Injuria cerebral precoz en la hemorragia subaracnoidea aneurismática: comprendiendo la fisiopatología para optimizar el manejo intensivo

Abstract

Early brain injury (EBI) following aneurysmal subarachnoid hemorrhage represents a critical phase of brain damage occurring within the first 72 hours after aneurysmal rupture. Traditionally underestimated in favor of delayed cerebral ischemia, EBI has emerged as a key determinant of both functional and vital prognosis in these patients.

EBI is characterized by a multifactorial cascade of events, including intracranial hypertension, global cerebral ischemia, disruption of the blood–brain barrier, cerebral edema, neurovascular inflammation, oxidative stress, and apoptosis, as well as alterations in cerebral blood flow autoregulation. Moreover, EBI is not confined to the brain: it triggers a systemic response that affects the cardiovascular system, lungs, immune system, and other peripheral organs, thereby amplifying secondary cerebral injury.

A comprehensive understanding of these mechanisms has driven the development of physiopathologically targeted therapeutic strategies aimed at preserving cerebral perfusion, oxygenation, and metabolism, controlling intracranial pressure, preventing epileptic seizures, and avoiding multiorgan failure. In this context, multimodal neuromonitoring has become an essential tool for tailoring real-time, individualized treatments.