Postoperative goal-directed therapy and development of acute kidney injury following major elective noncardiac surgery: post-hoc analysis of POM-O randomized controlled trial

Abstract

Background: The role of goal-directed therapy (GDT) in preventing creatinine rise following noncardiac surgery is unclear. We performed a post-hoc analysis of a randomized controlled trial to assess the relationship between postoperative optimization of oxygen delivery and development of acute kidney injury (AKI)/creatinine rise following noncardiac surgery. Methods: Patients were randomly assigned immediately postoperatively to receive either fluid and/or dobutamine therapy to maintain/restore their preoperative oxygen delivery, or protocolized standard care (oxygen delivery only recorded). Primary end point was serial changes in postoperative creatinine within 48 h postoperatively. Secondary outcomes were development of AKI (KDIGO criteria) and minimal creatinine rise (MCR; no decline from preoperative creatinine), related to all-cause morbidity and length of stay. Results: Postoperative reductions in serum creatinine were similar (P = 0.76) in patients randomized to GDT [10 µmol/L (95% confidence interval, CI: 17 to -1); n = 95] or protocolized care [8 µmol/L (95% CI: 17 to -6); n = 92]. Postoperative haemodynamic management was not associated with the development of MCR [78/187 (41.7%)] or AKI [13/187; (7.0%)]. Intraoperative requirement for norepinephrine was more likely in patients who developed postoperative rises in creatinine [relative risk (RR): 1.66 (95% CI: 1.04-2.67); P = 0.04], despite similar volumes of intraoperative fluid being administered. Persistently higher lactate during the intervention period was associated with AKI (mean difference: 1.15 mmol/L (95% CI: 0.48-1.81); P = 0.01]. Prolonged hospital stay was associated with AKI but not MCR [RR: 2.71 (95% CI: 1.51-4.87); P = 0.0008]. Conclusion: These data provide further insights into how perioperative haemodynamic alterations relate to postoperative increases in creatinine once systemic inflammation is established.

Keywords: acute kidney injury; cardiac output; noncardiac surgery; oxygen delivery.

Fig. 1.

Trial enrollment and analysis plan. RCT, randomized controlled trial.

Fig. 2.

Oxygen delivery stratified by postoperative creatinine rise and allocation to postoperative haemodynamic intervention. (A) Oxygen delivery, indexed and expressed as % individualized preoperative value. Mean values (95% CI) shown; numbers per group indicated within figure. Failure to reach preoperative oxygen delivery was associated with postoperative creatinine rise. Asterisk denotes P = 0.008, for comparison between mean oxygen delivery during intervention period (standardized to each patients’ preoperative value), by ANOVA. Post-hoc analysis showed a mean difference in standardized oxygen delivery between GDT and GDT-creatinine rise was 22% [(95% CI: 1–45); P = 0.05].

Fig. 3.

Kaplan–Meier plot showing relationship between development of early AKI and subsequent length of hospital stay.