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

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Fuller, Gordon. "Intracranial Pressure Monitoring in Severe Traumatic Brain Injury." Journal of the Intensive Care Society 14, no. 3 (July 2013): 266–68. http://dx.doi.org/10.1177/175114371301400319.

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12

Hutchinson, P. J., A. G. Kolias, M. Czosnyka, P. J. Kirkpatrick, J. D. Pickard, and D. K. Menon. "Intracranial pressure monitoring in severe traumatic brain injury." BMJ 346, feb15 1 (February 15, 2013): f1000. http://dx.doi.org/10.1136/bmj.f1000.

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13

Levitt, Michael R., Joshua W. Osbun, and Louis J. Kim. "Intracranial Pressure Monitoring in Severe Traumatic Brain Injury." World Neurosurgery 79, no. 5-6 (May 2013): 600–601. http://dx.doi.org/10.1016/j.wneu.2013.03.047.

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14

Meyfroidt, Geert. "Intracranial pressure monitoring in severe traumatic brain injury." Critical Care Medicine 40, no. 6 (June 2012): 1993–94. http://dx.doi.org/10.1097/ccm.0b013e31824c9188.

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15

Suasti, Ni Wayan Lisa. "Regulation and Intervention of Intracranial Pressure." Bioscientia Medicina : Journal of Biomedicine and Translational Research 5, no. 10 (November 3, 2021): 1194–200. http://dx.doi.org/10.32539/bsm.v5i10.421.

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Intracranial pressure is the total amount of pressure exerted by the brain, blood and cerebrocinal fluid in the rigid cranial space. Compliance is an indicator of the brain's tolerance for increased ICP, when compliance is exceeded, there will be a dramatic increase in the pressure/volume curve so that ICP will increase rapidly. In the injured brain, cerebral blood flow (CBF) is regulated to supply sufficient oxygen and substrates to the brain. Certain physiological factors such as hypercarbia, acidosis and hypoxemia cause vasodilation which causes an increase in CBF, seizure activity and fever will increase the level of brain metabolism and CBF. Cerebral edema is the most common cause of non-traumatic brain injury such as central nervous system infections, metabolic and systemic encephalopathy. Vasogenic brain edema occurs due to injury to the blood-brain barrier and increased capillary permeability in the area around the injury, or to inflammation, especially in CNS infections. Medical management of elevated intracranial pressure includes sedation, cerebrospinal fluid drainage, and osmotherapy with either mannitol or hypertonic salts.

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16

Mitchell, Pamela H., Catherine Kirkness, and Patricia A. Blissitt. "Cerebral Perfusion Pressure and Intracranial Pressure in Traumatic Brain Injury." Annual Review of Nursing Research 33, no. 1 (May 2015): 111–83. http://dx.doi.org/10.1891/0739-6686.33.111.

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Nearly 300,000 children and adults are hospitalized annually with traumatic brain injury (TBI) and monitored for many vital signs, including intracranial pressure (ICP) and cerebral perfusion pressure (CPP). Nurses use these monitored values to infer the risk of secondary brain injury. The purpose of this chapter is to review nursing research on the monitoring of ICP and CPP in TBI. In this context, nursing research is defined as the research conducted by nurse investigators or research about the variables ICP and CPP that pertains to the nursing care of the TBI patient, adult or child. A modified systematic review of the literature indicated that, except for sharp head rotation and prone positioning, there are no body positions or nursing activities that uniformly or nearly uniformly result in clinically relevant ICP increase or decrease. In the smaller number of studies in which CPP is also measured, there are few changes in CPP since arterial blood pressure generally increases along with ICP. Considerable individual variation occurs in controlled studies, suggesting that clinicians need to pay close attention to the cerebrodynamic responses of each patient to any care maneuver. We recommend that future research regarding nursing care and ICP/CPP in TBI patients needs to have a more integrated approach, examining comprehensive care in relation to short- and long-term outcomes and incorporating multimodality monitoring. Intervention trials of care aspects within nursing control, such as the reduction of environmental noise, early mobilization, and reduction of complications of immobility, are all sorely needed.

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17

Khadka, Nilam, Rajan Kumar Sharma, Rajiv Jha, and Prakash Bista. "Study of Intracranial Pressure Monitoring In Traumatic Brain Injury." Nepal Journal of Neuroscience 15, no. 2 (September 4, 2018): 23–29. http://dx.doi.org/10.3126/njn.v15i2.20982.

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Intracranial pressure monitoring is considered the standard of care for severe traumatic brain injury and is used frequently. However, the efficacy of treatment based on monitoring in improving the outcome has not been rigorously assessed. We conducted a trial in which we included 26 patients of all types of traumatic brain injury (TBI) and they were monitored for intracranial pressure by Conventional fluid filled system with a manometer (Group 1) and compared with the Fiber optic transducer-tipped intracranial pressure monitoring system (Group 2).The main aim of this study was to examine the relationship between Intracranial Pressure (ICP) monitoring and in-hospital mortality. The median length of stay in the ICU was similar in the two groups (12 days in the conventional pressure-monitoring group and 9 days in the new fiber optic group; P=0.25), the number of days of brain-specific treatments (e.g., administration of hyperosmolar fluids and the use of hyperventilation) in the ICU was similar in both groups. The distribution of serious adverse events was similar in the two groups. We concluded that ICP monitoring (as is any monitoring modality) is a useful guide for management. The outcomes are decided by the differences in management protocols that the knowledge of the said parameter brings about. ICP monitoring is recommended for the better management of traumatic brain injury and fiber optic ICP monitoring seems to be beneficial than using the conventional methods of ICP monitoring with manometer.Nepal Journal of Neuroscience, Volume 15, Number 2, 2018, page: 23-29

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18

Stiver, Shirley I., and Geoffrey T. Manley. "Prehospital management of traumatic brain injury." Neurosurgical Focus 25, no. 4 (October 2008): E5. http://dx.doi.org/10.3171/foc.2008.25.10.e5.

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The aim of this study was to review the current protocols of prehospital practice and their impact on outcome in the management of traumatic brain injury. A literature review of the National Library of Medicine encompassing the years 1980 to May 2008 was performed. The primary impact of a head injury sets in motion a cascade of secondary events that can worsen neurological injury and outcome. The goals of care during prehospital triage, stabilization, and transport are to recognize life-threatening raised intracranial pressure and to circumvent cerebral herniation. In that process, prevention of secondary injury and secondary insults is a major determinant of both short- and longterm outcome. Management of brain oxygenation, blood pressure, cerebral perfusion pressure, and raised intracranial pressure in the prehospital setting are discussed. Patient outcomes are dependent upon an organized trauma response system. Dispatch and transport timing, field stabilization, modes of transport, and destination levels of care are addressed. In addition, special considerations for mass casualty and disaster planning are outlined and recommendations are made regarding early response efforts and the ethical impact of aggressive prehospital resuscitation. The most sophisticated of emergency, operative, or intensive care units cannot reverse damage that has been set in motion by suboptimal protocols of triage and resuscitation, either at the injury scene or en route to the hospital. The quality of prehospital care is a major determinant of long-term outcome for patients with traumatic brain injury.

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19

Khanuja, Tanu, and Harikrishnan Narayanan Unni. "Intracranial pressure–based validation and analysis of traumatic brain injury using a new three-dimensional finite element human head model." Proceedings of the Institution of Mechanical Engineers, Part H: Journal of Engineering in Medicine 234, no. 1 (October 19, 2019): 3–15. http://dx.doi.org/10.1177/0954411919881526.

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Traumatic brain injuries are life-threatening injuries that can lead to long-term incapacitation and death. Over the years, numerous finite element human head models have been developed to understand the injury mechanisms of traumatic brain injuries. Many of these models are erroneous and used ellipsoidal or spherical geometries to represent brain. This work is focused on the development of high-quality, comprehensive three-dimensional finite element human head model with accurate representation of cerebral sulci and gyri structures in order to study traumatic brain injury mechanisms. Present geometry, predicated on magnetic resonance imaging data consist of three rudimentary components, that is, skull, cerebrospinal fluid with the ventricular system, and the soft tissues comprising the cerebrum, cerebellum, and brain stem. The brain is modeled as a hyperviscoelastic material. Meshed model with 10 nodes modified tetrahedral type element (C3D10M) is validated against two cadaver-based impact experiments by comparing the intracranial pressures at different locations of the head. Our results indicate a better agreement with cadaver results, specifically for the case of frontal and parietal intracranial pressure values. Existing literature focuses mostly on intracranial pressure validation, while the effects of von Mises stress on brain injury are not analyzed in detail. In this work, a detailed interpretation of neurological damage resulting from impact injury is performed by analyzing von Mises stress and intracranial pressure distribution across numerous segments of the brain. A reasonably good correlation with experimental data signifies the robustness of the model for predicting injury mechanisms based on clinical predictions of injury tolerance criteria.

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20

Shrestha, B., and G. Lakshmipathy. "Peak Systolic Velocity in Middle Cerebral Artery in Patients with Severe Traumatic Brain Injury as an Indicator of Detrimental Rise in Intracranial Pressure." Kathmandu University Medical Journal 19, no. 4 (December 31, 2021): 481–85. http://dx.doi.org/10.3126/kumj.v19i4.49782.

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Background Intracranial pressure (ICP) is the major concern for neurosurgeons while treating patients with severe traumatic brain injury, as any troublesome escalation in intracranial pressure heralds feared complications leading to definite morbidity or even mortality. Objective This study focuses on analyzing the correlation between peak systolic velocity in middle cerebral artery derived from transcranial doppler ultrasonographic spectral analysis and intracranial pressure values derived from invasive intracranial pressure monitoring system in a patient with severe traumatic brain injury. Method A prospective observational study was performed using a convenience sample technique including all adult patients with severe traumatic brain injury who had invasive intracranial monitors placed as part of their clinical care. Transcranial doppler ultrasonography was performed with a 2 MHz linear probe of ACUSON X300 ultrasound system while simultaneous intracranial pressure readings were obtained directly from invasive intracranial pressure monitoring. The association between peak systolic velocity in the middle cerebral artery and invasive intracranial pressure was assessed with Pearson’s correlation coefficient. Result One hundred one transcranial doppler ultrasound spectral analysis was performed on 26 individual patients. The mean age of the population involved in this study is 43.57 years ± S.D. 19.95 (range 18-78 years), with male preponderance in a ratio of 5.5:1. Pearson’s correlation coefficient of peak systolic velocity in middle cerebral artery and intracranial pressure was 0.715 (p < 0.000) demonstrating a significant positive correlation. With further evaluation of area under curve characteristics, peak systolic velocity in middle cerebral artery of 39.6 cm/s yielded the most favorable balance of test characteristics to diagnose elevation of intracranial pressure, with a resulting sensitivity of 82.1% and specificity of 84.4%. Conclusion Peak systolic velocity in middle cerebral artery can be explored further as a dependable screening tool to evaluate intracranial pressure among patients with severe traumatic brain injury in settings with unavailability of invasive intracranial pressure monitoring facilities.

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21

Bader, Mary Kay, Richard Arbour, and Sylvain Palmer. "Refractory Increased Intracranial Pressure in Severe Traumatic Brain Injury." AACN Clinical Issues: Advanced Practice in Acute and Critical Care 16, no. 4 (October 2005): 526–41. http://dx.doi.org/10.1097/00044067-200510000-00009.

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22

Stocchetti, Nino, Tommaso Zoerle, and Marco Carbonara. "Intracranial pressure management in patients with traumatic brain injury." Current Opinion in Critical Care 23, no. 2 (April 2017): 110–14. http://dx.doi.org/10.1097/mcc.0000000000000393.

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23

Tang, Andrew, Viraj Pandit, Vernard Fennell, Trevor Jones, Bellal Joseph, Terence O'Keeffe, Randall S. Friese, and Peter Rhee. "Intracranial pressure monitor in patients with traumatic brain injury." Journal of Surgical Research 194, no. 2 (April 2015): 565–70. http://dx.doi.org/10.1016/j.jss.2014.11.017.

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24

Beaumont, A., and A. Marmarou. "Treatment of raised intracranial pressure following traumatic brain injury." Critical Reviews in Neurosurgery 9, no. 4 (April 1999): 207–16. http://dx.doi.org/10.1007/s003290050135.

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25

Helbok, Raimund, G. Meyfroidt, and R. Beer. "Intracranial pressure thresholds in severe traumatic brain injury: Con." Intensive Care Medicine 44, no. 8 (July 5, 2018): 1318–20. http://dx.doi.org/10.1007/s00134-018-5249-y.

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26

Myburgh, John A. "Intracranial pressure thresholds in severe traumatic brain injury: Pro." Intensive Care Medicine 44, no. 8 (July 5, 2018): 1315–17. http://dx.doi.org/10.1007/s00134-018-5264-z.

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27

Sheth, Kevin N., Deborah M. Stein, Bizhan Aarabi, Peter Hu, Joseph A. Kufera, Thomas M. Scalea, and Daniel F. Hanley. "Intracranial Pressure Dose and Outcome in Traumatic Brain Injury." Neurocritical Care 18, no. 1 (October 9, 2012): 26–32. http://dx.doi.org/10.1007/s12028-012-9780-3.

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Bourdeaux, Chris, and Jules Brown. "Sodium Bicarbonate Lowers Intracranial Pressure After Traumatic Brain Injury." Neurocritical Care 13, no. 1 (April 27, 2010): 24–28. http://dx.doi.org/10.1007/s12028-010-9368-8.

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29

Risdall, Jane E., and David K. Menon. "Traumatic brain injury." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1562 (January 27, 2011): 241–50. http://dx.doi.org/10.1098/rstb.2010.0230.

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There is an increasing incidence of military traumatic brain injury (TBI), and similar injuries are seen in civilians in war zones or terrorist incidents. Indeed, blast-induced mild TBI has been referred to as the signature injury of the conflicts in Iraq and Afghanistan. Assessment involves schemes that are common in civilcian practice but, in common with civilian TBI, takes little account of information available from modern imaging (particularly diffusion tensor magnetic resonance imaging) and emerging biomarkers. The efficient logistics of clinical care delivery in the field may have a role in optimizing outcome. Clinical care has much in common with civilian TBI, but intracranial pressure monitoring is not always available, and protocols need to be modified to take account of this. In addition, severe early oedema has led to increasing use of decompressive craniectomy, and blast TBI may be associated with a higher incidence of vasospasm and pseudoaneurysm formation. Visual and/or auditory deficits are common, and there is a significant risk of post-traumatic epilepsy. TBI is rarely an isolated finding in this setting, and persistent post-concussive symptoms are commonly associated with post-traumatic stress disorder and chronic pain, a constellation of findings that has been called the polytrauma clinical triad.

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Shrestha, B., P. Shrestha, P. Ghale, and G. Lakshmipathy. "Correlation between Invasive Intracranial Pressure Monitoring and Optic Nerve Sheath Diameter in Patients with Traumatic Brain Injury." Kathmandu University Medical Journal 19, no. 2 (June 30, 2021): 221–24. http://dx.doi.org/10.3126/kumj.v19i2.49650.

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Background In management of patients with traumatic brain injury, intracranial pressure holds an important place. Any untoward rise in intracranial pressure portends dreaded complications. Hence, any delay in detecting the issue is considered unacceptable. Objective This study focuses on analyzing the correlation between ultrasound derived optic nerve sheath diameter and intracranial pressure values derived from invasive intracranial pressure monitoring system in a neurosurgical patient with severe traumatic brain injury. Method A prospective observational study was performed using a convenience sample technique including all adult patients with traumatic brain injury who had invasive intracranial monitors placed as part of their clinical care. Ocular ultrasound was performed with 5 - 7.5 MHz linear probe of ACUSON X300 ultrasound system while simultaneous intracranial pressure readings were obtained directly from an invasive intracranial pressure monitoring system. The association between optic nerve sheath diameter and invasive intracranial pressure reading was assessed with the Pearson’s correlation coefficient and a receiver operator characteristic curve was created to determine the optimal optic nerve sheath diameter cutoff to detect intracranial pressure > 15 cm H2O. Result One hundred and fifteen ocular ultrasounds were performed on 30 individual patients. The mean age of the population involved in this study is 42.13 years ± 1.89 with male preponderance in the ratio of 6:1. Pearson’s correlation coefficient of optic nerve sheath diameter and intracranial pressure was found to be 0.844 (p < 0.000) demonstrating a significant positive correlation. The area under the receiver operating characteristic curve was found to be 0.961 (95% confidence interval = 0.93 to 0.99). Based on analysis of the receiver operating characteristic curve, optic nerve sheath diameter > 4.85 mm performed best to detect intracranial pressure > 15 cm H2O with a sensitivity of 93.5% and specificity of 83%. Conclusion Optic nerve sheath diameter is a dependable screening tool to evaluate for elevated intracranial pressure among patients with traumatic nerve injury.

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Stocchetti, Nino. "Intracranial Pressure, Brain Vessels, and Consciousness Recovery in Traumatic Brain Injury." Anesthesia & Analgesia 109, no. 6 (December 2009): 1726–27. http://dx.doi.org/10.1213/ane.0b013e3181bdca25.

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Friess, Stuart H., Todd J. Kilbaugh, and Jimmy W. Huh. "Advanced Neuromonitoring and Imaging in Pediatric Traumatic Brain Injury." Critical Care Research and Practice 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/361310.

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While the cornerstone of monitoring following severe pediatric traumatic brain injury is serial neurologic examinations, vital signs, and intracranial pressure monitoring, additional techniques may provide useful insight into early detection of evolving brain injury. This paper provides an overview of recent advances in neuromonitoring, neuroimaging, and biomarker analysis of pediatric patients following traumatic brain injury.

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Lu, C. W., M. Czosnyka, J. S. Shieh, A. Smielewska, J. D. Pickard, and P. Smielewski. "Complexity of intracranial pressure correlates with outcome after traumatic brain injury." Brain 135, no. 8 (June 25, 2012): 2399–408. http://dx.doi.org/10.1093/brain/aws155.

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Berger-Pelleiter, Elyse, Marcel Émond, François Lauzier, Jean-François Shields, and Alexis F. Turgeon. "Hypertonic saline in severe traumatic brain injury: a systematic review and meta-analysis of randomized controlled trials." CJEM 18, no. 2 (March 2016): 112–20. http://dx.doi.org/10.1017/cem.2016.12.

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AbstractObjectivesHypertonic saline solutions are increasingly used to treat increased intracranial pressure following severe traumatic brain injury. However, whether hypertonic saline provides superior management of intracranial pressure and improves outcome is unclear. We thus conducted a systematic review to evaluate the effect of hypertonic saline in patients with severe traumatic brain injury.MethodsTwo researchers independently selected randomized controlled trials studying hypertonic saline in severe traumatic brain injury and collected data using a standardized abstraction form. No language restriction was applied. We searched MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, Scopus, Web of Science, and BIOSIS databases. We searched grey literature via OpenGrey and National Technical Information Service databases. We searched the references of included studies and relevant reviews for additional studies.ResultsEleven studies (1,820 patients) were included. Hypertonic saline did not decrease mortality (risk ratio 0.96, 95% confidence interval [CI] 0.83 to 1.11, I2=0%) or improve intracranial pressure control (weighted mean difference −1.25 mm Hg, 95% CI −4.18 to 1.68, I2=78%) as compared to any other solutions. Only one study reported monitoring for adverse events with hypertonic saline, finding no significant differences between comparison groups.ConclusionsWe observed no mortality benefit or effect on the control of intracranial pressure with the use of hypertonic saline when compared to other solutions. Based on the current level of evidence pertaining to mortality or control of intracranial pressure, hypertonic saline could thus not be recommended as a first-line agent for managing patients with severe traumatic brain injury.

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Beier, Alexandra D., and Peter B. Dirks. "Pediatric brainstem hemorrhages after traumatic brain injury." Journal of Neurosurgery: Pediatrics 14, no. 4 (October 2014): 421–24. http://dx.doi.org/10.3171/2014.7.peds13376.

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Traumatic brain injuries afflict a large number of pediatric patients. The most severe injuries lead to increased intracranial pressure and herniation, with resultant changes in the brainstem. Traumatic brainstem hemorrhages have previously been associated with poor neurological outcome and fatality. However, this report discusses 2 pediatric patients who sustained severe head trauma with subsequent brainstem hemorrhages, and yet experienced good neurological outcome; the possible mechanism is described.

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Markert, Ronald J., Jonathan M. Saxe, and Cathryn L. Chadwick. "Intracranial Pressure is a Better Predictor of Mortality than Cerebral Perfusion Pressure." Panamerican Journal of Trauma, Critical Care & Emergency Surgery 1, no. 1 (2012): 15–19. http://dx.doi.org/10.5005/jp-journals-10030-1004.

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ABSTRACT Objective To evaluate whether elevated intracranial pressure (ICP) or depressed cerebral perfusion pressure (CPP) is a better predictor of intracranial compartment syndrome and long-term functional outcomes in blunt traumatic brain injury. Methods This was a retrospective evaluation of data collected on 203 patients with blunt traumatic brain injury who were admitted to Miami Valley Hospital, a Level I trauma center, over a 2 years period, whose initial hospital management required an intracranial pressure monitor. Serial measurements of ICP and CPP were recorded during the patients hospital stay. These patients were then evaluated at 3,6,12 and 24 months post-injury to assess their outcome based on functional status, as defined by death vegetative state, severe disability, moderate disability and good recovery. Results Utilizing an ICP cut-off value of 25 or greater and a CPP value of less than 60 at any point during the patients hospital course, ICP elevation consistently correlated with a higher percentage of deaths and persistent vegetative state than a depression in CPP value. Outcomes as measured by severe or moderate disability where similar in both groups. However, neither measure approached statistical significance. Conclusion ICP appears to be a better predictor of intracranial compartment syndrome and extent of brain injury, predicting better than CPP values, the outcome of death or persistent vegetative state. This may help to predict prognosis, change management strategies and guide discussions with family, especially in the early phase of injury. How to cite this Article Markert RJ, Saxe JM, Chadwick CL. Intracranial Pressure is a Better Predictor of Mortality than Cerebral Perfusion Pressure. Panam J Trauma Critical Care Emerg Surg 2012;1(1):15-19.

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De Almeida, Andrea Garcia, Marco Antônio Stefani, and Carlos Alexandre Netto. "Hemodynamic and metabolic parameters in brain injury." JBNC - JORNAL BRASILEIRO DE NEUROCIRURGIA 21, no. 3 (March 19, 2018): 140–46. http://dx.doi.org/10.22290/jbnc.v21i3.839.

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Introduction: Indirect monitoring of brain metabolism through parameters such as cerebral perfusion pressure (CPP), intracranial pressure (ICP), arterial CO2 partial pressure (PaCO2) and mean arterial blood pressure (MABP) is necessary to guide treatment and to prevent secondary cerebral ischemia. The aim of the present study was to analyze the association between cerebral hemodynamic and metabolic parameters and the occurrence of traumatic brain ischemia. Methods: Thirty-one patients were prospectively assessed in the pediatric or adult intensive care unit of Hospital de Pronto Socorro (HPS), in Porto Alegre, Brasil, from April to December, 2003. Patients were 23 adults (aged 17 to 66 years-old ) and eight children (aged 3 to 13 years-old) with severe traumatic brain injury( TBI ) . Mean age was 24 years. The inclusioncriteria were Glasgow coma scale (GCS) below 8 and abnormal cranial computed tomography (CT) results. Intracranial pressure, mean arterial blood pressure, arterial CO2 partial pressure and cerebral perfusion pressure were recorded. Results: Cerebral ischemia was identified in 13 adults (56.5%) and in seven children (87.5%). High MABP was associated with mortality (P<=0.005) in children. High ICP (P= 0.03) and low CPP (P=0.007) in adults were associated with cerebral ischemia. Fourteen patients (45.2%) died: 13 adults (56.5%) and one child (12.5%). Adult patients with low CPP had a worse outcome with higher mortality rate (P=0.045). Conclusions: High ICP, high MABP and low CPP were associated with traumatic brain ischemia and higher mortality rate in these patients.

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Blissitt, Patricia A. "Controversies in the Management of Adults With Severe Traumatic Brain Injury." AACN Advanced Critical Care 23, no. 2 (April 1, 2012): 186–203. http://dx.doi.org/10.4037/nci.0b013e31824db4f3.

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Despite progress in the management of adults with severe traumatic brain injury, several controversies persist. Among the unresolved issues of greatest concern to neurocritical care clinicians and scientists are the following: (1) the best use of technological advances and the data obtained from multimodality monitoring; (2) the use of mannitol and hypertonic saline in the management of increased intracranial pressure; (3) the use of decompressive craniectomy and barbiturate coma in refractory increased intracranial pressure; (4) therapeutic hypothermia as a neuroprotectant; (5) anemia and the role of blood transfusion; and (6) venous thromboembolism prophylaxis in severe traumatic brain injury. Each of these strategies for managing severe traumatic brain injury, including the postulated mechanism(s) of action and beneficial effects of each intervention, adverse effects, the state of the science, and critical care nursing implications, is discussed.

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Faruq, Mohammad Omar. "ICU management of Traumatic Brain Injury." Bangladesh Critical Care Journal 10, no. 2 (October 18, 2022): 135–41. http://dx.doi.org/10.3329/bccj.v10i2.62207.

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Traumatic brain injury (TBI) can be defined as the disruption in brain function, or other evidence of brain pathology, caused by an external physical force. Management of TBI depends on, if the injury is focal or diffuse. Focal can be epidural or intra cerebral and diffuse lesions can present as multiple contusions/DAI. A basic understanding of anatomy of central nervous system and some working knowledge of physiology of brain help in management of TBI. According to severity there are three types of TBI patients. They are: mild (GCS 13-15), moderate (GCS 9-12) and severe (GCS 3-8). TBI may be primary or secondary. Primary injuries include contusion, hematoma, subarachnoid hemorrhage, diffuse axonal injury etc. Secondary injuries can manifest as cerebral oedema, raised intra cranial pressure etc. Airway management and cervical spine immobilization are important early steps in management. Hypoxia and hypercarbia must be avoided and attention is always paid to ventilation status of patients. Mean arterial pressure (MAP) should be monitored and maintained at 80-90 mm of Hg. Intracranial pressure (ICP) should be checked whenever feasible and monitored so raised ICP can be controlled. Adequate pain control and sedation, using mannitol, hypertonic saline should be used as needed to control raised ICP. Invasive ICP monitoring and cerebrospinal fluid diversion should be used in patient who decompensate and decision to do decompressive craniectomy is often made by neurosurgeons. Body temperature in TBI patients should be maintained under 37o C. Neurologic conditions like brainstem dysfunction, intracranial hypertension, altered level of consciousness etc. and respiratory conditions like ARDS, hypoxaemia , neurogenic pulmonary oedema etc. warrants endotracheal intubation and mechanical ventilation. TBI patients requiring haemo dialysis usually need special modification in protocol to avoid pulmonary oedema and fluctuation in blood pressure. Monitoring TBI patients is done by routine assessment of GCS, pupillary size and reaction, motor responses. ICP monitoring is to be done if feasible. By aggressive monitoring secondary brain injuries can be avoided or managed. Outcome of management of TBI patients in ICU depends on severity of primary and secondary injuries of brain, status of GCS on presentation, advanced age (>65yrs), presence or absence of co morbidities and severity of associated injuries. Bangladesh Crit Care J September 2022; 10(2): 135-141

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Hlatky, Roman, Alex B. Valadka, and Claudia S. Robertson. "Intracranial hypertension and cerebral ischemia after severe traumatic brain injury." Neurosurgical Focus 14, no. 4 (April 2003): 1–4. http://dx.doi.org/10.3171/foc.2003.14.4.2.

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Arterial hypotension and intracranial hypertension are detrimental to the injured brain. Although artificial elevation of cerebral perfusion pressure (CPP) has been advocated as a means to maintain an adequate cerebral blood flow (CBF), the optimal CPP for the treatment of severe traumatic brain injury (TBI) remains unclear. In addition, CBF evolves significantly over time after TBI, and CBF may vary considerably in patient to patient. For these reasons, a more useful approach may be to consider the optimal CPP in an individual patient at any given time, rather than having an arbitrary goal applied uniformly to all patients. Important information for optimizing CBF is provided by monitoring intracranial pressure in combination with assessment of the adequacy of CBF by using global indicators (for example, jugular oximetry), supplemented when appropriate by local data, such as brain tissue oxygen tension.

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Schmidt, Eric A., Marek Czosnyka, Luzius A. Steiner, Marcella Balestreri, Piotr Smielewski, Stefan K. Piechnik, Basil F. Matta, and John D. Pickard. "Asymmetry of pressure autoregulation after traumatic brain injury." Journal of Neurosurgery 99, no. 6 (December 2003): 991–98. http://dx.doi.org/10.3171/jns.2003.99.6.0991.

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Object. The aim of this study was to assess the asymmetry of autoregulation between the left and right sides of the brain by using bilateral transcranial Doppler ultrasonography in a cohort of patients with head injuries. Methods. Ninety-six patients with head injuries comprised the study population. All significant intracranial mass lesions were promptly removed. The patients were given medications to induce sedation and paralysis, and artificial ventilation. Arterial blood pressure (ABP) and intracranial pressure (ICP) were monitored in an invasive manner. A strategy based on the patient's cerebral perfusion pressure (CPP = ABP − ICP) was applied: CPP was maintained at a level higher than 70 mm Hg and ICP at a level lower than 25 mm Hg. The left and right middle cerebral arteries were insonated daily, and bilateral flow velocities (FVs) were recorded. The correlation coefficient between the CPP and FV, termed Mx, was calculated and time-averaged over each recording period on both sides. An Mx close to 1 signified that slow fluctuations in CPP produced synchronized slow changes in FV, indicating a defective autoregulation. An Mx close to 0 indicated preserved autoregulation. Computerized tomography scans in all patients were reviewed; the side on which the major brain lesion was located was noted and the extent of the midline shift was determined. Outcome was measured 6 months after discharge. The left—right difference in the Mx between the hemispheres was significantly higher in patients who died than in those who survived (0.16 ± 0.04 compared with 0.08 ± 0.01; p = 0.04). The left—right difference in the Mx was correlated with a midline shift (r = −0.42; p = 0.03). Autoregulation was worse on the side of the brain where the lesion was located (p < 0.035). Conclusions. The left—right difference in autoregulation is significantly associated with a fatal outcome. Autoregulation in the brain is worse on the side ipsilateral to the lesion and on the side of expansion in cases in which there is a midline shift.

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Alali, Aziz S., David Gomez, Chethan Sathya, Randall S. Burd, Todd G. Mainprize, Richard Moulton, Richard A. Falcone, Charles de Mestral, and Avery Nathens. "Intracranial pressure monitoring among children with severe traumatic brain injury." Journal of Neurosurgery: Pediatrics 16, no. 5 (November 2015): 523–32. http://dx.doi.org/10.3171/2015.3.peds14507.

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OBJECT Well-designed studies linking intracranial pressure (ICP) monitoring with improved outcomes among children with severe traumatic brain injury (TBI) are lacking. The main objective of this study was to examine the relationship between ICP monitoring in children and in-hospital mortality following severe TBI. METHODS An observational study was conducted using data derived from 153 adult or mixed (adult and pediatric) trauma centers participating in the American College of Surgeons (ACS) Trauma Quality Improvement Program (TQIP) and 29 pediatric trauma centers participating in the pediatric pilot TQIP between 2010 and 2012. Random-intercept multilevel modeling was used to examine the association between ICP monitoring and in-hospital mortality among children with severe TBI ≤16 years of age after adjusting for important confounders. This association was evaluated at the patient level and at the hospital level. In a sensitivity analysis, this association was reexamined in a propensity-matched cohort. RESULTS A total of 1705 children with severe TBI were included in the study cohort. The overall in-hospital mortality was 14.3% of patients (n = 243), whereas the mortality of the 273 patients (16%) who underwent invasive ICP monitoring was 11% (n = 30). After adjusting for patient- and hospital-level characteristics, ICP monitoring was associated with lower in-hospital mortality (adjusted OR 0.50; 95% CI 0.30–0.85; p = 0.01). It is possible that patients who were managed with ICP monitoring were selected because of an anticipated favorable or unfavorable outcome. To further address this potential selection bias, the analysis was repeated with the hospital-specific rate of ICP monitoring use as the exposure. The adjusted OR for death of children treated at high ICP–use hospitals was 0.49 compared with those treated at low ICP-use hospitals (95% CI 0.31–0.78; p = 0.003). Variations in ICP monitoring use accounted for 15.9% of the interhospital variation in mortality among children with severe TBI. Similar results were obtained after analyzing the data using propensity score-matching methods. CONCLUSIONS In this observational study, ICP monitoring use was associated with lower hospital mortality at both the patient and hospital levels. However, the contribution of variable ICP monitoring rates to interhospital variation in pediatric TBI mortality was modest.

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Rosenfeld, Jeffrey V., Piers A. W. Thomas, and Martin K. Hunn. "Intracranial pressure monitoring in severe traumatic brain injury: Quo Vadis?" ANZ Journal of Surgery 91, no. 12 (December 2021): 2568–70. http://dx.doi.org/10.1111/ans.17182.

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Shutter, Lori A., and Shelly D. Timmons. "Intracranial Pressure Rescued by Decompressive Surgery after Traumatic Brain Injury." New England Journal of Medicine 375, no. 12 (September 22, 2016): 1183–84. http://dx.doi.org/10.1056/nejme1609722.

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Dzyak, L. A., N. A. Zorin, A. G. Sirko, V. M. Suk, and V. I. Grishin. "Intracranial pressure monitoring in patients with severe traumatic brain injury." Ukrainian Neurosurgical Journal, no. 1 (March 17, 2008): 17–22. http://dx.doi.org/10.25305/unj.108856.

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Ropper, Alexander E., and John H. Chi. "Treatment of Traumatic Brain Injury Without Direct Intracranial Pressure Monitoring." Neurosurgery 72, no. 4 (April 2013): N19—N20. http://dx.doi.org/10.1227/01.neu.0000428424.83867.87.

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Vavilala, Monica S. "Intracranial pressure monitoring in meningitis: Thinking beyond traumatic brain injury*." Pediatric Critical Care Medicine 12, no. 6 (November 2011): 689–90. http://dx.doi.org/10.1097/pcc.0b013e31820ac0c4.

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Lazaridis, Christos, and Fernando D. Goldenberg. "Intracranial Pressure in Traumatic Brain Injury: From Thresholds to Heuristics." Critical Care Medicine 48, no. 8 (April 28, 2020): 1210–13. http://dx.doi.org/10.1097/ccm.0000000000004383.

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Kawoos, Usmah, Xu Meng, Shi-Min Huang, Arye Rosen, Richard M. McCarron, and Mikulas Chavko. "Telemetric Intracranial Pressure Monitoring in Blast-Induced Traumatic Brain Injury." IEEE Transactions on Biomedical Engineering 61, no. 3 (March 2014): 841–47. http://dx.doi.org/10.1109/tbme.2013.2291239.

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Melhem, Samer, Lori Shutter, and A. Kaynar. "A trial of intracranial pressure monitoring in traumatic brain injury." Critical Care 18, no. 1 (2014): 302. http://dx.doi.org/10.1186/cc13713.

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