摘要
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≤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. TNF αlevels 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 TNF α, 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.
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≤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. TNF αlevels 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 TNF α, 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.
