Effects on coagulation of intravenous crystalloid or colloid inpatients undergoing peripheral vascular surgery. Br J Anaesth ; 89 Burdett E, James M. New aspects of perioperative fluid therapy. Drug Discov Today Ther Strateg ; 2 Marwick C.
Fluid and Electrolyte Physiology and Therapy
BSE sets agenda for imported gelatin. JAMA ; Ljungstrom KG. Infusionsther Transfusionsmed ; 20 Intensive Care Med ; 28 A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med ; Burdett E. Eur J Anesthesiol ; [In press]. Sarkar S. Artificial blood.
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Liposome-encapsulated hemoglobin attenuates cardiac dysfunction and sympathetic activity during hypohemoglobinemic shock. Shock ; Hemorrhage and surgery cause a contraction of the extra cellular space needing replacement - evidence and implications. A systematic review. Surgery ; Such attitude is compounded by the inadequate knowledge, among the doctors, on the essentials of intravenous fluids like the electrolyte components [ 3 ]. Intravenous fluids are drugs, and like other drugs, there are potential complications.
In the acute setting where these fluids are commonplace, it is imperative that the practice aims at administering the right patient the right fluids, at the right volume and rate, with the right overall fluid balance. Water is the most important and abundant element of the human body, and the physiology that surrounds it is extensive.
The following principles are at best, the foundations toward an informed fluid practice. The percentage will vary depending on the gender and the fat content in the body. There is an inverse correlation between the water content of the body and the fat content as adipose tissue contains less water than lean tissue. This explains why women have lower percentages of water than men as they have a higher percentage of adipose tissue. Water in the body is functionally distributed among the two main body fluid compartments, the intracellular fluid ICF and the extracellular fluid ECF Figure 1.
Water crosses between the ICF and the ECF through aquaporin channels in the cell membrane to attain osmotic equilibrium. The cell membrane also contains active pumps and transporters that distribute individual solutes, including electrolytes. These electrolytes account for the effective osmolality tonicity that governs the water movement. The mechanisms of these electrolyte movements are further defined by the Gibbs-Donnan effect of the nondiffusible large anions like protein. The ECF is further divided into the interstitial fluid and the plasma compartments, the two separated by the capillary wall.
Except for plasma proteins and blood cells, the pores on the capillary wall permit the flux of water and small solutes. This contributes to the two compartments having almost similar electrolyte composition with only small differences contributed by the Gibbs-Donnan effect of the plasma proteins.
As a side note, these proteins are solids in the plasma, and the changes in their plasma load will affect the water-based measurements of plasma electrolyte concentrations [ 6 ]. A complex interaction of regulatory mechanisms from different organs helps the body to maintain an effective fluid volume in different circumstances.
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The key pathway that underpins this volume regulation is the hormonally mediated renin-angiotensin II-aldosterone-system RAAS , with the faster neutrally mediated baroreceptor reflex contributing an indirect role through its interplay of the pressure regulation. In the context of the fluid therapy scope of the chapter, the RAAS will be elaborated below. In the JGA, the reduced renal perfusion stimulates the granular cells of the afferent arteriole to secrete the proteolytic enzyme renin through a direct intrarenal baroreceptor activity and detection of reduced sodium chloride concentrations by the macula densa in the wall of the ascending limb of the loop of Henle.
Besides these mechanisms, the renin release is also controlled by renal sympathetic nerves and angiotensin II. Renin as an enzyme will then catalyze the conversion of angiotensinogen, a large protein produced in the liver, to angiotensin I, a decapeptide. Angiotensin I has little biologic activity apart from being the precursor to angiotensin II.
Its conversion to angiotensin II involves the removal of two amino acid moieties by the angiotensin-converting enzyme ACE. ACE is primarily located in the pulmonary capillaries, but it is also found in the kidney epithelial cells. The ultimate objective of the RAAS, through the activities of angiotensin II and aldosterone as summarized in Figure 3 , is the preservation of effective fluid volume and pressure. The RAAS demonstrates the strong interconnection between the body fluid and electrolytes in maintaining the fluid homeostasis.
In the acute setting, this interconnection is very relevant given the frequent alterations of the electrolyte contents of the body in the acute phase of illness. The assessment of electrolytes in the acute patients should, therefore, be comprehensive and extend beyond the laboratory results. For example, the assessment should also consider the potential electrolyte losses from the gastrointestinal tract, a common organ affected in acute illnesses [ 7 ]. The classic microcirculation model, based on the semipermeability of the capillary and postcapillary venule walls, and the presence of hydrostatic and oncotic pressure gradients across these walls had for long described the flux of fluids and electrolytes between the plasma and the interstitial fluid [ 8 , 9 ].
The identification of the endothelial glycocalyx layer, a web of membrane-bound glycoproteins and proteoglycans on the luminal side of endothelial cells, has now challenged the classic model [ 10 , 11 ]. The colloid oncotic pressure from the sub-glycocalyx space is a key determinant of the trans-capillary flow.
Appreciation of the dynamics of glycocalyx in the microcirculation of the acute cohort of patients will be integral in their fluid resuscitation and in future fluid research in such population [ 13 , 14 ]. The endothelial glycocalyx layer in healthy, equilibrium state A and damaged, leaky state B that leads to interstitial edema. The history of intravenous fluids began during the cholera pandemic in Europe in the s.
The success of Thomas Latta in using a saline solution to resuscitate dying cholera patients paved the way for the widespread use of intravenous fluids and the research to refine their contents [ 15 ]. The gelatins and other solutions with larger molecules only broke into the scene during the Second World War [ 19 ], although the first study in humans was performed in [ 20 ].
It is interesting that the history behind the most common type of fluids used, the 0. The present-day 0. The only possible connection to 0. From the above breakthroughs, the science of intravenous fluids has grown progressively, especially in the last couple of decades. Whether medicine will find an answer to the ideal intravenous fluid will be debatable, but more evidence has emerged in the comparison between the different types of fluids available.
Crystalloids are solutions containing salts in the form of electrolytes and small molecules. The composition of commonly available crystalloids is given in Table 1. Based on their differing compositions, crystalloids have been divided into saline solutions and balanced solutions. Saline solutions, chiefly the 0. The 0. These solutions achieve lower sodium and chloride concentrations through the addition of other electrolytes and buffers like lactate and acetate. The debate is ongoing as to which will be the better choice for the acute population of patients, saline or balanced solutions.
While saline is cheap and is still the most commonly used crystalloid in the world, there are significant concerns with its effect on acid-base balance and kidney function. The high chloride contents of saline contribute to the hyperchloremic or strong ion acidosis [ 25 , 26 , 27 ], and this has been well shown in different studies in different acute populations [ 28 , 29 , 30 ]. Lancet ; Determinants of long-term survival after major surgery and the adverse effect of postoperative complications.
Ann Surg ; Bellamy MC. Wet, dry or something else? Br J Anaesth ; Cannesson M, Gan TJ.
Pro: Peri-operative goal directed therapy is an essential part of an enhanced recovery protocol. Int Anaesth Res Soc ; Voldby AW, Brandstrup B. Fluid therapy in the perioperative setting — A clinical review. J Intensive Care ; Fluid therapy in critical illness. Extrem Physiol Med ; Fluid resuscitation with hydroxyethyl starches in patients with sepsis is associated with an increased incidence of acute kidney injury and use of renal replacement therapy: A systematic review and meta-analysis of the literature.
J Crit Care ; Colloids versus crystalloids for fluid resuscitation in critically ill patients. Hyperchloremia after noncardiac surgery is independently associated with increased morbidity and mortality: A propensity-matched cohort study. Anesth Analg ; Perioperative intravenous fluid therapy for adults. Ulster Med J ; Alves DR, Ribeiras R. Does fasting influence preload responsiveness in ASA 1 and 2 volunteers?
Braz J Anesthesiol ; Aditianingsih D, George YW. Guiding principles of fluid and volume therapy. Best Pract Res Clin Anaesthesiol ; Fluid overload is associated with an increased risk for day mortality in critically ill patients with renal replacement therapy: Data from the prospective FINNAKI study.
hospsagasnephy.gq Liberal or restrictive fluid administration in fast-track colonic surgery: A randomized, double-blind study. Clinical review: Goal-directed therapy-what is the evidence in surgical patients?