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

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.