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Anthony A Figaji - One of the best experts on this subject based on the ideXlab platform.
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a management algorithm for adult patients with both Brain oxygen and intracranial pressure monitoring the seattle international severe traumatic Brain injury consensus conference sibicc
Intensive Care Medicine, 2020Co-Authors: Randall M Chesnut, Sergio Aguilera, Andras Buki, Eileen M Bulger, Giuseppe Citerio, Jamie D Cooper, Ramon Diaz Arrastia, Michael N Diringer, Anthony A FigajiAbstract:Current guidelines for the treatment of adult severe traumatic Brain injury (sTBI) consist of high-quality evidence reports, but they are no longer accompanied by management protocols, as these require expert opinion to bridge the gap between published evidence and patient care. We aimed to establish a modern sTBI protocol for adult patients with both intracranial pressure (ICP) and Brain oxygen monitors in place. Our consensus working group consisted of 42 experienced and actively practicing sTBI opinion leaders from six continents. Having previously established a protocol for the treatment of patients with ICP monitoring alone, we addressed patients who have a Brain oxygen monitor in addition to an ICP monitor. The management protocols were developed through a Delphi-method-based consensus approach and were finalized at an in-person meeting. We established three distinct treatment protocols, each with three tiers whereby higher tiers involve therapies with higher risk. One protocol addresses the management of ICP elevation when Brain oxygenation is normal. A second addresses management of Brain Hypoxia with normal ICP. The third protocol addresses the situation when both intracranial hypertension and Brain Hypoxia are present. The panel considered issues pertaining to blood transfusion and ventilator management when designing the different algorithms. These protocols are intended to assist clinicians in the management of patients with both ICP and Brain oxygen monitors but they do not reflect either a standard-of-care or a substitute for thoughtful individualized management. These protocols should be used in conjunction with recommendations for basic care, management of critical neuroworsening and weaning treatment recently published in conjunction with the Seattle International Brain Injury Consensus Conference.
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Brain tissue oxygen tension monitoring in pediatric severe traumatic Brain injury part 1 relationship with outcome
Childs Nervous System, 2009Co-Authors: Anthony A Figaji, Peter Le D Roux, Eugene Zwane, Crispin Thompson, Graham A Fieggen, Andrew C Argent, Jonathan C PeterAbstract:Introduction Intracranial pressure (ICP) monitoring and cerebral perfusion pressure (CPP) management are the current standards to guide care of severe traumatic Brain injury (TBI). However, Brain Hypoxia and secondary Brain injury can occur despite optimal ICP and CPP. In this study, we used Brain tissue oxygen tension (PbtO(2)) monitoring to examine the association between multiple patient factors, including PbtO(2), and outcome in pediatric severe TBI. Materials and methods In this prospective observational study, 52 children (less than 15 years) with severe TBI were managed with continuous PbtO(2) and ICP monitoring. The relationships between outcome [Glasgow Outcome Score (GOS) and Pediatric Cerebral Performance Category Scale] and clinical, radiologic, treatment, and physiological variables, including PbtO(2), were examined using multiple logistic regression analysis. Results Outcome was favorable in 40 patients (77%) and unfavorable (mortality, 9.6%; n = 5) in 12 (23%). In univariate analysis, the following variables had a significant association with unfavorable outcome: initial GCS, computed tomography classification, ICP(peak), mICP(24), mICP, CPP(low), CPP( 1 h, the adjusted OR for poor outcome was 27.4 (95% confidence interval, 1.9-391). No variables apart from PbtO(2) were independently associated with mortality when controlled for PbtO(2). Conclusion Reduced PbtO(2) is shown to be an independent factor associated with poor outcome in pediatric severe TBI in the largest study to date. It appears to have a stronger association with outcome than conventionally evaluated measures.
Peter D Leroux - One of the best experts on this subject based on the ideXlab platform.
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Brain lactate metabolism in humans with subarachnoid hemorrhage
Stroke, 2012Co-Authors: Mauro Oddo, Joshua M Levine, Suzanne Frangos, Eileen Maloneywilensky, Roy Thomas Daniel, Marc Levivier, Emmanuel Carrera, Pierre J Magistretti, Peter D LerouxAbstract:Background and Purpose— Lactate is central for the regulation of Brain metabolism and is an alternative substrate to glucose after injury. Brain lactate metabolism in patients with subarachnoid hemorrhage has not been fully elucidated. Methods— Thirty-one subarachnoid hemorrhage patients monitored with cerebral microdialysis (CMD) and Brain oxygen (PbtO2) were studied. Samples with elevated CMD lactate (>4 mmol/L) were matched to PbtO2 and CMD pyruvate and categorized as hypoxic (PbtO2 119 μmol/L) versus nonhyperglycolytic. Results— Median per patient samples with elevated CMD lactate was 54% (interquartile range, 11%–80%). Lactate elevations were more often attributable to cerebral hyperglycolysis (78%; interquartile range, 5%–98%) than Brain Hypoxia (11%; interquartile range, 4%–75%). Mortality was associated with increased percentage of samples with elevated lactate and Brain Hypoxia (28% [interquartile range 9%–95%] in nonsurvivors versus 9% [interquartile range 3%–17%] in survivors; P =0.02) and lower percentage of elevated lactate and cerebral hyperglycolysis (13% [interquartile range, 1%–87%] versus 88% [interquartile range, 27%–99%]; P =0.07). Cerebral hyperglycolytic lactate production predicted good 6-month outcome (odds ratio for modified Rankin Scale score, 0–3 1.49; CI, 1.08–2.05; P =0.016), whereas increased lactate with Brain Hypoxia was associated with a reduced likelihood of good outcome (OR, 0.78; CI, 0.59–1.03; P =0.08). Conclusions— Brain lactate is frequently elevated in subarachnoid hemorrhage patients, predominantly because of hyperglycolysis rather than Hypoxia. A pattern of increased cerebral hyperglycolytic lactate was associated with good long-term recovery. Our data suggest that lactate may be used as an aerobic substrate by the injured human Brain.
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Brain tissue oxygen and outcome after severe traumatic Brain injury a systematic review
Critical Care Medicine, 2009Co-Authors: Eileen Maloneywilensky, Wei Yang, Vicente H Gracias, Arthur Itkin, Katherine Hoffman, Stephanie Bloom, Susan Christian, Peter D LerouxAbstract:Objective: In this study, available medical literature were reviewed to determine whether Brain Hypoxia as measured by Brain tissue oxygen (Bto 2 ) 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 BtO 2 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 Bto 2 monitor, 3) Brain Hypoxia defined as Bto 2 15 or 30 minutes, 4) 6-month outcome data, and 5) clear reporting of patient outcome associated with Bto 2 . For the analysis, each selected article had to have adequate data to determine odds ratios (ORs) and confidence intervals (Cls). 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 (Bto 2 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 Bto 2 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 Bto 2 probes are safe. These results imply that treating patients to increase Bto 2 may improve outcome after severe TBI. This question will require further study.
Pierre Bouzat - One of the best experts on this subject based on the ideXlab platform.
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mannitol improves Brain tissue oxygenation in a model of diffuse traumatic Brain injury
Critical Care Medicine, 2015Co-Authors: C Schilte, Pierre Bouzat, A Millet, Karin Pernetgallay, P Boucheix, Benjamin Lemasson, Emmanuel L Barbier, Jean Francois PayenAbstract:OBJECTIVES: Based on evidence supporting a potential relation between posttraumatic Brain Hypoxia and microcirculatory derangements with cell edema, we investigated the effects of the antiedematous agent mannitol on Brain tissue oxygenation in a model of diffuse traumatic Brain injury. DESIGN: Experimental study. SETTING: Neurosciences and physiology laboratories. SUBJECTS: Adult male Wistar rats. INTERVENTIONS: Thirty minutes after diffuse traumatic Brain injury (impact-acceleration model), rats were IV administered with either a saline solution (traumatic Brain injury-saline group) or 20% mannitol (1 g/kg) (traumatic Brain injury-mannitol group). Sham-saline and sham-mannitol groups received no insult. MEASUREMENTS AND MAIN RESULTS: Two series of experiments were conducted 2 hours after traumatic Brain injury (or equivalent) to investigate 1) the effect of mannitol on Brain edema and oxygenation, using a multiparametric magnetic resonance-based approach (n = 10 rats per group) to measure the apparent diffusion coefficient, tissue oxygen saturation, mean transit time, and blood volume fraction in the cortex and caudoputamen; 2) the effect of mannitol on Brain tissue PO2 and on venous oxygen saturation of the superior sagittal sinus (n = 5 rats per group); and 3) the cortical ultrastructural changes after treatment (n = 1 per group, taken from the first experiment). Compared with the sham-saline group, the traumatic Brain injury-saline group had significantly lower tissue oxygen saturation, Brain tissue PO2, and venous oxygen saturation of the superior sagittal sinus values concomitant with diffuse Brain edema. These effects were associated with microcirculatory collapse due to astrocyte swelling. Treatment with mannitol after traumatic Brain injury reversed all these effects. In the absence of traumatic Brain injury, mannitol had no effect on Brain oxygenation. Mean transit time and blood volume fraction were comparable between the four groups of rats. CONCLUSION: The development of posttraumatic Brain edema can limit the oxygen utilization by Brain tissue without evidence of Brain ischemia. Our findings indicate that an antiedematous agent such as mannitol can improve Brain tissue oxygenation, possibly by limiting astrocyte swelling and restoring capillary perfusion.
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changes in Brain tissue oxygenation after treatment of diffuse traumatic Brain injury by erythropoietin
Critical Care Medicine, 2013Co-Authors: Pierre Bouzat, A Millet, Yvonnick Boue, Karin Pernetgallay, Thibaut Trouvebuisson, Lucie GaidechevronnayAbstract:OBJECTIVES: To investigate the effects of recombinant human erythropoietin on Brain oxygenation in a model of diffuse traumatic Brain injury. DESIGN: Adult male Wistar rats. SETTING: Neurosciences and physiology laboratories. INTERVENTIONS: Thirty minutes after diffuse traumatic Brain injury (impact-acceleration model), rats were intravenously administered with either a saline solution or a recombinant human erythropoietin (5000 IU/kg). A third group received no traumatic Brain injury insult (sham-operated). MEASUREMENTS AND MAIN RESULTS: Three series of experiments were conducted 2 hours after traumatic Brain injury to investigate: 1) the effect of recombinant human erythropoietin on Brain edema using diffusion-weighted magnetic resonance imaging and measurements of apparent diffusion coefficient (n = 11 rats per group); local Brain oxygen saturation, mean transit time, and blood volume fraction were subsequently measured using a multiparametric magnetic resonance-based approach to estimate Brain oxygenation and Brain perfusion in the neocortex and caudoputamen; 2) the effect of recombinant human erythropoietin on Brain tissue PO₂ in similar experiments (n = 5 rats per group); and 3) the cortical ultrastructural changes after treatment (n = 1 rat per group). Compared with the sham-operated group, traumatic Brain injury saline rats showed a significant decrease in local Brain oxygen saturation and in Brain tissue PO₂ alongside Brain edema formation and microvascular lumen collapse at H2. Treatment with recombinant human erythropoietin reversed all of these traumatic Brain injury-induced changes. Brain perfusion (mean transit time and blood volume fraction) was comparable between the three groups of animals. CONCLUSION: Our findings indicate that Brain Hypoxia can be related to microcirculatory derangements and cell edema without evidence of Brain ischemia. These changes were reversed with post-traumatic administration of recombinant human erythropoietin, thus offering new perspectives in the use of this drug in Brain injury.
David K Menon - One of the best experts on this subject based on the ideXlab platform.
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Brain Hypoxia is associated with neuroglial injury in humans post cardiac arrest
Circulation Research, 2021Co-Authors: Ryan L Hoiland, Philip N Ainslie, Sharanjit Thiara, Denise Foster, Cheryl L Wellington, Jennifer Cooper, Sophie Stukas, Nicholas A Fergusson, Edward M Conway, David K MenonAbstract:Rationale: Secondary Brain Hypoxia portends significant mortality in ischemic Brain diseases, yet our understanding of hypoxic ischemic Brain injury (HIBI) pathophysiology in humans remains rudimentary. Objective: To quantify the impact of secondary Brain Hypoxia on injury to the neurovascular unit in patients with HIBI. Methods and Results: We conducted a prospective interventional study of invasive neuromonitoring in 18 post-cardiac arrest patients with HIBI. The partial pressures of Brain tissue O2 (PbtO2) and intracranial pressure were directly measured via intra-parenchymal micro-catheters. To isolate the cerebrovascular bed, we conducted paired sampling of arterial and jugular venous bulb blood and calculated the trans-cerebral release of biomarkers of neurovascular injury and inflammation in the HIBI patients and 14 healthy volunteers for control comparisons. Ten HIBI patients exhibited secondary Brain Hypoxia (PbtO2<20mmHg), while eight exhibited Brain normoxia (PbtO2≥20mmHg). In the patients with secondary Brain Hypoxia, we observed active cerebral release of glial fibrillary acidic protein (-161[ -3695 - -75] pg/mL; P=0.0078), neurofilament light chain (-231[-370 - -11] pg/mL; P=0.010), total tau (-32[-310 - -3] pg/mL; P=0.0039), neuron specific enolase (-14890[-148813 - -3311] pg/mL; P=0.0039), and ubiquitin carboxy-terminal hydrolase L1 (-14.7[-37.7 - -4.1] pg/mL; P=0.0059) indicating de novo neuroglial injury. This injury was unrelated to the systemic global ischemic burden or cerebral endothelial injury but rather was associated with cerebral release of interleukin-6 (-10.3[-43.0 - -4.2] pg/mL; P=0.0039). No cerebral release of the aforementioned biomarkers was observed in HIBI patients with Brain normoxia or the healthy volunteers. Hyperosmolar therapy in the patients with secondary Brain Hypoxia reduced the partial pressure of jugular venous O2-to-PbtO2 gradient (39.6[34.1-51.1] vs. 32.0[24.5-39.2] mmHg; P=0.0078) and increased PbtO2 (17.0[9.1-19.7] vs. 20.2[11.9-22.7] mmHg; P=0.039) suggesting improved cerebrovascular-to-parenchymal O2 transport. Conclusions: Secondary Brain Hypoxia is associated with de novo neuroglial injury and cerebral release of interleukin-6. Mitigating cerebrovascular-to-parenchymal limitations to O2 transport is a promising therapeutic strategy for HIBI patients with secondary Brain Hypoxia.
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Brain Hypoxia secondary to diffusion limitation in hypoxic ischemic Brain injury postcardiac arrest
Critical Care Medicine, 2020Co-Authors: Mypinder S Sekhon, Philip N Ainslie, David K Menon, Sharanjit Thiara, Danilo Cardim, Arun K Gupta, Ryan L Hoiland, Peter Gooderham, Donald E G GriesdaleAbstract:OBJECTIVES We sought to characterize 1) the difference in the diffusion gradient of cellular oxygen delivery and 2) the presence of diffusion limitation physiology in hypoxic-ischemic Brain injury patients with Brain Hypoxia, as defined by parenchymal Brain tissue oxygen tension less than 20 mm Hg versus normoxia (Brain tissue oxygen tension > 20 mm Hg). DESIGN Post hoc subanalysis of a prospective study in hypoxic-ischemic Brain injury patients dichotomized into those with Brain Hypoxia versus normoxia. SETTING Quaternary ICU. PATIENTS Fourteen adult hypoxic-ischemic Brain injury patients after cardiac arrest. INTERVENTIONS Patients underwent monitoring with Brain oxygen tension, intracranial pressure, cerebral perfusion pressure, mean arterial pressure, and jugular venous bulb oxygen saturation. Data were recorded in real time at 300Hz into the ICM+ monitoring software (Cambridge University Enterprises, Cambridge, United Kingdom). Simultaneous arterial and jugular venous bulb blood gas samples were recorded prospectively. MEASUREMENTS AND MAIN RESULTS Both the normoxia and Hypoxia groups consisted of seven patients. In the normoxia group, the mean Brain tissue oxygen tension, jugular venous bulb oxygen tension, and cerebral perfusion pressure were 29 mm Hg (SD, 9), 45 mm Hg (SD, 9), and 80 mm Hg (SD, 7), respectively. In the Hypoxia group, the mean Brain tissue oxygen tension, jugular venous bulb oxygen to Brain tissue oxygen tension gradient, and cerebral perfusion pressure were 14 mm Hg (SD, 4), 53 mm Hg (SD, 8), and 72 mm Hg (SD, 6), respectively. There were significant differences in the jugular venous bulb oxygen tension-Brain oxygen tension gradient (16 mm Hg [sd, 6] vs 39 mm Hg SD, 11]; p < 0.001) and in the relationship of jugular venous bulb oxygen tension-Brain oxygen tension gradient to cerebral perfusion pressure (p = 0.004) when comparing normoxia to Hypoxia. Each 1 mm Hg increase in cerebral perfusion pressure led to a decrease in the jugular venous bulb oxygen tension-Brain oxygen tension gradient by 0.36 mm Hg (95% CI, -0.54 to 0.18; p < 0.001) in the normoxia group, but no such relation was demonstrable in the Hypoxia group. CONCLUSIONS In hypoxic-ischemic Brain injury patients with Brain Hypoxia, there is an elevation in the jugular venous bulb oxygen tension-Brain oxygen tension gradient, which is not modulated by changes in cerebral perfusion pressure.
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the burden of Brain Hypoxia and optimal mean arterial pressure in patients with hypoxic ischemic Brain injury after cardiac arrest
Critical Care Medicine, 2019Co-Authors: Mypinder S Sekhon, David K Menon, Danilo Cardim, Arun K Gupta, Peter Gooderham, Penelope M A Brasher, Denise Foster, Marek Czosnyka, Peter Smielewski, Philip N AinslieAbstract:Objectives:In patients at risk of hypoxic ischemic Brain injury following cardiac arrest, we sought to: 1) characterize Brain oxygenation and determine the prevalence of Brain Hypoxia, 2) characterize autoregulation using the pressure reactivity index and identify the optimal mean arterial pressure,
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imaging of Brain Hypoxia in permanent and temporary middle cerebral artery occlusion in the rat using 18f fluoromisonidazole and positron emission tomography a pilot study
Journal of Cerebral Blood Flow and Metabolism, 2007Co-Authors: Masashi Takasawa, John S Beech, Tim D Fryer, Young T Hong, Jessica L Hughes, Keiji Igase, Simon P Jones, Rob Smith, Franklin I Aigbirhio, David K MenonAbstract:In acute stroke, the target of therapy is the severely hypoxic but salvageable tissue. Previous human studies using 18F-fluoromisonidazole and positron emission tomography (18F-FMISO PET) have shown high tracer retention indicative of tissue Hypoxia, which had normalized at repeat scan >48 h later. In the only validation study of 18F-FMISO, using ex vivo autoradiography in thread middle cerebral artery occluded (MCAo) rats, there was unexpected high uptake as late as 22 h after reperfusion, raising questions about the use of 18F-FMISO as a Hypoxia tracer. Here we report a pilot study of 18F-FMISO PET in experimental stroke. Spontaneous hypertensive rats were subjected to distal clip MCAo. Three-hour dynamic PET was performed in 7 rats: 3 normals, 1 with permanent MCAo (two sessions: 30 mins and 48 h after clip), and 3 with temporary MCAo (45 mins, n = 1; 120 mins, n = 2; scanning started 30 mins after clip removal). Experiments were terminated by perfusion—fixation for standard histopathology. Late tracer...
Lucie Gaidechevronnay - One of the best experts on this subject based on the ideXlab platform.
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changes in Brain tissue oxygenation after treatment of diffuse traumatic Brain injury by erythropoietin
Critical Care Medicine, 2013Co-Authors: Pierre Bouzat, A Millet, Yvonnick Boue, Karin Pernetgallay, Thibaut Trouvebuisson, Lucie GaidechevronnayAbstract:OBJECTIVES: To investigate the effects of recombinant human erythropoietin on Brain oxygenation in a model of diffuse traumatic Brain injury. DESIGN: Adult male Wistar rats. SETTING: Neurosciences and physiology laboratories. INTERVENTIONS: Thirty minutes after diffuse traumatic Brain injury (impact-acceleration model), rats were intravenously administered with either a saline solution or a recombinant human erythropoietin (5000 IU/kg). A third group received no traumatic Brain injury insult (sham-operated). MEASUREMENTS AND MAIN RESULTS: Three series of experiments were conducted 2 hours after traumatic Brain injury to investigate: 1) the effect of recombinant human erythropoietin on Brain edema using diffusion-weighted magnetic resonance imaging and measurements of apparent diffusion coefficient (n = 11 rats per group); local Brain oxygen saturation, mean transit time, and blood volume fraction were subsequently measured using a multiparametric magnetic resonance-based approach to estimate Brain oxygenation and Brain perfusion in the neocortex and caudoputamen; 2) the effect of recombinant human erythropoietin on Brain tissue PO₂ in similar experiments (n = 5 rats per group); and 3) the cortical ultrastructural changes after treatment (n = 1 rat per group). Compared with the sham-operated group, traumatic Brain injury saline rats showed a significant decrease in local Brain oxygen saturation and in Brain tissue PO₂ alongside Brain edema formation and microvascular lumen collapse at H2. Treatment with recombinant human erythropoietin reversed all of these traumatic Brain injury-induced changes. Brain perfusion (mean transit time and blood volume fraction) was comparable between the three groups of animals. CONCLUSION: Our findings indicate that Brain Hypoxia can be related to microcirculatory derangements and cell edema without evidence of Brain ischemia. These changes were reversed with post-traumatic administration of recombinant human erythropoietin, thus offering new perspectives in the use of this drug in Brain injury.