This project will investigate the following hypotheses: 1. That the hypermetabolic response (HMR) to burn injury in humans is a thermoregulatory response to increments in evaporative and radiational heat loss occurring mainly through the burn wound and that changes in catecholamine metabolism are secondary, and only facilitate the HMR. 2. That in nonseptic burn patients the increment in body temperature (TB) which is directly proportional to the size of the burn wound, reflects a shift upward in setpoint temperature (TSet). Burn patients without inhalation injury will be alternated (ratio 1:2) between treatment with occlusive dressings and no dressing. All wounds will be treated with topical Silvadene. Patients managed with dressings and one group without dressing will be exposed to comfort ambient temperature (TA) and 40% R.H. as selected by individual patients. The second open treatment group will be allowed to adjust the output from three 40W infrared heaters to achieve subjective comfort. Treatments will be started on admission and continue until wound closure is obtained. Unburned volunteers and healed burn patients will serve as controls. Once patients are hemodynamically stable, staged burn wound excision and grafting will begin. Ungraftable excised burn wounds will be covered with allograft or Biobrane. Partitional calorimetry will be performed weekly. The study sequence will begin in the AM after individual patients have been housed overnight in a metabolic chamber held at their established warmest comfortable, nonsweating TA, or with infrared heaters at appropriate settings. Baseline blood will be drawn for epinephrine (E) and norepinephrine (NE) assay, followed immediately by measurement of oxygen consumption rate (OCR), partitioned heat loss, rectal temperature (TR), average surface temperature (TSU), average skin temperature (TAS) and TB. From the data collected, the heat balance equation will be solved. Beginning at the highest comfortable TA or heater setting, the temperature of the chamber will be decreased in 2 C decrements or the infrared heater output by 20W, to establish the lowest comfortable TA or heater output. A metabolic study sequence will be run after a steady state is obtained following each change in TA or heater setting. Blood will be drawn for E and Ne assay at the end of each study sequence. The first subjective indication of coolness by the burn patients will be noted and step wise reduction in TA or heater setting continued until lack of patient cooperation demands termination. Other studies will include measurement of daily calorie and nitrogen intake, weekly 24 hour urinary nitrogen, E and NE excretion rates, and the effect of the cyclo-oxygenase inhibiter, ibuprofen on the febrile response and HMR of patients with burn injury. These studies should establish whether the thermoneutral zone (TNZ) is shifted upward for burn patients, and separate the primary and secondary drives for the HMR, i.e., increased evaporative and radiational heat loss, E and NE, fever, and TSet shift.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Project (R01)
Project #
5R01GM041694-02
Application #
3300033
Study Section
Surgery, Anesthesiology and Trauma Study Section (SAT)
Project Start
1989-06-01
Project End
1992-05-31
Budget Start
1990-06-01
Budget End
1991-05-31
Support Year
2
Fiscal Year
1990
Total Cost
Indirect Cost
Name
University of Arkansas for Medical Sciences
Department
Type
Schools of Medicine
DUNS #
City
Little Rock
State
AR
Country
United States
Zip Code
72205
Caldwell Jr, F T; Wallace, B H; Cone, J B (1994) The effect of wound management on the interaction of burn size, heat production, and rectal temperature. J Burn Care Rehabil 15:121-9
Cone, J B; Wallace, B H; Olsen, K M et al. (1993) The pharmacokinetics of ibuprofen after burn injury. J Burn Care Rehabil 14:666-9
Caldwell Jr, F T; Wallace, B H; Cone, J B et al. (1992) Control of the hypermetabolic response to burn injury using environmental factors. Ann Surg 215:485-90;discussion 490-1
Caldwell Jr, F T (1991) Etiology and control of postburn hypermetabolism: the 1991 presidential address to the American Burn Association. J Burn Care Rehabil 12:385-401
Wood, R H; Caldwell Jr, F T; Wallace, B H (1990) Effect of early feeding on the postburn hypermetabolic response in rats. J Trauma 30:S24-30