外伤后急性半球脑肿胀的手术治疗

目的 探讨外伤后急性大脑半球肿胀（ACHS）的治疗效果以及影响疗效的主要因素.方法 对38例外伤后急性半球脑肿胀病人的资料进行回顾性分析.所有患者均接受了去骨瓣减压手术.结果 大骨瓣减压术后,CT影像显示脑中线结构无明显移位、环池结构清晰.术后6个月按GOS评分标准评估：良好14例（占36.8%）、中残9例（占23.7%）、重残5例（占13.2%）、植物生存4例（占10.5%）、死亡6例（占15.8%）.结论 早期去骨瓣减压手术可改善患者预后,而脑肿胀合并急性硬膜下血肿、手术后出血性脑挫伤处血肿量明显增加以及出现创伤后大面积脑梗死的患者预后较差.     

重型颅脑损伤并发急性呼吸窘迫综合征的高危因素及综合治疗

目的 分析重型颅脑伤继发急性呼吸窘迫综合征(ARDS)的高危因素,根据高危因素采取综合治疗措施.方法 对我科近5 年来28 例重性颅脑损伤合并ARDS 的病人资料进行回顾性分析,对患者发病的高危因素及治疗方法 进行讨论.结果 28 例患者均诊断明确,16 例抢救成功,12 例死亡.结论 重型性颅脑损伤后并发ARDS ...     

去骨板减压术治疗的重型颅脑损伤出院时预后的影响因素

目的 探讨重型颅脑损伤去骨瓣减压术后出院时预后的影响因素。方法 回顾性分析2014年5月至2019年5月收治的150例重型颅脑损伤的临床资料,均行去骨板减压术治疗。出院时,根据GOS评分评估预后,4~5分为预后良好,1~3分为预后不良。采用多因素logistic回归分析检验预后影响因素。结果 150例中,出院时预后良好39例,预后不良111例。多因素logistic回归分析结果显示,入院时APACHEⅡ评分低、无瞳孔散大及入院时GCS评分较高及气管切开术是预后良好的独立评估指标（P<0.05）。结论 重型颅脑损伤病人预后影响因素很多,对于入院时APACHEⅡ评分较高、瞳孔散大、入院GCS评分较低的病人,应及早采取措施干预,以改善病人预后;另外,重型颅脑损伤建议尽早进行气管切开术     

重型颅脑损伤死亡相关因素分析

目的总结重型颅脑损伤患者的死亡率,探讨死亡的相关因素。方法建立颅脑损伤数据库,总结我科2000年1月至2005年12月之间收治的重型颅脑损伤患者的临床诊疗情况,并对影响患者死亡的相关临床特点进行比较分析。结果213例重型颅脑损伤患者中,车祸致伤152例(71.4%),手术103例(48.4%),其中血肿清除加标准大骨瓣减压术75例。GCS 3～5分患者死亡率61.2%,GCS 6～8分患者死亡率19.1%,总死亡率39.4%。外院转入99例(46.5%)。直接来院及入院时间在4h以内的患者死亡率明显下降。血糖明显升高(>13mmol/L)、上消化道出血和严重的低氧血症可以增加患者死亡率,尤其是晚期死亡者。结论在强化现场急救、规范住院治疗的基础上,完善转诊机制、减少转院、缩短入院时间,对降低重型颅脑损伤死亡率、尤其是早期(24h之内)的死亡,有重要意义。加强继发性损伤的治疗、预防并及时准确处理并发症,可以降低患者的中晚期死亡率。     

重型颅脑损伤并发脑梗死的危险因素分析

目的探讨重型颅脑损伤并发脑梗死的危险因素,为临床诊治提供参考。方法回顾性分析2015年1月至2016年12月收治的符合标准的172例重型颅脑损伤的临床资料,采用多因素Logistic回归分析检验危险因素。结果 172例中,44例并发脑梗死,128例无脑梗死。多因素Logistic回归分析表明脑疝、弥漫性脑肿胀、失血性休克是重型颅脑损伤并发脑梗死的独立危险因素。结论对于伴有脑疝、弥漫性脑肿胀、失血性休克的成人重型颅脑损伤,临床应注意防止脑梗死。     

重型颅脑损伤病人创伤后应激障碍的风险因素分析

目的 探讨重型颅脑损伤病人并发创伤后应激障碍（PTSD）的危险因素。方法 回顾性分析2020年1月至2022年2月收治的110例重型颅脑损伤的临床资料。出院前采用PTSD自评量表（PTSD-SS）评估PTSD情况,总分≥50分表示存在PTSD。结果 110例PTSD-SS评分总分（49.64±7.29）分,其中≥50分52例（47.27%）。多因素logistic回归分析显示,女性、低龄、家庭人均月收入低、非亲属照顾、无经济赔偿、合并颅内感染为重型颅脑损伤并发PTSD的独立影响因素（P<0.05）。根据多因素logistic回归分析结果构建PTSD列线图显示一致性指数为0.886,预测PTSD具有较高的应用价值。结论 重症颅脑损伤病人并发PTSD的风险较高,女性、年轻病人、收入低、非亲属照顾、无经济赔偿、合并颅内感染等因素会增加PTSD发生风险,临床应密切关注,识别PTSD风险因素,并给予有效的防治措施降低PTSD发生率。     

中重度颅脑损伤继发急性脑梗死的相关危险因素和预后分析

目的探讨中重度颅脑外伤患者继发急性外伤性脑梗死(PTCI)的危险因素和预后。方法回顾性分析218例中重度颅脑外伤患者的临床资料,其中27例伤后1周内出现PTCI。通过多因素Logistic回归分析,分析患者的性别、年龄、入院格拉斯哥昏迷量表(GCS)评分、是否合并脑疝、颅内压、血压、血气分析中CO2值、DIC评分、是否合并感染、有无实施去骨瓣减压术共10个因素与PTCI的关系,以及对患者预后的影响。结果经过统计学分析,患者的入院GCS评分、合并脑疝、颅高压、低血压、DIC评分是发生PTCI的独立危险因素,而年龄、性别、CO2值、合并感染以及有无实施去骨瓣减压术与PTCI无明显相关性。入院GCS评分低(3~5分)、合并脑疝、低血压、DIC评分≥5分、合并感染、继发PTCI是患者预后不良的独立预测因素。结论中重度颅脑外伤患者入院GCS评分、合并脑疝、颅高压、低血压、DIC评分是发生PTCI的独立危险因素;入院GCS评分低、合并脑疝、低血压、DIC评分≥5分、合并感染、继发PTCI的患者预后差,致残率高。     

Central nervous system microbleeds in the acute phase are associated with structural integrity by DTI one year after mild traumatic brain injury: A longitudinal study

Introduction

Several imaging modalities are under investigation to unravel the pathophysiological mystery of delayed performance deficits in patients after mild traumatic brain injury (mTBI). Although both imaging and neuropsychological studies have been conducted, only few data on longitudinal correlations of diffusion tensor imaging (DTI), susceptibility weighted imaging (SWI) and extensive neuropsychological testing exist.

重型颅脑损伤术后发生脑积水的危险因素分析

目的探讨重型颅脑损伤患者术后脑积水发生的危险因素。方法回顾性分析手术后276例重型颅脑损伤手术患者的临床资料。随访6个月后根据脑积水诊断标准,分为脑积水组(47例)和非脑积水组(229例),采用单因素分析和逐步Logistic回归分析,比较两组患者颅内脑挫裂伤、脑室出血、硬膜下血肿、硬膜外血肿、颅骨损伤、颅骨线型骨折、脑脊液蛋白水平及压力等因素。结果随访结果显示,重型颅脑损伤患者术后脑积水发生率为17.03%(47/276);单因素分析结果显示脑积水组和非脑积水组在年龄、脑室出血、硬膜下血肿、昏迷(有无、持续时间)、格拉斯哥昏迷评分(Glasgow Coma Scale,GCS)、去骨瓣减压术、创伤性蛛网膜下腔出血(traumatic subarachnoid hemorrhage,tSAH)、加尔维斯顿定位和失忆测试(Galveston Orientation and Amnesia Test,PTA)、功能独立性测评(Function Independent Measure,FIM)的差异均有统计学意义(P0.05);Logistic回归结果显示高龄、硬膜下血肿、昏迷时间长、GCS低分值,去骨瓣减压术与重型颅脑创伤后的脑积水的发生显著正相关。结论高龄、有硬膜下血肿、GCS评分低、接受去骨瓣减压术是重型颅脑创伤后脑积水的危险因素。     

重型颅脑损伤标准去骨瓣减压术后30 d内死亡的危险因素分析

目的 探讨重型颅脑损伤标准去骨瓣减压术后30d内死亡的危险因素.方法 回顾性分析2016年9月至2019年9月采用标准去骨瓣减压术治疗的145例重型颅脑损伤的临床资料.采用多因素logistic回归分析检验术后30 d内死亡的危险因素.结果 145例中,术后30 d内死亡43例,存活102例.多因素logistic回归...     

亚低温对重型颅脑创伤合并急性创伤性凝血病影响的临床研究

目的 研究亚低温对重型颅脑创伤(sTBI)合并急性创伤性凝血病(ATC)患者的影响及其临床意义.方法 83例sTBI合并AT℃患者随机分为亚低温治疗组42例、常规治疗组(对照组)41例.亚低温治疗组均于伤后24h内接受亚低温治疗.分别测量两组患者不同时间点的凝血酶原时间(PT)、部分凝血酶原时间(APTT)、凝血时间(TT)、纤维蛋白原(FIB)及D-二聚体水平,同时监测患者颅内压(ICP)以及生命体征、血气、血电解质及动脉血氧饱和度等,并根据GOS评估法判断预后.结果 亚低温治疗组患者PT、APTT、TT、FIB及D-二聚体与对照组相比差异无统计学意义(P＞0.05),而颅内压明显降低(P＜0.01);生命体征、血气、血电解质、动脉血氧饱和度差异无统计学意义,无严重并发症,病死率低,预后改善明显.结论 亚低温治疗不会增加sTBI合并ATC患者出现凝血障碍及纤溶亢进的风险,并且能有效地降低颅内压,具有肯定的脑保护作用,是一项安全有效的治疗措施.     

神经外科重型颅脑创伤急性期血压变异性对患者近期预后的影响研究

目的探讨神经外科重型颅脑创伤(TBI)急性期血压变异性对患者近期预后的影响。方法选取110例重型TBI患者作为研究对象,根据格拉斯哥预后(GOS)评分分为预后良好组(n=53)和预后不良组(n=57),对两组患者术后3d内的血压变异性进行对比分析。结果预后良好组的平均年龄明显低于预后不良组,GCS评分、APACHEⅡ评分均明显高于预后不良组,P0.05。预后良好组入院24h的收缩压标准差、舒张压标准差、收缩压变异系数均显著低于预后不良组,入院72h的收缩压标准差、舒张压标准差、收缩压变异系数、舒张压变异系数均显著低于预后不良组,P0.05。APACHEⅡ评分是患者预后的保护因素,TBI程度、72h SD(SBP)是患者预后的危险因素。结论急性期血压变异性与重型TBI患者的预后密切相关,其影响患者预后的独立危险因素。     

脑创伤患者预后的影响因素及与凝血酶-抗凝血酶复合物的相关性

目的 分析脑创伤患者预后的影响因素及其与术前凝血酶-抗凝血酶（TAT）复合物的相关性。方法 分析2019年1月—2021年1月在漯河市中心医院进行治疗的70例颅脑创伤患者,依据术后30 d内患者是否死亡将其分为生存组（n=48）和死亡组（n=22）,分析颅脑创伤患者死亡的影响因素,并分析术前TAT复合物水平与各影响因素的相关性及术前TAT复合物水平对颅脑创伤患者死亡的预测价值。结果 年龄大于等于60岁、受伤至手术时间小于10 h、入院格拉斯哥昏迷量表（GCS）评分小于5分、术前TAT复合物大于100 ng/mL、空腹血糖（FBG）大于10 mmol/L、手术时间≥大于等于3 h为颅脑创伤患者死亡的危险因素（P＜0.05）。术前TAT复合物水平与患者年龄、FBG水平和手术时间均呈正相关（P<0.05）,与受伤至手术时间、入院GCS评分均呈负相关（P<0.05）。术前TAT复合物水平对颅脑创伤患者死亡的受试者工作特征曲线下面积（AUC）为0.79,95％CI为0.723~0913,P<0.001,敏感度为80.32％,特异度为74.06％,最佳截断值为100 ng/mL,具有较佳的预测价值。结论 TAT复合物水平为颅脑创伤患者死亡的影响因素,且与其他一些影响因素存在相关性,对颅脑创伤患者死亡有较佳的预测价值。     

Neuropsychological support to relatives of patients with severe traumatic brain injury in the sub-acute phase

Many studies have reported emotional distress in relatives of patients with brain injury, but few studies have investigated neuropsychological interventions for relatives. The present study assessed the amount of neuropsychological support as well as the actual number of sessions with a neuropsychologist during rehabilitation in a sub-acute unit. The study also examined whether the amount of support was related to the condition of the patient or the relative at admission. The sample consisted of 26 patients and their closest relative, and measures included demographic variables as well as characteristics related to the patient: Glasgow Coma Scale, Injury Severity Score, Early Functional Abilities, Functional Independence Measure, Rancho Los Amigos; and to the relative: symptoms of anxiety and depression (SCL-90-R), quality of life (SF-36) and amount and number of sessions of neuropsychological support. On average, the relatives received about 18 units of 15 minutes and had six sessions with a neuropsychologist during hospitalisation. A total of 38% participated in group sessions. Relatives' symptoms of anxiety at admission were associated with the number of sessions as well as the amount of support, indicating that relatives with more symptoms of anxiety received more support during the hospitalisation.     

Endothelial dysfunction in acute brain injury and the development of cerebral ischemia

Cerebral ischemia (CeI) is a major complicating event after acute brain injury (ABI) in which endothelial dysfunction is a key player. This study evaluates cellular markers of endothelial function and in vivo reactive hyperemia in patients with ABI and their relationship to the development of cerebral ischemia. We studied cellular markers of endothelial dysfunction and the peripheral reactive hyperemia index (RHI) in 26 patients with ABI at admission and after 6 and 12 days, and compared these with those of healthy volunteers (n = 15). CeI was determined clinically or by computer tomography. In patients with ABI, RHI at admission was significantly reduced compared with healthy subjects (P = 0.003), coinciding with a decrease in circulating endothelial progenitor cells (EPC; P = 0.002). The RHI recovered in eight patients without development of CeI, but failed to fully recover by day 12 in three of four patients who developed CeI. Despite recovery of the RHI within 12 days in these patients (P = 0.003), EPC count remained significantly lower after 12 days in patients with ABI (P = 0.022). CD31⁺ T cells and endothelial microparticles were not different between controls and patients. No differences were noted in cellular markers of endothelial dysfunction in patients developing CeI and those not. In conclusion, patients with ABI exhibit impaired microvascular endothelial function measured as RHI and a decreased circulating level of EPC. © 2015 Wiley Periodicals, Inc.     

87例重症颅脑外伤患者急诊救治临床效果分析

目的：探讨重症颅脑损伤患者的急诊救治措施。方法将174例重度颅脑损伤患者随机分成对照组和观察组各87例。对照组采用常规急诊救治措施,观察组进行综合急救治疗。比较治疗前与治疗3、7 d后2组患者脑血流（Vm、PI、RI）变化,比较2组预后。结果治疗后第3、7天2组患者脑血流供应均有一定改善,其中观察组Vm、PI显著高于对照组,而RI显著低于对照组,P＜0·05。治疗3个月后,观察组生存率显著高于对照组,P＜0·05;观察组ADL分级为Ⅰ级和Ⅱ级的比例显著高于对照组,为Ⅳ级显著低于对照组,P＜0·05。结论采用综合的急诊救治措施治疗重症颅脑外伤患者能有效提高生存率并改善预后。     

Effects of closed traumatic brain injury and genetic factors on the development of Alzheimer's disease

In order to assess the impact of traumatic brain injury (TBI) and Apolipoprotein E (ApoE) allele frequency on the development of Alzheimer's disease (AD), we examined: (i) the incidence of AD pathology in 55 consecutive autopsy cases (mean age +/- SD 77.6 +/- 7.3 years) with residual closed TBI lesions and (ii) the frequency of TBI residuals in 53 age-matched autopsy proven AD cases. In both series, ApoE was evaluated from archival paraffin-embedded brain material. The results were as follows: (i) In the TBI series, 12.7% showed Consortium to Establish a Registry for Alzheimer's disease (CERAD) definite and 9.1% probable AD, only one with ApoEepsilon4. From the remaining 43 non-AD cases, three had ApoEepsilon4. The prevalence of 21.8% AD in this small autopsy cohort was significantly higher than 3.3% in a recent large clinical series and 14% in the general population over the age of 70. (ii) In the AD cohort with ApoEepsilon4 allele frequency of 30% similar to other AD series, residuals of TBI were seen in 4 brains (7.5%), all lacking the ApoEepsilon4 allele. TBI incidence was slightly higher than 8.5% in the clinical MIRAGE study. The results of this first retrospective autopsy study of TBI, ApoE allele frequency, and AD confirms clinical studies suggesting severe TBI to be a risk factor for the development of AD particularly in subjects lacking ApoEepsilon4.     

颅脑损伤患者深静脉血栓形成的危险因素分析及预防方法

目的探讨颅脑损伤患者深静脉血栓(DVT)形成的高危因素及预防方法。方法对3 6 2例颅脑损伤患者伤后每间隔1 0 d检查一次下肢血管彩超,发现DVT后给予及时治疗。对发生DVT与未发生DVT的患者进行年龄、疾病、卧床时间、性别等各因素的患病率进行对照分析。结果 3 6 2例患者发现DVT 4 8例,DVT患肢6 3侧,DVT患病率高血压者为1 7.5 0%(2 8/1 6 0),无高血压者9.9 0%(2 0/2 0 2),年龄<6 0岁者1 0.7 1%(3 3/3 0 8),>6 0岁者2 7.7 8%(1 5/5 4),糖尿病者2 5.3 0%(2 1/8 3),无糖尿病者9.6 8%(2 7/2 7 9);瘫痪肢体2 2.9 2%(4 4/1 9 2),未瘫痪肢体3.5 7%(1 9/5 3 2),卧床≤1 0 d时DVT患病率2.2 1%(8/3 6 2),≤2 0 d时7.4 6%(1 7/2 2 8),≤3 0 d时1 2.1 2%(2 4/1 9 8),≤4 0 d时2 4.4 3%(3 2/1 3 1),≤5 0 d时3 9.8 1%(4 3/1 0 8)。结论颅脑损伤患者DVT的发生与年龄、血压、血糖、肢体活动度、卧床时间等密切相关,与性别关系不大。高龄、高血压史、糖尿病史、瘫痪肢体、卧床时间>1 0 d等均是形成DVT的高危因素,而且卧床时间越长,形成DVT的风险越大。     

Temporal and egional profiles of cytoskeletal protein accumulation in the rat brain following traumatic brain injury

Abstract To characterize the cytoskeletal aberration due to traumatic injury, temporal and regional profiles of changes in immunoreactivity of microtubule-associated protein 2 (MAP2), neurofilament heavy subunit protein (NFH) and heat shock protein 72 (HSP72) were investigated after different magnitudes of traumatic brain injury by fluid percussion. The experimental rat brain was perfusion-fixed at 1, 6 and 24 hours after traumatic brain injury. Conventional histological staining has demonstrated that the mildest traumatic brain injury (1.0 atm) induced no neuronal loss at the impact site and that neuron loss was apparent when traumatic brain injury was increased to 4.3 atm. The mildest traumatic brain injury, however, caused a significant increase in HSP72 immunoreactivity in the superficial cortical layers at the impact site as early as 1 hour after the injury. In the case of severe traumatic brain injury (4.3 atm), neuron loss was apparent in the area at the impact site, but the increase in HSP72 immunoreactivity was moderate, and it was observed only after 6 hours in the deep cortical layers under the necrotic area. The increased immunostaining of MAP2 was demonstrated in damaged axons and neuronal perikarya in the wider area surrounding the impact site at 6 and 24 hours after the injury. Six and 24 hours after the injury, perikaryal accumulation of neurofilament was observed, and the accumulated neurofilament was mostly phosphorylated. These results indicate that the severe traumatic brain injury of 4.3 atm triggers the abnormal accumulation of cytoskeletal proteins in neuronal perikarya, most probably due to an impairment of axonal transport. It is implied that the increased expression of HSP72 may be involved in the protective process of neurons after traumatic brain injury.     

标准大骨瓣开颅减压术治疗重型颅脑损伤和大面积脑梗死(附49例报告)

目的探讨标准大骨瓣减压术治疗重型颅脑损伤和大面积脑梗死的临床效果。方法回顾性的分析2006年1月至2011年1月标准大骨瓣开颅减压术治疗的38例重型颅脑损伤和11例大面积脑梗死患者临床资料。结果出院时按GOS分级,38例重型颅脑损伤患者中,GOSⅠ级15例,Ⅱ~Ⅲ级4例,Ⅳ~Ⅴ级19例。11例大面积脑梗死患者中,GOSⅠ级4例,Ⅱ~Ⅲ级1例,Ⅳ~Ⅴ级6例。结论标准大骨瓣减压术是治疗重型颅脑损伤和大面积脑梗塞的有效方法。