Abstract DP289: Impaired Cerebral Autoregulation and Postoperative Acute Kidney Injury After Non-cardiac Surgery

Introduction: Interindividual variation in the lower limit of cerebral autoregulation (LLA) challenges fixed mean arterial pressure (MAP) targets. We assessed whether impaired cerebral autoregulation and hypoperfusion burden below the LLA are associated with acute kidney injury (AKI) after noncardiac surgery. Methods: Adults undergoing major noncardiac surgery had continuous intraarterial pressure and bifrontal nearinfrared spectroscopy monitoring. Bilateral frontoparietal near infrared spectroscopy monitoring of regional cerebral oxygen saturations (rSO2) and invasive MAP were captured intraoperatively and analysed using wavelet semblance. The LLA was defined as the MAP corresponding to the inflection point on semblance vs MAP plots, with semblance values >0.3 indicating impaired autoregulation. Hypoperfusion burden was quantified as the area under the curve for pressure values below the LLA (mmHg.min). The primary outcome was AKI (Kidney Disease: Improving Global Outcomes). Between group comparisons used t-tests or Wilcoxon rank–sum for continuous data and χ 2 /Fisher’s exact tests for categorical data; covariate adjusted associations were explored using multivariable logistic regression. Relevant ethics approvals were prospectively obtained (PAABLo: HREC/18/QPCH/48043, ACTRN12617001365358; Wavelet HREC/17/QPCH/33, ACTRN12617000834392) and all participants provided written informed consent. Results: One hundred and four patients contributed 19,416 monitored minutes. An LLA was identifiable in 85% (88/104). In those with a detectable LLA, the median LLA was 70 mmHg (IQR 56.3–77.5, Figure 1). Across all patients, 15% of monitored time occurred with mean arterial pressure below the LLA. AKI occurred in 16/101 (15.8%). Compared with patients without AKI, those with AKI had higher mean semblance consistent with impaired autoregulation (0.3 [IQR 0.2–0.4] vs 0.2 [0.1–0.3]; p=0.005), larger hypoperfusion burdens(AUC<LLA 235.7 mmHg.min [IQR 24.2–520.1] vs 42.0 mmHg.min [IQR 0.3–248.9]; p=0.033), and longer durations with pressure below the LLA (40.1 min [IQR 2.3–53.1] vs 9.8 min [IQR 0.5–39.2]; p=0.031). Conclusions: Impaired cerebral autoregulation and greater hypoperfusion burden below the patient specific LLA are associated with postoperative AKI. Marked interindividual LLA variability undermines one size fits all pressure targets and justifies randomised trials of personalised, autoregulation guided haemodynamic management.

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Journal
Stroke
Published
2026-01-29
DOI
https://doi.org/10.1161/str.57.suppl_1.dp289
Primary Topic
Traumatic Brain Injury and Neurovascular Disturbances
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article
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article

Abstract DP289: Impaired Cerebral Autoregulation and Postoperative Acute Kidney Injury After Non-cardiac Surgery

Jonathon Fanning, David Highton, Matthew Bright
Stroke
Traumatic Brain Injury and Neurovascular Disturbances
article

Abstract DP289: Impaired Cerebral Autoregulation and Postoperative Acute Kidney Injury After Non-cardiac Surgery

Jonathon Fanning, David Highton, Matthew Bright
article en

Abstract

Introduction: Interindividual variation in the lower limit of cerebral autoregulation (LLA) challenges fixed mean arterial pressure (MAP) targets. We assessed whether impaired cerebral autoregulation and hypoperfusion burden below the LLA are associated with acute kidney injury (AKI) after noncardiac surgery. Methods: Adults undergoing major noncardiac surgery had continuous intraarterial pressure and bifrontal nearinfrared spectroscopy monitoring. Bilateral frontoparietal near infrared spectroscopy monitoring of regional cerebral oxygen saturations (rSO2) and invasive MAP were captured intraoperatively and analysed using wavelet semblance. The LLA was defined as the MAP corresponding to the inflection point on semblance vs MAP plots, with semblance values >0.3 indicating impaired autoregulation. Hypoperfusion burden was quantified as the area under the curve for pressure values below the LLA (mmHg.min). The primary outcome was AKI (Kidney Disease: Improving Global Outcomes). Between group comparisons used t-tests or Wilcoxon rank–sum for continuous data and χ 2 /Fisher’s exact tests for categorical data; covariate adjusted associations were explored using multivariable logistic regression. Relevant ethics approvals were prospectively obtained (PAABLo: HREC/18/QPCH/48043, ACTRN12617001365358; Wavelet HREC/17/QPCH/33, ACTRN12617000834392) and all participants provided written informed consent. Results: One hundred and four patients contributed 19,416 monitored minutes. An LLA was identifiable in 85% (88/104). In those with a detectable LLA, the median LLA was 70 mmHg (IQR 56.3–77.5, Figure 1). Across all patients, 15% of monitored time occurred with mean arterial pressure below the LLA. AKI occurred in 16/101 (15.8%). Compared with patients without AKI, those with AKI had higher mean semblance consistent with impaired autoregulation (0.3 [IQR 0.2–0.4] vs 0.2 [0.1–0.3]; p=0.005), larger hypoperfusion burdens(AUC<LLA 235.7 mmHg.min [IQR 24.2–520.1] vs 42.0 mmHg.min [IQR 0.3–248.9]; p=0.033), and longer durations with pressure below the LLA (40.1 min [IQR 2.3–53.1] vs 9.8 min [IQR 0.5–39.2]; p=0.031). Conclusions: Impaired cerebral autoregulation and greater hypoperfusion burden below the patient specific LLA are associated with postoperative AKI. Marked interindividual LLA variability undermines one size fits all pressure targets and justifies randomised trials of personalised, autoregulation guided haemodynamic management.

StrokeVol. 57(Suppl_1)
The University of Queensland (AU), Princess Alexandra Hospital (AU), Prince Charles Hospital (AU)
Good health and well-being
Openalex Percentile: Top 74%
Traumatic Brain Injury and Neurovascular Disturbances
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