Association of peri-reperfusion oxygen exposure and early allograft dysfunction after deceased donor orthotopic liver transplantation: a retrospective cohort study

Le résumé fourni par la source

Hepatic insufficiency within a week of orthotopic liver transplantation (OLT), termed early allograft dysfunction (EAD), occurs in 20–25% of deceased donor OLT recipients and carries substantial morbidity and mortality. Ischemia reperfusion injury, in which reperfusion after ischemia provokes oxidative stress and inflammation, underlies EAD. We hypothesized higher peri-reperfusion oxygen exposure is associated with EAD. We conducted a retrospective single-center cohort study of 963 primary adult deceased-donor static cold storage OLT recipients, January 2014 to May 2022. The primary outcome was EAD (serum bilirubin, international normalized ratio, and aminotransferases). Peri-reperfusion oxygen exposure was assessed by median partial pressure of arterial oxygen (PaO 2 ) from 30 min before to 2 h after reperfusion. PaO 2 was examined continuously, and a data-derived dichotomized cutpoint was sought. Associations were evaluated by logistic regression adjusted for donor age, total ischemia time, recipient body mass index, alcohol-associated liver disease, and metabolic dysfunction-associated steatohepatitis, with missing data handled by multiple imputation. Sensitivity analyses addressed exposure timing, anesthesiologist inspired-oxygen preference, and early lactate clearance. EAD occurred in 199 of 963 recipients (21%). Modeled continuously, higher PaO 2 was associated with EAD after adjustment (adjusted OR 1.16 per 50 mmHg [95% CI 1.01–1.34]). The complete-case estimate was nearly identical but less precise (1.14 [95% CI 0.97–1.34]), with no detected departure from linearity ( p = 0.28, multiple imputation). The association could not be localized to the pre- or post-reperfusion window. The estimate changed little after adjusting for early lactate clearance, and the association remained evident within the low-inspired-oxygen stratum; the high-inspired-oxygen stratum was uninformative owing to limited exposure contrast. No cutpoint could be identified across the 205 candidate thresholds searched (complete cases; global p = 0.18). Higher peri-reperfusion PaO 2 was associated with EAD after adjustment; the association could not be statistically localized to the pre- or post-reperfusion window. Whether this reflects a modifiable causal factor, a marker of early graft dysfunction, or both remains uncertain. External validation and prospective trials are needed to determine whether conservative oxygen management reduces EAD risk.

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.