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TOTAL BURN CARE
2nd edition Reprinted with permission of Elsevier (excerpt from chapter 7, pages 78-79)
Pathophysiology of burn shock and burn edema Introduction and historical notes If left untreated, cutaneous thermal injury greater that one-third of the total body surface area (TBSA) invariably results in the severe and unique derangement of cardiovascular function called burn shock. Shock is defined as an abnormal physiologic state in which the flow of blood is insufficient to maintain adequate nutritive perfusion to meet cellular needs. Before the 19th century, it was demonstrated that after a burn, fluid is lost from the blood so that the blood becomes thicker; and in 1897, saline infusions for severe burns were first advocated.1,2 However, a real understanding of burn pathophysiology was not reached until the work of Frank Underhill.3 He demonstrated that unresuscitated burn shock correlates with greatly increased hematocrit values in burned patients, which are secondary to fluid and electrolyte loss after burn injury. The increased hematocrit values occurring shortly after severe burn were interpreted as a plasma volume deficit. Cope and Moore showed that the hypovolemia of burn injury resulted from fluid and protein translation into burned and nonburned tissues.4 Throughout the 20th century, both animal and clinical studies have established the importance of fluid resuscitation for burn shock. Investigations have focused on the rapid and massive fluid sequestration in the burn wound and the resultant hypovolemia. We now have an extensive experimental database on the circulatory and microcirculatory alterations associated with burn shock and edema generation in both the burn wound and nonburned tissues. During the last decade, research has focused on identifying and defining the release mechanisms and effects of the many inflammatory mediators produced and released after burn injury.5 It is now recognized that burn shock is a complex process of circulatory and microcirculatory dysfunction, not easily or fully repaired by fluid resuscitation. Severe burn injury results in significant hypovolemic shock and substantial tissue trauma, both of which cause the formation and release of many local and systemic mediators.6-8 Burn shock results from the interplay of hypovolemia and mediator action and continues as a significant pathophysiologic state, even if hypovolemia is corrected. Increases in pulmonary and systemic vascular resistance (SVR) and myocardial depression occur despite adequate preload and volume support.8-12 These physiologic changes can further exacerbate the whole body inflammatory response into a vicious cycle of accelerating organ dysfunction.7,8,13 Chapter 7 of "Total Burn Care, 2nd edition" examines our present understanding of the pathophysiology of the early events in burn shock, focusing on the many facets of organ and systemic effects directly resulting from the hypovolemia and circulating mediators. Inflammatory shock mediators, both local and systemic, that are implicated in the pathogenesis of burn shock include histamine, serotonin, kinins, oxygen free radicals, and products of the eicosanoid acid cascade - prostaglandins, thromboxanes, and interleukins. Additionally, certain hormones and mediators of cardiovascular function are elevated several-fold after burn injury; these include epinephrine, norepinephrine, vasopressin, angiotensin II, and neuropeptide-Y. Most certainly other mediators and factors are also involved. Understanding the complex mechanism of the pathophysiologic actions of these mediators may be of great relevance when optimally effective therapies are designed. The hope is that an improved early treatment of burn shock, perhaps through individualized fluid resuscitation protocols and methods of mediator blockade, can be developed to ameliorate or eliminate the incidence of organ dysfunction. Effective burn resuscitation and treatment of burn shock remain major challenges in modern medicine.
References 2. Haynes BW. The history of burn care. In: Boswick JAJ, ed. The Art and Science of Burn Care, 1987; 3-9 3. Underhill FP, Carrington GL, Kapsinov R, Pack GT. Blood concentration changes in extensive superficial burns, and their significance for systemic treatment. Arch Intern Med 1923; 32: 31-39 4. Cope O, Moore FD. The redistribution of body water and fluid therapy of the burned patient. Ann Surg 1947; 126: 1010-1045 5. Youn YK, LaLonde C, Demling R. The role of mediators in the response to thermal injury. World J Surg 1992; 16(1): 30-36 6. Aulick LH, Wilmore DW, Mason AD, Pruin BA. Influence of the burn wound on peripheral circulation in thermally injured patients. Am J Physiol 1977; 233: H520-H526 7. Settle JAD. Fluid therapy in burns. J Roy Soc Med 1982; 1(75): 7-11 8. Demling RH. Fluid replacement in burned patients. Surg Clin North Am 1987; 67: 15-30 9. Demling RH, Will JA, Belzer FO. Effect of major thermal injury on the pulmonary microcirculation. Surgery 1978; 83(6): 746-751 10. Baxter CR. Fluid volume and electrolyte changes of the early postburn period. Clin Plast Surg 1974; 1(4): 693-709 11. Baxter CR, Cook WA, Shires GT. Serum myocardial depressant factor of burn shock. Surg Forum 1966; 17: 103 12. Hilton JG, Marullo DS. Effects of thermal trauma on cardiac force of contraction. Burns Incl Therm Inj 1986; 12: 167-171 13. Clark WR. Death due to thermal trauma. In: Dolecek R. Brizio-Molteni L, Molteni A, Traber D, eds. Endocrinology of Thermal Trauma. Philadelphia, PA: Lea & Febiger, 1990: 6-27
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.
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