Portal blood flow

 
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Portal venous-systemic venous shunting of blood impairs delivery of portal substances to the liver. Shunting of this sort can occur as a result of congenital vascular anomalies (portosystemic shunts or portosystemic vascular anomalies, microvascular dysplasia), or secondary to acquired defects, such as chronic inflammatory disease with associated fibrosis. The decreased availability of normal hepatotrophic factors in portal blood can lead to hepatic atrophy. These abnormalities in hepatic blood flow are mostly diagnosed in dogs (Toulza et al 2006) and are infrequent in other species, including cats (Ruland et al 2009), horses (Fortier et al 1996), ruminants (Fortier et al 1996, Marçal et al 2008Kinde et al 2014) and camelids (Ivany et al 2002).

The clinicopathologic findings in these conditions results from:

  • Delivery of substances normally absorbed by the intestine and removed efficiently by hepatocytes after delivery from portal blood or normally filtered by the liver are now delivered directly to or stay in the systemic circulation.
  • Decreased hepatic functional mass resulting from reduced blood flow and decreased delivery of hepatotrophic factors (e.g. insulin, glucagon, epidermal growth factor).
  • Abnormalities in iron homeostasis resulting in functional iron deficiency.

 Laboratory detection of altered hepatic portal blood flow

Note that clinical pathologic findings in animals with altered hepatic portal blood flow are variable and some animals may show few or none of these abnormalities.

  • Increased concentrations of substances normally filtered by the liver directly to the systemic circulation.
    • Increased ammonia concentration, with decreased urea production and resulting ammonium urate crystalluria
    • Increased bile acids are seen in dogs with shunts (congenital, acquired) and microvascular dysplasia (Toulza et al 2006).
    • In one study in dogs and cats, measurement of fasting bile acids and ammonia was sensitive and specific for the diagnosis of shunts in dogs and cats. In dogs, high ammonia (>59 μmol/L) were slightly less sensitive than bile acids (>20 μmol/L) (86 versus 93%) but more specific (86 vs 67%).  In cats, high ammonia was less sensitive than bile acids (76 versus 100%) but slightly more specific (76 versus 71%) (Ruland et al 2010). Note, that measurement of post-prandial bile acid concentrations may have improved sensitivity at the expense of specificity (particularly in dogs).
  • Decreased hepatic functional mass resulting from reduced blood flow and decreased delivery of hepatotrophic factors (e.g. insulin, glucagon, epidermal growth factor).
  • Iron homeostasis defects which result in a “functional” iron deficiency (cause unknown, but some dogs have increased iron stores in the liver).
    • Microcytic hypochromic RBCs on a hemogram, possible siderocytes (iron-containing inclusions in RBCs).
    • Low iron and % saturation of transferrin on a chemistry panel
    • Note that some animals have an absolute iron deficiency with depletion of total body iron stores due to intestinal hemorrhage and chronic blood loss.
  • Other abnormalities:
    • RBC shape changes: Some dogs with shunts can have schistocytes in blood smears, presumably due to turbulent blood flow through the portal system.
    • Protein C: Studies have shown that protein C can act a biomarker of hepatic function and hepatoportal perfusion. This is because protein C concentrations appear to be governed by hepatic portal flow and are not only influenced by synthetic capability of the liver. Measurement of protein C activity can assist clinicians in:
      • Recognition of portosystemic shunts: 88% of dogs with shunts in one study had low protein C activity, i.e. <70% (reference interval 75-135%) (Toulza et al 2006). Note that the lowest protein C activity in this study was seen in dogs diagnosed with hepatic failure.
      • Help differentiate shunts from microvascular dysplasia, since portal blood flow is abnormal in the former and normal in the latter. In the above study, 30 of 35 dogs with microvascular dysplasia had protein C activity ≥ 70%.
      • Help with monitoring response to ligation of portosystemic vascular anomalies: In the above study, protein C activity increased to >70% in 10 of 15 dogs after shunt ligation (and all but 1 dog showed an increase in protein C activity) whereas serum bile acid concentrations remained increased in most of the dogs (Toulza et al 2006).
    • Altered liver enzymes: Also note, that many dogs with congenital shunts and microvascular dysplasia can have mildly increased liver enzymes (ALT, AST, and ALP most commonly). Bilirubin concentrations are usually normal in dogs with these two disorders. Animals with acquired shunts, secondary to chronic liver disease, can have increases in all liver enzymes and bilirubin (Toulza et al 2006).
    • Ascites: Animals with acquired defects in hepatic portal flow, e.g. those with fibrosis secondary to chronic active hepatitis, can develop a transudative effusion (low or high protein).
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