Hypermanganesemia is commonly recognized in human patients with
hepatic insufficiency and portosystemic shunting. Since
manganese is neurotoxic, increases in brain
manganese concentrations have been implicated in the development of
hepatic encephalopathy although a direct causative role has yet to be demonstrated. Evaluate
manganese concentrations in dogs with a naturally occurring congenital shunt before and after attenuation as well as longitudinally following the changes in
hepatic encephalopathy grade. Our study demonstrated that attenuation of the shunt resolved
encephalopathy, significantly reduced postprandial
bile acids, yet a hypermanganasemic state persisted. This study demonstrates that resolution of
hepatic encephalopathy can occur without the correction of hypermanganesemia, indicating that increased
manganese concentrations alone do not play a causative role in
encephalopathy. Our study further demonstrates the value of the canine congenital
portosystemic shunt as a naturally occurring spontaneous model of human
hepatic encephalopathy.