Partial Pressure Of Brain Tissue Oxygen Research Articles

Brain tissue oxygen partial pressure monitoring and prognosis of patients with traumatic brain injury: a meta-analysis.

To assess whether monitoring brain tissue oxygen partial pressure (PbtO2) or employing intracranial pressure (ICP)/cerebral perfusion pressure (CCP)-guided management improves patient outcomes, including mortality, hospital length of stay (LOS), mean daily ICP and mean daily CCP during the intensive care unit(ICU)stay. We searched the Web of Science, EMBASE, PubMed, Cochrane Library, and MEDLINE databases until December 12, 2023. Prospective randomized controlled and cohort studies were included. A meta-analysis was performed for the primary outcome measure, mortality, following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Eleven studies with a total of 37,492 patients were included. The mortality in the group with PbtO2 was 29.0% (odds ratio: 0.73;95% confidence interval [CI]:0.56-0.96; P = 0.03; I = 55%), demonstrating a significant benefit. The overall hospital LOS was longer in the PbtO2 group than that in the ICP/CPP group (mean difference:2.03; 95% CI:1.03-3.02; P<0.0001; I = 39%). The mean daily ICP in the PbtO2 monitoring group was lower than that in the ICP/CPP group (mean difference:-1.93; 95% CI: -3.61 to -0.24; P = 0.03; I = 41%). Moreover, PbtO2 monitoring did not improve the mean daily CPP (mean difference:2.43; 95%CI: -1.39 to 6.25;P = 0.21; I = 56%).Compared with ICP/CPP monitoring, PbtO2 monitoring reduced the mortality and the mean daily ICP in patients with severe traumatic brain injury; however, no significant effect was noted on the mean daily CPP. In contrast, ICP/CPP monitoring alone was associated with a short hospital stay.

Metabolism changes during direct revascularization in moyamoya disease: illustrative case.

Cerebral revascularization is recommended for patients with moyamoya disease (MMD) with reduced cerebral perfusion reserve and recurrent or progressive ischemic events. The standard surgical treatment for these patients is a low-flow bypass with or without indirect revascularization. The use of intraoperative monitoring of the metabolic profile using analytes such as glucose, lactate, pyruvate, and glycerol has not yet been described during cerebral artery bypass surgery for MMD-induced chronic cerebral ischemia. The authors aimed to describe an illustrative case using intraoperative microdialysis and brain tissue oxygen partial pressure (PbtO2) probes in a patient with MMD during direct revascularization. The patient's severe tissue hypoxia situation was confirmed by a PbtO2:partial pressure of oxygen (PaO2) ratio below 0.1 and anaerobic metabolism by a lactate:pyruvate ratio greater than 40. Following bypass, a rapid and sustained increase in PbtO2 up to normal values (PbtO2:PaO2 ratio between 0.1 and 0.35) and the normalization of cerebral energetic metabolism with a lactate/pyruvate ratio less than 20 was observed. The results show a quick improvement of regional cerebral hemodynamics due to the direct anastomosis procedure, reducing the incidence of subsequent ischemic stroke in pediatric and adult patients immediately.

Dynamic oxygen changes during status epilepticus and subsequent endogenous kindling.

ObjectiveBrain tissue oxygen (partial oxygen pressure [pO2]) levels are tightly regulated to stay within the normoxic zone, with deviations on either side resulting in impaired brain function. Whereas pathological events such as ischemic attacks and brief seizures have previously been shown to result in pO2 levels well below the normoxic zone, oxygen levels during prolonged status epilepticus (SE) and the subsequent endogenous kindling period are unknown.MethodsWe utilized two models of acquired temporal lobe epilepsy in rats: intrahippocampal kainic acid infusion and prolonged perforant pathway stimulation. Local tissue oxygen was measured in the dorsal hippocampus using an optode during and for several weeks following SE.ResultsWe observed hyperoxia in the hippocampus during induced SE in both models. Following termination of SE, 88% of rats initiated focal self‐generated spiking activity in the hippocampus within the first 7 days, which was associated with dynamic oxygen changes. Self‐generated and recurring epileptiform activity subsequently organized into higher‐frequency bursts that became progressively longer and were ultimately associated with behavioral seizures that became more severe with time and led to postictal hypoxia.SignificanceInduced SE and self‐generated recurrent epileptiform activity can have profound and opposing effects on brain tissue oxygenation that may serve as a biomarker for ongoing pathological activity in the brain.

Multimodal Monitoring Technologies for Pathophysiology and Management of Traumatic Brain Injury

Despite decades of efforts, severe traumatic brain injury (TBI) is still the leading cause for mortality and immobility of children and young adults worldwide and is a great burden to the health-care system. After injury, the oxygen supply is conventionally considered the monitoring parameter in a neurosurgical Intensive Care Unit. However, the overall mortality rate has only slightly improved since the late twentieth century. Evolving evidence suggests that dysfunction of oxygen utilization might be the underlying pathophysiology of secondary brain injury, which should also be a key parameter for multimodal monitoring and management after severe TBI. In this review, we summarize the current and advanced understanding of multimodal monitoring for severe TBI along with novel noninvasive technologies in this field. By continuously monitoring patients with severe TBI, the use of multimodal monitoring technologies including (but not limited to) computed tomography, cerebral microdialysis, near-infrared spectroscopy, magnetic resonance spectroscopy, high-performance liquid chromatography, and magnetic induction phase shift method will be crucial for observing disease changes such as intracranial pressure and brain tissue oxygen partial pressure as well as developing potential therapeutic strategies after severe TBI.

Hyperbaric oxygen therapy ameliorates acute brain injury after porcine intracerebral hemorrhage at high altitude.

IntroductionIntracerebral hemorrhage (ICH) at high altitude is not well understood to date. This study investigates the effects of high altitude on ICH, and examines the acute neuroprotection of hyperbaric oxygen (HBO) therapy against high-altitude ICH.MethodsMinipigs were placed in a hypobaric chamber for 72 h before the operation. ICH was induced by an infusion of autologous arterial blood (3 ml) into the right basal ganglia. Animals in the high-altitude ICH group received HBO therapy (2.5 ATA for 60 min) 30 min after ICH. Blood gas, blood glucose and brain tissue oxygen partial pressure (PbtO2) were monitored continuously for animals from all groups, as were microdialysis products including glucose, lactate, pyruvate and glutamate in perihematomal tissue from 3 to 12 h post-ICH.ResultsHigh-altitude ICH animals showed significantly lower PbtO2, higher lactate/pyruvate ratio (LPR) and glutamate levels than low-altitude ICH animals. More severe neurological deficits, brain edema and neuronal damage were also observed in high-altitude ICH. After HBO therapy, PbtO2 was significantly increased and LPR and glutamate levels were significantly decreased. Brain edema, neurological deficits and neuronal damage were also ameliorated.ConclusionsThe data suggested a more serious disturbance of tissue oxygenation and cerebral metabolism in the acute stage after ICH at high altitude. Early HBO treatment reduced acute brain injury, perhaps through a mechanism involving the amelioration of the derangement of cerebral oxygenation and metabolism following high-altitude ICH.

Quelle pression de perfusion cérébrale après traumatisme crânien chez l’enfant ?

The management of cerebral perfusion pressure (CPP) is the one of the main preoccupation for the care of paediatric traumatic brain injury (TBI). The physiology of cerebral autoregulation, CO2 vasoreactivity, cerebral metabolism changes with age as well as the brain compliance. Low CPP leads to high morbidity and mortality in pediatric TBI. The recent guidelines for the management of CPP for the paediatric TBI indicate a CPP threshold 40–50mmHg (infants for the lower and adolescent for the upper). But we must consider the importance of age-related differences in the arterial pressure and CPP. The best CPP is the one that allows to avoid cerebral ischaemia and oedema. In this way, the adaptation of optimal CPP must be individual. To assess this objective, interesting tools are available. Transcranial Doppler can be used to determine the best level of CPP. Other indicators can predict the impairment of autoregulation like pressure reactivity index (PRx) taking into consideration the respective changes in ICP and CPP. Measurement of brain tissue oxygen partial pressure is an other tool that can be used to determine the optimal CPP.

The Frontal Lobe and Thalamus Have Different Sensitivities to Hypoxia-Hypotension after Traumatic Brain Injury: A Microdialysis Study in Rats

After traumatic brain injury (TBI), lesions are anatomically heterogeneous, but the spatial heterogeneity of the post-traumatic brain's vulnerability to hypoxia-hypotension (HH) has been poorly studied. Our objective was to compare the effect of HH after TBI on brain energy metabolism into two regions: the frontal lobe and the thalamus. Twenty-eight Sprague-Dawley rats were randomized into four groups: sham, TBI (brain trauma alone, impact acceleration, 450-g weight drop from 1.8 m), HH (blood depletion to mean arterial pressure 40 mm Hg, FiO(2) 10%, 15 min), and TBI-HH (TBI followed by HH, 45-min delay). Cerebral perfusion pressure (CPP) was continuously measured. Brain microdialysis and brain tissue oxygen partial pressure (PtiO(2)) probes were both inserted stereotaxically into the right thalamus and frontal lobe. Except during the HH period, CPP was always above 60 mm Hg. During the hour following the HH period, significant increases in cerebral lactate-pyruvate ratio, glycerol, and glutamate were observed, and were always higher in the frontal lobe than in the thalamus (p<0.001). In the TBI-HH group and in the frontal lobe, increases in glutamate and glycerol were significantly higher than in the HH group (p<0.001). During the 30 min following the HH phase (reperfusion), an increase in PtiO(2) was observed. In the TBI-HH group, this increase was significantly lower in the frontal lobe than in the thalamus. These findings demonstrate that in the early post-traumatic period, the metabolic cerebral response to HH is higher in the frontal lobe than in the thalamus, and is worsened by TBI, suggesting a higher vulnerability for the frontal lobes.

A Surgical Model of Permanent and Transient Middle Cerebral Artery Stroke in the Sheep

BackgroundAnimal models are essential to study the pathophysiological changes associated with focal occlusive stroke and to investigate novel therapies. Currently used rodent models have yielded little clinical success, however large animal models may provide a more suitable alternative to improve clinical translation. We sought to develop a model of acute proximal middle cerebral artery (MCA) ischemic stroke in sheep, including both permanent occlusion and transient occlusion with reperfusion.Materials and Methods18 adult male and female Merino sheep were randomly allocated to one of three groups (n = 6/gp): 1) sham surgery; 2) permanent proximal MCA occlusion (MCAO); or 3) temporary MCAO with aneurysm clip. All animals had invasive arterial blood pressure, intracranial pressure and brain tissue oxygen monitoring. At 4 h following vessel occlusion or sham surgery animals were killed by perfusion fixation. Brains were processed for histopathological examination and infarct area determination. 6 further animals were randomized to either permanent (n = 3) or temporary MCAO (n = 3) and then had magnetic resonance imaging (MRI) at 4 h after MCAO.ResultsEvidence of ischemic injury in an MCA distribution was seen in all stroke animals. The ischemic lesion area was significantly larger after permanent (28.8%) compared with temporary MCAO (14.6%). Sham animals demonstrated no evidence of ischemic injury. There was a significant reduction in brain tissue oxygen partial pressure after permanent vessel occlusion between 30 and 210 mins after MCAO. MRI at 4 h demonstrated complete proximal MCA occlusion in the permanent MCAO animals with a diffusion deficit involving the whole right MCA territory, whereas temporary MCAO animals demonstrated MRA evidence of flow within the right MCA and smaller predominantly cortical diffusion deficits.ConclusionsProximal MCAO can be achieved in an ovine model of stroke via a surgical approach. Permanent occlusion creates larger infarct volumes, however aneurysm clip application allows for reperfusion.

Use of Serum Biomarkers to Predict Cerebral Hypoxia after Severe Traumatic Brain Injury

The management of severe traumatic brain injury (TBI) focuses on prevention and treatment of secondary insults such as cerebral hypoxia (CH). There are a number of biomarkers that are thought to play a part in secondary injury following severe TBI. This study evaluates the association between S100β, neuron-specific enolase (NSE), and glial fibrillary acidic protein (GFAP), detected in the serum of severe TBI patients and CH as measured by brain tissue oxygen partial pressure (Pbo(2)). Patients with severe TBI were prospectively enrolled. Pressure times time (PTD; mm Hg*h), measuring the depth and duration of CH, was calculated for 12-h periods for episodes of moderate (Pbo(2) < 20 mm Hg) and severe (Pbo(2) < 15 mm Hg) CH, and compared to serum levels of S100β, NSE, and GFAP drawn prior to periods of monitoring. An adjusted mixed model analysis was applied as was receiver operating characteristic (ROC) curve analysis. Of 76 patients enrolled, 24 had Pbo(2) monitoring. One hundred and thirty serum samples were matched with 12-h periods of monitoring. Significant associations were found in adjusted analyses between increasing serum levels of S100β (coefficient=0.57, 0.56; p<0.001), NSE (coefficient=0.48, 0.52; p<0.001), and GFAP (coefficient=0.29, 0.30; p=0.003 and 0.002), and increasing PTD of moderate (Pbo(2)<20 mm Hg) and severe (Pbo(2)<15 mm Hg) CH. AUCs for the prediction of moderate and severe CH were 0.62 and 0.66 for S100β, 0.55 and 0.71 for NSE, and 0.50 and 0.62 for GFAP, respectively. Specificities were between 76% and 90% for S100β and NSE. S100β, NSE, and GFAP demonstrate promise as candidate serum markers of impending CH. The fact that these biomarker elevations occur prior to the onset of clinical manifestations suggests that we may be able to predict imminent events following TBI. Given the morbidity of CH, early intervention and prevention may have a significant impact on outcomes and help guide decisions about the timing of interventions.

Fluctuation of Brain Tissue Oxygen Partial Pressure: A Biochemical Landmark in the Arctic Ground Squirrel's Spontaneous Arousal

Hibernation in the Arctic ground Squirrel (AGS) is a regulated, adaptive response to arctic environmental conditions. Problem statement: Regional brain Blood Flow (rCBF) has been observed to increase dramatically during arousal in hibernators. However, the real time dynamic change in PtO2 during arousal has not been studied, we hypothesized that PtO2 is Interdependent of Tbrain and a key component in the arousal process. Approach: Simultaneous in vivo measurements of PtO2 and brain temperature (Tbrain) in conjunction with oxygen consumption (V02) were conducted in the striatum of non-sedated, non-anesthetized Arctic ground squirrels during spontaneous arousal from hibernation. Results: A dramatic fluctuation of brain tissue oxygen partial pressure (PtO2) is associated with the complex phenomena of spontaneous arousal. In this study, we observed that: (1) a PtO2 elevation precedes changes in Tbrain and V02; (2) PtO2 changes do not correlate with changes in V02 during arousal and (3), endogenous O2 shift from O2 enriched blood to brain in hibernating AGS induces an arousal with the pharmaceutical chemical, efaproxiral (RSR-13). Conclusion: The four turning points of PtO2 appearing at different Tbrain during arousal suggest that changes in PtO2 are Tbrain interdependent and support the concept that arousal from hibernation is complex process invoking different feedbacks.

Effects of Hyperoxia on Brain Tissue Oxygen Tension in Non-Sedated, Non- Anesthetized Arctic Ground Squirrels: An Animal Model of Hyperoxic Stress

Arctic Ground Squirrels (AGS) are classic hibernators known for their tolerance to hypoxia. AGS have been studied as a model of hypoxia with potential as a medical research model. Problem statement: Their unique resistance to the stressors of low oxygen led us to hypothesize that AGS might also be adaptable to hyperoxia. Approach: This study examined the physiological pattern associated with hyperoxia in response to brain tissue oxygen partial pressure (PtO2), brain temperature (Tbrain), global oxygen consumption (VO2) and respiratory frequency (fR) using non-sedated and nonanesthetized Arctic Ground Squirrels (AGS) and rats. Results: We found that 1) 100% inspired oxygen (FiO2) increased the baseline values of brain PtO2 significantly in both summer euthermic AGS (24.4 ± 3.6-87.3 ± 3.6 mmHg, n=6) and in rats (18.2 ± 5.2-73.3 ± 5.2 mmHg, n = 3); PtO2 was significantly higher in AGS than in rats during hyperoxic exposure; 2) hyperoxic exposure had no effect on brain temperature in either AGS or rats, with the brain temperatures maintaining constancy before, during and after 100% O2 exposure; 3) systemic metabolic rates increased significantly during hyperoxic exposure in both euthermic AGS and rats; moreover, VO2 were significantly lower in AGS than in rats during hyperoxic exposure; 4) the respiratory rates for rats were maintained before, during and after 100% O2 exposure, while the respiratory responding patterns to hyperoxic exposure changed after exposure in AGS. AGS fR was significantly lower after hyperoxic exposure than before the exposure. Conclusion: These results suggest that hyperoxic ventilation induced PtO2 and VO2 differences between AGS and rats and led to altered respiratory patterns between these species. AGS and the rat serves as an excellent comparative model for hypoxic and hyperoxic stress studies of the brain.

Patient Transport and Brain Oxygen in Comatose Patients

Transport of critically ill intensive care unit patients may be hazardous. We examined whether brain oxygen (brain tissue oxygen partial pressure [PbtO2]) is influenced by transport to and from a follow-up head computed tomography (transport head computed tomography [tHCT]) scan. Forty-five patients (24 men, 21 women; Glasgow Coma Scale score < or =8; mean age, 47.3 +/- 19.0 years) who had a traumatic brain injury (n = 26) or subarachnoid hemorrhage (n = 19) were retrospectively identified from a prospective observational cohort of PbtO2 monitoring in a neurosurgical intensive care unit at a university-based level I trauma center. PbtO2, intracranial pressure, and cerebral perfusion pressure were monitored continuously and compared during the 3 hours before and after 100 tHCT scans. The mean PbtO2 before and after the tHCT scans for all 100 scans was 37.9 +/- 19.8 mm Hg and 33.9 +/- 17.2 mm Hg, respectively (P = .0001). A decrease in PbtO2 (>5%) occurred after 54 tHCTs (54%) and in 36 patients (80%). In instances in which a decrease occurred, the average decrease in mean, minimum, and maximum PbtO2 was 23.6%, 29%, and 18.1%, respectively. This decrease was greater when PbtO2 was compromised (<25 mm Hg) before tHCT. An episode of brain hypoxia (<15 mm Hg) was identified in the 3 hours before tHCT in 9 and after tHCT in 19 instances. On average, an episode of brain hypoxia was 46.6 +/- 16.0 (standard error) minutes longer after tHCT than before tHCT (P = .008). Multivariate analysis suggests that changes in lung function (PaO2/fraction of inspired oxygen [FiO2] ratio) may account for the reduced PbtO2 after tHCT (parameter estimate 0.45, 95% confidence interval: 0.024-0.871; P = .04). These data suggest that transport to and from the intensive care unit may adversely affect PbtO2. This deleterious effect is greater when PbtO2 is already compromised and may be associated with lung function.

The physiology behind direct brain oxygen monitors and practical aspects of their use

Secondary neuronal injury is implicated in poor outcome after acute neurological insults. Outcome can be improved with protocol-driven therapy. These therapies have largely been based on monitoring and control of intracranial pressure and the maintenance of an adequate cerebral perfusion pressure. In recent years, brain tissue oxygen partial pressure (PbtO2) monitoring has emerged as a clinically useful modality and a complement to intracranial pressure monitors. This review examines the physiology of PbtO2 monitors and practical aspects of their use.

Adaptive response of brain tissue oxygenation to environmental hypoxia in non-sedated, non-anesthetized arctic ground squirrels

The present study examined the physiological mechanisms of the responses of brain tissue oxygen partial pressure (P tO 2), brain temperature ( T brain), global oxygen consumption (V̇ O2), and respiratory frequency ( f R) to hypoxia in non-sedated and non-anesthetized arctic ground squirrels ( Spermophilus parryii, AGS) and rats. We found that (1) in contrast to oxygen partial pressure in blood (P aO 2), the baseline value of P tO 2 in summer euthermic AGS is significantly higher than in rats; (2) both P tO 2 and P aO 2 are dramatically reduced by inspired 8% O 2 in AGS and rats, but AGS have a greater capacity in P tO 2 to cope with environmental hypoxia; (3) metabolic rate before, during, and after hypoxic exposure is consistently lower in AGS than in rats; (4) the respiratory responding patterns to hypoxia in the two species differ in that f R decreases in AGS but increases in rats. These results suggest that (1) AGS have special mechanisms to maintain higher P tO 2 and lower P aO 2, and these levels in AGS represent a typical pattern of adaptation of heterothermic species to and a brain protection from hypoxia; (2) AGS brain responds to hypoxia through greater decreases in P tO 2 and decreased f R and ventilation. In contrast, rat brain responds to hypoxia by less reduction in P tO 2 and increased f R and ventilation.

Simultaneous measurement of brain tissue oxygen partial pressure, temperature, and global oxygen consumption during hibernation, arousal, and euthermy in non-sedated and non-anesthetized Arctic ground squirrels

This study reports an online temperature correction method for determining tissue oxygen partial pressure ( P t O 2 ) in the striatum and a novel simultaneous measurement of brain P t O 2 and temperature ( T brain) in conjunction with global oxygen consumption ( V O 2 ) in non-sedated and non-anesthetized freely moving Arctic ground squirrels (AGS, Spermophilus parryii). This method fills an important research gap—the lack of a suitable method for physiologic studies of tissue P O 2 in hibernating or other cool-blooded species. P t O 2 in AGS brain during euthermy (21.22 ± 2.06 mmHg) is significantly higher ( P = 0.016) than during hibernation (13.21 ± 0.46 mmHg) suggests brain oxygenation in the striatum is normoxic during euthermy and hypoxic during hibernation. These results in P t O 2 are different from blood oxygen partial pressure ( P a O 2 ) in AGS, which are significantly lower during euthermy than during hibernation and are actually hypoxic during euthermy and normoxic during hibernation in our previous study. This intriguing difference between the P O 2 of brain tissue and blood during these two physiological states suggests that regional mechanisms in the brain play a role in maintaining tissue oxygenation and protect against hypoxia during hibernation.

Monitoring of cerebral oxygenation with near infrared spectroscopy and tissue oxygen partial pressure during cardiopulmonary resuscitation in pigs

The present study was designed to compare cerebral oxygenation measured with near infrared spectroscopy and local brain tissue oxygen partial pressure, respectively, in pigs during cardiopulmonary resuscitation. Since tissue overlying the brain may have an impact on near infrared spectroscopy readings, we tested whether optode placement on intact skin or on the skull yielded comparable results. Twelve healthy pigs were anaesthetized and subjected to continuous haemodynamic, near infrared spectroscopy and brain tissue oxygen partial pressure monitoring. After 4 min of untreated ventricular fibrillation, cardiopulmonary resuscitation was started and arginine vasopressin was administered repeatedly three times. Near infrared spectroscopy values recorded were both the tissue oxygenation index and the tissue haemoglobin index as well as relative changes of chromophores (haemoglobin and cytochrome oxidase). Four animals served as control and were measured with both near infrared spectroscopy optodes mounted on the intact skin of the forehead, while in the remaining eight animals, one near infrared spectroscopy optode was implanted directly on the skull. Near infrared spectroscopy readings at the skin or at the skull differed consistently throughout the study period. After arginine vasopressin administration, near infrared spectroscopy values at the different locations showed a transient dissociation. In contrast to near infrared spectroscopy measured on intact skin, near infrared spectroscopy readings obtained from skull showed a significant correlation to brain tissue oxygen partial pressure values (r = 0.67, P < 0.001). Near infrared spectroscopy readings obtained from skin and skull differed largely after vasopressor administration. Near infrared spectroscopy optode placement therefore may have an important influence on the tissue region investigated.

The relationship between brain tissue oxygen partial pressure thresholds and microdialysis markers of ischaemia in traumatic brain injury

While cerebral ischaemia contributes significantly to secondary brain injury following trauma, there are no data on critical thresholds of brain tissue pO2 (PbO2) for metabolic compromise. The aim of this study was to identify ischaemic thresholds for changes in brain tissue lactate concentrations and lactate/pyruvate ratio. Eleven patients with severe traumatic brain injury, with brain tissue oxygen tension (NeurotrendTM) and microdialysis monitoring in place, were studied within the first 4 days following injury, over 4 h epochs during which physiology was carefully monitored and stabilised as part of a protocol involving transfusion of red cells. All patients were managed according to the Addenbrooke's Hospital Neuro-critical Care Unit head injury algorithm. Data for brain PbO2, and microdialysate glucose, lactate and pyruvate were measured over 20-minute intervals. Relationships between PbO2 and brain lactate level as well as lactate/pyruvate ratio were examined, and the significance of relationships assessed using non-parametric statistical methods. The eleven patients had a mean age of 34 years (range: 17 – 64), a median post-resuscitation GCS of 9 (range: 4 – 13) and 55% were female. Seven patients had the monitors placed in structurally normal-appearing tissue on CT scan, while in four patients the monitors were in abnormal tissue. Pooled mean ( standard deviation) PbO2 was 2.15 1.3 kPa, lactate 2.77 1.58 mmol/l, pyruvate 105 52 mol/l, and L/P ratio 26.6 5.4. There were no significant differences between normal and abnormal tissue, but PbO2 was less than 1 kPa only in abnormal tissue. Fitting with a Lowess function appeared to show an inflection point for increases in lactate at PbO2 below 1.5 kPa (Fig 1;). While the relationship between PbO2 and L/P ratio was also statistically significant (Spearman-Rank : - 0.358, p < 0.001), clear PbO2 threshold levels were less well defined. Brain tissue oxygen displays a threshold at about 1.5 kPa below which brain lactate increases in abnormal tissue. The absence of clear increases in L/P ratio below this threshold raises the possibility that brain lactate elevation in these areas may not entirely be due to tissue hypoxia. As PbO2 in normal tissue did not drop below 1 kPa, our data may be less representative of physiology in these areas. Further investigation is required in patients with low PbO2.

Packed red blood cell transfusion increases local cerebral oxygenation*

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. Prospective observational study. A neurosurgical intensive care unit at a university-based level I trauma center and tertiary care hospital. 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. None. 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). 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.

Treatment of Traumatic Brain Injury: One Size Does Not Fit All

Treatment of Traumatic Brain Injury: One Size Does Not Fit All

Prone position in subarachnoid hemorrhage patients with acute respiratory distress syndrome: effects on cerebral tissue oxygenation and intracranial pressure.

To analyze the effect of prone position on cerebral perfusion pressure and brain tissue oxygen partial pressure in subarachnoid hemorrhage patients with acute respiratory distress syndrome (ARDS). Clinical study with retrospective data analysis. Neurosurgical intensive care unit of a primary level university hospital. Sixteen patients treated for intracranial aneurysm rupture with initial Hunt and Hess grade III or worse who developed ARDS within 2 wks after the bleeding. Routine neurosurgical intensive care treatment for subarachnoid hemorrhage and posthemorrhagic vasospasm including cerebral monitoring with continuous intracranial pressure and brain tissue oxygen partial pressure recordings. Hemodynamics, arterial oxygenation, ventilatory setting, intracranial pressure, cerebral perfusion pressure, and brain tissue oxygen partial pressure in the supine as well as in the prone position were analyzed and compared. A significant increase in Pao(2) from 97.3 +/- 20.7 torr (mean +/- sd) in the supine position to 126.6 +/- 31.7 torr in the prone position was joined by a significant increase in brain tissue oxygen partial pressure from 26.8 +/- 10.9 torr to 31.6 +/- 12.2 torr (both p <.0001), whereas intracranial pressure increased from 9.3 +/- 5.2 mm Hg to 14.8 +/- 6.7 mm Hg and cerebral perfusion pressure decreased from 73.0 +/- 10.5 mm Hg to 67.7 +/- 10.7 mm Hg (both p <.0001). The beneficial effect of prone positioning on cerebral tissue oxygenation by increasing arterial oxygenation appears to outweigh the expected adverse effect of prone positioning on cerebral tissue oxygenation by decreasing cerebral perfusion pressure in ARDS patients.