J Trauma
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Case Reports
Serial debridement and allografting of facial burns: a method of controlling spontaneous healing.
Management of severe partial-thickness facial burns is difficult and not ideal. Over the past 4 years, 18 patients have undergone serial debridements and allografting at regular intervals until re-epithelialization occurred. Twelve patients required one procedure and two patients required two procedures. ⋯ Only four patients required scar revision procedures. Three desired cosmetic improvement, and one required functional improvement. The use of serial debridements and allografting controls facial burn healing, as well as producing good cosmetic and functional results.
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Numerous formulas have been used to estimate the calorie requirements of hypermetabolic burned patients. With the recent development of instrumentation for indirect calorimetric measurements, questions have been raised concerning the validity and accuracy of the early equations. Because metabolic rate decreases during the course of wound healing, we attempted to determine the magnitude of hypermetabolism and the accuracy of the Curreri formula in patients with various wound sizes. ⋯ The measured REE was 27, 35, and 50% greater than the BEE in Groups 1, 2, and 3, respectively (p less than 0.001). The ACEE underestimated REE by 7% in Group 1, and overestimated REE by 13 and 35% in Groups 2 and 3, respectively (p less than 0.001). Resting energy expenditure should be measured at regular intervals in individuals with open burn wounds greater than 10% BSA in order to adjust nutritional support appropriately.
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The purpose of this study was to determine whether or not thromboxane A2 (TXA2) was necessary or sufficient for the development of end-organ pathology during graded bacteremia. Pulmonary artery catheters were placed in 21 adult male pigs under pentobarbital anesthesia and breathing room air. After a control period, animals were studied in four groups: Group 1, anesthesia only; Group 2, infusion of 1 X 10(9) ml Aeromonas hydrophila which was gradually increased from 0.2 ml/kg/hr to 4.0 ml/kg/hr over 4 hours; Group 3, pretreatment with SQ 29,548 (TXA2 antagonist) then Aeromonas h. infusion; Group 4, infusion of U46619 (TXA2 agonist) to pulmonary artery pressures measured in Group 2. ⋯ The results indicated that physiologic thromboxane A2 agonist (Group 4) was sufficient alone to cause pulmonary inflammation. Thromboxane A2 was neither necessary nor sufficient for significant renal, hepatic, pulmonary, or splenic pathology to occur in graded bacteremia, manifested in similar microanatomic abnormalities in these organs in Groups 2 and 3 and in Groups 1 and 4. Pulmonary leukocyte infiltration was significantly increased in Group 3 compared to all other groups, suggesting that TXA2 impairs inflammatory responses.