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Updated: Jun 13, 2026
A Bedside, Single Burr Hole Approach to Multimodality Monitoring in Severe Brain Injury
Published on: March 26, 2019
Brain tissue oxygen-directed management and outcome in patients with severe traumatic brain injury
Alejandro M Spiotta1, Michael F Stiefel, Vicente H Gracias
1Department of Neurosurgery, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Object:
The object of this study was to determine whether brain tissue oxygen (PbtO(2))-based therapy or intracranial pressure (ICP)/cerebral perfusion pressure (CPP)-based therapy is associated with improved patient outcome after severe traumatic brain injury (TBI).
Methods:
Seventy patients with severe TBI (postresuscitation GCS score < or = 8), admitted to a neurosurgical intensive care unit at a university-based Level I trauma center and tertiary care hospital and managed with an ICP and PbtO(2) monitor (mean age 40 +/- 19 years [SD]) were compared with 53 historical controls who received only an ICP monitor (mean age 43 +/- 18 years). Therapy for both patient groups was aimed to maintain ICP < 20 mm Hg and CPP > 60 mm Hg. Patients with PbtO(2) monitors also had therapy to maintain PbtO(2) > 20 mm Hg.
Results:
Data were obtained from 12,148 hours of continuous ICP monitoring and 6,816 hours of continuous PbtO(2) monitoring. The mean daily ICP and CPP and the frequency of elevated ICP (> 20 mm Hg) or suboptimal CPP (< 60 mm Hg) episodes were similar in each group. The mortality rate was significantly lower in patients who received PbtO(2)-directed care (25.7%) than in those who received conventional ICP and CPP-based therapy (45.3%, p < 0.05). Overall, 40% of patients receiving ICP/CPP-guided management and 64.3% of those receiving PbtO(2)-guided management had a favorable short-term outcome (p = 0.01). Among patients who received PbtO(2)-directed therapy, mortality was associated with lower mean daily PbtO(2) (p < 0.05), longer durations of compromised brain oxygen (PbtO(2) < 20 mm Hg, p = 0.013) and brain hypoxia (PbtO(2) < 15 mm Hg, p = 0.001), more episodes and a longer cumulative duration of compromised PbtO(2) (p < 0.001), and less successful treatment of compromised PbtO(2) (p = 0.03).
Conclusions:
These results suggest that PbtO(2)-based therapy, particularly when compromised PbtO(2) can be corrected, may be associated with reduced patient mortality and improved patient outcome after severe TBI.
