Pathogenesis of intracranial hypertension in acute liver failure: inflammation, ammonia and cerebral blood flow.

R.A. Jalan*, S. Olde Damink, P.C. Hayes, N.E.P. Deutz, A. Lee

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


BACKGROUND/AIMS: The study aims were to determine the role of inflammation in the pathogenesis of increased intracranial pressure (ICP) in patients with acute liver failure (ALF) and its interplay with cerebral blood flow (CBF) and ammonia. METHODS: Twenty-one patients with ALF were studied from the time they were ventilated for grade 4 encephalopathy until receiving specific treatment for increased ICP. Depending upon the ICP, the patients were divided into two groups; those that required specific treatment (ICP>20 mmHg, group 1: n=8, ICP: 32 (28-54) mmHg); and those that did not (ICP< or =20 mmHg, group 2: n=13, ICP: 15 (10-20) mmHg). RESULTS: Inflammatory markers, arterial ammonia and CBF were significantly higher in the group 1 patients. TNFalpha levels correlated with CBF (r=0.80). Four patients from group 2 developed surges of increased ICP (32 (15-112) hours from enrolment). These were associated increases in markers of inflammation and TNFalpha, and an increase in CBF. There was no change in these inflammatory markers, CBF or ICP in the other 9 group 2 patients. CONCLUSIONS: The results of this study suggest that inflammation plays an important synergistic role in the pathogenesis of increased ICP possibly through its effects on CBF.
Original languageEnglish
Pages (from-to)613-20
JournalJournal of Hepatology
Issue number4
Publication statusPublished - 1 Jan 2004

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