<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>17(2)</volume><submitter>Mazeraud A</submitter><pubmed_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 includ</pubmed_abstract><journal>Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics</journal><pagination>392-403</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7283452</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Septic-Associated Encephalopathy: a Comprehensive Review.</pubmed_title><pmcid>PMC7283452</pmcid><pubmed_authors>Mazeraud A</pubmed_authors><pubmed_authors>Bozza FA</pubmed_authors><pubmed_authors>Bouchereau E</pubmed_authors><pubmed_authors>Benghanem S</pubmed_authors><pubmed_authors>Sharshar T</pubmed_authors><pubmed_authors>Righy C</pubmed_authors></additional><is_claimable>false</is_claimable><name>Septic-Associated Encephalopathy: a Comprehensive Review.</name><description>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 includ</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Apr</publication><modification>2025-04-22T00:48:17.783Z</modification><creation>2022-02-09T10:13:16.385Z</creation></dates><accession>S-EPMC7283452</accession><cross_references><pubmed>32378026</pubmed><doi>10.1007/s13311-020-00862-1</doi></cross_references></HashMap>