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Michael F. Stiefel, Alejandro Spiotta, Vincent H. Gracias, Alicia M. Garuffe, Oscar Guillamondegui, Eileen Maloney-Wilensky, Stephanie Bloom, M. Sean Grady and Peter D. LeRoux

Object. An intracranial pressure (ICP) monitor, from which cerebral perfusion pressure (CPP) is estimated, is recommended in the care of severe traumatic brain injury (TBI). Nevertheless, optimal ICP and CPP management may not always prevent cerebral ischemia, which adversely influences patient outcome. The authors therefore determined whether the addition of a brain tissue oxygen tension (PO2) monitor in the treatment of TBI was associated with an improved patient outcome.

Methods. Patients with severe TBI (Glasgow Coma Scale [GCS] score < 8) who had been admitted to a Level I trauma center were evaluated as part of a prospective observational database. Patients treated with ICP and brain tissue PO2 monitoring were compared with historical controls matched for age, pathological features, admission GCS score, and Injury Severity Score who had undergone ICP monitoring alone. Therapy in both patient groups was aimed at maintaining an ICP less than 20 mm Hg and a CPP greater than 60 mm Hg. Among patients whose brain tissue PO2 was monitored, oxygenation was maintained at levels greater than 25 mm Hg. Twenty-five patients with a mean age of 44 ± 14 years were treated using an ICP monitor alone. Twenty-eight patients with a mean age of 38 ± 18 years underwent brain tissue PO2-directed care. The mean daily ICP and CPP levels were similar in each group. The mortality rate in patients treated using conventional ICP and CPP management was 44%. Patients who also underwent brain tissue PO2 monitoring had a significantly reduced mortality rate of 25% (p < 0.05).

Conclusions. The use of both ICP and brain tissue PO2 monitors and therapy directed at brain tissue PO2 is associated with reduced patient death following severe TBI.

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Jason H. Huang, Eric L. Zager, Jun Zhang, Robert F. Groff IV, Bryan J. Pfister, Akiva S. Cohen, M. Sean Grady, Eileen Maloney-Wilensky and Douglas H. Smith

Object

Although neuron transplantation to repair the nervous system has shown promise in animal models, there are few practical sources of viable neurons for clinical application and insufficient approaches to bridge extensive nerve damage in patients. Therefore, the authors sought a clinically relevant source of neurons that could be engineered into transplantable nervous tissue constructs. The authors chose to evaluate human dorsal root ganglion (DRG) neurons due to their robustness in culture.

Methods

Cervical DRGs were harvested from 16 live patients following elective ganglionectomies, and thoracic DRGs were harvested from 4 organ donor patients. Following harvest, the DRGs were digested in a dispase–collagenase treatment to dissociate neurons for culture. In addition, dissociated human DRG neurons were placed in a specially designed axon expansion chamber that induces continuous mechanical tension on axon fascicles spanning 2 populations of neurons originally plated ∼ 100 μm apart.

Results

The adult human DRG neurons, positively identified by neuronal markers, survived at least 3 months in culture while maintaining the ability to generate action potentials. Stretch-growth of axon fascicles in the expansion chamber occurred at the rate of 1 mm/day to a length of 1 cm, creating the first engineered living human nervous tissue constructs.

Conclusions

These data demonstrate the promise of adult human DRG neurons as an alternative transplant material due to their availability, viability, and capacity to be engineered. Also, these data show the feasibility of harvesting DRGs from living patients as a source of neurons for autologous transplant as well as from organ donors to serve as an allograft source of neurons.

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Kaitlin Peace, Eileen Maloney-Wilensky, Suzanne Frangos, Marianne Hujcs, Joshua Levine, W. Andrew Kofke, Wei Yang and Peter D. Le Roux

Object

Follow-up head CT scans are important in neurocritical care but involve intrahospital transport that may be associated with potential hazards including a deleterious effect on brain tissue oxygen pressure (PbtO2). Portable head CT (pHCT) scans offer an alternative imaging technique without a need for patient transport. In this study, the investigators examined the effects of pHCT scans on intracranial pressure (ICP), cerebral perfusion pressure (CPP), and PbtO2 in patients with severe brain injury.

Methods

Fifty-seven pHCT scans were obtained in 34 patients (mean age of 42 ± 15 years) who underwent continuous ICP, CPP, and PbtO2 monitoring in the neuro intensive care unit at a university-based Level I trauma center. Patient ICU records were retrospectively reviewed and physiological data obtained during the 3 hours before and after pHCT scans were examined.

Results

Before pHCT, the mean ICP and CPP were 14.3 ± 7.4 and 78.9 ± 20.2 mm Hg, respectively. Portable HCT had little effect on ICP (mean ICP 14.1 ± 6.6 mm Hg, p = 0.84) and CPP (mean CPP 81.0 ± 19.8 mm Hg, p = 0.59). The mean PbtO2 was similar before and after pHCT (33.2 ± 17.0 mm Hg and 31.6 ± 15.9 mm Hg, respectively; p = 0.6). Ten episodes of brain hypoxia (PbtO2 < 15 mm Hg) were observed before pHCT; these episodes prompted scans. Brain hypoxia persisted in 5 patients after pHCT despite treatment. No new episodes of brain hypoxia were observed during or after pHCT.

Conclusions

These data suggest that pHCT scans do not have a detectable effect on a critically ill patient's ICP, CPP, or PbtO2.

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Michael F. Stiefel, Joshua D. Udoetuk, Alejandro M. Spiotta, Vicente H. Gracias, Aaron Goldberg, Eileen Maloney-Wilensky, Stephanie Bloom and Peter D. Le Roux

Object

Control of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is the foundation of traumatic brain injury (TBI) management. In this study, the authors examined whether conventional ICP- and CPP-guided neurocritical care ensures adequate brain tissue O2 in the first 6 hours after resuscitation.

Methods

Resuscitated patients with severe TBI (Glasgow Coma Scale score ≤ 8 and Injury Severity Scale score ≥ 16) who were admitted to a Level I trauma center and who underwent brain tissue O2 monitoring within 6 hours of injury were evaluated as part of a prospective observational database. Therapy was directed to maintain an ICP of 25 mm Hg or less and a CPP of 60 mm Hg or higher.

Data from a group of 25 patients that included 19 men and six women (mean age 39 ± 20 years) were examined. After resuscitation, ICP was 25 mm Hg or less in 84% and CPP was 60 mm Hg or greater in 88% of the patients. Brain O2 probes were allowed to stabilize; the initial brain tissue O2 level was 25 mm Hg or less in 68% of the patients, 20 mm Hg or less in 56%, and 10 mm Hg or less in 36%. Nearly one third (29%) of patients with ICP readings of 25 mm Hg or less and 27% with CPP levels of 60 mm Hg or greater had severe cerebral hypoxia (brain tissue O2 ≤10 mm Hg). Nineteen patients had both optimal ICP (≤25 mm Hg) and CPP (> 60 mm Hg); brain tissue O2 was 20 mm Hg or less in 47% and 10 mm Hg or less in 21% of these patients. The mortality rate was higher in patients with reduced brain tissue O2.

Conclusions

Brain resuscitation based on current neurocritical care standards (that is, control of ICP and CPP) does not prevent cerebral hypoxia in some patients. This finding may help explain why secondary neuronal injury occurs in some patients with adequate CPP and suggests that the definition of adequate brain resuscitation after TBI may need to be reconsidered.

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Matthew R. Sanborn, Stephen R. Thom, Leif-Erik Bohman, Sherman C. Stein, Joshua M. Levine, Tatyana Milovanova, Eileen Maloney-Wilensky, Suzanne Frangos and Monisha A. Kumar

Object

Microparticles (MPs), small membrane fragments shed from various cell types, have been implicated in thrombosis, inflammation, and endothelial dysfunction. Their involvement in subarachnoid hemorrhage (SAH) and the development of cerebral infarction and clinical deterioration caused by delayed cerebral ischemia (DCI) remain ill defined. The authors sought to quantify the magnitude of elevations in MPs, delineate the temporal dynamics of elevation, and analyze the correlation between MPs and DCI in patients with SAH.

Methods

On the day of hemorrhage and on Days 1, 3, 5, 7, and 10 after hemorrhage, peripheral blood samples were drawn from 22 patients with SAH. Plasma samples were labeled with Annexin V and CD142, CD41a, CD235a, CD146, CD66b, or von Willebrand factor (vWF) and were quantified by flow cytometry. Clinical data, including the 3-month extended Glasgow Outcome Scale (GOS-E) scores, infarction as measured on MRI at 14 days after SAH, and vasospasm as measured by transcranial Doppler ultrasonography and angiography, were collected and compared with the MP burden.

Results

When averaged over time, all MP subtypes were elevated relative to controls. The CD235a+(erythrocyte)−, CD66b+(neutrophil)−, and vWF-associated MPs peaked on the day of hemorrhage and quickly declined. The CD142+(tissue factor [TF])–associated MPs and CD146+(endothelial cell)–associated MPs were significantly elevated throughout the study period. There was a strong negative correlation between TF-expressing and endothelial-derived MPs at Day 1 after SAH and the risk of infarction at Day 14 after SAH.

Conclusions

Microparticles of various subtypes are elevated following SAH; however, the temporal profile of this elevation varies by subtype. Those subtypes closely associated with thrombosis and endothelial dysfunction, for example, CD145+(TF)-associated MPs and CD146+(endothelial cell)–associated MPs, had the most durable response and demonstrated a significant negative correlation with radiographic infarction at 14 days after SAH. Levels of these MPs predict infarction as early as Day 1 post-SAH.

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Michael F. Stiefel, Gregory G. Heuer, John M. Abrahams, Stephanie Bloom, Michelle J. Smith, Eileen Maloney-Wilensky, M. Sean Grady and Peter D. Leroux

Object. Nimodipine has been shown to improve neurological outcome after subarachnoid hemorrhage (SAH); the mechanism of this improvement, however, is uncertain. In addition, adverse systemic effects such as hypotension have been described. The authors investigated the effect of nimodipine on brain tissue PO2.

Methods. Patients in whom Hunt and Hess Grade IV or V SAH had occurred who underwent aneurysm occlusion and had stable blood pressure were prospectively evaluated using continuous brain tissue PO2 monitoring. Nimodipine (60 mg) was delivered through a nasogastric or Dobhoff tube every 4 hours. Data were obtained from 11 patients and measurements of brain tissue PO2, intracranial pressure (ICP), mean arterial blood pressure (MABP), and cerebral perfusion pressure (CPP) were recorded every 15 minutes.

Nimodipine resulted in a significant reduction in brain tissue PO2 in seven (64%) of 11 patients. The baseline PO2 before nimodipine administration was 38.4 ± 10.9 mm Hg. The baseline MABP and CPP were 90 ± 20 and 84 ± 19 mm Hg, respectively. The greatest reduction in brain tissue PO2 occurred 15 minutes after administration, when the mean pressure was 26.9 ± 7.7 mm Hg (p < 0.05). The PO2 remained suppressed at 30 minutes (27.5 ± 7.7 mm Hg [p < 0.05]) and at 60 minutes (29.7 ± 11.1 mm Hg [p < 0.05]) after nimodipine administration but returned to baseline levels 2 hours later. In the seven patients in whom brain tissue PO2 decreased, other physiological variables such as arterial saturation, end-tidal CO2, heart rate, MABP, ICP, and CPP did not demonstrate any association with the nimodipine-induced reduction in PO2. In four patients PO2 remained stable and none of these patients had a significant increase in brain tissue PO2.

Conclusions. Although nimodipine use is associated with improved outcome following SAH, in some patients it can temporarily reduce brain tissue PO2.

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Michael F. Stiefel, Gregory G. Heuer, Michelle J. Smith, Stephanie Bloom, Eileen Maloney-Wilensky, Vincente H. Gracias, M. Sean Grady and Peter D. Leroux

Object. Medically intractable intracranial hypertension is a major cause of morbidity and mortality after severe brain injury. One potential treatment for intracranial hypertension is decompressive hemicraniectomy (DCH). Whether and when to use DCH, however, remain unclear. The authors therefore studied the effects of DCH on cerebral O2 to develop a better understanding of the effects of this treatment on the recovery from injury and disease.

Methods. The study focused on seven patients (mean age 30.6 ± 9.7 years) admitted to the hospital after traumatic brain injury (five patients) or subarachnoid hemorrhage (two patients) as part of a prospective observational database at a Level I trauma center. At admission the Glasgow Coma Scale (GCS) score was 6 or less in all patients. Patients received continuous monitoring of intracranial pressure (ICP), cerebral perfusion pressure (CPP), blood pressure, and arterial O2 saturation. Cerebral oxygenation was measured using the commercially available Licox Brain Tissue Oxygen Monitoring System manufactured by Integra NeuroSciences. A DCH was performed when the patient's ICP remained elevated despite maximal medical management.

Conclusions. All patients tolerated DCH without complications. Before the operation, the mean ICP was elevated in all patients (26 ± 4 mm Hg), despite maximal medical management. After surgery, there was an immediate and sustained decrease in ICP (19 ± 11 mm Hg) and an increase in CPP (81 ± 17 mm Hg). Following DCH, cerebral oxygenation improved from a mean of 21.2 ± 13.8 mm Hg to 45.5 ± 25.4 mm Hg, a 114.8% increase. The change in brain tissue O2 and the change in ICP after DCH demonstrated only a modest relationship (r2 = 0.3). These results indicate that the use of DCH in the treatment of severe brain injury is associated with a significant improvement in brain O2.

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Alejandro M. Spiotta, Michael F. Stiefel, Vicente H. Gracias, Alicia M. Garuffe, W. Andrew Kofke, Eileen Maloney-Wilensky, Andrea B. Troxel, Joshua M. Levine and Peter D. Le Roux

Object

The object of this study was to determine whether brain tissue oxygen (PbtO2)–based therapy or intracranial pressure (ICP)/cerebral perfusion pressure (CPP)–based therapy is associated with improved patient outcome after severe traumatic brain injury (TBI).

Methods

Seventy patients with severe TBI (postresuscitation GCS score ≤ 8), admitted to a neurosurgical intensive care unit at a university-based Level I trauma center and tertiary care hospital and managed with an ICP and PbtO2 monitor (mean age 40 ± 19 years [SD]) were compared with 53 historical controls who received only an ICP monitor (mean age 43 ± 18 years). Therapy for both patient groups was aimed to maintain ICP < 20 mm Hg and CPP > 60 mm Hg. Patients with PbtO2 monitors also had therapy to maintain PbtO2 > 20 mm Hg.

Results

Data were obtained from 12,148 hours of continuous ICP monitoring and 6,816 hours of continuous PbtO2 monitoring. The mean daily ICP and CPP and the frequency of elevated ICP (> 20 mm Hg) or suboptimal CPP (< 60 mm Hg) episodes were similar in each group. The mortality rate was significantly lower in patients who received PbtO2-directed care (25.7%) than in those who received conventional ICP and CPP–based therapy (45.3%, p < 0.05). Overall, 40% of patients receiving ICP/CPP–guided management and 64.3% of those receiving PbtO2–guided management had a favorable short-term outcome (p = 0.01). Among patients who received PbtO2-directed therapy, mortality was associated with lower mean daily PbtO2 (p < 0.05), longer durations of compromised brain oxygen (PbtO2 < 20 mm Hg, p = 0.013) and brain hypoxia (PbtO2 < 15 mm Hg, p = 0.001), more episodes and a longer cumulative duration of compromised PbtO2 (p < 0.001), and less successful treatment of compromised PbtO2 (p = 0.03).

Conclusions

These results suggest that PbtO2-based therapy, particularly when compromised PbtO2 can be corrected, may be associated with reduced patient mortality and improved patient outcome after severe TBI.