The Ignored Role of Intraoperative Hypotension in Producing Postoperative Acute Kidney Injury-An Obligatory Appeal for More Preventative Nephrology

Abstract

Our recent experiences suggest and show a link between IOH and postoperative AKI. Sun et al. (2015) recently demonstrated that postoperative AKI was associated with sustained intraoperative hypotensive periods of MAP <55 and <60 mm Hg, respectively, in a graded pattern. Our experiences and new emerging Surgery-AKI literature provide an impetus for clinical trials to be set up and completed to determine whether interventions that promptly treat IOH, or better still that prevent IOH, and that are tailored to suit individual patient physiology, would reduce the risk of AKI. We posit that IOH is a neglected cause of postoperative AKI. We call for a preventative nephrology paradigm shift and the targeting of MAP ≥ 60 mm Hg and/or SBP ≥ 90 mm Hg during surgical procedures. Particularly in sub-Saharan Africa with its paucity of renal replacement therapy options to manage kidney failure, every effort to limit AKI, SORO-ESRD and exacerbation of kidney dysfunction in general, must be vigorously applied.

Hospital-acquired nephrotoxic exposures in the precipitation of acute kidney injury – A case series analysis and a call for more preventative nephrology practices

“…Fortunately, during the laparotomy procedure to evacuate the abscess, intra-operative blood pressures were maintained with MABP generally >80 mm Hg and consequently, the patient was saved the additional precipitating factor of intraoperative hypotension. We and several other investigators have highlighted recently, in several publications, the neglected, potent, and yet preventable role of intraoperative hypotension in the causation of post-operative AKI (12)(13)(14)(15)(16). Case II: This 77-year-old Caucasian female patient had CKD stage IIIB with serum creatinine serum creatinine of 1.57-1.67 mg/dL (eGFR = 30-32 mL/min/1.73m 2 BSA).…”

“…Subsequently, the combination of concurrent ACE inhibition (enalapril), concurrent diuretic (hydrochlorothiazide) and the exposure to seven doses of intravenous NSAID (ketorolac) had completed the well described phenomenon of "triple whammy" nephrotoxicity (22)(23)(24)(25)(26). To further exacerbate this scenario, the patient during the anterior resection of the rectal mass experienced significant intraoperative hypotension, a factor that has now been acknowledged to be a neglected yet potent factor in the pathogenesis of post-operative AKI (12)(13)(14)(15)(16). We dubbed this phenomenon as the previously unrecognized syndrome of "quadruple whammy" (27)(28)(29).…”

Postoperative Acute Kidney Injury in Abdominal Operations: a Critical Appraisal

“…In the cited Bijker report, all analyses were repeated using time variables of 5 and 10 min for the minimal episode of intraoperative hypotension duration [4]. In our previous reports, we demonstrated intraoperative hypotension as measured by systolic arterial pressure changes over contiguous periods sometimes exceeding 1-2 h [5,6].…”

“…Whether they would still have enough AKI cases to power the regression analysis is open to question. Intraoperative hypotension must be avoided to mitigate postoperative AKI [4][5][6]. Postoperative AKI, as demonstrated in the study, drives cost of care and is associated with significant 90-day mortality [1].…”

Identifying Risk Factors for Acute Kidney Injury After Pediatric Cardiac Surgery

“…4 Most importantly, the authors did not provide the intraoperative hemodynamic data, especially the occurrence of hypotension, a known causative factor of postoperative AKI. 5 Patterson et al determined that reduced renal perfusion pressure by a lower mean arterial pressure and a higher central venous pressure was also a significant predictor of AKI after pediatric cardiac surgery. 6 Furthermore, the multivariable model in Lee et al's study only included the preoperative vasoactive inotrope score, not the intraoperative vasoactive inotrope score.…”