Fluid management for the prevention and attenuation of acute kidney injury

Abstract

In patients with acute kidney injury (AKI), optimization of systemic haemodynamics is central to the clinical management. However, considerable debate exists regarding the efficacy, nature, extent and duration of fluid resuscitation, particularly when the patient has undergone major surgery or is in septic shock. Crucially, volume resuscitation might be required to maintain or restore cardiac output. However, resultant fluid accumulation and tissue oedema can substantially contribute to ongoing organ dysfunction and, particularly in patients developing AKI, serious clinical consequences. In this Review, we discuss the conflict between the desire to achieve adequate resuscitation of shock and the need to mitigate the harmful effects of fluid overload. In patients with AKI, limiting and resolving fluid overload might prompt earlier use of renal replacement therapy. However, rapid or early excessive fluid removal with diuretics or extracorporeal therapy might lead to hypovolaemia and recurrent renal injury. Optimal management might involve a period of guided fluid resuscitation, followed by management of an even fluid balance and, finally, an appropriate rate of fluid removal. To obtain best clinical outcomes, serial fluid status assessment and careful definition of cardiovascular and renal targets will be required during fluid resuscitation and removal.

Low Systemic Oxygen Delivery and BP and Risk of Progression of Early AKI

“…An increase of cumulative fluid balance by .1 L/d after AKI had developed was associated with an odds ratio of AKI III of 6.09 and a 95% confidence interval of 2.39 to 15.52. Previous studies have shown similar associations between fluid accumulation and harm (38)(39)(40)(41)(42), and, almost 10 years ago, an RCT in patients with acute lung injury confirmed that a conservative strategy of fluid management improved lung function without causing severe AKI (43). Importantly, we did not determine whether fluid accumulation was attributable to fluid administration or reduced urine production.…”

Reduction of Tubular Flow Rate as a Mechanism of Oliguria in the Early Phase of Endotoxemia Revealed by Intravital Imaging

“…This proviso on the response to fluid resuscitation may be associated with the fluid overload conditions in AKI. 12,[38][39][40] Fluid resuscitation in participants with scores of 3 or 4 may induce positively balanced fluid retention because of strongly exaggerated output. Indeed, better responses to intravenous fluid resuscitation were observed at 6 hours than at 24 hours after LPS injection.…”

“…4,5 Although basic research has identified several pathways involved in the mechanism of AKI, including inflammation 6,7 and alterations in microcirculation, 8,9 thus enabling the development of new therapeutic strategies, specific treatments that can improve AKI outcome are not yet clinically available. [10][11][12] Notably, only modest histologic changes in the kidney gave been observed in patients with sepsis and in animal models of sepsis, 13,14 whereas septic AKI has a high mortality rate. These results strongly underscore the need for further investigations of AKI by physiologic rather than by pathologic approaches.…”

Shock Management for Cardio-surgical Intensive Care Unit Patient: The Silver Days

“…39 The underlying mechanism seems to be a consecutive reduction in renal blood flow and glomerular filtration rate by a high venous pressure. 39,40 Of note, there is no good correlation between CVP and fluid responsiveness [41][42][43] and therefore other preload variables should be used. 44 Since fluid overload leads to increased morbidity in acute respiratory distress syndrome, 45 pancreatitis 46 and sepsis, 47 the authors recommend a conservative fluid regime with fluids being administered preferably after assessing responsiveness.…”