s A.I.S.F. Annual Meeting (Rome, February 25th−26th, 2010) / Digestive and Liver Disease 42 Suppl. 1 (2010) S1–S51 S19 with normal spleen diameter (p 20 ppm or a rise by 12 ppm above baseline following glucose administration was considered as positive. IP was evaluated by the (51)Cr-EDTA permeability test. SIBO prevalence in LC was compared with healthy controls and correlated with LC severity and IP. Results: Twenty-nine out of 56 LC patients had SIBO vs 2 of the 48 healthy controls (51.8% vs 4%, p< 0.0001). SIBO prevalence correlated with the severity of LC (68.2% of Child C pts vs. 56.2% of Child B and 31.2% of Child A pts), with the presence of ascites (66% in ascitic pts vs. 27% in non-ascitic pts), and with a history of SBP (92% of patients with SBP vs. 48% of those without SBP). A significant correlation was found between presence of SIBO and altered IP: it was weak for Child A but significant for Child B and C pts (R = 0.07, NS; R = 0.35, p = 0.005; R = 0.29, p = 0.03, respectively). Conclusions: SIBO seems to have a higher prevalence in LC, correlates with LC severity and altered IP. This association suggests that SIBO may affect intestinal permeability of splancnic vessels and/or peritoneal membranes leading to SBP outbreak in LC. Future interventional studies are needed to confirm these preliminary data. T.N.13 PREDICTORS OF OUTCOME IN CIRRHOTICS ADMITTED TO INTENSIVE CARE UNIT (ICU); SURVIVORS EXHIBITED SIGNIFICANT RISE OF SERUM SODIUM LEVELS AND A FALL IN LACTATE LEVELS AT 48 HOURS M. Garcovich1,2, V. Vemala1, A. Davenport1, E. Dionigi1, S. Shaw1, B. Agarwal1, A.K. Burroughs1. Sheila Sherlock Liver Centre, Royal Free Hospital, London, UK; Dipartimento di Medicina Interna, Universita Cattolica del Sacro Cuor, Rome, Italy Background: Critically ill cirrhotics admitted to ICU have poor prognosis. Factors known to portend worse outcome include mechanical ventilation, development of shock, renal failure and increasing number of organ failure. While a negative impact on mortality of low serum sodium level is observed in stable cirrhotics active on the waiting list for liver transplant, the impact of admission serum sodium and its changes during the course of an acute illness in these patients is not well known. Methods: We retrospective studied a cohort of cirrhotics admitted to ICU between 2005−08 at the Royal Free Hospital. Data were collected on demographic variables, aetiology of liver disease, liver-specific prognostic scores; Child–Turcotte–Pugh (CTP), Model for end-stage liver disease (MELD), United Kingdom model for end-stage liver disease (UKELD), acute physiological score and chronic health points (APACHE II) and sequential organ failure assessment score (SOFA). In addition, data were also collected for serum Na+ and Lactate levels at 0 (on admission) and at 48 hrs. Results: Currently 67 of 125 patients have been enrolled. 51/67 (76.1%) survived ICU. The non-survivors (16/67) had similar demographics as the survivors, had significantly higher mean MELD, UKELD, SOFA and APACHE II scores, and higher admission lactate. Total CTP score was not different between the groups but serum bilirubin level and prothrombin time were significantly higher in the non-survivors. Although the admission Na+ levels in survivors and non survivors were similar, a significant elevation was observed at 48 hrs in the survivors. The trend for serum lactate levels showed a similar pattern i.e., the survivors showed significant reductions at 48 hrs. Conclusions: The reasons for this observed rise in serum Na+ at 48 hrs in the survivors are not obvious. It may signify a better preserved water balance in patients with less severe underlying liver disease. T.N.14 COLLAGEN PROPORTIONATE AREA IN ASSESSING THE AMOUNT OF FIBROSIS IN CHRONIC LIVER DISEASE: DOES HIGH RESOLUTION COMPARED TO CONVENTIONAL IMAGE CAPTURING AND ANALYSIS ALTERS ITS RESULTS? L. Andreana1, G. Isgro1, M. Garcovich1, A. Hall2, F. Grillo2, A.P. Dhillon2, A.K. Burroughs1, T.V. Luong2. The Sheila Sherlock Liver Centre and University Dept. of Surgery, Royal Free Hospital, London, UK; Dept. of Histopathology, Royal Free Hospital,