Skip to content

Selenium to Improve Neurological Outcome After Cardiac Arrest

Effect of High Dose Selenium on Inflammation and Neurological Outcome After Cardiac Arrest: A Randomized, Double Blind Placebo Controlled Phase 2a Study

Status
Withdrawn
Phases
Phase 2
Study type
Interventional
Source
ClinicalTrials.gov
Registry ID
NCT01390506
Acronym
SCPR
Enrollment
0
Registered
2011-07-11
Start date
2017-01-31
Completion date
2019-07-31
Last updated
2017-12-13

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Cardiac Arrest

Keywords

cardiac arrest, resuscitation, neurological outcome

Brief summary

After cardiac arrest and successful resuscitation it can happen that the brain function of a patient is impaired because the brain was without oxygen for a prolonged period of time. Several strategies have been studied to improve brain function after cardiac arrest. Cooling of the patients is routinely used today. The trace element selenium has several biological functions and is important for defense mechanisms against oxidative stress, which occurs after cardiac arrest and successful resuscitation. critically ill patients have low selenium blood levels. Therefore the investigators hypothesize that giving selenium after cardiac arrest and successful resuscitation might improve brain function.

Detailed description

When cardiopulmonary resuscitation results in the return of spontaneous circulation, intensive care is required to optimize neurological recovery. The pathophysiological reactions that follow hypoxic brain injury are complex, and the mechanisms by which ischemia causes neuronal death leading to postanoxic encephalopathy are only partly understood to date. Therapeutic hypothermia improves brain function after cardiopulmonary resuscitation. Injury however can be ongoing even after the return of spontaneous circulation, giving the clinician an additional window of opportunity to treat and protect the injured brain \[5\]. Therefore there is an unmet clinical need for further therapeutic strategies. Strategies to counteract the deleterious effects of oxygen-derived free radicals after cerebral reperfusion have been studied for long. The trace element selenium is part of the enzyme glutathione peroxidase which belongs to the endogenous defence mechanisms against oxidative stress. Clinical data suggest that supplementation of selenium may be beneficial in critically ill patients and in neurodegenerative diseases including, among others, Parkinson's disease, stroke, and epilepsy, where oxidative stress plays an important pathophysiological role. In SIRS, sepsis and septic shock doses up to 4000µg per day have been proven to be safe A recent retrospective analysis supported the hypothesis that early administration of selenium may improve neurological outcome after cardiac arrest. Therefore the purpose of this study is to explore the influence of early administration of selenium on neurological outcome after cardiopulmonary resuscitation by a randomized, placebo-controlled, single-center study.

Interventions

Di-sodium-selenite-pentahydrate (Na 2SeO3.5H2O) in 0,9% sodium chloride is administered intravenously at a does of 3000µg on day 0, 2000µg on day 1 and 2 and at a dose of 1000µg per day on day 3-6.

DRUGPlacebo

0,9% sodium chloride is administered intravenously

Sponsors

Medical University of Graz
Lead SponsorOTHER

Study design

Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
PREVENTION
Masking
QUADRUPLE (Subject, Caregiver, Investigator, Outcomes Assessor)

Eligibility

Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No

Inclusion criteria

* Cardiac arrest * Successful Resuscitation * Age \>18

Exclusion criteria

* Polytrauma * Pregnancy * Any condition that makes it likely that the patient will not survive 24 hours

Design outcomes

Primary

MeasureTime frameDescription
neuron specific enolase72 hoursReduction of neuron specific enolase below by more than 4.4 µg/l at 72 hours after admission to the hospital

Secondary

MeasureTime frameDescription
inflammation7 daysReduction of C-reactive protein, procalcitonin, interleukin 6
oxidative stress markers7 daysReduction in peroxide, peroxidase, OLAB, MDA-LDL IG, TAC, ADMA, selenium and glutathione peroxidase levels
neurological function6 monthsImprovement of NIH stroke scale and Glasgow Pittsburgh Performance score
Selenium blood levels7 daysIncrease in selenium levels in whole blood
glutathion peroxidase plasma levels7 daysImprovement in glutathion peroxidase plasma levels

Countries

Austria

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026