scholarly journals Traumatic Brain Injury Patients Mortality and Serum Total Antioxidant Capacity

2020 ◽  
Vol 10 (2) ◽  
pp. 110 ◽  
Author(s):  
Leonardo Lorente ◽  
María M. Martín ◽  
Antonia Pérez-Cejas ◽  
Agustín F. González-Rivero ◽  
Pedro Abreu-González ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Antioxidant Capacity ◽  
Total Antioxidant Capacity ◽  
Injury Severity ◽  
Early Mortality ◽  
Secondary Brain Injury ◽  
Total Antioxidant ◽  
Time Of Admission

Objective: Oxidation is involved in secondary brain injury after traumatic brain injury (TBI). Increased concentrations of total antioxidant capacity (TAC) in blood at the time of admission for TBI have been found in non-surviving patients. The main objective of this study was to determine the role of serum TAC levels at any time during the first week of TBI for the prediction of early mortality. Methods: Isolated (<10 points in non-cranial aspects of Injury Severity Score) and severe (<9 points in Glasgow Coma Scale) TBI patients were included. Serum TAC concentrations at days 1, 4, and 8 of TBI were determined. The end-point study was 30-day mortality. Results: Higher serum TAC levels at days 1 (p < 0.001), 4 (p < 0.001), and 8 (p = 0.002) of TBI were found in non-surviving (n = 34) than in surviving patients (n = 90). The area under curve (95% Confidence Interval) for prediction of 30-day mortality by serum TAC concentrations at days 1, 4, and 8 of TBI were 0.79 (0.71–0.86; p < 0.001), 0.87 (0.79–0.93; p < 0.001), and 0.76 (0.67–0.84; p = 0.006) respectively. Conclusions: The novelty of our study was the ability to predict 30-day mortality by serum TAC concentrations at any time during the first week of TBI.

Prognostic value of total antioxidant capacity to predict functional outcome in traumatic brain injury patients

2017 ◽  
Vol 55 (11) ◽  
Author(s):  
Ana Rodríguez-Rodríguez ◽  
Juan José Egea-Guerrero ◽  
Ángel Vilches-Arenas ◽  
Elena Gordillo-Escobar ◽  
Zaida Ruiz de Azúa-López ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Antioxidant Capacity ◽  
Functional Outcome ◽  
Total Antioxidant Capacity ◽  
Prognostic Value ◽  
Total Antioxidant

scholarly journals Total antioxidant capacity is associated with mortality of patients with severe traumatic brain injury

BMC Neurology ◽  
2015 ◽  
Vol 15 (1) ◽  
Author(s):  
Leonardo Lorente ◽  
María M. Martín ◽  
Teresa Almeida ◽  
Pedro Abreu-González ◽  
Luis Ramos ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Antioxidant Capacity ◽  
Severe Traumatic Brain Injury ◽  
Total Antioxidant Capacity ◽  
Total Antioxidant

scholarly journals High Serum Caspase-Cleaved Cytokeratin-18 Levels and Mortality of Traumatic Brain Injury Patients

2019 ◽  
Vol 9 (10) ◽  
pp. 269 ◽  
Author(s):  
Leonardo Lorente ◽  
María M. Martín ◽  
Agustín F. González-Rivero ◽  
Antonia Pérez-Cejas ◽  
Mónica Argueso ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Glasgow Coma Scale ◽  
Area Under The Curve ◽  
High Serum ◽  
Early Mortality ◽  
Cytokeratin 18 ◽  
New Findings ◽  
Severe Tbi ◽  
Time Of Admission

Objective: Apoptosis increases in traumatic brain injury (TBI). Caspase-cleaved cytokeratin (CCCK)-18 in blood during apoptosis could appear. At the time of admission due to TBI, higher blood CCCK-18 levels were found in non-surviving than in surviving patients. Therefore, the objective of our study was to analyze whether serum CCCK-18 levels determined during the first week after TBI could predict early mortality (at 30 days). Methods: Severe TBI patients were included (considering severe when Glasgow Coma Scale < 9) in this observational and multicentre study. Serum CCCK-18 levels were determined at day 1 of TBI, and at days 4 and 8 after TBI. Results: Serum CCCK-18 levels at day 1 of TBI, and in the days 4 and 8 after TBI were higher (p < 0.001) in non-surviving than in surviving patients (34 and 90 patients, respectively) and could predict early mortality (p < 0.001 in the area under the curve). Conclusions: The new findings from our study were that serum CCCK-18 levels at any moment of the first week of TBI were higher in non-surviving patients and were able to predict early mortality.

Role of total antioxidant capacity in the differential growth of human embryos in vitro

2006 ◽  
Vol 86 (2) ◽  
pp. 304-309 ◽  
Author(s):  
Mohamed Bedaiwy ◽  
Ashok Agarwal ◽  
Tamer M. Said ◽  
Jeffery M. Goldberg ◽  
Rakesh K. Sharma ◽  
...  
Keyword(s):  
Antioxidant Capacity ◽  
Total Antioxidant Capacity ◽  
Human Embryos ◽  
Differential Growth ◽  
Total Antioxidant

The Role of Free Radicals in Traumatic Brain Injury

2012 ◽  
Vol 15 (3) ◽  
pp. 253-263 ◽  
Author(s):  
Karen M. O’Connell ◽  
Marguerite T. Littleton-Kearney
Keyword(s):  
Traumatic Brain Injury ◽  
Free Radicals ◽  
Free Radical ◽  
Brain Injury ◽  
Current Knowledge ◽  
Cellular Level ◽  
Secondary Brain Injury ◽  
Secondary Injury ◽  
The Military

Traumatic brain injury (TBI) is a significant cause of death and disability in both the civilian and the military populations. The primary impact causes initial tissue damage, which initiates biochemical cascades, known as secondary injury, that expand the damage. Free radicals are implicated as major contributors to the secondary injury. Our review of recent rodent and human research reveals the prominent role of the free radicals superoxide anion, nitric oxide, and peroxynitrite in secondary brain injury. Much of our current knowledge is based on rodent studies, and the authors identified a gap in the translation of findings from rodent to human TBI. Rodent models are an effective method for elucidating specific mechanisms of free radical-induced injury at the cellular level in a well-controlled environment. However, human TBI does not occur in a vacuum, and variables controlled in the laboratory may affect the injury progression. Additionally, multiple experimental TBI models are accepted in rodent research, and no one model fully reproduces the heterogeneous injury seen in humans. Free radical levels are measured indirectly in human studies based on assumptions from the findings from rodent studies that use direct free radical measurements. Further study in humans should be directed toward large samples to validate the findings in rodent studies. Data obtained from these studies may lead to more targeted treatment to interrupt the secondary injury cascades.

Differential growth of human embryos in vitro: Role of total antioxidant capacity

2004 ◽  
Vol 82 ◽  
pp. S195-S196 ◽  
Author(s):  
M.A. Bedaiwy ◽  
A. Agarwal ◽  
T.M. Said ◽  
S. Worley ◽  
J. Thornton ◽  
...  
Keyword(s):  
Antioxidant Capacity ◽  
Total Antioxidant Capacity ◽  
Human Embryos ◽  
Differential Growth ◽  
Total Antioxidant

The Management of Traumatic Brain Injury

2018 ◽  
pp. 83-96
Author(s):  
Jeremy G. Stone ◽  
David M. Panczykowski ◽  
David O. Okonkwo
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Clinical Assessment ◽  
Cerebral Perfusion ◽  
Injury Severity ◽  
Secondary Brain Injury ◽  
Second Line ◽  
Injury Management ◽  
Imaging Characteristics ◽  
System P

The management of traumatic brain injury necessitates a multidisciplinary approach with medical and surgical therapies employed based on rapid clinical assessment of injury severity and imaging characteristics. Therapy aims to prevent secondary brain injury through multifactorial interventions primarily focusing on prevention of cerebral hypoxemia and aggressive control of intracranial pressure (ICP). This chapter covers epidemiology, pathophysiology, clinical assessment, and both medical and surgical management of traumatic brain injury. Management topics include appropriate monitoring, first- and second-line therapy for ICP and cerebral perfusion pressure, hypoxia, seizure prophylaxis, hyperpyrexia, glycemic control, fluids and electrolytes, nutrition, and prophylaxis for venous thromboembolism and the gastrointestinal system.

scholarly journals Decreased Superoxide Dismutase Concentrations (SOD) in Plasma and CSF and Increased Circulating Total Antioxidant Capacity (TAC) Are Associated with Unfavorable Neurological Outcome after Aneurysmal Subarachnoid Hemorrhage

2021 ◽  
Vol 10 (6) ◽  
pp. 1188
Author(s):  
Harald Krenzlin ◽  
Dominik Wesp ◽  
Jan Schmitt ◽  
Christina Frenz ◽  
Elena Kurz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Antioxidant Capacity ◽  
Neurological Outcome ◽  
Total Antioxidant Capacity ◽  
Early Brain Injury ◽  
Fisher Grade ◽  
Total Antioxidant

Background: Subarachnoid hemorrhage (SAH) is a devastating disease with high morbidity and mortality. Hypoxia-induced changes and hemoglobin accumulation within the subarachnoid space are thought to lead to oxidative stress, early brain injury, and delayed vasospasm. This study aimed to evaluate the antioxidant status and its impact on neurological outcome in patients with aneurysmal SAH. Methods: In this prospective observational study, 29 patients with aneurysmal SAH were included (mean age 54.7 ± 12.4). Blood and cerebrospinal fluid (CSF) samples were collected on days (d) 1, 3, and 7. In addition, 29 patients without intracranial hemorrhage served as controls. The antioxidant system was analyzed by glutathione peroxidase (GSH-Px; U/L) and total and free glutathione-sulfhydryl (GSH; mg/L) in the plasma. Superoxide dismutase (SOD, U/mL) and total antioxidant capacity (TAC, µmol/L) were measured in the serum and CSF. Clinical data were compiled on admission (Hunt and Hess grade, Fisher grade, and GCS). Neurological and cognitive outcome (modified Rankin scale (mRS), Glasgow Outcome Scale Extended (GOSE) and Montreal Cognitive Assessment (MoCA)) was assessed after 6 weeks (6 w) and 6 months (6 m). Results: Plasma levels of SOD increased from day 1 to 7 after SAH (d1: 1.22 ± 0.36 U/L; d3: 1.25 ± 0.33 U/L, p = 0.99; d7: 1.52 ± 0.4 U/L, p = 0.019) and were significantly higher compared to controls (1.11 ± 0.27 U/L) at day 7 (p < 0.001). Concordantly, CSF levels of SOD increased from day 1 to 7 after SAH (d1: 1.22 ± 0.41 U/L; d3: 1.77 ± 0.73 U/L, p = 0.10; d7: 2.37 ± 1.29 U/L, p < 0.0001) without becoming significantly different compared to controls (1.74 ± 0.8 U/L, p = 0.09). Mean plasma TAC at day 1 (d1: 77.87 ± 49.72 µmol/L) was not statistically different compared to controls (46.74 ± 32.42 µmol/L, p = 0.25). TAC remained unchanged from day 1 to 7 (d3: 92.64 ± 68.58 µmol/L, p = 0.86; d7: 74.07 ± 54.95 µmol/L, p = 0.8) in plasma. TAC in CSF steeply declined from day 1 to 7 in patients with SAH becoming significantly different from controls at days 3 and 7 (d3: 177.3 ± 108.7 µmol/L, p = 0.0046; d7: 85.35 ± 103.9 µmol/L, p < 0.0001). Decreased SOD levels in plasma and CSF are associated with a worse neurological outcome 6 weeks (mRS: CSF p = 0.0001; plasma p = 0.027/GOSE: CSF p = 0.001; plasma p = 0.001) and 6 months (mRS: CSF p = 0.001; plasma p = 0.09/GOSE: CSF p = 0.001; plasma p = 0.001) after SAH. Increased plasma TAC correlated with a worse neurological outcome 6 weeks (mRS: p = 0.001/GOSE p = 0.001) and 6 months (mRS p = 0.001/GOSE p = 0.001) after SAH. Conclusion: In our study, a reduction in the antioxidative enzyme SOD and elevated TAC were associated with a poorer neurological outcome reflected by mRS and GOSE at 6 weeks and 6 months after SAH. A lower initial SOD CSF concentration was associated with the late deterioration of cognitive ability. These findings support the mounting evidence of the role of oxidative stress in early brain injury formation and unfavorable outcome after SAH.

Sign in / Sign up

Export Citation Format

Share Document