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Portosystemic Shunts and Microvascular Dysplasia
Geraldine Hunt, BVSc, MVetClinStud, PhD, FACVSc

School of Veterinary Medicine, University of California Davis, Davis, CA, USA

Etiology with primary PVH‐MVD (but no CPSS) may develop
acquired shunts within the first few years of life due to
Portosystemic shunting refers to a condition where chronic portal hypertension, in which case they fall into a
blood bypasses the liver and travels from the hepatic category termed “noncirrhotic portal hypertension.”
portal circulation to the systemic circulation through
one or more connections that can occur at a microvascu- Classification and Anatomy
lar or macrovascular level.
Congenital portosystemic shunts (CPSS) occur as a Portosystemic shunts are classified according to three
result of an error in embryonic development where criteria:
primordial vessels either develop abnormal connections congenital versus acquired
or fail to undergo atresia. This has been shown to have a ● single versus multiple
genetic basis in some breeds, including the Maltese, Irish ● macroscopic versus microscopic.
wolfhound, and Cairn terrier. Inheritance, as assessed by ●
pedigree analysis and test‐mating, appears to be complex – Congential portosystemic shunts are further classified
either digenic or polygenic with variable expression. according to their point of origin as either extrahepatic
Rarely, intrahepatic shunts may result from failure of (originating from the hepatic portal vein or one of its
the ductus venosus to close. This is most commonly source vessels) or intrahepatic (originating from one of the
reported in Irish wolfhounds (considered to be digenic in hepatic branches of the portal vein). Extrahepatic shunts
this breed). Left‐divisional shunts may be encountered in are described by their origin and insertion (e.g., portocaval,
any breed, but it is unclear how often these represent splenoazygous). A subset of extrahepatic shunts that insert
failure of the ductus venosus to close, versus other vascu- into the phrenic or hepatic vein has recently been charac-
lar malformations. terized in various countries. Intrahepatic shunts are typi-
Acquired shunts develop as a result of increased cally described according to the division of the portal vein
vascular resistance within the portal system, the hepatic from which they arise (left, central, and right‐divisional).
sinusoids or the hepatic veins (in the face of normal A subset of dogs with CPSS have portal aplasia and no
central venous pressure). The most common cause is demonstrable portal circulation to their liver. In these
hepatic fibrosis/cirrhosis, although other conditions cases, the shunt represents the only outlet from the por-
such as portal vein thrombosis, periportal neoplasia, tal circulation, inserting directly into the systemic venous
hepatic arteriovenous fistula, and dynamic hepatic circulation. Unfortunately, there is no surgical option for
vascular occlusion are sometimes encountered. these patients. This anatomic variant may be associated
Microvascular dysplasia (MVD, which has more recently with other malformations such as interruption of the
been termed portal vein hypoplasia (PVH) without portal caudal vena cava with azygous continuation, abdominal
hypertension, refers to abnormal development or absence situs inversus, and segmentation of the spleen.
of the portal microvasculature within the liver. As different Acquired shunts are usually multiple and generally
authors use different terminology, this spectrum of condi- extrahepatic. Multiple intrahepatic shunts have been
tions will be referred to henceforth as PVH‐MVD. PVH‐ identified in patients following thrombogenic coil occlu-
MVD may occur with or without CPSS. Dogs and cats sion of intrahepatic shunts but it is not yet known

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical