RÉSUMÉ
Sepsis-associated encephalopathy, which presents as delirium and coma, is a significant complication of sepsis characterized by acute brain dysfunction. The presence of inflammatory pathological changes in the brain of sepsis patients and animal models has been recognized since the 1920 s, initially attributed to the entry of microbial toxins into the brain. In the early 2000 s, attention shifted towards the impact of oxidative stress, the cholinergic system, and cytokines on brain function following sepsis onset. More recently, sepsis-associated encephalopathy has been defined as a diffuse brain dysfunction not directly caused by pathogenic infection of the brain. Currently, there is no evidence-based standard for diagnosing sepsis-associated encephalopathy, and clinical management is primarily focused on symptomatic and supportive measures. This review aims to explore the pathophysiology of sepsis-associated encephalopathy and establish the connection between pathophysiological mechanisms and clinical characteristics. We hope that this work will spark the interest of researchers from various fields and contribute to the advancement of sepsis-associated encephalopathy research.