Relevant bibliographies by topics / Traumatic brain injury; intracranial pressure

Academic literature on the topic 'Traumatic brain injury; intracranial pressure'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Traumatic brain injury; intracranial pressure"

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Fan, Jun-Yu, Catherine Kirkness, Paolo Vicini, Robert Burr, and Pamela Mitchell. "Intracranial Pressure Waveform Morphology and Intracranial Adaptive Capacity." American Journal of Critical Care 17, no. 6 (November 1, 2008): 545–54. http://dx.doi.org/10.4037/ajcc2008.17.6.545.

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Background Intracranial hypertension due to primary and secondary injuries is a prime concern when providing care to patients with severe traumatic brain injury. Increases in intracranial pressure vary depending on compensatory processes within the craniospinal space, also referred to as intracranial adaptive capacity. In patients with traumatic brain injury and decreased intracranial adaptive capacity, intracranial pressure increases disproportionately in response to a variety of stimuli. However, no well-validated measures are available in clinical practice to predict the development of such an increase. Objectives To examine whether P2 elevation, quantified by determining the P2:P1 ratio (=0.8) of the intracranial pressure pulse waveform, is a unique predictor of disproportionate increases in intracranial pressure on a beat-by-beat basis in the 30 minutes preceding the elevation in patients with severe traumatic brain injury, within 48 hours after deployment of an intracranial pressure monitor. Methods A total of 38 patients with severe traumatic brain injury were sampled from a randomized controlled trial of cerebral perfusion pressure management in patients with traumatic brain injury or subarachnoid hemorrhage. Results The P2 elevation was not only present before the disproportionate increase in pressure, but also appeared in the comparison data set (within-subject without such a pressure increase). Conclusions P2 elevation is not a reliable clinical indicator to predict an impending disproportionate increase in intracranial pressure.
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Romner, Bertil, and Per-Olof Grände. "Intracranial pressure monitoring in traumatic brain injury." Nature Reviews Neurology 9, no. 4 (March 12, 2013): 185–86. http://dx.doi.org/10.1038/nrneurol.2013.37.

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Prasad, G. Lakshmi. "Intracranial Pressure Monitoring in Traumatic Brain Injury." World Neurosurgery 100 (April 2017): 702–3. http://dx.doi.org/10.1016/j.wneu.2016.12.096.

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Noble, Kim A. "Traumatic Brain Injury and Increased Intracranial Pressure." Journal of PeriAnesthesia Nursing 25, no. 4 (August 2010): 242–50. http://dx.doi.org/10.1016/j.jopan.2010.05.008.

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Smith, Martin. "Monitoring Intracranial Pressure in Traumatic Brain Injury." Anesthesia & Analgesia 106, no. 1 (January 2008): 240–48. http://dx.doi.org/10.1213/01.ane.0000297296.52006.8e.

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Hariri, Robert J., Andrew D. Firlick, Scott R. Shepard, Douglas S. Cohen, Philip S. Barie, John M. Emery, and Jamshid B. G. Ghajar. "Traumatic brain injury, hemorrhagic shock, and fluid resuscitation: effects on intracranial pressure and brain compliance." Journal of Neurosurgery 79, no. 3 (September 1993): 421–27. http://dx.doi.org/10.3171/jns.1993.79.3.0421.

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✓ Intracranial hypertension following traumatic brain injury is associated with considerable morbidity and mortality. Hemorrhagic hypovolemia commonly coexists with head injury in this population of patients. Therapy directed at correcting hypovolemic shock includes vigorous volume expansion with crystalloid solutions. It is hypothesized that, following traumatic brain injury, cerebrovascular dysfunction results in rapid loss of brain compliance, resulting in increased sensitivity to cerebrovascular venous pressure. Increased central venous pressure (CVP) occurring with vigorous crystalloid resuscitation may therefore contribute to the loss of brain compliance and the development of intracranial hypertension. The authors tested this hypothesis in miniature swine subjected to traumatic brain injury, hemorrhage, and resuscitation. Elevated CVP following resuscitation from hemorrhage to a high CVP significantly worsened intracranial hypertension in animals with concurrent traumatic brain injury, as compared to animals subjected to traumatic brain injury alone (mean ± standard error of the mean: 33.0 ± 2.0 vs. 20.0 ± 2.0 mm Hg, p < 0.05) or to animals subjected to the combination of traumatic brain injury, hemorrhage, and resuscitation to a low CVP (33.0 ± 2.0 vs. 24.0 ± 2.0 mm Hg, p < 0.05). These data support the hypothesis that reduction in brain compliance can occur secondary to elevation of CVP following resuscitation from hemorrhagic shock. This may worsen intracranial hypertension in patients with traumatic brain injury and hemorrhagic shock.
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Flower, Oliver, and Simon Hellings. "Sedation in Traumatic Brain Injury." Emergency Medicine International 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/637171.

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Several different classes of sedative agents are used in the management of patients with traumatic brain injury (TBI). These agents are used at induction of anaesthesia, to maintain sedation, to reduce elevated intracranial pressure, to terminate seizure activity and facilitate ventilation. The intent of their use is to prevent secondary brain injury by facilitating and optimising ventilation, reducing cerebral metabolic rate and reducing intracranial pressure. There is limited evidence available as to the best choice of sedative agents in TBI, with each agent having specific advantages and disadvantages. This review discusses these agents and offers evidence-based guidance as to the appropriate context in which each agent may be used. Propofol, benzodiazepines, narcotics, barbiturates, etomidate, ketamine, and dexmedetomidine are reviewed and compared.
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Apetrei, Al Cosmin, A. Şt Iencean, A. Iordache, B. Iliescu, and Ion Poeata. "Intracranial pressure monitoring in severe traumatic brain injury." Romanian Neurosurgery 21, no. 2 (June 1, 2014): 193–99. http://dx.doi.org/10.2478/romneu-2014-0021.

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AbstractIntracranial pressure monitoring seems to be an indispensable stage in management of severe traumatic brain injured patient. Since 2009, this technique completes our trauma protocol. The study has been carried out from 2011 to 2013 in Prof. Dr. N. Oblu hospital in Iasi. There have been included in the study patients with severe craniocerebral trauma, who had traumatic brain lesions CT detected and Glasgow score between 3 and 8. The age ranged from 16 to 60, an average of 35.5 years old. 50% of the studied cases had a favorable outcome. Diagrams associated to this category of patients showed increases in intracranial pressure above normal values but without repeated values above 50 mm Hg. Most of those patients had a good evolution under medical treatment. Monitoring intracranial pressure is an extremely useful stage in treating intracranial high pressure in traumatology and it should be included in the equipment of any intensive therapy section caring traumatic patients
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Link, Caroline, Ana Flávia Botelho, Thomas Markus Dhaese, Gustavo Frigieri, José Carlos Rebuglio Vellosa, and Leonardo Christiaan Welling. "Noninvasive intracranial pressure in patients with traumatic brain injury." Research, Society and Development 11, no. 10 (August 12, 2022): e471111033106. http://dx.doi.org/10.33448/rsd-v11i10.33106.

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Monitoring and treatment of intracranial pressure are extremely important procedures in the management of patients with traumatic brain injury. The monitoring methods currently marketed are invasive and are not suitable for all patients. In addition to the risks offered, they are not available on all services. This study aims to describe the cases of five patients with traumatic brain injury of different severity who underwent noninvasive monitoring of intracranial pressure in the acute phase of the injury, relating the changes identified with the clinical picture presented. Patients showed important changes in intracranial pressure wave morphology, possibly related to the lesions, clinical presentation and therapeutic interventions used.
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Marshall, Lawrence F. "Pediatric traumatic brain injury and elevated intracranial pressure." Journal of Neurosurgery: Pediatrics 2, no. 4 (October 2008): 237–38. http://dx.doi.org/10.3171/ped.2008.2.10.237.

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Dissertations / Theses on the topic "Traumatic brain injury; intracranial pressure"

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Donnelly, Joseph. "Intracranial monitoring after severe traumatic brain injury." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/271422.

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Intracranial monitoring after severe traumatic brain injury offers the possibility for early detection and amelioration of physiological insults. In this thesis, I explore cerebral insults due raised intracranial pressure, decreased cerebral perfusion pressure and impaired cerebral pressure reactivity after traumatic brain injury. In chapter 2, the importance of intracranial pressure, cerebral perfusion pressure and pressure reactivity in regulating the cerebral circulation is elucidated along with a summary of the existing evidence supporting intracranial monitoring in traumatic brain injury. In chapter 4, intracranial pressure, cerebral perfusion pressure, and pressure reactivity insults are demonstrated to be common, prognostically important, and responsive to long-term changes in management policies. Further, while these insults often occur independently, coexisting insults portend worse prognosis. In chapter 5, I examine possible imaging antecedents of raised intracranial pressure and demonstrate that initial subarachnoid haemorrhage is associated with the subsequent development of elevated intracranial pressure. In addition, elevated glucose during the intensive care stay is associated with worse pressure reactivity. Cortical blood flow and brain tissue oxygenation are demonstrated to be sensitive to increases in intracranial pressure in chapter 6. In chapter 7, a method is proposed to estimate the cerebral perfusion pressure limits of reactivity in real-time, which may allow for more nuanced intensive care treatment. Finally, I explore a recently developed visualisation technique for intracranial physiological insults and apply it to the cerebral perfusion pressure limits of reactivity. Taken together, this thesis outlines the scope, risk factors and consequences of intracranial insults after severe traumatic brain injury. Novel signal processing applications are presented that may serve to facilitate a physiological, personalised and precision approach to patient therapy.
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Rohlwink, Ursula Karin. "Paediatric traumatic Brain Injury: The relationship between Intracranial Pressure and Brain Oxygenation." Master's thesis, University of Cape Town, 2009. http://hdl.handle.net/11427/2889.

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Introduction: Intracranial pressure (ICP) monitoring is a cornerstone of care for patients with severe traumatic brain injury (TBI). The primary goal of ICP treatment is to preserve brain oxygenation, and since brain oxygenation is usually not measured, the control of ICP is used as a surrogate marker. However studies indicating that cerebral hypoxia/ischemia may occur in the face of adequate ICP and cerebral perfusion pressure (CPP) suggest that the interaction between ICP and brain oxygenation is poorly understood and warrants further investigation. This is of particular importance in the context of children in whom the interpretation of relationships between intracranial factors is even more complex due to changing physiological norms with age. To date little scientific data exists in children and treatment threshold values are often extrapolated from adult guidelines. This study aims to better understand the relationship between ICP and brain oxygenation measured as brain tissue oxygen tension (PbtO2) in a large paediatric cohort suffering from severe TBI. Specifically analysis 1) investigated ICP and PbtO2 profiles over time following TBI, 2) examined the relationship between ICP and PbtO2 from time-linked paired observations, 3) explored various critical thresholds for ICP and PbtO2, and 4) interrogated digital data trends depicting the relationship between ICP and PbtO2. The level of agreement between hourly recorded and high frequency electronic data for ICP and PbtO2 was also evaluated. Method: Paired ICP and PbtO2 data from 75 children with severe TBI were tested with correlation and regression. Additional analyses controlled for mean arterial pressure (MAP), arterial partial pressure of oxygen (PaO2), CPP, arterial partial pressure of carbon dioxide (PaCO2) and haemoglobin (Hb) using multivariate logistic regression analysis and general estimating equations. Various thresholds for ICP were examined; these included age-related thresholds to account for the potential influence of age. Receiver-operating curves (ROCs) were used to graphically demonstrate the relationships between various thresholds of ICP and various definitions of low PbtO2. These were constructed for pooled and individual patient data. Interrogation of electronically recorded data allowed for case illustrations examining the relationship between ICP and PbtO2 at selected time points. Hourly and electronic data were compared using Bland and Altman plots and by contrasting the frequency of ICP and PbtO2 perturbations recorded with each system. 5 Result: Analyses using over 8300 hours of paired observations revealed a weak relationship between ICP and PbtO2, with an initially positive but weak slope (r = 0.05) that trended downwards only at higher values of ICP. Controlling for inter-individual differences, as well as MAP, CPP, PaO2, PaCO2 and Hb did not strengthen this association. This poor relationship was further reflected in the examination of threshold ICP values with ROCs, no singular critical ICP threshold for compromised brain oxygenation was discernible. Using age-based thresholds did not improve this relationship and individual patient ROCs demonstrated inter-individual heterogeneity in the relationship between ICP and PbtO2. However, it was clear that in individual patients ICP did exhibit a strong negative relationship with PbtO2 at particular time points, but various different relationships between the 2 variables were also demonstrated. A high level of agreement was found between hourly and electronic data. Conclusion: These results suggest that the relationship between ICP and PbtO2 is highly complex. Although the relationship in individual children at specific time points may be strong, pooled data for the entire cohort of patients, and even for individual patients, suggest only a weak relationship. This is likely because several other factors affect PbtO2 outside of ICP, and some factors affect both independently of each other. These results suggest that more study should be directed at optimising ICP thresholds for treatment in children. The use of complimentary monitoring modalities may assist in this task. Depending on the adequacy of measures of brain perfusion, metabolism or oxygenation, it is possible that targeting a range of ICP values in individual patients may be appropriate; however this would require detailed investigation.
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Elf, Kristin. "Secondary Insults in Neurointensive Care of Patients with Traumatic Brain Injury." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4837.

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Fan, Jun-Yu. "Intracranial pressure waveform analysis in traumatic brain injury : an approach to determining parameters capable of prediction decreased intracranial adaptive capacity /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/7312.

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Wu, Zhizhen. "Flexible Microsensors based on polysilicon thin film for Monitoring Traumatic Brain Injury (TBI)." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1512045589967871.

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Pahren, Laura. "PHM for Biomedical Analytics: A Case Study on Neurophysiologic Data from Patients with Traumatic Brain Injury." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1490352193060328.

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Nyholm, Lena. "Quality systems to avoid secondary brain injury in neurointensive care." Doctoral thesis, Uppsala universitet, Neurokirurgi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-253005.

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Outcome after traumatic brain injury (TBI) depends on the extent of primary cell death and on the development of secondary brain injury. The general aim of this thesis was to find strategies and quality systems to minimize the extent of secondary insults in neurointensive care (NIC). An established standardized management protocol system, multimodality monitoring and computerized data collection, and analysis systems were used. The Uppsala TBI register was established for regular monitoring of NIC quality indexes. For 2008-2010 the proportion of patients improving during NIC was 60-80%, whereas 10% deteriorated. The percentage of ‘talk and die’ cases was < 1%. The occurrences of secondary insults were less than 5% of good monitoring time (GMT) for intracranial pressure (ICP) > 25 mmHg, cerebral perfusion pressure (CPP) < 50 mmHg and systolic blood pressure < 100 mmHg. Favorable outcome was achieved by 64% of adults. Nurse checklists of secondary insult occurrence were introduced. Evaluation of the use of nursing checklists showed that the nurses documented their assessments in 84-85% of the shifts and duration of monitoring time at insult level was significantly longer when secondary insults were reported regarding ICP, CPP and temperature. The use of nurse checklist was found to be feasible and accurate.  A clinical tool to avoid secondary insults related to nursing interventions was developed. Secondary brain insults occurred in about 10% of nursing interventions. There were substantial variations between patients. The risk ratios of developing an ICP insult were 4.7 when baseline ICP ≥ 15 mmHg, 2.9 when ICP amplitude ≥ 6 mmHg and 1.7 when pressure autoregulation ≥ 0.3. Hyperthermia, which is a known frequent secondary insult, was studied. Hyperthermia was most common on Day 7 after admission and 90% of the TBI patients had hyperthermia during the first 10 days at the NIC unit. The effects of hyperthermia on intracranial dynamics (ICP, brain energy metabolism and BtipO2) were small but individual differences were observed. Hyperthermia increased ICP slightly more when temperature increased in the groups with low compliance and impaired pressure autoregulation. Ischemic pattern was never observed in the microdialysis samples. The treatment of hyperthermia may be individualized and guided by multimodality monitoring.
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Dodge, Lydia. "Investigating the effects of acute intracranial pressure and brain oxygenation on neuropsychological outcomes 12 months after severe pediatric traumatic brain injury." Master's thesis, Faculty of Humanities, 2019. http://hdl.handle.net/11427/30832.

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Traumatic brain injury (TBI) is one of the major causes of mortality and morbidity among children and adolescents all over the world and studies suggest a higher incidence of pediatric TBI (pTBI), as well as poorer post-TBI outcomes, in countries with extreme levels of socioeconomic inequality such as South Africa. pTBI leads to a multitude of long-term adverse outcomes in a wide range of domains and in general, a dose-response pattern is evident. Multiple acute and post-acute stage predictors of outcome have been investigated, however acute stage neurological and neurosurgical variables are relatively absent from this knowledge base. This study was conducted to better understand the heterogeneity in outcomes of pTBI: it aimed to investigate the nature and severity of neuropsychological deficits in pTBI patients one year after injury and to investigate the association between acute stage physiological changes in intracranial pressure (ICP) and brain tissue oxygenation (PbtO2) and neuropsychological outcomes one year after pTBI. Results of the study indicated that children who sustained TBI performed significantly poorer than healthy, matched controls on multiple cognitive, behavioural and quality of life domains, however, neither acute ICP nor PbtO2 reliably predicted within-TBI group performance. The results of the study emphasise the poor relationship of ICP and PbtO2, and the complexity of the relationship between acute physiological variables and outcomes after pTBI. Further studies of this kind should be done on large sample sizes and include multiple physiological variables.
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Tume, Lyvonne Nicole. "The effect of intensive care nursing interventions on the intracranial pressure in children with moderate to severe traumatic brain injury." Thesis, Liverpool John Moores University, 2009. http://researchonline.ljmu.ac.uk/5951/.

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Objective The aim of this study was to examine the effects of selected routine nursing interventions - endotracheal suctioning and manual ventilation (ETSMV), log-rolling, eye care, mouth care and washing - on the intracranial pressure (ICP) in children with traumatic brain injury. Design Prospective observational study over three years. Setting Single tertiary paediatric intensive care unit in the North West of England. Patients Twenty five children with moderate to severe closed traumatic brain injury and intraparenchymal intracranial pressure monitoring in intensive care (2 -17 years of age). Interventions Routine nursing care interventions. Measurements and main results ICP measured one minute before the procedure, at the maximal value during the procedure and five minutes after the procedure was recorded for the purpose of this study. Time to recovery was also recorded, in minutes. A total of 25 measurements (the first one in each child) in the first 36 hours of the child's PICU admission were analysed. Both ETSMV and log-rolling were associated with clinically and statistically significant changes in ICP from baseline to maximal ICP (p=0.005) and maximal to 5-minute post ICP (p=0.001) for ETSMV and (p < 0.001) baseline to maximal ICP and (p=0.002) for maximal to post-procedure ICP for log-rolling. During ETSMV and logrolling 70% of children exceeded the 20mmHg clinical treatment threshold during the interventions. During both ETSMV and log-rolling children with higher baseline ICPs ( > 15mmHg) showed higher maximal ICPs (but not ICP rise), suggesting a linear relationship between baseline and maximal ICP, although this was more pronounced during turning. One third of the children had not returned to their baseline ICP by 5 minutes after ETSMV, compared with 60% children after log-rolling. Neither eye care nor mouth care showed any clinically significant effects on ICP in these children, suggesting these procedures are not noxious and are tolerated very well. However, there was only a small number of washing episodes reported in this study therefore the observations are not conclusive. Conclusions Endotracheal suctioning and log-rolling in moderate to severe traumatic brain injured children can cause significant intracranial instability and should only be performed as required and with careful planning and execution. Eye and mouth care and washing appear to be well tolerated interventions and could be performed when necessary.
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Flynn, Liam Martin Clint. "Physiological responses to brain tissue hypoxia and blood flow after acute brain injury." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31268.

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This thesis explores physiological changes occurring after acute brain injury. The first two chapters focus on traumatic brain injury (TBI), a significant cause of disability and death worldwide. I discuss the evidence behind current management of secondary brain injury with emphasis on partial brain oxygen tension (PbtO2) and intracranial pressure (ICP). The second chapter describes a subgroup analysis of the effect of hypothermia on ICP and PbtO2 in 17 patients enrolled to the Eurotherm3235 trial. There was a mean decrease in ICP of 4.1 mmHg (n=9, p < 0.02) and a mean decrease in PbtO2 (7.8 ± 3.1 mmHg (p < 0.05)) in the hypothermia group that was not present in controls. The findings support previous studies in demonstrating a decrease in ICP with hypothermia. Decreased PbtO2 could partially explain worse outcomes seen in the hypothermia group in the Eurotherm3235 trial. Further analysis of PbtO2 and ICP guided treatment is needed. The third chapter focuses on delayed cerebral ischaemia (DCI) after aneurysmal subarachnoid haemorrhage (aSAH), another form of acute brain injury that causes significant morbidity and mortality. I include a background of alpha-calcitonin gene-related peptide (αCGRP), a potential treatment of DCI, along with results from a systematic review and meta-analysis of nine experimental models investigating αCGRP. The meta-analysis demonstrates a 40.8 ± 8.2% increase in cerebral vessel diameter in those animals treated with αCGRP compared with controls (p < 0.0005, 95% CI 23.7 to 57.9). Neurobehavioural scores were reported in four publications and showed a Physiological responses to brain tissue hypoxia and blood flow after acute brain injury standardised mean difference of 1.31 in favour of αCGRP (CI -0.49 to 3.12). I conclude that αCGRP reduces cerebral vessel narrowing seen after SAH in animal studies but note that there is insufficient evidence to determine its effect on functional outcomes. A review of previous trials of αCGRP administration in humans is included, in addition to an original retrospective analysis of CSF concentrations of αCGRP in humans. Enzyme-linked immunosorbent assay of CSF (n = 22) was unable to detect αCGRP in any sample, which contrasts with previous studies and was likely secondary to study methodology. Finally, I summarise by discussing a protocol I designed for a dose-toxicity study involving the intraventricular administration of αCGRP to patients with aSAH and provide some recommendations for future research. This protocol was based upon the systematic review and was submitted to the Medical Research Council's DPFS funding stream during the PhD.
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Books on the topic "Traumatic brain injury; intracranial pressure"

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Marmarou, Anthony, Ross Bullock, Cees Avezaat, Alexander Baethmann, Donald Becker, Mario Brock, Julian Hoff, Hajime Nagai, Hans-J. Reulen, and Graham Teasdale, eds. Intracranial Pressure and Neuromonitoring in Brain Injury. Vienna: Springer Vienna, 1998. http://dx.doi.org/10.1007/978-3-7091-6475-4.

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Ratcliff, Jonathan J., and David W. Wright. Neuroprotection for Traumatic Brain Injury. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0008.

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Traumatic brain injury (TBI) is a common, clinically complex, heterogeneous global public health problem. Neuroprotection strategies focus on preventing secondary injury by creating a physiologic environment devoid of extremes while targeting normal physiologic parameters. Careful attention must be paid to aggressively avoid and treat hypoxia, hypotension, hypoglycemia, intracranial hypertension, and cerebral hypoperfusion (low cerebral perfusion pressure). Aggressive management of intracranial pressure and cerebral perfusion pressure through optimal patient positioning, appropriate use of sedation and analgesia, and administration of hyperosmolar therapy remain the hallmark for the care of the TBI patient. Surgical decompressive craniectomy and hypothermia hold promise but remain controversial and should be used in carefully selected clinical situations. Early identification of injury progression is aided through careful monitoring by clinical examination and cerebral physiological monitoring. Multimodal monitoring provides an early warning system to guide appropriate clinical responses to identified deranged physiology.
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Gibson, Alistair A., and Peter J. D. Andrews. Management of traumatic brain injury. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0343.

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Traumatic brain injury (TBI) is a leading cause of death and disability worldwide and although young male adults are at particular risk, it affects all ages. TBI often occurs in the presence of significant extracranial injuries and immediate management focuses on the ABCs—airway with cervical spine control, breathing, and circulation. Best outcomes are achieved by management in centres that can offer comprehensive neurological critical care and appropriate management for extracranial injuries. If patients require transfer from an admitting hospital to a specialist centre, the transfer must be carried out by an appropriately skilled and equipped transport team. The focus of specific TBI management is on the avoidance of secondary injury to the brain. The principles of management are to avoid hypotension and hypoxia, control intracranial pressure and maintain cerebral perfusion pressure above 60 mmHg. Management of increased intracranial pressure is generally by a stepwise approach starting with sedation and analgesia, lung protective mechanical ventilation to normocarbia in a 30° head-up position, maintenance of oxygenation, and blood pressure. Additional measures include paralysis with a neuromuscular blocking agent, CSF drainage via an external ventricular drain, osmolar therapy with mannitol or hypertonic saline, and moderate hypothermia. Refractory intracranial hypertension may be treated surgically with decompressive craniectomy or medically with high dose barbiturate sedation. General supportive measures include provision of adequate nutrition preferably by the enteral route, thromboembolism prophylaxis, skin and bowel care, and management of all extracranial injuries.
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Wecksell, Matthew, and Kenneth Fomberstein. Traumatic Brain Injury and C-Spine Management. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0020.

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Traumatic brain injury encompasses two different types of pathology: that caused at the time of the initial physical insult, called primary injury, and then further, secondary injury caused by either host cellular responses such as oxidative injury and inflammation or by physiological insults such as ischemia, hypoxia, hypo- or hypercapnia, intracranial hypertension, and hypo- or hyperglycemia. While primary injury falls to the realm of public health (e.g., encouraging helmet use for sports, discouraging impaired driving, etc.), many secondary injuries are avoidable with proper medical management. As the stem case for this chapter, an older patient experiences a fall and is incoherent on presentation to the emergency room. This case concerns her initial management, stabilization, diagnosis, and airway management. With progression of her traumatic brain injury, the authors discuss intracranial pressure management, surgical management, and resuscitation as well as likely postoperative sequelae.
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Aisiku, Imoigele, and Claudia S. Robertson. Epidemiology and pathophysiology of traumatic brain injury. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0341.

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Although medical management of traumatic brain injury (TBI) may have improved in developed countries, TBI is still a major cause of mortality and morbidity. The demographics are skewed towards the younger patient population, and affects males more than females, but in general follow a bimodal distribution with peaks affecting young adults and the elderly. As a result, the loss of functional years is devastating. Pathology due to brain trauma is a complex two-hit phenomenon, frequently divided into ‘primary’ and ‘secondary’ injury. Hypoxia, ischaemia, and inflammation all play a role, and the importance of each component varies between patients and in an individual patient over time. The initial injury may increase intracranial pressure and reduce cerebral perfusion due to the presence of mass lesions or diffuse brain swelling. Further secondary insults, such as hypotension, reduced cerebral perfusion pressure, hypoxia, or fever may exacerbate swelling and inflammation, and further compromise cerebral perfusion. Although there are currently no specific effective treatments for TBI, an improved understanding of the pathophysiology may eventually lead to treatments that will reduce mortality and improve long-term functional outcome.
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Mathews, Letha, and John Barwise. Refractory Intracranial Hypertension. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0067.

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Intracranial pressure remains constant in adults at 10–15 mmHg under normal conditions with some fluctuations associated with respirations, coughing, sneezing, and so forth. Refractory intracranial hypertension (ICH) is defined by recurrent episodes of intracranial pressure elevation above 20 mmHg for sustained periods (10–15 min) despite medical therapy. The common causes of ICH are traumatic brain injury, brain tumors, subarachnoid hemorrhage, and brain infarction from arterial occlusion, cerebral venous thrombosis, and anoxic encephalopathy. Intracranial infections, abscesses, acute liver encephalopathy, and idiopathic ICH are also recognized causes of ICH. For the purposes of this chapter, the discussion is limited to ICH related to traumatic brain injury.
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Rhodes, Jonathan K. J., and Peter J. D. Andrews. Intracranial pressure monitoring in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0223.

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Intracranial pressure (ICP) measurement is an established monitoring modality in the ICU and can aid prognostication after acute brain injury. ICP monitoring is recommended in all patients with severe traumatic brain injury (TBI), and an abnormal cranial computed tomographic (CT) scan and the ability to control ICP is associated with improved outcome after TBI. The lessons from TBI studies can also be applied to other acute pathologies of the central nervous system where ICP can be increased. ICP measurement can warn of impending disaster and allow intervention. Furthermore, measurement of ICP allows the calculation of cerebral perfusion pressure (CPP) and maintenance of CPP may help to ensure adequate cerebral oxygen delivery. Various systems exist to monitor ICP. A recent trial in two South American countries suggested that ICP-guided management and management guided by clinical examination and repeated imaging produced equivalent outcomes. Although this trial currently provides the best evidence regarding the impact of monitoring ICP on outcome following TBI, but because of the inadequate power and questionable external validity, the generalizability of the results remain to be confirmed.
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Prout, Jeremy, Tanya Jones, and Daniel Martin. Neuroanaesthesia and neurocritical care. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199609956.003.0022.

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This chapter describes the general conduct of anaesthesia for neurosurgery with particular reference to techniques for reducing intracranial pressure, safe positioning, and recognition and management of air embolus. Management for specific common procedures such as shunt surgery, haematomas, traumatic brain injury and pituitary surgery is described. Neurosurgical conditions such as cerebral aneurysms and arteriovenous malformations may be managed in neuroradiology and the special considerations for the provision of anaesthesia for these cases are detailed. The principles of management of traumatic brain injury in critical care which aim to reduce secondary brain injury are explained.
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Ferioli, Simona, and Lori Shutter. Normal anatomy and physiology of the brain. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0219.

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An understanding of the normal anatomy of the brain is essential to the diagnosis of a number of conditions that may be encountered in patients in the intensive care unit (ICU). Common structural cerebral conditions causing patients to be admitted to the ICU include cerebral trauma (traumatic brain injury), cerebrovascular accidents (both ischaemic and haemorrhagic), and infections. Cerebral conditions with a structural basis occurring after admission to the ICU are not as common as functional abnormalities, such as delirium, and peripheral complications, such as critical illness neuropathy and myopathy. An understanding of brain physiology, in particular factors that control or influence intracranial pressure (ICP) and cerebral blood flow (CBF) underpin much of the theory behind the management of acute brain injuries and syndromes.
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Adam, Sheila, Sue Osborne, and John Welch. Neurological problems. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199696260.003.0008.

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This chapter provides an overview of the care and management of neurological disorders commonly seen in critical care, starting with an outline of the anatomy and physiology of the nervous system. The concepts of awareness, consciousness, and arousal, and the use of the Glasgow Coma Scale (GCS) to assess conscious level are discussed. The management and monitoring of raised intracranial pressure, cerebral perfusion pressure, and the impact on cerebral blood flow are detailed. The management of sodium and water balance, including diabetes insipidus, is outlined. There are overviews of the management and nursing of patients who have suffered traumatic brain injury, subarachnoid haemorrhage, status epilepticus, myasthenia gravis, Guillain–Barré syndrome, meningitis, encephalitis, and intracranial abcess. The concept, ethics, and testing of brainstem death, organ donation, and the care of the family are detailed.
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Book chapters on the topic "Traumatic brain injury; intracranial pressure"

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Dahl, Bent Lob. "Intracranial Pressure Reduction." In Management of Severe Traumatic Brain Injury, 139–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28126-6_27.

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Reinstrup, Peter. "Intracranial Pressure (ICP)." In Management of Severe Traumatic Brain Injury, 157–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28126-6_30.

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Dahl, Bent Lob, and Kristian Dahl Friesgaard. "Intracranial Pressure Reduction." In Management of Severe Traumatic Brain Injury, 245–51. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39383-0_37.

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Andersen, B. J., and A. Marmarou. "Isolated Stimulation of Glycolysis Following Traumatic Brain Injury." In Intracranial Pressure VII, 575–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73987-3_149.

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Lu, J., A. Marmarou, S. Choi, A. Maas, G. Murray, and E. W. Steyerberg. "Mortality from traumatic brain injury." In Intracranial Pressure and Brain Monitoring XII, 281–85. Vienna: Springer Vienna, 2005. http://dx.doi.org/10.1007/3-211-32318-x_58.

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Reinstrup, Peter. "Intracranial Pressure (ICP): Theoretical and Practical Aspects." In Management of Severe Traumatic Brain Injury, 267–77. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39383-0_40.

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Tanno, H., L. Pitts, and L. J. Noble. "Breakdown of the Blood-Brain Barrier to Horseradish Peroxidase After Experimental Post-Traumatic Hypoxic Brain Injury." In Intracranial Pressure VIII, 148–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77789-9_32.

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Hutchinson, P. J. "Microdialysis in traumatic brain injury — methodology and pathophysiology." In Intracranial Pressure and Brain Monitoring XII, 441–45. Vienna: Springer Vienna, 2005. http://dx.doi.org/10.1007/3-211-32318-x_91.

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Katayama, Y., M. K. Cheung, A. Alves, and D. P. Becker. "Ion Fluxes and Cell Swelling in Experimental Traumatic Brain Injury: The Role of Excitatory Amino Acids." In Intracranial Pressure VII, 584–88. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-73987-3_151.

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McKeating, E. Grant, P. J. D. Andrews, and L. Mascia. "Leukocyte Adhesion Molecule Profiles and Outcome after Traumatic Brain Injury." In Intracranial Pressure and Neuromonitoring in Brain Injury, 200–202. Vienna: Springer Vienna, 1998. http://dx.doi.org/10.1007/978-3-7091-6475-4_57.

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Conference papers on the topic "Traumatic brain injury; intracranial pressure"

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Mendelson, Asher A., Christopher Gillis, William Henderson, Juan J. Ronco, and Donald E. Griesdale. "Intracranial Pressure Monitors In Traumatic Brain Injury: A Systematic Review." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4728.

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Sotudeh Chafi, M., G. Karami, and M. Ziejewski. "Simulation of Blast-Head Interactions to Study Traumatic Brain Injury." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-41629.

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This paper presents a methodology for predicting the mechanical damage inflicted on the brain by a high explosive (HE) detonation and leading to traumatic brain injury (TBI). A brain model, with its complexity, is used in the computational procedure. The processes of HE detonation and shock propagation in the air, as well as their interaction with the head, are modeled by an Arbitrary Lagrangian Eulerian (ALE) multi-material formulation, together with a penalty-based fluid/structure interaction algorithm. This methodology provides intracranial pressure and maximum shear stress within the microscale time frame for this highly dynamic phenomenon. Two scenarios are simulated. In one scenario, the brain is in close proximity to a 1lb trinitrotoluene (TNT) explosion, and the other to a 0.5lb explosion. The resulting countercoup intracranial pressure-time histories, from the 1 lb TNT explosive scenario, demonstrates that pressure falls below −100 kPa. This can cause cavitation bubbles and damage to the brain tissue. The simulations also predict that the areas of high pressure and shear stress concentration are consistent with those of clinical observations. These resulted intracranial pressure and shear stress responses are the parameters to examine against injury criterions thresholds.
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Huang, Shi-Min, Mohammad-Reza Tofighi, and Arye Rosen. "Novel microwave techniques for non-invasive intracranial pressure monitoring following traumatic brain injury." In 2014 IEEE Benjamin Franklin Symposium on Microwave and Antenna Sub-systems for Radar, Telecommunications, and Biomedical Applications (BenMAS). IEEE, 2014. http://dx.doi.org/10.1109/benmas.2014.7529466.

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Mengling Feng, Zhuo Zhang, Cuntai Guan, D. R. Hardoon, N. K. K. King, Boon Chuan Pang, and Beng Ti Ang. "Utilization of temporal information for intracranial pressure development trend forecasting in traumatic brain injury." In 2012 34th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2012. http://dx.doi.org/10.1109/embc.2012.6346826.

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Meng, X., M. R. Tofighi, and A. Rosen. "Digital microwave system for monitoring intracranial pressure in hydrocephalic and traumatic brain injury patients." In 2011 IEEE/MTT-S International Microwave Symposium - MTT 2011. IEEE, 2011. http://dx.doi.org/10.1109/mwsym.2011.5972638.

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Meng, X., M. R. Tofighi, and A. Rosen. "Digital microwave system for monitoring intracranial pressure in hydrocephalic and traumatic brain injury patients." In 2011 IEEE/MTT-S International Microwave Symposium - MTT 2011. IEEE, 2011. http://dx.doi.org/10.1109/mwsym.2011.5973306.

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Kazimierska, Agnieszka, Agnieszka Uryga, Cyprian Mataczynski, Malgorzata Burzynska, Arkadiusz Ziolkowski, Andrzej Rusiecki, and Magdalena Kasprowicz. "Analysis of the Shape of Intracranial Pressure Pulse Waveform in Traumatic Brain Injury Patients." In 2021 43rd Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2021. http://dx.doi.org/10.1109/embc46164.2021.9630516.

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Chafi, M. S., G. Karami, and M. Ziejewski. "Computation of Blast-Induced Traumatic Brain Injury." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204882.

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In this paper, an integrated numerical approach is introduced to determine the human brain responses when the head is exposed to blast explosions. The procedure is based on a 3D non-linear finite element method (FEM) that implements a simultaneous conduction of explosive detonation, shock wave propagation, and blast-brain interaction of the confronting human head. Due to the fact that there is no reported experimental data on blast-head interactions, several important checkpoints should be made before trusting the brain responses resulting from the blast modeling. These checkpoints include; a) a validated human head FEM subjected to impact loading; b) a validated air-free blast propagation model; and c) the verified blast waves-solid interactions. The simulations presented in this paper satisfy the above-mentioned requirements and checkpoints. The head model employed here has been validated again impact loadings. In this respect, Chafi et al. [1] have examined the head model against the brain intracranial pressure, and brain’s strains under different impact loadings of cadaveric experimental tests of Hardy et al. [2]. In another report, Chafi et al. [3] has examined the air-blast and blast-object simulations using Arbitrary Lagrangian Eulerian (ALE) multi-material and Fluid-Solid Interaction (FSI) formulations. The predicted results of blast propagation matched very well with those of experimental data proving that this computational solid-fluid algorithm is able to accurately predict the blast wave propagation in the medium and the response of the structure to blast loading. Various aspects of blast wave propagations in air as well as when barriers such as solid walls are encountered have been studied. With the head model included, different scenarios have been assumed to capture an appropriate picture of the brain response at a constant stand-off distance of nearly 80cm (2.62 feet) from the explosion core. The impact of brain response due to severity of the blast under different amounts of the explosive material, TNT (0.0838, 0.205, and 0.5lb) is examined. The accuracy of the modeling can provide the information to design protection facilities for human head for the hostile environments.
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Ott, Kyle, Liming Voo, Andrew Merkle, Alexander Iwaskiw, Alexis Wickwire, Brock Wester, and Robert Armiger. "Experimental Determination of Pressure Wave Transmission to the Brain During Head-Neck Blast Tests." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14834.

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Traumatic Brain Injury (TBI) has been the termed the “signature injury” in wounded soldiers in recent military operations [1]. Evidence has shown a strong association between TBI and blast loading to the head due to exposure to explosive events [2, 3]. Head injury mechanisms in a primary blast environment remain elusive and are the subject of much speculation and hypotheses. However, brain injury mechanisms have traditionally been attributed to either a direct impact or a rapid head acceleration or deceleration. Extensive research has been performed regarding the effects of blunt trauma and inertial loading on head injuries [4, 5]. Direct impacts to the head can largely be described based on linear acceleration measurements that correlate to skull fracture and focal brain injuries [6]. Computational head modeling of blunt impact events has shown that the linear acceleration response correlates well with increases in brain pressure [7]. Intracranial pressure, therefore, has been one of the major quantities investigated for correlation to blast induced TBI injury mechanisms [8–14].
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Rezaei, Asghar, Hesam Sarvghad-Moghaddam, Ashkan Eslaminejad, Mariusz Ziejewski, and Ghodrat Karami. "Skull Deformation Has No Impact on the Variation of Brain Intracranial Pressure." In ASME 2016 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/imece2016-67518.

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Skull deformation and vibration has been hypothesized to be an injury mechanism when the human head undergoes an impact scenario. The extent that skull deformation may increase the risk of traumatic brain injury, however, is not well understood. This computational study explains whether skull deformation has any impact on the variation of intracranial pressure (ICP). To this end, a finite element head model including major anatomical components of the human head was employed. The head model has been validated against ICP variations on the brain. The impact simulations were carried out using a rigid cylindrical impactor. The scenarios were frontal impacts with the impactor hitting the forehead of the head model at two impact severity levels. In order to examine the effect of skull elasticity on the stress wave propagation inside the cranium under an external applied force, the skull was also taken as a rigid body with the same density as the elastic one, and the result were compared with those obtained with the deformable skull. For the two cases, the variation of ICPs at the coup and countercoup sites were recorded and compared. The results of the study showed that, for the case studies presented here, the deformation of skull didn’t increase the level of ICP inside the brain. It was concluded that the skull rapid body motion might be responsible for brain injuries.
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Reports on the topic "Traumatic brain injury; intracranial pressure"

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VandeVord, Pamela. Measuring Intracranial Pressure and Correlation with Severity of Blast Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada566717.

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VandeVord, Pamela J. Measuring Intracranial Pressure and Correlation with Severity of Blast Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, January 2013. http://dx.doi.org/10.21236/ada583513.

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Nyein, Michelle K., Amanda M. Jason, Li Yu, Claudio M. Pita, John D. Joannopoulos, David F. Moore, and Raul A. Radovitzky. In Silico Investigation of Intracranial Blast Mitigation with Relevance to Military Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, September 2010. http://dx.doi.org/10.21236/ada533075.

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Ford, Corey C., and Paul Allen Taylor. Modeling and simulation of blast-induced, early-time intracranial wave physics leading to traumatic brain injury. Office of Scientific and Technical Information (OSTI), February 2008. http://dx.doi.org/10.2172/1028900.

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Morykwas, Michael. Treatment of Traumatic Brain Injury by Localized Application of Subatmospheric Pressure to the Site of Cortical Impact. Fort Belvoir, VA: Defense Technical Information Center, July 2010. http://dx.doi.org/10.21236/ada542618.

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Morykwas, Michael. Treatment of Traumatic Brain Injury by Localized Application of Subatmospheric Pressure to the Site of Cortical Impact. Fort Belvoir, VA: Defense Technical Information Center, July 2011. http://dx.doi.org/10.21236/ada573367.

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Morykwas, Michael. Treatment of Traumatic Brain Injury by Localized Application of Subatmospheric Pressure to the Site of Cortical Impact. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada580603.

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Morykwas, Michael. Treatment of Traumatic Brain Injury by Localized Application of Sub-atmospheric Pressure to the Site of Cortical Impact. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada583375.

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ANDRADE, RAUL RIBEIRO, Edla Vitória Santos Pereira, Igor Hudson Albuquerque e. Aguiar, Olavo Barbosa de Oliveira Neto, FABIANO TIMBÓ BARBOSA, OÃO GUSTAVO ROCHA PEIXOTO SANTOS, and CÉLIO FERNANDO SOUSA. Effectiveness of Early Tracheostomy compared with Late Tracheostomy Or Prolonged Orotracheal Intubation in Traumatic Brain Injury: Protocol of Umbrella Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0096.

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Review question / Objective: What is the effectiveness of Early Tracheostomy compared with Late Tracheostomy Or Prolonged Orotracheal Intubation in Traumatic Brain Injury? Eligibility criteria: The inclusion criteria are (P) studies with patients above 18 years old, male or female, who had a severe traumatic brain injury and who need advanced airway support; (I) patient undergoing early tracheostomy (less than 10 days of orotraqueal intubation); (C) patient undergoing late tracheostomy (after 10 days of orotraqueal intubation) or undergoing prolonged intubation; (O) With data about mortality, time on ICU stay, on Hospital stay and time free of mechanical ventilation, complications related a health care services (pneumonia, septicemia, candidemia, Pressure ulcers, thromboembolic events and time using antibiotics), Quality of life (scores about neurological functions); e (S) Systematic reviews. No language restrictions. The exclusion criteria are data about mortality without data about time and follow up (In Hospital or after discharge?). We will contact the authors of studies without data enough to make a decision or without full text available, If we do not have answers we will exclude the study.
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Newman-Toker, David E., Susan M. Peterson, Shervin Badihian, Ahmed Hassoon, Najlla Nassery, Donna Parizadeh, Lisa M. Wilson, et al. Diagnostic Errors in the Emergency Department: A Systematic Review. Agency for Healthcare Research and Quality (AHRQ), December 2022. http://dx.doi.org/10.23970/ahrqepccer258.

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Objectives. Diagnostic errors are a known patient safety concern across all clinical settings, including the emergency department (ED). We conducted a systematic review to determine the most frequent diseases and clinical presentations associated with diagnostic errors (and resulting harms) in the ED, measure error and harm frequency, as well as assess causal factors. Methods. We searched PubMed®, Cumulative Index to Nursing and Allied Health Literature (CINAHL®), and Embase® from January 2000 through September 2021. We included research studies and targeted grey literature reporting diagnostic errors or misdiagnosis-related harms in EDs in the United States or other developed countries with ED care deemed comparable by a technical expert panel. We applied standard definitions for diagnostic errors, misdiagnosis-related harms (adverse events), and serious harms (permanent disability or death). Preventability was determined by original study authors or differences in harms across groups. Two reviewers independently screened search results for eligibility; serially extracted data regarding common diseases, error/harm rates, and causes/risk factors; and independently assessed risk of bias of included studies. We synthesized results for each question and extrapolated U.S. estimates. We present 95 percent confidence intervals (CIs) or plausible range (PR) bounds, as appropriate. Results. We identified 19,127 citations and included 279 studies. The top 15 clinical conditions associated with serious misdiagnosis-related harms (accounting for 68% [95% CI 66 to 71] of serious harms) were (1) stroke, (2) myocardial infarction, (3) aortic aneurysm and dissection, (4) spinal cord compression and injury, (5) venous thromboembolism, (6/7 – tie) meningitis and encephalitis, (6/7 – tie) sepsis, (8) lung cancer, (9) traumatic brain injury and traumatic intracranial hemorrhage, (10) arterial thromboembolism, (11) spinal and intracranial abscess, (12) cardiac arrhythmia, (13) pneumonia, (14) gastrointestinal perforation and rupture, and (15) intestinal obstruction. Average disease-specific error rates ranged from 1.5 percent (myocardial infarction) to 56 percent (spinal abscess), with additional variation by clinical presentation (e.g., missed stroke average 17%, but 4% for weakness and 40% for dizziness/vertigo). There was also wide, superimposed variation by hospital (e.g., missed myocardial infarction 0% to 29% across hospitals within a single study). An estimated 5.7 percent (95% CI 4.4 to 7.1) of all ED visits had at least one diagnostic error. Estimated preventable adverse event rates were as follows: any harm severity (2.0%, 95% CI 1.0 to 3.6), any serious harms (0.3%, PR 0.1 to 0.7), and deaths (0.2%, PR 0.1 to 0.4). While most disease-specific error rates derived from mainly U.S.-based studies, overall error and harm rates were derived from three prospective studies conducted outside the United States (in Canada, Spain, and Switzerland, with combined n=1,758). If overall rates are generalizable to all U.S. ED visits (130 million, 95% CI 116 to 144), this would translate to 7.4 million (PR 5.1 to 10.2) ED diagnostic errors annually; 2.6 million (PR 1.1 to 5.2) diagnostic adverse events with preventable harms; and 371,000 (PR 142,000 to 909,000) serious misdiagnosis-related harms, including more than 100,000 permanent, high-severity disabilities and 250,000 deaths. Although errors were often multifactorial, 89 percent (95% CI 88 to 90) of diagnostic error malpractice claims involved failures of clinical decision-making or judgment, regardless of the underlying disease present. Key process failures were errors in diagnostic assessment, test ordering, and test interpretation. Most often these were attributed to inadequate knowledge, skills, or reasoning, particularly in “atypical” or otherwise subtle case presentations. Limitations included use of malpractice claims and incident reports for distribution of diseases leading to serious harms, reliance on a small number of non-U.S. studies for overall (disease-agnostic) diagnostic error and harm rates, and methodologic variability across studies in measuring disease-specific rates, determining preventability, and assessing causal factors. Conclusions. Although estimated ED error rates are low (and comparable to those found in other clinical settings), the number of patients potentially impacted is large. Not all diagnostic errors or harms are preventable, but wide variability in diagnostic error rates across diseases, symptoms, and hospitals suggests improvement is possible. With 130 million U.S. ED visits, estimated rates for diagnostic error (5.7%), misdiagnosis-related harms (2.0%), and serious misdiagnosis-related harms (0.3%) could translate to more than 7 million errors, 2.5 million harms, and 350,000 patients suffering potentially preventable permanent disability or death. Over two-thirds of serious harms are attributable to just 15 diseases and linked to cognitive errors, particularly in cases with “atypical” manifestations. Scalable solutions to enhance bedside diagnostic processes are needed, and these should target the most commonly misdiagnosed clinical presentations of key diseases causing serious harms. New studies should confirm overall rates are representative of current U.S.-based ED practice and focus on identified evidence gaps (errors among common diseases with lower-severity harms, pediatric ED errors and harms, dynamic systems factors such as overcrowding, and false positives). Policy changes to consider based on this review include: (1) standardizing measurement and research results reporting to maximize comparability of measures of diagnostic error and misdiagnosis-related harms; (2) creating a National Diagnostic Performance Dashboard to track performance; and (3) using multiple policy levers (e.g., research funding, public accountability, payment reforms) to facilitate the rapid development and deployment of solutions to address this critically important patient safety concern.
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