高压氧治疗颅脑损伤致脑室积气一例

临床资料:患者,男,20岁,因车祸伤后昏迷2 h就诊,诊断为左额颞硬膜下血肿、左额颞叶脑挫伤、蛛网膜下腔出血.急诊行左额颞硬膜下血肿清除术、去骨瓣减压术.术后患者清醒,并于术后1个月开始行高压氧治疗及康复治疗,患者病情逐渐恢复.高压氧治疗1个月后,复查头CT示:颅骨呈术后改变,颅脑损伤恢复期,未见颅内积气.患者出院后继续在门诊行高压氧治疗.     

飞行员头部外伤后坐过山车致颅内硬膜下血肿一例

一、临床资料 患者,男性,35岁,运-8飞行员,飞行时间1000 h.2011年1月2日乘坐单位大巴车外出,因急刹车右侧颞顶部碰撞到前座后背,当时无头痛、头晕,无意识障碍,局部无红肿、头皮撕裂,未就诊.2月6日陪孩子坐过山车,头部无碰撞伤.2月7日排便时感头痛、头昏,站立不稳,自行休息后减轻,但头痛、头昏持续存在,且逐渐加重.2月14日到体系医院就诊,头颅CT示:右侧额颞顶部亚急性硬膜下血肿.查体:四肢自主活动,肌力左右侧、上下肢均正常.血尿便常规、空腹血糖、血脂均正常.ECG示:窦性心动过缓,心率49次/min.入院后脱水治疗,行硬膜下血肿钻孔引流术.     

颅脑外伤伴迟发性颅内血肿32例临床分析

外伤性迟发性颅内血肿(delayed traumatic intracerebral hematoma,DTICH)是指头部外伤后首次CT检查未发现颅内血肿,经过一段时间后再次检查而发现血肿,或清除颅内血肿后复查在不同部位又出现血肿者,临床上其发生率较低,但因病情进展隐匿,易延误诊治.密切观察病情变化并及时复查头颅CT是诊治本病的关键.武警江苏总队医院神经外科2004年6月- 2008年6月共收治DTICH 32例(占同期颅脑损伤的6.8%),现对病历资料回顾性分析如下.     

慢性硬膜下血肿术后并发短期运动性失语1例

病例男性,58岁,汉族,1个月前存在雪地行走摔伤,左颞顶部首先触地,硬冰路面,当时头颅 CT提示未见明显异常;5d前感头部胀痛,休息后无缓解,间断出现恶心,进行性加重;入院前1 d头颅CT提示“左额颞顶部慢性硬膜下血肿”,并以该诊断收住入院。积极术前准备后,在局麻下行“左额颞顶部慢性硬膜下血肿钻孔冲洗引流术”,手术顺利。术后第1d下午突然出现言语含混不清,右下肢功能障碍,恶心、呕吐胃内容物1次,量多,查体发现右侧病理征阳性,急查头颅CT提示“左侧脑实质结构不甚均匀,内囊后肢及颞叶局部密度减低模糊,CT值约26 HU,同侧额颞部及枕顶部有小弧形低密度影,左侧侧脑室变窄中闭塞,中线结构向右略移位”。     

迟发性颅内血肿的CT检查

目的:分析迟发性颅内血肿的临床表现、CT复查指征及预后。对象与方法:36例颅脑外伤后临床症状进行性加重的迟发性颅内血肿患者均经CT复查,并与第1次CT检查所见比较。结果:经CT复查发现36例颅内血肿,其中,脑内血肿16例(19个病灶),硬膜下血肿7例(伴蛛网膜下腔出血1例),硬膜外血肿9例,以及混合性血肿4例。结论:当颅脑外伤病人临床症状进行性加重时,择期进行CT复查可以发现第1次CT检查未发现的颅内血肿。     

跨窦骨瓣开颅术治疗骑跨静脉窦硬膜外血肿

目的 探讨骑跨静脉窦硬膜外血肿的手术治疗策略及疗效.方法 对43例骑跨静脉窦硬膜外血肿病例的临床资料、手术方式和预后进行回顾性分析.43例患者均采用跨窦骨瓣开颅,骨瓣复位,窦旁(周)硬脑膜悬吊于骨瓣相应位置的骨孔上.结果 43例术后第3、6天头部CT扫描显示血肿无复发、无残留,骨瓣无移位.出院时GOS预后评分:术后死亡1例,重度残疾1例,中度残疾2例,恢复良好39例.结论 跨窦骨瓣开颅术是治疗骑跨静脉窦硬膜外血肿的一种安全而且有效的方法.     

颅脑外伤后颅内并发症86例分析

我院自1995～1998年共收治颅脑外伤后颅内并发症病人86例,其中迟发性血肿58例,硬膜下积液6例,外伤性血管闭塞20例,脂肪栓塞2例。现报告如下。临床资料一般资料：本组男63例,女23例,年龄1～76岁,平均38．3岁。致伤原因：车祸致伤61冽,摔伤10例,坠落伤11例,打击伤4例。7例合并胸腹外伤,9例合并四肢骨折。受伤至入院时间为2～17小时,出现迟发性神经系统症状的时间为受伤后5小时～15天,均经头颅CT复查证实有颅内并发症的发生。并发症的部位及类型：58例迟发血肿中硬膜外37例、硬膜下13例、脑内8例;6例硬膜下积液均集中于额颞顶部…     

额颞部巨大蛛网膜囊肿1例处理体会

1 临床资料患者,男,18岁,以“5公里跑步后头痛、恶心2小时”人院。查体:神志清,精神差,表情痛苦疲惫,语言正常,四肢肌力、肌张力正常,生理反射存在,病理反射未引出。头颅CT示:左额颞部颅骨下方巨大低密度混杂阴影,形状不规则,量约200ml。CT报告:左额颞部巨大硬膜下血肿,考虑诊断:左额颞部巨大蛛网膜囊肿并囊内出血。急诊行硬膜下血肿钻孔引流术。近血肿底边(颞底)钻孔,术中引流出血性液体约200 ml,生理盐水反复冲洗血肿腔,术后引流管持续引流。患者第2天感头痛、头晕、烦躁,复查头颅CT示:除原硬膜下空     

飞行员副鼻窦炎致眶尖综合征2例护理体会

1 临床资料 病例1,男,29岁,歼击机飞行员,受凉后出现咽痛、鼻塞、鼻腔内异物感。抗感冒治疗好转。数日后出现左颞顶部剧烈疼痛,左眼胀痛、复视。于1993年5月21日住我院。检查:视力左0.6,右1.2,左眼外突,左眼球向内、上、下方向活动受限,球结膜充血,左瞳孔散大,对光反射迟钝。鼻腔检查未见异常,头颅CT、脑动脉     

CT在颅内血肿微创治疗前后的应用价值(附32例报告)

目的探讨CT在颅内血肿微创治疗前后的临床应用价值. 资料与方法对32例颅内血肿患者于微创术前做CT定位和术后CT复查评价.32例中,外伤性硬膜外血肿12例,外伤性硬膜下血肿5例,高血压脑出血12例,其他原因致颅内血肿3例. 结果外伤性颅内血肿17例(硬膜外12例,硬膜下5例)微创治疗满意,无后遗症,尤其是硬膜外血肿效果更佳.高血压及其他原因所致颅内血肿15例中,微创治疗成功12例,死亡2例,1例因术后有活动性出血且出血量大而行手术开颅清除血肿.成功的12例中5例有后遗症. 结论术前CT定位和选择最佳适应证是微创治疗成功的术后CT复查是评价微创治疗效果的有效方法.     

飞行员肺隔离症的诊断、治疗及医学鉴定原则——附二例临床病例

目的 探讨肺隔离症的影像学表现、治疗和飞行员的医学鉴定原则. 方法 回顾分析两例确诊为肺隔离症的飞行员的临床诊治过程及医学鉴定,并进行相关文献复习. 结果 肺隔离症临床症状不典型,1例叶外型肺隔离症无任何临床症状,在体检过程中发现;另1例叶内型肺隔离症反复咯血,多次按肺炎等诊治,存在误诊、漏诊.影像学检查对诊断有重要意义,其中胸部X线片多作为初筛,薄层CT、CT增强及血管重建对发现异常动脉有意义,但最可靠的方法为主动脉血管造影检查.对诊断明确者多主张积极治疗,本文中1例叶内型肺隔症者采用先进的经导管动脉栓塞治疗,最终恢复飞行;另1例叶外型肺隔离症者已恢复飞行至最高年限. 结论 肺隔离症临床少见,飞行员更是罕见,易误诊、漏诊,应重视年度体检中胸部X线检查.肺隔离症在无临床症状的非战斗机飞行员可个别评定,有临床症状者采用微创介入治疗对肺功能影响小,有望恢复飞行.同时提示航空医师加强对少见先天性疾病的诊断意识,治疗时综合考虑各种治疗手段对飞行能力的影响,一些先进的治疗方法能最大限度地挽救飞行员的职业生涯.     

Major depressive disorder with psychotic features in an aviator after head trauma

We present a case in which a Naval aviator suffered an unusual sequence of neuropsychiatric symptoms after head trauma. He demonstrated subtle deficits on several measures 1 mo after the trauma. Repeat testing at 8 mo showed apparent recovery, and the patient was cleared to return to flight status. Unbeknownst to medical staff, the patient was still experiencing difficulties. He was found in a severely debilitated state and exhibiting psychotic features 12 mo after his initial trauma. The patient was hospitalized in a psychiatric ward, and with prolonged inpatient and outpatient treatment, he eventually recovered.     

飞行人员先天性心脏病的临床诊治与医学鉴定

目的 探讨飞行人员先天性心脏病的诊断治疗及医学鉴定.方法 回顾性分析1993年1月-2010年10月在我院住院的12例飞行人员先天性心脏病病例的临床特点、预后及其医学鉴定结论.结果 12例中：①3例室间隔缺损,2例主动脉二瓣畸形,1例冠状动脉-肺动脉瘘,均未作特殊处理,鉴定结论：飞行不合格.②1例卵圆孔未闭,空中机械师,未作特殊处理,鉴定结论：飞行合格;1例主动脉瓣二瓣畸形,未作特殊处理,鉴定结论：原机种合格.③1例房间隔缺损,外科修补后,鉴定结论：飞行不合格.④1例动脉导管未闭及2例房间隔缺损,均给予介入封堵治疗.其中1例动脉导管未闭及1例房间隔缺损患者经过6～14月地面观察及严格体检后,鉴定结论：飞行合格;另1例房间隔缺损患者尚处于地面观察期,鉴定结论：暂时飞行不合格.结论 飞行人员确诊先天性心脏病后,应结合临床分型、飞行机种及预后处理,进行个体化医学鉴定;封堵介入方法治疗先天性心脏病,创伤小,成功率高,治愈患者可考虑重新放飞.     

Cases from the aerospace medicine residents' teaching file. Case #26. A fighter pilot with a single left frontal lobe infarction and probable mitral valve prolapse and supraventricular arrhythmias

A fighter pilot with a single left frontal lobe infarction and probable mitral valve prolapse and supraventricular arrhythmias is presented. He was found unfit for flying duties as a fighter pilot, but because of his experience and expertise he was restricted to flying with a qualified copilot in aircraft other than fighters, with regular aeromedical followup.     

一例战斗机飞行员深静脉血栓形成并文献复习

目的探讨深静脉血栓形成与飞行的关系、诊断方法和预防措施。方法结合收治的1例男性高性能战斗机飞行员的临床资料及复习文献,对深静脉血栓形成与飞行的关系及发生机制进行综合分析。结果该飞行员入院前2月无诱因出现右下肢疼痛,当地医院行抗炎药物治疗15d,疼痛减轻。入院前2周出现咳嗽、咯血伴左侧胸痛,无发热。经血管超声、肺部CT等检查,诊断为:深静脉血栓形成;肺栓塞。给予抗凝等治疗后症状缓解。3个月后,一般日常活动无明显不适出院。结论:飞行不合格。结论战斗机的高载荷造成血管壁的轻微损伤,抗荷服对血管的压迫造成的血流淤滞,座舱内缺氧、振动、有毒气体及电磁辐射可能是促进飞行员静脉血栓形成的原因。     

颅脑损伤后癫痫发作的航空医学鉴定——附病例报告二例

目的 通过回顾性分析民航飞行员颅脑损伤病例及社区病例相关文献,探讨不同程度的颅脑损伤后不同时间段癫痫的发病率和颅脑损伤后癫痫发作的高危因素,以期指导民用航空人员颅脑损伤的医学鉴定.方法 获取并回顾相关颅脑损伤后癫痫发作的流行病学研究,获得社区颅脑损伤病例共9475例,其中重度605例,中度1955例,轻度6915例;民航飞行员重度颅脑损伤申请特许鉴定病例2例.分析并探讨颅脑损伤后癫痫发作的航空医学鉴定.结果 ①重度颅脑损伤后癫痫发病率高于中度,中度高于轻度.②颅脑损伤后随时间推移癫痫发作可能性逐步降低;轻度颅脑损伤1年后癫痫年发病率小于1%,中度颅脑损伤3年后癫痫年发病率小于1%,重度颅脑损伤8年后癫痫年发病率小于1%.③颅脑损伤后癫痫发作高危因素有:脑挫伤、硬膜下血肿、凹陷性骨折及意识丧失或损伤后遗忘大于24 h.④两名颅脑损伤飞行员经及时有效治疗后恢复良好,各项检查未见异常,密切随访期间未见癫痫发作.其中1名飞行员于伤后第4年特许合格,安全飞行2年(1800 h),未见癫痫发作;另1名于伤后第9年特许合格,安全飞行4年(1600 h),未见癫痫发作.结论 根据1%法则,颅脑损伤治愈后,若各项检查未见异常,轻度颅脑损伤1年后可评定为合格,中度3年后可评定为合格,重度8年后可考虑有或无限制的合格鉴定. Abstract： Objective To investigate the incidence of various grade of posttraumatic epilepsy in different time and risk factors by analyzing cerebral trauma cases of civil pilots and correlative literatures.The conclusion is expected to contribute to the aviation medical assessment for the civil pilot with posttraumatic epilepsy. Methods For analyzing epidemiology studies of posttraumatic epilepsy 9475 cases of civilians' posttraumatic epilepsy (include 605 severe, 1955 moderate and 6915 mild traumatic brain injury cases) were reviewed. Besides, 2 epilepsy cases of civil pilots with severe traumatic brain injury, who were specially applied for assessment, were also analyzed to investigate the application in aeromedical assessment. Results ①The severer traumatic brain injury the higher incidence of posttraumatic epilepsy. ②The possibility of posttraumatic epilepsy seizure was gradully diminished with time. The incidence of posttraumatic epilepsy could reduce to lower than 1% after 1, 3 or 8 years corresponding to the mild,moderate and severe traumatic brain injury. ③ The high risk factors of posttraumatic epilepsy included brain contusion, subdural hematoma, depressed fracture, loss of consciousness or post traumatic amnesia more than 24 h and early seizure. The close follow-up showed that 2 pilots well recovered by timely treatment and no more abnormities and seizure happened. One pilot was permitted for co-piloting at the 4th year of injury and had no epilepsy seizure in his safe flying for 2 years (1800 h). Another pilot returned to his qualified flight at the 9th year and had safely flied as pilot instructor for 4 years ( 1600 h) without seizure.Conclusions By applying 1% rule in aeromedical assessment, the mild traumatic brain injured pilot would be suggested to fit for flying by 1-year recovery and 3-year recovery for the moderate if no more abnormities were diagnosed. For the severe injured pilot, the flying qualification could be considered with or without limitation by 8-year recovery.     

CT for acute stage of closed head injury

Brain damage after head injury can be classified by its time course. Primary damage that includes acute subdural hematoma (SDH), acute epidural hematoma (EDH), and intraaxial lesions that include contusions, diffuse axonal injury (DAI), and intracranial hemorrhage (ICH), occurs at the moment of impact and is thought to be irreversible. Secondary damage that includes herniations, diffuse cerebral swelling, and secondary infarction and hemorrhage, evolves hours or days after injury as a consequence of systemic or intracranial complications. The duration and severity of secondary damage influence outcome. Head injury management is focused on preventing, detecting, and correcting such secondary damage. CT has been widely used for the neuromonitoring of head trauma. CT is the gold standard for the detection of intracranial abnormalities and is a safe method for survey. While MRI is more sensitive and accurate in diagnosing cerebral pathology, CT is considered the most critical imaging technique for the management of closed head-injured patients in the acute stage. In this article, we review the imaging findings and literature of various lesions of closed head injury in the acute stage.     

Atlas occipitalization in a supersonic fighter pilot involved in a midair collision: a case report

We report a case of a midair collision between two F16 fighter aircraft, in which one pilot survived and the other was ejected upon impact and his remains recovered from sea. In autopsy, no patholgy was detected, other than the expected evidence of mechanical trauma. No defects in the aircraft or faults in the parachute or ejection mechanism were found. Reconstruction of the shattered skull base and the cervical vertebrae revealed fusion of the atlanto-occipital joint (occipitalization) and a left paracondylar process. The effective diameter of the spinal canal was decreased by the abnormal articulation. Such malformations can cause a wide range of neurologic deficits. Considering the skill and alertness needed to operate a supersonic fighter aircraft, with the pressure applied by the heavy protective head gear and various G forces endured by the spinal column during flight, we postulate that the collision was related to the pilot's sudden incapacitation.     

Comparison of non-sedated brain MRI and CT for the detection of acute traumatic injury in children 6 years of age or less

CT is considered the first-line study for acute intracranial injury in children because of its availability, detection of acute hemorrhage, and lack of sedation. An MRI study with rapidly acquired sequences can obviate the need for sedation and radiation. We compared the detection rate of rapid non-sedated brain MRI to CT for traumatic head injury in young children. We reviewed a series of children 6 years of age or less who presented to our ED during a 5-year period with head trauma and received a non-sedated brain MRI and CT within 24 h of injury. Most MRI studies were limited to triplane T2 and susceptibility sequences. Two neuroradiologists reviewed the MRIs and CTs and assessed the following findings: fracture, epidural hematoma (EDH)/subdural hematoma (SDH), subarachnoid hemorrhage (SAH), intraventricular hemorrhage (IVH), and parenchymal injury. Thirty of 33 patients had radiologically identified traumatic injuries. There was an overall agreement of 82 % between the two modalities. Skull fracture was the only injury subtype which had a statistically significant difference in detection between CT and MRI (p?=?0.0001), with MRI missing 14 of 21 fractures detected on CT. While not statistically significant, MRI had a higher detection rate of EDH/SDH (p?=?0.34), SAH (p?=?0.07), and parenchymal injuries (p?=?0.50). Non-sedated MRI has similar detection rates to CT for intracranial injury in young children presenting with acute head trauma and may be an alternative to CT in select patients.     

Capsular and thalamic infarction caused by tentorial herniation subsequent to head trauma

Summary Five patients (4 male and 1 female) were observed to have capsular and thalamic infarction ascribed to descending transtentorial herniation (DTH) caused by head injury. A lucid interval immediately after the trauma and the presence of an epidural hematoma (EDH) characterized all five cases. At the time of hospitalization consciousness was seriously impaired and signs of cerebral herniation were apparent. Two to four days after the trauma, low attenuation in the computed tomography (CT) images pinpointed intracerebral damage in the anterolateral part of the thalamus and in the internal capsule on the same side as that of the EDH in three patients, and in the other two patients bilateral thalamic and capsular damage was noted. The low attenuation implicated the perforating arteries, that is the anterior thalamoperforating and anterior choroidal arteries, suggesting infarcted regions caused by occlusion of these arteries. Findings in the present study suggest that arterial occlusion in closed head injury may result from DTH. Moreover, infarction may be attributed to the delayed effects of injury.