Outcome After Decompressive Craniectomy in Different Pathologies

详细信息    查看全文

• 作者：Thomas Kapapa¹ ; ^{thomas.kapapa@uniklinik-ulm.de" class="auth_mail" title="E-mail the corresponding author} ; Christine Brand¹ ; Christian Rainer Wirtz¹ ; Dieter Woischneck²
• 关键词：Indication ; Malignant cerebral infarction ; Stroke ; Subarachnoid hemorrhage ; Survival
• 刊名：World Neurosurgery
• 出版年：2016
• 出版时间：September 2016
• 年：2016
• 卷：93
• 期：Complete
• 页码：389-397
• 全文大小：7741 K

文摘

We compare the outcome after decompressive craniectomy for various neurologic diseases with the final common pathway of coma, compression of the basal cisterns, a midline shift, or refractory intracranial hypertension.

Methods

Between January 2005 and June 2009, 134 patients underwent decompressive craniectomy for traumatic brain injury (n = 74), intracerebral hemorrhage (n = 21), spontaneous subarachnoid hemorrhage (n = 11), malignant cerebral infarction (n = 27), or encephalitis (n = 1). The outcome was classified at discharge and up to 12 months after treatment in accordance with the Glasgow Outcome Scale (GOS), as well as the Glasgow Coma Scale, Marshall classification, or National Institutes of Health Stroke Scale. Significance was established as P ≤ 0.05.

Results

Median and mean scores on the Glasgow Coma Scale at time of neurosurgical assessment in all patients were ≤7. Midline shift was reduced in each subset as a result of surgery (mean, 0.26–0.46 cm; P ≤ 0.049). Overall outcome based on the median GOS score at discharge ranged from death to severe disability. After 12 months, the median range narrowed to a range of death to persistent vegetative state. At various time points, mean GOS score was not found to differ significantly between the subsets. Unfavorable outcome after 3 months was found in a smaller group of patients after traumatic brain injury than was found in patients with other diseases (P = 0.016).

Conclusions

The outcome after decompressive craniectomy does not differ significantly in different diseases once the final pathophysiologic pathway of refractory intracranial hypertension, coma, compression of the basal cisterns, or midline shift has been reached.