The timing of
decompressive craniectomy for the treatment of increased intracranial pressure (ICP) after
traumatic brain injury (TBI) is a widely discussed clinical issue. Although we showed recently that early
decompression is beneficial following experimental TBI, it remains unclear to what degree
decompression craniectomy reduces secondary brain damage and if
craniectomy is still beneficial when it is delayed by several hours as often inevitable during daily clinical practice. The aim of the current study was therefore to investigate the influence of
craniectomy on secondary
contusion expansion and
brain edema formation and to determine the therapeutic window of
craniectomy. Male C57/Bl6 mice were subjected to controlled cortical impact injury.
Contusion volume,
brain edema formation, and opening of the blood-brain barrier were investigated 2, 6, 12, and 24 h and 7 days after
trauma. The effect of
decompression craniectomy on secondary brain damage was studied in control mice (closed skull) and in animals craniotomized immediately or with a delay of 1, 3, or 8 h after
trauma. Twenty-four hours after
trauma, the time point of maximal lesion expansion (+60% vs. 15 min after
trauma) and
brain edema formation (+3.0% water content vs.
sham),
contusion volume in craniotomized mice did not show any secondary expansion; that is,
contusion volume was similar to that observed in mice sacrificed immediately after
trauma (18.3 +/- 5.3 vs. 22.2 +/- 1.4 mm(3)). Furthermore,
brain edema formation was reduced by 52% in craniotomized animals. The beneficial effect of
craniectomy was still present even when treatment was delayed by up to 3 h after
trauma (p < 0.05). The current study clearly demonstrates that early
craniectomy prevents secondary brain damage and significantly reduces
brain edema formation after experimental TBI. Evaluation of early
craniectomy as a therapeutic option after TBI in humans may therefore be indicated.