Intravenous Fluid Therapy in Traumatic Brain Injury And

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Journal compilation © 2014 Trauma Research Center, Shiraz University of Medical Sciences,

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Bull Emerg Trauma 2014;2(1):3-14.Review Article

Intravenous Fluid Therapy in Traumatic Brain Injury and

Decompressive Craniectomy

Hernando Raphael Alvis-Miranda1 , Sandra Milena Castellar-Leones1 , Luis Rafael Moscote-Salazar 2*

1University of Cartagena, Colombia, South America.

2Department of Neurosurgery, University of Cartagena, Colombia, South America.

Corresponding au thor: Luis Rafael M os cot e-Salazar

Address: Universityof Cartagena, Cartagena de Indias,Colombia,South America.e-mail:[email protected]

Received: November 9, 2013

Revised: November 15, 2013Accepted: November 28, 2013

The patient with head trauma is a challenge for the emergency physician and for the neurosurgeon. Currentlytraumatic brain injury constitutes a public health problem. Knowledge of the various supportive therapeuticstrategies in the pre-hospital and pre-operative stages is essential for optimal care. The immediate rapid infusionof large volumes of crystalloids to restore blood volume and blood pressure is now the standard treatment of patients with combined traumatic brain injury (TBI) and hemorrhagic shock (HS). The fluid in patients w ithbrain trauma and especially in patients with brain injur y is a critical issue. In this context we present a review

of the literature about the history, physiology of current fluid preparations, and a discussion regarding the useof fluid therapy in traumatic brain injury and decompressive craniectomy.

Keywords: Brain trauma; Colloid solutions;Fluid resuscitation.

Please cite this pa pe r as:

Alvis-Miranda HR, Castellar-LeonesSM, Moscote-Salazar LR. Intravenous Fluid Therapy in Traumatic Brain Injury andDecompressive Craniectomy. Bull Emerg Trauma. 2014;2(1):3-14.

Introduction

raumatic brain injury (TBI) is a major public

health problem and a leading cause of deathand disability [1]. It is frequently accompanied byhaemorrhagic shock (HS) [2-5]. The mechanism f oradverse outcome in patients with combined TBI andHS may be due in part to the secondary ischemicinjuryof already vulnerable brain following loss of cerebralauto-regulation and or to adverse effects of TB I itself on the normal compensatory response to HS [6].Rapid infusion as quickly as possible of large volumesof crystalloids to restore blood volume and bloodpressure is now the standard treatment for patients

with combined TBI and HS [7,8]. Perioperative fluidadministration is an important aspect of surgical care,but is often poorly understood [9-13], and continues

to be an empirical exercise, with nagging questionsabout its efficacy and complications [14].

Fluid therapy (FT), as the name implies is a treatmentwith fluids [15]. The final goal of fluid managementis to optimize the circulatory system to ensure thesufficient delivery of oxygen to organs [16]. FT isneeded for the following conditions:

1. Normal maintenance;2. Blood or fluid loss due to wounds, drains,induced diuresis etc;3. Third space losses socalled fluid sequestrationin tissue oedema or ileus;4.Increased systemic requirements resulting from

fever and hypermetabolic state.TF should be tailored to match these requirements[17].Intravenous (IV) fluids may be broadlyclassified

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4 Bull Emerg Tr auma 2014;2(1)

Alv is- Mir and a HR et al

into colloid and crystalloid solutions. They havevery different physical, chemical, and physiologicalcharacteristics. Colloid solutions can be natural(albumin) or synthetics (gelatins, dextrans, andhydroxyethyl starches).

Goal-directed fluid therapy (GDT) aimed atoptimizing cardiac output and oxygen delivery has

been shown to improve the outcome of high-risksurgical patients [18].Most information presented herein is derived

from the fluid management for the surgical patientin general, and those who were critically ill, such astrauma patients. Primary studies on preoperativefluid therapy for decomprssive craniectomy (DC) aresparse.

The fluid management for patients undergoingelective major surgery, e.g., neurotrauma surgery,is controversial [19-21]. During the perioperativeperiod, many pathophysiological changes occur thatalter the normal efficiency of fluid homeostasis.Despite this, perioperative fluid prescription is oftenpoor, being based on an insufficient knowledge of water and electrolyte requirements and distribution[22-25]. Perioperatively, crystalloids, colloids andblood components are required to meet the ongoinglosses and for maintaining cardiovascular stability tosustain adequate tissue perfusion [26,27].

Intravenous fluids maintain hydration whilepatients are unable to drink and replace losses thatoccur as a result of surgery [28]. Severity of illness,

magnitude and duration of surgery, comorbiditiesand the host response to injury, influence theperioperative fluid needs. Although the principlegoal of fluid administration is to maintain adequatetissue perfusion and the perils of over and under-resuscitation are well documented, there are nostandards of care guiding for perioperative fluidadministration [28].The aim of this work is to reviewthe current topics of fluid management in patientswith traumatic brain injury and the candidates f ordecompressive craniectomy.

History of Modern Fluid TherapyThe intravenous fluid therapy (IVF) first gained

importance in the treatment of cholera in the1830s [29-34], with the reports of William BrookeO’Shaughnessy on his terminal cholera patients’blood observations [29]. Their blood were thick andobscure, thus concluded that there was water deficitin those patients [31]. Aiming to replace the corporalfluid loss, the 0.9% physiologic saline solution wasused for surgical patients. The perioperative useof IVF to compensate for the injurious effects of

anaesthesia began in1880s. Clinical improvementswere consequently noted, though the adverse effects

of saline were observed. Thomas Latta was the first toadminister intravenously water and salt solutions todying patients with no favorable results [29,35]. Theuse of different mixes of water and salt in conjunctionwith the poor hygienic practices of those days ,did notprove safe, thus the fluid therapy did not initiallygain acceptance [15].

In 1880, Sidney Ringer observed the differentprotoplasmic activity of sodium, calcium, potassiumand chloride salts, and introduced Ringer’s solution[15]. George Crile in 1899, using a hemorrhagic shockanimal model, studied the solution and recommendedit in warm form. War injuries during the First WorldWar were treated with primitive saline and colloidsolutions. The Gum arabic, a natural colloid from the

Acacia se negalis tree used by W.C. Cannon, was a highpoint colloid [15].

In 1924, the intravenous "drip" was introduced byRudolph Matas. In 1930, Hartmann and Senna inorder to avoid the hyperchloremic acidosis resultingfrom the use of Ringer´s solutions [36], added sodiumlactate, allowing sodium to be linked to the excessivechloride. This facilitated the lactate metabolism,thus, giving rise to the Hartman solution or Ringer-lactate. The work of Ringer, Hartmann, and othersemphasized the importance of the composition of IV fluids and laid the foundations for the balancedsolutions in use today [37]. During the Second WorldWar, blood and plasma were massively administered,even in the battlefield, aimed at prolonging the lives

of injured soldiers. In general, FT has been changingcontinuously, depending on current trends [15]. Asthe metabolic response to injury was increasinglyinvestigated in the 1940s and 1950s, the cause of post-operative oliguria was widely debated by Moore andShires, the most prominent surgeons [37]. DuringVietnam War, the preservation of renal function,became a therapeutic objective, thus, allowing the useof large amounts of crystalloid for the hemorrhagicshock in the Da Nang Army Hospital. At this timepulmonary complications called Da Nang lung orwet lung syndrome, previous denominations of thepresent Adult Respiratory Distress Syndrome (ARDS),was observed which derived from prescribing largevolumes of fluids.

These differences in opinion, coupled with reportson survival of injured soldiers from the Korean warwho received large IV fluid infusions, dictated thesurgical practice of liberal IV fluid administrationuntil very recently [37]. Recent research in fluidtherapy has explored the concept of fluid restriction.Shoemaker and col leagues also pioneered the conceptof fluid administration to achieve supranormal

indices of cardiorespiratory function, which has ledto the advent of goal-directed fluid therapy [37].

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Fluid therapy in traumatic brain injury

Alongside the development of balanced solutions, therenewed focus on perioperative fluid therapy has ledto IVF administration being guided by physiologicalprinciples with a new consideration of the lessonsgleaned from history [37]. With military medicineadvances, fluid therapy has attracted particularattention, and become increasingly important when

it is combined with hemotherapy. But, with no clearideas about the proper volume. Currently, fluidtherapy stills with largecontroversies.

Fluid PhysiologyThe fundamentals governing fluid and electrolyte

management in patients date to the 19th century [38].In the first half of the 20th century work by Gambleand Darrow and colleagues defined the electrolytecontent of extracellular, intracellular and interstitialfluid compartments [38]. The body of adult humancontains 60% water, of which two-third is intracellularand the remaining one- third is in the extracellularspace, which in turn is divided between intravascularand extravascular or interstitial compartments[39,40].

The interstitial compartment is actually a matrix,a collagen/gel substance that allows the interstitiumto provide structural rigidity which resists againstgravity and can maintain structural integrity duringextracellular volume depletion. The collagen/gelinterstitial space, especially in skin and connective tissue,is an important reservoir of extracellular fluid [38].

The total intravascular volume, also referred toas blood volume, is approximately 5 liters of which2 liters (40%) form intracellular structures such asred and white cells and platelets and 3 liters(60%)constitute extracellular component (plasma) [39,40].Extracellular compartment is important for oxygenand nutrients transport, and the elimination of carbonic anhydride and other products from cellularmetabolism. Another compartment is transcellularthat includes fluids not equilibrated with the otherfluids, and constitutes synovial, cerebrospinal fluids,gastrointestinal secretions, etc. This compartmentthrough the lymphatic system returns the fluids to theintravascular space[40].

The cells and the intravascular space have membranesthat preserve their structural integrity and allow themolecule and fluid interchange between differentcompartments. The main function of membranesis to preserve osmolarity and the electronegativityin of each compartment. The cell wall separatesthe intracellular space from the extracellularcompartment. The capillary endothelium and thewalls of arteries and veins divide the extracellular

compartment into the intravascular and the interstitialareas such as tissue or extravascular compartments.

Water moves freely through cell and vessel walls andenters al l these compartments. The energy-dependentNa/K adenosine triphosphatase in cell walls extrudesNa+ and Cl- and maintains a sodium gradient acrossthe cell membrane with Na+ as an extracellularion. The capillary endothelium is freely permeableto small ions such as Na+ and Cl-, but is relatively

impermeable to larger molecules such as albuminand the semisynthetic colloids like gelatin andstarch, which normally remain in the intravascularspace. Plasma is a solution in water of inorganic ionsincluding predominantly sodium chloride, simplemolecules such as urea, and larger organic moleculeslike albumin and the globulins. Plasma and interstitialfluid are highly interchangeable. Fluid exchangethrough a capillary is regulated by Starling’s law, whichmathematically summarizes the forces governing theflow of fluid out of blood vessels into surroundingtissues, and expressed asQf = Kf [(Pc − Pi) − R(πc − πi)].

Where Qf is the total fluid flux out of capillaries (notthe quantity, but just the speed of water movement[16]) and Kf is the filtration coefficient (the productof the membrane conductance and the membranesurface area), Pc is intravascular hydrostatic pressure,Pi is interstitial hydrostatic pressure, πc is colloidosmotic pressure within the vasculature, πi isinterstitial colloid osmotic pressure gradient across thevessel wall, and R is the oncotic reflection coefficient,the tendency of a membrane to impede the passage of

oncotically active particles (Starling, 1896) [16,41]. Rof 0 indicates a membrane that is totally permeableto protein while R of 1 represents a membrane thatcompletelyprevents protein diffusion.

Distribution terminates when the balance of thehydrostatic pressure and the osmotic pressure canceleach other out. Because the interstitium consists notonly of free space but also of absorbent gel, capturedwater in the gel does not contribute to lowering theosmotic pressure in the interstitium [16]. Therefore,the osmotic pressure does not easily change until thegel is saturated by flow of water. This is a mechanismof edema formation. Thus, Starling’s law does notdetermine the distribution ratio between plasma andinterstitium, it just explains the movement of waterthrough the capillary wall [16].

The original interpretation of an equilibriumincluding fluid reabsorption at the venous end of themicrocirculation is now known to be incorrect throughactual measurement of the pressures involved. Rather,a steady state is involved,with a level of permeability toplasma proteins in the microvascular walls. Net fluidmovement occurs in the vessels from the intravascular

to the perivascular space [42]. The fluid transfer ismediated by the endothelial glycocalyx layer (EGL),



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a physiological entity discovered and studied over thepast 30 years [43]. A model for fluid transfer acrossthe EGL [44] accounts for the discrepancies observedin fluid transfer as predicated by Starling's originalequation, and proposes a modified hypothesis basedon pressures involving the generation of fluid throughthe glycocalyx rather than the interstitial space [45]

modifying the Starlingequation to:Qf = (Pc – Pi)-R (πc – πg)Where Pi and πg are the hydrostatic and osmotic

pressures respectively, exerted by the formation of ultrafiltrate across the glycocalyx [46]. While the EGLis the conduit for water passage from the intravascularto the extravascular space, plasma proteins cross theendothelial barrier through a separate pathway, thelargepore system[46].

This model is perturbed by a number of factorsduring anesthesia and surgery. Patients scheduled f orsurgery are presented with a variety of conditions thatresult in altered fluid distribution. Many anestheticdrugs like IV induction medications and volatileanesthetics cause vasodilation, leading to a reductionin the ratio between the circulating volume and thecapacity of the intravascular space, or myocardialimpairment, causing a reduction in flow through thecirculation.

Fluid shifts between compartments may also reducethe circulating volume representing third-space lossesand loss of intravascular fluid into the interstitiumbecause of altered endothelial permeability in sepsis

and inflammatory states .[39]The following section is devoted to a resume of themain characteristics of different kind of solutions.

Crystalloids

A crystalloid fluid is a solution of small wa ter-soluble molecules that can diffuse easily acrosssemi-permeable membranes. The properties of thesesolutions are largely determined by their tonicity(osmolality relative to plasma) and their sodiumcontent (affecting their distribution within bodycompartments) [47]. They redistribute throughoutthe extracellular fluid (ECF) compartment, of which75% is interstitial fluid. This suggests that 4 litres of crystalloid are required to replace a blood loss of 1litre. [48] Studies have shown that the volume kineticsof infused crystalloid solutions differ betweennormovolaemic and hypovolaemic patients. [49]

IV infusions of isotonic saline solution only expandthe intravascular space by a maximum of one-thirdof the volume used in normal subjects, with only16% left after 30 minutes. The volume of crystalloidrequired to replace an acute blood loss remains

3-4-fold because of redistribution into, and rapidelimination from, the ECF [48].

Isotoni c Solutions

Isotonic or iso-osmolar solutions,with an osmolality≈300 mOsm/L, such as sodium chloride 0.9%(normal saline), Ringer’s solution or plasmalyte, donot change plasma osmolality and do not increasebrain water content [50]. They also contain sodiumat physiological plasma concentrations. These fluids

distribute freely within the ECF compartment causinglittle change in sodium concentration and osmolality.As a result, this limits the movement of water out of the extracellular fluid (ECF) into the intracellularfluid (ICF) compartment and vice versa. Commerciallactated Ringer’s solution is not truly iso-osmolarwith respect to plasma. Its measured osmolality is⋲254 mOsmol/kg, which explains why administrationof large volumes can reduce plasma osmolality andincrease brain water content and intracranial pressure(ICP). [50]

Hypo tonic Solutions

Large amounts of hypo-osmolar or hypotonic fluidsreduce plasma osmolality, drive water across theblood brain barrier (BBB), and increase cerebral watercontent and ICP. A solution of 5% dextrose (D5W)is essentially water since the sugar is metabolizedvery quickly and provides free water which dispersesthroughout the intracellular and extracellularcompartments with little use as a resuscitative fluid[50]. Therefore , hypo-osmolar crystalloids (0.45%NaCl or D5W) should be avoided in neurosurgical

patients [50].

Hyp ertonic cr ystalloids: Mannitol and hypertonic saline

Osmotherapy agents such as hypertonic saline(HTS) are currently used in the treatment of patientswith post-traumatic cerebral edema and raised ICPresulting from TBI [51].It is believed to have aparticularly useful role in the treatment of ICP whilstadministering small volume fluid resuscitation [52].HTS solutions typically improve cardiovascularoutput as well as cerebral oxygenation whilst reducingcerebral oedema. Hypertonicity seems to affect someinnate immune-cell functions, specifically neutrophilburst activity in preclinicalstudies, probably providingbeneficial impact on modulation of the inflammatoryresponse to trauma [53-58].

Clinical studies however do not provide compellingevidence to support the use of HTS either for TBIor for haemorrhagic shock. A small randomizedclinical trial (RCT) reported a significant reductionin mortality when comparing a 250 ml bolus of HTS/ dextran with isotonic saline in 222 patients withhaemorrhagic shock [59]. But many other RCTs

have not demonstrated reduction in mortality inthis group of patients [60-63], including the most



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recent and largest RCT comparing HTS, HTS/ dextran and normal saline. This trial recruited twoseparate cohorts, one with TBI (n = 1087) [64] andthe other with haemorrhagic shock (n = 853) [65];with primary endpoints of neurological outcome at6 months after TBI and 28 day survival respectively.The TBI study was terminated early due to futility,

as interim analysis was unable to demonstratean improvement in neurological status or indeedmortality at 6 months. Another study demonstratedno significant difference in mortality at 28 days, andwas terminated early for concerns of potential (albeitstatistically non-significant) increase in mortalityobserved with a subgroup of patients receiving HTSbut no blood transfusions within the first 24 h [65].Wade et al., [66] undertook a cohort analysis of individual patient data from a previous prospectiverandomized double-blinded trial to evaluateimprovements in survival at 24 hours and dischargeafter initial treatment with HSD in patients whohad TBI (head region Abbreviated Injury Score ≥4)and hypotension (systolic blood pressure ≤90 mmHg). They found that treatment with HSD resultedin survival until discharge of 37.9% (39 of 103)compared with 26.9% (32 of 119) with standardcare ( p=0.080). Using logistic regression, adjustingfor trial and potential confounding variables, thetreatment effect can be summarized by the odds ratioof 2.12 ( p=0.048) for survival until discharge. Theyconcluded that patients with traumatic brain injuries

in the presence of hypotension and receiving HSDareabout twice as likelyto survive as those who receivestandard of care.

Rockswold et al., [67] examined the effect of hypertonic saline on ICP, cerebral perfusion pressure(CPP), and brain tissue oxygen tension (PbtO2), andfound that hypertonic saline as a single osmotic agentdecreased ICP while improving CPP and PbtO2 inpatients with severe traumatic brain injury. Patientswith higher baseline ICP and lower CPP levelsresponded to hypertonic saline more significantly.

Colloids

Colloids are fluids with larger, more insolublemolecules that do not readily cross semi-permeablemembranes, across which they exert oncotic pressure.Water is drawn in from the interstitial and ICF byosmosis. Their movement out of the intravascularspace and their duration of action is dependent ontheir molecular weight, shape, ionic charge and thecapillary permeability [47]. Apart from albumin,all colloids are polymers and contain particles withdifferent molecular weights [48]. They may increase

plasma volume by more than the volume infused,because of their higher osmolality; hence the term

plasma expanders [48]. Studies suggest they can causesignificant impairment of clot formation activity[68,69].

Albumin

Albumin is a multifunctional, non-glycosylated,negatively charged plasma protein, with a molecular

weight of 69 kD. It is a biological therapeutic,manufactured from an inherently variable materialsource using a variety of purification techniques.Albumin is an effective volume expander, has notbeen associated with allergic-type reactions, andhas no intrinsic effects on clotting [50]. Its use asreanimation fluid has not been linked to bettersurvival compared with the synthetic colloids, a factthat together with costs, discredits its use in criticallyill patients [70]. There are in different concentrations:iso-oncotic (4-5% albumin) and hyper-oncotic (20%albumin). The later has adverse renal events.

Synthetic colloidsGelatins

Gelatin products are semi-synthetic colloids derivedfrom bovine collagen and prepared as polydispersivesolutions by multiple chemical modifications [48,71].Gelatins for volume therapy have been withdrawnfrom the US market due to the high rate of anaphylacticreactions [71]. Conventional gelatin preparationshave a mean molecular weight of 30-35kDa and a lowmolecular mass range. Their intravascular persistence

is short (2-3 hours), particularly for the urea-linkedgelatins, with rapid renal excretion (80% molecules< 20 kDa). Since the cross-linked gelatin moleculescontain negative charges, chloride concentrations of the solvent solution are reduced in contrast to othertypes of colloid. Since the latter fact results in slighthyposmolality, infusion of large amounts of gelatinsolutionsmay reduce plasmaosmolality and ultimatelyfoster the genesis of intracellular edema [71]. Therapid urinary excretion of gelatin is associated withincreased diuresis and has to be substituted byadequate crystalloid infusion to prevent dehydration.Gelatin infusion may furthermore increase bloodviscosity and facilitate red blood cell aggregationwithout influencing the results of crossmatching.Severe anaphylactoid reactions are low (thoughmore likely with gelatins than with other colloids),and usually occur only with rapid infusions (1/13000for succinylated gelatin; 1/2000 for urea-linkedgela tin), although much less with newer f ormulations.Reactions are usually mild (incidence < 0.4%).(48)Clinically, they have little effect on coagulation [48].

DextranesThese are neutral, high-molecular-weight



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glucopolysaccharides based on glucose monomers.Dextranes are derived from the action of the bacterium

Le uc onostoc mese nteroides on a sucrose medium viathe dextran sucrose enzyme. This produces a groupof branched polysaccharides of 200,000 glucose units.Subsequent partial hydrolysis produces moleculesof mean MW 40, 60, 70 and 110 kDa, with half-lives

ranging from 15 minutes to several days. They aremainly excreted via the kidneys (70%), with the restmetabolized by endogenous dextranase. They arerelatively cheap (£4-5 per 500 ml).

Dextran 40 is hyperoncotic and initially acts as aplasma expander before its rapid elimination by thekidney. Its main use is in promoting peripheral bloodflow in cases of prophylaxis for deep vein thrombosisand arterial insufficiency. Dextran 70 and 110 aremainly used for plasma expansion; 6% dextran 110 isno longer available clinically. Blood flow improvementresults from a reduction in blood viscosity, possiblyby coating the vascular endothelium and cellularelements of blood, thus reducing their interaction.Dextrans inhibit platelet adhesiveness, enhancefibrinolysis and may reduce factor VIII activity. Dosesabove 1.5 g/kg cause bleeding tendency. Initial useshould be limited to 500 – 1000 ml with a restrictionof 10 – 20 ml/kg/day thereafter.

Modern solutions do not interfere with blood cross-matching or cause roleaux formation, which was afeature of the early, very high MW dextrans. Theycan impair renal function by tubular obstruction

from dextran casts. This is usually seen with dextran40 combined with hypovolaemia and pre-existingrenal dysfunction. They can also cause an osmoticdiuresis. Severe anaphylactic reactions like immunecomplex type III can occur resulting from prior cross-immunization against bacterial antigens f ormingdextran reactive antibodies. The incidence of 1/4500is reduced with monovalent hapten pre-treatment(injection of 3 g dextran 1) to 1/84000. This blocksthe antigen-binding sites of circulating antidextranantibodies, preventing formation of immunecomplexes with subsequent infusions of dextran 40or 70. Dextran 1 (MW 1000 Da) is not available inthe UK[48].

Hydroxye thy l star ch( HE S)

HES is a semi-synthetic colloid, related to glycogen

The mean molecular weight of the different HESpreparations ranges from 70 and 670 kDa. Followinginfusion of HES, small molecules 8;

Low < 8

Concentration High 10%;

Low 6%.



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the standard’ maintenance volume in neurosurgicalpatients (2.000 mL/day of 0.45 normal saline in 5%dextrose) increases serum osmolality over abouta week [72]. Thus the old concept of benefit fromfluid restriction was simply a consequence of anincreased osmotic gradient over time [50]. Theavailable data indicate that volume replacement and

expansion will have no effect on cerebral edemaas long as normal serum osmolality is maintained,and cerebral hydrostatic pressures are not markedlyincreased due to true volume overload and elevatedright heart pressures. Whether this is achieved w ithcrystalloid or colloid seems uncertain, althoughthe osmolality of the selected fluid is crucial. Aspreviously mentioned, lactated Ringer’s solution isnot strictly iso-osmotic (measured osmolality 252-255 mOsmol/kg), particularly when administered topatients whose baseline osmolality has been increasedby hyperosmolar fluids (mannitol, HS) [50].

In TBI, a blunt or penetrating injury incitesmechanical and autodigestive destruction of thenormally tightly intact endothelium of the blood brainbarrier [73]. This allows uncontrolled movement of fluid and serum proteins into the brain parenchyma,eventually leading to vasogenic cerebral edema andincreased ICP. It has been shown that in critically illpatients, there is increased leakage of albumin acrossthe capillary wall [74]. In the brain, this increasedextravasation of albumin could lead to heightenedinterstitial oncotic pressure and exacerbate cerebral

edema.

Pr e-hospital

In nine randomised controlled trials and one cohortstudy of pre-hospital fluid treatment in patients w ithTBI [75], hypertonic crystalloids and colloid solutionswere not more effective than isotonic saline [76].In a combined polytrauma model of uncontrol ledhaemorrhage and TBI in swine, Teranishi et al.,[6] investigated if pre-hospital administration of the haemoglobin based oxygen carrier HBOC-201will improve tissue oxygenation and physiologicparameters compared to LR solution. They f oundthat mean TBI force (2.4±0.1 atm; means ± standarderror of the mean) and blood loss (22.5±1.7 mL/ kg) were similar between groups. Survival at the 6hendpoint was similar in all groups (≈50%). Cerebralperfusion pressure (CPP) and brain tissue oxygentension were significantly greater in HBOC-201 ascompared with LR animals ( p


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Mortality was assessed after 10 and 28 days, 6 and18 months. They found that the total fluid balancewas positive on days 1-3, and negative on days 4-10,and the crystalloid balance was negative from day2. The mean serum albumin was 38±6 g/L. Colloidsconstituted 40-60% of the total fluids given per day.Furosemide was administered to 94% of all patients.

Severe organ failure defined as SOFA≥3 was evidentonly for respiratory failure, which was observed in29% with none developing renal failure.After 28 days,mortality was 11% and, after 18 months, it was 14%.Thus, a protocol including albumin administrationcombined with a neutral to a slightly negative fluidbalance wasassociated with lowmortality in patientswith severe TBI despite a relatively high frequency(29%) of respiratory failure, assessed by the SOFA.Acute lung injury (ALI) and ARDS are reportedcommonly after TBI and their appearance isassociated with fluid management. ALI and ARDS areconsidered as independent factors for mortality [85-88].

A single equimolar infusion of 7.45% hypertonicsaline solution is as effective as 20% mannitol indecreasing ICP in patients with brain injury [79].In the Taiwan guidelines for TBI management, withneeded massive fluid transfusion, it is recommendedthat normal saline is better than lactated Ringer'ssolution (grade D). Fresh frozen plasma is onlyindicated for coagulopathy and not used as a regularvolume expander (grade C). Hypertonic saline may

be useful in patients with complication of severe TBIand systemic shock (grade D) [89].The Saline versus Albumin Fluid Evaluation (SAFE)

study was an international trial that randomizedcritically ill patients to either 4% albumin ornormal saline fluid resuscitation for 28 days [89].Although there was no overall difference in 28-daymortality between the 2 groups, there was a trendtoward increased mortality in patients with traumarandomized to albumin resuscitation. This increasedmortality appeared to be driven by patients withtrauma with TBI compared with those with traumawithout TBI. A post hoc analysis of patients withTBI randomized during the SAFE study confirmedthat resuscitation with albumin was associated w ithincreased mortality at 24 months compared withnormal saline [90-92]. This increased risk was entirelydriven by patients with severe TBI, defined as GCS ≤8.Sekhon et al., [91] in their study on 171 patientsattemted to determine if there was an associationbetween synthetic colloids and mortality in patientswith severe TBI,and found that patients receivingpentastarch had higher acute physiology and chronic

health II scores (23.9 vs 21.6, p


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• Give carbohydrate drinks.• Avoid bowel preparation.

Peri-operative:• Use fluid management technologies to deliver

individualized goal directed fluid therapy.• Avoid crystalloid excess (salt and water overload).

Maintenance’ fluid, if utilized, should be limitedto less than 2 ml/kg/hr including any drug

infusions.The use of isotonic balanced electrolytesuch as Hartmann’s solution will minimizehyperchloraemic acidosis.

Post-operative: Avoid post-operative i.v.fluids when it is possible. Always ask the question; ‘what are we giving

fluids for?Maintenance fluid? -Push early drinking and

eating; Replacement fluid? ; Considering oral before

i.v. and prescribing oral fluidsResuscitation fluids? ; Using goal directed fluid

therapy

Physiological responses during the pe ri op erati ve phase

In the critically ill, effectsof surgery per se and itsassociated changes in the hormonal milieu interne areexaggerated by a systemic inflammatory response withdevelopment of capillary leak. This leads to difficult-to-balance losses into the interstitium and frequently

visible oedema formation. Resulting abnormalitiesof fluid and electrolyte balance in the critically ill arepurposefully or involuntarily influenced, in addition,by nutritional support and measures that affect acid – base homeostasis [79].

Surgery alters fluid balance [39], generates asystemic inflammatory response which increasesoxygen consumption, and is associated with increasein cardiac output and oxygen delivery. Failure to meetthe metabolic demands of recovery from surgery isassociated with increased morbidity and mortality[95]. The stress response to surgery and trauma

involves a number of different physiological reactions.Importantly, the renine-angiotensine-aldosteronesystem is stimulated, leading to increased sodium andfluid retention, decreased urinary output and alteredfluid balance. In addition, the activated inflammatoryresponse causes vasodilatation and increasedpermeability of capillary wall [47]. This affects theintravascular duration of fluids administration, withincreased capillary leak of fluids into the interstitialtissues. As a result, the perioperative period is a timewhen the body’s management of fluids is dramaticallyaltered and needs to be considered carefully whenprescribing fluids [47].

In conclusion, perioperative fluid therapy continuesto be an exercise in empiricism, with naggingquestions about its efficacy and complications. Thereare no evidence-based guidelines or standards of care for the management of fluid therapy in patientsundergoing decompressive craniectomy. Knowledgeof the properties of the various available IV f luids, andthe awareness of the pathophysiology of endothelial,parenchymal and endocrine alterations emerging inTBI should guide i.v. fluid administration, to reach

a good medium that favors better neurological,morbidity and mortality outcomes.

Conflict of Interest: None declared.

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