We appreciate Dr Ripollés et al.'s1 interest in our study.2 They kindly recognise that the results of our trial are of great importance in routine clinical practice. Our work adds to the paucity of prospective trials studying postoperative acute kidney injury, as defined by current consensus definitions, after major abdominal surgery.3 In their letter, they highlight three aspects regarding the administration of fluids during the perioperative period that are considered particularly important. We would like to comment on these aspects as they apply to our study.
First of all, we agree completely with the recommendations for anaesthetic practice in patients undergoing major abdominal surgery with an Enhanced Recovery after Surgery (ERAS) programme. Some of these measures are aimed to minimise prolonged fasting and mechanical colon preparation to avoid preoperative hypovolaemia. In fact, during the last few years, we have implemented an ERAS pathway. However, as stated in the discussion section of our article, when we designed our study, the implementation of this strategy was not possible at our institution.
With regards to the pharmacokinetic properties of crystalloid solutions, we acknowledge that the volume effect of these types of fluids is low (although higher for isotonic saline than for Ringer's lactate) and transient. However, most studies on this topic have been performed by infusion of volume over a short period of time, usually shorter than an hour, in healthy anaesthetised study participants. Our experimental intervention was quite unlike this and was planned as a fluid infusion for maintenance in awake study participants, following the terminology of a conceptual model recently published.4 Additionally, the functional fluid deficit in patients undergoing ERAS fasting guidelines has been estimated to be 2.5 to 3 ml kg−1. Our preoperative infusion (1.5 ml kg−1 h−1 for 12 h, roughly six times the fluid deficit) was not administered to increase or maintain cardiac output during surgery but to avoid hypovolaemia before the induction of general anaesthesia. We agree with Dr Ripollés et al. that the choice of isotonic saline instead of a balanced solution may have been a confounding factor. However, we could not detect any adverse event of the infusion of isotonic saline at the dose rate specified in our protocol.
Finally, we would like to remark that the intervention in our trial was preoperative. The intraoperative management of our patients, as stated in the Methods section of our manuscript, was standardised for both groups. A rational and individualised use of volume therapy, avoiding both overload and hypoperfusion, implies the measurement of changes in dynamic indices. When we designed our trial, this type of haemodynamic monitoring was not available at our institution, so for our study, we choose a pragmatic design with an easy intervention. The infusion of fluids and vasopressors guided by haemodynamic goals can decrease the incidence of hypovolaemia and renal hypoperfusion, and thus, at least theoretically, the incidence of acute kidney injury. However, information from the medical literature regarding this issue is still controversial and a matter of current debate. Although some authors have reported a decrease in the incidence of acute kidney injury,5 others could not demonstrate this.6,7 We agree with Dr Ripollés et al.'s statement that judicious perioperative administration of fluids is essential to reduce postoperative complications, but in our opinion, the best strategy to achieve it is still an unresolved issue.
Acknowledgements relating to this article
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Conflicts of interest: none.
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