![]() The degree of peripheral muscle protein net balance, taking into account synthesis and breakdown, was quantified using stable isotope tracers. We propose that the time between operations was indicative when donor sites were healed and thereby allowed determination of wound healing. ![]() 13, 14, 16 We further determined time between operations as a measure for wound healing/re-epithelization. Sepsis was defined as a positive blood culture or pathologic tissue identifying the pathogen during hospitalization or at autopsy, in combination with at least 3 of the following: leucocytosis or leucopenia (>12,000 or 38.5 or 150 BPM in children), refractory hypotension (systolic BP 240 mg/dl), and enteral feeding intolerance (residuals > 200 cc/hr or diarrhea > 1 L/day) as previously published. Patient demographics (age, date of burn and admission, sex, burn size and depth of burn) and concomitant injuries such as inhalation injury, sepsis, morbidity, and mortality were recorded. Parenteral nutrition was only given in rare instances if the patient could not tolerate tube feeds. 13– 15 The nutritional route of choice in our patient population was enteral nutrition via a duodenal (Dobhof) or nasogastric tube. The intake was calculated as 1500 kcal/m 2 body surface + 1500 kcal/m 2 area burn as previously published. This procedure was repeated until all open wound areas were covered with autologous skin.Īll patients underwent the same nutritional treatment according to a standardized protocol. After the first operative procedure, patients were taken back to the operation theater when donor sites were healed. Any remaining open areas were covered with homograft. Within 48 hours of admission, all patients underwent total burn wound excision and the wounds were covered with autograft. If needed, patients were resuscitated according to the Galveston formula with 5000 cc/m 2 TBSA burned + 2000 cc/m 2 TBSA lactated Ringer’s solution given in increments over the first 24 hours. The purpose of the present study was to characterize the pathophysiologic responses postburn in terms of hypermetabolism, inflammation, hormonal and body composition changes, organ function, and muscle protein synthesis in a large prospective clinical trial in order to understand pathophysiologic mechanisms and develop new specific treatment options to improve outcome of severely burned patients.Īll thermally injured children with burns over 30% of their total body surface area (TBSA) who required surgery and consented to an IRB-approved experimental protocol between 19, and were admitted to our burn unit and required at least one surgical intervention were included in this study. 12 Several clinical trials with the goal to correct hormonal dysbalances in critically ill patients have been ineffective or even harmful because of a lack of understanding of the pathophysiologic mechanisms.ĭespite the identification and delineation of fragments of the postburn responses, no large prospective clinical trial examining the major responses during the postburn acute phase has been conducted. ![]() 12 The long-term phase encompasses the hypothalamic suppression of the endocrine axes which contributes to the low serum levels of the subsequent target organ hormones. 12 The acute phase is characterized by low effector hormones due to target-organ resistance. 11 In critically ill patients, a biphasic endocrine response is present, which encompasses an acute and a long-term phase. The hypothalamic-pituitary-organ-hormonal axis acts as a regulator of many organ and cellular functions however, it has been suggested that a hormonal dysbalance is present following a burn injury. Hypermetabolism is further associated with alterations in the endocrinologic response. 1, 4, 8 The hypermetabolic response is associated with a marked acute phase response that persists for 8–12 weeks after the initial insult. 4– 7 This hypermetabolic response begins on the fifth day post-injury and continues up to 24 months postburn causing loss of lean body mass (LBM), loss of bone density, muscle weakness, and poor wound healing. 3 The hypermetabolic response following major burn is characterized by a hyperdynamic response with increased body temperature, oxygen and glucose consumption, CO 2 production, glycogenolysis, proteolysis, lipolysis, and futile substrate cycling. 1, 3 The inflammatory response starts immediately after burn and persists for up to several months. 1, 2 There is growing evidence that pathophysiologic responses that occur immediately or early after burn will affect long-term outcome of severely burned patients. We and others have shown that after a severe thermal injury, patients are hypermetabolic, disabled, and debilitated over a period of at least 24 months. Despite improvements in mortality over the last decade, postburn morbidity is tremendous and remains a challenge for clinicians.
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