Admission glucose and coagulopathy occurrence in patients with traumatic brain injury

被引:64
作者
Alexiou, George A. [1 ]
Lianos, Georgios [2 ]
Fotakopoulos, George [1 ]
Michos, Evaggelos [1 ]
Pachatouridis, Dimitrios [1 ]
Voulgaris, Spyridon [1 ]
机构
[1] Univ Hosp Ioannina, Dept Neurosurg, Ioannina, Greece
[2] Univ Hosp Ioannina, Dept Surg, Ioannina, Greece
关键词
Coagulopathy; glucose; traumatic brain injury; HYPERGLYCEMIA;
D O I
10.3109/02699052.2014.888769
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Introduction: Coagulopathy after traumatic brain injury (TBI) is a frequent event and is associated with patients' prognosis. TBI is also associated with a stress response that includes hyperglycemia. This study investigated if coagulopathy occurrence is associated with admission blood glucose levels in patients with TBI. Methods: This study retrospectively evaluated patients with TBI who were admitted to a neurosurgical department over a 4-year period. Coagulopathy was defined as an aPTT >40 seconds and/or INR >1.2 and/or a platelet count <120*10(9) per litre. Results: One-hundred and forty-nine patients were included in the study. Thirty-four patients developed coagulopathy. Patients with coagulopathy had significantly lower haemoglobin levels, increased INR and increased aPTT. Patients with severe TBI had more frequent coagulopathy. Patients with severe TBI had significant higher serum glucose levels compared to patients with mild TBI. Using ROC curves it was found that a serum glucose of 151 mg dl(-1) was the threshold for the discrimination of patients that developed coagulopathy. Logistic regression analysis revealed that serum glucose greater than 151 mg dl(-1) and haemoglobin levels lower than 12.4 mg dL(-1) were significantly associated with coagulopathy occurrence. Conclusion: Coagulopathy frequently occur after TBI. Patients with lower GCS score and lower haemoglobin levels and increased blood glucose levels at admission are at greater risk.
引用
收藏
页码:438 / 441
页数:4
相关论文
共 25 条
[1]   The Bcl-2 protein family: Arbiters of cell survival [J].
Adams, JM ;
Cory, S .
SCIENCE, 1998, 281 (5381) :1322-1326
[2]  
[Anonymous], 2011, CRITICAL CARE
[3]  
Bochicchio GV, 2005, AM SURGEON, V71, P171
[4]  
Brealey David, 2009, J Diabetes Sci Technol, V3, P1250
[5]   Induction of apoptosis by high proinsulin and glucose in cultured human umbilical vein endothelial cells is mediated by reactive oxygen species [J].
Du, XL ;
Sui, GZ ;
Stockklauser-Färber, K ;
Weiss, J ;
Zink, S ;
Schwippert, B ;
Wu, QX ;
Tschöpe, D ;
Rösen, P .
DIABETOLOGIA, 1998, 41 (03) :249-256
[6]   Roles of mitochondria in health and disease [J].
Duchen, MR .
DIABETES, 2004, 53 :S96-S102
[7]   Coagulation disorders after traumatic brain injury [J].
Harhangi, B. S. ;
Kompanje, E. J. O. ;
Leebeek, F. W. G. ;
Maas, A. I. R. .
ACTA NEUROCHIRURGICA, 2008, 150 (02) :165-175
[8]   The exclusive use of coagulation factor concentrates enables reversal of coagulopathy and decreases transfusion rates in patients with major blunt trauma [J].
Innerhofer, Petra ;
Westermann, Isabella ;
Tauber, Helmuth ;
Breitkopf, Robert ;
Fries, Dietmar ;
Kastenberger, Tobias ;
El Attal, Rene ;
Strasak, Alexander ;
Mittermayr, Markus .
INJURY-INTERNATIONAL JOURNAL OF THE CARE OF THE INJURED, 2013, 44 (02) :209-216
[9]   The impact of hyperglycemia on patients with severe brain injury [J].
Jeremitsky, E ;
Omert, LA ;
Dunham, CM ;
Wilberger, J ;
Rodriguez, A .
JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE, 2005, 58 (01) :47-50
[10]   Coagulopathy After Traumatic Brain Injury [J].
Laroche, Mathieu ;
Kutcher, Matthew E. ;
Huang, Michael C. ;
Cohen, Mitchell Jay ;
Manley, Geoffrey T. .
NEUROSURGERY, 2012, 70 (06) :1334-1345