Obesity is Associated with Reduced Brain Tissue Oxygen Tension After Severe Brain Injury

Abstract

BackgroundObesity 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 (PbtO2) may result in poor outcome after brain injury. We tested the hypothesis that obesity is associated with compromised PbtO2 after severe brain injury.MethodsPatients with severe brain injury (GCS score ≤ 8) who underwent continuous PbtO2 monitoring were retrospectively identified from a prospective single-center database. Patients, were classified by body mass index (BMI = weight (kg)/m2) and were included if they were obese (BMI ≥ 30) or non-obese (BMI = <30).ResultsSixty-nine patients (mean age 46.4 ± 17.0 years) were included. Mean daily PbtO2 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 PbtO2 and mean daily maximum PbtO2 measurements also were significantly lower in obese patients than in non-obese patients. Univariate predictors of compromised PbtO2 (defined as minutes PbtO2 < 20 mmHg) included elevated BMI (P = 0.02), presence of ARDS (P < 0.01), mean PaO2 (P < 0.01), maximum FiO2 (P < 0.01), mean PaO2:FiO2 (P < 0.01), and mean CVP (P < 0.01). In multivariable analysis, BMI was significantly associated with compromised PbtO2 (P = 0.02). Sex, age, and mean CVP were also identified as significant predictors of compromised PbtO2; ARDS and PF ratio were not.ConclusionsIn patients with severe brain injury, obesity was found to be an independent predictor of compromised PbtO2. This effect may be mediated through obesity-related pulmonary dysfunction and inadequate compensatory mechanisms.