<abstract xmlns="http://www.w3.org/1999/xhtml"><p>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.</p></abstract>

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.

Oxidative Stress and Antioxidant Therapy in Critically Ill Polytrauma Patients with Severe Head Injury

Clinic of Anaesthesia and Intensive Care, Emergency County Hospital ”Pius Brînzeu”, Timişoara, Romania

Faculty of Medicine, ”Victor Babeş” University of Medicine and Pharmacy, Timişoara, Romania

Faculty of Chemistry, Biology, Geography, West University of Timişoara, Timişoara, Romania

The Journal of Critical Care Medicine

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

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...

Oxidative Stress and Antioxidant Therapy in Critically Ill Polytrauma Patients with Severe Head Injury

Pubblicato online: 06 ago 2015

Pagine: 83 - 91

Ricevuto: 08 apr 2015

Accettato: 16 lug 2015

DOI: https://doi.org/10.1515/jccm-2015-0014

Parole chiave
antioxidant therapy, oxidative stress, traumatic brain injury, multiple trauma patients

© Loredana Luca et al.

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Oxidative Stress and Antioxidant Therapy in Critically Ill Polytrauma Patients with Severe Head Injury

Pubblicato online: 06 ago 2015

Pagine: 83 - 91

Ricevuto: 08 apr 2015

Accettato: 16 lug 2015

DOI: https://doi.org/10.1515/jccm-2015-0014

Parole chiaveantioxidant therapy, oxidative stress, traumatic brain injury, multiple trauma patients

© Loredana Luca et al.

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Parole chiave
antioxidant therapy, oxidative stress, traumatic brain injury, multiple trauma patients