TY - JOUR
T1 - Obesity is associated with reduced brain tissue oxygen tension after severe brain injury
AU - Kumar, Monisha A.
AU - Chanderraj, Rishi
AU - Gant, Ryan
AU - Butler, Christi
AU - Frangos, Suzanne
AU - Maloney-Wilensky, Eileen
AU - Faerber, Jennifer
AU - Kofke, W. Andrew
AU - Levine, Joshua M.
AU - LeRoux, Peter
N1 - Funding Information:
Acknowledgments We acknowledge the valuable contributions of the nurses in the Neurosurgical Intensive Care Unit at the Hospital of the University of Pennsylvania in caring for our patients as well as their help in data acquisition. This study is supported by Research Grants from Integra Neurosciences (PDLR) and the Mary Elisabeth Groff Surgical and Medical Research Trust (PDLR). PDL is a member of Integra Lifesciences’s Speaker’s Bureau.
PY - 2012/4
Y1 - 2012/4
N2 - Background Obesity has been associated with compromised tissue oxygenation and reduced organ perfusion. The brain is critically dependent on oxygen delivery, and reduced brain tissue oxygen tension (P btO 2) may result in poor outcome after brain injury. We tested the hypothesis that obesity is associated with compromised P btO 2 after severe brain injury. Methods Patients with severe brain injury (GCS score ≤ 8) who underwent continuous P btO 2 monitoring were retrospectively identified from a prospective single-center database. Patients, were classified by body mass index (BMI = weight (kg)/m 2) and were included if they were obese (BMI ≥ 30) or non-obese (BMI = <30). Results Sixty-nine patients (mean age 46.4 ± 17.0 years) were included. Mean daily P btO 2 was 25.8 (9.6) mmHg for the 28 obese and 31.8 (12.3) mmHg for the 41 non-obese patients (P = 0.03). Initial P btO 2 and mean daily maximum P btO 2 measurements also were significantly lower in obese patients than in non-obese patients. Univariate predictors of compromised P btO 2 (defined as minutes P btO 2 < 20 mmHg) included elevated BMI (P = 0.02), presence of ARDS (P < 0.01), mean PaO 2 (P < 0.01), maximum FiO 2 (P < 0.01), mean PaO 2:FiO 2 (P < 0.01), and mean CVP (P < 0.01). In multivariable analysis, BMI was significantly associated with compromised P btO 2 (P = 0.02). Sex, age, and mean CVP were also identified as significant predictors of compromised P btO 2; ARDS and PF ratio were not. Conclusions In patients with severe brain injury, obesity was found to be an independent predictor of compromised P btO 2. This effect may be mediated through obesity-related pulmonary dysfunction and inadequate compensatory mechanisms.
AB - Background Obesity has been associated with compromised tissue oxygenation and reduced organ perfusion. The brain is critically dependent on oxygen delivery, and reduced brain tissue oxygen tension (P btO 2) may result in poor outcome after brain injury. We tested the hypothesis that obesity is associated with compromised P btO 2 after severe brain injury. Methods Patients with severe brain injury (GCS score ≤ 8) who underwent continuous P btO 2 monitoring were retrospectively identified from a prospective single-center database. Patients, were classified by body mass index (BMI = weight (kg)/m 2) and were included if they were obese (BMI ≥ 30) or non-obese (BMI = <30). Results Sixty-nine patients (mean age 46.4 ± 17.0 years) were included. Mean daily P btO 2 was 25.8 (9.6) mmHg for the 28 obese and 31.8 (12.3) mmHg for the 41 non-obese patients (P = 0.03). Initial P btO 2 and mean daily maximum P btO 2 measurements also were significantly lower in obese patients than in non-obese patients. Univariate predictors of compromised P btO 2 (defined as minutes P btO 2 < 20 mmHg) included elevated BMI (P = 0.02), presence of ARDS (P < 0.01), mean PaO 2 (P < 0.01), maximum FiO 2 (P < 0.01), mean PaO 2:FiO 2 (P < 0.01), and mean CVP (P < 0.01). In multivariable analysis, BMI was significantly associated with compromised P btO 2 (P = 0.02). Sex, age, and mean CVP were also identified as significant predictors of compromised P btO 2; ARDS and PF ratio were not. Conclusions In patients with severe brain injury, obesity was found to be an independent predictor of compromised P btO 2. This effect may be mediated through obesity-related pulmonary dysfunction and inadequate compensatory mechanisms.
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U2 - 10.1007/s12028-011-9576-x
DO - 10.1007/s12028-011-9576-x
M3 - Article
C2 - 21748506
AN - SCOPUS:84860881255
SN - 1541-6933
VL - 16
SP - 286
EP - 293
JO - Neurocritical Care
JF - Neurocritical Care
IS - 2
ER -