Glial fibrillary acidic protein injury and multiple trauma in serum after traumatic brain

被引:167
作者
Pelinka, LE
Kroepfl, A
Schmidhammer, R
Krenn, M
Buchinger, W
Redl, H
Raabe, A
机构
[1] Ludwig Boltzmann Inst Expt & Clin Traumatol, Austrian Workers Compensat Board, A-1200 Vienna, Austria
[2] AUVA, Trauma Hosp Liz, Linz, Austria
[3] Mistelbach Gen Hosp, Dept Traumatol, Mistelbach, Austria
[4] Waldviertel Clin, Dept Traumatol, Horn, Austria
[5] Goethe Univ Frankfurt, Neuroctr, Dept Neurosurg, D-6000 Frankfurt, Germany
来源
JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE | 2004年 / 57卷 / 05期
关键词
secondary brain damage; multiple trauma; brain specificity; intracranial pressure cerebral perfusion; pressure; outcome;
D O I
10.1097/01.TA.0000108998.48026.C3
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Background. This study aimed to determine whether glial fibrillary acidic protein (GFAP) is released after traumatic brain injury (TBI), whether GFAP is related to brain injury severity and outcome after TBI, and whether GFAP is released after multiple trauma without TBI. Methods:. This prospective study enrolled 114 patients who had TBI with or without multiple trauma (n = 101) or multiple trauma without TBI (n 13), as verified by computerized tomography. Daily GFAP measurement began at admission (< 12 hours after trauma) and continued for the duration of intensive care (1-22 days). Documentation included categorization of computerized tomography according to Marshall classification, based on daily highest intracranial pressure (ICP), lowest cerebral perfusion pressure (CPP), lowest mean arterial pressure (MAP), and 3-month Glasgow Outcome Score (GOS). Results: The GFAP concentration was lower for diffuse injury 2 than for diffuse injury 4 (p < 0.0005) or nonevacuated mass lesions larger than than 25 mL (p < 0.005), lower for a ICP less than 25 mm Hg than for a ICP of 25 mm Hg or more, lower for a CPP of 60 mm Hg or more than for a CPP of 60 mm Hg or less, lower for a MAP of 60 mm Hg or more than for a MAP less than 60 mm Hg (all p < 0.0005), and lower for a GOS of 1 or 2 than for a GOS of 3, 4 (p < 0.05), or 5 (p < 0.0005). After TBI, GFAP was higher in nonsurvivors (n = 39) than in survivors (n = 62) (p < 0.005). After multiple trauma without TBI, GFAP remained normal. Conclusion: The findings showed that GFAP is released after TBI, that GFAP is related to brain injury severity and outcome after TBI, and that GFAP is not released after multiple trauma without brain injury.
引用
收藏
页码:1006 / 1012
页数:7
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