Selenium to Improve Neurological Outcome After Cardiac Arrest

Cardiac Arrest Clinical Trial

— SCPR  

Official title:

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

Clinical Trial Details — Status: Withdrawn

Administrative data

• NCT number: NCT01390506
• Other study ID #: SCRP2011
• Secondary ID: 2011-001074-26
• Status: Withdrawn
• Phase: Phase 2
• First received: July 4, 2011
• Last updated: December 12, 2017
• Start date: January 2017
• Est. completion date: July 2019

Study information

• Verified date: December 2017
• Source: Medical University of Graz
• Contact: n/a
• Is FDA regulated: No
• Study type: Interventional

Clinical Trial 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.

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.

Recruitment information / eligibility

• Status: Withdrawn
• Enrollment: 0
• Est. completion date: July 2019
• Est. primary completion date: July 2018
• Accepts healthy volunteers: No
• Gender: All
• Age group: 18 Years and older

Eligibility

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

Related Conditions & MeSH terms

• Cardiac Arrest
• Heart Arrest

Intervention

Drug:
• Sodium-selenite
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.
• Placebo
0,9% sodium chloride is administered intravenously

Locations

Country	Name	City	State
Austria	Department of Internal Medicine, Medical University of Graz	Graz

Sponsors (1)

Lead Sponsor	Collaborator
Medical University of Graz

Country where clinical trial is conducted

Austria, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	neuron specific enolase	Reduction of neuron specific enolase below by more than 4.4 µg/l at 72 hours after admission to the hospital	72 hours
Secondary	inflammation	Reduction of C-reactive protein, procalcitonin, interleukin 6	7 days
Secondary	oxidative stress markers	Reduction in peroxide, peroxidase, OLAB, MDA-LDL IG, TAC, ADMA, selenium and glutathione peroxidase levels	7 days
Secondary	neurological function	Improvement of NIH stroke scale and Glasgow Pittsburgh Performance score	6 months
Secondary	Selenium blood levels	Increase in selenium levels in whole blood	7 days
Secondary	glutathion peroxidase plasma levels	Improvement in glutathion peroxidase plasma levels	7 days