• Rajiv Jalan, Steven W M Olde Damink, Peter C Hayes, Nicolaas E P Deutz, and Alistair Lee.
• Liver Failure Group, Institute of Hepatology, Royal Free and University College London Medical School and University College London Hospitals, 69-75 Chenies Mews, London WC1E 6HX, UK. r.jalan@ucl.ac.uk
• J. Hepatol. 2004 Oct 1; 41 (4): 613-20.

Background/AimsThe 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.MethodsTwenty-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).ResultsInflammatory 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.ConclusionsThe results of this study suggest that inflammation plays an important synergistic role in the pathogenesis of increased ICP possibly through its effects on CBF.

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