Evidence map›Paper›PMID 31440996›Full record

ArticleNeurocritical care2020

High-Dose Intravenous Ascorbic Acid: Ready for Prime Time in Traumatic Brain Injury?

Stefan W Leichtle, Anand K Sarma, Micheal Strein, Vishal Yajnik, Dennis Rivet, Adam Sima, Gretchen M Brophy

Open access · bronzeAbstract readEditorial
PubMed Publisher
In one paragraph

Article in Neurocritical care, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 30% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 14 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Stefan W LeichtleDivision of Acute Care Surgical Services, Department of Surgery, Virginia Commonwealth University School of Medicine, Richmond, USA. stefan.leichtle@vcuhealth.org.ORCID http://orcid.org/0000-0002-6774-0682
Anand K SarmaDepartment of Neurology, Wake Forest School of Medicine, Winston-Salem, USA.
Micheal StreinDepartment of Pharmacotherapy and Outcomes Sciences, Virginia Commonwealth University School of Pharmacy, Richmond, USA.
Vishal YajnikDivision of Critical Care, Department of Anesthesiology, Virginia Commonwealth University School of Medicine, Richmond, USA.
Dennis RivetDepartment of Neurosurgery, Virginia Commonwealth University School of Medicine, Richmond, USA.
Adam SimaDepartment of Biostatistics, Virginia Commonwealth University, Richmond, USA.
Gretchen M BrophyDepartment of Pharmacotherapy and Outcomes Sciences, Virginia Commonwealth University School of Pharmacy, Richmond, USA.
Virginia Commonwealth University · USWake Forest University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) is one of the leading public health problems in the USA and worldwide. It is the number one cause of death and disability in children and adults between ages 1-44. Despite efforts to prevent TBIs, the incidence continues to rise. Secondary brain injury occurs in the first hours and days after the initial impact and is the most effective target for intervention. Inflammatory processes and oxidative stress play an important role in the pathomechanism of TBI and are exacerbated by impaired endogenous defense mechanisms, including depletion of antioxidants. As a reducing agent, free radical scavenger, and co-factor in numerous biosynthetic reactions, ascorbic acid (AA, vitamin C) is an essential nutrient that rapidly becomes depleted in states of critical illness. The administration of high-dose intravenous (IV) AA has demonstrated benefits in numerous preclinical models in the areas of trauma, critical care, wound healing, and hematology. A safe and inexpensive treatment, high-dose IV AA administration gained recent attention in studies demonstrating an associated mortality reduction in septic shock patients. High-quality data on the effects of high-dose IV AA on TBI are lacking. Historic data in a small number of patients demonstrate acute and profound AA deficiency in patients with central nervous system pathology, particularly TBI, and a strong correlation between low AA concentrations and poor outcomes. While replenishing deficient AA stores in TBI patients should improve the brain's ability to tolerate oxidative stress, high-dose IV AA may prove an effective strategy to prevent or mitigate secondary brain injury due to its ability to impede lipid peroxidation, scavenge reactive oxygen species, suppress inflammatory mediators, stabilize the endothelium, and reduce brain edema. The existing preclinical data and limited clinical data suggest that high-dose IV AA may be effective in lowering oxidative stress and decreasing cerebral edema. Whether this translates into improved clinical outcomes will depend on identifying the ideal target patient population and possible treatment combinations, factors that need to be evaluated in future clinical studies. With its excellent safety profile and low cost, high-dose IV AA is ready to be evaluated in the early treatment of TBI patients to mitigate secondary brain injury and improve outcomes.

Indexed as

Administration, IntravenousAntioxidantsAscorbic AcidBrain Injuries, TraumaticCell DeathDose-Response Relationship, DrugHumansLipid PeroxidationOxidative StressReactive Oxygen SpeciesAntioxidantsAscorbic AcidReactive Oxygen SpeciesAntioxidantAscorbic acidFree radical scavengerOxidative stressSecondary brain injuryTraumatic brain injuryVitamin C

Identifiers

PMID31440996
OpenAlexW2969543812

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.