Anemia and brain oxygen after severe traumatic brain injury

Purpose: To investigate the relationship between hemoglobin (Hgb) and brain tissue oxygen tension (PbtO2) after severe traumatic brain injury (TBI) and to examine its impact on outcome. Methods: This was a retrospective analysis of a prospective cohort of severe TBI patients whose PbtO2 was monitored. The relationship between Hgb—categorized into four quartiles (≤9; 9-10; 10.1-11; >11g/dl)—and PbtO2 was analyzed using mixed-effects models. Anemia with compromised PbtO2 was defined as episodes of Hgb≤9g/dl with simultaneous PbtO211g/dl as the reference level, and controlling for important physiologic covariates (CPP, PaO2, PaCO2), Hgb≤9g/dl was the only Hgb level that was associated with lower PbtO2 (coefficient −6.53 (95% CI −9.13; −3.94), p<0.001). Anemia with simultaneous PbtO2<20mmHg, but not anemia alone, increased the risk of unfavorable outcome (odds ratio 6.24 (95% CI 1.61; 24.22), p=0.008), controlling for age, GCS, Marshall CT grade, and APACHE II score. Conclusions: In this cohort of severe TBI patients whose PbtO2 was monitored, a Hgb level no greater than 9g/dl was associated with compromised PbtO2. Anemia with simultaneous compromised PbtO2, but not anemia alone, was a risk factor for unfavorable outcome, irrespective of injury severit

Brain Tissue Hypoxia is a Strong Predictor of Outcome after Severe Traumatic Brain Injury Independent from Elevated Intracranial Pressure

Introduction: Low brain tissue oxygen pressure (PbtO2) is associated with worse outcome in patients with severe traumatic brain injury (TBI). However, it is unclear whether brain tissue hypoxia is merely a marker of injury severity or a predictor of prognosis, independent from intracranial pressure (ICP) and injury severity. Hypothesis: We hypothesized that brain tissue hypoxia was an independent predictor of outcome in patients wih severe TBI, irrespective of elevated ICP and of the severity of cerebral and systemic injury. Methods: This observational study was conducted at the Neurological ICU, Hospital of the University of Pennsylvania, an academic level I trauma center. Patients admitted with severe TBI who had PbtO2 and ICP monitoring were included in the study. PbtO2, ICP, mean arterial pressure (MAP) and cerebral perfusion pressure (CPP = MAP-ICP) were monitored continuously and recorded prospectively every 30 min. Using linear interpolation, duration and cumulative dose (area under the curve, AUC) of brain tissue hypoxia (PbtO2 &lt; 15 mm Hg), elevated ICP &gt;20 mm Hg and low CPP &lt;60 mm Hg were calculated, and the association with outcome at hospital discharge, dichotomized as good (Glasgow Outcome Score [GOS] 4-5) vs. poor (GOS 1-3), was analyzed. Results: A total of 103 consecutive patients, monitored for an average of 5 days, was studied. Brain tissue hypoxia was observed in 66 (64%) patients despite ICP was &lt; 20 mm Hg and CPP &gt; 60 mm Hg (72 +/- 39% and 49 +/- 41% of brain hypoxic time, respectively). Compared with patients with good outcome, those with poor outcome had a longer duration of brain hypoxia (1.7 +/- 3.7 vs. 8.3 +/- 15.9 hrs, P&lt;0.01), as well as a longer duration (11.5 +/- 16.5 vs. 21.6 +/- 29.6 hrs, P=0.03) and a greater cumulative dose (56 +/- 93 vs. 143 +/- 218 mm Hg*hrs, P&lt;0.01) of elevated ICP. By multivariable logistic regression, admission Glasgow Coma Scale (OR, 0.83, 95% CI: 0.70-0.99, P=0.04), Marshall CT score (OR 2.42, 95% CI: 1.42-4.11, P&lt;0.01), APACHE II (OR 1.20, 95% CI: 1.03-1.43, P=0.03), and the duration of brain tissue hypoxia (OR 1.13; 95% CI: 1.01-1.27; P=0.04) were all significantly associated with poor outcome. No independent association was found between the AUC for elevated ICP and outcome (OR 1.01, 95% CI 0.97-1.02, P=0.11) in our prospective cohort. Conclusions: In patients with severe TBI, brain tissue hypoxia is frequent, despite normal ICP and CPP, and is associated with poor outcome, independent of intracranial hypertension and the severity of cerebral and systemic injury. Our findings indicate that PbtO2 is a strong physiologic prognostic marker after TBI. Further study is warranted to examine whether PbtO2-directed therapy improves outcome in severely head-injured patients

Continuous non-invasive optical monitoring of cerebral blood flow and oxidative metabolism after acute brain injury

Rapid detection of ischemic conditions at the bedside can improve treatment of acute brain injury. In this observational study of 11 critically ill brain-injured adults, we employed a monitoring approach that interleaves time-resolved near-infrared spectroscopy (TR-NIRS) measurements of cerebral oxygen saturation and oxygen extraction fraction (OEF) with diffuse correlation spectroscopy (DCS) measurement of cerebral blood flow (CBF). Using this approach, we demonstrate the clinical promise of non-invasive, continuous optical monitoring of changes in CBF and cerebral metabolic rate of oxygen (CMRO ). In addition, the optical CBF and CMRO measures were compared to invasive brain tissue oxygen tension (PbtO ), thermal diffusion flowmetry CBF, and cerebral microdialysis measures obtained concurrently. The optical CBF and CMRO information successfully distinguished between ischemic, hypermetabolic, and hyperemic conditions that arose spontaneously during patient care. Moreover, CBF monitoring during pressor-induced changes of mean arterial blood pressure enabled assessment of cerebral autoregulation. In total, the findings suggest that this hybrid non-invasive neurometabolic optical monitor (NNOM) can facilitate clinical detection of adverse physiological changes in brain injured patients that are otherwise difficult to measure with conventional bedside monitoring techniques