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Page last updated 8-04-04

© COPYRIGHT 2004 ALL RIGHTS RESERVED TOTALBURNCARE.COM

TOTAL BURN CARE  2nd edition
Copyright© 2001 Elsevier Science
Edited by Dr. David N. Herndon

Reprinted with permission of Elsevier


(excerpt from chapter 8, pages 88, 90)

Fluid resuscitation and early management
Glenn D Warden

Introduction

   Proper fluid management is critical to the survival of the victim of a major thermal injury.  In the 1940's, hypovolemic shock or shock-induced renal failure was the leading cause of death after burn injury.  Today, with our current knowledge of the massive fluid shifts and vascular changes that occur during burn shock, mortality related to burn-induced volume loss has decreased considerably.  Although a vigorous approach to fluid therapy has ensued in the last 20 years and fewer deaths are occurring in the first 24-48 hours post-burn, the fact remains that approximately 50% of the deaths occur within the first 10 days following burn injury from a multitude of causes, one the most significant being inadequate fluid resuscitation therapy.1  Knowledge of fluid management following burn shock resuscitation is also important and is often over-looked in burn education.

Pathophysiology of Burn Injury

   Modern fluid resuscitation formulas originate from experimental studies in the pathophysiology of burn shock.  Burn shock is both hypovolemic shock and cellular shock, and is characterized by specific hemodynamic changes including decreased cardiac output, extracellular fluid, plasma volume and oliguria.  As in the treatment of other forms of shock, the primary goal is to restore and preserve tissue perfusion in order to avoid ischemia.  However, in burn shock, resuscitation is complicated by obligatory burn edema, and the voluminous transvascular fluid shifts which result from a major burn are unique to thermal trauma.

   Although the exact pathophysiology of the postburn vascular changes and fluid shifts is unknown, one major component of burn shock is the increase in total body capillary permeability.  Direct thermal injury results in marked changes in the microcirculation.  Most of the changes occur locally at the burn site, when maximal edema formation occurs at about 8-12 hours post-injury in smaller burns and 12-24 hours post-injury in major thermal injuries.  The rate of progression of tissue edema is dependent upon the adequacy of resuscitation.

Resuscitation from Burn Shock

   Fluid resuscitation is aimed at supporting the patient throughout the initial 24-hour to 48-hour period of hypovolemia.  The primary goal of therapy is to replace the fluid sequestered as a result of thermal injury.  The critical concept in burn shock is that massive fluid shifts can occur even though total body water remains unchanged.  What actually changes is the volume of each fluid compartment, intracellular and interstitial volumes increasing at the expense of plasma volume and blood volume.  In light of all the studies on different fluid regimens, the question still remains: 'What is the best formula for resuscitation of the burn patient?'

   It is quite clear that the edema process is accentuated by the resuscitation fluid.  The magnitude of edema will be affected by the amount and type of fluid administered.25  The National Institutes of Health consensus summary on fluid resuscitation in 1978 was not in agreement in regard to a specific formula; however, there was consensus in regard to two major issues - the guidelines used during the resuscitation process and the type of fluid used.  In regard to the guidelines, the consensus was to give the least amount of fluid necessary to maintain adequate organ perfusion.  The volume infused should be continually titrated so as to avoid both under-resuscitation and over-resuscitation.26,27  As for the optimum type of fluid, there is no question that replacement of the extracellular salt lost into the burned tissue and into the cell is essential for successful resuscitation.19,21

Summary

   The volume necessary to resuscitate burn patients is dependent upon injury severity, age, physiological status, and associated injury.  Consequently, the volume predicted by a resuscitation formula must commonly be modified according to the individual's response to therapy.  In optimizing fluid resuscitation in severely burned patient, the amount of fluid should be just enough to maintain vital organ function without producing iatrogenic pathological changes.  The composition of the resuscitation fluid, within limitations, in the first 24 hours postburn probably makes very little difference; however, it should be individualized to the particular patient.  The utilization if the beneficial properties of hypertonic, crystalloid, and colloid solutions at various times postburn will minimize the amount of edema formation.  The rate of administration of resuscitation fluids should maintain urine outputs of 30-50 cc in adults and 1-2 cc/kg in children.  When a child weighs 30-50 kg, the urine output should be maintained at the adult level.  Fluid resuscitation based on our current knowledge of the massive fluid shifts and vascular changes that occur following burn injury has markedly decreased mortality related to burn-induced volume loss.  The failure rate for adequate resuscitation is <5% even for patients with burns >85% TBSA.  These improved statistics, however, are derived from experience in burn centers where there is substantial knowledge of the pathophysiology of burn injury.  Inadequate volume replacement in major burns is, unfortunately, common when clinicians lack sufficient knowledge and experience in this area.

Areas of burn shock research that need further attention include:

1.  the definition of the postburn course of capillary permeability changes, and identification of humoral or cellular factors influencing these changes;
2.  the identification and evaluation of pharmacological agents that can significantly alter capillary leakage;
3.  elucidation of the relationships between resuscitation fluid composition and pulmonary function changes; and
4.  the effect of resuscitation on late organ dysfunction, such as post-resuscitation wound, renal, and pulmonary complications.87

 

References
1.  Artz CP, Moncrief JA. The burn problem. In: Artz CP, Moncrief JA, eds. The Treatment of Burns. Philadelphia: WB Saunders, 1969: 1-22

19. Neely AN, Nathan P, Highsmith RF. Plasma proteolytic activity following burns. J Trauma 1988; 28: 362-367

21. Moyer CA, Margraf HW, Monafo WW. Burn shock and extravascular sodium deficiency: treatment with Ringer's solution with lactate. Arch Surg 1965; 90: 799-811

25. Hilton JG. Effects of fluid resuscitation on total fluid loss following thermal injury. Surg Gynecol Obstet 1981; 152: 441-447

26. Schwartz SL. Consensus summary on fluid resuscitation. J Trauma 1979; 19(11 Suppl): 876-877

27. Shires GT. Proceedings of the Second NIH Workshop on Burn Management. J Trauma 1979; 19(11 Suppl): 862-863

87. Pruitt BA Jr. Fluid resuscitation of extensively burned patients. J Trauma 1981; 21(Suppl): 690-692


This article was excerpted from the book Total Burn Care, 2nd edition (2001), edited by David N. Herndon, M.D. and is posted with permission from Elsevier.
Single copies of this article may be downloaded or copied only for the reader's personal research and study.

(This link takes you to the "Total Burn Care" page at the publishers web site.)
TOTAL BURN CARE  2nd ed.

 

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