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 h after collapse, after exclusion of primary non-hypoxic hepatopathy. Analyses were restricted to patients alive at 72 h 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 h 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.