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Perioperativefluidtherapyrecommendationsformajorabdominalsurgery.ViaRICArecommendationsrevisited.PartI:Physiolo....

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DOI:10.1016/j.redare.2017.02.009

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Rev Esp Anestesiol Reanim. 2017;xxx(xx):xxx---xxx

www.elsevier.es/redar

Revista Española de Anestesiologíay Reanimación

SPECIAL ARTICLE

Perioperative fluid therapy recommendations formajor abdominal surgery. Via RICA recommendationsrevisited. Part I: Physiological background�,��

Recomendaciones de fluidoterapia perioperatoria para la cirugía abdominalmayor. Revisión de las recomendaciones de la Vía RICA. Parte I:Fundamentos fisiológicos

J. Ripollés-Melchor a,∗, D. Chappellb, Á. Espinosa c, M.G. Mhytend,A. Abad-Gurumeta a, S.D. Bergesee, R. Casans-Francés f, J.M. Calvo-Vecino g

a Departamento de Anestesia, Hospital Universitario Infanta Leonor, Universidad Complutense de Madrid, Madrid, Spainb Departamento de Anestesia, Hospital Universitario LMU de Múnich, Múnich, Germanyc Departamento de Anestesia Cardiovascular y Torácica, y Cuidados Intensivos, Bahrain Defence Force Hospital, Riffa, Bahraind University College London Hospital, National Institute of Health Research, Biomedical Research Centre, Londres, United

Kingdome Departamento de Anestesia y Neurocirugía, Wexner Medical Center, The Ohio State University, Columbus, OH, United Statesf Departamento de Anestesia, Hospital Clínico Universitario Lozano Blesa, Zaragoza, Spaing Departamento de Anestesia, Complejo Asistencial de Salamanca, Universidad de Salamanca, Salamanca, Spain

Received 21 January 2017; accepted 8 February 2017

� Please cite this article as: Ripollés-Melchor J, Chappell D,Espinosa Á, Mhyten MG, Abad-Gurumeta A, Bergese SD, et al.Recomendaciones de fluidoterapia perioperatoria para la cirugíaabdominal mayor. Revisión de las recomendaciones de la Vía RICA.Parte I: Fundamentos fisiológicos. Rev Esp Anestesiol Reanim. 2017.http://dx.doi.org/10.1016/j.redar.2017.02.008

�� This article belongs to the Continuing Medical Training Programin Anesthesiology and Reanimation. The evaluation of the questionsin this article can be made through the Internet by accessing thetraining section of the following website: www.elsevier.es/redar.

∗ Corresponding author.E-mail address: ripo542@gmail.com (J. Ripollés-Melchor).

Introduction

About 230 million patients undergo surgery each year.1

Reported mortality rates for elective non-cardiac surgeryrange from 1% to 4%.2 Although less than 15% of in-patient procedures are performed in high-risk patients, suchpatients account for 80% of deaths.3

Since postoperative complications lead to a decrease inlong-term survival and an increase in hospital costs,4,5 dif-ferent perioperative strategies have been introduced in anattempt to reduce these complications and improve qualitypatient recovery. In the late 1990s, Henrik Kehlet introduceda comprehensive concept of perioperative care, known as

2341-1929/© 2017 Sociedad Espanola de Anestesiologıa, Reanimacion y Terapeutica del Dolor. Published by Elsevier Espana, S.L.U. All rightsreserved.

REDARE-800; No. of Pages 11

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2 J. Ripollés-Melchor et al.

Hypovolemia

Perioperative volume load

Fluid

overload

Optim

al

Po

sto

pe

rative

co

mp

lica

tio

ns

Figure 1 Association between perioperative administrationof fluids and postoperative complications.

‘enhanced recovery after surgery’ (ERAS), or the EnhancedRecovery Protocol (ERP),6 aimed at reducing surgery-relatedphysical and psychological stress,7 which in turn reducesthe rate of perioperative complications,8 and ultimatelyhastens full recovery.9 In 2014, the Spanish Ministry ofHealth published a suite of recommendations on perioper-ative management of patients undergoing major abdominalsurgery within ERP (RICA).10,11

Perioperative fluid management is one of the most widelydiscussed topics,12 especially in major surgeries associ-ated with considerable stress response, altered capillarypermeability, and large fluid shifts. Fluid therapy is a com-plex intervention at multiple levels.13 The maintenanceof appropriate fluid levels in the perioperative period iscrucial.14,15 Postoperative increase in body weight, a signof hypervolemia and a manifestation of interstitial oedema,is strongly correlated with postoperative complications,16---19

including the pulmonary, cardiac, gastrointestinal,20,21 andrenal19,22. Hypovolemia leads to tissue hypoperfusion andaltered organ function. Therefore, both hyper- and hypo-volemia can contribute to morbidity and mortality23

(Fig. 1).The following review aims to expand and revisit the fluid

therapy recommendations included in RICA11 from a physio-logical point of view.

Physiological background

Body fluid distribution

Water makes up approximately 60% of the total bodyweight in the adult,24 although the ratio of water toadipose tissue varies widely with weight, age and gen-der. Water is distributed in the two main compartmentsof the body: the intracellular compartment (the largest,representing about two thirds of body water), and theextracellular compartment, comprising the plasma andthe interstitial compartments. The interstitial compart-ment is actually a matrix, a collagen/gel substance thatgives the interstitium its structural rigidity and resistance

Intravascular

3L

Vascular endothelium

5%

De

xtr

ose

Iso

ton

ic

cry

sta

lloid

Iso

on

co

tic

co

lloid

Extravascular

(intersticial space)

12L

Extravascular

(intracelular space)

30 L

Figure 2 Compartmental distribution of intravenous fluids.

to gravity, and can maintain structural integrity duringextracellular volume depletion. The collagen/gel intersti-tial space is an important reservoir of extracellular fluid(Fig. 2).

The endothelial surface layer

The Starling principle governs the displacement of fluidsbetween vascular and interstitial spaces, and is determinedby the balance between the hydrostatic pressure and colloidosmotic pressure in both spaces.25 It does not really deter-mine the plasma/interstitium distribution ratio, but ratherexplains the movement of water across the capillary wall.26

Hence, the classic Starling principle was modified to accom-modate the ‘‘glycocalyx concept’’, in which not only theendothelial cell line, but also the surface layer of the vascu-lar endothelium as the physiologically active barrier.27 Thisgoes against the original Starling principle, in which only theendothelial cell line is responsible for the vascular barrierfunction.25

The vascular endothelium is the key barrier betweenthe intravascular and interstitial spaces. The movement ofwater and solutes between these two compartments occursthrough a double capillary membrane, and can follow themodified Starling equation and the so called ‘‘glycocalyx-Junction-break model’’.28 The vascular endothelium is asingle cell layer covering the luminal face of all blood ves-sels. On the vascular side of the endothelial cells lies acontinuous layer of glycosaminoglycan chains, membrane-bound proteoglycans and glycoproteins that collectivelyform the endothelial glycocalyx. This basal skeleton bindsalbumin, forming an endothelial surface layer interactingdynamically with all blood constituents.29 It has now beenestablished that the endothelial glycocalyx, besides beinga physical barrier between the blood and the middle layerof the vessels or tissue in the case of capillaries, has akey role in maintaining vascular homeostasis, contribut-ing to vascular tone regulation and mechanical impulse

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Perioperative fluid therapy recommendations for major abdominal surgery 3

transduction, and is also responsible for variations in redblood cell velocity.30 Furthermore, it participates in numer-ous physiological processes, including vascular permeability,adhesion of leukocytes to the vessel wall, transmissionof shear stress, and modulation of inflammatory andhaemostatic processes.31,32 The endothelial glycocalyx isconsidered the natural gateway to the interstitial space.33

Under physiological conditions, the endothelial surface layer(ESL) has a thickness of approximately 1 �m and bindsapproximately 800 mL of blood plasma, so that plasmavolume can be divided into 2 parts: circulating and non-circulating. Physiologically, the ESL has been estimated tocomprise as much as 25% of the total intravascular space.34

The presence of a healthy vascular membrane maintains abarrier to prevent excessive fluid shifts.35 It acts as a pri-mary molecular filter, retaining proteins and generating aneffective oncotic gradient.36 A small space between the wallof the anatomical vessel and the ESL remains almost freeof proteins,37 so that fluid loss across the vascular barrieris limited by oncotic pressure gradient within the ESL34,38

(Fig. 3).

Preserving the glycocalyx

There are two prerequisites for a functioning vascular bar-rier: an intact endothelial glycocalyx, and a sufficiently highconcentration of albumin which is able to bind (electrostat-ically) to the endothelial glycocalyx, thereby forming a tightmeshwork hindering passage of colloids through the ESL.29

The intact vascular barrier cannot be penetrated by largemolecules and proteins in relevant amounts, and it thereforeenables the circulation to generate a positive intravascu-lar blood pressure without excessive loss of fluid into theinterstitial space.33

The endothelial glycocalyx structure is fairly stable underphysiological conditions, maintaining a balance between thesynthesis of new glycans and shear-dependent shedding ofexiting glycans. Degradation of the endothelial glycocalyxis associated with capillary leakage and oedema formation;this can occur in inflammatory states, including perioper-ative states, ischaemia---reperfusion, sepsis, or trauma.39,40

Thus, the preservation of the glycocalyx must be consid-ered in any perioperative fluid therapy strategy32 in orderto minimize fluid displacement. Administration of exces-sive fluids will result in hypervolemia33 and a subsequentincrease in intravascular hydrostatic pressure resulting inthe release of certain substances, such as atrial natriureticpeptides, which can damage the endothelial glycocalyx.41,42

Fluid shifts from the intravascular to the interstitial spacecan be classified into 2 types33: type 1, occurring evenwhen the vascular barrier is intact, including the pas-sage of an almost protein-free fluid in the interstitium;and type 2, which consists of fluids containing proteinclose to plasma concentration, crossing an altered vascularbarrier.33 Following surgery, this shift occurs for 3 rea-sons: First, increased protein permeability of capillaries andvenules by endothelial damage caused by mechanical stressor inflammation due surgical manipulation.43,44 Secondly,reperfusion injury and inflammatory mediators that alter thevascular barrier.39,45,46 Thirdly, iatrogenic hypervolemia.47

Type 1 fluid shifting should be minimized by adequate

Figure 3 Electronic microscope image of a left ventricularmyocardial capillary in a rat model (a) perfused with an alcianblue 8GX staining solution, or (b) treated with hyaluronidasebefore staining. Bar = 1 �m. (Courtesy of B.M. van den Berg[38]).

monitoring and limitation of fluids. Reducing the endocrineand immune response that leads to surgery can decreaseglycocalyx disruption45 and limit type 2 alterations.33 Pro-phylactic fluid boluses to anticipate acute bleeding or toextend intravascular blood volume in a normovolaemicpatient is unreasonable.48 Selecting the right fluid for eachsituation is key. Rehm et al. infused a large colloidal bolus toexpand blood volume, and observed a reduced intravascularvolume effect of around 40% of the infused amount. As theother 60% seems to have been shifted towards the interstitialcompartment, generating tissue oedema.47 This applica-tion of iso-oncotic colloids outside a proper indicationsignificantly reduced the total volume of the endothe-lial surface layer to 1/3 of the initial value, presumablyaltering vascular biology33; likewise, liberal administra-tion of crystalloid solution without proper indication canresult in pronounced extravasation.49 The association ofinadequate fluid (both in type and quantity) and surgicalstress causes a decrease in plasma albumin,50 and promotesinflammation, glycocalyx degradation, and the formation ofinterstitial oedema due to vascular leakage.51 Therefore,

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4 J. Ripollés-Melchor et al.

fluid must be chosen in accordance with the compartmentis it needed to fill: colloids for intravascular space, andcrystalloid for the extracellular space, to replace insen-sible losses and urine output. It becomes apparent thataccurate measurement of perioperative fluid losses is essen-tial.

Intraoperative fluid loss

A conventional infusion regimen during major surgery shouldbe based on physiological considerations. Patients under-going major abdominal surgery often receive preoperativecrystalloid loading, e.g. 2 mL/kg/h of fasting, and thenadditional crystalloids to replace blood losses. Frequentlypatients receive 4---8 mL/kg/h of crystalloid, based onsuspected ongoing losses, such as third spacing and perspi-ration. This formula may result in basal crystalloid infusionrates of up to 20 mL/kg/h, which means 1.6 litres in an 80 kgadult.

Fluid shift is a common phenomenon during and aftersurgical procedures; however, preoperative fluid deficit andperioperative insensible losses are usually overestimatedfor 3 reasons: the belief in the existence of the so-called‘‘third space’’; preoperative fasting; and insensible lossesdue to surgical body exposure. Despite the evidence, themisleading concept of a third anatomic space that shouldbe refilled persists. The third space refers to sequestrationof fluid in a non-functional extracellular space that is beyondosmotic equilibrium with the vascular space; however, clas-sical third-space fluid losses have never been measureddirectly, and actually do not exist.52

In the last 50 years, many studies have reported highfluid loss due to perspiration in major abdominal surgery:(bodyweight + 40) (kg) × 1 (mL/kg/h).53 Lamke et al. exper-imentally evaluated insensible perspiration and showed thatit was highly overestimated; they calculated that baselineevaporation during extended abdominal surgery was approx-imately 0.5---1 mL/kg/h at the most.54

The impact of preoperative fasting is also seriouslyoverestimated. Even after prolonged pre-operative fasting,patients remain intravascularly normovolaemic55; preoper-ative fasting, therefore, does not increase the proportion ofresponders to a PLR test.56,57

Maintenance fluid therapy

A maintenance balanced fluid therapy isrecommended in order to avoid fluid overload

‘‘The objective of care is to maintain normal physiologyand normal function of organs, with a normal blood vol-ume, functional body water and electrolytes. This can neverbe achieved by inundation’’.58 These principles proposed byMoore and Shires in the 1960s remain in force today. Manyrecent trials and papers have addressed the important issueof restrictive versus liberal fluid strategies in the perioper-ative setting.59,60 The difficulty of interpreting the differentresults originates from the lack of definition and standardcriteria for ‘‘restrictive’’ and ‘‘liberal’’ fluid management,and has prevented the development of guidelines for peri-operative fixed-volume regimens.61 Rahbari et al. proposed

standardized definitions for the terms standard, restrictiveand supplemental fluid therapy. A meta-analysis suggeststhat in patients undergoing colorectal resection, restrictiverather than standard fluid substitution reduces postopera-tive morbidity (OR 0.41 (95% CI 0.22---0.77); P = 0.005), butit included only 4 small studies, involving a total of 393patients.53 Varadhan and Lobo proposed a new classificationof perioperative fluid management, defining it as balanced(1.75-2-75 L/24 h) or imbalanced. The balanced group pre-sented a 59% reduction in risk of developing complicationsand a shorter length of stay.62 Recently published clinicalpractice guidelines, using the same definitions, found simi-lar results. Their recommendation was to perform balancedfluid maintenance until the start of oral tolerance. Remark-ably, they even found a decreased hospital stay of more than2 days.63

Maintenance fluid should be administered to maintain apatient’s pre-operative weight by replacing ongoing losses,such as from urine and insensible perspiration. Infusion ofbalanced crystalloid should not normally exceed 3 mL/kg/h,as perspiration losses are typically only 0.5---1.0 mL/kg/heven during major abdominal surgery.64

Recently, perioperative fluid utilization and associatedoutcomes of colorectal surgery were evaluated by a retro-spective analysis of 106,900 patients in US Premier ResearchDatabase. The analysis revealed that both highly restric-tive and liberal fluid strategies used on the first operativeday result in worse outcomes compared to a zero-balancefluid therapy.65 The findings suggest that an applicable,protocol-based approach to optimal fluid management mayimprove outcomes, and confirm the traditional fluid volumeinfused vs. complications curve (Fig. 2). As stated by theBritish Consensus Guidelines for Intravenous Fluid Therapyin Adult Surgical Patients,66 correction of volume deficit dur-ing major surgery should be directed towards a particulargoal.

The upcoming results of the RELIEF study (NCT01424150)might determine whether liberal or restrictive maintenancefluid therapy is more beneficial. This will be the largestperioperative fluid study to date, a randomized controlledtrial of liberal (intraoperative and first 24 h ≈ 5 L) vs. restric-tive (intraoperative and first 24 h ≈ 2.5 L) fluid therapy inover 2800 patients undergoing elective intra-abdominalsurgery.

Crystalloids

The most widely used intravenous crystalloid is still 0.9%saline.67 The use of the term ‘‘normal’’ may have con-tributed to the widespread acceptance of 0.9% saline intoclinical practice. Despite being referred to as ‘‘normal’’,0.9% saline is not physiologically ‘‘normal’’ at all.68

Firstly, compared to human serum, saline has nearly 10%higher Na concentration and 50% higher Cl concentra-tion. Secondly, the strong ion difference (SID) of 0.9%saline is ‘‘zero’’ and differs completely from that ofplasma (approx. +40). Large volume infusions of 0.9%saline can cause hyperchloraemic acidosis,69 which is asso-ciated with reduced gastric blood flow, reduced mucosalpH70 and delayed recovery of gut function.16,71 Further-more, hypochloraemia may also adversely affect renal

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Perioperative fluid therapy recommendations for major abdominal surgery 5

Table 1 Characteristics of common crystalloid solutions compared to human plasma.

Plasma 0.9%saline

Ringer’s lactate(lactatebufferedsolution)

Ionosteril®

(acetatebufferedsolution)

SterofundinISO

®(acetate

& malatebufferedsolution)

PlasmaLyte148

®(acetate

& gluconatebufferedsolution)

Sodium (mmol/l) 136---145 154 130 137 145 140Potassium (mmol/l) 3.5---5.0 4 4 4 5Magnesium (mmol/l) 0.8---1.0 1.25 1 1.5Calcium (mmol/l) 2.2---2.6 3 1.65 2.5Chloride (mmol/l) 98---106 154 109 110 127 98Acetate (mmol/l) 36.8 24 27Gluconate (mmol/l) 23Lactate (mmol/l) 28Malate (mmol/l) 5eSID (mEq/l) 42 28 36.8 25.5 50Theoretical

osmolarity(mosmol/l)

291 308 273 291 309 295

Actual or measuredosmolality(mosmol/kg H2O)

287 286 256 270 Not stated 271

pH 7.35---7.45 4.5---7 5.0---7 6.9---7.9 5.1---5.9 4---8

Plasma Lyte 148 (Baxter Healthcare, Toongabie, NSW, Australia); Ringer’s Lactate (Baxter Healthcare, Deerfield, IL, USA); Ionosteril(Fresenius Medical Care, Schweinfurt, Germany); Sterofundin ISO (Braun Melsungen AG, Melsungen, Germany).

function due to renal vasoconstriction,72 mediated pri-marily by effects on afferent and intrarenal arterialvessels.73,74

Unlike 0.9% saline, buffered crystalloid solutions containphysiological or near physiological amounts of chloride. Thekey differences between 0.9% saline and buffered/balancedcrystalloids is the presence of metabolizable anions, such aslactate, acetate, malate or gluconate, which act as physi-ological buffers to generate bicarbonate. Despite the factthat buffered crystalloid fluids more closely resemble thecomposition of human plasma, no perfectly balanced orphysiologically ‘‘normal’’ crystalloid fluid is currently avail-able (Table 1).

There are few studies comparing the effect of 0.9% salineand buffered/balanced crystalloids during the perioperativeperiod.75 Most randomized trials to date have included fewpatients and analyzed physiological and/or biochemical out-comes. These studies showed balanced crystalloid infusionto have a better biochemical profile, but could not demon-strate a difference in either postoperative complicationsor hospital length of stay.74,76 Recently, the Saline versusPlasma-Lyte for Intravenous Fluid Therapy (SPLIT) researchprogram77 showed that the use of a buffered crystalloidcompared with saline did not reduce the risk of acute kid-ney injury (AKI) in patients admitted to intensive care units(9.6% vs. 9.2%).78 Within the SPLIT program, a single-centre,double-blind, crossover trial in 1380 major surgical patientswas unable to show a decrease in AKI: 52 (10.9%) patientsin the Plasma-Lyte 148

®group compared to 59 (9.3%) in the

0.9% saline group developed postoperative AKI.79

Despite this, giving several litres of 0.9% saline willresult in hyperchloraemia, so continuing this fluid strat-egy is not rational.80 RICA11 and NICE guidelines,81

and the recently published German volume ther-apy guidelines, recommend avoiding saline 0.9%both during the perioperative period and both duringICU.82

Colloids versus crystalloids for stroke volumeoptimization

Current best practice seems to be the combination of a fixedcrystalloid administration (the combination of maintenanceand replacement solutions) and a rational goal-directedapproach to resuscitation fluids.83 However, only 2 RCTshave specifically studied which fluid maintenance strat-egy was more effective in the context of goal-directedhaemodynamic therapy (GDHT).84,85 The results of thesestudies were contradictory. Futier et al. randomize 70patients undergoing major abdominal surgery to 6 mL/kg/hor 12 mL/kg/h of crystalloid (a more conservative liberalfluid strategy); in both groups, fluid bolus was adminis-tered when respiratory variation in peak aortic flow velocitywas greater than 13%. The restrictive fluid strategy wasassociated with an increase in the incidence of patientswith hypovolemia and postoperative complications. Loboet al., meanwhile, showed that the infusion of 4 mL/kg/hcompared to 12 mL/kg/h of lactated Ringer’s solution asmaintenance fluid during GDHT with DO2- and lactate-guided

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6 J. Ripollés-Melchor et al.

Perioperative fluid

therapy plan

Preoperative insensible

losses are usually

overestimated

Impact of preoperative

fasting is usually

overestimated

Long fasting periods must

be avoided

Intaoperative insensible

fluid losses by body

exposures are usually

overestimated

The so called “third space”

do not exist

Hipervolemia must be

avoided

A near zero fluid balance is the goal for maintenance fluid therapy

Macro hemodynamics Microcirculation

Acute kidney injury

paralytic ileus

Postoperative

weith gain is

associated with

complications

and mortality

Crystalloids and colloidsDifferent solutions with different indications

Infusion of crystalloid for

maintenance should not

excess 3 ml/kg/h

0.9% saline must be

avoidedBalanced crystalloid

solutions are more

physiological

Colloids have a higher

plasma-expanding

property than crystalloids

Goal directed

hemodynamic therapy

with colloidIn the preoperative

setting, colloids are not

associated with AKI

Inadecuate fluid therapy is

associated with complications

Routine bowel preparation

must be avoided

If performed, iso-osmotic

agents are prefered

Figure 4 Perioperative fluid therapy protocol.

optimization reduced the incidence of major complicationsby 52%. In both trials, the restrictive group would beconsidered liberal according to today’s criteria. This illus-trates the difficulty of comparing different fluid therapystrategies using different haemodynamic targets, differentmonitoring technique, and different therapies. However,there is indirect evidence that a liberal maintenance fluidtherapy together with GDHT is less effective86,87 thanGDHT accompanied by a restrictive maintenance fluid ther-apy.

The controversy regarding the choice of fluids inrelation to stroke volume (SV) optimization persists.88---90

Nevertheless, because there are few RCTs conductedin the perioperative period comparing colloids versuscrystalloids,90---92 we need to keep the focus on thepathophysiology.93 It is accepted that colloids have a higherplasma-expanding property than crystalloids, as they remainin the intravascular compartment due to large molecularweight and difficulty crossing the endothelium.94---96 In thespecific setting of acute bleeding, colloids have a volume

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Perioperative fluid therapy recommendations for major abdominal surgery 7

effect of more than 90%.97 However, a colloid only behaveslike a colloid when the glycocalyx is intact and the patientis in need of intravascular expansion. The benefit of colloidsin the setting of an intact glycocalyx in a patient undergo-ing volume optimization during major surgery or after majorhaemorrhage may be very different from the risk of colloidsduring the stabilization phase of severe sepsis with glycoca-lyx shedding and disruption.98 Hypervolaemia degrades theglycocalyx and allows colloids to escape from the intravas-cular compartment.27

In the setting of GDHT, less fluid should be requiredto achieve specific haemodynamic goals (Fig. 4). Recently,Kanda el al. showed that colloid infusion was associated withsignificant increases in systolic blood pressure, left ventricu-lar end-diastolic volume, SV, and cardiac output (CO).99 Wuet al. demonstrated no difference between crystalloids orcolloids, in macro-haemodynamic terms, when resuscitat-ing animals with haemorrhagic shock, while only syntheticcolloids improved intestinal perfusion,100 which it is seri-ously compromised in patients with haemorrhage. An idealresuscitation fluid should not only be effective in restoringboth macrocirculation and microcirculation, but should alsocause less reperfusion injury.101 Chen et al. reported thatthe expander that came closest to this definition was 6%HES 130/0.4. This solution was associated with less oxida-tive stress and a milder inflammatory response in the liver,intestine, lungs, and brain compared with gelatines and HES200/0.5, after resuscitation from haemorrhagic shock.102

HES 130/0.4 has positive effects on ischaemia/reperfusioninjury,103,104 microcirculation, tissue oxygenation,100,105,106

and immunity107,108; it also impairs endothelial and epithelialbarrier integrity,109 and the haemodynamic balance.99,110,111

Administration of colloids within GDHT is knownto reduce the amount of perioperative fluidsadministered,110,111 which is closely related to volumeoverload and postoperative complications.16 Consider-ing existing evidence, (patho)physiology, and findingfrom trials, there is no justification for increasing crys-talloid infusion rates in patients that appear to beclinically hypovolaemic during surgery, despite a goodextracellular fluid balance,33 particularly because thecolloid controversy stems from the septic patient,112,113

who differs from the perioperative patient in so manyways.114 Moreover, the association between infusion ofcolloids and AKI in the perioperative setting has not beenproved.115,116

Conclusions

Fluid therapy is a key element in perioperative patientmanagement. An adequate understanding of pathophysi-ology will guide fluid administration in terms of quantityand type. Maintenance fluid therapy should be restricted,as volume overload leads to an increase in perioperativecomplications.

Ethical disclosures

Protection of human and animal subjects. The authorsstate that no experiments have been performed on humansor animals for this research.

Confidentiality of data. The authors state that no patientdata appears in this article.

Right to privacy and informed consent. The authors statethat no patient data appears in this article.

Conflict of interest

JRM received travel funding from Deltex Medical and hono-raria for lectures from Fresenius Kabi, Edwards Lifesciences,Deltex Medical and Merck Sharp & Dohme. DC Honoraria forlectures and academia studies from BBraun, Fresenius Kabi,Grifols, and LFB Biomedikaments. MM is a member of theEditorial Board of the BJA; Co-Editor-in-Chief of Perioper-ative medicine and a paid Consultant for Deltex Medicaland Edwards Lifesciences. MM has run educational meet-ings that have received grants from Deltex Medical, EdwardsLifesciences, LidCo, Cheetah and Pulsion (www.ebpom.org).MM’s University Chair is Sponsored by Smiths Medical. MM is aDirector of The Bloomsbury Innovation Group. RCF: receivedhonoraria and travel funding for lectures from Merck Sharp& Dohme and Deltex Medical. JMCV received honoraria andtravel funding for lectures from Merck Sharp & Dohme, Del-tex Medical and Fresenius Kabi. AE, AAG, SB state no conflictof interest.

Funding

None declared.

Acknowledgements

Professor Jean-Louis Vincent, Professor of Intensive CareMedicine (Université Libre de Bruxelles,) Depart. of Inten-sive Care, Erasme University Hospital, Brussels, Belgium.Professor Can Ince, Dept. of Intensive Care, Erasmus MedicalCenter. Erasmus University of Rotterdam, the Netherlands.Bernard M. van den Berg, Ph.D. Depart. of Internal Medicine(Nephrology) Leiden University Medical Center, Leiden, theNetherlands. Professor Hans Vink, CArdiovascular ResearchInstitute Maastricht (CARIM), Depart. of Vascular Medicineat the Academic Medical Center, Amsterdam, the Nether-lands. Professor Ignacio García Monge, Dept. of IntensiveCare, Hospital SAS de Jerez, Experimental Research Unitof Hospital SAS de Jerez, Spain. Professor Susana GonzálezSuárez, Dept. of Anesthesiology, Vall d’Hebrón Univer-sity Hospital, Barcelona, Spain. Eugenio Martínez Hurtado,Infanta Leonor University Hospital, Madrid, Spain. Profe-sor Vladimir Cerny, Dept. of Anesthesiology, PerioperativeMedicine and Intensive Care J.E. Purkinje University,Masaryk Hospital Usti nad Labem, Czech Republic. Profes-sor José Manuel Ramírez Rodríguez, Depart. of ColorectalSurgery, Lozano Blesa University Hospital, Zaragoza, Spain.Alix Zuleta-Alarcón, Dept. of Anesthesiology and CriticalCare,The Ohio State University Hospital, Columbus, USA.Teresa de la Torre Aragonés, professional librarian, InfantaLeonor University Hospital, Madrid, Spain. GERM: GrupoEspanol de Rehabilitación Multimodal; Enhanced RecoveryAfter Surgery (ERAS) Spain Chapter; and EAR Group (Evi-dence Anesthesia Review Group).

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8 J. Ripollés-Melchor et al.

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