Send to

Choose Destination
Neurosurgery. 2010 Jul;67(1):65-72; discussion 72. doi: 10.1227/01.NEU.0000370604.30037.F5.

Cerebral blood flow and metabolism following decompressive craniectomy for control of increased intracranial pressure.

Author information

Acute Brain Injury Research Laboratory, Department of Neurosurgery, Rambam Medical Center, Faculty of Medicine, The Technion-Israel Institute of Technology, Haifa, Israel.



Decompressive craniectomy (DC) is a common practice for control of intracranial pressure (ICP) following traumatic brain injury (TBI), although the impact of this procedure on the fate of operated patients is still controversial.


Cerebral blood flow (CBF) and metabolic rates were monitored prospectively and daily as a surrogate of neuronal viability in 36 TBI patients treated by DC and compared with those of 86 nonoperated patients. DC was performed either on admission (n=29) or within 48 hours of admission (n=7).


DC successfully controlled ICP levels and maintained CBF within a normal range although the cerebral metabolic rate of oxygen (CMRO2) was significantly lower in this group. In 7 patients, pre- and postoperative recordings showed a significant ICP decrease that correlated with CBF augmentation but not with concurrent improvement of CMRO2 that remained particularly low. Logistic regression analysis of all investigated variables showed that DC was not associated with higher mortality despite more severe injuries in this group. However, operated patients were 7-fold more likely to have poor functional outcomes than nonoperated patients. Good functional outcome was strongly associated with higher CMRO2 but not with higher CBF values. CMRO2 levels were significantly lower in the DC group, even after adjustment for injury severity, and showed a progressive and sustained trend of deterioration significantly different from that of the non-DC group.


These results suggest that DC may enhance survival in the presence of severe brain swelling, although it is unlikely to represent an adequate answer to mitochondrial damage responsible for cellular energy crisis and edema.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Silverchair Information Systems
Loading ...
Support Center