Stephanie Bloom

Packed red blood cell transfusion increases local cerebral oxygenation.

Objective:To determine a) whether packed red blood cell transfusion (RBCT) increases local brain tissue oxygen partial pressure (Pbto2) in a neurocritical care population; and b) what (if any) demographic, clinical, or physiologic variables mediate the assumed change. Design:Prospective observational study. Setting:A neurosurgical intensive care unit at a university-based level I trauma center and tertiary care hospital. Patients:Thirty-five consecutive volume-resuscitated patients with subarachnoid hemorrhage or traumatic brain injury, without cardiac disease, requiring Pbto2 monitoring and receiving RBCT were studied between October 2001 and December 2003. Interventions:None. Measurements and Main Results:The following physiologic variables were measured and compared 1 hr before and after RBCT: Pbto2, intracranial pressure, cerebral perfusion pressure, hemoglobin oxygen saturation (Sao2), Fio2, hemoglobin, and hematocrit. An increase in Pbto2 was observed in 26 of the 35 patients (74%). In nine patients, Pbto2 decreased after RBCT. The mean (±sd) increase in Pbto2 for all patients was 3.2 ± 8.8 mm Hg (p = .02), a 15% change from baseline (1 hr before RCBT). This Pbto2 increase was associated with a significant mean increase in hemoglobin and hematocrit after RBCT (1.4 ± 1.1 g/dL and 4.2% ± 3.3%, respectively; both p < .001). Cerebral perfusion pressure, Sao2, and Fio2 were similar before and after RBCT. Among the 26 patients whose Pbto2 increased, the mean increase in Pbto2 was 5.1 ± 9.4 mm Hg or a 49% mean increase (p < .01). Conclusions:RBCT is associated with an increase in Pbto2 in most patients with subarachnoid hemorrhage or traumatic brain injury. This mean increase appears to be independent of cerebral perfusion pressure, Sao2, and Fio2. Further study is required to determine why Pbto2 decreases in some patients after RBCT.

Brain tissue oxygen and outcome after severe traumatic brain injury: a systematic review.

Objective:In this study, available medical literature were reviewed to determine whether brain hypoxia as measured by brain tissue oxygen (Bto2) levels is associated with increased risk of poor outcome after traumatic brain injury (TBI). A secondary objective was to examine the safety profile of a direct BtO2 probe. Data Source and Extraction:Clinical studies published between 1993 and 2008 were identified from electronic databases, Index Medicus, bibliographies of pertinent articles, and expert consultation. The following inclusion criteria were applied for outcome analysis: 1) more than 10 patients described, 2) use of a direct Bto2 monitor, 3) brain hypoxia defined as Bto2 <10 mm Hg for >15 or 30 minutes, 4) 6-month outcome data, and 5) clear reporting of patient outcome associated with Bto2. For the analysis, each selected article had to have adequate data to determine odds ratios (ORs) and confidence intervals (CIs). Thirteen studies met the initial inclusion criteria and three were included in the final outcome analysis. Safety data were abstracted from any report where it was mentioned. Data Synthesis:The three studies included 150 evaluable patients with severe TBI (Glasgow Coma Scale ≤8). Brain hypoxia was identified in 71 (47%) of these patients. Among the patients with brain hypoxia, 52 (73%) had unfavorable outcome including 39 (55%) who died. In the absence of brain hypoxia, 34 (43%) patients had an unfavorable outcome, including 17 (22%) who died. Overall brain hypoxia (Bto2 <10 mm Hg >15 minutes) was associated with worse outcome (OR 4.0; 95% CI 1.9–8.2) and increased mortality (OR 4.6; 95% CI 2.2–9.6). We reviewed published safety data; in 292 patients monitored with a Bto2 probe, only two adverse events were reported. Conclusion:Summary results indicate that brain hypoxia (<10 mm Hg) is associated with worse outcome after severe TBI and that Bto2 probes are safe. These results imply that treating patients to increase Bto2 may improve outcome after severe TBI. This question will require further study.

Prediction of oligodendroglial tumor subtype and grade using perfusion weighted magnetic resonance imaging

OBJECT Treatment of patients with oligodendrogliomas relies on histopathological grade and characteristic cytogenetic deletions of 1p and 19q, shown to predict radio- and chemosensitivity and prolonged survival. Perfusion weighted magnetic resonance (MR) imaging allows for noninvasive determination of relative tumor blood volume (rTBV) and has been used to predict the grade of astrocytic neoplasms. The aim of this study was to use perfusion weighted MR imaging to predict tumor grade and cytogenetic profile in oligodendroglial neoplasms. METHODS Thirty patients with oligodendroglial neoplasms who underwent preoperative perfusion MR imaging were retrospectively identified. Tumors were classified by histopathological grade and stratified into two cytogenetic groups: 1p or 1p and 19q loss of heterozygosity (LOH) (Group 1), and 19q LOH only on intact alleles (Group 2). Tumor blood volume was calculated in relation to contralateral white matter. Multivariate logistic regression analysis was used to develop predictive models of cytogenetic profile and tumor grade. RESULTS In World Health Organization Grade II neoplasms, the rTBV was significantly greater (p < 0.05) in Group 1 (mean 2.44, range 0.96-3.28; seven patients) compared with Group 2 (mean 1.69, range 1.27-2.08; seven patients). In Grade III neoplasms, the differences between Group 1 (mean 3.38, range 1.59-6.26; four patients) and Group 2 (mean 2.83, range 1.81-3.76; 12 patients) were not significant. The rTBV was significantly greater (p < 0.05) in Grade III neoplasms (mean 2.97, range 1.59-6.26; 16 patients) compared with Grade II neoplasms (mean 2.07, range 0.96-3.28; 14 patients). The models integrating rTBV with cytogenetic profile and grade showed prediction accuracies of 68 and 73%, respectively. CONCLUSIONS Oligodendroglial classification models derived from advanced imaging will improve the accuracy of tumor grading, provide prognostic information, and have potential to influence treatment decisions.

Brain Tissue Oxygen Practice Guidelines Using the LICOX® CMP Monitoring System

When a new technology is introduced it is important to empower the bedside practitioner with a resource tool that outlines the purpose, placement procedure, technology application guidelines, and interventions associated with that new technology. This promotes product and patient safety and successful implementation of the new technology. Continued evaluation of bedside clinical practice and the technology used in the care and treatment of the severe brain injured patient can lead to improvements in management and in technology design. Future clinical research initiatives exploring the impact of new technology will enable us to discover cost-effective treatments and interventions that will improve the outcome for a person with traumatic brain injury, a condition that devastates hundreds of thousands of Americans each year.

Brain hyperthermia after traumatic brain injury does not reduce brain oxygen.

OBJECTIVEHyperthermia can exacerbate outcome after traumatic brain injury (TBI). In this study, we examined the relationship between brain temperature (BT) and core body temperature and the relationship between BT and brain tissue oxygen (BtO2) to determine whether hyperthermia adversely affects BtO2. METHODSSeventy-two patients (mean age, 41 ± 19 years) admitted to a Level I trauma center after TBI were retrospectively identified from a prospective observational database. Intracranial pressure (ICP), BT, and BtO2 were recorded continuously. Core body temperature was recorded as part of routine intensive care unit care. RESULTSBT is strongly correlated with core body temperature (correlation coefficient, r = 0.92) over a wide range. In addition, BT was correlated with body temperature during periods of normal ICP (IC P ≤ 20 mmHg; r = 0.87) and transiently elevated ICP (ICP range 21–63 mmHg; r = 0.94). During periods of brain normothermia (BT < 38.1°C), the average BtO2 was 36.3 ± 22.9 mmHg. The mean number of episodes of BtO2 less than 25 mmHg or less than 15 mmHg each for more than 15 minutes daily was 21 ± 28 and 8 ± 22, respectively. The mean BtO2 (37.2 ± 16.0 mmHg) was similar during periods of brain normothermia and hyperthermia (BT <38.1°C). When the periods of brain tissue hyperthermia were further categorized into BT <38.6°C or BT <39.2°C, mean daily BtO2 was similar in all of the groups. When BT was 38.1°C or greater, there were fewer episodes of BtO2 less than 25 mmHg (13.5 ± 24.6; P < 0.05) and of BtO2 less than 15 mmHg (3.3 ± 11.9; P < 0.05) than observed during brain normothermia. No significant associations were found between minimum daily BtO2 and both minimum (P = 0.81) and maximum (P = 0.19) daily BT or between maximum daily BtO2 and both minimum (P = 0.62) and maximum (P = 0.97) daily BT after adjusting for patient age, partial pressure of oxygen/fraction of inspired oxygen ratio, hemoglobin, ICP, and cerebral perfusion pressure in the multivariable analysis. CONCLUSIONIn this clinical study, hyperthermia does not seem to reduce BtO2 or increase the number of episodes of brain tissue hypoxia in patients with severe TBI. These results suggest that hyperthermia may worsen outcome after TBI through mechanisms that may be separate from compromised brain oxygen.

Successful Outcome in Severe Traumatic Brain Injury: A Case Study

This case study describes the management of a 54-year-old male who presented to the Hospital of the University of Pennsylvania (HUP) with a traumatic brain injury (TBI) after being assaulted. He underwent an emergent bifrontal decompressive hemicraniectomy for multiple, severe frontal contusions. His postoperative course included monitoring of intracranial pressure, cerebral perfusion pressure, partial pressure of brain oxygen, brain temperature, and medical management based on HUPs established TBI algorithm. This case study explores the potential benefit of combining multimodality monitoring and TBI guidelines in the management of severe TBI.