RHC 2014;5(1)7-22.html

Reviews in Health Care 2014; 5(1): 7-22

Techniques

Narrative review

Fluid therapy in neurotrauma: basic and clinical concepts

Hernando Raphael Alvis-Miranda 1, Andres M. Rubiano 2, Juan C. Puyana 3, Gabriel Alcala-Cerra 1, Luis Rafael Moscote-Salazar 1

1 Universidad de Cartagena, Cartagena de Indias, Colombia

2 MEDITECH Foundation. Hospital Universitario de Neiva, Colombia

3 Director of Surgical ICU, director of the Surgical Critical Care Program at the University of Pittsburgh Medical Center at Presbyterian Hospital, Pittsburgh, USA

Abstract

The patient with head trauma is a challenge for the emergency physician and for the neurosurgeon. Currently traumatic brain injury constitutes a public health problem. Knowledge of the various therapeutic strategies to provide support in the prehospital and perioperative are essential for optimal care. Rapid infusion of large volumes of crystalloids to restore blood volume and blood pressure quickly is now the standard treatment for patients with combined TBI and HS The fluid in patients with brain and especially in the carrier of brain injury is a critical topic; we present a review of the literature about the history, physiology of current fluid preparations, and a discussion regard the use of fluid therapy in traumatic brain injury and decompressive craniectomy.

Keywords

Brain trauma; Colloid solutions; Fluid resuscitation

Corresponding author

Dr: Luis Rafael Moscote-Salazar

mineurocirujano@aol.com

Disclosure

The Authors have no financial competing interest to declare.

Introduction

Traumatic brain injury (TBI) is a major public health problem and a leading cause of death and disability [1]. It is frequently accompanied by hemorrhagic shock (HS) [2-5]. The mechanism for adverse outcome in patients with combined TBI and HS may be due in part to secondary ischemic injury to the already vulnerable brain following loss of cerebral auto-regulation and/or to adverse effects of TBI itself on the normal compensatory response to HS [6]. Rapid infusion of large volumes of crystalloids to restore blood volume and blood pressure quickly is now the standard treatment for patients with combined TBI and HS [7,8]. Perioperative fluid administration is an important aspect of surgical care, but is often poorly understood [9-13], and continue to be an exercise in empiricism, with nagging questions about efficacy and complications [14].

Fluid therapy (FT), as the name implies is a treatment with fluids, thus, is a drug [15]. The final goal of fluid management is to optimize the circulatory system to ensure the sufficient delivery of oxygen to organs [16]. FT is needed for the following requirements:

  1. Normal maintenance;
  2. Blood or fluid loss (wounds, drains, induced dieresis, etc);
  3. “Third space losses” (fluid sequestration in tissue edema or ileus); and
  4. Increased systemic requirements due to fever and hypermetabolic state.

TF should be tailored to match these requirements [17]. Intravenous (IV) fluids may broadly be classified into colloid and crystalloid solutions. They have very different physical, chemical, and physiological characteristics. Colloid solutions can be natural (albumin) or synthetics (gelatins, dextranes, and hydroxyethyl starches).

Goal-directed fluid therapy (GDT) aimed at optimizing cardiac output and oxygen delivery has been shown to improve outcome for high-risk surgical patients [18]. The majority of the information presented here is derived from the fluid management for the surgical patient in general, and those critically ill, such as trauma patient. Primary studies on preoperative fluid therapy for DC are sparse.

The fluid management for patients undergoing elective major surgery, e.g., neurotrauma surgery, is controversial [19-21]. During the perioperative period, many pathophysiological changes occur that alter the normal efficiency of fluid homeostasis. Despite this, perioperative fluid prescription is often poor, being based on an insufficient knowledge of water and electrolyte requirements and distribution [22-25]. Perioperatively, crystalloids, colloids and blood components are required to meet the ongoing losses and for maintaining cardiovascular stability to sustain adequate tissue perfusion [26,27].

Intravenous fluids maintain hydration while patients are unable to drink and replace losses that occur as a result of surgery [28]. Severity of illness, magnitude and duration of surgery, comorbidities and the host response to injury, influence the perioperative fluid needs. Although the principle goal of fluid administration is to maintain adequate tissue perfusion and the perils of over and under-resuscitation are well documented, there are no standards of care guiding perioperative fluid administration [28]. The aim of this work is to review current topics of fluid management in the patients with traumatic brain injury and those who are candidate to decompressive craniectomy.

History of modern fluid therapy

IVF first gained therapeutic importance in the treatment of cholera in the 1830s [29-34], with the reports of William Brooke O’Shaughnessy about his terminal cholera patients’ blood observations [29]. Their blood were “thick and obscure”, thus concluding there was water deficit in those patients [31]. Aiming to replace the corporal fluid loses was prepared the misnamed 0.9% physiologic saline solution for surgical patients.

From the 1880s, IVF began to be administered perioperatively to compensate for the “injurious” effects of anesthesia. Clinical improvements were consequently noted, though the adverse effects of saline were observed. Thomas Latta was the first to administrate intravenously water and salt solutions to dying patients with no great results [29,35]. Water and salt solutions were randomly mixed and in conjunction with the poor hygienic practices of those times, the FT initially wasn’t firmly instituted [15].

In 1880, Sidney Ringer observed the different protoplasmic activity of sodium, calcium, potassium and chloride salts, and originating “Ringer’s solution” [15]. George Crile in 1899, with a hemorrhagic shock animal model, studied the reanimation, recommend it in warm way. In the First World War, took place treatments of war injuries with primitive saline and colloid solutions. The Gum Arabic, a natural colloid from the Acacia senegalis tree used by W.C. Cannon, was a highlighted colloid [15].

In 1924, the intravenous “drip” was introduced by Rudolph Matas. In 1930, Hartmann and Senna looking for evading the hyperchloremic acidosis derived from the use of Ringer´s solutions [36], added sodium lactate, allowing sodium to be linked to the excess of chloride, facilitating the lactate metabolism, and thus, giving origin to the Hartman solution or Ringer-lactate. The work of Ringer, Hartmann, and others emphasized the importance of the composition of IV fluids and laid the foundations for the balanced solutions in use today [37]. During the Second World War, blood and plasma were massively administrated, even in the battlefield, with the aim to enhance injured soldier surviving. In general, FT has been continuously in change, depending on current trends [15]. As the metabolic response to injury was increasingly investigated in the 1940s and 1950s, the cause of post-operative oliguria was debated widely with the most prominent surgeons being Moore and Shires [37]. During Vietnam War, the preservation of renal function, becomes a therapeutic objective, thus, were protocolized the use of large amounts of crystalloid for the hemorrhagic shock in the Da Nang Army Hospital. In this moment, took place the observations of pulmonary complications derived from those large volumes of fluids, generating the “Da Nang lung”, “wet lung syndrome”, previous denominations of the today Adult Respiratory Distress Syndrome (ARDS).

These differences in opinion, coupled with reports of injured soldiers from the Korean War receiving large IV fluid infusions and surviving, dictated the surgical practice of liberal IV fluid administration until very recently [37]. Newer work in fluid therapy has explored the concept of fluid restriction. Shoemaker and colleagues also pioneered the concept of fluid administration to achieve supranormal indices of cardiorespiratory function, which has led to the advent of goal-directed fluid therapy [37]. Alongside the development of balanced solutions, the renewed focus on perioperative fluid therapy has led to IVF administration being guided by physiological principles with a new consideration of the lessons gleaned from history [37]. With military medicine advances, fluid therapy is going catching more, and more attention, being important to receive fluid therapy plus hemotherapy, but, with no clear ideas about the proper volume. Currently, fluid therapy stills with large controversies.

Fluid physiology

The fundamentals governing fluid and electrolyte management in patients date to the 19th century [38]. In the first half of the 20th century work by Gamble and Darrow and colleagues defined the electrolyte content of extracellular, intracellular and interstitial fluid compartments [38]. 60% of the human adult body is composed by water, two-thirds of this is intracellular water, and the remaining third is the extracellular compartment, which in turn is divided between intravascular and extravascular or interstitial compartments [39,40]. The interstitial compartment is actually a matrix, a collagen/gel substance that allows the interstitium to provide structural rigidity which resists gravity and can maintain structural integrity during extracellular volume depletion. The collagen/gel interstitial space, especially in skin and connective tissue, is an important reservoir of extracellular fluid [38]. The total intravascular volume, also referred as blood volume, has approximately 5 l and has intracellular (red and white cells and platelets: 40%; 2 l) and extracellular (plasma: 60%; 3 l) components [39,40]. Extracellular compartment is important for oxygen and nutrients transport, and the elimination of carbonic anhydride and other products from cellular metabolism. There is another compartment, the transcellular, which is composed by fluids not equilibrated with the other fluids, and it is constituted by synovial, cerebrospinal fluids, gastrointestinal secretions, etc. This compartment through the lymphatic system returns the fluids to the intravascular space [40].

The cells and the intravascular space have membranes that preserve their structural integrity and allow the molecule and fluid interchange between different compartments. The main objective of membranes is preserve osmolarity and the electronegativity of each one of the compartments. The cell wall separates the intracellular compartment from the extracellular compartment. The capillary endothelium and the walls of arteries and veins divide the extracellular compartment into the intravascular and the interstitial (tissue or extravascular) compartments. Water moves freely through cell and vessel walls and is distributed throughout all these compartments. The energy-dependent Na/K adenosine triphosphatase in cell walls extrudes Na+ and Cl- and maintains a sodium gradient across the cell membrane: Na+ is an extracellular ion. The capillary endothelium is freely permeable to small ions such as Na+ and Cl-, but is relatively impermeable to larger molecules such as albumin and the semisynthetic colloids, e.g., gelatins and starches, which are therefore normally theoretically maintained in the intravascular space. Plasma is a solution in water of inorganic ions (predominantly sodium chloride), simple molecules such as urea, and larger organic molecules such as albumin and the globulins. Plasma volume and interstitial fluid volume is highly exchangeable. Fluid exchange through a capillary is regulated by Starling’s law, which mathematically summarizes the forces governing the flow of fluid out of blood vessels into surrounding tissues, states that:

Qf = Kf x [(Pc - Pi) - R (πc - πi)]

Where Qf is the total fluid flux out of capillaries (not represent the quantity, but just the speed of water movement [16]) and Kf is the filtration coefficient (the product of the membrane conductance and the membrane surface area), Pc is intravascular hydrostatic pressure, Pi is interstitial hydrostatic pressure, πc is colloid osmotic pressure within the vasculature, πi is interstitial colloid osmotic pressure gradient across the vessel wall, and R is the oncotic reflection coefficient, the tendency of a membrane to impede the passage of oncotically active particles [16,41].

A R of 0 indicates a membrane that is totally permeable to protein while a R of 1 indicates a membrane that completely prevents protein diffusion. Distribution terminates when the balance of the hydrostatic pressure and the osmotic pressure cancel each other out. Because the interstitium consists not only of free space but also of absorbent gel, captured water in the gel does not contribute to lowering the osmotic pressure in the interstitium [16]. Therefore, the osmotic pressure does not easily change until the gel is saturated by water movement. This is a mechanism of edema formation. Thus, Starling’s law does not determine the distribution ratio between plasma and interstitium, it just explains the movement of water through the capillary wall [16].

The original interpretation of an equilibrium including fluid re-absorption at the venous end of the microcirculation is now known to be incorrect through actual measurement of the pressures involved. Rather, a steady state is involved, with a level of permeability to plasma proteins in the microvascular walls. Net fluid movement occurs in the vessels from the intravascular to the perivascular components [42]. The fluid transfer is mediated by the endothelial glycocalyx layer (EGL), a physiological entity discovered and studied over the past 30 years [43]. A model for fluid transfer across the EGL [44] accounts for the discrepancies observed in fluid transfer as predicated by Starling’s original equation, and proposes a modified hypothesis based on pressures involving the generation of fluid through the glycocalyx rather than the interstitial space [45] modifying the Starling equation to:

Qf = (Pc - Pi) – R x (πc – πg)

Where Pi and πg are the hydrostatic and osmotic pressures, respectively, exerted by the ultrafiltrate formed across the glycocalyx [46]. While the EGL is the conduit for water passage from the intravascular to the extravascular space, plasma proteins cross the endothelial barrier through a separate pathway, the large pore system [46]. This model is perturbed by a number of factors during anesthesia and surgery. Patients present for surgery with a variety of conditions that result in altered fluid distribution. Many anesthetic drugs (e.g., IV induction drugs and volatile anesthetics) cause vasodilation, leading to a reduction in the ratio between the circulating volume and the capacity of the intravascular space, or myocardial impairment, leading to a reduction in flow through the circulation. Fluid shifts between compartments may also reduce the circulating volume (third-space losses and loss of intravascular fluid into the interstitium because of altered endothelial permeability in sepsis and inflammatory states) [39].

In the next items, it will be presented a resume of the main characteristics of different kind of solutions.

Crystalloids

A crystalloid fluid is a solution of small water-soluble molecules that can diffuse easily across semi-permeable membranes. The properties of these solutions are largely determined by their tonicity (osmolality relative to plasma) and their sodium content (affecting their distribution within body compartments) [47]. They redistribute throughout the ECF compartment, of which 75% is interstitial fluid. This suggests that 4 liters of crystalloid are required to replace a blood loss of 1 liter [48]. Studies have shown that the volume kinetics of infused crystalloid solutions differ between normovolemic and hypovolemic patients [49].

IV infusions of isotonic saline solution only expand the intravascular space by a maximum of one-third of the volume used in normal subjects, with only 16% left after 30 minutes. The volume of crystalloid required to replace an acute blood loss remains 3-4 fold because of redistribution into, and rapid elimination from, the ECF [48].

Isotonic 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, do not change plasma osmolality and do not increase brain water content [50]. They also contain sodium at physiological plasma concentrations. These fluids distribute freely within the extracellular fluid (ECF) compartment causing little change in sodium concentration and osmolality. As a result this limits the movement of water out of the ECF into the ICF compartment and viceversa. Commercial lactated Ringer’s solution is not truly iso-osmolar with respect to plasma. Its measured osmolality is 254 mOsmol/kg, which explains why administration of large volumes can reduce plasma osmolality and increase brain water content and ICP [50].

Hypotonic solutions

Large amounts of hypo-osmolar or hypotonic fluids reduce plasma osmolality, drive water across the BBB, and increase cerebral water content and ICP. 5% dextrose (D5W) is essentially water (the sugar is metabolized very quickly), provides free water which disperses throughout the intracellular and extracellular compartments, and has little use as a resuscitative fluid [50]. As a consequence, hypo-osmolar crystalloids (0.45% NaCl or D5W) should be avoided in neurosurgical patients [50].

Hypertonic crystalloids: mannitol and hypertonic saline

Osmotherapy agents such as hypertonic saline (HTS) are currently being used in the treatment of patients with post-traumatic cerebral edema and raised intracranial pressure (ICP) resulting from TBI [51]. It’s said to have a particularly useful role for the treatment of ICP whilst administering small volume fluid resuscitation [52]. HTS solutions typically improve cardiovascular output as well as cerebral oxygenation whilst reducing cerebral edema. Hypertonicity seems to affect some innate immune-cell functions, specifically neutrophil burst activity in preclinical studies, probably this could have beneficial effects on modulation of the inflammatory response to trauma [53-58].

Clinical studies however do not provide compelling evidence to support the use of HTS either for TBI or for hemorrhagic shock. One small RCT (n = 222) reported a significant reduction in mortality when comparing a 250 ml bolus of HTS/dextran with isotonic saline in 222 patients with hemorrhagic shock [59]. But many other RCTs have not demonstrated mortality benefit in this group of patients [60-63], including the most recent and largest RCT comparing HTS, HTS/dextran and normal saline. This trial recruited two separate cohorts, one with TBI (n = 1087) [64] and one with hemorrhagic shock (n = 853) [65]; with primary endpoints of neurological outcome at 6 months after TBI and 28 day survival, respectively. The TBI study was terminated early due to futility, as interim analysis was unable to demonstrate an improvement in neurological status or indeed mortality at 6 months. The second study demonstrated no significant difference in mortality at 28 days, and was terminated early for concerns of potential (albeit statistically non-significant) increase in mortality observed with a subgroup of patients receiving HTS but no blood transfusions within the first 24 h [65].

Wade et al. [66] undertook a cohort analysis of individual patient data from a previous prospective randomized double-blinded trial to evaluate improvements in survival at 24 hours and discharge after initial treatment with HSD in patients who had TBI (head region Abbreviated Injury Score ≥4) and hypotension (systolic blood pressure ≤90 mm Hg). Found that treatment with HSD resulted in a survival until discharge of 37.9% (39 of 103) compared with 26.9% (32 of 119) with standard of care (p = 0.080). Using logistic regression, adjusting for trial and potential confounding variables, the treatment effect can be summarized by the odds ratio of 2.12 (p = 0.048) for survival until discharge. They conclude that patients who have traumatic brain injuries in the presence of hypotension and receive HSD are about twice as likely to survive as those who receive standard of care.

Rockswold et al. [67] examined the effect of hypertonic saline on ICP, cerebral perfusion pressure (CPP), and brain tissue oxygen tension (PbtO2), and found that hypertonic saline as a single osmotic agent decreased ICP while improving CPP and PbtO2 in patients with severe traumatic brain injury. Patients with higher baseline ICP and lower CPP levels responded to hypertonic saline more significantly.

Colloids

Colloids are fluids with larger, more insoluble molecules that do not readily cross semi-permeable membranes, across which they exert oncotic pressure. Water is drawn in from the interstitial and ICF by osmosis. Their movement out of the intravascular space and their duration of action depend on their molecular weight, shape, ionic charge and the capillary permeability [47]. Apart from albumin, all colloids are polymers and contain particles with a range of 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 cause significant 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. Albumin is a biological therapeutic, manufactured from an inherently variable source material using a variety of purification techniques. Albumin is an effective volume expander, has not been associated with allergic-type reactions, and has no intrinsic effects on clotting [50]. Its use as reanimation fluid has not been linked to better surviving in compared with the synthetic colloids, fact that together with costs, discredits its use in critically ill patients [70]. There are different concentrations: iso-oncotic (4-5% albumin) and hyper-oncotic (20% albumin). The later has adverse renal events.

Sintetic colloids

Gelatins

Gelatin products are semi-synthetic colloids derived from bovine collagen and prepared as polydispersive solutions by multiple chemical modifications [48,71]. Gelatins for volume therapy have been withdrawn from the US market due to the high rate of anaphylactic reactions [71]. Conventional gelatin preparations have a mean molecular weight of 30-35kDa and a low molecular mass range. Their intravascular persistence is short (2-3 hours), particularly for the urea-linked gelatins, which are excreted rapidly renally (80% molecules < 20 kDa). Since the cross-linked gelatin molecules contain negative charges, chloride concentrations of the solvent solution are reduced in contrast to other types of colloid. Since the latter fact results in slight hyposmolality, infusion of large amounts of gelatin solutions may reduce plasma osmolality and ultimately foster the genesis of intracellular edema [71]. The rapid urinary excretion of gelatin is associated with increased diuresis and has to be substituted by adequate crystalloid infusion to prevent dehydration. Gelatin infusion may furthermore increase blood viscosity and facilitate red blood cell aggregation without influencing the results of crossmatching.

Severe anaphylactoid reactions are low (though more likely with gelatins than with other colloids), and usually occur only with rapid infusions (1/13000 for succinyl ated gelatin; 1/2000 for urea-linked gelatin), though much less with newer formulations. Reactions are usually mild (incidence < 0.4%) [48]. Clinically, they have little effect on coagulation [48].

Dextranes

These are neutral, high-molecular-weight glucopolysaccharides based on glucose monomers. Dextranes are derived from the action of the bacterium Leuconostoc mesenteroides on a sucrose medium via the dextran sucrose enzyme. This produces a group of branched polysaccharides of 200,000 glucose units. Subsequent partial hydrolysis produces molecules of mean MW 40, 60, 70 and 110 kDa, with half-lives ranging from 15 minutes to several days. They are mainly excreted via the kidneys (70%), with the rest metabolized by endogenous dextranase. They are relatively cheap (4-5 £/500 ml).

Dextran 40 is hyperoncotic and initially acts as a plasma expander before its rapid elimination by the kidney. Its main use is in promoting peripheral blood flow (e.g. in prophylaxis for deep vein thrombosis and arterial insufficiency). Dextran 70 and 110 are mainly used for plasma expansion; 6% dextran 110 is no longer available clinically. Improvement in blood flow results from a reduction in blood viscosity, possibly by coating the vascular endothelium and cellular elements of blood, thus reducing their interaction. Dextrans inhibit platelet adhesiveness, enhance fibrinolysis and may reduce factor VIII activity. Doses above 1.5 g/kg produce a bleeding tendency. Initial use should be limited to 500-1000 ml with a restriction of 10-20 ml/kg/day thereafter.

Modern solutions do not interfere with blood cross-matching or cause roleaux formation, which was a feature of the early, very high MW dextrans. They can impair renal function by tubular obstruction from dextran casts. This is usually seen with dextran 40 combined with hypovolaemia and pre-existing renal dysfunction. They can also cause an osmotic diuresis. Severe anaphylactic reactions can occur (immune complex type III), resulting from prior cross-immunization against bacterial antigens forming dextranreactive antibodies. The incidence of 1/4,500 is reduced with monovalent hapten pre-treatment (injection of 3 g dextran 1) to 1/84,000. This blocks the antigen-binding sites of circulating antidextran antibodies, preventing formation of immune complexes with subsequent infusions of dextran 40 or 70 [48].

Hydroxyethyl starch

HES was used extensively to treat wounded soldiers during the Vietnam War [71]. HES are semi-synthetic colloids related to glycogen. The raw material for the production of HES is amylopectin, a highly branched polymer of glucose, derived from either waxy-maize or potato starch [71], which are etherified with hydroxyethyl groups into the D-glucose units. HES has a much lower viscosity than dextran or gelatin, but does not reach the low viscosity of albumin. The mean molecular weight of the different HES preparations ranges between 70 and 670 kDa. Following infusion of HES, small molecules <60 kDa are filtrated into the urine, whereas larger molecules are degraded by plasma amylase.

MWw [kDa]

High (450–480);

Medium (130–200);

Low (40–70)

Degree of substitution

High (0.6–0.7);

Low (0.4–0.5)

C2:C6 ratio

High > 8;

Low < 8

Concentration

High 10%;

Low 6%.

Table 1. Classification of hydroxyethyl starch preparations

The kinetics of this degradation are mainly determined by the molar substitution and the C2/C6 ratio (i.e. the quotient of the numbers of glucose residues hydroxyethylated at positions 2 and 6, respectively) [71]. A high molar substitution and a high C2/C6 ratio make the HES molecule less susceptible to plasma amylase, and thus increase the intravascular half-life of HES molecules. Part of the HES is stored within the reticulo-endothelial system and slowly degraded to CO2 and water [71].

However, massive infusion of old, high-molecular-weight preparations with a high degree of substitution (particularly heta- and hexastarch) may be associated with excessive tissue storage. With modern preparations (i.e. 6% HES 130/0.4), no plasma accumulation and greatly reduced tissue storage have been reported in the literature [71]. The reduction in viscosity of HES solutions results from the globular structure associated with the high degree of branching [71].They are classified as shown in Table 1.

They are hydrolyzed to smaller molecules by amylase and renal elimination is rapid for polymers over 50 kDa. The action of amylase is suppressed by higher degrees of substitution and with greater etherification at the C2 versus C6 position. Intravascular half-life is thus maximized especially when the initial MW is high. As well as persistent plasma expansion, HES plug capillary leaks induced by sepsis and major trauma and restore macrophage function after hemorrhagic shock. Compared with 20% albumin in these patients, 10% HES significantly improves hemodynamic parameters in the systemic and microcirculation (splanchnic perfusion) [48].

Fluid therapy and traumatic brain injury

Clinically acceptable fluid restriction has little effect on edema formation. The first human study on fluid therapy demonstrated that reducing by 50% the standard maintenance volume in neurosurgical patients (2,000 ml/day of 0.45 normal saline in 5% dextrose) increases serum osmolality over about a week [72]. Thus the old concept of benefit from fluid restriction was simply a consequence of an increased osmotic gradient over time [50].The available data indicate that volume replacement and expansion will have no effect on cerebral edema as long as normal serum osmolality is maintained, and as long as cerebral hydrostatic pressures are not markedly increased (e.g. due to true volume overload and elevated right heart pressures). Whether this is achieved with crystalloid or colloid seems irrelevant, although the osmolality of the selected fluid is crucial. As previously mentioned, lactated Ringer’s solution is not strictly iso-osmotic (measured osmolality 252-255 mOsmol/kg), particularly when administered to patients whose baseline osmolality has been increased by hyperosmolar fluids (mannitol, HS) [50].

In TBI, a blunt or penetrating injury incites mechanical and autodigestive destruction of the normally tightly intact endothelium of the blood brain barrier [73]. This allows uncontrolled movement of fluid and serum proteins into the brain parenchyma, eventually leading to vasogenic cerebral edema and increased ICP. It has been shown that in critically ill patients, there is increased leakage of albumin across the capillary wall [74]. In the brain, this increased extravasation of albumin could lead to increased interstitial oncotic pressure and exacerbate cerebral edema.

Pre-hospital

In nine randomised controlled trials and one cohort study of pre-hospital fluid treatment in patients with TBI [75], hypertonic crystalloids and colloid solutions were not more effective than isotonic saline [76]. In a combined polytrauma model of uncontrolled hemorrhage and TBI in swine, Teranishi et al. [6] investigated if pre-hospital administration of the hemoglobin based oxygen carrier HBOC-201 will improve tissue oxygenation and physiologic parameters compared to LRsolution. They found that mean TBI force (2.4 ± 0.1 atm; means ± standard error of the mean) and blood loss (22.5 ± 1.7 ml/kg) were similar between groups. Survival at the 6h endpoint was similar in all groups (≈50%). Cerebral perfusion pressure (CPP) and brain tissue oxygen tension were significantly greater in HBOC-201 as compared with LR animals (p < 0.005). Mean arterial pressure (MAP) and mean pulmonary artery pressure (MPAP) were not significantly different amongst groups. Blood transfusion requirements were delayed in HBOC-201 animals. Animals treated with HBOC-201 or LR showed no immunohistopathological differences in glial fibrillary acidic protein (GFAP) and microtubule-associated protein 2 (MAP-2). Severity of subarachnoid and intraparenchymal hemorrhages were similar for HBOC and LR groups. They conclude that in their polytrauma swine model of uncontrolled hemorrhage and TBI with a 30 minute delay to hospital arrival, pre-hospital resuscitation with one bolus of HBOC-201 indicated short term benefits in systemic and cerebrovascular physiological parameters. True clinical benefits of this strategy need to be confirmed on TBI and hemorrhagic shock patients.

In-hospital

A defined strategy for volume replacement and fluid balance that includes maintenance of normovolemia and colloid osmotic pressure in combination with a neutral to a slightly negative fluid balance is a cornerstone of the intracranial pressure ICP-targeted therapy for severe TBI [77]. In contrast to hemorrhage and hemorrhagic shock, possibilities for life-saving interventions are very limited in CNS injury. The significant contribution of HS to brain injury mortality further illustrates the role of hemorrhage control in reducing mortality in trauma patients [78].

Crystalloid resuscitation should be targeting a corridor of safety, avoiding both extremes of overt hypovolaemia and fluid overload. While avoidance of edema formation is a prime objective and concern in visceral surgery, efforts to restrict fluids, such as forced hypovolaemia, are associated with oliguria and occasionally renal shutdown, and may impair nutritional microvascular blood flow in other vascular beds such as the splanchnic circulation. Fluid excess, on the other hand, is presumably a cause of perioperative morbidity and mortality [79]. Sequelae of volume overload are particularly well known, and the pathophysiological cascades of events have been worked out best for the patient with aggressive crystalloid resuscitation after major trauma. Manifestations of crystalloid overload might include ARDS and brain edema in the patient with concomitant head injury [80-84].

Wahlström et al. [77] analyzed the occurrence of organ failure and mortality in patients with severe TBI treated by a protocol that includes defined strategies for fluid therapy (albumin administration to maintain normal colloid osmotic pressure and advocates a neutral to slightly negative fluid balance). Ninety-three patients with severe TBI and Glasgow Coma Scale ≤ 8 were included during 1998-2001. Medical records of the first 10 days were retrieved. Organ dysfunction was evaluated with the Sequential Organ Failure Assessment (SOFA) score. Mortality was assessed after 10 and 28 days, 6 and 18 months. They found that the total fluid balance was positive on days 1-3 and negative on days 4-10. The crystalloid balance was negative from day 2. The mean serum albumin was 38 ± 6 g/l. Colloids constituted 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 evident only for respiratory failure, which was observed in 29%. None developed renal failure. After 28 days, mortality was 11% and, after 18 months, it was 14%. Thus, a protocol including albumin administration in combination with a neutral to a slightly negative fluid balance was associated with low mortality in patients with severe TBI in spite of a relatively high frequency (29%) of respiratory failure, assessed with the SOFA. Acute lung injury (ALI) and ARDS are reported commonly after TBI and their appearance is associated with fluid management. ALI and ARDS are considered as independent factors for mortality [85-88].

A single equimolar infusion of 7.45% hypertonic saline solution is as effective as 20% mannitol in decreasing ICP in patients with brain injury [79]. In the Taiwan guidelines for TBI management, when it is needed massive fluid transfusion, recommends that normal saline is better than lactated Ringer’s solution (grade D). Fresh frozen plasma is only indicated for coagulopathy and not recommended to be used as a regular volume expander (grade C). Hypertonic saline may be useful in patients who have complication of severe TBI and systemic shock (grade D) [89].

The Saline versus Albumin Fluid Evaluation (SAFE) study was an international trial that randomized critically ill patients to either 4% albumin or normal saline fluid resuscitation for 28 days [89]. Although there was no overall difference in 28-day mortality between the 2 groups, there was a trend toward increased mortality in patients with trauma randomized to albumin resuscitation. This increased mortality appeared to be driven by patients with trauma with TBI compared with those patients with trauma without TBI. A post hoc analysis of patients with TBI randomized during the SAFE study confirmed that resuscitation with albumin was associated with increased mortality at 24 months when compared with normal saline [90,91]. This increased risk was entirely driven by patients with severe TBI, defined as GCS ≤ 8.

Sekhon et al. [91] in their study (n=171) looking for determine if there is an association between synthetic colloids and mortality in patients with severe TBI, found that patients receiving pentastarch had higher Acute Physiology and Chronic Health II scores (23.9 vs. 21.6, p < 0.01), frequency of craniotomy (42.5% vs. 21.6%, p = 0.02), longer duration of intensive care unit stay (12 vs. 4 days, p < 0.01), and mechanical ventilation (10 vs. 3 days, p < 0.01). On unadjusted Cox regression, patients in the highest quintile of cumulative pentastarch administration had a higher rate of mortality compared with those receiving no colloid (HR = 3.8; CI95% = 1.2-12.4; p = 0.03]. However, this relationship did not persist in the final multivariable model [HR = 1.0; CI95% = 0.25-4.1; p = 0.98]. They conclude that there was no association between cumulative exposure to pentastarch and mortality in patients with severe TBI.

Elliot et al. [51] in a study focused on the hypothesis that hypertonic saline-induced improvements in histological outcome are time dependent and may be associated with alterations in astrocyte hypertrophy after cortical contusion injury, examined histopathological changes at 7 days after controlled cortical impact (CCI) injury in a rat model. They found that hypertonic saline treatment reduced tissue loss that correlated with attenuated astrocyte hypertrophy characterized by reductions in astrocyte immunoreactivity without changes in the number of astrocytes after CCI injury. Delayed treatment of hypertonic saline resulted in the greatest reduction in tissue loss compared to all other treatments (0.9% normal saline – NS, n = 12; 7.5% hypertonic saline – HS, n = 15; delayed NS, n=3; delayed HS, n=4; or no treatment – CCI control, n=18) indicating that there is a therapeutic window for hypertonic saline use after TBI.

Hypertonic/hyperoncotic solutions

Recently, attention has been directed at hypertonic/hyperoncotic solutions (typically hypertonic hetastarch or dextran solutions). Because of the hemodynamic stabilizing properties of these fluids in hypovolaemic shock, administration in patients with trauma and TBI might be particularly advantageous for the prevention of secondary ischemic brain damage. Small volumes of such solutions can restore normovolaemia rapidly, without increasing ICP. They have been successfully used to treat intracranial hypertension in TBI patients [66], and in others neurosurgical acute emergencies (SAH [92] and stroke [93]).

Fluid therapy for decompressive craniectomy

Some general principles of enhanced recovery fluid management and recommendations of the enhanced recovery partnership [94]:

Pre-operative:

  • Maintain good pre-operative hydration;
  • Give carbohydrate drinks;
  • Avoid bowel preparation.

Perioperative:

  • Use fluid management technologies to deliver individualized goal directed fluid therapy;
  • Avoid crystalloid excess (salt and water overload). Maintenance fluid, if utilized, should be limited to less than 2 ml/kg/h including any drug infusions. The use of isotonic balanced electrolyte solution (e.g. Hartmann’s) will minimize hyperchloraemic 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? Consider oral before IV and consider prescribing oral fluids;
    • Resuscitation fluids? Use goal directed fluid therapy.

Physiological responses during the perioperative phase

In the critically ill, effects of surgery per se and its associated changes in the hormonal milieu interne are exaggerated by a systemic inflammatory response with development of capillary leak. This leads to difficult to balance losses into the interstitium and frequently visible edema formation. Resulting abnormalities of fluid and electrolyte balance in the critically ill are purposefully or involuntarily influenced, in addition, by nutritional support and measures that affect acid–base homeostasis [79].

Surgery alters fluid balance [39], generates a systemic inflammatory response which increases oxygen consumption, and is associated with increase in cardiac output and oxygen delivery. An inability to meet the metabolic demands of recovery from surgery is associated with increased morbidity and mortality [95]. The stress response to surgery and trauma involves a number of different physiological reactions. Importantly, the renine-angiotensine-aldosterone system is stimulated, leading to increased sodium and fluid retention, decreased urinary output and altered fluid balance. In addition, the activated inflammatory response causes vasodilatation and increased capillary wall permeability [47]. This affects the intravascular duration of fluids given, with increased capillary leak of fluids into the interstitial tissues. As a result, the perioperative period is a time when the body’s management of fluids is dramatically altered and needs to be considered carefully when prescribing and giving fluids [47].

Conclusions

Perioperative fluid therapy continues to be an exercise in empiricism, with nagging questions about efficacy and complications. There are no evidence-based guidelines or standards of care for the management of fluid therapy in patients who will underwent to decompressive craniectomy.

Knowledge of the properties of the various available IV fluids, and the knowledge of the pathophysiology of endothelial, parenchymal and endocrine alterations which happen in TBI should guide their administration, to reach a good medium which propitiate allow better neurological, morbidity and mortality outcomes.

Question for further research

Development of an evidence based guidelines or standard of care for the management of fluid therapy in patients who will underwent to decompressive craniectomy.

The review in brief

Clinical question

To review current topics of fluid management in the patients with traumatic brain injury and those who are candidate to decompressive craniectomy

Type of review

Narrative

Search of the literature

PubMed

Conclusion

Perioperative fluid therapy continues to be an exercise in empiricism, with nagging questions about efficacy and complications. There are no evidence-based guidelines or standards of care for the management of fluid therapy in patients who will underwent to decompressive craniectomy. Knowledge of the properties of the various available IV fluids, and the knowledge of the pathophysiology of endothelial, parenchymal and endocrine alterations which happen in TBI should guide their administration, to reach a good medium which propitiate allow better neurological, morbidity and mortality outcomes.

Limitations

The absence of evidence-based guidelines or standards of care

References

1. Sharma D, Vavilala MS. Perioperative management of adult traumatic brain injury. Anesthesiol Clin 2012; 30: 333-46; http://dx.doi.org/10.1016/j.anclin.2012.04.003

2. Langlois JA, Rutland-Brown W, Wald MM. The epidemiology and impact of traumatic brain injury: a brief overview. J Head Trauma Rehabil 2006; 21: 375-8

3. Shackford SR, Zhuang J, Schmoker J. Intravenous fluid tonicity: effect on intracranial pressure, cerebral blood flow, and cerebral oxygen delivery in focal brain injury. J Neurosurg 1992; 76: 91-8

4. Gennarelli TA, Champion HR, Copes WS, et al. Comparison of mortality, morbidity, and severity of 59,713 head injured patients with 114,447 patients with extracranial injuries. J Trauma 1994; 37: 962-8

5. McMahon CG, Yates DW, Campbell FM, et al. Unexpected contribution of moderate traumatic brain injury to death after major trauma. J Trauma 1999; 47: 891-5

6. Teranishi K, Scultetus A, Haque A, et al. Traumatic brain injury and severe uncontrolled haemorrhage with short delay pre-hospital resuscitation in a swine model. Injury 2012; 43: 585-93; http://dx.doi.org/10.1016/j.injury.2010.09.042

7. Bullock R, Chesnut RM, Clifton G, et al. Guidelines for the management of severe head injury. Brain Trauma Foundation. Eur J Emerg Med 1996; 3: 109-27

8. Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. II. J Neurotrauma 2007; 24 Suppl 1: S14-20

9. Dick F, Erdoes G, Opfermann P, et al. Delayed volume resuscitation during initial management of ruptured abdominal aortic aneurysm. J Vasc Surg 2013; 57: 943-50; http://dx.doi.org/10.1016/j.jvs.2012.09.072

10. Assaad S, Popescu W, Perrino A. Fluid management in thoracic surgery. Curr Opin Anaesthesiol 2013; 26: 31-9; http://dx.doi.org/10.1097/ACO.0b013e32835c5cf5

11. Moore E, Bellomo R, Nichol A. The meaning of acute kidney injury and its relevance to intensive care and anaesthesia. Anaesth Intensive Care 2012; 40: 929-48

12. Ivashkov Y, Bhananker SM. Perioperative management of pediatric trauma patients. Int J Crit Illn Inj Sci 2012; 2: 143-8; http://dx.doi.org/10.4103/2229-5151.100891

13. Searl CP, Perrino A. Fluid management in thoracic surgery. Anesthesiol Clin 2012; 30: 641-55; http://dx.doi.org/10.1016/j.anclin.2012.08.009

14. Svensen CH, Rodhe PM, Prough DS. Pharmacokinetic aspects of fluid therapy. Best Pract Res Clin Anaesthesiol 2009; 23: 213-24

15. González Posada MÁ, Quintana Díaz M. Fluidoterapia en el paciente politraumático. InfoColloids 2010; 8. Available at: http://www.fresenius-kabi.es/pdf/info_colloides/InfoColloids 8-FLUIDOETERAPIA EN EL PACIENTE POLITRAUMÁTICO-Ene10.pdf

16. Iijima T. Complexity of blood volume control system and its implications in perioperative fluid management. J Anesth 2009; 23: 534-42; http://dx.doi.org/10.1007/s00540-009-0797-5

17. Kerridge RK. Perioperative patient management. Best Pract Res Clin Obstet Gynaecol 2006; 20: 23-40

18. Shoemaker WC, Appel PL, Kram HB, et al. Prospective trial of supranormal values of survivors as therapeutic goals in high-risk surgical patients. Chest 1988; 94: 1176-86

19. Bellamy MC. Wet, dry or something else? Br J Anaesth 2006; 97: 755-7

20. Li Y. Perioperative goal-directed fluid therapy: grand progress and controversy. Zhonghua Wei Chang Wai Ke Za Zhi 2012; 15: 540-3

21. Haas S, Eichhorn V, Hasbach T, et al. Goal-directed fluid therapy using stroke volume variation does not result in pulmonary fluid overload in thoracic surgery requiring one-lung ventilation. Crit Care Res Pract 2012; 2012: 687018; http://dx.doi.org/10.1155/2012/687018

22. Knighton J, Smith GB. Perioperative Fluid Therapy. Anaesth Intensive Care 2003; 4: 324-6

23. Warrillow SJ, Weinberg L, Parker F, et al. Perioperative fluid prescription, complications and outcomes in major elective open gastrointestinal surgery. Anaesth Intensive Care 2010; 38: 259-65

24. De Silva AN, Scibelli T, Itobi E, et al. Improving perioperative fluid management in a large teaching hospital: pragmatic studies on the effects of changing practice. Proc Nutr Soc 2010; 69: 499-507; http://dx.doi.org/10.1017/S0029665110003824

25. Walsh SR, Cook EJ, Bentley R, et al. Perioperative fluid management: prospective audit. Int J Clin Pract 2008; 62: 492-7

26. Arya VK. Basics of fluid and blood transfusion therapy in paediatric surgical patients. Indian J Anaesth 2012; 56: 454-62; http://dx.doi.org/10.4103/0019-5049.103960

27. Chowdhury AH, Cox EF, Francis ST, et al. A randomized, controlled, double-blind crossover study on the effects of 2-L infusions of 0.9% saline and plasma-lyte® 148 on renal blood flow velocity and renal cortical tissue perfusion in healthy volunteers. Ann Surg 2012; 256: 18-24; http://dx.doi.org/10.1097/SLA.0b013e318256be72

28. Chong PC, Greco EF, Stothart D, et al. Substantial variation of both opinions and practice regarding perioperative fluid resuscitation. Can J Surg 2009; 52: 207-14

29. Baskett TF. William O’Shaughnessy, Thomas Latta and the origins of intravenous saline. Resuscitation 2002; 55: 231-4

30. Howard-Jones N. Cholera therapy in the nineteenth century. J Hist Med Allied Sci 1972; 27: 373-95

31. Cosnett JE. The origins of intravenous fluid therapy. Lancet 1989; 1: 768-71

32. Kleinman RE, Barness LA, Finberg L. History of pediatric nutrition and fluid therapy. Pediatr Res 2003; 54: 762-72

33. Mengoli LR. Excerpts from the history of postoperative fluid therapy. Am J Surg 1971; 121: 311-21

34. Foëx BA. How the cholera epidemic of 1831 resulted in a new technique for fluid resuscitation. Emerg Med J 2003; 20: 316-8

35. Latta T. Malignant cholera. Documents communicated by the Central Board of Health, London, relative to the treatment of cholera by the copious injection of aqueous and saline fluids into the veins. Lancet 1832; 18: 274-7

36. Neville KA, Sandeman DJ, Rubinstein A, et al. Prevention of Hyponatremia during Maintenance Intravenous Fluid Administration: A Prospective Randomized Study of Fluid Type versus Fluid Rate. J Pediatr 2010; 156: 313-9; http://dx.doi.org/10.1016/j.jpeds.2009.07.059

37. Srinivasa S, Hill AG. Perioperative Fluid Administration: Historical Highlights and Implications for Practice. Ann Surg 2012; 256: 1113-8; http://dx.doi.org/10.1097/SLA.0b013e31825a2f22

38. Friedman A. Fluid and electrolyte therapy: a primer. Pediatr Nephrol 2010; 25: 843-6; http://dx.doi.org/10.1007/s00467-009-1189-7

39. Grocott MPW, Mythen MG, Gan TJ. Perioperative fluid management and clinical outcomes in adults. Anesth Analg 2005; 100: 1093-106

40. Datta R, Chaturvedi R. Fluid therapy in trauma. Med J Armed Forces India 2010; 66: 312-6

41. Prough DS, Olsson J, Svensén C. Crystalloid Solutions. In: Winslow RM, Robert M. Winslow, editors. Oxford: Academic Press; 2006; pp. 126-38

42. Michel CC. Starling: the formulation of his hypothesis of microvascular fluid exchange and its significance after 100 years. Exp Physiol 1997; 82: 1-30

43. Weinbaum S, Tarbell JM, Damiano ER. The structure and function of the endothelial glycocalyx layer. Annu Rev Biomed Eng 2007; 9: 121-67

44. Adamson RH, Lenz JF, Zhang X, et al. Oncotic pressures opposing filtration across non-fenestrated rat microvessels. J Physiol 2004; 557: 889-907

45. Levick JR. Revision of the Starling principle: new views of tissue fluid balance. J Physiol 2004; 557: 704

46. Farrugia A. Albumin Usage in Clinical Medicine: Tradition or Therapeutic? Transfus Med Rev 2010; 24: 53-63; http://dx.doi.org/10.1016/j.tmrv.2009.09.005

47. Cook S-C, Brown J. Perioperative fluid therapy. Anaesth. Intensive Care Med 2009; 10: 573-5

48. Gutteridge G. Crystalloids, colloids, blood, blood products and blood substitutes. Anaesth Intensive Care Med 2004; 5: 42-6

49. Gondos T, Marjanek Z, Ulakcsai Z, et al. Short-term effectiveness of different volume replacement therapies in postoperative hypovolaemic patients. Eur J Anaesthesiol 2010; 27: 794-800; http://dx.doi.org/10.1097/EJA.0b013e32833b3504

50. Tommasino C, Picozzi V. Volume and electrolyte management. Best Pract Res Clin Anaesthesiol 2007; 21: 497-516

51. Elliott MB, Jallo JJ, Barbe MF, et al. Hypertonic saline attenuates tissue loss and astrocyte hypertrophy in a model of traumatic brain injury. Brain Res 2009; 1305: 183-91; http://dx.doi.org/10.1016/j.brainres.2009.09.104

52. Hashiguchi N, Lum L, Romeril E, et al. Hypertonic saline resuscitation: efficacy may require early treatment in severely injured patients. J Trauma 2007; 62: 299-306

53. Powers KA, Woo J, Khadaroo RG, et al. Hypertonic resuscitation of hemorrhagic shock upregulates the anti-inflammatory response by alveolar macrophages. Surgery 2003; 134: 312-8

54. Rizoli SB, Kapus A, Parodo J, et al. Hypertonicity prevents lipopolysaccharide-stimulated CD11b/CD18 expression in human neutrophils in vitro: role for p38 inhibition. J Trauma 1999; 46: 794-8

55. Angle N, Hoyt DB, Coimbra R, et al. Hypertonic saline resuscitation diminishes lung injury by suppressing neutrophil activation after hemorrhagic shock. Shock 1998; 9: 164-70

56. Homma H, Deitch EA, Feketeova E, et al. Small volume resuscitation with hypertonic saline is more effective in ameliorating trauma-hemorrhagic shock-induced lung injury, neutrophil activation and red blood cell dysfunction than pancreatitic protease inhibition. J Trauma 2005; 59: 266-72

57. Deitch EA, Shi HP, Feketeova E, et al. Hypertonic saline resuscitation limits neutrophil activation after trauma-hemorrhagic shock. Shock 2003; 19: 328-33

58. Deree J, Martins JO, Leedom A, et al. Hypertonic saline and pentoxifylline reduces hemorrhagic shock resuscitation-induced pulmonary inflammation through attenuation of neutrophil degranulation and proinflammatory mediator synthesis. J Trauma 2007; 62: 104-11

59. Younes RN, Aun F, Ching CT, et al. Prognostic factors to predict outcome following the administration of hypertonic/hyperoncotic solution in hypovolemic patients. Shock 1997; 7: 79-83

60. Maningas PA, Mattox KL, Pepe PE, et al. Hypertonic saline-dextran solutions for the prehospital management of traumatic hypotension. Am J Surg 1989; 157: 528-33

61. Vassar MJ, Perry CA, Gannaway WL, et al. 7.5% sodium chloride/dextran for resuscitation of trauma patients undergoing helicopter transport. Arch Surg 1991; 126: 1065-72

62. Younes RN, Aun F, Accioly CQ, et al. Hypertonic solutions in the treatment of hypovolemic shock: a prospective, randomized study in patients admitted to the emergency room. Surgery 1992; 111: 380-5

63. Jousi M, Reitala J, Lund V, et al. The role of pre-hospital blood gas analysis in trauma resuscitation. World J Emerg Surg 2010; 5: 10; http://dx.doi.org/10.1186/1749-7922-5-10

64. Bulger EM, May S, Brasel KJ, et al. Out-of-hospital hypertonic resuscitation following severe traumatic brain injury: a randomized controlled trial. JAMA 2010; 304: 1455-64; http://dx.doi.org/10.1001/jama.2010.1405

65. Bulger EM, May S, Kerby JD, et al. Out-of-hospital hypertonic resuscitation after traumatic hypovolemic shock: a randomized, placebo controlled trial. Ann Surg 2011; 253: 431-41; http://dx.doi.org/10.1097/SLA.0b013e3181fcdb22

66. Wade CE, Grady JJ, Kramer GC, et al. Individual patient cohort analysis of the efficacy of hypertonic saline/dextran in patients with traumatic brain injury and hypotension. J Trauma 1997; 42: S61-5

67. Rockswold GL, Solid CA, Paredes-Andrade E, et al. Hypertonic saline and its effect on intracranial pressure, cerebral perfusion pressure, and brain tissue oxygen. Neurosurgery 2009; 65: 1035-41; http://dx.doi.org/10.1227/01.NEU.0000359533.16214.04

68. Witt L, Osthaus WA, Jahn W, et al. Isovolaemic hemodilution with gelatin and hydroxyethylstarch 130/0.42: effects on hemostasis in piglets. Paediatr Anaesth 2012; 22: 379-85; http://dx.doi.org/10.1111/j.1460-9592.2012.03798.x

69. Mauch J, Madjdpour C, Kutter APN, et al. Effect of rapid fluid resuscitation using crystalloids or colloids on hemostasis in piglets. Paediatr Anaesth 2013; 23: 258-64; http://dx.doi.org/10.1111/pan.12106

70. Schortgen F, Girou E, Deye N, et al. The risk associated with hyperoncotic colloids in patients with shock. Intensive Care Med 2008; 34: 2157-68; http://dx.doi.org/10.1007/s00134-008-1225-2

71. Ertmer C, Rehberg S, Van Aken H, et al. Relevance of non-albumin colloids in intensive care medicine. Best Pract Res Clin Anaesthesiol 2009; 23: 193-212

72. Shenkin HA, Bezier HS, Bouzarth WF. Restricted fluid intake. Rational management of the neurosurgical patient. J Neurosurg 1976; 45: 432-6

73. Werner C, Engelhard K. Pathophysiology of traumatic brain injury. Br J Anaesth 2007; 99: 4-9

74. Greenhalgh DG, Housinger TA, Kagan RJ, et al. Maintenance of serum albumin levels in pediatric burn patients: a prospective, randomized trial. J Trauma 1995; 39: 67-73

75. Tan PG, Cincotta M, Clavisi O, et al. Prehospital fluid management in traumatic brain injury. Emerg Med Australas 2011; 23: 665-76; http://dx.doi.org/10.1111/j.1742-6723.2011.01455.x

76. Rosenfeld J V, Maas AI, Bragge P, et al. Early management of severe traumatic brain injury. Lancet 2012; 380: 1088-98; http://dx.doi.org/10.1016/S0140-6736(12)60864-2

77. Rodling Wahlström M, Olivecrona M, Nyström F, et al. Fluid therapy and the use of albumin in the treatment of severe traumatic brain injury. Acta Anaesthesiol Scand 2009; 53: 18-25; http://dx.doi.org/10.1111/j.1399-6576.2008.01798.x

78. Geeraedts Jr. LMG, Kaasjager HAH, van Vugt AB, et al. Exsanguination in trauma: A review of diagnostics and treatment options. Injury 2009; 40: 11-20; http://dx.doi.org/10.1016/j.injury.2008.10.007

79. Bauer M, Kortgen A, Hartog C, et al. Isotonic and hypertonic crystalloid solutions in the critically ill. Best Pract Res Clin Anaesthesiol 2009; 23: 173-81

80. Hariri RJ, Firlick AD, Shepard SR, et al. Traumatic brain injury, hemorrhagic shock, and fluid resuscitation: effects on intracranial pressure and brain compliance. J Neurosurg 1993; 79: 421-7

81. Modig J. Advantages of dextran 70 over Ringer acetate solution in shock treatment and in prevention of adult respiratory distress syndrome. A randomized study in man after traumatic-haemorrhagic shock. Resuscitation 1983; 10: 219-26

82. Feinstein AJ, Patel MB, Sanui M, et al. Resuscitation with pressors after traumatic brain injury. J Am Coll Surg 2005; 201: 536-45

83. Wiedemann HP, Wheeler AP, Bernard GR, et al. Comparison of two fluid-management strategies in acute lung injury N Engl J Med 2006; 354: 2564-75

84. Cotton BA, Guy JS, Morris JA, et al. The cellular, metabolic, and systemic consequences of aggressive fluid resuscitation strategies. Shock 2006; 26: 115-21

85. Contant CF, Valadka AB, Gopinath SP, et al. Adult respiratory distress syndrome: a complication of induced hypertension after severe head injury. J Neurosurg 2001; 95: 560-8

86. Bratton SL, Davis RL. Acute lung injury in isolated traumatic brain injury. J Neurosurg 2001; 95: 560-8

87. Holland MC, Mackersie RC, Morabito D, et al. The development of acute lung injury is associated with worse neurologic outcome in patients with severe traumatic brain injury. J Trauma 2003; 55: 106-11

88. Lee K, Rincon F. Pulmonary complications in patients with severe brain injury. Crit Care Res Pract 2012; 2012: 207247; http://dx.doi.org/10.1155/2012/207247

89. Finfer S, Bellomo R, Boyce N, et al. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004; 350: 2247-56

90. Myburgh J, Cooper DJ, Finfer S, et al. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. N Engl J Med 2007; 357: 874-84

91. Sekhon MS, Dhingra KV, Sekhon IS, et al. The safety of synthetic colloid in critically ill patients with severe traumatic brain injuries. J Crit Care 2011; 26: 357-62; http://dx.doi.org/10.1016/j.jcrc.2010.12.001

92. Bentsen G, Breivik H, Lundar T, et al. Predictable reduction of intracranial hypertension with hypertonic saline hydroxyethyl starch: a prospective clinical trial in critically ill patients with subarachnoid haemorrhage. Acta Anaesthesiol Scand 2004; 48: 1089-95

93. Schwarz S, Schwab S, Bertram M, et al. Effects of hypertonic saline hydroxyethyl starch solution and mannitol in patients with increased intracranial pressure after stroke. Stroke 1998; 29: 1550-5

94. Mythen MG, Swart M, Acheson N, et al. Perioperative fluid management: Consensus statement from the enhanced recovery partnership. Perioper Med 2012; 1: 2; http://dx.doi.org/10.1186/2047-0525-1-2

95. Shoemaker WC, Appel PL, Kram HB. Role of oxygen debt in the development of organ failure sepsis, and death in high-risk surgical patients. Chest 1992; 102: 208-15

Refbacks

  • There are currently no refbacks.




© SEEd srl