Oxidative Stress and Antioxidant Therapy in Critically Ill Polytrauma Patients with Severe Head Injury
Traumatic Brain Injury (TBI) is one of the leading causes of death among critically ill patients from the Intensive Care Units (ICU). After primary traumatic injuries, secondary complications occur, which are responsible for the progressive degradation of the clinical status in this type of patients...
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| Format: | Article |
| Language: | English |
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Sciendo
2015-05-01
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| Series: | The Journal of Critical Care Medicine |
| Subjects: | |
| Online Access: | https://doi.org/10.1515/jccm-2015-0014 |
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| author | Luca Loredana Rogobete Alexandru Florin Bedreag Ovidiu Horea |
| author_facet | Luca Loredana Rogobete Alexandru Florin Bedreag Ovidiu Horea |
| author_sort | Luca Loredana |
| collection | DOAJ |
| description | Traumatic Brain Injury (TBI) is one of the leading causes of death among critically ill patients from the Intensive Care Units (ICU). After primary traumatic injuries, secondary complications occur, which are responsible for the progressive degradation of the clinical status in this type of patients. These include severe inflammation, biochemical and physiological imbalances and disruption of the cellular functionality. The redox cellular potential is determined by the oxidant/antioxidant ratio. Redox potential is disturbed in case of TBI leading to oxidative stress (OS). A series of agression factors that accumulate after primary traumatic injuries lead to secondary lesions represented by brain ischemia and hypoxia, inflammatory and metabolic factors, coagulopathy, microvascular damage, neurotransmitter accumulation, blood-brain barrier disruption, excitotoxic damage, blood-spinal cord barrier damage, and mitochondrial dysfunctions. A cascade of pathophysiological events lead to accelerated production of free radicals (FR) that further sustain the OS. To minimize the OS and restore normal oxidant/antioxidant ratio, a series of antioxidant substances is recommended to be administrated (vitamin C, vitamin E, resveratrol, N-acetylcysteine). In this paper we present the biochemical and pathophysiological mechanism of action of FR in patients with TBI and the antioxidant therapy available. |
| first_indexed | 2024-03-09T09:27:18Z |
| format | Article |
| id | doaj.art-ba12f409f87745289df2467c07b87211 |
| institution | Directory Open Access Journal |
| issn | 2393-1817 |
| language | English |
| last_indexed | 2024-03-09T09:27:18Z |
| publishDate | 2015-05-01 |
| publisher | Sciendo |
| record_format | Article |
| series | The Journal of Critical Care Medicine |
| spelling | doaj.art-ba12f409f87745289df2467c07b872112023-12-02T05:48:24ZengSciendoThe Journal of Critical Care Medicine2393-18172015-05-0113839110.1515/jccm-2015-0014jccm-2015-0014Oxidative Stress and Antioxidant Therapy in Critically Ill Polytrauma Patients with Severe Head InjuryLuca Loredana0Rogobete Alexandru Florin1Bedreag Ovidiu Horea2 Clinic of Anaesthesia and Intensive Care, Emergency County Hospital ”Pius Brînzeu”, Timişoara, Romania Clinic of Anaesthesia and Intensive Care, Emergency County Hospital ”Pius Brînzeu”, Timişoara, Romania Clinic of Anaesthesia and Intensive Care, Emergency County Hospital ”Pius Brînzeu”, Timişoara, RomaniaTraumatic Brain Injury (TBI) is one of the leading causes of death among critically ill patients from the Intensive Care Units (ICU). After primary traumatic injuries, secondary complications occur, which are responsible for the progressive degradation of the clinical status in this type of patients. These include severe inflammation, biochemical and physiological imbalances and disruption of the cellular functionality. The redox cellular potential is determined by the oxidant/antioxidant ratio. Redox potential is disturbed in case of TBI leading to oxidative stress (OS). A series of agression factors that accumulate after primary traumatic injuries lead to secondary lesions represented by brain ischemia and hypoxia, inflammatory and metabolic factors, coagulopathy, microvascular damage, neurotransmitter accumulation, blood-brain barrier disruption, excitotoxic damage, blood-spinal cord barrier damage, and mitochondrial dysfunctions. A cascade of pathophysiological events lead to accelerated production of free radicals (FR) that further sustain the OS. To minimize the OS and restore normal oxidant/antioxidant ratio, a series of antioxidant substances is recommended to be administrated (vitamin C, vitamin E, resveratrol, N-acetylcysteine). In this paper we present the biochemical and pathophysiological mechanism of action of FR in patients with TBI and the antioxidant therapy available.https://doi.org/10.1515/jccm-2015-0014antioxidant therapyoxidative stresstraumatic brain injurymultiple trauma patients |
| spellingShingle | Luca Loredana Rogobete Alexandru Florin Bedreag Ovidiu Horea Oxidative Stress and Antioxidant Therapy in Critically Ill Polytrauma Patients with Severe Head Injury The Journal of Critical Care Medicine antioxidant therapy oxidative stress traumatic brain injury multiple trauma patients |
| title | Oxidative Stress and Antioxidant Therapy in Critically Ill Polytrauma Patients with Severe Head Injury |
| title_full | Oxidative Stress and Antioxidant Therapy in Critically Ill Polytrauma Patients with Severe Head Injury |
| title_fullStr | Oxidative Stress and Antioxidant Therapy in Critically Ill Polytrauma Patients with Severe Head Injury |
| title_full_unstemmed | Oxidative Stress and Antioxidant Therapy in Critically Ill Polytrauma Patients with Severe Head Injury |
| title_short | Oxidative Stress and Antioxidant Therapy in Critically Ill Polytrauma Patients with Severe Head Injury |
| title_sort | oxidative stress and antioxidant therapy in critically ill polytrauma patients with severe head injury |
| topic | antioxidant therapy oxidative stress traumatic brain injury multiple trauma patients |
| url | https://doi.org/10.1515/jccm-2015-0014 |
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