Clinical review: Traumatic brain injury in patients receiving antiplatelet medication
Abstract As the population ages, emergency physicians are confronted with a growing number of trauma patients receiving antithrombotic and antiplatelet medication prior to injury. In cases of traumatic brain injury, pre-injury treatment with anticoagulants has been associated with an increased risk...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Beynon, Christopher [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2012 |
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| Schlagwörter: |
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| Anmerkung: |
© BioMed Central Ltd 2012 |
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| Übergeordnetes Werk: |
Enthalten in: Critical care - London : BioMed Central, 1997, 16(2012), 4 vom: 26. Juli |
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| Übergeordnetes Werk: |
volume:16 ; year:2012 ; number:4 ; day:26 ; month:07 |
| Links: |
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| DOI / URN: |
10.1186/cc11292 |
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SPR029842859 |
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| 520 | |a Abstract As the population ages, emergency physicians are confronted with a growing number of trauma patients receiving antithrombotic and antiplatelet medication prior to injury. In cases of traumatic brain injury, pre-injury treatment with anticoagulants has been associated with an increased risk of posttraumatic intracranial haemorrhage. Since high age itself is a well-recognised risk factor in traumatic brain injury, this population is at special risk for increased morbidity and mortality. The effects of antiplatelet medication on coagulation pathways in posttraumatic intracranial haemorrhage are not well understood, but available data suggest that the use of these agents increases the risk of an unfavourable outcome, especially in cases of severe traumatic brain injury. Standard laboratory investigations are insufficient to evaluate platelet activity, but new assays for monitoring platelet activity have been developed. Commonly used interventions to restore platelet activity include platelet transfusion and application of haemostatic drugs. Nevertheless, controlled clinical trials have not been carried out and, therefore, clinical practice guidelines are not available. In addition to the risks of the acute trauma, patients are at risk for cardiac events such as life-threatening stent thrombosis if antiplatelet therapy is withdrawn. In this review article, we summarize the pathophysiologic mechanisms of the most commonly used antiplatelet agents and analyse results of studies on the effects of this treatment on patients with traumatic brain injury. Additionally, we focus on opportunities to counteract antiplatelet effects in those patients as well as on considerations regarding the withdrawal of antiplatelet therapy. In those chronically ill patients, an interdisciplinary approach involving intensivists, neurosurgeons as well as cardiologists is often mandatory. | ||
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| 700 | 1 | |a Hertle, Daniel N |4 aut | |
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| 700 | 1 | |a Sakowitz, Oliver W |4 aut | |
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10.1186/cc11292 doi (DE-627)SPR029842859 (SPR)cc11292-e DE-627 ger DE-627 rakwb eng Beynon, Christopher verfasserin aut Clinical review: Traumatic brain injury in patients receiving antiplatelet medication 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2012 Abstract As the population ages, emergency physicians are confronted with a growing number of trauma patients receiving antithrombotic and antiplatelet medication prior to injury. In cases of traumatic brain injury, pre-injury treatment with anticoagulants has been associated with an increased risk of posttraumatic intracranial haemorrhage. Since high age itself is a well-recognised risk factor in traumatic brain injury, this population is at special risk for increased morbidity and mortality. The effects of antiplatelet medication on coagulation pathways in posttraumatic intracranial haemorrhage are not well understood, but available data suggest that the use of these agents increases the risk of an unfavourable outcome, especially in cases of severe traumatic brain injury. Standard laboratory investigations are insufficient to evaluate platelet activity, but new assays for monitoring platelet activity have been developed. Commonly used interventions to restore platelet activity include platelet transfusion and application of haemostatic drugs. Nevertheless, controlled clinical trials have not been carried out and, therefore, clinical practice guidelines are not available. In addition to the risks of the acute trauma, patients are at risk for cardiac events such as life-threatening stent thrombosis if antiplatelet therapy is withdrawn. In this review article, we summarize the pathophysiologic mechanisms of the most commonly used antiplatelet agents and analyse results of studies on the effects of this treatment on patients with traumatic brain injury. Additionally, we focus on opportunities to counteract antiplatelet effects in those patients as well as on considerations regarding the withdrawal of antiplatelet therapy. In those chronically ill patients, an interdisciplinary approach involving intensivists, neurosurgeons as well as cardiologists is often mandatory. Traumatic Brain Injury (dpeaa)DE-He213 Clopidogrel (dpeaa)DE-He213 Antiplatelet Therapy (dpeaa)DE-He213 Abciximab (dpeaa)DE-He213 Antiplatelet Agent (dpeaa)DE-He213 Hertle, Daniel N aut Unterberg, Andreas W aut Sakowitz, Oliver W aut Enthalten in Critical care London : BioMed Central, 1997 16(2012), 4 vom: 26. Juli (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:16 year:2012 number:4 day:26 month:07 https://dx.doi.org/10.1186/cc11292 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2012 4 26 07 |
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10.1186/cc11292 doi (DE-627)SPR029842859 (SPR)cc11292-e DE-627 ger DE-627 rakwb eng Beynon, Christopher verfasserin aut Clinical review: Traumatic brain injury in patients receiving antiplatelet medication 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2012 Abstract As the population ages, emergency physicians are confronted with a growing number of trauma patients receiving antithrombotic and antiplatelet medication prior to injury. In cases of traumatic brain injury, pre-injury treatment with anticoagulants has been associated with an increased risk of posttraumatic intracranial haemorrhage. Since high age itself is a well-recognised risk factor in traumatic brain injury, this population is at special risk for increased morbidity and mortality. The effects of antiplatelet medication on coagulation pathways in posttraumatic intracranial haemorrhage are not well understood, but available data suggest that the use of these agents increases the risk of an unfavourable outcome, especially in cases of severe traumatic brain injury. Standard laboratory investigations are insufficient to evaluate platelet activity, but new assays for monitoring platelet activity have been developed. Commonly used interventions to restore platelet activity include platelet transfusion and application of haemostatic drugs. Nevertheless, controlled clinical trials have not been carried out and, therefore, clinical practice guidelines are not available. In addition to the risks of the acute trauma, patients are at risk for cardiac events such as life-threatening stent thrombosis if antiplatelet therapy is withdrawn. In this review article, we summarize the pathophysiologic mechanisms of the most commonly used antiplatelet agents and analyse results of studies on the effects of this treatment on patients with traumatic brain injury. Additionally, we focus on opportunities to counteract antiplatelet effects in those patients as well as on considerations regarding the withdrawal of antiplatelet therapy. In those chronically ill patients, an interdisciplinary approach involving intensivists, neurosurgeons as well as cardiologists is often mandatory. Traumatic Brain Injury (dpeaa)DE-He213 Clopidogrel (dpeaa)DE-He213 Antiplatelet Therapy (dpeaa)DE-He213 Abciximab (dpeaa)DE-He213 Antiplatelet Agent (dpeaa)DE-He213 Hertle, Daniel N aut Unterberg, Andreas W aut Sakowitz, Oliver W aut Enthalten in Critical care London : BioMed Central, 1997 16(2012), 4 vom: 26. Juli (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:16 year:2012 number:4 day:26 month:07 https://dx.doi.org/10.1186/cc11292 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2012 4 26 07 |
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10.1186/cc11292 doi (DE-627)SPR029842859 (SPR)cc11292-e DE-627 ger DE-627 rakwb eng Beynon, Christopher verfasserin aut Clinical review: Traumatic brain injury in patients receiving antiplatelet medication 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2012 Abstract As the population ages, emergency physicians are confronted with a growing number of trauma patients receiving antithrombotic and antiplatelet medication prior to injury. In cases of traumatic brain injury, pre-injury treatment with anticoagulants has been associated with an increased risk of posttraumatic intracranial haemorrhage. Since high age itself is a well-recognised risk factor in traumatic brain injury, this population is at special risk for increased morbidity and mortality. The effects of antiplatelet medication on coagulation pathways in posttraumatic intracranial haemorrhage are not well understood, but available data suggest that the use of these agents increases the risk of an unfavourable outcome, especially in cases of severe traumatic brain injury. Standard laboratory investigations are insufficient to evaluate platelet activity, but new assays for monitoring platelet activity have been developed. Commonly used interventions to restore platelet activity include platelet transfusion and application of haemostatic drugs. Nevertheless, controlled clinical trials have not been carried out and, therefore, clinical practice guidelines are not available. In addition to the risks of the acute trauma, patients are at risk for cardiac events such as life-threatening stent thrombosis if antiplatelet therapy is withdrawn. In this review article, we summarize the pathophysiologic mechanisms of the most commonly used antiplatelet agents and analyse results of studies on the effects of this treatment on patients with traumatic brain injury. Additionally, we focus on opportunities to counteract antiplatelet effects in those patients as well as on considerations regarding the withdrawal of antiplatelet therapy. In those chronically ill patients, an interdisciplinary approach involving intensivists, neurosurgeons as well as cardiologists is often mandatory. Traumatic Brain Injury (dpeaa)DE-He213 Clopidogrel (dpeaa)DE-He213 Antiplatelet Therapy (dpeaa)DE-He213 Abciximab (dpeaa)DE-He213 Antiplatelet Agent (dpeaa)DE-He213 Hertle, Daniel N aut Unterberg, Andreas W aut Sakowitz, Oliver W aut Enthalten in Critical care London : BioMed Central, 1997 16(2012), 4 vom: 26. Juli (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:16 year:2012 number:4 day:26 month:07 https://dx.doi.org/10.1186/cc11292 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2012 4 26 07 |
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10.1186/cc11292 doi (DE-627)SPR029842859 (SPR)cc11292-e DE-627 ger DE-627 rakwb eng Beynon, Christopher verfasserin aut Clinical review: Traumatic brain injury in patients receiving antiplatelet medication 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2012 Abstract As the population ages, emergency physicians are confronted with a growing number of trauma patients receiving antithrombotic and antiplatelet medication prior to injury. In cases of traumatic brain injury, pre-injury treatment with anticoagulants has been associated with an increased risk of posttraumatic intracranial haemorrhage. Since high age itself is a well-recognised risk factor in traumatic brain injury, this population is at special risk for increased morbidity and mortality. The effects of antiplatelet medication on coagulation pathways in posttraumatic intracranial haemorrhage are not well understood, but available data suggest that the use of these agents increases the risk of an unfavourable outcome, especially in cases of severe traumatic brain injury. Standard laboratory investigations are insufficient to evaluate platelet activity, but new assays for monitoring platelet activity have been developed. Commonly used interventions to restore platelet activity include platelet transfusion and application of haemostatic drugs. Nevertheless, controlled clinical trials have not been carried out and, therefore, clinical practice guidelines are not available. In addition to the risks of the acute trauma, patients are at risk for cardiac events such as life-threatening stent thrombosis if antiplatelet therapy is withdrawn. In this review article, we summarize the pathophysiologic mechanisms of the most commonly used antiplatelet agents and analyse results of studies on the effects of this treatment on patients with traumatic brain injury. Additionally, we focus on opportunities to counteract antiplatelet effects in those patients as well as on considerations regarding the withdrawal of antiplatelet therapy. In those chronically ill patients, an interdisciplinary approach involving intensivists, neurosurgeons as well as cardiologists is often mandatory. Traumatic Brain Injury (dpeaa)DE-He213 Clopidogrel (dpeaa)DE-He213 Antiplatelet Therapy (dpeaa)DE-He213 Abciximab (dpeaa)DE-He213 Antiplatelet Agent (dpeaa)DE-He213 Hertle, Daniel N aut Unterberg, Andreas W aut Sakowitz, Oliver W aut Enthalten in Critical care London : BioMed Central, 1997 16(2012), 4 vom: 26. Juli (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:16 year:2012 number:4 day:26 month:07 https://dx.doi.org/10.1186/cc11292 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2012 4 26 07 |
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10.1186/cc11292 doi (DE-627)SPR029842859 (SPR)cc11292-e DE-627 ger DE-627 rakwb eng Beynon, Christopher verfasserin aut Clinical review: Traumatic brain injury in patients receiving antiplatelet medication 2012 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2012 Abstract As the population ages, emergency physicians are confronted with a growing number of trauma patients receiving antithrombotic and antiplatelet medication prior to injury. In cases of traumatic brain injury, pre-injury treatment with anticoagulants has been associated with an increased risk of posttraumatic intracranial haemorrhage. Since high age itself is a well-recognised risk factor in traumatic brain injury, this population is at special risk for increased morbidity and mortality. The effects of antiplatelet medication on coagulation pathways in posttraumatic intracranial haemorrhage are not well understood, but available data suggest that the use of these agents increases the risk of an unfavourable outcome, especially in cases of severe traumatic brain injury. Standard laboratory investigations are insufficient to evaluate platelet activity, but new assays for monitoring platelet activity have been developed. Commonly used interventions to restore platelet activity include platelet transfusion and application of haemostatic drugs. Nevertheless, controlled clinical trials have not been carried out and, therefore, clinical practice guidelines are not available. In addition to the risks of the acute trauma, patients are at risk for cardiac events such as life-threatening stent thrombosis if antiplatelet therapy is withdrawn. In this review article, we summarize the pathophysiologic mechanisms of the most commonly used antiplatelet agents and analyse results of studies on the effects of this treatment on patients with traumatic brain injury. Additionally, we focus on opportunities to counteract antiplatelet effects in those patients as well as on considerations regarding the withdrawal of antiplatelet therapy. In those chronically ill patients, an interdisciplinary approach involving intensivists, neurosurgeons as well as cardiologists is often mandatory. Traumatic Brain Injury (dpeaa)DE-He213 Clopidogrel (dpeaa)DE-He213 Antiplatelet Therapy (dpeaa)DE-He213 Abciximab (dpeaa)DE-He213 Antiplatelet Agent (dpeaa)DE-He213 Hertle, Daniel N aut Unterberg, Andreas W aut Sakowitz, Oliver W aut Enthalten in Critical care London : BioMed Central, 1997 16(2012), 4 vom: 26. Juli (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:16 year:2012 number:4 day:26 month:07 https://dx.doi.org/10.1186/cc11292 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2012 4 26 07 |
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Abstract As the population ages, emergency physicians are confronted with a growing number of trauma patients receiving antithrombotic and antiplatelet medication prior to injury. In cases of traumatic brain injury, pre-injury treatment with anticoagulants has been associated with an increased risk of posttraumatic intracranial haemorrhage. Since high age itself is a well-recognised risk factor in traumatic brain injury, this population is at special risk for increased morbidity and mortality. The effects of antiplatelet medication on coagulation pathways in posttraumatic intracranial haemorrhage are not well understood, but available data suggest that the use of these agents increases the risk of an unfavourable outcome, especially in cases of severe traumatic brain injury. Standard laboratory investigations are insufficient to evaluate platelet activity, but new assays for monitoring platelet activity have been developed. Commonly used interventions to restore platelet activity include platelet transfusion and application of haemostatic drugs. Nevertheless, controlled clinical trials have not been carried out and, therefore, clinical practice guidelines are not available. In addition to the risks of the acute trauma, patients are at risk for cardiac events such as life-threatening stent thrombosis if antiplatelet therapy is withdrawn. In this review article, we summarize the pathophysiologic mechanisms of the most commonly used antiplatelet agents and analyse results of studies on the effects of this treatment on patients with traumatic brain injury. Additionally, we focus on opportunities to counteract antiplatelet effects in those patients as well as on considerations regarding the withdrawal of antiplatelet therapy. In those chronically ill patients, an interdisciplinary approach involving intensivists, neurosurgeons as well as cardiologists is often mandatory. © BioMed Central Ltd 2012 |
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Abstract As the population ages, emergency physicians are confronted with a growing number of trauma patients receiving antithrombotic and antiplatelet medication prior to injury. In cases of traumatic brain injury, pre-injury treatment with anticoagulants has been associated with an increased risk of posttraumatic intracranial haemorrhage. Since high age itself is a well-recognised risk factor in traumatic brain injury, this population is at special risk for increased morbidity and mortality. The effects of antiplatelet medication on coagulation pathways in posttraumatic intracranial haemorrhage are not well understood, but available data suggest that the use of these agents increases the risk of an unfavourable outcome, especially in cases of severe traumatic brain injury. Standard laboratory investigations are insufficient to evaluate platelet activity, but new assays for monitoring platelet activity have been developed. Commonly used interventions to restore platelet activity include platelet transfusion and application of haemostatic drugs. Nevertheless, controlled clinical trials have not been carried out and, therefore, clinical practice guidelines are not available. In addition to the risks of the acute trauma, patients are at risk for cardiac events such as life-threatening stent thrombosis if antiplatelet therapy is withdrawn. In this review article, we summarize the pathophysiologic mechanisms of the most commonly used antiplatelet agents and analyse results of studies on the effects of this treatment on patients with traumatic brain injury. Additionally, we focus on opportunities to counteract antiplatelet effects in those patients as well as on considerations regarding the withdrawal of antiplatelet therapy. In those chronically ill patients, an interdisciplinary approach involving intensivists, neurosurgeons as well as cardiologists is often mandatory. © BioMed Central Ltd 2012 |
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Abstract As the population ages, emergency physicians are confronted with a growing number of trauma patients receiving antithrombotic and antiplatelet medication prior to injury. In cases of traumatic brain injury, pre-injury treatment with anticoagulants has been associated with an increased risk of posttraumatic intracranial haemorrhage. Since high age itself is a well-recognised risk factor in traumatic brain injury, this population is at special risk for increased morbidity and mortality. The effects of antiplatelet medication on coagulation pathways in posttraumatic intracranial haemorrhage are not well understood, but available data suggest that the use of these agents increases the risk of an unfavourable outcome, especially in cases of severe traumatic brain injury. Standard laboratory investigations are insufficient to evaluate platelet activity, but new assays for monitoring platelet activity have been developed. Commonly used interventions to restore platelet activity include platelet transfusion and application of haemostatic drugs. Nevertheless, controlled clinical trials have not been carried out and, therefore, clinical practice guidelines are not available. In addition to the risks of the acute trauma, patients are at risk for cardiac events such as life-threatening stent thrombosis if antiplatelet therapy is withdrawn. In this review article, we summarize the pathophysiologic mechanisms of the most commonly used antiplatelet agents and analyse results of studies on the effects of this treatment on patients with traumatic brain injury. Additionally, we focus on opportunities to counteract antiplatelet effects in those patients as well as on considerations regarding the withdrawal of antiplatelet therapy. In those chronically ill patients, an interdisciplinary approach involving intensivists, neurosurgeons as well as cardiologists is often mandatory. © BioMed Central Ltd 2012 |
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