ATI BURN MODULE.pdf

I. DEFINITION Burn injuries are the most severe form of trauma to the integumentary system. It results from excessive exposure to thermal, electrical, chemical or radioactive agents causing protein denaturation and increased vascular permeability. II. EPIDEMIOLOGY Although the prognosis and life expectancy of individuals with burn injuries have dramatically increased in recent years, the epidemiology of burns remains basically the same. There is a peak incidence in children 1 to 5 years of age, is due primarily to burns from hot liquids. While in adolescents and adults, the primary cause of burn injuries is due to accidents with flammable liquids, with men between the ages of 17 and 30 having the highest incidence of injury. III. ETIOLOGY The depth and percent of tissue destruction caused by injury vary widely depending on the duration and intensity of exposure to the agent. Thermal injuries are due to the exposure of the skin to extreme hot or cold objects. Chemical injuries maybe due to strong acids and alkalis, cresols, phosphorus and phenols. All produce necrosis that may extend slowly for several hours. In electrical burns on the other hand maybe from contact with malfunctioning electrical wiring or even lightning. Radiation injury is due to too much exposure to ultraviolet rays and radioactive elements such as Uranium and Radium. IV. PATHOPHYSIOLOGY Thermal destruction of the skin causes a chain of events that may be classified as local and systemic. The amount of tissue destroyed depends on local and systemic reactions to heat damage, the duration and intensity of thermal exposure and the characteristics of the area burned. The basic pathophysiologic consideration in the burn injury is the destruction of capillary and vascular integrity, which results in the formation of edema with loss of protein-rich intravascular fluid into the intercellular spaces. One of the major concerns of the physical therapists on the burn team is the patient’s splinting of the injured part to prevent movement, owing to pain. This results in an even greater accumulation of edema in the area as well as stiffness of the joints and immobility of tendons, muscles within the burned area. From the protein-rich exudates, collagen fibers will attempt to form and to organize into adhesions that will further limit the range of motion and movement of involved tissue if active physical therapy intervention is not implemented. A. LOCAL EFFECTS OF HEAT INJURY It is very difficult, even for the most experienced to determine with certainty the depth of burn for 3-5days post burn. Shortly following the burn injury, histamine is released into the local area which causes intense vasoconstriction and within a few hours, there is vasodilation and increased capillary permeability which permits plasma to escape into the wound. Damaged cells swell and platelets and leukocytes aggregate and stick to vessel walls, causing thrombosis and ischemia and further damage.