The current literature covers the role of selenium in metabolic processes and the importance of correcting its level in various diseases and critical conditions, including acute cerebral damage due to severe traumatic brain injury (TBI) and sepsis-associated encephalopathy (SAE). Numerous experimental animal studies have demonstrated that selenium has protective properties and blocks the mechanisms of apoptosis, and is involved in maintaining the functional activity of neurons and inhibits astrogliosis. The study of the selenium content in the blood of patients with acute cerebral damage due to severe TBI and sepsis with verified SAE, and the development of schemes of replacement selenium therapy will improve outcomes, both in increasing survival and in reducing the resuscitation bed-day and the number of neurological deficits in the future.