Pathogenesis of sepsis-associated encephalopathy: more than blood-brain barrier dysfunction

Abstract

Sepsis-associated encephalopathy is a common neurological complication of sepsis and is responsible for higher mortality and poorer long-term outcomes in septic patients. Sepsis-associated encephalopathy symptoms can range from mild delirium to deep coma, which occurs in up to 70% of patients in intensive care units. The pathological changes in the brain associated with sepsis include cerebral ischaemia, cerebral haemorrhage, abscess and progressive multifocal necrotic leukoencephalopathy. Several mechanisms are involved in the pathogenesis of sepsis-associated encephalopathy, such as blood-brain barrier dysfunction, cerebral blood flow impairment, glial cell activation, leukocyte transmigration, and neurotransmitter disturbances. These events are interrelated and influence each other, therefore they do not act as independent factors. This review is focused on new evidence showing the pathological process of sepsis-associated encephalopathy.

Keywords: Blood–brain barrier; Cerebral blood flow; Glial cell activation; Leukocyte transmigration; Neurotransmitter disturbances; Sepsis-associated encephalopathy.