Objective To observe effect of intra- and post-operative mild hypothermia using an ice blanket on patients with severe traumatic brain injury (sTBI). Methods Twenty sTBI patients with Glasgow Coma Scale (GCS) of 3-8 points were included and were assigned to either ice bag cooling (Bag group) or ice blanket cooling (Blanket group) (n=10 each) according to random number table. Patients in Bag group had temperature reduction by placing ice bag over great vessels, whereas in Blanket group an ice blanket (temperature was set as the nasopharyngeal temperature of 33℃-34℃) was employed to have temperature reduction. Hypothermia therapy in the two group groups was initiated from the beginning of operation and continued for 48 hours after operation. Intracranial pressure, cerebral perfusion pressure (CPP) and GCS in both groups were recorded respectively at 10 minutes before operation (T0) and at 8, 12, 24, 48 and 72 hours after operation (T1, T2, T3, T4 and T5). Venous blood of the two groups was harvested to assay the serum concentration of neuronspecific enolase (NSE), myelin basic protein (MBP) and S-100β at T0, T3, T4, T5 and at 96 hours after operation (T6) by ELISA method. Glasgow Outcome Scale (GOS) was evaluated at postoperative six months. Results In Bag group, body temperature (T1-T5) of the patients had no significant decrease (P>0.05) and NSE (T3-T6), S-100β (T3-T6) and MBP (T4-T6) were increased (P<0.05 or 0.01) when compared with those in T0; intracranial pressure (T2-T5) was increased (P<0.05) and CPP (T3-T5) was lowered (P<0.05) when compared with those in T1. In Blanket group, body temperature (T1-T6) of the patients presented was decreased significantly (P<0.01) and NSE (T3-T6), MBP (T5-T6) and S-100β (T4-T6) were increased (P<0.05 or 0.01) when compared those in T0; intracranial pressure (T2-T6) was increased (P<0.05 ) and CPP had no significant changes (P>0.05) when compared with those in T1. By contrast with those in the same time points in Bag group, lower body temperature (T1-T5) (P<0.001), lower intracranial pressure (T2-T5), higher CPP (T3-T5) as well as lower NSE (T4-T6), MBP (T4-T6) and S-100β (T6) were observed in Blanket group (P<0.05 or 0.01). Changes of GCS and GOS in the two groups were no significance (P>0.05). Conclusion Intraoperative and postoperative mild hypothermia therapy using an ice blanket may alleviate the degree of brain injury in sTBI patients."/>
冰毯术中、术后亚低温治疗重型创伤性脑损伤的疗效
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Abstract:Objective To observe effect of intra- and post-operative mild hypothermia using an ice blanket on patients with severe traumatic brain injury (sTBI). Methods Twenty sTBI patients with Glasgow Coma Scale (GCS) of 3-8 points were included and were assigned to either ice bag cooling (Bag group) or ice blanket cooling (Blanket group) (n=10 each) according to random number table. Patients in Bag group had temperature reduction by placing ice bag over great vessels, whereas in Blanket group an ice blanket (temperature was set as the nasopharyngeal temperature of 33℃-34℃) was employed to have temperature reduction. Hypothermia therapy in the two group groups was initiated from the beginning of operation and continued for 48 hours after operation. Intracranial pressure, cerebral perfusion pressure (CPP) and GCS in both groups were recorded respectively at 10 minutes before operation (T0) and at 8, 12, 24, 48 and 72 hours after operation (T1, T2, T3, T4 and T5). Venous blood of the two groups was harvested to assay the serum concentration of neuronspecific enolase (NSE), myelin basic protein (MBP) and S-100β at T0, T3, T4, T5 and at 96 hours after operation (T6) by ELISA method. Glasgow Outcome Scale (GOS) was evaluated at postoperative six months. Results In Bag group, body temperature (T1-T5) of the patients had no significant decrease (P>0.05) and NSE (T3-T6), S-100β (T3-T6) and MBP (T4-T6) were increased (P<0.05 or 0.01) when compared with those in T0; intracranial pressure (T2-T5) was increased (P<0.05) and CPP (T3-T5) was lowered (P<0.05) when compared with those in T1. In Blanket group, body temperature (T1-T6) of the patients presented was decreased significantly (P<0.01) and NSE (T3-T6), MBP (T5-T6) and S-100β (T4-T6) were increased (P<0.05 or 0.01) when compared those in T0; intracranial pressure (T2-T6) was increased (P<0.05 ) and CPP had no significant changes (P>0.05) when compared with those in T1. By contrast with those in the same time points in Bag group, lower body temperature (T1-T5) (P<0.001), lower intracranial pressure (T2-T5), higher CPP (T3-T5) as well as lower NSE (T4-T6), MBP (T4-T6) and S-100β (T6) were observed in Blanket group (P<0.05 or 0.01). Changes of GCS and GOS in the two groups were no significance (P>0.05). Conclusion Intraoperative and postoperative mild hypothermia therapy using an ice blanket may alleviate the degree of brain injury in sTBI patients.
YUE Sheng,WANG Zhi-ping,ZHOU Mai-tao et al. Effect of intra-and post-operative mild hypothermia with ice blanket in treatment of severe traumatic brain injury[J]. CHINESE JOURNAL OF TRAUMA, 2013, 29(9): 815-819.
[1]Sahuquillo J, Vilalta A. Cooling the injured brain: how does moderate hypothermia influence the pathophysiology of traumatic brain injury. Curr Pharm Des, 2007, 13(22):2310-2322.
[2]Diller KR, Zhu L. Hypothermia therapy for brain injury. Annu Rev Biomed Eng, 2009, 11:135-162.
[3]Murillo-Cabezas F, Muñoz-Sánchez MA, Rincón-Ferrari MD, et al. The prognostic value of the temporal course of S100 beta protein in post-acute severe brain injury: a prospective and observational study. Brain Inj, 2010, 24(4):609-619.
[4]Zhang H, Zhou M, Zhang J, et al. Initiation time of post-ischemic hypothermia on the therapeutic effect in cerebral ischemic injury. Neurol Res, 2009, 31(4):336-339.
[5]Clifton GL, Valadka A, Zygun D, et al. Very early hypothermia induction in patients with severe brain injury (the National Acute Brain Injury Study: Hypothermia II): a randomised trial. Lancet Neurol, 2010, 10(2):131-139.
[6]Peterson K, Carson S, Carney N. Hypothermia treatment for traumatic brain injury: a systematic review and meta-analysis. J Neurotrauma, 2008, 25(1):62-71.
[7]Berger RP, Beers SR, Richichi R, et al. Serum biomarker concentrations and outcome after pediatric traumatic brain injury. J Neurotrauma, 2007, 24(12): 1793-1801.
[8]Vos PE, Lamers KJ, Hendriks JC, et al. Glial and neuronal proteins in serum predict outcome after severe traumatic brain injury. Neurology, 2004, 62(8):1303-1310.
[9]Wunderlich MT, Wallesch CW, Goertler M. Release of neurobiochemical markers of brain damage is related to the neurovascular status on admission and the site of arterial occlusion in acute ischemic stroke. J Neurol Sci, 2004, 227(1):49-53.
[10]Palmio J, Huuhka M, Laine S, et al. Electroconvulsive therapy and biomarkers of neuronal injury and plasticity: serum levels of neuron-specific enolase and S-100 b protein. Psychiatry Res, 2010, 177(1-2):97-100.
[11]Woertgen C, Rothoerl RD, Brawanski A. Early S-100 B serum level correlates to quality of life in patients after severe head injury. Brain Inj, 2002, 16(9):807-816.