Neuroimaging in sepsis induced brain dysfunction: association with clinical and laboratory findings.

Objective: Incidence and patterns of brain lesions of sepsisinduced brain dysfunction (SIBD) have been well-defined. Our objective was to provide findings from brain magnetic resonance imaging (MRI) and voxel-based morphometry (VBM) of the brain in patients showing neurological alterations due to sepsis and relate it to the inflammatory and disease severity markers of SIBD. Methods: In this prospective observational study, 93 SIBD patients (45 men, 48 women; 50.6±12.7 year-old) were enrolled. Patients underwent a neurological examination and brain MRI. Several severity-of-disease scoring systems were used for evaluation of patient outcome. Serum levels of a panel of mediators [IL-1 β, IL-6, IL-8, IL-10, IL-12, IL-17, IFN-γ, TNF-α, complement factor Bb, C4d, C5a, iC3b, amyloid-b 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. Results: MRI 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. Multivariate regression analysis identified an association between reduced IL-12 level and occurrence of coma. Conclusion: Neuronal loss predominantly occurs in limbic and visceral pain perception regions of SIBD patients. Complement breakdown products, IL-12, and p-tau stand out as adverse neuroimaging and neurological outcome markers for SIBD. This work was supported by Scientific Research Projects Coordination Unit of Istanbul University. Project number 35165 and 46960. [ABSTRACT FROM AUTHOR]