去骨瓣减压造成继发性脑损伤54例临床分析

时间:2020-10-10 13:12:47 药学毕业论文 我要投稿

去骨瓣减压造成继发性脑损伤54例临床分析

【关键词】 ,颅内血肿
Clinical analysis of secondary brain damage of 54 cases after decompressive craniectomy
  【Abstract】 AIM: To study the causes of secondary brain injury and how to treat the injury after decompressive craniectomy. METHODS: Two hundred and sixtyseven intracranial hematoma patients with frontaltemporal decompressive craniectomy, were divided into 3 groups according to the size of the bone window group Ⅰ, 5 cm×7 cm×~6 cm×11 cm (n=72); group Ⅱ, 7 cm×12 cm~11 cm×14 cm (n=103); group Ⅲ 12 cm×15 cm or larger. Language function and upper limb motor function opposite to the side of hematoma before and after operation were recorded and compared. RESULTS: Secondary brain damage happened in 54 of all the patients. 35.9% (37/103) patients with mediumsized bone window had secondary brain damage, while the incidence of secondary brain damage for patients with smaller or larger size of bone window was 10.3%(7/12) and 10.9%(10/92), respectively. No such damage was observed in those patients whose dura had been repaired. CONCLUSION: Attention should be paid to the brain damage after decompressive craniectomy. The patients with mediumsized bone window have a high incidence rate of secondary brain damage. Protecting the vein and bone flap above functional domain and repairing the dura are good solutions to prevent the secondary brain injury.
  【Keywords】 intracranial hematoma;bone flap decompression; secondary brain injury
  【摘要】 目的: 探讨去骨瓣减压术引起继发性脑损害的原因和解决方法. 方法: 1994/2004收治的颅内血肿行额颞部去骨瓣减压患者267例,根据骨窗大小将所有患者分为3组,Ⅰ组5 cm×7 cm~6 cm×11 cm (n=72),Ⅱ组7 cm×12 cm~11 cm×14 cm (n=103),Ⅲ组12 cm×15 cm 以上(n=92),记录术前、术后早期血肿对侧上肢运动或语言功能与术后的比较. 结果: 发生继发性脑损害54例. 中等大小骨窗的病例继发性损害的发生率为35.9%(37/103),较小或较大的骨窗继发性损害的发生率较低,分别为10.3%(7/72)和10.9%(10/92),修补硬膜者无继发性损害. 结论: 继发于去骨瓣减压的脑损害应引起注意,中等大小骨窗的病例较易发生. 保护静脉,保护功能区上方的骨瓣和减张修补硬膜是预防继发性脑损害发生的好方法.
  【关键词】 颅内血肿;去骨瓣减压术;继发性脑损害
  0引言
  去骨瓣减压是神经外科治疗严重的'颅脑损伤,增加颅腔容积,缓解颅内压增高的常用有效手段. 但由于血肿清除急性减压后,脑组织缺血再灌注所致的脑肿胀,可造成脑组织由减压窗呈蕈样膨出,引起脑组织的嵌顿,导致局部脑组织的水肿加重[1],脑组织发生缺血坏死,由此而引起了由于去骨瓣减压而造成的新的神经功能损害. 这种功能损害的发生很容易笼统地归结为颅脑外伤所致. 我科54例发生继发于去骨瓣减压造成的脑组织由骨窗部疝出而引发的神经功能障碍如下.
1对象和方法
  1.1对象
  199409/200409颅脑损伤后行额颞部去骨瓣减压267(男182,女85)例,年龄4~72(平均37.6)岁. 单纯硬膜外血肿94例;硬膜下血肿及脑挫裂伤141例;硬膜外合并硬膜下血肿32例. 右侧血肿176例,左侧血肿91例. 手术采用“马蹄形”或“倒问号”切口,行额颞部的骨瓣或骨窗. 其中37例取自体颞肌筋膜行硬脑膜减张修补术,其余病例均行放射状剪开硬膜,未予修补.
  1.2方法
  本组病例均选择的是行单侧额颞部去骨瓣减压并存活出院的病例. 入选病例来院时或术后早期血肿对侧上肢有活动或躁动或刺激后有活动的记录. 术后4 d,患者骨窗对侧上肢肌力下降,甚至为0级,同时CT扫描提示有骨窗部脑膨出. CT排除皮层下有新的脑损伤. 若为优势半球侧血肿,入院时及术后早期和后期同时观察运动性语言的改变. 根据手术记录中的骨窗大小,将所有病例分为3组;第1组骨窗大小范围5 cm×7 cm~6 cm×11 cm,共72例(27%),右侧42例,左侧30例;第2组骨窗大小范围7 cm×12 cm~11 cm×14 cm,共103例(38.6%),右侧69例,左侧34例;第3组病例骨窗大小范围在12 cm×15 cm以上,共92例(34.5%),右侧65例,左侧27例. 修补硬膜37例,第1组4例,第2组19例,第3组14例.