The systemic inflammatory response syndrome in acute liver failure

Citation
N. Rolando et al., The systemic inflammatory response syndrome in acute liver failure, HEPATOLOGY, 32(4), 2000, pp. 734-739
Citations number
47
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
HEPATOLOGY
ISSN journal
02709139 → ACNP
Volume
32
Issue
4
Year of publication
2000
Part
1
Pages
734 - 739
Database
ISI
SICI code
0270-9139(200010)32:4<734:TSIRSI>2.0.ZU;2-7
Abstract
The systemic inflammatory response syndrome (SIRS) in acute liver failure ( ALF), in which infection is common, has not been studied. In this study, SI RS components were recorded on admission and during episodes of infection, in 887 ALF patients admitted to a single center during an 11-year period. O verall, 504 (56.8%) patients manifested a SIRS during their illness, with a maximum of 1, 2, and 3 concurrent SIRS components in 166, 238, and 100 pat ients, respectively. In 353 (39.8%) patients who did not become infected, a SIRS on admission was associated with a more critical illness, subsequent worsening of encephalopathy, and death. infected patients more often develo ped a SIRS and one of greater magnitude. The magnitude of the SIRS in 273 p atients with bacterial infection correlated with mortality, being 16.7%, 28 .4%, 41.2%, and 64.7% in patients with 0, 1, 2, and 3 maximum concurrent SI RS components, respectively. Similar correlations with mortality were seen for SIRS associated with fungal infection, bacteremia, and bacterial chest infection. Fifty-nine percent of patients with severe sepsis died, as did 9 8% of those with septic shock. A significant association was found between progressive encephalopathy and infection. Infected patients with progressiv e encephalopathy manifested more SIRS components than other infected patien ts. For patients with a SIRS, the proportions of infected and noninfected p atients manifesting worsening encephalopathy were similar. In ALF, the SIRS , whether or not precipitated by infection, appears to be implicated in the progression of encephalopathy, reducing the chances of transplantation and conferring a poorer prognosis.