The lecture duration is 23min.
0.5 CPD Points, 0.5 CEUs, 0.5 CME credits approval pending.
Accredited by CPDUK, CBRN and Provider Pending.
You can watch this lecture for free! For premium features, including a CPD/CME accredited certificate, to use time-coded note taking or get downloadable slides, you will need a fair price subscription.
Sepsis-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 but also with worse long-term outcomes, including cognitive impairment and psychological disorders. The pathophysiology of SAE is complex, involving schematically neuro-inflammatory (i.e. endothelial activation, blood-brain barrier dysfunction microglial activation) and ischemic processes due to microcirculatory and microcirculatory dysfunction, which both end-up to neuronal dysfunction. Some brain regions are more liable to these processes, including the brainstem, the limbic system, and the hippocampus. The brainstem dysfunction could account for increased mortality and arousal impairment; the limbic dysfunction for long-term psychological disorders; and the hippocampal and frontal dysfunction for the long-term cognitive impairment. SAE is mostly diagnosed clinically with using validated scales for coma or delirium. Electroencephalogram could be useful for SAE detection, monitoring and assessment of its severity. There is no established specific treatment for SAE. Statines and dexmedetodmidine have not been shown to be beneficial. Its prevention and treatment rely mainly on the control of sepsis and risk factor of delirium.
Emergency Medicine Doctors
Emergency Medicine Nurses
Paramedics
Rural GP's
Upon completion of this activity, you should be able to:
None.