Abstract
Sepsis-associated encephalopathy (SAE) is characterized by diffuse cerebral dysfunction caused by a systemic inflammatory response to infection. SAE can be reversible after recovery from sepsis or can result in long-term cognitive impairments. SAE has a detrimental effect on the prognosis of septic patients. Although the exact pathophysiology of SAE remains unknown, several mechanisms have been proposed in animal and clinical studies. Animal studies suggest that neuroinflammation, oxidative stress, blood–brain barrier (BBB) disruption, impairment of cerebrovascular autoregulation, alteration of neurotransmission, mitochondrial dysfunction, and neuronal apoptosis are involved in the pathophysiology of SAE, whereas clinical studies suggest neuroinflammation, BBB disruption, oxidative stress in the brain, impairment of cerebrovascular autoregulation, and alteration of neurotransmission as underlying mechanisms. Systemic insults such as other organ dysfunction and metabolic abnormalities may also play a role in the pathophysiology of SAE, as suggested by a retrospective analysis of a large prospective multicenter database. However, there is a discrepancy in the hypothesized pathophysiology of SAE between animal and clinical studies. This discrepancy may stem from differences in the diagnosis of SAE between animals and humans. Clinically, the diagnosis of SAE is based on symptoms, whereas changes in mental status are difficult to detect in animals. Further research is necessary to clarify the pathophysiology of SAE.
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Fujita, M., Tsuruta, R. (2019). Sepsis and Sepsis-Associated Encephalopathy: Its Pathophysiology from Bench to Bed. In: Kinoshita, K. (eds) Neurocritical Care . Springer, Singapore. https://doi.org/10.1007/978-981-13-7272-8_14
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