重型颅脑损伤开颅术中急性脑膨出原因及防治

急性脑膨出是外伤性颅脑损伤开颅术中较常遇到的问题,愈后较差.本院1995年至2003年,颅脑开颅术中发生急性脑膨出19例,分析其原因及防治措施.     

重型颅脑损伤开颅术中急性脑膨出的防治

目的探讨重型颅脑损伤开颅术中急性脑膨出的原因及对策。方法对120例重型颅脑损伤开颅术中急性脑膨出的原因、对策及预后进行回顾性分析。结果（1）迟发血肿65例，其中同侧脑内血肿10例，硬膜外血肿8例，对侧硬膜外血肿21例，硬膜下血肿10例，脑内血肿9例，大脑纵裂血肿7例；（2）急性弥漫性脑肿胀40例；（3）外伤性大面积脑梗死15例；（4）复合伤患者有30例。合并胸部、腹部及四肢骨折，有明显的低血压和低血氧症状；（5）术中操作不当，误诊误治10例。结论重型颅脑损伤开颅术中急性脑膨出的主要原因有迟发性颅内血肿，弥漫性脑肿胀，严重脑水肿，广泛脑梗死，术中操作不当，对病情的误诊误治，麻醉问题等。根据不同的原因进行正确处理，可以降低急性脑膨出的重残率及病死率。     

重型颅脑损伤术中急性脑膨出的原因及应对措施

目的探讨重型颅脑损伤术中急性脑膨出的原因及处理方法。方法回顾性分析21例重型颅脑损伤术中急性脑膨出患者的临床资料。结果术中急性脑膨出主要原因为迟发性颅内血肿13例,急性弥漫性脑肿胀4例,外伤性大面积脑梗死2例,广泛性脑挫裂伤1例,严重脑组织缺血缺氧1例;经对脑膨出原因综合处理后均关颅成功。术后给予综合治疗,格拉斯哥预后(GOS)标准评定,患者存活11例(52.4%),其中良好4例,轻残3例,中、重残3例,植物生存1例;死亡10例(47.6%)。结论术前准确评估、术中准确判断并及时处理,为重度颅脑损伤术中急性脑膨出有效防治措施,可减低致残及死亡率,改善患者预后。     

重型颅脑损伤开颅术中急性脑膨出防治策略

重型颅脑损伤开颅术中发生急性脑膨出，病情危重，病因复杂，处理棘手。过去一般认为，颅脑外伤术中发生脑膨出是急性脑肿胀引起的，死亡率几乎达100％。近15年来笔者加强了对颅脑外伤开颅术中急性脑膨出原因的观察研究，发现这种急性脑膨出，除急性脑肿胀外尚有很大一部分是由颅内迟发性异位血肿等其他原因引起。针对病因，结合综合治疗，疗效较好。现报告如下。     

重型颅脑损伤术中急性脑膨出的救治

目的探讨重型颅脑损伤开颅手术过程中出现急性脑膨出的原因与治疗方法。方法对78例重型颅脑损伤术中急性脑膨出患者进行回顾性调查,并对其原因、诊疗措施与预后进行分析。结果在重型颅脑损伤开颅手术过程中出现急性脑膨出．必须根据不同的发病原因分别采取相对应的治疗措施。只要条件允许,应先抓紧时间复查头颅CT,不宜盲目进行手术探查。不允许在原因未明的情况下盲目切除大块脑组织做内减压术或强行关颅。结论根据不同发病原因分析处理本病,有助于提高诊疗水平及改善预后。     

重型颅脑损伤术中急性脑膨出的分析

急性脑膨出是重型颅脑损伤手术中较常见的问题,预后差,死亡率高,术中处理比较棘手.本院1997年5月至2004年5月颅脑损伤病人术中出现急性脑膨出共21例,现分析报告如下.     

31例重型颅脑损伤术中急性脑膨出的防治

重型颅脑损伤开颅术中急性脑膨出较为常见，由于病情危重．若处理不当．往往预后不良．死亡率很高。本文回顾自1998年1月至2005年9月本院收录的31例术中出现急性脑膨出的重型颅脑损伤患者的临床资料．分析其形成原因并探讨防治措施．     

重度颅脑损伤术中急性脑膨出的成因及其防治

目的 探讨重度颅脑损伤术中急性脑膨出的形成原因及防治措施。方法 对手术中出现急性脑膨出的28例重度颅脑损伤病人进行回顾性分析并复习文献,总结其形成机理及诱发因素,易发疾病以及其防治方法和疗效。结果 急性硬膜下血肿伴严重广泛脑挫裂伤病人术中最易发生急性脑膨出。其主要原因为弥漫性脑肿胀;其次为颅内迟发性血肿;长时间脑疝、低血压、失血性休克、缺血缺氧等也是重要因素。早期施行气管内插管等保持呼吸道通畅,尽早手术及应用脱水剂、缓慢降低颅内压,术中适当控制血压,过度通气,清除颅内迟发性血肿及积极治疗其并发症,纠正全身缺血缺氧状态等是防治术中急性脑膨出的有效措施。结论 针对不同病因,早期积极采取相应防治措施,可有效地防治重型颅脑损伤术中脑膨出的发生,减少重残率和死亡率。     

重型颅脑损伤术中脑膨出原因分析及防治措施

术中急性脑膨出是重型颅脑损伤术中常见而严重现象，临床并非少见，其预后较差。国内外资料显示，重型颅脑损伤术中急性脑膨出的病死率高达70％。因此，对术中急性脑膨出进行原因分析及采取相应的防治措施显得十分必要。     

112例重型颅脑损伤术中急性脑膨出的诊治体会

目的 探讨重型颅脑损伤开颅术中急性脑膨出的原因、防治措施与预后关系. 方法 回顾性分析本院近年来收治的112例重型颅脑损伤开颅术中急性脑膨出病例的临床资料,总结其原因和防治经验. 结果 迟发性颅内血肿、弥漫性脑肿胀是颅脑损伤术中急性脑膨出的主要原因.术后6个月根据格拉斯哥预后评分（GOS）评定：恢复良好20例,中残14例,重残16例,植物生存14例,死亡48例,死亡率42.9％. 结论 正确认识重型颅脑手术中急性脑膨出的原因,采取各种措施积极降低颅内压,提高生存率,改善预后.     

超声在颅脑损伤术中急性脑膨出时的应用

目的探讨超声检查在重型颅脑损伤开颅术中急性脑膨出时应用价值。方法比较重型颅脑损伤开颅术中出现脑膨出时行床边超声检查组与CT检查组．对比分析两组发现颅内再出血阳性率、开颅手术时间及6月后功能恢复的差异。结果超声检查组与CT检查组在发现颅内再出血阳性率无显著性差异（x2=0．183,P〉0．05）;超声检查组手术时间显著低于CT检查组（x^2=4．861,P〈O．05）;超声检查组术后神经功能恢复显著优于CT检查组（x^2=6．593,P〈O．05）。结论术中超声检查可及时判断急性脑膨出的原因,并为清除颅内血肿实施导向,能避免遗漏血肿、缩短手术时间,对提高手术效果、改善患者预后有重要临床意义。     

双侧开颅在重型颅脑损伤术中急性脑膨出的应用

目的 探讨重度颅脑损伤急性脑膨出的原因及最佳治疗方案.方法 回顾性分析26例采用双侧开颅治疗重度颅脑损伤术中急性脑膨出患者的临床资料.结果 恢复良好4例,中残5例,重残2例,植物生存3例,死亡12例.结论 迟发性颅内血肿和急性弥漫性脑肿胀是颅脑损伤开颅术中急性脑膨出的主要原因,而采用双侧开颅可明显提高抢救成功率和患者的生存质量.     

创伤性结肠损伤的特点及诊治体会

目的探讨创伤性结肠损伤的特点和救治体会。方法回顾分析我院1995年1月~2003年12月结肠外伤48例的临床资料。结果结肠损伤中刀刺伤占71%,腹部钝性伤占25%,火器伤4%。合并多发伤或多脏器伤35例,一期修补或切除吻合46例,结肠局部切除 近端造口2例,手术死亡1例,十二指肠损伤漏诊1例,术后死亡3例,切口感染及脂肪液化7例,严重腹腔感染3例。结论结肠损伤以开放性穿透性损伤为多见,常伴有其他脏器伤,且结肠损伤具有一定的隐匿性,易误诊、漏诊,引起严重感染,影响愈合。治疗上强调尽早手术,术中探查应全面仔细,谨防遗漏,一期修补或切除吻合对绝大多数结肠损伤是安全可靠的。     

Nimodipine in traumatic subarachnoid haemorrhage: A re-analysis of the HIT I and HIT II trials

Summary Two large randomised controlled trials have been performed to study the effect of the calcium antagonist nimodipine on the outcome of severe head injury, HIT I [1] amd HIT II [4]. Both trials showed a modest and statistically non-significant increase in the proportion of favourable outcomes in patients treated with nimodipine. A subgroup analysis of the HIT II trial [4, 5] suggested, however, that there could be a substantial protective effect of nimodipine in patients with traumatic subarachnoid haemorrhage (SAH). This report provides a re-analysis of the HIT I data to see whether it provides confirmatory evidence of the subgroup effect observed in HIT II. This involved performing a central review of the CT scans for the HIT I patients, to identify those individuals with evidence of traumatic SAH. The sample size was small, but the HIT I data gave no support to the hypothesis that nimodipine is protective in the traumatic SAH subgroup, where 69% of patients had a poor outcome on placebo and 74% of patients had a poor outcome on nimodipine. The data do not exclude the possibility of a clinically relevant beneficial effect of nimodipine in the traumatic SAH subgroup, but further data are required to provide a definitive answer.In addition, we present a pooled analysis of the data from the two trials, which suggests that the overall benefit of treating unselected head injured patients with nimodipine is unlikely to be clinically relevant.     

Mild traumatic brain injury and anxiety sequelae: a review of the literature

There is scattered but significant psychological and neuropsychological evidence to suggest that mild traumatic brain injury (mild TBI) plays a notable role in the emergence and expression of anxiety. Conversely, there is also empirical evidence to indicate that anxiety may exert a pronounced impact on the prognosis and course of recovery of an individual who has sustained a mild TBI. Although the relationship between mild TBI and anxiety remains unclear, the present body of research attempts to elucidate a number of aspects regarding this topic. Overall, the mild TBI research is rife with inconsistencies concerning prevalence rates, the magnitude and implications of this issue and, in the case of PTSD, even whether certain diagnoses can exist at all. This review obviates the need for greater consistencies across studies, especially between varying disciplines, and calls for a shift from studies overly focused on categorical classification to those concerned with dimensional conceptualization.     

Prediction of the level of cognitive functional independence in acute care following traumatic brain injury

Primary objective: To determine a predictive model for cognitive functional outcome of patients with traumatic brain injury (TBI) at discharge from acute care.

Methods and procedure: Three hundred and thirty-five patients were included in this analysis. Variables considered were age, education, initial score on the Glasgow Coma Scale (GCS), duration of post-traumatic amnesia (PTA), cerebral imaging results and the need for neurosurgical intervention.

Experimental interventions: Functional Independence Measure (FIM).

Main outcomes and results: Results of this analysis indicated better cognitive FIM at discharge from acute care settings for patients with TBI when PTA was less than 24 hours, when level of education was higher, when no parietal lesion was identified, when no neurosurgical intervention was required, for patients with TBI who were younger and who presented with a higher GCS score upon admission.

Conclusions: This model will help to plan resource allocation for treatment and discharge planning within the first weeks following TBI.     

The incidence of acute kidney injury in patients with traumatic brain injury

There is limited information on the incidence of acute kidney injury (AKI) in patients with traumatic brain injury (TBI) although AKI may contribute to morbidity and mortality. We investigated the incidence of AKI in patients with moderate and severe TBI and the association of AKI with risk factors and outcomes in these patients.

We studied all TBI patients over 16 years of age admitted to the two designated trauma hospitals in the state of Victoria, Australia from 1 January to 31 December 2008. Patients were included if they had head trauma and presented with a Glasgow coma scale (GCS) <13. Prospectively collected data from the hospital trauma registries, ICUs, and pathology databases were analyzed retrospectively. Risk injury failure loss end (RIFLE) criteria were used to categorize renal function.

The incidence of AKI was 9.2% (19/207). Patients who developed AKI were older, had higher severity of illness scores, and a lower GCS. Overall 42.1% of these patients died in hospital compared with 18.1% in patients without AKI. In univariable linear regression analysis, age, severity of illness, and admitting hospital were associated with AKI. After multivariable logistic regression, the occurrence of AKI was associated with age (p < 0.001) and higher APACHE III scores (p = 0.016).

AKI is relatively common even in patients with TBI. Its association with age and APACHE III scores helps identify patients at higher risk of AKI.     

Comparison of functional outcome following acute care in young, middle-aged and elderly patients with traumatic brain injury

Primary objective: To compare functional physical and cognitive outcome of patients in three age groups with mild, moderate and severe traumatic brain injury (TBI) at discharge from acute care.

Research design: Retrospective database review.

Methods and procedures: Scores on the Extended Glasgow Outcome Scale (GOSE) and on the FIM™ instrument,1 discharge destination and length-of-stay (LOS) were gathered and compared for 2327 patients with TBI admitted to a level 1 trauma hospital from 1997-2003 divided into three age groups; 971 patients between 18-39 years, 672 between 40-59 years and 684 aged 60-99 years.

Main outcomes and results: Relative to younger adults with similar TBI severity, elderly patients showed worse outcome on the GOSE and FIM™ instrument (physical and cognitive ratings) and longer LOS. No difference was observed between the young and middle-aged groups except for cognitive FIM™ ratings and LOS for severe TBI. A higher percentage of elderly patients went to in-patient rehabilitation, to long-term care facilities or died compared to young and middle-aged patients. A higher number of young and middle-aged patients were discharged home.

Conclusions: Further development of services in early rehabilitation as well as post-rehabilitation geared to the specific needs of the elderly patient with TBI is required as the population ages.     

Short-term lack of cerebral perfusion with good outcome. Advantages of early intracranial pressure monitoring

A 21-year-old man was injured by a tailboard of a truck. He suffered a severe head injury with bilateral depressed skull fractures necessitating surgical decompression. On admission to the hospital the patient showed bending to pain stimuli (Glasgow Coma Score 5). Anisocoria was noticed from the beginning. Initial intracranial pressure (ICP), measured 3 hours after injury, was 30 mm Hg, and the cerebral perfusion pressure (CPP) was 70 mm Hg. During surgical elevation of the skull fracture on the right side an unexplainable rise of ICP to values of 100 mm Hg occurred, which corresponded to the mean arterial blood pressure (MAP). At the same time both pupils were dilated and fixed indicating a lack of cerebral perfusion. Due to immediate trephination of the opposite side, the ICP was lowered to values below 20 mm Hg, and sufficient cerebral perfusion (above 50 mm Hg) was regained. The patient showed a good recovery and was transferred to a rehabilitation center 5 weeks after injury.This case report emphasizes the importance of early and continuous intracranial pressure monitoring for adequate therapy in neurosurgical emergencies.