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Year : 2016  |  Volume : 6  |  Issue : 2  |  Page : 54-55

Ideal resuscitation fluid in hypovolemia: The quest is on and miles to go!

Department of Anesthesiology, North Bengal Medical College, Siliguri, West Bengal, India

Date of Web Publication26-May-2016

Correspondence Address:
Mohanchandra Mandal
Department of Anesthesiology, North Bengal Medical College, Sushrutanagar, Siliguri - 734 012, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2229-5151.183020

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How to cite this article:
Mandal M. Ideal resuscitation fluid in hypovolemia: The quest is on and miles to go!. Int J Crit Illn Inj Sci 2016;6:54-5

How to cite this URL:
Mandal M. Ideal resuscitation fluid in hypovolemia: The quest is on and miles to go!. Int J Crit Illn Inj Sci [serial online] 2016 [cited 2023 Mar 27];6:54-5. Available from: https://www.ijciis.org/text.asp?2016/6/2/54/183020

Hypovolemia is defined as a decrease in the blood volume resulting from loss of blood, plasma and/or plasma water, thereby causing a loss of intravascular content and resulting in a potential limitation of tissue perfusion.[1] It is often seen in case of severe dehydration or blood loss owing to trauma or surgery. If left untreated, this 'hypovolemic shock' can result in hypoxic tissue damage, organ failure, and ultimately, death. Activation of sympathetic nervous system (homeostatic response) results in peripheral vasoconstriction and tachycardia thereby trying to preserve blood flow to vital organs and maintain blood pressure up to a certain degree of hypovolemia. Hence, in patients of trauma, only when the magnitude of blood loss approaches half the circulating volume or that occurs rapidly, there can be a relation between the cardiac output and blood pressure.

Recently, there is paradigm shift from the 'static model' of classifying shock by percentage of blood volume loss to the 'dynamic model' of monitoring the response to initial intravenous fluid resuscitation with division into 'rapid-, transient- and non-responders'.[2] It helps understanding the status of any on-going bleeding or volume loss, the need for transfusion and surgery, and explore the possibility of non-hemorrhagic causes like tension pneumothorax and pericardial tamponade contributing to non-response. Fluid-responsiveness is arbitrarily defined as a 15% or more increase in cardiac output in response to a fluid challenge, and patients are divided into 'responders' and 'nonresponders', accordingly.[1]

Till the bleeding is controlled, the physician tries to maintain oxygen delivery to tissues thus limiting tissue hypoxia, inflammation, and organ dysfunction. This effort involves the use of fluid resuscitation, vasopressors, and blood transfusion. Currently, volume expansion aims at increasing global blood flow, with the hope that such an increase will improve flow to the microcirculation increasing oxygen availability to the tissues.[1] Although fluid resuscitation is the first step to restore tissue perfusion in severe hemorrhagic shock, it remains a matter of controversy for decades whether colloids or crystalloids, and more specifically, which colloid, should be used. The choice of fluid for resuscitation, the target of hemodynamic goals for hemorrhage control, and the optimal prevention of traumatic coagulopathy are questions that remain to be answered.[3]

The use of either colloids or crystalloids did not result in a significant difference regarding 28-day mortality in patients with hypovolemia in ICU settings.[4] A recent Cochrane meta-analysis failed to demonstrate that colloids reduce the risk of death compared to resuscitation with crystalloids.[5] Colloids have 'dual advantage' over crystalloids in that the former can induce a more rapid and persistent plasma expansion and quickly achieve circulatory goals owing to its larger increase in oncotic pressure.[3] The predefined hemodynamic endpoints are achieved earlier with less volume of colloids.[1]

Despite little published evidence suggesting specific advantages over other intravenous fluids, and emerging evidence of harm in septic and critically ill patients, the colloidal fluids remain a popular choice for perioperative fluid therapy. The 'urea-linked gelatins'- the 'polygeline' has short (2-3 hours) intravascular persistence and tendency of extravasation.[6] Large volume of gelatin promotes intracellular edema as a result of decreased plasma osmolality owing to the reduction of chloride concentration of solvent solution by interaction with negative charges of cross-linked gelatin molecules. Moreover, rapid renal excretion (80% molecules <20 kDa) of gelatins can increase diuresis which has to be replenished with adequate crystalloid infusion to prevent dehydration. Gelatin infusion may furthermore increase the blood viscosity and facilitate red blood cell aggregation.[7] Current evidence clearly shows increased acute kidney injury (AKI) and use of renal replacement therapy (RRT) associated with the use of hydroxyethyl starches (HES). In light of lack of evidence and potential for dose-related deleterious effects (coagulopathy, accumulation in skin and liver, induction of inflammation and oxidative stress, and development of AKI) gelatins and HES should be avoided.[8]

Following some reports about serious adverse effects of colloids as resuscitation fluids, currently there is 'resurgence of crystalloids'. Saline (0.9% NaCl), the cheapest of all fluids, is still by far the most commonly used fluids for resuscitation. However, treating perioperative patients and trauma victims with large volumes of chloride-rich crystalloids (e.g., normal saline) leads to hyperchloremic metabolic acidosis which may hike the incidence of AKI owing to decreased renal blood flow and renal cortical hypoperfusion.[8] Balanced salt solutions ('chloride-restricted' crystalloids containing acetate, lactate or gluconate and mimicking the composition of extracellular fluid) has shown no harmful effects in any particular type of patient.[8],[9] However, such solution have demerits of hypotonicity, hyperlactatemia, and metabolic alkalosis.[1]

All resuscitation fluids can contribute to the formation of interstitial edema, especially under different inflammatory conditions and confounding medical scenario in which such fluids are used excessively.[10] As resuscitation with crystalloid solution necessitates larger volume it has more propensity of generating tissue edema and abdominal compartment syndrome. Excessive tissue hydration has been blamed for a higher incidence of postoperative nausea and anastomotic dehiscence after abdominal surgery.[3]

With current evidence, no ideal resuscitation fluid exists. It is better to observe the patient's response to volume infusion than to follow blindly any specific rule as every patient responds differently to fluid therapy. Therapy should target physiologic goals of hemodynamic stabilization. Improved outcomes have been noted with the use of 'goal-directed' therapy over 'fluid-liberal' approach. In the critical care and anesthesia setting, choosing the type of fluid to resuscitate patients has become a difficult decision, and clinical practice is largely influenced by the clinician's preference, with marked regional variation. Based on patho-physiology of hypovolemia, new-generation fluids should be developed with a focus of research on improving oxygen-carrying capacity by using hemoglobin-based oxygen carriers and with an emphasis on limiting the proinflammatory effects of fluids.


The authors would like to thank Dr. Dipanjan Bagchi, Consultant Anesthesiologist, Howrah District Hospital, Howrah, West Bengal, India for his contribution during revision after first submission.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Gruartmonera G, Mesquidaa J, Inceb C. Fluid therapy and the hypovolemic microcirculation. Curr Opin Crit Care 2015;21:276-84.  Back to cited text no. 1
Kam CW, Lai CH, Lam SK, So FL, Lau CL, Cheung KH. What are the ten new commandments in severe polytrauma management? World J Emerg Med 2010;1:85-92.  Back to cited text no. 2
Bouglé A, Harrois A, Duranteau J. Resuscitative strategies in traumatic hemorrhagic shock. Ann Intensive Care 2013;3:1.  Back to cited text no. 3
Annane D, Siami S, Jaber S, Martin C, Elatrous S, Declère AD, et al. CRISTAL Investigators. Effects of fluid resuscitation with colloids vs crystalloids on mortality in critically ill patients presenting with hypovolemic shock: The CRISTAL randomized trial. JAMA 2013;310:1809-17.  Back to cited text no. 4
Perel P, Roberts I. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev 2011;CD000567.  Back to cited text no. 5
Gillies MA, Habicher M, Jhanji S, Sander M, Mythen M, Hamilton M, et al. Incidence of postoperative death and acute kidney injury associated with i.v. 6% hydroxyethyl starch use: Systematic review and meta-analysis. Br J Anaesth 2014;112:25-34.  Back to cited text no. 6
Alvis-Miranda HR, Castellar-Leones SM, Moscote-Salazar LR. Intravenous fluid therapy in traumatic brain injury and decompressive craniectomy. Bull Emerg Trauma 2014;2:3-14.  Back to cited text no. 7
Lira A, Pinsky MR. Choices in fluid type and volume during resuscitation: Impact on patient outcomes. Ann Intensive Care 2014;4:38.  Back to cited text no. 8
Raghunathan K, Murray PT, Beattie WS, Lobo DN, Myburgh J, Sladen R, et al.; ADQI XII Investigators Group. Choice of fluid in acute illness: What should be given? An international consensus. Br J Anaesth 2014;113:772-83.  Back to cited text no. 9
Myburgh JA, Mythen MG. Resuscitation Fluids. N Engl J Med 2013;369:1243-51.  Back to cited text no. 10

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