Skin consists of two layers: the epidermis and dermis. In the very young and the elderly, the skin thickness is less than that of a person in the prime of life. Skin thickness also varies significantly throughout the body. The skin is very thick in the palm of the hand and the sole of the foot. The upper part of the back is thicker than other parts of the body. Thus exposure to same temperature for same duration will lead to different depths of injury in different parts of the body.

Skin functions as a semipermeable barrier to evaporative water loss. Other functions of the skin include protection from the adversities of the environment, control of body temperature, sensation, and excretion. Partial-thickness thermal injury can result in disruption of the barrier function and contribute to free water deficits. The effect may be significant in moderate to large burns.

Thermal injury results in a spectrum of local and systemic homeostatic derangements that contribute to burn shock. These include disruption of normal cell membrane function, hormonal alterations, changes in tissue acid-base balance, hemodynamic changes, and hematologic derangement. 5

Fluid and electrolyte abnormalities seen in burn shock are largely the result of alterations of cell membrane potentials with intracellular flux of water and sodium and extracellular migration of potassium secondary to dysfunction of the sodium pump. In burns of greater than 60 percent of body surface area, depression of cardiac output is frequently observed with lack of response to aggressive volume resuscitation. Although disputed by others, Baxter and Shires have explained this phenomenon on the basis of circulating myocardial depressants.6 Also, there is increased systemic vascular resistance. A significant metabolic acidosis may be present in early stages of a large burn injury.

Hematologic derangements associated with massive thermal injury vary from an increase in hematocrit with increased blood viscosity during the early phase followed by anemia from erythrocyte extravasation and destruction. However, transfusion is infrequently required for patients with isolated burn injury. 3

Thermal injury is a progressive injury. Local effects of thermal injury include liberation of vasoactive substances, disruption of cellular function, and edema formation. The systemic response consists of responses by the neurohormonal axis and profound alterations of all organ systems. Substances implicated in these events are histamine, kinin, serotonin, arachidonic acid metabolites, and free oxygen radicals. These substances exert their primary effects at the local level and cause progression of the burn wound. Preservation of the blood supply by decreasing the inflammatory response has been attempted with pharmacologic manipulations using drugs such as nonsteroidal anti-inflammatories.5

Although many factors may influence prognosis, the severity of the burn, presence of inhalation injury, associated injuries, patient's age, preexisting disease, and acute organ system failure are most important.2 The burn's size and depth are functions of the burning agent, its temperature, and the duration of exposure. Cell damage occurs at a temperature greater than 45°C (113°F) owing to denaturation of cellular protein. The burn wound is described as having three zones: the zone of coagulation, where tissue is irreversibly destroyed with thrombosis of blood vessels; the zone of stasis, where there is stagnation of the microcirculation; and the zone of hyperemia, where there is increased blood flow. The zone of stasis can become progressively more hypoxemic and ischemic if resuscitation is not adequate. In the zone of hyperemia, there is minimal damage to the cells and spontaneous recovery is likely.

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