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Erschienen in:
01.06.2011 | Original Article
Medical Management of Compromised Brain Oxygen in Patients with Severe Traumatic Brain Injury
Erschienen in: Neurocritical Care | Ausgabe 3/2011
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Background
Brain tissue oxygen (PbtO2) monitoring is used in severe traumatic brain injury (TBI) patients. How brain reduced PbtO2 should be treated and its response to treatment is not clearly defined. We examined which medical therapies restore normal PbtO2 in TBI patients.
Methods
Forty-nine (mean age 40 ± 19 years) patients with severe TBI (Glasgow Coma Scale [GCS] ≤ 8) admitted to a University-affiliated, Level I trauma center who had at least one episode of compromised brain oxygen (PbtO2 <25 mmHg for >10 min), were retrospectively identified from a prospective observational cohort study. Intracranial pressure (ICP), cerebral perfusion pressure (CPP), and PbtO2 were monitored continuously. Episodes of compromised PbtO2 and brain hypoxia (PbtO2 <15 mmHg for >10 min) and the medical interventions that improved PbtO2 were identified.
Results
Five hundred and sixty-four episodes of compromised PbtO2 were identified from 260 days of PbtO2 monitoring. Medical management used in a “cause-directed” manner successfully reversed 72% of the episodes of compromised PbtO2, defined as restoration of a “normal” PbtO2 (i.e. ≥25 mmHg). Ventilator manipulation, CPP augmentation, and sedation were the most frequent interventions. Increasing FiO2 restored PbtO2 80% of the time. CPP augmentation and sedation were effective in 73 and 66% of episodes of compromised brain oxygen, respectively. ICP reduction using mannitol was effective in 73% of treated episodes, though was used only when PbtO2 was compromised in the setting of elevated ICP. Successful medical treatment of brain hypoxia was associated with decreased mortality. Survivors (n = 38) had a 71% rate of response to treatment and non-survivors (n = 11) had a 44% rate of response (P = 0.01).
Conclusion
Reduced PbtO2 may occur in TBI patients despite efforts to maintain CPP. Medical interventions other than those to treat ICP and CPP can improve PbtO2. This may increase the number of therapies for severe TBI in the ICU.