Neurological complications of sepsis

Piva, Simone; Bertoni, Michele; Gitti, Nicola; Rasulo, Frank; Latronico, Nicola

doi:10.1097/mcc.0000000000001022

Cited by 17 publications

(9 citation statements)

References 113 publications

(133 reference statements)

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“…The Glasgow coma scores are often used to assess and monitor such types of neurological impairment [ 39 ]. Sometimes, the nervous system may be the first to show signs of dysfunction, particularly in elderly and immunocompromised patients, leading to a variety of clinical syndromes including sepsis-associated encephalopathy (SAE), seizures, stroke, and neuromuscular disorders [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Skin Lesions with Loss of Tissue and Cutaneous-Onset Sepsis: The Skin Infection–Sepsis Relationship

Pătrașcu,

Vâță,

Temelie-Olinici

et al. 2024

Diagnostics

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Infectious and inflammatory dermatoses featuring skin lesions with loss of tissue expose skin layers to microbial invasions, disrupt the normal skin microbiome, and potentially lead to sepsis. However, literature data on the incidence of cutaneous-onset sepsis are scarce. This retrospective observational study assessed hospital admissions for primary skin lesions without bacterial infections and sepsis during 2020–2022 in the largest emergency hospital in NE Romania. Of 509 patients, 441 had infected lesions, 78 had sepsis caused by venous ulcers from microbial eczema cellulitis, superinfected bullous dermatoses, erysipelas, and erythroderma. Cultured samples revealed S. aureus, P. aeruginosa, and E. coli; and K. pneumoniae and S. β-hemolytic associated with sepsis, even if this was rarer. Clinical manifestations included ulcerations, erosions, fissures, excoriations, bullae, vesicles, pruritus, tumefaction, edema, fever, chills, pain, adenopathy, and mildly altered mental status. Underlying chronic heart failure, atrial fibrillation, anemia, and type-1 diabetes mellitus were comorbidities associated with infection and sepsis. Significant associations and risk factors, including their combined effects, are discussed to draw attention to the need for further research and adequate management to prevent sepsis in adult patients of any age presenting with infected skin lesions (especially cellulitis) and comorbidities (especially type 1 diabetes mellitus and anemia).

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Section: Discussionmentioning

confidence: 99%

Skin Lesions with Loss of Tissue and Cutaneous-Onset Sepsis: The Skin Infection–Sepsis Relationship

Pătrașcu,

Vâță,

Temelie-Olinici

et al. 2024

Diagnostics

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“…Systemic inflammatory disorders, such as those caused by uncontrolled bacterial or viral infections, are associated with cognitive and memory impairment and exacerbation of neurocognitive diseases (1)(2)(3)(4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

“…It affects 19 million patients worldwide annually ( 8 ). Of these, half recover, one-third die within the next year, and one-sixth subsequently develop severe persistent neurological impairments ( 2 , 3 , 9 ). Clinical management of patients ( 10 ) does not include the treatment or prevention of neurological disorders, although it is an area of intense research ( 11 ).…”

Section: Introductionmentioning

confidence: 99%

Retinal response to systemic inflammation differs between sexes and neurons

Rodríguez-Ramírez,

Norte-Muñoz,

Lucas-Ruiz

et al. 2024

Front. Immunol.

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BackgroundNeurological dysfunction and glial activation are common in severe infections such as sepsis. There is a sexual dimorphism in the response to systemic inflammation in both patients and animal models, but there are few comparative studies. Here, we investigate the effect of systemic inflammation induced by intraperitoneal administration of lipopolysaccharide (LPS) on the retina of male and female mice and determine whether antagonism of the NLRP3 inflammasome and the extrinsic pathway of apoptosis have protective effects on the retina.MethodsA single intraperitoneal injection of LPS (5 mg/kg) was administered to two months old C57BL/6J male and female mice. Retinas were examined longitudinally in vivo using electroretinography and spectral domain optical coherence tomography. Retinal ganglion cell (RGC) survival and microglial activation were analysed in flat-mounts. Retinal extracts were used for flow cytometric analysis of CD45 and CD11b positive cells. Matched plasma and retinal levels of proinflammatory cytokines were measured by ELISA. Retinal function and RGC survival were assessed in animals treated with P2X7R and TNFR1 antagonists alone or in combination.ResultsIn LPS-treated animals of both sexes, there was transient retinal dysfunction, loss of vision-forming but not non-vision forming RGCs, retinal swelling, microglial activation, cell infiltration, and increases in TNF and IL-1β. Compared to females, males showed higher vision-forming RGC death, slower functional recovery, and overexpression of lymphotoxin alpha in their retinas. P2X7R and TNFR1 antagonism, alone or in combination, rescued vision-forming RGCs. P2X7R antagonism also rescued retinal function. Response to treatment was better in females than in males.ConclusionsSystemic LPS has neuronal and sex-specific adverse effects in the mouse retina, which are counteracted by targeting the NLRP3 inflammasome and the extrinsic pathway of apoptosis. Our results highlight the need to analyse males and females in preclinical studies of inflammatory diseases affecting the central nervous system

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“…Similarly, recent studies indicate that adults who survive a variety of infections severe enough to require hospitalization have a significantly increased risk of developing dementia over the next 10–20 years ( Sipilä et al, 2021 ; Bohn et al, 2023 ). Severe sepsis in the elderly approximately triples the risk of the development of moderate to strong new cognitive impairment in this population ( Peters van Ton et al, 2022 ; Piva et al, 2023 ). These findings in humans are recapitulated in a mouse model of intraperitoneal infection with Listeria monocytogenes followed by amoxicillin treatment ( Cassidy et al, 2023 ).…”

Section: Introductionmentioning

confidence: 99%

“…The most extreme manifestation of septic encephalopathy occurs in deep septic shock with bilateral hippocampal necrosis as a consequence of watershed infarctions ( Tauber et al, 2017 ). Pathophysiological mechanisms have been discussed in detail in several recent publications ( Perry et al, 2003 ; Tauber et al, 2017 , 2021 ; Robba et al, 2018 ; Too et al, 2021 ; Sekino et al, 2022 ; Dumbuya et al, 2023 ; Barichello et al, 2023 ; Piva et al, 2023 ). This review will focus on biomarkers of septic encephalopathy which have already been successfully applied in clinical practice and which show promise as prognostic markers in older patients.…”

Section: Introductionmentioning

confidence: 99%

Septic encephalopathy in the elderly – biomarkers of potential clinical utility

Schütze,

Drevets,

Tauber

et al. 2023

Front. Cell. Neurosci.

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Next to acute sickness behavior, septic encephalopathy is the most frequent involvement of the brain during infection. It is characterized by a cross-talk of pro-inflammatory cells across the blood–brain barrier, by microglial activation and leukocyte migration, but not by the entry of infecting organisms into the brain tissue. Septic encephalopathy is very frequent in older persons because of their limited cognitive reserve. The predominant clinical manifestation is delirium, whereas focal neurological signs and symptoms are absent. Electroencephalography is a very sensitive method to detect functional abnormalities, but these abnormalities are not specific for septic encephalopathy and of limited prognostic value. Routine cerebral imaging by computer tomography usually fails to visualize the subtle abnormalities produced by septic involvement of the brain. Magnetic resonance imaging is by far more sensitive to detect vasogenic edema, diffuse axonal injury or small ischemic lesions. Routine laboratory parameters most suitable to monitor sepsis, but not specific for septic encephalopathy, are C-reactive protein and procalcitonin. The additional measurement of interleukin (IL)-6, IL-8, IL-10 and tumor necrosis factor-α increases the accuracy to predict delirium and an unfavorable outcome. The most promising laboratory parameters to quantify neuronal and axonal injury caused by septic encephalopathy are neurofilament light chains (NfL) and S100B protein. Neuron-specific enolase (NSE) plasma concentrations are strongly influenced by hemolysis. We propose to determine NSE only in non-hemolytic plasma or serum samples for the estimation of outcome in septic encephalopathy.

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Neurological complications of sepsis

Cited by 17 publications

References 113 publications

Skin Lesions with Loss of Tissue and Cutaneous-Onset Sepsis: The Skin Infection–Sepsis Relationship

Skin Lesions with Loss of Tissue and Cutaneous-Onset Sepsis: The Skin Infection–Sepsis Relationship

Retinal response to systemic inflammation differs between sexes and neurons

Septic encephalopathy in the elderly – biomarkers of potential clinical utility

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