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非类固醇治疗的头部损伤患者的代谢和营养后遗症。

Metabolic and nutritional sequelae in the non-steroid treated head injury patient.

作者信息

Young B, Ott L, Norton J, Tibbs P, Rapp R, McClain C, Dempsey R

出版信息

Neurosurgery. 1985 Nov;17(5):784-91. doi: 10.1227/00006123-198511000-00010.

Abstract

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.

摘要

对16例未接受类固醇治疗的重型颅脑损伤患者的能量产生、底物氧化、血清蛋白水平及体重变化进行了研究。患者从入院至出院平均接受了31.3天的评估。测得的平均能量消耗(MEE)为预测能量消耗的1.40±0.5倍。在第2周实现了热量平衡[摄入热量=消耗热量]。尽管实现了热量平衡且每天每千克体重至少给予1.5克蛋白质,但平均氮平衡仍为负。只有2例患者氮平衡为正。这些患者接受的总千卡热量平均为MEE的1.43倍,每千克体重给予2.3克蛋白质。伤后3周内脂肪和蛋白质氧化超过了脂肪和蛋白质的摄入量。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。初始视黄醇结合蛋白水平在正常范围内,且随时间增加。体重显著下降(平均15.6±5.9磅)。颅脑损伤引发了一种严重的创伤反应,表现为能量消耗增加、氮平衡为负、体重减轻、低白蛋白血症及底物氧化改变。这种反应似乎仅由颅脑损伤引起,而非糖皮质激素的使用所致。

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