To the Editor:
We read with interest the recently published study by Arslan-Carlon et al. in Anesthesiology.1 This primary objective of this randomized, controlled trial (N = 283) was to determine whether a goal-directed fluid therapy approach would result in a lower incidence of postoperative ileus compared with a standard fluid therapy approach in patients undergoing open radical cystectomy. All patients had an arterial line coupled to an advanced hemodynamic monitoring device (EV-1000, Edwards Lifesciences, USA) to monitor advanced hemodynamic variables before, during, and immediately after surgery. No statistically significant difference in this primary outcome was found between the two groups. Interestingly, however, the authors identified a relative negative impact of goal-directed fluid therapy on acute kidney injury (AKI) incidence (secondary outcome) with more patients in the goal-directed fluid therapy group who experienced AKI (56% vs. 40%, P = 0.005). We do appreciate the statistical insignificance noted after taking into account Bonferroni adjustments (P = 0.170) because this is rarely done. We congratulate the authors for having performed such a rigorous study. We have, however, two main comments for any interested readers.
First, although many clinicians throughout the world may use a similar hemodynamic algorithm that calls for fluid, vasopressor, or inotrope administration if stroke volume variation is greater than 12%, mean arterial pressure (MAP) less than 60 mmHg, or cardiac index less than 2.5 l · min–1 · m–2, there have been at least two large randomized, controlled trials demonstrating that targeting a higher arterial pressure during surgery is associated with less postoperative AKI. The first, from Futier et al.,2 reported a lower incidence of organ dysfunction in the group of patients with a targeted systolic arterial pressure closer to the patient’s baseline value compared with the control group. The second, from Wu et al.,3 demonstrated that targeting a MAP level between 80 and 95 mmHg in chronically hypertensive patients reduces postoperative AKI compared with two other MAP levels (65 to 79 and 96 to 110 mmHg). Additionally, French national guidelines recommend maintenance of a MAP target greater than 70 mmHg to prevent AKI in patients with chronic hypertension (which is the case in more than 60% of the current study population).4 As a result, the MAP level targeted in the current hemodynamic algorithm may have been too low and could be responsible for the higher incidence of AKI.
Second, because both groups were monitored with an advanced hemodynamic monitor, we would have greatly appreciated summaries of advanced hemodynamic variables to better understand the results. It would be useful if the authors could provide mean MAP, stroke volume, cardiac index, and stroke volume variation during the case and also the percentage of procedure time the patients were hypotensive as defined using their algorithm of MAP less than 60 mmHg and the percentage of procedure time with a stroke volume variation greater than 12%. It is quite evident that clinicians’ compliance with the application of hemodynamic protocols remains poor, ranging between 62% and 87%, even within ideal study conditions.5,6 Compliance of less than 50% to protocols is reported in daily practice across different medical specialties, but at least 80% adherence is required to observe improved clinical outcomes.7–9 As a result, having hemodynamic data would allow readers to assess protocol compliance and determine whether advanced hemodynamic variables were well optimized throughout the perioperative period.
Dr. Joosten has been a consultant for Edwards Lifesciences (Irvine, California), Aguettant Laboratoire (Lyon, France), and Fresenius Kabi GmbH (Bad Homburg, Germany). Dr. Legrand has received consulting fees from Novartis (Bale, Switzerland), lecture fees from Baxter (Lessines, Belgium) and Fresenius Kabi GmbH, and research support from Sphingotec (Hennigsdorf, Germany). The other authors declare no competing interests.