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Preoperative fluid loading in major abdominal surgery

Ripollés-Melchor, Javier; Álvarez-Baena, Lucía; Espinosa, Ángel; Calvo-Vecino, José María

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European Journal of Anaesthesiology: January 2017 - Volume 34 - Issue 1 - p 43-44
doi: 10.1097/EJA.0000000000000512
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Recently, Serrano et al.1 evaluated the effectiveness of preoperative administration of physiological saline as a measure to reduce postoperative acute kidney injury in patients undergoing major abdominal surgery. Although it is based on a somewhat arbitrary assumption, that is, the fact that the administration of saline decreases the incidence of contrast-induced nephropathy, they hypothesise that preoperative administration of 0.9% saline could reduce the incidence of acute kidney injury. The results of this study are of great importance in routine clinical practice. Although Serrano et al.1 showed that preoperative administration of physiological saline does not diminish the incidence of postoperative acute kidney injury, this practice is common in operating rooms all around the world.

The most important factor for preventing postoperative acute kidney injury is the elimination of ischaemic or nephrotoxic triggers in at-risk patients. The most effective means of prevention is to ensure an adequate intravascular volume and cardiac output, as dehydration and renal hypoperfusion could lead to renal medullary hypoperfusion. Therefore, the basic preventive general strategy of the acute kidney injury is to identify patients with renal injury risk by monitoring haemodynamics and diuresis, correcting hypovolaemia with electrolyte replacement and avoiding nephrotoxic drugs. On this basis, considering the major studies of Bundgaard-Nielsen et al.,2 which showed that a large proportion of anaesthetised patients had a relative hypovolaemia, or rather, were responders to volume (it does not necessarily indicate that they needed volume), Serrano et al.1 hypothesised that preoperative administration of physiological saline could restore relative hypovolaemia that may be present in patients undergoing major abdominal surgery. The development of postoperative acute kidney injury has been demonstrated as an independent risk factor of morbidity and mortality; even minimal increases in serum creatinine have been associated with an increase in mortality.3 It is obvious that the research into factors that may reduce the incidence of acute kidney injury becomes relevant. However, regarding the administration of fluids in the perioperative period, three aspects should be considered as particularly important.

First, in the era of enhanced recovery programmes, a large proportion of patients reach the operating room in a normovolaemic state. Therefore, preoperative measures that could lead to hypovolaemia, such as prolonged fasting or mechanical preparation of the colon, are currently not recommended. Second, the permanence of a crystalloid in the intravascular space is about 20%4; as a result, it is unlikely that preoperative administration of physiological saline will increase or maintain cardiac output during surgery if it is not accompanied by goal-directed haemodynamic therapy. Moreover, Serrano et al.1 found no significant differences in postoperative chloraemia because of saline administration; these solutions contain a supraphysiological concentration of chloride, and hyperchloraemia caused by large-volume administration of saline-based solutions may adversely affect kidney function because of renal vasoconstriction, and decreased renal blood flow and glomerular filtration rate.5

Finally, renal hypoperfusion is often the initial insult in perioperative acute kidney injury, which importantly can lead to a reduction in medullary blood flow.2 The outer medulla, because of its high metabolic demands, is particularly vulnerable to renal hypoperfusion and hypoxia. Up to 80% of patients with postoperative acute kidney injury presented some episode of perioperative haemodynamic instability.2 Fluid therapy is aimed at restoring systemic blood pressure and cardiac output. Occult hypovolaemia occurs frequently during surgery, and contributes to inadequate tissue perfusion and the development of postoperative complications. Therefore, administering fluids and vasopressors guided by haemodynamic goals (goal-directed haemodynamic therapy) could reduce the incidence of situations of hypovolaemia and renal hypoperfusion, and thus theoretically could reduce the incidence of acute kidney injury. Prowle et al.6 demonstrated in a meta-analysis that using perioperative goal-directed therapy decreased the incidence of postoperative acute kidney injury, and notably, determined that this was more evident in those studies in which the same amount of fluid was administered in both the control and the intervention groups, and when the intervention was accompanied by inotropes. Nonetheless, this has not been proved in a recent meta-analysis.7 Cardiovascular monitoring may be required to recognise haemodynamic changes and to allow the timely institution of fluids, vasopressor and/or inotropic support. However, because of the possible adverse effects of excessive fluid administration, it seems reasonable to maintain adequate preload to ensure an adequate cardiac output and adequate oxygen delivery to the tissues, rather than to maximise the stroke volume. This is currently known as individualised goal-directed haemodynamic therapy.

Judicious perioperative administration of fluids is essential to reduce postoperative complications. The work of Serrano et al.1 indicates that preoperative fluid administration does not provide benefits, consequently it must be assessed individually, and always considering the administration of fluids such as the administration of a drug.

Acknowledgements relating to this article

Assistance with the letter: none.

Financial support and sponsorship: none.

Conflicts of interest: none.


1. Serrano AB, Candela-Toha AM, Zamora J, et al. Preoperative hydration with 0.9% normal saline to prevent acute kidney injury after major elective open abdominal surgery: a randomised controlled trial. Eur J Anaesthesiol 2016; 33:436–443.
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© 2017 European Society of Anaesthesiology