Local effects

The initiation of burn injury begins with damage to or loss of the victim's skin, which acts as an interface with the physical environment. The skin, which is the largest organ in the body, is not just a passive envelope, but a physiologically and immunologically active organ. In the immediate zone of injury, microcirculatory thrombosis and protein coagulation result in tissue death. A zone of ischemia exists between dead and living tissue in the early postburn period ( iDemJln..g...,1.990). Impaired blood flow can persist in this zone of ischemia even after restoration of systemic hemodynamic parameters. The hallmark of tissue reaction in this zone is edema formation.

Local edema formation is a result of three pathophysiological vascular changes: loss of microvascular integrity resulting in fluid flux into the interstitium, impairment of cell membrane function resulting in cell swelling as a result of loss of cell membrane potential, and hypoproteinemia coupled with increased osmotic pressure in burned tissue. Derangement of cell membrane potential and sodium-potassium pump function also occurs systematically and may contribute to remote organ dysfunction, causing edema in non-burn tissue (Griswold 1994). The purpose of fluid resuscitation in the early postburn period is re-expansion of plasma volume within the extracellular space. This hinges on delivery of adequate amounts of sodium ion into the extracellular space so that cellular transmembrane potentials return to normal.

While restoration of the sodium-potassium pump is central to control of intracellular swelling, edema is also exacerbated by the hypoproteinemia-based reduction in colloid oncotic pressure. Burn wound edema begins almost immediately, and non-burn tissue edema starts after 4 to 8 h. Human and animal studies demonstrate that the renin-angiotensin-aldosterone axis is appropriately responsive to postburn changes in plasma volume ( G,oie..,et..a/ 1996). Therefore, after restoration of plasma volume, sympathetic activity may play a predominant role in regulating renal blood flow.

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