Background: Experimental data indicate that destructive oxidative events reach their peak within the first 24 h after trauma in head injury (HI) and that brain damage occurring due to this impact can be the cause of death or irreversible permanent disabilities in affected patients.
Methods: Venous blood samples were obtained from 50 HI patients within 24 h of trauma onset and from 30 age- and sex-matched normal controls (NC). Patients were divided into three different neurological outcome groups: those who died within 10 days of trauma (D), and those with severe neurological deficits (SD) or mild/no neurological deficits (MD) at 90 days after trauma. Early oxidative changes in erythrocytes were assessed by estimating an indicator of lipid peroxidative damage - thiobarbituric acid-reactive substances (TBARS) - and antioxidants [reduced glutathione (GSH) levels and superoxide dismutase (SOD) activity].
Results: In the D group, erythrocyte TBARS levels were significantly higher compared to the NC, SD and MD groups (p<0.001); GSH levels were significantly lower compared to the NC (p<0.001) and MD (p<0.01) groups and SOD activity was significantly higher than in the NC (p<0.01) and MD (p<0.01) groups. In the SD group, TBARS levels were significantly higher than in the NC (p<0.001) and MD (p<0.05) groups; GSH levels were significantly lower than in the NC (p<0.001) and MD (p<0.01) groups and SOD activity was higher compared to the NC and MD (p<0.01) groups. In the MD group, TBARS levels were significantly higher and GSH levels significantly lower compared to the NC group (p<0.001). However, we did not observe any significant change in SOD activity compared to the NC group.
Conclusions: These findings indicate that early oxidative changes may reflect the severity of neurological insult and provide an early indication of patient outcome in traumatic HI.