Acute kidney injury (AKI) remains one of the most common serious complications after noncardiac surgery, and intraoperative hypotension (IOH) is consistently identified as a modifiable risk factor. Observational studies show a consistent, roughly dose-response association between IOH, particularly at mean arterial pressures below 60-65 mmHg, and postoperative AKI, with stronger associations in patients with limited renal reserve. Definitions of IOH vary widely, which complicates the comparison of studies and the translation of thresholds into clinical targets. Randomized trials of individualized or higher blood pressure targets have generally not confirmed a kidney-protective benefit, and pooled analyses with trial sequential analysis have not demonstrated that higher targets reduce AKI. This narrative review examines how IOH definitions evolved, summarizes the conflicting intervention evidence, and assesses the controversies that shape current practice. The review concludes that avoiding severe and sustained hypotension remains reasonable, whereas current randomized trial evidence does not support a general kidney-protective benefit of higher or individualized blood pressure targets. This conclusion is provisional and is tempered by the methodologic and causal uncertainties.
Study objective To evaluate the first-hour arterial-to-end-tidal carbon dioxide gradient as a marker of recorded 90-day mortality, distinguishing association, component interpretation and incremental prediction. Design Retrospective cohort study. Setting INSPIRE v1.4.2, covering surgery from 2011 to 2020. Patients Adults undergoing their first eligible intracranial operation with arterial carbon dioxide tension (PaCO₂) recorded within 60 min of anesthesia start. End-tidal carbon dioxide (ETCO₂) was paired within ±5 min. Measurements The outcome was database-recorded all-cause death within 90 days. Firth regression evaluated the gradient without conditioning on either component. The revised principal association model included clinical covariates and contemporaneous mean arterial pressure, heart rate and minute ventilation. Component and internally validated prediction models were secondary. Main results Among 1907 patients, 95 deaths were recorded. The clinical gradient odds ratio (OR) per 5 mmHg was 1.38 (95% confidence interval [CI], 1.09–1.73). The revised principal association model included 1830 patients and 92 events (OR, 1.34; 95% CI, 1.06–1.69). Conditional component estimates did not establish predominance of either component. Adding the gradient to clinical variables, contemporaneous physiology and ETCO₂ changed optimism-corrected area under the curve from 0.832 to 0.833, without improving the Brier score. Conclusions A larger first-hour gradient was associated with recorded mortality in patients selected for early paired monitoring. Within the evaluated models and metrics, incremental prediction was limited. These findings do not establish a causal mechanism, treatment target or externally validated prediction tool.
