Update on hypoxic-ischemic brain injury: Prognosis and management

Hypoxic-ischemic brain injury (HIBI) can occur after cardiac arrest, asphyxiation, carbon monoxide poisoning, and diffuse brain injury. While it is a major cause of mortality and morbidity, there is no consensus on its management. Therefore, I performed a literature review to analyze HIBI pathophysiology, clinical progression, imaging, treatment, and prognosis with a goal to deepen our understanding of best treatment and prognostication options. A search was performed in PubMed, Scopus, Google scholar, EMBASE, and Crossref. The pathophysiology of HIBI consists of the primary insult due to cessation of cerebral oxygen delivery and a secondary hit due to reperfusion injury. The poor clinical prognostic factors are: Absent or extensor motor response, bilaterally absent pupillary light reflex, bilaterally absent corneal reflex, and early status myoclonus. Electroencephalogram can aid in prognostication, while magnetic resonance imaging may reveal restricted diffusion. Treatment guidelines for HIBI have been debated, particularly regarding hyperoxia vs normoxia, hypocapnia vs normocapnia, high-normal mean arterial pressure (MAP) vs low-normal MAP, and hypothermia vs normothermia. Core treatment principles include maintaining normoxia and normocapnia through ventilation, targeting a MAP of 65 mmHg, preventing fever, managing seizures, and providing neurorehabilitation.