Metabolic Brain Disease

, 24:5

The brain in acute liver failure. A tortuous path from hyperammonemia to cerebral edema

Authors

  • Peter Nissen Bjerring
    • Dept. Hepatology, section A-2121, RigshospitaletUniversity Hospital of Copenhagen
  • Martin Eefsen
    • Dept. Hepatology, section A-2121, RigshospitaletUniversity Hospital of Copenhagen
  • Bent Adel Hansen
    • Dept. Hepatology, section A-2121, RigshospitaletUniversity Hospital of Copenhagen
    • Dept. Hepatology, section A-2121, RigshospitaletUniversity Hospital of Copenhagen
Original Paper

DOI: 10.1007/s11011-008-9116-3

Cite this article as:
Bjerring, P.N., Eefsen, M., Hansen, B.A. et al. Metab Brain Dis (2009) 24: 5. doi:10.1007/s11011-008-9116-3

Abstract

Acute liver failure (ALF) is a condition with an unfavourable prognosis. Multiorgan failure and circulatory collapse are frequent causes of death, but cerebral edema and intracranial hypertension (ICH) are also common complications with a high risk of fatal outcome. The underlying pathogenesis has been extensively studied and although the development of cerebral edema and ICH is of a complex and multifactorial nature, it is well established that ammonia plays a pivotal role. This review will focus on the effects of hyperammonemia on neurotransmission, mitochondrial function, oxidative stress, inflammation and regulation of cerebral blood flow. Finally, potential therapeutic targets and future perspectives are briefly discussed.

Keywords

Acute liver failureCerebral edemaHyperammonemiaIntracranial hypertension

Copyright information

© Springer Science+Business Media, LLC 2008