Neuroanatomy of sepsis-associated encephalopathy

Abstract

This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2017. Other selected articles can be found online at http://ccforum.com/series/annualupdate2017. Further information about the Annual Update in Intensive Care and Emergency Medicine is available from http://www.springer.com/series/8901.Originally published in the Annual Update in Intensive Care and Emergency Medicine 2017. The number of authors differs in the two versions due to constraints regarding the number of authors in the Annual Update in Intensive Care and Emergency Medicine. In the Annual Update version of the review, the three senior authors appear in the acknowledgement section. In the Critical Care version, these three senior authors appear as full authors of the manuscript. All authors helped draft and revise the manuscript for critical intellectual content.

Astroglia in Sepsis Associated Encephalopathy

“…The main histopathologic changes in the brain during sepsis include infarctions, petechial and small focal hemorrhages, septic-embolic abscesses and septicopyemic microabscesses, signs of disseminated intravascular coagulation (DIC) syndrome with fibrinous microthrombi, multifocal necrotizing leukoencephalopathy, selective necrosis and apoptosis of neurones in the regions most sensitive to ischemia and neurotoxicity with more prominent hippocampal and brainstem damage, proliferation of astrocytes and microglia in the cerebral cortex, diffuse perivascular and cytotoxic oedema, BBB damage and reactive neuroinflammation [22][23][24][25][26]. In this regard, the signal example can be septic endocarditis characterized by microbial emboli entering the brain parenchyma and causing ischemic infarction foci in conjunction with formation of abscesses.…”

“…Development of sickness behaviour is associated with pro-inflammatory factors, such as interleukin (IL)-1α, IL-1β, tumour necrosis factor-α (TNF)-α and IL-6 with particular role attributed to IL-1 [39]. In rodents, the systemic or central IL-1β administration induces typical behavioural and neuro-endocrine symptoms of sickness behaviour [40] due to an activation of hypothalamic-pituitary-adrenal axis and adrenergic system [22]. Sickness behaviour acquires maladaptive features with increased severity and duration [30].…”

Sepsis: developing new alternatives to reduce neuroinflammation and attenuate brain injury

“…Both in sepsis and septic shock, the CNS becomes vulnerable due to the breach of the BBB followed by inflammatory and neurotoxic processes . Patients experience an alteration of mental functions, ranging from delirium to coma; this syndrome is known as SAE.…”

“…As stated above, sepsis leads to an exacerbated neuroinflammatory response that may promote an acute and long‐term dysfunction in the brainstem, amygdala, and hippocampus leading to psychological disarrays, cognitive injury, and even death. An effective anti‐neuroinflammatory treatment may improve the prognosis of sepsis patients . Various murine models that resemble the NI that accompanies sepsis have been developed, which are presented in Table .…”

Bioenergy Crisis in Coronavirus Diseases?

“…Mitochondrial dysfunction related to microcirculatory dysfunction [8], with an inhibition of mitochondrial respiratory chain and a decrease of oxygen utilization, remains poorly understood [25]. An increased level of proinflammatory cytokines (such as TNF, interleukins, etc.)…”