Hypoxic hepatitis after cardiac arrest is associated with 30-day mortality, poor neurological outcome and non-occlusive mesenteric ischemia

Background and aims Abdominal organ dysfunction after cardiac arrest may reflect hepatosplanchnic hypoperfusion. Hypoxic hepatitis may indicate severe systemic hypoperfusion and a hepatosplanchnic ischemic phenotype. We assessed hypoxic hepatitis occurrence and associations with 30-day mortality, favourable neurological outcome and non-occlusive mesenteric ischemia after conventional and extracorporeal cardiopulmonary resuscitation (CPR, ECPR). Methods We performed a retrospective single-centre cohort study of adult patients admitted after cardiac arrest between 11/2020 and 02/2026. Hypoxic hepatitis was defined as peak aspartate or alanine aminotransferase ≥20 times the sex-specific upper limit of normal within 72 hours after collapse, after exclusion of primary non-hypoxic hepatopathy. Analyses were restricted to patients alive at 72 hours and performed separately for CPR and ECPR using adjusted Cox proportional hazards and logistic regression models. Results Among 835 patients, hypoxic hepatitis occurred in 58/702 CPR patients (8.3%) and 29/133 ECPR patients (21.8%). In the CPR cohort, hypoxic hepatitis was associated with higher 30-day mortality (adjusted HR 1.63, 95% CI 1.11–2.42), lower odds of favourable neurological survival (adjusted OR 0.33, 95% CI 0.17–0.64) and higher odds of non-occlusive mesenteric ischemia (adjusted OR 7.02, 95% CI 2.61–18.89). Corresponding adjusted estimates in ECPR patients were HR 2.65 (95% CI 1.44–4.90), OR 0.09 (95% CI 0.02–0.33) and OR 3.99 (95% CI 1.35–11.78), respectively. Conclusion Among patients alive 72 hours after cardiac arrest, hypoxic hepatitis was associated with increased 30-day mortality, poor neurological outcome and non-occlusive mesenteric ischemia and may help identify a hepatosplanchnic high-risk phenotype after both CPR and ECPR.