Hemofiltration in Acute Liver Failure: Substition with Electrolyte Solution Versus Normal Animal Ultrafiltrate
Current knowledge of the pathogenesis of hepatic coma suggests that putative toxins such as ammonia, mercaptans, and aromatic amino acids play a major role, while the contribution of deficient liver-dependent factors is as yet unsettled. To determine the role of deficient factors, functionally anhepatic pigs undergoing hemofiltration with reinfusion of a standard electrolyse solution were compared with another group of animals treated with hemofiltration with reinfusion of ultrafiltrate obtained from normal pigs. A third control group underwent a sham hemofiltration procedure. Hemofiltration was started 18 h after functional hepatectomy and continued for 4 h twice daily until death or for 60 h. The mean duration of survival after functional hepatectomy was 47 h for standard hemofiltration, 35 h for hemofiltration with normal animal fluid reinfusion, and 33 h for controls. Clearances of putative toxins were identical (∼ 80 ml/min) in both hemofiltration procedures, resulting in equal reductions in blood tyrosine concentrations in comparison to controls. During standard hemofiltration, levels of blood ammonia fell significantly lower than in controls; reinfusion of the ammonia precursor urea apparently prevented such a fall in blood ammonia concentrations in hemofiltation with normal animal fluid reinfusion.
We conclude that attempts to correct deficient factors in hepatic insufficiency (as in cross dialysis, cross circulation, plasmapheresis, etc.) entail the risk of inadvertently supplying toxin precursors; in addition, lowering blood ammonia might be more important than correction of aromatic amino acid profiles.
KeywordsHepatic Encephalopathy Acute Liver Failure Blood Ammonia Hepatic Coma Acute Hepatic Failure
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