Thermal Burns

Published on 10/02/2015 by admin

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Last modified 10/02/2015

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189 Thermal Burns

Pathophysiology

Knowing the anatomy of the skin is essential to understanding burn pathophysiology (Fig. 189.1). Burns are classified according to the depth of injury (Table 189.1 and Fig. 189.2). First- and second-degree burns are partial-thickness burns and have a better prognosis. Full-thickness burns (third and fourth degree) are insensate and require skin grafts (unless <1 cm) or reconstruction because of destruction of the epidermis and dermis. Based on the depth of the burn, the ability to heal can be predicted. Because the dermis itself is the living tissue, the depth of burn into the dermis determines how likely wounds are to heal and what degree of scarring can be expected.

The severity of the burn depends on the duration of contact with the burn agent, the heat and conductivity of tissues, the heat of the burn agent, heat transfer (conduction, convection, or radiation), and the heat capacity of the burn agent.

Burns damage by two methods: first, by direct injury to the cellular structure of the tissue and, second, by the release of local mediators. Three zones are discussed with burn injuries: the zone of coagulation, the zone of stasis, and the zone of hyperemia. The zone of coagulation is the necrotic area of cell death as a result of direct thermal injury. Surrounding this area is the zone of stasis, which has decreased blood flow and is at risk for cell death within 24 hours but may initially appear as living tissue. Cell mediators such as thromboxane A2 are predominantly responsible for transforming this area into the zone of coagulation. Outside this zone is the zone of hyperemia. The zone of hyperemia is defined as the outside area of tissue affected by the burn, usually blanching on touch, but with intact blood flow and high potential to recover from the initial insult.

The secondary effects of burns, such as histamine release and edema, are thought to result from cellular mediators. Aggregated platelets from the burn release serotonin, whereas histamine is derived from mast cells within the burned skin.

Presenting Signs and Symptoms

Frequently, occupational exposure causes burns. Direct contact with flame, scalds, injuries caused by heated equipment or arc welding, gasoline fires, and cooking accidents are all common. In children or elderly patients with burn injuries, the concern for abuse is always present (see the “Red Flags” box).

One issue that is often of concern is the depth of burns. Determining between deep partial-thickness and superficial partial-thickness burns is difficult because it may take time for a definitive area of demarcation to develop. The usual method of distinction, blistering (which occurs with deep partial-thickness burns, or second-degree burns), can be delayed; however, it is the only distinction that is available early. Third-degree burns are insensate.

With all burn patients, assessment of the airway is critical. Signs of deep injury are stridor, soot in the mouth, and singed nasal hairs; any of these signs should indicate the need for close monitoring and more aggressive airway management. Swelling can occur rapidly in burned tissues, so signs of airway involvement should suggest earlier intubation because decompensation may occur rapidly.