etiology
Portosystemic shunts abnormal vascular connections between the hepatic portal vein (the blood vessel that connects the gastrointestinal
tract with the liver) and the systemic circulation. Such anomalies cause blood in the gastrointestinal track to be diverted
past the liver, thereby limiting the liver's vital functions in metabolism and detoxification of compounds and the body's
defenses against intestinally derived pathogens. This effectively exposes the body to toxic by-products of digestion (toxins
and bacteria) and often times mimics the effects of liver failure. Portosystemic shunts can be present at birth (i.e. congenital)
or acquired as the result of another disease process later in life. Congenital shunts are more common; representing approximately
75% of all canine cases, and generally result from anatomic abnormalities of the portal vasculature or persistence of fetal
vessels. One or occasionally two vessels are involved, and the shunts are classified according to their location as either
outside of (extrahepatic) or within (intrahepatic) the liver.