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Resuscitation Fluids — NEJM

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Resuscitation Fluids — NEJM


Critical Care Medicine

Resuscitation Fluids

John A. Myburgh, M.B., B.Ch., Ph.D., and Michael G. Mythen, M.D., M.B., B.S.
N Engl J Med 2013; 369:1243-1251September 26, 2013DOI: 10.1056/NEJMra1208627
Article
References
Fluid resuscitation with colloid and crystalloid solutions is a ubiquitous intervention in acute medicine. The selection and use of resuscitation fluids is based on physiological principles, but clinical practice is determined largely by clinician preference, with marked regional variation. No ideal resuscitation fluid exists. There is emerging evidence that the type and dose of resuscitation fluid may affect patient-centered outcomes. Despite what may be inferred from physiological principles, colloid solutions do not offer substantive advantages over crystalloid solutions with respect to hemodynamic effects. Albumin is regarded as the reference colloid solution, but its cost is a limitation to its use. Although albumin has been determined to be safe for use as a resuscitation fluid in most critically ill patients and may have a role in early sepsis, its use is associated with increased mortality among patients with traumatic brain injury. The use of hydroxyethyl starch (HES) solutions is associated with increased rates of renal-replacement therapy and adverse events among patients in the intensive care unit (ICU). There is no evidence to recommend the use of other semisynthetic colloid solutions. Balanced salt solutions are pragmatic initial resuscitation fluids, although there is little direct evidence regarding their comparative safety and efficacy. The use of normal saline has been associated with the development of metabolic acidosis and acute kidney injury. The safety of hypertonic solutions has not been established. All resuscitation fluids can contribute to the formation of interstitial edema, particularly under inflammatory conditions in which resuscitation fluids are used excessively. Critical care physicians should consider the use of resuscitation fluids as they would the use of any other intravenous drug. The selection of the specific fluid should be based on indications, contraindications, and potential toxic effects in order to maximize efficacy and minimize toxicity.

History of Fluid Resuscitation

In 1832, Robert Lewins described the effects of the intravenous administration of an alkalinized salt solution in treating patients during the cholera pandemic. He observed that “the quantity necessary to be injected will probably be found to depend upon on the quantity of serum lost; the object being to place the patient in nearly his ordinary state as to the quantity of blood circulating in the vessels.”1 The observations of Lewins are as relevant today as they were nearly 200 years ago. Asanguinous fluid resuscitation in the modern era was advanced by Alexis Hartmann, who modified a physiologic salt solution developed in 1885 by Sidney Ringer for rehydration of children with gastroenteritis.2 With the development of blood fractionation in 1941, human albumin was used for the first time in large quantities for resuscitation of patients who were burned during the attack on Pearl Harbor in the same year. Today, asanguinous fluids are used in almost all patients undergoing general anesthesia for major surgery, in patients with severe trauma and burns, and in patients in the ICU. It is one of the most ubiquitous interventions in acute medicine. Fluid therapy is only one component of a complex hemodynamic resuscitation strategy. It is targeted primarily at restoring intravascular volume. Since venous return is in equilibrium with cardiac output, sympathetically mediated responses regulate both efferent capacitance (venous) and afferent conductance (arterial) circulations in addition to myocardial contractility.3 Adjunctive therapies to fluid resuscitation, such as the use of catecholamines to augment cardiac contraction and venous return, need to be considered early to support the failing circulation.4 In addition, changes to the microcirculation in vital organs vary widely over time and under different pathologic states, and the effects of fluid administration on end-organ function should be considered along with effects on intravascular volume.

The Physiology of Fluid Resuscitation

For decades, clinicians have based their selection of resuscitation fluids on the classic compartment model — specifically, the intracellular fluid compartment and the interstitial and intravascular components of the extracellular fluid compartment and the factors that dictate fluid distribution across these compartments. In 1896, English physiologist Ernest Starling found that capillaries and postcapillary venules acted as a semipermeable membrane absorbing fluid from the interstitial space.5 This principle was adapted to identify the hydrostatic and oncotic pressure gradients across the semipermeable membrane as the principal determinants of transvascular exchange.6 Recent descriptions have questioned these classic models.7 A web of membrane-bound glycoproteins and proteoglycans on the luminal side of endothelial cells has been identified as the endothelial glycocalyx layer8 (Figure 1Figure 1Role of the Endothelial Glycocalyx Layer in the Use of Resuscitation Fluids.). The subglycocalyx space produces a colloid oncotic pressure that is an important determinant of transcapillary flow. Nonfenestrated capillaries throughout the interstitial space have been identified, indicating that absorption of fluid does not occur through venous capillaries but that fluid from the interstitial space, which enters through a small number of large pores, is returned to the circulation primarily as lymph that is regulated through sympathetically mediated responses.9 The structure and function of the endothelial glycocalyx layer are key determinants of membrane permeability in various vascular organ systems. The integrity, or “leakiness,” of this layer, and thereby the potential for the development of interstitial edema, varies substantially among organ systems, particularly under inflammatory conditions, such as sepsis,10 and after surgery or trauma, when resuscitation fluids are commonly used.

The Ideal Resuscitation Fluid

The ideal resuscitation fluid should be one that produces a predictable and sustained increase in intravascular volume, has a chemical composition as close as possible to that of extracellular fluid, is metabolized and completely excreted without accumulation in tissues, does not produce adverse metabolic or systemic effects, and is cost-effective in terms of improving patient outcomes. Currently, there is no such fluid available for clinical use. Resuscitation fluids are broadly categorized into colloid and crystalloid solutions (Table 1Table 1Types and Compositions of Resuscitation Fluids.). Colloid solutions are suspensions of molecules within a carrier solution that are relatively incapable of crossing the healthy semipermeable capillary membrane owing to the molecular weight of the molecules. Crystalloids are solutions of ions that are freely permeable but contain concentrations of sodium and chloride that determine the tonicity of the fluid. Proponents of colloid solutions have argued that colloids are more effective in expanding intravascular volume because they are retained within the intravascular space and maintain colloid oncotic pressure. The volume-sparing effect of colloids, as compared with crystalloids, is considered to be an advantage, which is conventionally described in a 1:3 ratio of colloids to crystalloids to maintain intravascular volume. Semisynthetic colloids have a shorter duration of effect than human albumin solutions but are actively metabolized and excreted. Proponents of crystalloid solutions have argued that colloids, in particular human albumin, are expensive and impractical to use as resuscitation fluids, particularly under field-type conditions. Crystalloids are inexpensive and widely available and have an established, although unproven, role as first-line resuscitation fluids. However, the use of crystalloids has classically been associated with the development of clinically significant interstitial edema.

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Source Information

From the University of New South Wales, the Division of Critical Care and Trauma, George Institute for Global Health, and the Department of Intensive Care Medicine, St. George Hospital — all in Sydney (J.A.M.); and the National Institute for Health Research, University College London Hospitals Biomedical Research Centre, London (M.G.M.).
Address reprint requests to Dr. Myburgh at the Department of Intensive Care Medicine, St. George Hospital, Gray St., Kogarah 2217, Sydney, NSW, Australia, or at .

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