Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury
Background Raised intracranial pressure (ICP) is a prominent cause of morbidity and mortality after severe traumatic brain injury (TBI). However, in the clinical setting, little is known about the cerebral physiological response to severe and prolonged increases in ICP. Methods Thirty-three severe T...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Donnelly, Joseph [verfasserIn] Smielewski, Peter [verfasserIn] Adams, Hadie [verfasserIn] Zeiler, Frederick A. [verfasserIn] Cardim, Danilo [verfasserIn] Liu, Xiuyun [verfasserIn] Fedriga, Marta [verfasserIn] Hutchinson, Peter [verfasserIn] Menon, David K. [verfasserIn] Czosnyka, Marek [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2019 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Neurocritical care - New York, NY : Springer, 2004, 32(2019), 2 vom: 25. Juni, Seite 437-447 |
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| Übergeordnetes Werk: |
volume:32 ; year:2019 ; number:2 ; day:25 ; month:06 ; pages:437-447 |
| Links: |
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| DOI / URN: |
10.1007/s12028-019-00748-x |
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| Katalog-ID: |
SPR039155854 |
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| 245 | 1 | 0 | |a Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury |
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| 520 | |a Background Raised intracranial pressure (ICP) is a prominent cause of morbidity and mortality after severe traumatic brain injury (TBI). However, in the clinical setting, little is known about the cerebral physiological response to severe and prolonged increases in ICP. Methods Thirty-three severe TBI patients from a single center who developed severe refractory intracranial hypertension (ICP > 40 mm Hg for longer than 1 h) with ICP, arterial blood pressure, and brain tissue oxygenation ($ P_{BT} %$ O_{2} $) monitoring (subcohort, n = 9) were selected for retrospective review. Secondary parameters reflecting autoregulation (including pressure reactivity index—PRx, which was available in 24 cases), cerebrospinal compensatory reserve (RAP), and ICP pulse amplitude were calculated. Results PRx deteriorated from 0.06 ± 0.26 a.u. at baseline levels of ICP to 0.57 ± 0.24 a.u. (p < 0.0001) at high levels of ICP (> 50 mm Hg). In 4 cases, PRx was impaired (> 0.25 a.u.) before ICP was raised above 25 mm Hg. Concurrently, $ P_{BT} %$ O_{2} $ decreased from 27.3 ± 7.32 mm Hg at baseline ICP to 12.68 ± 7.09 mm Hg at high levels of ICP (p < 0.001). The pulse amplitude of the ICP waveform increased with increasing ICP but showed an ‘upper breakpoint’—whereby further increases in ICP lead to decreases in pulse amplitude—in 6 out of the 33 patients. Discussion Severe intracranial hypertension after TBI leads to decreased brain oxygenation, impaired pressure reactivity, and changes in the pulse amplitude of ICP. Impaired pressure reactivity may denote increased risk of developing refractory intracranial hypertension in some patients. | ||
| 650 | 4 | |a Traumatic brain injury |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Intracranial pressure |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cerebral hemodynamics |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Autoregulation |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cerebral oxygenation |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cerebral perfusion pressure |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Intracranial hypertension |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Smielewski, Peter |e verfasserin |4 aut | |
| 700 | 1 | |a Adams, Hadie |e verfasserin |4 aut | |
| 700 | 1 | |a Zeiler, Frederick A. |e verfasserin |4 aut | |
| 700 | 1 | |a Cardim, Danilo |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Xiuyun |e verfasserin |4 aut | |
| 700 | 1 | |a Fedriga, Marta |e verfasserin |4 aut | |
| 700 | 1 | |a Hutchinson, Peter |e verfasserin |4 aut | |
| 700 | 1 | |a Menon, David K. |e verfasserin |4 aut | |
| 700 | 1 | |a Czosnyka, Marek |e verfasserin |4 aut | |
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10.1007/s12028-019-00748-x doi (DE-627)SPR039155854 (SPR)s12028-019-00748-x-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Donnelly, Joseph verfasserin aut Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Raised intracranial pressure (ICP) is a prominent cause of morbidity and mortality after severe traumatic brain injury (TBI). However, in the clinical setting, little is known about the cerebral physiological response to severe and prolonged increases in ICP. Methods Thirty-three severe TBI patients from a single center who developed severe refractory intracranial hypertension (ICP > 40 mm Hg for longer than 1 h) with ICP, arterial blood pressure, and brain tissue oxygenation ($ P_{BT} %$ O_{2} $) monitoring (subcohort, n = 9) were selected for retrospective review. Secondary parameters reflecting autoregulation (including pressure reactivity index—PRx, which was available in 24 cases), cerebrospinal compensatory reserve (RAP), and ICP pulse amplitude were calculated. Results PRx deteriorated from 0.06 ± 0.26 a.u. at baseline levels of ICP to 0.57 ± 0.24 a.u. (p < 0.0001) at high levels of ICP (> 50 mm Hg). In 4 cases, PRx was impaired (> 0.25 a.u.) before ICP was raised above 25 mm Hg. Concurrently, $ P_{BT} %$ O_{2} $ decreased from 27.3 ± 7.32 mm Hg at baseline ICP to 12.68 ± 7.09 mm Hg at high levels of ICP (p < 0.001). The pulse amplitude of the ICP waveform increased with increasing ICP but showed an ‘upper breakpoint’—whereby further increases in ICP lead to decreases in pulse amplitude—in 6 out of the 33 patients. Discussion Severe intracranial hypertension after TBI leads to decreased brain oxygenation, impaired pressure reactivity, and changes in the pulse amplitude of ICP. Impaired pressure reactivity may denote increased risk of developing refractory intracranial hypertension in some patients. Traumatic brain injury (dpeaa)DE-He213 Intracranial pressure (dpeaa)DE-He213 Cerebral hemodynamics (dpeaa)DE-He213 Autoregulation (dpeaa)DE-He213 Cerebral oxygenation (dpeaa)DE-He213 Cerebral perfusion pressure (dpeaa)DE-He213 Intracranial hypertension (dpeaa)DE-He213 Smielewski, Peter verfasserin aut Adams, Hadie verfasserin aut Zeiler, Frederick A. verfasserin aut Cardim, Danilo verfasserin aut Liu, Xiuyun verfasserin aut Fedriga, Marta verfasserin aut Hutchinson, Peter verfasserin aut Menon, David K. verfasserin aut Czosnyka, Marek verfasserin aut Enthalten in Neurocritical care New York, NY : Springer, 2004 32(2019), 2 vom: 25. Juni, Seite 437-447 (DE-627)478509855 (DE-600)2176033-0 1556-0961 nnns volume:32 year:2019 number:2 day:25 month:06 pages:437-447 https://dx.doi.org/10.1007/s12028-019-00748-x kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 32 2019 2 25 06 437-447 |
| spelling |
10.1007/s12028-019-00748-x doi (DE-627)SPR039155854 (SPR)s12028-019-00748-x-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Donnelly, Joseph verfasserin aut Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Raised intracranial pressure (ICP) is a prominent cause of morbidity and mortality after severe traumatic brain injury (TBI). However, in the clinical setting, little is known about the cerebral physiological response to severe and prolonged increases in ICP. Methods Thirty-three severe TBI patients from a single center who developed severe refractory intracranial hypertension (ICP > 40 mm Hg for longer than 1 h) with ICP, arterial blood pressure, and brain tissue oxygenation ($ P_{BT} %$ O_{2} $) monitoring (subcohort, n = 9) were selected for retrospective review. Secondary parameters reflecting autoregulation (including pressure reactivity index—PRx, which was available in 24 cases), cerebrospinal compensatory reserve (RAP), and ICP pulse amplitude were calculated. Results PRx deteriorated from 0.06 ± 0.26 a.u. at baseline levels of ICP to 0.57 ± 0.24 a.u. (p < 0.0001) at high levels of ICP (> 50 mm Hg). In 4 cases, PRx was impaired (> 0.25 a.u.) before ICP was raised above 25 mm Hg. Concurrently, $ P_{BT} %$ O_{2} $ decreased from 27.3 ± 7.32 mm Hg at baseline ICP to 12.68 ± 7.09 mm Hg at high levels of ICP (p < 0.001). The pulse amplitude of the ICP waveform increased with increasing ICP but showed an ‘upper breakpoint’—whereby further increases in ICP lead to decreases in pulse amplitude—in 6 out of the 33 patients. Discussion Severe intracranial hypertension after TBI leads to decreased brain oxygenation, impaired pressure reactivity, and changes in the pulse amplitude of ICP. Impaired pressure reactivity may denote increased risk of developing refractory intracranial hypertension in some patients. Traumatic brain injury (dpeaa)DE-He213 Intracranial pressure (dpeaa)DE-He213 Cerebral hemodynamics (dpeaa)DE-He213 Autoregulation (dpeaa)DE-He213 Cerebral oxygenation (dpeaa)DE-He213 Cerebral perfusion pressure (dpeaa)DE-He213 Intracranial hypertension (dpeaa)DE-He213 Smielewski, Peter verfasserin aut Adams, Hadie verfasserin aut Zeiler, Frederick A. verfasserin aut Cardim, Danilo verfasserin aut Liu, Xiuyun verfasserin aut Fedriga, Marta verfasserin aut Hutchinson, Peter verfasserin aut Menon, David K. verfasserin aut Czosnyka, Marek verfasserin aut Enthalten in Neurocritical care New York, NY : Springer, 2004 32(2019), 2 vom: 25. Juni, Seite 437-447 (DE-627)478509855 (DE-600)2176033-0 1556-0961 nnns volume:32 year:2019 number:2 day:25 month:06 pages:437-447 https://dx.doi.org/10.1007/s12028-019-00748-x kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 32 2019 2 25 06 437-447 |
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10.1007/s12028-019-00748-x doi (DE-627)SPR039155854 (SPR)s12028-019-00748-x-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Donnelly, Joseph verfasserin aut Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Raised intracranial pressure (ICP) is a prominent cause of morbidity and mortality after severe traumatic brain injury (TBI). However, in the clinical setting, little is known about the cerebral physiological response to severe and prolonged increases in ICP. Methods Thirty-three severe TBI patients from a single center who developed severe refractory intracranial hypertension (ICP > 40 mm Hg for longer than 1 h) with ICP, arterial blood pressure, and brain tissue oxygenation ($ P_{BT} %$ O_{2} $) monitoring (subcohort, n = 9) were selected for retrospective review. Secondary parameters reflecting autoregulation (including pressure reactivity index—PRx, which was available in 24 cases), cerebrospinal compensatory reserve (RAP), and ICP pulse amplitude were calculated. Results PRx deteriorated from 0.06 ± 0.26 a.u. at baseline levels of ICP to 0.57 ± 0.24 a.u. (p < 0.0001) at high levels of ICP (> 50 mm Hg). In 4 cases, PRx was impaired (> 0.25 a.u.) before ICP was raised above 25 mm Hg. Concurrently, $ P_{BT} %$ O_{2} $ decreased from 27.3 ± 7.32 mm Hg at baseline ICP to 12.68 ± 7.09 mm Hg at high levels of ICP (p < 0.001). The pulse amplitude of the ICP waveform increased with increasing ICP but showed an ‘upper breakpoint’—whereby further increases in ICP lead to decreases in pulse amplitude—in 6 out of the 33 patients. Discussion Severe intracranial hypertension after TBI leads to decreased brain oxygenation, impaired pressure reactivity, and changes in the pulse amplitude of ICP. Impaired pressure reactivity may denote increased risk of developing refractory intracranial hypertension in some patients. Traumatic brain injury (dpeaa)DE-He213 Intracranial pressure (dpeaa)DE-He213 Cerebral hemodynamics (dpeaa)DE-He213 Autoregulation (dpeaa)DE-He213 Cerebral oxygenation (dpeaa)DE-He213 Cerebral perfusion pressure (dpeaa)DE-He213 Intracranial hypertension (dpeaa)DE-He213 Smielewski, Peter verfasserin aut Adams, Hadie verfasserin aut Zeiler, Frederick A. verfasserin aut Cardim, Danilo verfasserin aut Liu, Xiuyun verfasserin aut Fedriga, Marta verfasserin aut Hutchinson, Peter verfasserin aut Menon, David K. verfasserin aut Czosnyka, Marek verfasserin aut Enthalten in Neurocritical care New York, NY : Springer, 2004 32(2019), 2 vom: 25. Juni, Seite 437-447 (DE-627)478509855 (DE-600)2176033-0 1556-0961 nnns volume:32 year:2019 number:2 day:25 month:06 pages:437-447 https://dx.doi.org/10.1007/s12028-019-00748-x kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 32 2019 2 25 06 437-447 |
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10.1007/s12028-019-00748-x doi (DE-627)SPR039155854 (SPR)s12028-019-00748-x-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Donnelly, Joseph verfasserin aut Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Raised intracranial pressure (ICP) is a prominent cause of morbidity and mortality after severe traumatic brain injury (TBI). However, in the clinical setting, little is known about the cerebral physiological response to severe and prolonged increases in ICP. Methods Thirty-three severe TBI patients from a single center who developed severe refractory intracranial hypertension (ICP > 40 mm Hg for longer than 1 h) with ICP, arterial blood pressure, and brain tissue oxygenation ($ P_{BT} %$ O_{2} $) monitoring (subcohort, n = 9) were selected for retrospective review. Secondary parameters reflecting autoregulation (including pressure reactivity index—PRx, which was available in 24 cases), cerebrospinal compensatory reserve (RAP), and ICP pulse amplitude were calculated. Results PRx deteriorated from 0.06 ± 0.26 a.u. at baseline levels of ICP to 0.57 ± 0.24 a.u. (p < 0.0001) at high levels of ICP (> 50 mm Hg). In 4 cases, PRx was impaired (> 0.25 a.u.) before ICP was raised above 25 mm Hg. Concurrently, $ P_{BT} %$ O_{2} $ decreased from 27.3 ± 7.32 mm Hg at baseline ICP to 12.68 ± 7.09 mm Hg at high levels of ICP (p < 0.001). The pulse amplitude of the ICP waveform increased with increasing ICP but showed an ‘upper breakpoint’—whereby further increases in ICP lead to decreases in pulse amplitude—in 6 out of the 33 patients. Discussion Severe intracranial hypertension after TBI leads to decreased brain oxygenation, impaired pressure reactivity, and changes in the pulse amplitude of ICP. Impaired pressure reactivity may denote increased risk of developing refractory intracranial hypertension in some patients. Traumatic brain injury (dpeaa)DE-He213 Intracranial pressure (dpeaa)DE-He213 Cerebral hemodynamics (dpeaa)DE-He213 Autoregulation (dpeaa)DE-He213 Cerebral oxygenation (dpeaa)DE-He213 Cerebral perfusion pressure (dpeaa)DE-He213 Intracranial hypertension (dpeaa)DE-He213 Smielewski, Peter verfasserin aut Adams, Hadie verfasserin aut Zeiler, Frederick A. verfasserin aut Cardim, Danilo verfasserin aut Liu, Xiuyun verfasserin aut Fedriga, Marta verfasserin aut Hutchinson, Peter verfasserin aut Menon, David K. verfasserin aut Czosnyka, Marek verfasserin aut Enthalten in Neurocritical care New York, NY : Springer, 2004 32(2019), 2 vom: 25. Juni, Seite 437-447 (DE-627)478509855 (DE-600)2176033-0 1556-0961 nnns volume:32 year:2019 number:2 day:25 month:06 pages:437-447 https://dx.doi.org/10.1007/s12028-019-00748-x kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 32 2019 2 25 06 437-447 |
| allfieldsSound |
10.1007/s12028-019-00748-x doi (DE-627)SPR039155854 (SPR)s12028-019-00748-x-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Donnelly, Joseph verfasserin aut Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Raised intracranial pressure (ICP) is a prominent cause of morbidity and mortality after severe traumatic brain injury (TBI). However, in the clinical setting, little is known about the cerebral physiological response to severe and prolonged increases in ICP. Methods Thirty-three severe TBI patients from a single center who developed severe refractory intracranial hypertension (ICP > 40 mm Hg for longer than 1 h) with ICP, arterial blood pressure, and brain tissue oxygenation ($ P_{BT} %$ O_{2} $) monitoring (subcohort, n = 9) were selected for retrospective review. Secondary parameters reflecting autoregulation (including pressure reactivity index—PRx, which was available in 24 cases), cerebrospinal compensatory reserve (RAP), and ICP pulse amplitude were calculated. Results PRx deteriorated from 0.06 ± 0.26 a.u. at baseline levels of ICP to 0.57 ± 0.24 a.u. (p < 0.0001) at high levels of ICP (> 50 mm Hg). In 4 cases, PRx was impaired (> 0.25 a.u.) before ICP was raised above 25 mm Hg. Concurrently, $ P_{BT} %$ O_{2} $ decreased from 27.3 ± 7.32 mm Hg at baseline ICP to 12.68 ± 7.09 mm Hg at high levels of ICP (p < 0.001). The pulse amplitude of the ICP waveform increased with increasing ICP but showed an ‘upper breakpoint’—whereby further increases in ICP lead to decreases in pulse amplitude—in 6 out of the 33 patients. Discussion Severe intracranial hypertension after TBI leads to decreased brain oxygenation, impaired pressure reactivity, and changes in the pulse amplitude of ICP. Impaired pressure reactivity may denote increased risk of developing refractory intracranial hypertension in some patients. Traumatic brain injury (dpeaa)DE-He213 Intracranial pressure (dpeaa)DE-He213 Cerebral hemodynamics (dpeaa)DE-He213 Autoregulation (dpeaa)DE-He213 Cerebral oxygenation (dpeaa)DE-He213 Cerebral perfusion pressure (dpeaa)DE-He213 Intracranial hypertension (dpeaa)DE-He213 Smielewski, Peter verfasserin aut Adams, Hadie verfasserin aut Zeiler, Frederick A. verfasserin aut Cardim, Danilo verfasserin aut Liu, Xiuyun verfasserin aut Fedriga, Marta verfasserin aut Hutchinson, Peter verfasserin aut Menon, David K. verfasserin aut Czosnyka, Marek verfasserin aut Enthalten in Neurocritical care New York, NY : Springer, 2004 32(2019), 2 vom: 25. Juni, Seite 437-447 (DE-627)478509855 (DE-600)2176033-0 1556-0961 nnns volume:32 year:2019 number:2 day:25 month:06 pages:437-447 https://dx.doi.org/10.1007/s12028-019-00748-x kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 32 2019 2 25 06 437-447 |
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Enthalten in Neurocritical care 32(2019), 2 vom: 25. Juni, Seite 437-447 volume:32 year:2019 number:2 day:25 month:06 pages:437-447 |
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Traumatic brain injury Intracranial pressure Cerebral hemodynamics Autoregulation Cerebral oxygenation Cerebral perfusion pressure Intracranial hypertension |
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Donnelly, Joseph @@aut@@ Smielewski, Peter @@aut@@ Adams, Hadie @@aut@@ Zeiler, Frederick A. @@aut@@ Cardim, Danilo @@aut@@ Liu, Xiuyun @@aut@@ Fedriga, Marta @@aut@@ Hutchinson, Peter @@aut@@ Menon, David K. @@aut@@ Czosnyka, Marek @@aut@@ |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR039155854</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519084854.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2019 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s12028-019-00748-x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR039155854</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s12028-019-00748-x-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.90</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Donnelly, Joseph</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2019</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Raised intracranial pressure (ICP) is a prominent cause of morbidity and mortality after severe traumatic brain injury (TBI). However, in the clinical setting, little is known about the cerebral physiological response to severe and prolonged increases in ICP. Methods Thirty-three severe TBI patients from a single center who developed severe refractory intracranial hypertension (ICP > 40 mm Hg for longer than 1 h) with ICP, arterial blood pressure, and brain tissue oxygenation ($ P_{BT} %$ O_{2} $) monitoring (subcohort, n = 9) were selected for retrospective review. Secondary parameters reflecting autoregulation (including pressure reactivity index—PRx, which was available in 24 cases), cerebrospinal compensatory reserve (RAP), and ICP pulse amplitude were calculated. Results PRx deteriorated from 0.06 ± 0.26 a.u. at baseline levels of ICP to 0.57 ± 0.24 a.u. (p < 0.0001) at high levels of ICP (> 50 mm Hg). In 4 cases, PRx was impaired (> 0.25 a.u.) before ICP was raised above 25 mm Hg. Concurrently, $ P_{BT} %$ O_{2} $ decreased from 27.3 ± 7.32 mm Hg at baseline ICP to 12.68 ± 7.09 mm Hg at high levels of ICP (p < 0.001). The pulse amplitude of the ICP waveform increased with increasing ICP but showed an ‘upper breakpoint’—whereby further increases in ICP lead to decreases in pulse amplitude—in 6 out of the 33 patients. Discussion Severe intracranial hypertension after TBI leads to decreased brain oxygenation, impaired pressure reactivity, and changes in the pulse amplitude of ICP. 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Donnelly, Joseph |
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Donnelly, Joseph ddc 610 bkl 44.90 misc Traumatic brain injury misc Intracranial pressure misc Cerebral hemodynamics misc Autoregulation misc Cerebral oxygenation misc Cerebral perfusion pressure misc Intracranial hypertension Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury |
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610 ASE 44.90 bkl Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury Traumatic brain injury (dpeaa)DE-He213 Intracranial pressure (dpeaa)DE-He213 Cerebral hemodynamics (dpeaa)DE-He213 Autoregulation (dpeaa)DE-He213 Cerebral oxygenation (dpeaa)DE-He213 Cerebral perfusion pressure (dpeaa)DE-He213 Intracranial hypertension (dpeaa)DE-He213 |
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ddc 610 bkl 44.90 misc Traumatic brain injury misc Intracranial pressure misc Cerebral hemodynamics misc Autoregulation misc Cerebral oxygenation misc Cerebral perfusion pressure misc Intracranial hypertension |
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ddc 610 bkl 44.90 misc Traumatic brain injury misc Intracranial pressure misc Cerebral hemodynamics misc Autoregulation misc Cerebral oxygenation misc Cerebral perfusion pressure misc Intracranial hypertension |
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Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury |
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Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury |
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Donnelly, Joseph |
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Neurocritical care |
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Donnelly, Joseph Smielewski, Peter Adams, Hadie Zeiler, Frederick A. Cardim, Danilo Liu, Xiuyun Fedriga, Marta Hutchinson, Peter Menon, David K. Czosnyka, Marek |
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10.1007/s12028-019-00748-x |
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610 |
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observations on the cerebral effects of refractory intracranial hypertension after severe traumatic brain injury |
| title_auth |
Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury |
| abstract |
Background Raised intracranial pressure (ICP) is a prominent cause of morbidity and mortality after severe traumatic brain injury (TBI). However, in the clinical setting, little is known about the cerebral physiological response to severe and prolonged increases in ICP. Methods Thirty-three severe TBI patients from a single center who developed severe refractory intracranial hypertension (ICP > 40 mm Hg for longer than 1 h) with ICP, arterial blood pressure, and brain tissue oxygenation ($ P_{BT} %$ O_{2} $) monitoring (subcohort, n = 9) were selected for retrospective review. Secondary parameters reflecting autoregulation (including pressure reactivity index—PRx, which was available in 24 cases), cerebrospinal compensatory reserve (RAP), and ICP pulse amplitude were calculated. Results PRx deteriorated from 0.06 ± 0.26 a.u. at baseline levels of ICP to 0.57 ± 0.24 a.u. (p < 0.0001) at high levels of ICP (> 50 mm Hg). In 4 cases, PRx was impaired (> 0.25 a.u.) before ICP was raised above 25 mm Hg. Concurrently, $ P_{BT} %$ O_{2} $ decreased from 27.3 ± 7.32 mm Hg at baseline ICP to 12.68 ± 7.09 mm Hg at high levels of ICP (p < 0.001). The pulse amplitude of the ICP waveform increased with increasing ICP but showed an ‘upper breakpoint’—whereby further increases in ICP lead to decreases in pulse amplitude—in 6 out of the 33 patients. Discussion Severe intracranial hypertension after TBI leads to decreased brain oxygenation, impaired pressure reactivity, and changes in the pulse amplitude of ICP. Impaired pressure reactivity may denote increased risk of developing refractory intracranial hypertension in some patients. |
| abstractGer |
Background Raised intracranial pressure (ICP) is a prominent cause of morbidity and mortality after severe traumatic brain injury (TBI). However, in the clinical setting, little is known about the cerebral physiological response to severe and prolonged increases in ICP. Methods Thirty-three severe TBI patients from a single center who developed severe refractory intracranial hypertension (ICP > 40 mm Hg for longer than 1 h) with ICP, arterial blood pressure, and brain tissue oxygenation ($ P_{BT} %$ O_{2} $) monitoring (subcohort, n = 9) were selected for retrospective review. Secondary parameters reflecting autoregulation (including pressure reactivity index—PRx, which was available in 24 cases), cerebrospinal compensatory reserve (RAP), and ICP pulse amplitude were calculated. Results PRx deteriorated from 0.06 ± 0.26 a.u. at baseline levels of ICP to 0.57 ± 0.24 a.u. (p < 0.0001) at high levels of ICP (> 50 mm Hg). In 4 cases, PRx was impaired (> 0.25 a.u.) before ICP was raised above 25 mm Hg. Concurrently, $ P_{BT} %$ O_{2} $ decreased from 27.3 ± 7.32 mm Hg at baseline ICP to 12.68 ± 7.09 mm Hg at high levels of ICP (p < 0.001). The pulse amplitude of the ICP waveform increased with increasing ICP but showed an ‘upper breakpoint’—whereby further increases in ICP lead to decreases in pulse amplitude—in 6 out of the 33 patients. Discussion Severe intracranial hypertension after TBI leads to decreased brain oxygenation, impaired pressure reactivity, and changes in the pulse amplitude of ICP. Impaired pressure reactivity may denote increased risk of developing refractory intracranial hypertension in some patients. |
| abstract_unstemmed |
Background Raised intracranial pressure (ICP) is a prominent cause of morbidity and mortality after severe traumatic brain injury (TBI). However, in the clinical setting, little is known about the cerebral physiological response to severe and prolonged increases in ICP. Methods Thirty-three severe TBI patients from a single center who developed severe refractory intracranial hypertension (ICP > 40 mm Hg for longer than 1 h) with ICP, arterial blood pressure, and brain tissue oxygenation ($ P_{BT} %$ O_{2} $) monitoring (subcohort, n = 9) were selected for retrospective review. Secondary parameters reflecting autoregulation (including pressure reactivity index—PRx, which was available in 24 cases), cerebrospinal compensatory reserve (RAP), and ICP pulse amplitude were calculated. Results PRx deteriorated from 0.06 ± 0.26 a.u. at baseline levels of ICP to 0.57 ± 0.24 a.u. (p < 0.0001) at high levels of ICP (> 50 mm Hg). In 4 cases, PRx was impaired (> 0.25 a.u.) before ICP was raised above 25 mm Hg. Concurrently, $ P_{BT} %$ O_{2} $ decreased from 27.3 ± 7.32 mm Hg at baseline ICP to 12.68 ± 7.09 mm Hg at high levels of ICP (p < 0.001). The pulse amplitude of the ICP waveform increased with increasing ICP but showed an ‘upper breakpoint’—whereby further increases in ICP lead to decreases in pulse amplitude—in 6 out of the 33 patients. Discussion Severe intracranial hypertension after TBI leads to decreased brain oxygenation, impaired pressure reactivity, and changes in the pulse amplitude of ICP. Impaired pressure reactivity may denote increased risk of developing refractory intracranial hypertension in some patients. |
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Observations on the Cerebral Effects of Refractory Intracranial Hypertension After Severe Traumatic Brain Injury |
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Smielewski, Peter Adams, Hadie Zeiler, Frederick A. Cardim, Danilo Liu, Xiuyun Fedriga, Marta Hutchinson, Peter Menon, David K. Czosnyka, Marek |
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| score |
7.4027834 |