Ventilator-induced brain injury: another iatrogenic complication of mechanical ventilation

Mechanical ventilation is life-saving, but is increasingly recognized to be involved in adverse neurological outcomes. Ventilator-associated brain injury (VABI) refers to primary brain dysfunction directly attributable to mechanical ventilation, independent of sedation, hypoxemia, or sepsis. This review summarizes current evidence on the pathophysiology, clinical impact, monitoring strategies, and potential therapeutic interventions for VABI.

A growing number of preclinical and clinical studies suggest that mechanical ventilation contributes to hippocampal apoptosis, maladaptive vagal and purinergic signaling, neuroinflammation, blood-brain barrier disruption, altered CO 2 regulation, and nasal airflow abolition. Clinically, VABI may manifest as delirium, disordered sleep, prolonged weaning, and long-term cognitive impairment. Monitoring tools such as electroencephalography, near-infrared spectroscopy, cerebral biomarkers, Doppler ultrasound, and MRI offer complementary but indirect insights. As of today, preventive and therapeutic strategies focus on lung-protective ventilation, limited sedation, early mobilization, and good quality sleep promotion. Some innovative approaches such restoration of nasal airflow, phrenic and vagal stimulation remain experimental.

VABI is increasingly recognized as a critical research frontier in critical care medicine. Awareness of its mechanisms and clinical impact should prompt ICU clinicians to integrate brain-oriented practices into routine care. Future trials are needed to evaluate preventive strategies and improve long-term cognitive and functional outcomes for ICU survivors.