• Neurocritical care · Feb 2019

    Observational Study

    Neuroimaging Findings in Sepsis-Induced Brain Dysfunction: Association with Clinical and Laboratory Findings.

    • Günseli Orhun, Figen Esen, ÖzcanPerihan ErginPEDepartment of Anesthesiology and Intensive Care, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey., Serra Sencer, Başar Bilgiç, Canan Ulusoy, Handan Noyan, Melike Küçükerden, Achmet Ali, Mehmet Barburoğlu, and Erdem Tüzün.
    • Department of Anesthesiology and Intensive Care, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey. gunseli_orhun@hotmail.com.
    • Neurocrit Care. 2019 Feb 1; 30 (1): 106117106-117.

    BackgroundIncidence and patterns of brain lesions of sepsis-induced brain dysfunction (SIBD) have been well defined. Our objective was to investigate the associations between neuroimaging features of SIBD patients and well-known neuroinflammation and neurodegeneration factors.MethodsIn this prospective observational study, 93 SIBD patients (45 men, 48 women; 50.6 ± 12.7 years old) were enrolled. Patients underwent a neurological examination and brain magnetic resonance imaging (MRI). Severity-of-disease scoring systems (APACHE II, SOFA, and SAPS II) and neurological outcome scoring system (GOSE) were used. Also, serum levels of a panel of mediators [IL-1β, IL-6, IL-8, IL-10, IL-12, IL-17, IFN-γ, TNF-α, complement factor Bb, C4d, C5a, iC3b, amyloid-β peptides, total tau, phosphorylated tau (p-tau), S100b, neuron-specific enolase] were measured by ELISA. Voxel-based morphometry (VBM) was employed to available patients for assessment of neuronal loss pattern in SIBD.ResultsMRI of SIBD patients were normal (n = 27, 29%) or showed brain lesions (n = 51, 54.9%) or brain atrophy (n = 15, 16.1%). VBM analysis showed neuronal loss in the insula, cingulate cortex, frontal lobe, precuneus, and thalamus. Patients with abnormal MRI findings had worse APACHE II, SOFA, GOSE scores, increased prevalence of delirium and mortality. Presence of MRI lesions was associated with reduced C5a and iC3b levels and brain atrophy was associated with increased p-tau levels. Regression analysis identified an association between C5a levels and presence of lesion on MRI and p-tau levels and the presence of atrophy on MRI.ConclusionsNeuronal loss predominantly occurs in limbic and visceral pain perception regions of SIBD patients. Complement breakdown products and p-tau stand out as adverse neuroimaging outcome markers for SIBD.

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