TY - JOUR
T1 - Medical management of compromised brain oxygen in patients with severe traumatic brain injury
AU - Bohman, Leif Erik
AU - Heuer, Gregory G.
AU - MacYszyn, Lukascz
AU - Maloney-Wilensky, Eileen
AU - Frangos, Suzanne
AU - Le Roux, Peter D.
AU - Kofke, Andrew
AU - Levine, Joshua M.
AU - Stiefel, Michael F.
N1 - Funding Information:
Acknowledgments This article was supported by Research Grants from the Integra Foundation (PDL), Integra Neurosciences (PDL), and the Mary Elisabeth Groff Surgical and Medical Research Trust (PDL). PDL is a member of Integra’s Speaker’s Bureau.
PY - 2011/6
Y1 - 2011/6
N2 - 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 PbtO 2 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.
AB - 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 PbtO 2 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.
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U2 - 10.1007/s12028-011-9526-7
DO - 10.1007/s12028-011-9526-7
M3 - Article
C2 - 21394543
AN - SCOPUS:79955870408
SN - 1541-6933
VL - 14
SP - 361
EP - 369
JO - Neurocritical Care
JF - Neurocritical Care
IS - 3
ER -