| Literature DB >> 32378026 |
Aurélien Mazeraud1,2,3, Cássia Righy1,4, Eleonore Bouchereau1,2,3, Sarah Benghanem3,5, Fernando Augusto Bozza6, Tarek Sharshar7,8.
Abstract
Septic-associated encephalopathy (SAE) is a key manifestation of sepsis, ranging from delirium to coma and occurring in up to 70% of patients admitted to the ICU. SAE is associated with higher ICU and hospital mortality, and also with poorer long-term outcomes, including cognitive and functional outcomes. The pathophysiology of SAE is complex, and it may involve neurotransmitter dysfunction, inflammatory and ischemic lesions to the brain, microglial activation, and blood-brain barrier dysfunction. Delirium (which is included in the SAE spectrum) is mostly diagnosed with validated scales in the ICU population. There is no established treatment for SAE; benzodiazepines should generally be avoided in this setting. Nonpharmacological prevention and management is key for treating SAE; it includes avoiding oversedation (mainly with benzodiazepines), early mobilization, and sleep promotion.Entities:
Keywords: Sepsis; blood–brain barrier; microglia; neuroanatomy; neuroinflammation; sepsis-associated encephalopathy
Mesh:
Year: 2020 PMID: 32378026 PMCID: PMC7283452 DOI: 10.1007/s13311-020-00862-1
Source DB: PubMed Journal: Neurotherapeutics ISSN: 1878-7479 Impact factor: 7.620