Cerebral oxygenation following decompressive hemicraniectomy for the treatment of refractory intracranial hypertension

2004 ◽  
Vol 101 (2) ◽  
pp. 241-247 ◽  
Author(s):  
Michael F. Stiefel ◽  
Gregory G. Heuer ◽  
Michelle J. Smith ◽  
Stephanie Bloom ◽  
Eileen Maloney-Wilensky ◽  
...  
Keyword(s):  
Brain Injury ◽  
Intracranial Hypertension ◽  
Brain Tissue ◽  
Medical Management ◽  
Cerebral Oxygenation ◽  
Severe Brain Injury ◽  
Content Type ◽  
Decompressive Hemicraniectomy ◽  
Gcs Score ◽  
Fine Print

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.

Effects of hyperbaric oxygen therapy on cerebral oxygenation and mitochondrial function following moderate lateral fluid-percussion injury in rats

2004 ◽  
Vol 101 (3) ◽  
pp. 499-504 ◽  
Author(s):  
Wilson P. Daugherty ◽  
Joseph E. Levasseur ◽  
Dong Sun ◽  
Gaylan L. Rockswold ◽  
M. Ross Bullock
Keyword(s):  
Brain Injury ◽  
Redox Potential ◽  
Brain Tissue ◽  
Mitochondrial Function ◽  
Cerebral Oxygenation ◽  
Brain Tissue Oxygenation ◽  
Content Type ◽  
Fluid Percussion ◽  
Lateral Fluid Percussion ◽  
Fine Print

Object. In the current study, the authors examined the effects of hyperbaric O2 (HBO) following fluid-percussion brain injury and its implications on brain tissue oxygenation (PO2) and O2 consumption (VO2) and mitochondrial function (redox potential). Methods. Cerebral tissue PO2 was measured following induction of a lateral fluid-percussion brain injury in rats. Hyperbaric O2 treatment (100% O2 at 1.5 ata) significantly increased brain tissue PO2 in both injured and sham-injured animals. For VO2 and redox potential experiments, animals were treated using 30% O2 or HBO therapy for 1 or 4 hours (that is, 4 hours 30% O2 or 1 hour HBO and 3 hours 100% O2). Microrespirometer measurements of VO2 demonstrated significant increases following HBO treatment in both injured and sham-injured animals when compared with animals that underwent 30% O2 treatment. Mitochondrial redox potential, as measured by Alamar blue fluorescence, demonstrated injury-induced reductions at 1 hour postinjury. These reductions were partially reversed at 4 hours postinjury in animals treated with 30% O2 and completely reversed at 4 hours postinjury in animals on HBO therapy when compared with animals treated for only 1 hour. Conclusions. Analysis of data in the current study demonstrates that HBO significantly increases brain tissue PO2 after injury. Nonetheless, treatment with HBO was insufficient to overcome injury-induced reductions in mitochondrial redox potential at 1 hour postinjury but was able to restore redox potential by 4 hours postinjury. Furthermore, HBO induced an increase in VO2 in both injured and sham-injured animals. Taken together, these data demonstrate that mitochondrial function is depressed by injury and that the recovery of aerobic metabolic function may be enhanced by treatment with HBO.

Measurement of brain tissue oxygenation performed using positron emission tomography scanning to validate a novel monitoring method

2002 ◽  
Vol 96 (2) ◽  
pp. 263-268 ◽  
Author(s):  
Arun K. Gupta ◽  
Peter J. Hutchinson ◽  
Tim Fryer ◽  
Pippa G. Al-Rawi ◽  
Dot A. Parry ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Brain Injury ◽  
Brain Tissue ◽  
Tissue Oxygenation ◽  
Emission Tomography ◽  
Brain Tissue Oxygenation ◽  
Content Type ◽  
Positron Emission ◽  
Pet Scans ◽  
Fine Print

Object. The benefits of measuring cerebral oxygenation in patients with brain injury are well accepted; however, jugular bulb oximetry, which is currently the most popular monitoring technique used has several shortcomings. The goal of this study was to validate the use of a new multiparameter sensor that measures brain tissue oxygenation and metabolism (Neurotrend) by comparing it with positron emission tomography (PET) scanning. Methods. A Neurotrend sensor was inserted into the frontal region of the brain in 19 patients admitted to the neurointensive care unit. After a period of stabilization, the patients were transferred to the PET scanner suite where C15O, 15O2, and H215O PET scans were obtained to facilitate calculation of regional cerebral blood volume, O2 metabolism, blood flow, and O2 extraction fraction (OEF). Patients were given hyperventilation therapy to decrease arterial CO2 by approximately 1 kPa (7.5 mm Hg) and the same sequence of PET scans was repeated. For each scanning sequence, end-capillary O2 tension (PvO2) was calculated from the OEF and compared with the reading of brain tissue O2 pressure (PbO2) provided by the sensor. In three patients the sensor was inserted into areas of contusion and these patients were eliminated from the analysis. In the subset of 16 patients in whom the sensor was placed in healthy brain, no correlation was found between the absolute values of PbO2 and PvO2 (r = 0.2, p = 0.29); however a significant correlation was obtained between the change in PbO2 (ΔPbO2) and the change in PvO2 (ΔPvO2) produced by hyperventilation in a 20-mm region of interest around the sensor (ρ = 0.78, p = 0.0035). Conclusions. The lack of correlation between the absolute values of PbO2 and PvO2 indicates that PbO2 cannot be used as a substitute for PvO2. Nevertheless, the positive correlation between ΔPbO2 and ΔPvO2 when the sensor had been inserted into healthy brain suggests that tissue PO2 monitoring may provide a useful tool to assess the effect of therapeutic interventions in brain injury.

Cerebral tissue PO2 and SjvO2 changes during moderate hyperventilation in patients with severe traumatic brain injury

2002 ◽  
Vol 96 (1) ◽  
pp. 97-102 ◽  
Author(s):  
Roberto Imberti ◽  
Guido Bellinzona ◽  
Martin Langer
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Severe Traumatic Brain Injury ◽  
Cerebral Perfusion ◽  
Content Type ◽  
Secondary Damage ◽  
Tissue Po2 ◽  
Two Parameters ◽  
Fine Print

Object. The aim of this study was to investigate the effects of moderate hyperventilation on intracranial pressure (ICP), jugular venous oxygen saturation ([SjvO2], an index of global cerebral perfusion), and brain tissue PO2 (an index of local cerebral perfusion). Methods. Ninety-four tests consisting of 20-minute periods of moderate hyperventilation (27–32 mm Hg) were performed on different days in 36 patients with severe traumatic brain injury (Glasgow Coma Scale score ≤ 8). Moderate hyperventilation resulted in a significant reduction in average ICP, but in seven tests performed in five patients it was ineffective. The response of SjvO2 and brain tissue PO2 to CO2 changes was widely variable and unpredictable. After 20 minutes of moderate hyperventilation in most tests (79.8%), both SjvO2 and brain tissue PO2 values remained above the lower limits of normality (50% and 10 mm Hg, respectively). In contrast, in 15 tests performed in six patients (16.6% of the studied population) brain tissue PO2 decreased below 10 mm Hg although the corresponding SjvO2 values were greater than 50%. The reduction of brain tissue PO2 below 10 mm Hg was favored by the low prehyperventilation values (10 tests), higher CO2 reactivity, and, possibly, by lower prehyperventilation values of cerebral perfusion pressure. In five of those 15 tests, the prehyperventilation values of SjvO2 were greater than 70%, a condition of relative hyperemia. The SjvO2 decreased below 50% in four tests; the corresponding brain tissue PO2 values were less than 10 mm Hg in three of those tests, whereas in the fourth, the jugular venous O2 desaturation was not detected by brain tissue PO2. The analysis of the simultaneous relative changes (prehyperventilation — posthyperventilation) of SjvO2 and brain tissue PO2 showed that in most tests (75.5%) there was a reduction of both SjvO2 and brain tissue PO2. In two tests moderate hyperventilation resulted in an increase of both SjvO2 and brain tissue PO2. In the remaining 17 tests a redistribution of the cerebral blood flow was observed, leading to changes in SjvO2 and brain tissue PO2 in opposite directions. Conclusions. Hyperventilation, even if moderate, can frequently result in harmful local reductions of cerebral perfusion that cannot be detected by assessing SjvO2. Therefore, hyperventilation should be used with caution and should not be considered safe. This study confirms that SjvO2 and brain tissue PO2 are two parameters that provide complementary information on brain oxygenation that is useful to reduce the risk of secondary damage. Changes in SjvO2 and brain tissue PO2 in opposite directions indicate that data obtained from brain tissue PO2 monitoring cannot be extrapolated to evaluate the global cerebral perfusion.

Association between elevated brain tissue glycerol levels and poor outcome following severe traumatic brain injury

2005 ◽  
Vol 103 (2) ◽  
pp. 233-238 ◽  
Author(s):  
Tobias Clausen ◽  
Oscar Luis Alves ◽  
Michael Reinert ◽  
Egon Doppenberg ◽  
Alois Zauner ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Severe Traumatic Brain Injury ◽  
Time Course ◽  
Glycerol Concentration ◽  
Significant Information ◽  
Content Type ◽  
Significant Difference ◽  
Fine Print

Object. Glycerol is considered to be a marker of cell membrane degradation and thus cellular lysis. Recently, it has become feasible to measure via microdialysis cerebral extracellular fluid (ECF) glycerol concentrations at the patient's bedside. Therefore the aim of this study was to investigate the ECF concentration and time course of glycerol after severe traumatic brain injury (TBI) and its relationship to patient outcome and other monitoring parameters. Methods. As soon as possible after injury for up to 4 days, 76 severely head-injured patients were monitored using a microdialysis probe (cerebral glycerol) and a Neurotrend sensor (brain tissue PO2) in uninjured brain tissue confirmed by computerized tomography scanning. The mean brain tissue glycerol concentration in all monitored patients decreased significantly from 206 ± 31 µmol/L on Day 1 to 9 ± 3 µmol/L on Day 4 after injury (p < 0.0001). Note, however, that there was no significant difference in the time course between patients with a favorable outcome (Glasgow Outcome Scale [GOS] Scores 4 and 5) and those with an unfavorable outcome (GOS Scores 1–3). Significantly increased glycerol concentrations were observed when brain tissue PO2 was less than 10 mm Hg or when cerebral perfusion pressure was less than 70 mm Hg. Conclusions. Based on results in the present study one can infer that microdialysate glycerol is a marker of severe tissue damage, as seen immediately after brain injury or during profound tissue hypoxia. Given that brain tissue glycerol levels do not yet add new clinically significant information, however, routine monitoring of this parameter following traumatic brain injury needs further validation.

Intercenter variance in clinical trials of head trauma—experience of the National Acute Brain Injury Study: Hypothermia

2001 ◽  
Vol 95 (5) ◽  
pp. 751-755 ◽  
Author(s):  
Guy L. Clifton ◽  
Sung C. Choi ◽  
Emmy R. Miller ◽  
Harvey S. Levin ◽  
Kenneth R. Smith ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Brain Injury ◽  
Phase Iii ◽  
Severe Brain Injury ◽  
Quality Of Data ◽  
Content Type ◽  
Physiological Variables ◽  
Arterial Blood ◽  
Present On Admission ◽  
Fine Print

Object. In a recently conducted trial of hypothermia in patients with severe brain injury, differences were found in the effects of hypothermia treatment among various centers. This analysis explores the reasons for such differences. Methods. The authors reviewed data obtained in 392 patients treated for severe brain injury. Prerandomization variables, critical physiological variables, treatment variables, and accrual methodologies were investigated among various centers. Hypothermia was found to be detrimental in patients older than the age of 45 years, beneficial in patients younger than 45 years of age in whom hypothermia was present on admission, and without effect in those in whom normothermia was documented on admission. Marginally significant differences (p < 0.054) in the intercenter outcomes of hypothermia-treated patients were likely the result of wide differences in the percentage of patients older than 45 years of age and in the percentage of patients in whom hypothermia was present on admission among centers. The trial sensitivity was likely diminished by significant differences in the incidence of mean arterial blood pressure (MABP) less than 70 mm Hg (p < 0.001) and cerebral perfusion pressure (CPP) less than 50 mm Hg (p < 0.05) but not intracranial pressure (ICP) greater than 25 mm Hg (not significant) among patients in the various centers. Hours of vasopressor usage (p < 0.03) and morphine dose (p < 0.001) and the percentage of dehydrated patients varied significantly among centers (p < 0.001). The participation of small centers increased intercenter variance and diminished the quality of data. Conclusions. For Phase III clinical trials we recommend: 1) a detailed protocol specifying fluid and MABP, ICP, and CPP management; 2) continuous monitoring of protocol compliance; 3) a run-in period for new centers to test accrual and protocol adherence; and 4) inclusion of only centers in which patients are regularly randomized.

Relative importance of hypertension compared with hypervolemia for increasing cerebral oxygenation in patients with cerebral vasospasm after subarachnoid hemorrhage

2005 ◽  
Vol 103 (6) ◽  
pp. 974-981 ◽  
Author(s):  
Andreas Raabe ◽  
Jügen Beck ◽  
Mike Keller ◽  
Hartmuth Vatter ◽  
Michael Zimmermann ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Brain Tissue ◽  
Cerebral Vasospasm ◽  
Moderate Hypertension ◽  
Cerebral Oxygenation ◽  
Brain Oxygenation ◽  
Content Type ◽  
Arterial Blood ◽  
Hypertension Therapy ◽  
Fine Print

Object. Hypervolemia and hypertension therapy is routinely used for prophylaxis and treatment of symptomatic cerebral vasospasm at many institutions. Nevertheless, there is an ongoing debate about the preferred modality (hypervolemia, hypertension, or both), the degree of therapy (moderate or aggressive), and the risk or benefit of hypervolemia, moderate hypertension, and aggressive hypertension in patients following subarachnoid hemorrhage. Methods. Monitoring data and patient charts for 45 patients were retrospectively searched to identify periods of hypervolemia, moderate hypertension, or aggressive hypertension. Measurements of central venous pressure, fluid input, urine output, arterial blood pressure, intracranial pressure, and oxygen partial pressure (PO2) in the brain tissue were extracted from periods ranging from 1 hour to 24 hours. For these periods, the change in brain tissue PO2 and the incidence of complications were analyzed. During the 55 periods of moderate hypertension, an increase in brain tissue PO2 was found in 50 cases (90%), with complications occurring in three patients (8%). During the 25 periods of hypervolemia, an increase in brain oxygenation was found during three intervals (12%), with complications occurring in nine patients (53%). During the 10 periods of aggressive hypervolemic hypertension, an increase in brain oxygenation was found during six of the intervals (60%), with complications in five patients (50%). Conclusions. When hypervolemia treatment is applied as in this study, it may be associated with increased risks. Note, however, that further studies are needed to determine the role of this therapeutic modality in the care of patients with cerebral vasospasm. In poor-grade patients, moderate hypertension (cerebral perfusion pressure 80–120 mm Hg) in a normovolemic, hemodiluted patient is an effective method of improving cerebral oxygenation and is associated with a lower complication rate compared with hypervolemia or aggressive hypertension therapy.

Influence of oxygen therapy on glucose—lactate metabolism after diffuse brain injury

2004 ◽  
Vol 101 (2) ◽  
pp. 323-329 ◽  
Author(s):  
Michael Reinert ◽  
Benoit Schaller ◽  
Hans Rudolf Widmer ◽  
Rolf Seiler ◽  
Ross Bullock
Keyword(s):  
Brain Injury ◽  
Brain Tissue ◽  
Brain Metabolism ◽  
Arterial Line ◽  
Content Type ◽  
Diffuse Brain Injury ◽  
Lactate Levels ◽  
The Brain ◽  
Fine Print ◽  
Diffuse Brain

Object. Severe traumatic brain injury (TBI) imposes a huge metabolic load on brain tissue, which can be summarized initially as a state of hypermetabolism and hyperglycolysis. In experiments O2 consumption has been shown to increase early after trauma, especially in the presence of high lactate levels and forced O2 availability. In recent clinical studies the effect of increasing O2 availability on brain metabolism has been analyzed. By their nature, however, clinical trauma models suffer from a heterogeneous injury distribution. The aim of this study was to analyze, in a standardized diffuse brain injury model, the effect of increasing the fraction of inspired O2 on brain glucose and lactate levels, and to compare this effect with the metabolism of the noninjured sham-operated brain. Methods. A diffuse severe TBI model developed by Foda and Maramarou, et al., in which a 420-g weight is dropped from a height of 2 m was used in this study. Forty-one male Wistar rats each weighing approximately 300 g were included. Anesthesized rats were monitored by placing a femoral arterial line for blood pressure and blood was drawn for a blood gas analysis. Two time periods were defined: Period A was defined as preinjury and Period B as postinjury. During Period B two levels of fraction of inspired oxygen (FiO2) were studied: air (FiO2 0.21) and oxygen (FiO2 1). Four groups were studied including sham-operated animals: air-air-sham (AAS); air-O2-sham (AOS); air-air-trauma (AAT); and air-O2-trauma (AOT). In six rats the effect of increasing the FiO2 on serum glucose and lactate was analyzed. During Period B lactate values in the brain determined using microdialysis were significantly lower (p < 0.05) in the AOT group than in the AAT group and glucose values in the brain determined using microdialysis were significantly higher (p < 0.04). No differences were demonstrated in the other groups. Increasing the FiO2 had no significant effect on the serum levels of glucose and lactate. Conclusions. Increasing the FiO2 influences dialysate glucose and lactate levels in injured brain tissue. Using an FiO2 of 1 influences brain metabolism in such a way that lactate is significantly reduced and glucose significantly increased. No changes in dialysate glucose and lactate values were found in the noninjured brain.

The effect of nimodipine on cerebral oxygenation in patients with poor-grade subarachnoid hemorrhage

2004 ◽  
Vol 101 (4) ◽  
pp. 594-599 ◽  
Author(s):  
Michael F. Stiefel ◽  
Gregory G. Heuer ◽  
John M. Abrahams ◽  
Stephanie Bloom ◽  
Michelle J. Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Brain Tissue ◽  
Cerebral Oxygenation ◽  
Content Type ◽  
Poor Grade ◽  
Physiological Variables ◽  
Arterial Blood ◽  
End Tidal ◽  
Fine Print

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.

Regional cerebrovascular and metabolic effects of hyperventilation after severe traumatic brain injury

2002 ◽  
Vol 96 (1) ◽  
pp. 103-108 ◽  
Author(s):  
Michael N. Diringer ◽  
Tom O. Videen ◽  
Kent Yundt ◽  
Allyson R. Zazulia ◽  
Venkatesh Aiyagari ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Metabolic Rate ◽  
Severe Traumatic Brain Injury ◽  
Content Type ◽  
Severe Tbi ◽  
The Mean ◽  
Gcs Score ◽  
Energy Failure ◽  
Fine Print

Object. Recently, concern has been raised that hyperventilation following severe traumatic brain injury (TBI) could lead to cerebral ischemia. In acute ischemic stroke, in which the baseline metabolic rate is normal, reduction in cerebral blood flow (CBF) below a threshold of 18 to 20 ml/100 g/min is associated with energy failure. In severe TBI, however, the metabolic rate of cerebral oxygen (CMRO2) is low. The authors previously reported that moderate hyperventilation lowered global hemispheric CBF to 25 ml/100 g/min but did not alter CMRO2. In the present study they sought to determine if hyperventilation lowers CBF below the ischemic threshold of 18 to 20 ml/100 g/min in any brain region and if those reductions cause energy failure (defined as a fall in CMRO2). Methods. Two groups of patients were studied. The moderate hyperventilation group (nine patients) underwent hyperventilation to PaCO2 of 30 ± 2 mm Hg early after TBI, regardless of intracranial pressure (ICP). The severe hyperventilation group (four patients) underwent hyperventilation to PaCO2 of 25 ± 2 mm Hg 1 to 5 days postinjury while ICP was elevated (20–30 mm Hg). The ICP, mean arterial blood pressure, and jugular venous O2 content were monitored, and cerebral perfusion pressure was maintained at 70 mm Hg or higher by using vasopressors when needed. All data are given as the mean ± standard deviation unless specified otherwise. The moderate hyperventilation group was studied 11.2 ± 1.6 hours (range 8–14 hours) postinjury, the admission Glasgow Coma Scale (GCS) score was 5.6 ± 1.8, the mean age was 27 ± 9 years, and eight of the nine patients were men. In the severe hyperventilation group, the admission GCS score was 4.3 ± 1.5, the mean age was 31 ± 6 years, and all patients were men. Positron emission tomography measurements of regional CBF, cerebral blood volume, CMRO2, and oxygen extraction fraction (OEF) were obtained before and during hyperventilation. In all 13 patients an automated search routine was used to identify 2.1-cm spherical nonoverlapping regions with CBF values below thresholds of 20, 15, and 10 ml/100 g/min during hyperventilation, and the change in CMRO2 in those regions was determined. In the regions in which CBF was less than 20 ml/100 g/min during hyperventilation, it fell from 26 ± 6.2 to 13.7 ± 1 ml/100 g/min (p < 0.0001), OEF rose from 0.31 to 0.59 (p < 0.0001), and CMRO2 was unchanged (1.12 ± 0.29 compared with 1.14 ± 0.03 ml/100 g/min; p = 0.8). In the regions in which CBF was less than 15 ml/100 g/min during hyperventilation, it fell from 23.3 ± 6.6 to 11.1 ± 1.2 ml/100 g/min (p < 0.0001), OEF rose from 0.31 to 0.63 (p < 0.0001), and CMRO2 was unchanged (0.98 ± 0.19 compared with 0.97 ± 0.23 ml/100 g/min; p = 0.92). In the regions in which CBF was less than 10 ml/100 g/min during hyperventilation, it fell from 18.2 ± 4.5 to 8.1 ± 0 ml/100 g/min (p < 0.0001), OEF rose from 0.3 to 0.71 (p < 0.0001), and CMRO2 was unchanged (0.78 ± 0.26 compared with 0.84 ± 0.32 ml/100 g/min; p = 0.64). Conclusions. After severe TBI, brief hyperventilation produced large reductions in CBF but not energy failure, even in regions in which CBF fell below the threshold for energy failure defined in acute ischemia. Oxygen metabolism was preserved due to the low baseline metabolic rate and compensatory increases in OEF; thus, these reductions in CBF are unlikely to cause further brain injury.

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