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Postoperative acute kidney injury

A never-ending challenge

Navarro, Lais H.; Chew, Michelle S.

European Journal of Anaesthesiology (EJA): September 2018 - Volume 35 - Issue 9 - p 639–640
doi: 10.1097/EJA.0000000000000862
Invited commentary
Free

From the Botucatu Medical School, UNESP, Botucatu, Sao Paulo, Brazil (LHN) and Department of Anaesthesia and Intensive Care, Medical and Health Sciences, Linköping University Hospital, Linköping, Sweden (MSC)

Correspondence to Dr Michelle S. Chew, Department of Anaesthesia and Intensive Care, Medical and Health Sciences, Linköping University Hospital, S-58185 Linköping, Sweden E-mail: michelle.chew@liu.se

This Invited Commentary accompanies the following article:

Furrer MA, Schneider MP, Löffel LM, et al. Impact of intra-operative fluid and noradrenaline administration on early postoperative renal function after cystectomy and urinary diversion. A retrospective observational cohort study. Eur J Anaesthesiol 2018; 35:641–649.

Acute kidney injury (AKI) is a potentially reversible and important contributor to postoperative morbidity and mortality. Its pathophysiology is likely to be multifactorial,1 with the inflammatory response and peri-operative hypovolaemia playing important pathophysiological roles. Intra-operative hypotension is also a demonstrated independent risk factor for postoperative AKI, presumably through renal hypoperfusion and a subsequent reduction in medullary blood flow. Indeed, it has been shown that most patients presenting with postoperative AKI have had at least one episode of peri-operative haemodynamic instability.2 Current evidence also supports a time dependent relationship between the duration of intra-operative hypotension and AKI.3,4

It therefore makes intuitive sense that in their study presented in this month's issue of the European Journal of Anaesthesiology, Furrer et al.5 investigated the role of fluid administration and noradrenaline use and their relationship to early postoperative AKI in patients undergoing cystectomy and urinary diversion. The authors also aimed to identify other contributing risk factors for postoperative AKI in those patients. Although the retrospective nature of the study inherently raises the possibility of bias, there are several important messages:

  1. Lower infusion rates of crystalloids were associated with the development of AKI postoperatively;
  2. Noradrenaline administration at a median dose of about 2.1 μg kg−1 h−1 (=low dose) was not a significant predictor of postoperative AKI;
  3. Age, sex, higher pre-operative haemoglobin (Hb) and pre-operative antihypertensive medications were important factors associated with postoperative AKI.

It is notable that, after age, the amount (ml kg−1) of administered crystalloids intra-operatively was the largest independent risk factor for postoperative AKI. Fluids and the need for vasopressors in the peri-operative period may contribute to changes in postoperative renal function. The type of fluid, for example, may influence the postoperative renal outcomes. It is well known that colloids may impair renal function in critically ill, septic patients. Similarly, patients with pre-operative renal dysfunctions should not be treated with this type of fluid. Furrer et al. noted that the administration of colloids was not associated with AKI; however, this subfinding should be interpreted cautiously, as the total volume (median 500 ml) and the amount (median 6.5 ml kg−1 bodyweight) was very low in patients who received colloids. Further, only a minority of patients (8.6%, n=66) received colloids at all, usually for replacement of severe blood loss.

Given the impact of hypotension on postoperative AKI, the use of vasopressors to counteract intra-operative hypotension seems appropriate. Noradrenaline, for example, has been shown to improve renal blood flow, glomerular filtration rate and urine output when used judiciously. Within the dose limits used in this study, and notwithstanding the limitations of the retrospective study design, it seems that noradrenaline is not associated with AKI in this group of high-risk patients.

The finding that increased pre-operative Hb was associated with AKI in the study by Furrer et al. is interesting and somewhat counterintuitive. It is not supported by previous studies.6 These findings may indicate that patients in the AKI group were more likely to be dehydrated prior to surgery, exacerbated by the restrictive fluid strategy that the patients were exposed to. In fact, pre-operative volume status is typically unknown and should not be presumed to be either adequate or inadequate. Blood volume varies considerably between patients depending on sex, weight and oxygen consumption. Moreover, effective circulatory volume varies when patients are under anaesthesia. Furrer et al. do not provide information on pre-operative hydration status and how this may have influenced the risk of postoperative AKI.5

Finally, Weir et al.7 discussed the potential role of peri-operative blood pressure (BP) lability in relation to the risk of postoperative renal dysfunction and 30-day mortality. The authors emphasised the influence of the peri-operative BP as a modifiable risk factor for postoperative AKI. It is possible that some of the patients in the Furrer et al. study were being treated with antihypertensive drugs and had poorer control of their BP before and during surgery, and that this was not accounted for in the study. Moreover, in a retrospective study, Kendale et al.8 found that lower pre-operative BP was associated with reduced postoperative estimated glomerular filtration rate and increased rates of AKI. Their findings suggested that extremes of baseline BP, and not only hypertension, are associated with peri-operative harm. Thus, the chronic use of antihypertensive drugs aiming for a very strict BP control may also be harmful to some of the AKI high-risk patients.

Based on their results, Furrer et al. provided an informative simulated graph in their Fig. 1, showing the probability of AKI given a mean administered volume of colloids of 0.7 ml kg−1, a mean duration of surgery of 386 min, a mean pre-operative plasma creatinine value of 95 μmol l−1, and a mean pre-operative Hb value of 127 g l−1 and stratified to the amount of noradrenaline administered. That the probabilities of developing AKI according to different infusion rates of crystalloids follow the same patterns regardless of whether antihypertensive medications were used add to the robustness of the findings of this study with regard to crystalloid fluid therapy. Whilst the findings of Furrer et al. may not be considered conclusive, the evidence suggests that a restrictive fluid strategy may be harmful. The impact of the volume of intra-operative crystalloids administered, with adequate adjustment for the use of vasopressors, pre-operative hydration status and other potential risk factors for kidney injury, are logical future lines of inquiry in prospective studies.

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Acknowledgements relating to this article

Assistance with the commentary: none.

Financial support and sponsorship: none.

Conflicts of interest: none.

Comment from the Editor: this Invited Commentary was checked and accepted by the editors, but was not sent for external peer review. MSC is an Associate Editor of the European Journal of Anaesthesiology.

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References

1. McKinlay J, Tyson E, Forni LG. Renal complications of anaesthesia. Anaesthesia 2018; 73 (suppl 1):85–94.
2. Calvert S, Shaw A. Perioperative acute kidney injury. Perioper Med 2012; 1:6.
3. Sun LY, Wijeysundera DN, Tait GA, et al. Association of intraoperative hypotension with acute kidney injury after elective noncardiac surgery. Anesthesiology 2015; 123:515–523.
4. Walsh M, Devereaux PJ, Garg AX, et al. Relationship between intraoperative mean arterial pressure and clinical outcomes after noncardiac surgery: toward an empirical definition of hypotension. Anesthesiology 2013; 119:507–515.
5. Furrer MA, Schneider MP, Löffel LM, et al. Impact of intra-operative fluid and noradrenaline administration on early postoperative renal function after cystectomy and urinary diversion: a retrospective observational cohort study. Eur J Anaesthesiol 2018; 35:641–649.
6. Walsh M, Garg AX, Devereaux PJ, et al. The association between perioperative hemoglobin and acute kidney injury in patients having noncardiac surgery. Anesth Analg 2013; 117:924–931.
7. Weir MR, Aronson S, Avery EG, et al. Acute kidney injury following cardiac surgery: role of perioperative blood pressure control. Am J Nephrol 2011; 33:438–452.
8. Kendale SM, Lapis PN, Melhem SM, et al. The association between preoperative variables, including blood pressure, and postoperative kidney function. Anaesthesia 2016; 71:1417–1423.
© 2018 European Society of Anaesthesiology