Category:Liver - Developmental Pathology

Portosystemic Shunt

Hepatic microvascular dysplasia

• Small intrahepatic portal vessels and portal endothelial hyperplasia which allows abnormal communication between portal and systemic circulation.
• Can develop as a separate entity or in conjunction with a portosystemic shunt.
• Can cause c/s similar to those of PSS.
• Vomiting, diarrhoea, urinary tract changes associated with ammonium biurate urolithiasis, stunted growth, prolonged recovery from anesthesia.
• Average age of presentation =3yrs.
• Mainly small dogs, esp. Yorkies
• Females>males

Histology

• • Arteriolarization of central veins
  • smooth muscle proliferation (segmental) within the walls of central veins
  • random distribution of small calibre vessels
  • endothelial hyperplasia within portal triads
  • dilation of periacinar vascular spaces.
  • May also see decreased diameter of intrahepatic veins.
• Can’t be accurately distinguished from PSS alone.
• Seen in older dogs than PSS
• Higher MCV, serum postprandial bile acid concentrations, serum albumin and cholesterol concentrations when PSS and HMD together, compared to HMD alone.

Idiopathic noncirrhotic portal hypertension

JAVMA paper

• Portal hypertension
• Sustained impairment of forward venous flow anywhere along the path from the portal vein to the right side of the heart.
• Luminal (thrombosis, parasites) or extraluminal obstruction (hepatic fibrosis or nodular regeneration) or relative restriction of flow due to massive portal volume overload (arterioportal fistulas).
• Hepatomegaly associated with posthepatic obstruction
• Microhepatica – associated with prehepatic/hepatic causes.
• Hepatic encephalopathy and GI bleeding not associated with posthepatic causes.
• Most common causes are RHS heart failure and severe diffuse hepatobiliary disease that results in cirrhosis.

Histology

• indistinguishable from microvascular dysplasia or surgically created portosystemic shunts
  • Portal triad arteriole proliferation
  • portal veins small to large
  • variable portal triad fibrosis
  • hepatic lobule size variation
  • arterioles scattered throughout hepatic parenchyma
  • portal veins – small
  • expanded perivenular connective tissue by arterioles and distended lymphatics.