Central Retinal Artery Occlusion Leading to Diagnosis of Eosinophilic Granulomatous Polyangiitis After Adenovirus Vector COVID-19 Vaccination.

Purpose: To present a case of central retinal artery occlusion (CRAO) leading to the diagnosis of eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome) within 1 week of an adenovirus vector COVID-19 vaccination. Methods: A case was reviewed. Results: A 50-year-old man with atopic dermatitis and asthma presented with acute painless vision loss in 1 eye. An examination and imaging findings showed CRAO. Further evaluation found eosinophilia and elevated inflammatory markers. A workup for vasculitis showed elevated cytoplasmic-antineutrophil cytoplasmic antibody, perinuclear-antineutrophil cytoplasmic antibody, myeloperoxidase antibody, rheumatoid factor, and total immunoglobulin E. Skin biopsies were consistent with eosinophilic granulomatosis with polyangiitis. Steroids, cyclophosphamide, and mepolizumab were initiated. At 1 year, the patient's systemic symptoms had improved but his vision had not. Conclusions: Few reports exist of CRAO associated with eosinophilic granulomatosis with polyangiitis, with no other instances related to an adenovirus vector COVID-19 vaccination. Treating a systemic vasculitis early can be vision saving in the fellow eye and prevent systemic life-threatening complications.

Unexplained Vision Loss Associated With Intraocular Silicone Oil Tamponade in Rhegmatogenous Retinal Detachment Repair.

Purpose: To evaluate the visual outcomes with unexplained vision loss during or after silicone oil (SO) tamponade. Methods: This multicenter retrospective case series comprised patients with unexplained vision loss associated with SO tamponade or its removal. Eyes with other clear secondary identifiable causes of vision loss were excluded. Results: Twenty-nine eyes of 28 patients (64% male) were identified. The mean age was 50 ± 13 years (range, 13-78 years). The mean duration of SO tamponade was 148 ± 38 days. Eighteen eyes (62%) developed unexplained vision loss while under SO; 11 (38%) had vision loss after SO removal. The most common optical coherence tomography (OCT) finding was ganglion cell layer (GCL) thinning (55%). Eyes with vision loss after SO removal had a mean logMAR best-corrected visual acuity (BCVA) of 0.6 ± 0.7 (Snellen 20/85) before SO tamponade and 1.2 ± 0.4 (20/340) before SO removal. By the last follow-up after SO removal, the BCVA had improved to 1.1 ± 0.4 (20/235). In eyes with vision loss after SO removal, the BCVA before SO removal was 0.7 ± 0.7 (20/104), which deteriorated to 1.4 ± 0.4 (20/458) 1 month after SO removal. By the last follow-up, the BCVA had improved to 1.0 ± 0.5 (20/219). Conclusions: Unexplained vision loss can occur during SO tamponade or after SO removal. Vision loss was associated with 1000-centistoke and 5000-centistoke oil and occurred in macula-off and macula-on retinal detachments. The duration of tamponade was 3 months or longer in the majority of eyes. Most eyes had GCL thinning on OCT. Gradual visual recovery can occur yet is often incomplete.

Complete and Early Vitrectomy for Endophthalmitis After Cataract Surgery: An Alternative Treatment Paradigm.

PURPOSE: In this study, we report the treatment outcomes of complete and early vitrectomy for endophthalmitis (CEVE) after cataract surgery as the predominate initial treatment, accompanied by systemic antibiotics and retreatment of persistent or recurrent purulence (CEVE+). PATIENTS AND METHODS: Clinical features and microbiological factors were retrospectively reviewed in 62 eyes of 62 patients who were treated for acute postcataract endophthalmitis (APCE) occurring within three weeks of cataract surgery at Retina Specialists of Alabama, between 2007 and 2017. RESULTS: Visual acuity on presentation included light perception (LP) in 18 eyes (29%) and hand motion (HM) in 23 eyes (37%). Initial treatment was maximum possible vitrectomy in 48 eyes (77%) and tap-and-inject in 14 eyes (23%), with 38 eyes (61%) receiving two or more treatments. Cultures for the first intervention were positive in 49 eyes (79%) and virulent in 18 eyes (29%). At a median follow-up time of five months, final visual acuity was ≥20/40 in 49 eyes (79%), between 20/50 and 5/200 in seven eyes (11%), and <5/200 in six eyes (10%). Virulence was the strongest predictor of poor visual outcome. Retinal detachment occurred in four eyes (6%), likely from necrotic retinal defects in each case. CONCLUSION: Complete and early vitrectomy is a safe and effective initial treatment for APCE. When accompanied by systemic antibiotics and retreatment (CEVE+) of recurrent media opacification, it improves recovery of 20/40 or better visual acuity by approximately 50% compared to a predominantly tap-and-inject treatment paradigm. We recommend CEVE for fundus-obscuring APCE (~75% of all cases) whenever the view is inadequate to rule out macular distress.

Mitochondrial DNA has a pro-inflammatory role in AMD.

Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in the elderly of industrialized nations, and there is increasing evidence to support a role for chronic inflammation in its pathogenesis. Mitochondrial DNA (mtDNA) has been recently reported to be pro-inflammatory in various diseases such as Alzheimer's and heart failure. Here, we report that intracellular mtDNA induces ARPE-19 cells to secrete inflammatory cytokines IL-6 and IL-8, which have been consistently associated with AMD onset and progression. The induction was dependent on the size of mtDNA, but not on specific sequence. Oxidative stress plays a major role in the development of AMD, and our findings indicate that mtDNA induces IL-6 and IL-8 more potently when oxidized. Cytokine induction was mediated by STING (Stimulator of Interferon Genes) and NF-κB as evidenced by abrogation of the cytokine response with the use of specific inhibitors (siRNA and BAY 11-7082, respectively). Finally, mtDNA primed the NLRP3 inflammasome. This study contributes to our understanding of the potential pro-inflammatory role of mtDNA in the pathogenesis of AMD.