Franco M. Recchia

Purpose To describe novel retinal findings in an infant with muscle–eye–brain disease and suggest a novel mechanism for congenital retinal detachment. Methods Case report. Results A 7-week-old, white, female infant presented with total retinal detachment, peripheral retinal avascularity, and neovascularization of the right eye. In the left eye, there was hypoplastic optic nerve, no identifiable foveal avascular zone, and a small area of avascularity in the temporal peripheral retina. Genetic testing ultimately confirmed the diagnosis of muscle–eye–brain disease, a disorder of aberrant neuronal migration. Conclusion This case describes retinal findings that, to our knowledge, have not been reported in previous cases of muscle–eye–brain disease: peripheral avascularity, leading to retinal detachment in one eye, and foveal dysplasia. It is speculated that aberrant retinal vasculogenesis arose from disordered migration and patterning of retinal neurons.

Fireworks-related injuries are frequently seen among patients admitted to the emergency department because fireworks are a popular means of expression during Independence Day and other celebrations in the United States. In 2006, a total of 11 deaths and approximately 9200 emergency department admissions resulted from fireworks-related injuries, with most affecting boys and 36% of injuries occurring in individuals younger than 15 years.¹ An estimated 1400 cases annually involve injury to the eyes.² A disproportionate number of cases of severe ocular morbidity and visual impairment are caused by bottle rockets.^3,4

Purpose.: Comparative retinal gene expression analysis in two rodent models of oxygen-induced retinopathy (OIR) was performed to identify the genes and pathways involved in retinal neovascularization. Methods.: Three independent experimental runs were conducted for each species, according to standard protocols for induction of OIR. Total retinal RNA was isolated at two time points, corresponding to the early response to relative hypoxia (P13 in mouse, P15 in rat) and to the later phase of maximum retinal neovascularization (P18 in mouse, P20 in rat) and was used to prepare labeled probes for hybridization. Gene expression was compared between normal and experimental conditions for each species at each time point. Probesets with a false-discovery rate of ≤0.05 were considered significantly different and were classified as cellular functions or biological pathways. Changes in expression of selected genes were confirmed by quantitative rtPCR. Results.: At the early time point, there were changes in 43 genes in each species, with two in common. Increased expression of members of the VEGF and ephrin receptor signaling pathways were identified in both models. At the later time point, there were changes in 26 genes in the rat and in 1622 in the mouse, with 13 in common. Four pathways were identified in both models. Conclusions.: Genes and pathways known to be involved in angiogenesis, as well as other biologically plausible genes and pathways, were identified. This work serves as a comprehensive resource for the study of retinal neovascularization and identification of potential rational targets for antiangiogenic therapy.

To determine the prevalence of prior or current usage of COX-2 inhibitors among patients with retinal venous occlusion (RVO). Records of all patients with RVO and control patients matched by age and gender without the diagnosis of RVO seen in a retina referral practice between May 1999 and October 2004 were reviewed. Prevalence of COX-2 inhibitor usage was compared. Multivariable analysis was used to assess the independent correlation of COX-2 inhibitor usage with RVO. A total of 111 consecutive patients with RVO and 316 controls without RVO were identified. There was no significant difference in race or presence of hypertension between cases and controls. Ten of the RVO patients (9%) had a history of using COX-2 inhibitors. Of these 10 patients, one had a central RVO, one had a hemi-central RVO, and eight had a branch RVO. Thirty-nine of the 321 controls (12%) had a history of COX-2 inhibitor use. The prevalence of COX-2 inhibitor usage among RVO patients was not significantly different from that of controls (9% versus 12%; P = 0.37). In a multivariable analysis adjusting for effects of age, gender, hypertension, diabetes, and cardiovascular disease, the association of COX-2 inhibitor usage and RVO was still not significant (P = 0.48). A few patients with RVO had prior or concurrent use of COX-2 inhibitors. The prevalence of COX-2 inhibitor usage does not appear to be significantly higher in patients with RVO.

Purpose: To describe the optical coherence tomography (OCT) findings for patients with a history of retinopathy of prematurity (ROP). Methods: Clinical records, fundus photographs, and OCT findings for consecutive patients aged 8 years and older who had a history of ROP were reviewed. The main outcome measures were best-corrected visual acuity, central foveal thickness (CFT), macular anatomy, and foveal contour by OCT. Results: Twenty eyes of 12 patients (median age, 15 years) were studied. Median gestational age at birth was 25 weeks. Six eyes had received peripheral retinal ablation for threshold ROP. Median best-corrected visual acuity was 20/40 (range, 20/20 to counting fingers). CFT was >220 μm in 70% of eyes and >240 μm in 35% of eyes. In all eyes, foveal contour was abnormal, with foveal depression either absent (n = 7 [35%]) or shallow (n = 13 [65%]). Preservation of multiple inner retinal layers within the fovea was seen in 14 eyes (70%). Vitreomacular traction or subretinal fluid was not seen in any eye. Conclusions: Anomalies in foveal anatomy by OCT may be a vestige of prematurity, appear to be independent of prior retinopexy, and can still be associated with excellent visual acuity.

To evaluate the incidence of self-reported decrease in visual acuity within 7 days of photodynamic therapy (PDT) for choroidal neovascularization secondary to age-related macular degeneration (AMD) and to describe the anatomical and clinical course of patients with documented significant visual loss. Consecutive records of all patients with exudative AMD treated with PDT over a 16-month period at a community-based retina referral practice were reviewed for instances of self-reported visual change within 7 days of treatment. The primary outcome measure was Snellen visual acuity. Secondary outcome measures were fluorescein angiography (FA) and anatomical findings. Among 1,894 PDT treatments performed for 821 patients, there were 32 instances (for 30 patients) of self-reported visual change within 7 days of PDT. A decrease in > or =2 lines of Snellen visual acuity was documented for 10 patients (1.2% of patients or 0.5% of treatments), and all occurred within 3 days of PDT (median, 1 day) in all patients. Median pre-PDT vision was 20/60 (range, 20/50 to 20/200). Vision within 3 days after PDT was 20/100 or worse in all 10 cases and counting fingers or worse in 3. Subretinal hemorrhage occurred in four cases. FA of eyes without hemorrhage showed a circular area of choroidal hypoperfusion (corresponding to the PDT spot) in all five eyes with persistence of the hypofluorescence up to 4 months later. Visual improvement after the initial acute decrease was seen in 3 patients (30%; 95% confidence interval, 7-65%) by 3 months after PDT. Acute visual decrease after PDT for AMD is uncommon. Visual recovery may occur in some patients, but a precise estimate is difficult to determine given the small sample size.

Research from JAMA Ophthalmology — Changing Trends in the Microbiologic Aspects of Postcataract Endophthalmitis