Sepsis-associated encephalopathy: not just delirium

Zampieri, Fernando Godinho; Park, Marcelo; Machado, Fábio Prates; Azevedo, Luciano César Pontes

doi:10.1590/s1807-59322011001000024

Cited by 81 publications

(71 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…CLP induces a polymicrobial sepsis that mimics human sepsis, and has contributed to the understanding of its pathogenesis (Hubbard et al 2005). Using this model, previous studies have implicated neuronal damage, endothelial dysfunction, neurotransmission imbalance, blood brain barrier disruption, and cytokine dysregulation in the cognitive deficits induced by sepsis (Imamura et al 2011;Zampieri et al 2011). Among many putative inflammatory cytokines involved, TNF-α is one of the most relevant (Clark et al 2010).…”

Section: Introductionmentioning

confidence: 99%

TNFR1 absence protects against memory deficit induced by sepsis possibly through over-expression of hippocampal BDNF

et al. 2014

View full text Add to dashboard Cite

The involvement of TNF-α type 1 receptor (TNFR1) in memory deficits induced by sepsis was explored by using TNFR1 knockout (KO) mice. We reported that wild type (WT) mice presented memory deficits in the novel object recognition test 10 days after sepsis induced by cecum ligation and perforation (CLP). These deficits were not observed in TNFR1 KO mice. The involvement of serum and brain cytokines TNF-α, IL-1β, IL-6, IFN-γ and IL-10 was then investigated. TNFR1 KO mice had higher serum levels of TNF-α and IL-1β, and brain levels of TNF-α than WT mice. After CLP, the brain levels of TNF-α, IL-1β, IL-6 and IFN-γ increased in both WT and KO mice. Our next step was to determine the expression of inflammatory cytokines, BDNF and TrKb in the hippocampus. The absence of TNFR1 in mice subjected to polymicrobial sepsis resulted in higher BDNF expression in the hippocampus. In conclusion, after CLP, memory is preserved in the absence of TNFR1. This finding was associated with increased BDNF expression in the hippocampus.

show abstract

Section: Introductionmentioning

confidence: 99%

TNFR1 absence protects against memory deficit induced by sepsis possibly through over-expression of hippocampal BDNF

et al. 2014

View full text Add to dashboard Cite

show abstract

“…dysfunction [116]. However, it has been difficult to visualize the pathological state of DIC because of a lack of an effective biomarker [117]. Our present findings developed a novel approach to analyze the pathological state of brain blood vessels in SE.…”

Section: Application Of Nir In Vivo Imaging To Pathological Analyses mentioning

confidence: 98%

In Vivo Imaging of Septic Encephalopathy

Imamura¹,

Murakami²,

Matsumoto³

et al. 2017

Sepsis

View full text Add to dashboard Cite

Septic encephalopathy is a devastating symptom of severe sepsis. Many studies have been performed to uncover the pathophysiological mechanisms of septic encephalopathy; however, novel technical approaches are still required to overcome this complex symptom. Because patients are suffering from severe cognitive impairment, coma, or delirium, which burden not only patients but also caregivers, overcoming septic encephalopathy is still a major social problem worldwide, especially in the intensive care. Septic encephalopathy seems to be caused by cytokine invasion and/or oxidative stress into the brain, and this pathological state leads to imbalance of neurotransmitters. In addition to this pathophysiology, septic encephalopathy causes complicated symptoms (e.g., ischemic stroke, edema, and aberrant sensory function). For these pathophysiological mechanisms, electrophysiology using animal models, positron emission tomography (PET), computed tomography, and magnetic resonance imaging for septic patients has provided important clues. However, the research for septic encephalopathy is currently confronted with the difficulty of complex symptoms. To overcome this situation, in this chapter, we introduce our novel methods for in vivo imaging of septic encephalopathy using near infrared (NIR) nanoparticles, quantum dots. In addition to our recent progress, we propose a strategy for the future approach to in vivo imaging of septic encephalopathy.

show abstract

“…The distinction between delirium and septic encephalopathy is uncertain at this time, as some argue that sepsisassociated encephalopathy is a different pathophysiological process that may overlap with clinical signs of delirium [62]. Many consider septic encephalopathy a common type of delirium that is rooted in the underlying pathophysiological underpinnings of the septic state (systemic inflammatory and coagulopathic disturbances).…”

Section: Definition Risk Factors and Monitoring For Deliriummentioning

confidence: 99%

Pharmacological and Nonpharmacological Management of Delirium in Critically Ill Patients

2012

View full text Add to dashboard Cite

Delirium is a common yet under-diagnosed syndrome of acute brain dysfunction, which is characterized by inattention, fluctuating mental status, altered level of consciousness, or disorganized thinking. Although our recognition of risk factors for delirium has progressed, our understanding of the underlying pathophysiologic mechanisms remains limited. Improvements in monitoring and assessment for delirium (particularly in the intensive care setting) have resulted in validated and reliable tools such as arousal scales and bedside delirium monitoring instruments. Once delirium is recognized and the modifiable risk factors are addressed, the next step in management (if delirium persists) is often pharmacological intervention. The sedatives, analgesics, and hypnotics most often used in the intensive care unit (ICU) to achieve patient comfort are all too frequently deliriogenic, resulting in a longer duration of ICU and hospital stay, and increased costs. Therefore, identification of safe and efficacious agents to reduce the incidence, duration, and severity of ICU delirium is a hot topic in critical care. Recognizing that there are no medications approved by the Food and Drug Administration (FDA) for the prevention or treatment of delirium, we chose anti-psychotics and alpha-2 agonists as the general pharmacological focus of this article because both were subjects of relatively recent data and ongoing clinical trials. Emerging pharmacological strategies for addressing delirium must be combined with nonpharmacological approaches (such as daily spontaneous awakening trials and spontaneous breathing trials) and early mobility (combined with the increasingly popular approach called: Awakening and Breathing Coordination, Delirium Monitoring, Early Mobility, and Exercise [ABCDE] of critical care) to develop evidence-based approaches that will ensure safer and faster recovery of the sickest patients in our healthcare system.

show abstract

Sepsis-associated encephalopathy: not just delirium

Cited by 81 publications

References 67 publications

TNFR1 absence protects against memory deficit induced by sepsis possibly through over-expression of hippocampal BDNF

TNFR1 absence protects against memory deficit induced by sepsis possibly through over-expression of hippocampal BDNF

In Vivo Imaging of Septic Encephalopathy

Pharmacological and Nonpharmacological Management of Delirium in Critically Ill Patients

Contact Info

Product

Resources

About