Sepsis-associated encephalopathy (SAE), also known as sepsis-associated brain dysfunction or septic encephalopathy, is a type of infectious disease-associated encephalopathy (IDAE).[1][2][3][4] It is an umbrella term referring to neurological complications following sepsis.[1] The condition is common but poorly understood.[2][3] Approximately 70% of people with sepsis experience SAE.[1] The diagnosis of SAE is difficult, with no well-established biomarkers, and it is currently a diagnosis of exclusion based on clinical symptoms.[1][2] However, electroencephalogram (EEG) may be helpful in aiding diagnosis.[2]

Acute symptoms of SAE can include sickness behavior, lethargy, delirium, cognitive, memory, and attention impairment, depression, anxiety, agitation, motor problems, seizures, and, in severe cases, coma.[1][2] Post-acute symptoms of SAE can include cognitive and memory deficits and neuromyopathy, among others.[1]

There are currently no well-accepted treatments for the prevention or treatment of SAE symptoms, and treatment is largely symptom-based.[1][2] In the acute phase, certain medications may aggravate symptoms and may be avoided, such as anticholinergics, antihistamines, sedatives, benzodiazepines, antipsychotics, and anticonvulsants (in those without seizures).[1] Certain medications such as statins, the antidepressant fluoxetine, and resveratrol may reduce neuroinflammation and the acute and long-term symptoms of SAE.[1] However, these findings are based on animal studies, and more research is needed in this area.[1][2] In addition to the preceding, the serotonin 5-HT2 receptor agonist and serotonergic psychedelic 25H-NBOMe has been found to attenuate sepsis-associated depressive-like behavior in rodents, as measured by the forced swim test (FST).[5][6]

The term "sepsis-associated encephalopathy" was first used by 1990 and this was when the first comprehensive study of this condition was published.[7][4]

See also

References

  1. ^ a b c d e f g h i j Barbosa-Silva MC, Lima MN, Battaglini D, Robba C, Pelosi P, Rocco PR, Maron-Gutierrez T (July 2021). "Infectious disease-associated encephalopathies". Crit Care. 25 (1): 236. doi:10.1186/s13054-021-03659-6. PMC 8259088. PMID 34229735.
  2. ^ a b c d e f g Pan S, Lv Z, Wang R, Shu H, Yuan S, Yu Y, Shang Y (2022). "Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment". Oxid Med Cell Longev. 2022: 1328729. doi:10.1155/2022/1328729. PMC 9433216. PMID 36062193.
  3. ^ a b Chaudhry N, Duggal AK (2014). "Sepsis Associated Encephalopathy". Adv Med. 2014: 762320. doi:10.1155/2014/762320. PMC 4590973. PMID 26556425.
  4. ^ a b Wilson JX, Young GB (May 2003). "Progress in clinical neurosciences: sepsis-associated encephalopathy: evolving concepts". Can J Neurol Sci. 30 (2): 98–105. doi:10.1017/s031716710005335x. PMID 12774948.
  5. ^ Werle I, Bertoglio LJ (December 2024). "Psychedelics: A review of their effects on recalled aversive memories and fear/anxiety expression in rodents". Neurosci Biobehav Rev. 167: 105899. doi:10.1016/j.neubiorev.2024.105899. PMID 39305969.
  6. ^ Ferri BG, de Novais CO, Rojas VC, Estevam ES, Dos Santos GJ, Cardoso RR, Nogueira ES, Oliveira PF, de Barros WA, de Fátima Â, Vilela Giusti FC, Giusti-Paiva A (June 2024). "Psychedelic 25H-NBOMe attenuates post-sepsis depression in rats". Neurosci Lett. 834: 137845. doi:10.1016/j.neulet.2024.137845. PMID 38821202.
  7. ^ Young GB, Bolton CF, Austin TW, Archibald YM, Gonder J, Wells GA (December 1990). "The encephalopathy associated with septic illness". Clin Invest Med. 13 (6): 297–304. PMID 2078909.



Allikas: http://en.wikipedia.org/wiki/Sepsis-associated_encephalopathy
No tags for this post.