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.
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.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
PREVENTION
Masking
QUADRUPLE
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.
0,9% sodium chloride is administered intravenously
Department of Internal Medicine, Medical University of Graz
Graz, Austria
neuron specific enolase
Reduction of neuron specific enolase below by more than 4.4 µg/l at 72 hours after admission to the hospital
Time frame: 72 hours
inflammation
Reduction of C-reactive protein, procalcitonin, interleukin 6
Time frame: 7 days
oxidative stress markers
Reduction in peroxide, peroxidase, OLAB, MDA-LDL IG, TAC, ADMA, selenium and glutathione peroxidase levels
Time frame: 7 days
neurological function
Improvement of NIH stroke scale and Glasgow Pittsburgh Performance score
Time frame: 6 months
Selenium blood levels
Increase in selenium levels in whole blood
Time frame: 7 days
glutathion peroxidase plasma levels
Improvement in glutathion peroxidase plasma levels
Time frame: 7 days
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