Burn shock

Abstract

The approach to fluid resuscitation in burn shock continues to be refined in step with improved knowledge of the complex fluid, electrolyte, and protein shifts that characterize this form of shock. Local burn tissue and generalized nonburn tissue edema occur initially after injury because of the release of histamine, which causes increased microvascular permeability. Subsequent edema formation in burned and nonburned tissue occurs according to distinctly different mechanisms. Burn tissue edema forms because of direct thermal injury to endothelial cells and increased burn tissue osmolarity. Nonburn tissue edema is attributed to severe hypoproteinemia caused by protein flux into burn-injured tissue. Interstitial protein depletion in nonburn tissue also increases the ease of water transport into the interstitial space. Cell damage occurs with ischemia caused by decreased perfusion. More cell damage can occur with reperfusion and the subsequent formation of oxygen radicals. Fluid therapy is designed to support the patient's cardiovascular system so as to restore and maintain tissue perfusion. General formulas serve as guidelines for the amount of fluid to infuse; however, fluid therapy should be tailored to the individual patient's needs based on factors such as extensiveness of burns, extremes of age, inhalation injury, pre-existing cardiopulmonary disease, and delayed fluid resuscitation. Ringer's lactate solution is the most common fluid used in the early postburn period. The addition of colloid to resuscitation efforts should begin as microvascular permeability is restored or immediately if the patient presents in frank shock. Continuous monitoring is necessary to judge the adequacy of fluid replacement.