Management of Increased Intracranial Pressure
Opinion statement After brain injury, neurologic intensive care focuses on the detection and treatment of secondary brain insults that may compound the initial injury. Increased intracranial pressure (ICP) contributes to secondary brain injury by causing brain ischemia, hypoxia, and metabolic dysfun...
Ausführliche Beschreibung
Autor*in: |
Sandsmark, Danielle K. [verfasserIn] Sheth, Kevin N. [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2014 |
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Schlagwörter: |
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Übergeordnetes Werk: |
Enthalten in: Current treatment options in neurology - Philadelphia, Pa. : Current Science Inc., 1999, 16(2014), 2 vom: 04. Jan. |
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Übergeordnetes Werk: |
volume:16 ; year:2014 ; number:2 ; day:04 ; month:01 |
Links: |
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DOI / URN: |
10.1007/s11940-013-0272-3 |
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Katalog-ID: |
SPR023072512 |
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520 | |a Opinion statement After brain injury, neurologic intensive care focuses on the detection and treatment of secondary brain insults that may compound the initial injury. Increased intracranial pressure (ICP) contributes to secondary brain injury by causing brain ischemia, hypoxia, and metabolic dysfunction. Because ICP is easily measured at the bedside, it is the target of numerous pharmacologic and surgical interventions in efforts to improve brain physiology and limit secondary injury. However, ICP may not adequately reflect the metabolic health of the underlying brain tissue, particularly in cases of focal brain injury. As a result, ICP control alone may be insufficient to impact patients’ long-term recovery. Further studies are needed to better understand the combination of cerebral, hemodynamic, and metabolic markers that are best utilized to ensure optimal brain and systemic recovery and overall patient outcome after brain injury. | ||
650 | 4 | |a Intracranial pressure |7 (dpeaa)DE-He213 | |
650 | 4 | |a Treatment |7 (dpeaa)DE-He213 | |
650 | 4 | |a Traumatic brain injury |7 (dpeaa)DE-He213 | |
650 | 4 | |a Stroke |7 (dpeaa)DE-He213 | |
650 | 4 | |a Craniectomy |7 (dpeaa)DE-He213 | |
650 | 4 | |a Cerebrospinal fluid |7 (dpeaa)DE-He213 | |
650 | 4 | |a Brain edema |7 (dpeaa)DE-He213 | |
650 | 4 | |a Osmotic therapy |7 (dpeaa)DE-He213 | |
650 | 4 | |a Ventriculostomy |7 (dpeaa)DE-He213 | |
700 | 1 | |a Sheth, Kevin N. |e verfasserin |4 aut | |
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10.1007/s11940-013-0272-3 doi (DE-627)SPR023072512 (SPR)s11940-013-0272-3-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Sandsmark, Danielle K. verfasserin aut Management of Increased Intracranial Pressure 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Opinion statement After brain injury, neurologic intensive care focuses on the detection and treatment of secondary brain insults that may compound the initial injury. Increased intracranial pressure (ICP) contributes to secondary brain injury by causing brain ischemia, hypoxia, and metabolic dysfunction. Because ICP is easily measured at the bedside, it is the target of numerous pharmacologic and surgical interventions in efforts to improve brain physiology and limit secondary injury. However, ICP may not adequately reflect the metabolic health of the underlying brain tissue, particularly in cases of focal brain injury. As a result, ICP control alone may be insufficient to impact patients’ long-term recovery. Further studies are needed to better understand the combination of cerebral, hemodynamic, and metabolic markers that are best utilized to ensure optimal brain and systemic recovery and overall patient outcome after brain injury. Intracranial pressure (dpeaa)DE-He213 Treatment (dpeaa)DE-He213 Traumatic brain injury (dpeaa)DE-He213 Stroke (dpeaa)DE-He213 Craniectomy (dpeaa)DE-He213 Cerebrospinal fluid (dpeaa)DE-He213 Brain edema (dpeaa)DE-He213 Osmotic therapy (dpeaa)DE-He213 Ventriculostomy (dpeaa)DE-He213 Sheth, Kevin N. verfasserin aut Enthalten in Current treatment options in neurology Philadelphia, Pa. : Current Science Inc., 1999 16(2014), 2 vom: 04. Jan. (DE-627)345859839 (DE-600)2076603-8 1534-3138 nnns volume:16 year:2014 number:2 day:04 month:01 https://dx.doi.org/10.1007/s11940-013-0272-3 lizenzpflichtig 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 16 2014 2 04 01 |
spelling |
10.1007/s11940-013-0272-3 doi (DE-627)SPR023072512 (SPR)s11940-013-0272-3-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Sandsmark, Danielle K. verfasserin aut Management of Increased Intracranial Pressure 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Opinion statement After brain injury, neurologic intensive care focuses on the detection and treatment of secondary brain insults that may compound the initial injury. Increased intracranial pressure (ICP) contributes to secondary brain injury by causing brain ischemia, hypoxia, and metabolic dysfunction. Because ICP is easily measured at the bedside, it is the target of numerous pharmacologic and surgical interventions in efforts to improve brain physiology and limit secondary injury. However, ICP may not adequately reflect the metabolic health of the underlying brain tissue, particularly in cases of focal brain injury. As a result, ICP control alone may be insufficient to impact patients’ long-term recovery. Further studies are needed to better understand the combination of cerebral, hemodynamic, and metabolic markers that are best utilized to ensure optimal brain and systemic recovery and overall patient outcome after brain injury. Intracranial pressure (dpeaa)DE-He213 Treatment (dpeaa)DE-He213 Traumatic brain injury (dpeaa)DE-He213 Stroke (dpeaa)DE-He213 Craniectomy (dpeaa)DE-He213 Cerebrospinal fluid (dpeaa)DE-He213 Brain edema (dpeaa)DE-He213 Osmotic therapy (dpeaa)DE-He213 Ventriculostomy (dpeaa)DE-He213 Sheth, Kevin N. verfasserin aut Enthalten in Current treatment options in neurology Philadelphia, Pa. : Current Science Inc., 1999 16(2014), 2 vom: 04. Jan. (DE-627)345859839 (DE-600)2076603-8 1534-3138 nnns volume:16 year:2014 number:2 day:04 month:01 https://dx.doi.org/10.1007/s11940-013-0272-3 lizenzpflichtig 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 16 2014 2 04 01 |
allfields_unstemmed |
10.1007/s11940-013-0272-3 doi (DE-627)SPR023072512 (SPR)s11940-013-0272-3-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Sandsmark, Danielle K. verfasserin aut Management of Increased Intracranial Pressure 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Opinion statement After brain injury, neurologic intensive care focuses on the detection and treatment of secondary brain insults that may compound the initial injury. Increased intracranial pressure (ICP) contributes to secondary brain injury by causing brain ischemia, hypoxia, and metabolic dysfunction. Because ICP is easily measured at the bedside, it is the target of numerous pharmacologic and surgical interventions in efforts to improve brain physiology and limit secondary injury. However, ICP may not adequately reflect the metabolic health of the underlying brain tissue, particularly in cases of focal brain injury. As a result, ICP control alone may be insufficient to impact patients’ long-term recovery. Further studies are needed to better understand the combination of cerebral, hemodynamic, and metabolic markers that are best utilized to ensure optimal brain and systemic recovery and overall patient outcome after brain injury. Intracranial pressure (dpeaa)DE-He213 Treatment (dpeaa)DE-He213 Traumatic brain injury (dpeaa)DE-He213 Stroke (dpeaa)DE-He213 Craniectomy (dpeaa)DE-He213 Cerebrospinal fluid (dpeaa)DE-He213 Brain edema (dpeaa)DE-He213 Osmotic therapy (dpeaa)DE-He213 Ventriculostomy (dpeaa)DE-He213 Sheth, Kevin N. verfasserin aut Enthalten in Current treatment options in neurology Philadelphia, Pa. : Current Science Inc., 1999 16(2014), 2 vom: 04. Jan. (DE-627)345859839 (DE-600)2076603-8 1534-3138 nnns volume:16 year:2014 number:2 day:04 month:01 https://dx.doi.org/10.1007/s11940-013-0272-3 lizenzpflichtig 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 16 2014 2 04 01 |
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10.1007/s11940-013-0272-3 doi (DE-627)SPR023072512 (SPR)s11940-013-0272-3-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Sandsmark, Danielle K. verfasserin aut Management of Increased Intracranial Pressure 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Opinion statement After brain injury, neurologic intensive care focuses on the detection and treatment of secondary brain insults that may compound the initial injury. Increased intracranial pressure (ICP) contributes to secondary brain injury by causing brain ischemia, hypoxia, and metabolic dysfunction. Because ICP is easily measured at the bedside, it is the target of numerous pharmacologic and surgical interventions in efforts to improve brain physiology and limit secondary injury. However, ICP may not adequately reflect the metabolic health of the underlying brain tissue, particularly in cases of focal brain injury. As a result, ICP control alone may be insufficient to impact patients’ long-term recovery. Further studies are needed to better understand the combination of cerebral, hemodynamic, and metabolic markers that are best utilized to ensure optimal brain and systemic recovery and overall patient outcome after brain injury. Intracranial pressure (dpeaa)DE-He213 Treatment (dpeaa)DE-He213 Traumatic brain injury (dpeaa)DE-He213 Stroke (dpeaa)DE-He213 Craniectomy (dpeaa)DE-He213 Cerebrospinal fluid (dpeaa)DE-He213 Brain edema (dpeaa)DE-He213 Osmotic therapy (dpeaa)DE-He213 Ventriculostomy (dpeaa)DE-He213 Sheth, Kevin N. verfasserin aut Enthalten in Current treatment options in neurology Philadelphia, Pa. : Current Science Inc., 1999 16(2014), 2 vom: 04. Jan. (DE-627)345859839 (DE-600)2076603-8 1534-3138 nnns volume:16 year:2014 number:2 day:04 month:01 https://dx.doi.org/10.1007/s11940-013-0272-3 lizenzpflichtig 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 16 2014 2 04 01 |
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10.1007/s11940-013-0272-3 doi (DE-627)SPR023072512 (SPR)s11940-013-0272-3-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Sandsmark, Danielle K. verfasserin aut Management of Increased Intracranial Pressure 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Opinion statement After brain injury, neurologic intensive care focuses on the detection and treatment of secondary brain insults that may compound the initial injury. Increased intracranial pressure (ICP) contributes to secondary brain injury by causing brain ischemia, hypoxia, and metabolic dysfunction. Because ICP is easily measured at the bedside, it is the target of numerous pharmacologic and surgical interventions in efforts to improve brain physiology and limit secondary injury. However, ICP may not adequately reflect the metabolic health of the underlying brain tissue, particularly in cases of focal brain injury. As a result, ICP control alone may be insufficient to impact patients’ long-term recovery. Further studies are needed to better understand the combination of cerebral, hemodynamic, and metabolic markers that are best utilized to ensure optimal brain and systemic recovery and overall patient outcome after brain injury. Intracranial pressure (dpeaa)DE-He213 Treatment (dpeaa)DE-He213 Traumatic brain injury (dpeaa)DE-He213 Stroke (dpeaa)DE-He213 Craniectomy (dpeaa)DE-He213 Cerebrospinal fluid (dpeaa)DE-He213 Brain edema (dpeaa)DE-He213 Osmotic therapy (dpeaa)DE-He213 Ventriculostomy (dpeaa)DE-He213 Sheth, Kevin N. verfasserin aut Enthalten in Current treatment options in neurology Philadelphia, Pa. : Current Science Inc., 1999 16(2014), 2 vom: 04. Jan. (DE-627)345859839 (DE-600)2076603-8 1534-3138 nnns volume:16 year:2014 number:2 day:04 month:01 https://dx.doi.org/10.1007/s11940-013-0272-3 lizenzpflichtig 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 16 2014 2 04 01 |
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topic_facet |
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container_title |
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Sandsmark, Danielle K. @@aut@@ Sheth, Kevin N. @@aut@@ |
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Sandsmark, Danielle K. |
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Sandsmark, Danielle K. ddc 610 bkl 44.90 misc Intracranial pressure misc Treatment misc Traumatic brain injury misc Stroke misc Craniectomy misc Cerebrospinal fluid misc Brain edema misc Osmotic therapy misc Ventriculostomy Management of Increased Intracranial Pressure |
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610 ASE 44.90 bkl Management of Increased Intracranial Pressure Intracranial pressure (dpeaa)DE-He213 Treatment (dpeaa)DE-He213 Traumatic brain injury (dpeaa)DE-He213 Stroke (dpeaa)DE-He213 Craniectomy (dpeaa)DE-He213 Cerebrospinal fluid (dpeaa)DE-He213 Brain edema (dpeaa)DE-He213 Osmotic therapy (dpeaa)DE-He213 Ventriculostomy (dpeaa)DE-He213 |
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ddc 610 bkl 44.90 misc Intracranial pressure misc Treatment misc Traumatic brain injury misc Stroke misc Craniectomy misc Cerebrospinal fluid misc Brain edema misc Osmotic therapy misc Ventriculostomy |
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ddc 610 bkl 44.90 misc Intracranial pressure misc Treatment misc Traumatic brain injury misc Stroke misc Craniectomy misc Cerebrospinal fluid misc Brain edema misc Osmotic therapy misc Ventriculostomy |
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management of increased intracranial pressure |
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Management of Increased Intracranial Pressure |
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Opinion statement After brain injury, neurologic intensive care focuses on the detection and treatment of secondary brain insults that may compound the initial injury. Increased intracranial pressure (ICP) contributes to secondary brain injury by causing brain ischemia, hypoxia, and metabolic dysfunction. Because ICP is easily measured at the bedside, it is the target of numerous pharmacologic and surgical interventions in efforts to improve brain physiology and limit secondary injury. However, ICP may not adequately reflect the metabolic health of the underlying brain tissue, particularly in cases of focal brain injury. As a result, ICP control alone may be insufficient to impact patients’ long-term recovery. Further studies are needed to better understand the combination of cerebral, hemodynamic, and metabolic markers that are best utilized to ensure optimal brain and systemic recovery and overall patient outcome after brain injury. |
abstractGer |
Opinion statement After brain injury, neurologic intensive care focuses on the detection and treatment of secondary brain insults that may compound the initial injury. Increased intracranial pressure (ICP) contributes to secondary brain injury by causing brain ischemia, hypoxia, and metabolic dysfunction. Because ICP is easily measured at the bedside, it is the target of numerous pharmacologic and surgical interventions in efforts to improve brain physiology and limit secondary injury. However, ICP may not adequately reflect the metabolic health of the underlying brain tissue, particularly in cases of focal brain injury. As a result, ICP control alone may be insufficient to impact patients’ long-term recovery. Further studies are needed to better understand the combination of cerebral, hemodynamic, and metabolic markers that are best utilized to ensure optimal brain and systemic recovery and overall patient outcome after brain injury. |
abstract_unstemmed |
Opinion statement After brain injury, neurologic intensive care focuses on the detection and treatment of secondary brain insults that may compound the initial injury. Increased intracranial pressure (ICP) contributes to secondary brain injury by causing brain ischemia, hypoxia, and metabolic dysfunction. Because ICP is easily measured at the bedside, it is the target of numerous pharmacologic and surgical interventions in efforts to improve brain physiology and limit secondary injury. However, ICP may not adequately reflect the metabolic health of the underlying brain tissue, particularly in cases of focal brain injury. As a result, ICP control alone may be insufficient to impact patients’ long-term recovery. Further studies are needed to better understand the combination of cerebral, hemodynamic, and metabolic markers that are best utilized to ensure optimal brain and systemic recovery and overall patient outcome after brain injury. |
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Management of Increased Intracranial Pressure |
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