Kyota Fukazawa1, Yoshitsugu Yamada2, Edward Gologorsky3, Kristopher L Arheart4, Ernesto A Pretto1. 1. Department of Anesthesiology, Preoperative and Pain Management. 2. Division of Biostatistics, University of Miami, Leonard Miller School of Medicine and Jackson Memorial Hospital, Miami, FL. 3. Department of Anesthesiology, Preoperative and Pain Management. Electronic address: egologorsky@med.miami.edu. 4. Department of Anesthesiology and Pain Management Centre, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Abstract
OBJECTIVES: The authors' current understanding of the phenomenon of significant and sustained decrease in arterial pressure following liver graft reperfusion (postreperfusion syndrome [PRS]), is derived from relatively small observational reports, and no large scale analysis of PRS exists up to date. This study investigated its incidence, risk factors, temporal course of hemodynamic recovery, and its impact on functional graft outcome. DESIGN: Retrospective observational study of 1,024 electronic records of orthotopic liver transplant recipients. SETTING: Major transplant center. MEASUREMENTS: Out of 1,024, 715 records satisfied the inclusion criteria. Data were analyzed by multivariable Cox's proportional hazard model to identify risk factors for PRS. Hemodynamic recovery patterns and functional graft outcomes were compared between the cohorts of interest (intraoperative PRS) and control (no intraoperative PRS) after propensity score-matching. Association between donor risk index and hemodynamic recovery after hepatic artery reperfusion was analyzed by a multivariable regression model. RESULTS: The overall incidence of PRS was 31.6% with associated mortality of 0.3%. Independent risk factors for PRS included older donor age, higher donor risk index, and lower central venous pressure at reperfusion. Hemodynamic recovery after PRS following portal vein reperfusion was delayed until hepatic artery reperfusion. The slope of hemodynamic recovery, expressed as %MAP/min, correlated negatively with donor risk index (p=0.014). Immediate and 1-year graft survival rates were similar in both cohorts. CONCLUSIONS: Host hemodynamic response to graft reperfusion appeared to be phasic: initial abrupt hypotension after portal vein reperfusion was followed by a period of gradual decline of blood pressure until hepatic artery reperfusion, and sustained hemodynamic recovery afterwards. The slope of hemodynamic recovery correlated negatively with the donor risk index. PRS was not associated with deterioration of post-transplant graft survival and function.
OBJECTIVES: The authors' current understanding of the phenomenon of significant and sustained decrease in arterial pressure following liver graft reperfusion (postreperfusion syndrome [PRS]), is derived from relatively small observational reports, and no large scale analysis of PRS exists up to date. This study investigated its incidence, risk factors, temporal course of hemodynamic recovery, and its impact on functional graft outcome. DESIGN: Retrospective observational study of 1,024 electronic records of orthotopic liver transplant recipients. SETTING: Major transplant center. MEASUREMENTS: Out of 1,024, 715 records satisfied the inclusion criteria. Data were analyzed by multivariable Cox's proportional hazard model to identify risk factors for PRS. Hemodynamic recovery patterns and functional graft outcomes were compared between the cohorts of interest (intraoperative PRS) and control (no intraoperative PRS) after propensity score-matching. Association between donor risk index and hemodynamic recovery after hepatic artery reperfusion was analyzed by a multivariable regression model. RESULTS: The overall incidence of PRS was 31.6% with associated mortality of 0.3%. Independent risk factors for PRS included older donor age, higher donor risk index, and lower central venous pressure at reperfusion. Hemodynamic recovery after PRS following portal vein reperfusion was delayed until hepatic artery reperfusion. The slope of hemodynamic recovery, expressed as %MAP/min, correlated negatively with donor risk index (p=0.014). Immediate and 1-year graft survival rates were similar in both cohorts. CONCLUSIONS: Host hemodynamic response to graft reperfusion appeared to be phasic: initial abrupt hypotension after portal vein reperfusion was followed by a period of gradual decline of blood pressure until hepatic artery reperfusion, and sustained hemodynamic recovery afterwards. The slope of hemodynamic recovery correlated negatively with the donor risk index. PRS was not associated with deterioration of post-transplant graft survival and function.
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