Pathophysiology of burn shock and burn edema

Burns covering more than one-third of the total body surface area lead to the unique derangements of cardiovascular function known as burn shock. Burn shock results from the interplay of direct tissue injury, hypovolemia, and release of multiple mediators of inflammation. Starling forces change to favor fluid extravasation from blood to injured and uninjured tissue. Rapid edema formation is predominantly due to the development of strongly negative interstitial fluid pressure, an increase in microvascular permeability, glycocalyx loss, and endothelial activation. The type, timing, and total volume of fluid used to resuscitate the burn shock affect the nature of these fluid shifts. Recent studies showed that crystalloid resuscitation exacerbates glycocalyx damage and thus microvascular leakage. Nevertheless, further research is required to define better treatments that ameliorate the burn edema. Key circulatory factors that alter microvascular permeability, cause vasoconstriction, depolarize cellular membranes, and depress myocardial function need to be determined.