OBJECTIVEThe aim of this study was to report the etiology, clinical features, microbiology, surgical outcome, and predictors of outcome of spontaneous subdural empyema (SDE).METHODSThe authors conducted a retrospective study in a tertiary hospital. Children up to 18 years of age, with a diagnosis of SDE with infective etiology, were included in the present cohort. Patients with posttraumatic, postsurgery, and tubercular origin of SDE were excluded from the study. The Glasgow Outcome Scale was used for outcome assessment at the end of 3 months. For analysis purposes, the demographic data, clinical features, radiological data, microbiology, type of surgery, and complication data were categorized, and univariate and multivariable logistic regression analyses were performed to identify the factors associated with outcome.RESULTSNinety-eight children were included in the study and the mean age was 10.9 years. Otogenic origin (34.7%) was the most common source of infection, followed by meningitis (14.3%). The mean duration of symptoms was 12 days. Seventy-six children presented with Glasgow Coma Scale (GCS) score > 8 and the supratentorial location was the most common location. Almost 75% of the children underwent craniotomy or craniectomy and the rest had burr-hole evacuation. Beta-hemolytic Streptococcus (10%) was the most common organism isolated. Cerebral venous thrombosis (CVT; 10.2%) was the most frequent complication in this cohort. The other complications were infarction (6.1%), new-onset seizure (4.1%), and bone flap osteomyelitis (4.1%). Thirteen cases had a recurrence of pus collection, which was more common in the craniotomy group than in the burr-hole group. Age (p = 0.02), GCS score ≤ 8 (OR 8.15, p = 0.001), CVT (OR 15.17, p = 0.001), and presence of infarction (OR 7, p = 0.05) were strongly associated with unfavorable outcome. In multivariable logistic regression analysis, only GCS score ≤ 8 (p = 0.01), CVT (p = 0.02), and presence of infarction (p = 0.04) had a significant impact on unfavorable outcome.CONCLUSIONSPrompt diagnosis and immediate intervention is the goal of management of SDE, especially in children as a delay in diagnosis can result in unconsciousness and secondary complications such as CVT and infarction, which adversely affect outcome.

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Background and Purpose: Presurgical prediction of H3K27M mutation in diffuse midline gliomas (DMGs) on MRI is desirable. The purpose of this study is to elaborate conventional MRI (cMRI) features of H3K27M-mutant DMGs and identify features that could discriminate them from wild-type (WT) DMGs. Methods: CMRI features of 123 patients with DMG were evaluated conforming to the institutional research protocols. Multimodality MRI was performed on 1.5 or 3.0 Tesla MR Scanners with imaging protocol, including T1-weighted (w), T2w, fluid-attenuated inversion recovery, diffusion-weighted, susceptibility-weighted, and postcontrast T1w sequences. Pertinent cMRI features were annotated along the lines of Visually AcceSAble Rembrandt Images features, and Intra Tumoral Susceptibility Signal score (ITSS) was evaluated. R software was used for statistical analysis. Results: Sixty-one DMGs were H3K27M-mutant (mutant DMGs). The patients in the H3K27M-mutant DMG group were younger compared to the WT-DMG group (mean age 24.13 ± 13.13 years vs. 35.79±18.74 years) (p = 0.016). The two groups differed on five cMRI features--(1) enhancement quality (p = 0.032), (2) thickness of enhancing margin (p = 0.05), (3) proportion of edema (p = 0.002), (4) definition of noncontrast-enhancing tumor (NCET) margin (p = 0.001), and (5) cortical invasion (p = 0.037). The mutant DMGs showed greater enhancement and greater thickness of enhancing margin, while the WT DMGs exhibited significantly larger edema proportion with poorly defined NCET margins and cortical invasion. ITSS was not significantly different among the groups. Conclusion: CMRI features like enhancement quality, the thickness of the enhancing margin, proportion of edema, definition of NCET margin, and cortical invasion can discriminate between the H3K27M-mutant and WT DMGs.

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