Sánchez-Rodríguez EC, López VJ. Hypoxic ischemic encephalopathy (HIE). Front Neurol. 2024 Jul 23;15:1389703.
Hypoxic ischemic encephalopathy (HIE) is a neurological condition caused by a lack of oxygen (hypoxia) and blood flow (ischemia) to the brain, usually occurring during critical events such as birth complications, cardiac arrest, or severe respiratory failure. They are often associated with complications during childbirth, such as umbilical cord problems, placental abruption, or maternal hypotension. A lack of oxygen and nutrients causes brain cells to run out of energy, causing them to die or become non-functional. Ischemia can initiate a cascade of inflammatory processes that exacerbate neuronal injury.
When HBOT is applied immediately, it can promote penumbra survival, modulate cytokine storm, modify inflammatory cascades, restore mitochondrial function, inhibit apoptosis, restore cellular communication and cytoskeletal function, reinstall kinase system and tissue functioning, reduce cytotoxicity. edema, stimulate microcirculation and provide an antioxidant effect. All these secondary mechanisms help to rescue, save and protect the marginal tissue.
Conclusion
HIE is a critical condition that requires rapid recognition and intervention to mitigate brain damage and support recovery. Advances in treatment, such as therapeutic hypothermia, have improved outcomes for affected individuals, but continued research is essential for further understanding and management.
When used timely, HBOT is a non-invasive adjunctive treatment that can preserve marginal tissue affected by ischemia, hypoxia, meet the metabolic needs of the penumbra, reduce inflammatory cascades, prevent expansion of damaged tissue, and modulate ischemia. reperfusion injury.