Orbital Fat Density as a Diagnostic Tool in Pre-Septal and Orbital Cellulitis.

PURPOSE: To evaluate the usefulness of measuring orbital fat density in identifying post-septal involvement when initial differential diagnosis between orbital and periorbital cellulitis (OC and POC) is unclear. MATERIALS AND METHODS: Retrospective study of patients with clinical diagnosis of OC or POC who underwent contrast-enhanced computerized tomographic scans over a span of 10 years. Intraconal orbital fat density was measured with Hounsfield units (HU) in six areas on axial scans consisting of nasal and temporal intraconal sites. These measurements correlated with the initial and final diagnoses. Main outcome measures were HU values at the initial and final diagnoses. RESULTS: Fifty-seven patients were included. Mean HU measurement was -52 ± 18 HU for the involved side vs. -63 ± 13 for the uninvolved side (P < .001). The values were higher in cases of a final diagnosis of OC in the involved side (P < .001). The HU values were significantly higher in the nasal vs. the temporal locations of each orbit bilaterally (P < .001). The initial POC diagnosis of 20 patients (35%) was revised to OC. CONCLUSION: Intraconal fat density measurements can assist in the primary assessment of orbital involvement in patients with an uncertain initial diagnosis, with a HU value higher than -50 is suggestive of orbital involvement.

Elevated cfDNA after exercise is derived primarily from mature polymorphonuclear neutrophils, with a minor contribution of cardiomyocytes.

Strenuous physical exercise causes a massive elevation in the concentration of circulating cell-free DNA (cfDNA), which correlates with effort intensity and duration. The cellular sources and physiological drivers of this phenomenon are unknown. Using methylation patterns of cfDNA and associated histones, we show that cfDNA in exercise originates mostly in extramedullary polymorphonuclear neutrophils. Strikingly, cardiomyocyte cfDNA concentration increases after a marathon, consistent with elevated troponin levels and indicating low-level, delayed cardiac cell death. Physical impact, low oxygen levels, and elevated core body temperature contribute to neutrophil cfDNA release, while muscle contraction, increased heart rate, ß-adrenergic signaling, or steroid treatment fail to cause elevation of cfDNA. Physical training reduces neutrophil cfDNA release after a standard exercise, revealing an inverse relationship between exercise-induced cfDNA release and training level. We speculate that the release of cfDNA from neutrophils in exercise relates to the activation of neutrophils in the context of exercise-induced muscle damage.