P70 Cui bono? Can we retrospectively identify risk factors for futility in AD/ACLF at ICU admission?

<h3>Introduction</h3> Acute decompensation (AD) is common among patients with cirrhosis, with rising admission numbers over the last decade.4 It may progress to acute-on-chronic liver failure (ACLF), carrying a high risk of short-term mortality1. Early intervention and organ support in the ICU are key to improving outcomes in this high-risk population. Identifying those who are unlikely to benefit from ICU admission can be difficult. The aim of this study was to identify patient characteristics for whom ICU admission did not improve outcome. <h3>Methods</h3> A retrospective analysis was performed of all patients admitted from hospital admission points to the QE Liver ICU with AD or ACLF from October 2022–2024. Patients with non-cirrhotic portal hypertension, inter-hospital ICU transfers for variceal management, cirrhosis in a previous liver transplant and pregnancy-related liver decompensation were excluded. Characteristics of ICU survivors vs non-survivors were assessed, including day 3 CLIF-C ACLF scores. <h3>Discussion</h3> 56 patients were identified. Patient demographics and clinical features are shown in table 1. Most patients were admitted from a ward and already had ACLF, with less than a quarter already active on the transplant list. Sepsis and upper gastrointestinal bleeding were precipitants in over 67% of admissions. Median ICU LoS was 4.0 days (0.3 – 11.0), and ICU survival was 38/56 (67.9%). At admission, non-survivors were not distinguished by any metric aside from admission bilirubin, significantly higher in non-survivors. All patients survived to d3. Though bilirubin at d3 remained significantly higher in non-survivors and all 5 in-ICU-transplant patients survived, there was no evidence of survival through hepatic recompensation when comparing matched d0–3 bilirubin or d0–3 INR (data not shown). On the other hand, failure to resolve multi-organ failure was evident in non-survivors as d3 ACLF numbers, ACLF severity by grade or score, was significantly higher in non-survivors (despite being similar between groups at admission). In keeping with this, the d3 use of vasopressors and RRT was significantly higher in non-survivors, and was associated with significantly higher d3 white cell counts. <h3>Conclusion</h3> We found no distinguishing features other than admission bilirubin that could potentially help discriminate ICU non-survivors. We reconfirmed the importance of dynamic ACLF trajectory on outcome as d3, but not d0 metrics, were significantly different between groups. It remains unclear why some ACLF patients resolve multiple-organ failure while others do not, though d3 survivors had significantly lower bone marrow markers of inflammation. <h3>References</h3> Moreau, Richard, <i>et al</i>. EASL clinical practice guidelines on acute-on-chronic liver failure. <i>Journal of Hepatology</i> 79(2):461–491. Jalan R, Saliba F, Pavesi M, Amoros A, Moreau R, Ginès P, <i>et al</i>. Development and validation of a prognostic score to predict mortality in patients with acute-on-chronic liver failure. <i>J Hepatol.</i> 2014 Nov;61(5):1038–1047. Engelmann C, Thomsen KL, Zakeri N, <i>et al</i>. Validation of CLIF-C ACLF score to define a threshold for futility of intensive care support for patients with acute-on-chronic liver failure. <i>Crit Care.</i> 2018;22:254. https://doi.org/10.1186/s13054–018-2156–0