汶川地震中颅脑损伤现场急救的临床分析

目的 探讨"5·12"汶川大地震中颅脑损伤伤员现场伤情特点和急救中的经验教训,为地震致颅脑损伤的现场急救提供临床经验.方法 回顾性总结自2008年5月12日至2008年5月13日汶川大地震后在重灾区北川和安县现场急救的120例颅脑损伤伤员的临床资料,对致伤原因、伤情分类、救治方法 、合并症、治疗措施等进行分析.结果 120例伤员中70例因头皮挫裂伤仅予现场处理,清创缝合,预后良好,余伤员急诊处理后转入后方综合性医院住院治疗.住院伤员行开颅手术治疗40例,非手术治疗10例,住院5～16d后康复出院46例,死亡4例.结论 现场正确处理判断地震致颅脑损伤伤员伤情且积极救治是提高救治水平的关键,并可最大程度地挽救生命,减少损失.     

地震后颅脑创伤患者的治疗分析

5.12四川汶川8.0级大地震造成大量的人员伤亡.南于灾区地形复杂、山体滑坡、交通中断,救援非常困难,很多伤员在伤后几天才被救出,或者因当地条件有限,未能及时获得专科救治,因此地震所致的颅脑创伤治疗与一般的处理不尽相同,特别是伤口的处理.     

地震中颅脑创伤伤员的救治

汶川强烈地震造成大量伤员,如颅脑创伤、胸腹损伤、脊柱和四肢损伤等,造成伤亡的原因多为坠物砸伤或挤压伤,其中颅脑创伤是地震伤亡中死亡率最高的损伤类型之一,因此,早期的正确救治对挽救伤员的生命至关重要,及早采取有效的救治措施和恰当的康复手段可有效预防相关并发症,最大限度恢复伤员的功能,减少残疾.     

汶川特大地震颅脑创伤临床救治分析

目的 总结汶川特大地震中颅脑外伤的临床类型及特点、救治经验.方法 对5.12汶川特大地震中四川大学华西医院神经外科收治的182例伤员资料、流行病学、致伤原因、分类、伤情、救助时间、合并症、并发症、治疗和预后等进行分析.结果 男102例,女80例,建筑物砸伤是最主要的致伤原因,其次为挤压伤;按GCS评分:轻型129例,占70.9%;中型32例,占17.6%.,重型21例,占11.5%.伤口开放占68.7%;合并叫肢及脊柱骨折占16.5%,伤口感染18例占7.4%,急性肾功衰竭3例(1.2%).手术治疗者40例.出院或转科时GOS评估:5分121例(66.5%),4分38例(20.8%),3分或以下23例(9.7%),死亡5例,死亡率3.3%.结论 重伤伤员院前抢救率低,院内以轻、中型颅脑创伤为主,合并症多,伤口感染率高;多学科联合早期、有序规范救治有重要意义.     

地震致颅脑创伤的研究进展

地震致颅脑损伤是地震伤害中仅次于肢体骨折的损伤类型,具有伤员数量多,致伤机制复杂,伤情变化快,救援难度大,死亡伤残率高等特点。致伤原因以钝性伤害为主,全身复合伤多见。妇女、儿童和老人是地震颅脑损伤的高危人群。针对不同类型的地震灾害,因地、因时制宜开展救援,可增加伤员救治的预见性,增强可控性,降低死残率。建立医疗机构间专项协作网络平台,有益于地震致颅脑损伤的研究和管理。     

颅脑交通伤合并胸腹腔脏器损伤的救治

在所有致伤原因中,道路交通伤(roadtraffcin鄄jury,RTI)占50%～60%,至今仍呈上升趋势[1～3]。在因RTI而致死的患者中有50%～70%为颅脑创伤,其合并胸腹腔脏器损伤时,伤情则更严重,抢救更为困难,死亡率高达40%以上[4]。1995年1月～2001年6月我科救治这类伤员51例,现将其救治体会总结如下。1临床资料1.1一般资料本组颅脑交通伤合并胸腹腔脏器损伤51例,其中男39例,女12例,年龄9～67岁。伤后就诊时间20min至5h,来院时GCS3～8分27例,9～12分16例,13～15分8例。颅脑伤均经CT确诊,其中开放性颅脑损伤6例,闭合性颅脑损伤45例;脑挫裂伤17例,颅内…     

120例中重型颅脑损伤合并多发伤患者的救治分析

目的探讨中重型颅脑损伤合并多发伤患者的临床特点及其救治策略。方法对120例中重型颅脑损伤合并多发伤患者的临床资料进行回顾性分析。结果 120例患者中,恢复良好61例(50.8%),中度残疾15例(12.5%),重度残疾8例(6.7%),植物生存及昏迷状态下自动出院21例(17.5%),死亡15例(12.5%),其中8例于入院24h内死亡。结论在多发伤一体化急救模式下,抓好院前院内急救环节,积极合理地手术干预,重视重症监护及后期综合治疗,对于提高颅脑损伤合并多发伤患者的救治成功率有积极意义。     

面颅伤救治的临床研究

目的研究面颅伤临床特征、救治方法和疗效.方法对250例面颅伤患者采用放射影像学诊断、常规面颅X线照片和CT、MRI脑扫描.个别进行脑部正电子发射计算机断层扫描(PET),同时常规血气分析,部分呼吸监护,了解和纠正伤后低氧血症.对30例患者行颅脑彩色多普勒超声血流显像检测,了解伤后脑血流改变.结果本组250例经救治后痊愈225例(90%),中残24例( 9.6% ),死亡1例(0.4%).生存者均无明显的颌面部畸形和功能障碍.结论颌面部软组织开放伤,早期彻底清创,一期愈合,防止疤痕挛缩;错位骨折及时复位固定,防止骨性畸形.低氧血症是面颅伤患者死亡的主要原因,也是致残的重要因素.     

重型颅脑损伤90例死亡原因分析

目的探讨重型颅脑损伤死亡原因和救治经验。方法2007年1月至2011年1月收治的重型颅脑损伤病人761例,死亡10例,对90例死亡患者的临床资料进行回顾性分析。结果重型颅脑损伤病人761例,死亡90例,死亡率11．8％。其中GCS3—5分死亡65例,GCS6~8分死亡25例。伤后1～3d内死亡24例,4～6d死亡19例,7~9d死亡26例,10～30d死亡21例。结论早期诊断,综合救治,积极预防并发症是救治重型颅脑损伤的关键。     

汶川地震336例颅脑损伤患者的救治分析

目的 总结和探讨地震发生后一线医院收治的颅脑损伤患者特点及救治经验.方法 将336例地震颅脑损伤患者通过GCS评分法初筛,按伤情程度分为重、中、轻3型,予以药物治疗和医学观察;伤口行止血包扎和清创;复合伤行相关处置;重型颅脑损伤中开颅手术4例,死亡1例.结果 本组病例中,轻型颅脑损伤206例,恢复良好201例;中型颅脑损伤122例,恢复良好11例;重型颅脑损伤8例,恢复良好1例,死亡4例.结论 地震所致颅脑损伤具有致伤机制复杂,合并损伤多,病情变化快的特点,提高一线医院灾害应对能力和应急储备,对于及时抢救危重颅脑损伤患者,提高抢救存活率,最大限度的降低死残率均有着极其重要的现实意义.     

汶川大地震颅脑损伤的时空特点及救治策略

目的 分析汶川大地震颅脑外伤患者的时空特点、复合伤情的分布,探讨救治时机和治疗方式的选择.方法 对成都军区总医院神经外科自2008年5月12日至6月2日收治的汶川地震中92例颅脑外伤患者的诊治情况进行回顾性分析.结果 收治的92例地震颅脑损伤患者均来自成都西北部平原地区,其中早期12 h内收治76例,共开展手术10例.治愈47例,转外省治疗31例,住院治疗11例,死亡3例.结论 汶川地震中颅脑损伤患者多为早期损伤,病情变化快.早期开展急救手术治疗可以提高救治成功率.     

Role of tumor necrosis factor receptor-1 in the death of retinal ganglion cells following optic nerve crush injury in mice

To assess the specific role of tumor necrosis factor (TNF) death receptor signaling in the induction of retinal ganglion cell (RGC) death, optic nerves of mice deficient for TNF receptor-1 (TNF-R1-/-) and control mice (C57BL/6J) were unilaterally subjected to crush injury. Counts of RGCs and their axons 6 weeks after the injury demonstrated that their loss was significantly less in TNF-R1-/- mice compared to controls. The most prominent decrease in neuronal loss detected in TNF-R1-/- mice was beyond the initial 2-week period after the injury. This time period was correlated with the period of glial activation and increased glial immunolabeling for TNF-alpha in these eyes. No further protection against neuronal loss was detectable in TNF-R1-/- mice treated with D-JNKI1, a specific inhibitor of c-Jun N-terminal protein kinase (JNK). However, anti-JNK treatment of control animals provided a significant protection against neuronal loss during the same secondary degeneration period. Phospho-JNK immunolabeling of RGCs in control mice subjected to optic nerve crush significantly decreased following their treatment with D-JNKI1, and anti-JNK treatment protected RGCs from degeneration in these animals, similar to the lack of TNF-R1. These findings provide evidence that TNF death receptor signaling is involved in the secondary degeneration of RGCs following optic nerve injury, and is associated with JNK signaling. Since secondarily degenerating neurons are viable targets for neuroprotection, inhibition of TNF death receptor signaling may be an effective strategy to protect RGCs in several neurodegenerative injuries.     

Influence of injury severity on the rate and magnitude of the T lymphocyte and neuronal response to facial nerve axotomy

The temporal relationship between severity of peripheral axonal injury and T lymphocyte trafficking to the neuronal cell bodies of origin in the brain has been unclear. We sought to test the hypothesis that greater neuronal death induced by disparate forms of peripheral nerve injury would result in differential patterns of T cell infiltration and duration at the cell bodies of origin in the brain and that these measures would correlate with the magnitude of neuronal death over time and cumulative neuronal loss. To test this hypothesis, we compared the time course of CD3(+) T cell infiltration and neuronal death (assessed by CD11b(+) perineuronal microglial phagocytic clusters) following axonal crush versus axonal resection injuries, two extreme variations of facial nerve axotomy that result in mild versus severe neuronal loss, respectively, in the facial motor nucleus. We also quantified the number of facial motor neurons present at 49 days post-injury to determine whether differences in the levels of neuronal death between nerve crush and resection correlated with differences in cumulative neuronal loss. Between 1 and 7 days post-injury when levels of neuronal death were minimal, we found that the rate of accumulation and magnitude of the T cell response was similar following nerve crush and resection. Differences in the T cell response were apparent by 14 days post-injury when the level of neuronal death following resection was substantially greater than that seen in crush injury. For nerve resection, the peak of neuronal death at 14 days post-resection was followed by a maximal T cell response one week later at 21 days. Differences in the level of neuronal death between the two injuries across the time course tested reflected differences in cumulative neuronal loss at 49 days post-injury. Altogether, these data suggest that the trafficking of T cells to the injured FMN is dependent upon the severity of peripheral nerve injury and associated neuronal death.     

The effect of MS-818, a pyrimidine compound,on the regeneration of peripheral nerve fibers of mice after a crush injury

One of the pyrimidine compounds, 2-piperadino-6-methyl-5-oxo-5,6-dihydro(7H)pyrrolo[3,4-d]pyrimidine (MS-818), has neurotropic effects in vitro. Therefore, we studied the effect of MS-818 on the regeneration of the peroneal nerve in C57BL/6J mice after a crush injury. Two test groups, which received a daily intraperitoneal injection of 5 mg/kg or 10 mg/kg MS-818, respectively, were compared with controls, which received daily intraperitoneal injections of physiological saline, over a 14-day period. The maximum foot-width ratio (crushed side/uncrushed side) was obtained on days 1, 8 and 14 after the crush injury, and the various morphometric parameters were evaluated at both 5 and 10 mm distal to the proximal portion of the crush site. The significant effects of MS-818 included a larger maximum foot width (P<0.04) and a greater number of unmyelinated axons per nerve at both levels (P<0.003) in both test groups than in controls. MS-818 had no significant effects on body weight, the increase of total transverse fascicular area after the crush injury, the total number of myelinated fibers with their size distributions, or the number of nuclei of Schwann cells and macrophages. Therefore, we conclude that MS-818 promotes axonal sprouting and elongation after a crush injury in mice.     

Number, size, and class of peripheral nerve fibers regenerating after crush, multiple crush, and graft

Morphometric characterization of fiber regeneration in a distal nerve after focal proximal nerve injury may provide useful clinical information and insights about underlying neurobiologic mechanisms. The myelinated (MF) and unmyelinated (UF) fibers of peroneal nerve of groups of mice were assessed 9 months after crush, graft, and multiple crush injury of the proximal sciatic nerve: number and size distribution of axon areas, myelin areas, and fiber diameters. After crush, number of regenerated MF and UF was almost identical to that of controls. Their size distribution had almost returned to normal. After graft and multiple crush, fiber number had returned to normal or was significantly increased beyond normal but there were only a few large fibers present. This may be explained by: (a) disproportionate regeneration of small-diameter compared to large-diameter classes of fibers; (b) misdirected regrowth of fibers, so that functional reinnervation was not established, resulting in failure of development or retrograde atrophy and degeneration; or (c) cellular alterations at the site of injury or in the distal nerve which inhibited neural outgrowth or elongation or did not inhibit outgrowth but retarded or prevented maturation. We conclude that explanation (b) is involved, and that there is some evidence favoring the roles of (a) and (c).     

地震致头皮损伤感染伤口的分析

目的 探讨地震灾害引起的开放性头皮损伤伤口感染的原因、病原菌分布、药敏特点和治疗措施.方法 回顾分析5.12汶川地震后,四川大学华西医院各科收治的82例头皮伤口感染的临床和病原学资料.结果 全组82例患者中,43例(52.4%)被检出伤口感染.感染的伤口多数伴有严重污染及异物存留,并且首次清创时间明显延迟.感染的病原菌菌株59株,革兰阳性金黄色葡萄球菌26株(44.06%),表皮葡萄球菌12株(20.33%),革兰阴性的阴沟肠杆菌13株(22.06%),肺炎克雷伯杆菌3株(5.08%),深红沙雷氏菌5株(8.47%).经彻底清创,换药,应用敏感抗生素治疗后,伤口愈合良好.结论 地震引起的颅脑外伤头皮伤口感染率明显增高,以革兰阳性的金黄色葡萄球菌感染为主.早期彻底清创,营养支持,应用敏感抗生素能提高治疗效果.     

Posttraumatic stress reactions after single and double trauma

This study evaluated the severity and symptom profile of posttraumatic stress reactions of 202 adults exposed in 1988 to political violence in Azerbaijan and/or the earthquake in Armenia. High rates of severe posttraumatic stress reactions were found among the most highly exposed individuals, irrespective of the type of trauma. There was no difference in symptom profile for subjects exposed to earthquake versus violence. These similarities in severity and symptom profile may be attributable to common features of the exposures, which included experiencing life-threat and witnessing injury, mutilation and death. Recent prior exposure to violence contributed to the severity of reaction to the earthquake. The high rates of chronic and severe posttraumatic stress reactions in Armenia constitute a major public mental health problem.     

Recovery of Brightness Discrimination in Adult Rats despite Progressive Loss of Retrogradely Labelled Retinal Ganglion Cells after Controlled Optic Nerve Crush

Restoration of brightness discrimination was studied in adult rats after controlled crush of the optic nerve in order to further characterize a recently introduced experimental brain injury model. Mild, moderate or severe crush of the optic nerve produced partial or complete loss of the ability to perform a brightness discrimination task. Two to three weeks following mild injury we observed nearly complete spontaneous behavioural recovery whereas recovery was more limited after moderate and totally absent after severe crush. Horseradish peroxidase (HRP) injected into the superior colliculus was transported retrogradely across the lesion site and accumulated in retinal ganglion cells (RGCs). Two days following mild, moderate or severe crush, 28, 23 and 8% respectively of RGCs were found to be labelled with HRP, indicating that they are still connected with their target and are therefore presumably intact. RGC loss affected all areas of the retina homogeneously. At postoperative day 14, the number of morphologically'intact'RGCs declined even further to 11% in the mild injury group, despite our observation of recovery of vision to near-normal levels. The mechanism whereby such impressive neuronal plasticity is achieved despite the rather small number of intact RGCs is still unknown. However, further studies of the crush model using additional behavioural, morphological and electrophysiological techniques may allow us to determine more clearly the biological basis of recovery of function after central nervous system injury.     

急性颅脑损伤后血清内源性类洋地黄物质含量变化

目的 探讨颅脑损伤后血清内源性类洋地黄物质（ＥＤＬＳ）含量变化及其机理和临床意义。方法 采用放免法检测６３例急性颅脑外伤患者血清ＥＤＬＳ浓度变化,对其中１９便作动态观测,１６例行手术前后对比,２３例与预后进行相关分析。结果 不同程度脑外伤皇２４小时内血清ＥＬＤＳ均升高,以轻伤组最为典型;随着损伤程度的加剧,少数病例ＥＤＬＳ不变甚至下降,术后或随伤情的恢复,ＥＤＬＳ多同步下降,不同病病理类型的脑损伤