Synergism Among Toxic Factors and Other Endogenous Abnormalities in Hepatic Encephalopathy

  • Leslie Zieve


The abnormalities that occur in fulminant hepatic failure are acid-base shifts such as respiratory and metabolic alkalosis, electrolyte depletion, hypoxia, hypoglycemia, hypo-volemia, hypotension, cerebral edema, pulmonary edema, cardiac arrhythmias, renal failure, coagulation abnormalities, often disseminated intravascular coagulation, bleeding diathesis, and infections. Additional abnormalities are associated with the development of hepatic encephalopathy (HE). The affinity of hemoglobin for oxygen is decreased. Pyruvate, lactate, citrate, and α-ketoglutarate are increased in blood and spinal fluid. α-ketoglutarate, fumarate, malate, and oxaloacetate are decreased in the brain. Cerebral blood flow and oxygen and glucose utilization are decreased. Brain ATP utilization is decreased. Ammonia accumulates in the blood and tissues. Ammonia utilization rates are increased. Glutamine and α-ketoglutaramate are increased in the brain and spinal fluid. Mercaptans, fatty acids, and amino acids accumulate in the blood and tissues. The highest plasma amino acid levels are observed with methionine, phenylalanine, tyrosine, and free tryptophan. The tyrosine derivatives, tyramine and phenols, are increased in the plasma. Neurotransmitters are decreased in muscle and brain, while their metabolites — glutamine, asparagine, homovanillic acid, and 5-hydroxy-indolacetic acid — are increased in the spinal fluid. Finally, false neurotransmitters such as octopamine accumulate in the blood and tissues.


Hepatic Encephalopathy Fulminant Hepatic Failure Octanoic Acid Dimethyl Sulfide Blood Ammonia 
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Copyright information

© Springer Verlag Berlin Heidelberg 1981

Authors and Affiliations

  • Leslie Zieve
    • 1
  1. 1.Department of MedicineHennepin County Medical CenterMinneapolisUSA

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