P139 Acute liver failure survival and non-survival trajectories

<h3>Background</h3> Acute liver failure (ALF) survival and mortality are thought primarily linked to hepatic function. <h3>Aim</h3> To characterise ALF recovery and mortality trajectories and the role of hepatic recovery in that. <h3>Methods</h3> We examined an ALF series of 37 patients treated between May 2022 and April 2024 for recovery and mortality trajectories according to ALF aetiology, Kings College Criteria (KCC), multi-organ failure (MOF) severity and type.1 Hepatic recovery was assessed by INR or hyperammonaemia, glucose/insulin dependence and mounting C-reactive protein responses when INR was confounded. <h3>Results</h3> Overall survival (table 1) was 31/37 (84%): 9/37 (51%) were transplanted (100% survival) whereas transplant-free survival (TFS) was 12/37 (32%). 23/37 (59.9%) had paracetamol hepatotoxicity (POD). 27/37 (72.9%) fulfilled Kings College criteria (KCC), significantly more commonly in non-POD (13/22 (59.1%) vs 14/15 (93.3%), p=0.028). All 10 KCC-ve patients survived (9/10 POD). TFS was 2/27 (7.4%) amongst KCC+ve, both POD. Consequently, TFS was significantly lower for non-PODs (p = 0.011). Mortality occurred in non-PODs that were unsuitable for transplant (prohibitive social circumstances &amp;/or medical co-morbidities (5/6), (non-malignant) non-transplant aetiologies (1/6)). All 6 deaths occurred in patients where TFS remained a clinical aim. ICU LoS was significantly lower in non-survivors (4.5d (4 – 11) vs 10d (6 – 17), p=0.03). No cranial deaths occured. Symptomatic DIC occurred within 24h of death in 4/6 (67%) patients, in one as part of viral triggered HLH; vasoplegia, low cardiac output state, metabolic failure despite haemofiltration, and ongoing hepatic failure reflected terminal decline. Low cardiac output state contributed to death in 2 more patients over 60, though prolonged DIC dominated futility determination in one. In the other case, respiratory compromise from cardiac failure coupled with chronic co-morbidity determined futility. Pancreatitis and mesenteric thrombosis contributed to hyperlactatemia, vasoplegia and ongoing hepatic insufficiency in another. 2 probable cases of bacterial sepsis were drivers of DIC and vasoplegia. Ventilator associated pneumonia contributed to respiratory failure in one, an unidentified source in another. Improving hepatic function was noted pre-mortem in 3/6 (50%) deaths. <h3>Conclusion</h3> In this series, mortality in KCC+ ALF was high, confined to non-POD aetiologies. Mortality trajectories were complex, not related to cranial complications and didn’t necessarily feature refractory hepatic failure. Treatment or hyperinflammation generated new pathologies that re-directed to mortality trajectories even if hepatic function was recovering. Prolonged ICU treatment in non-transplant suitable KCC+ patients is advisable to provide opportunities for MOF reversal and hepatic recompensation when complications can be avoided. <h3>Reference</h3> https://doi.org/10.1016/S0168–8278(25)00486–6