title: The use of antioxidants in the treatment of traumatic brain injury.
abstract: OBJECTIVE
  The aim of this study was to discuss secondary traumatic brain injury, the mitochondria and the use of antioxidants as a treatment.
  
  
  BACKGROUND
  One of the leading causes of death globally is traumatic brain injury, affecting individuals in all demographics. Traumatic brain injury is produced by an external blunt force or penetration resulting in alterations in brain function or pathology. Often, with a traumatic brain injury, secondary injury causes additional damage to the brain tissue that can have further impact on recovery and the quality of life. Secondary injury occurs when metabolic and physiologic processes alter after initial injury and includes increased release of toxic free radicals that cause damage to adjacent tissues and can eventually lead to neuronal necrosis. Although antioxidants in the tissues can reduce free radical damage, the magnitude of increased free radicals overwhelms the body's reduced defence mechanisms. Supplementing the body's natural supply of antioxidants, such as coenzyme Q10, can attenuate oxidative damage caused by reactive oxygen species.
  
  
  METHODS
  Discussion paper.
  
  
  METHODS
  Research literature published from 2011-2016 in PubMed, CINAHL and Cochrane.
  
  
  CONCLUSIONS
  Prompt and accurate assessment of patients with traumatic brain injury by nurses is important to ensure optimal recovery and reduced lasting disability. Thus, it is imperative that nurses be knowledgeable about the secondary injury that occurs after a traumatic brain injury and aware of possible antioxidant treatments.
  
  
  CONCLUSIONS
  The use of antioxidants has potential to reduce the magnitude of secondary injury in patients who experience a traumatic brain injury.
authors.affiliation: Internal Medicine, Prairie Star Medicine, Lenexa, Kansas, USA.
authors.forename: Whitney
authors.initials: W
authors.lastname: Venegoni
authors.affiliation: School of Nursing, University of Kansas, Kansas, USA.
authors.forename: Qiuhua
authors.initials: Q
authors.lastname: Shen
authors.affiliation: School of Nursing, University of Kansas, Kansas, USA.
authors.forename: Amanda R
authors.identifier: http://orcid.org/0000-0002-7791-5861
authors.initials: AR
authors.lastname: Thimmesch
authors.affiliation: School of Nursing, University of Kansas, Kansas, USA.
authors.forename: Meredith
authors.initials: M
authors.lastname: Bell
authors.affiliation: School of Nursing, University of Kansas, Kansas, USA.
authors.forename: John B
authors.initials: JB
authors.lastname: Hiebert
authors.affiliation: School of Nursing, University of Kansas, Kansas, USA.
authors.forename: Janet D
authors.initials: JD
authors.lastname: Pierce
mesh_terms: D000975:Antioxidants / Q000627:therapeutic use*; D000070642:Brain Injuries, Traumatic / Q000188:drug therapy* / Q000378:metabolism / Q000451:nursing / Q000503:physiopathology; D006801:Humans; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species
keywords: antioxidant; mitochondria; nursing; oxidative stress; secondary injury; traumatic brain injury