Metabolic and nutritional sequelae in the non-steroid treated head injury patient.
Metabolic and nutritional sequelae in the non-steroid treated head injury patient.
复制标题
非类固醇治疗的头部损伤患者的代谢和营养后遗症。
作者：
Byron Young;L. Ott;J. Norton;Phillip A. Tibbs;Robert P. Rapp;Craig J. McClain;Robert J. Dempsey
研究人员对 16 名接受非类固醇治疗的严重颅脑损伤患者的能量产生、底物氧化、血清蛋白水平和体重变化进行了研究。患者从入院到出院平均需要 31.3 天接受评估。平均测量能量消耗 (MEE) 是预测能量消耗的 1.40 +/- 0.5 倍。第 2 周实现热量平衡 [摄入的热量 = 消耗的热量]。尽管热量平衡并且每天每公斤体重摄入至少 1.5 克蛋白质，但平均氮平衡为负值。只有 2 名患者出现正氮平衡。这些患者平均摄入的热量是 MEE 的 1.43 倍，每公斤体重摄入的蛋白质是 2.3 克。受伤后 3 周内，脂肪和蛋白质的氧化超过了蛋白质和脂肪的施用量。白蛋白水平从入院时的平均 3.09 +/- 0.2 降至 2 周内的 1.98 +/- 0.4。最初的视黄醇结合蛋白水平在正常范围内，并且水平随着时间的推移而增加。体重明显减轻（平均 15.6 +/- 5.9 磅）。头部损伤会引起严重的创伤反应，表现为能量消耗增加、负氮平衡、体重减轻、低蛋白血症和底物氧化改变。这种反应似乎是由头部损伤单独引起的，而不是由于使用皮质类固醇引起的。
Energy production, substrate oxidation, serum protein levels, and weight change were studied in 16 non-steroid treated patients with severe head injury. Patients were evaluated during an average of 31.3 days from hospital admission to discharge. The mean measured energy expenditure (MEE) was 1.40 +/- 0.5 times predicted energy expenditure. Caloric balance [calories received = calories expended] was achieved by the 2nd week. Despite caloric balance and the administration of at least 1.5 g of protein per kg of body weight per day, the mean nitrogen balance was negative. There was a positive nitrogen balance in only 2 patients. These patients received a mean of 1.43 times the MEE in total kilocalories and 2.3 g of protein per kg of body weight. Fat and protein oxidation exceeded protein and fat administration for 3 weeks postinjury. Albumin levels dropped from a mean of 3.09 +/- 0.2 on admission to 1.98 +/- 0.4 within 2 weeks. The initial retinol binding protein levels were within the normal range, and the levels increased over time. There was marked weight loss (mean, 15.6 +/- 5.9 lb). Head injury induces a profound traumatic response identified by increased energy expenditure, a negative nitrogen balance, weight loss, hypoalbuminemia, and altered substrate oxidation. This response seems to be caused by the head injury alone and is not due to the administration of corticosteroids.