Purpose To ascertain the anatomic factors that help achieve non-surgical sealing in full thickness macular hole (FTMH). Methods Retrospective collaborative study of FTMH that closed without surgical intervention. Results A total of 78 patients (mean age 57.9 years) included 18 patients with blunt ocular trauma, 18 patients that received topical or intravitreal therapies and 42 patients with idiopathic FTMH. Mean±SD of the initial corrected visual acuity (VA) in logMAR improved from 0.65±0.54 to 0.34±0.45 (p<0.001) at a mean follow-up of 33.8±37.1 months. FTMH reopened in seven eyes (9.0%) after a mean of 8.6 months. Vitreomacular traction was noted in 12 eyes (15.8%), perifoveal posterior vitreous detachment in 42 (53.8%), foveal epiretinal membrane in 10 (12.8%), cystoid macular oedema (CME) in 49 (62.8%) and subretinal fluid (SRF) in 20 (25.6%). By multivariate analysis, initial VA correlated to the height (p<0.001) and narrowest diameter of the hole (p<0.001) while final VA correlated to the basal diameter (p<0.001). Time for closure of FTMH (median 2.8 months) correlated to the narrowest diameter (p<0.001) and the presence of SRF (p=0.001). Mean time for closure (in months) was 1.6 for eyes with trauma, 4.3 for eyes without trauma but with therapy for CME, 4.4 for eyes without trauma and without therapy in less than 200 µm in size and 24.7 for more than 200 µm. Conclusion Our data suggest an observation period in new onset FTMH for non-surgical closure, in the setting of trauma, treatment of CME and size <200 µm.

Background: The optimal timing of pars plana vitrectomy (PPV) following ocular trauma is an ongoing debate. Early vitrectomy post-trauma enables the rapid assessment of retinal disease by removing the scaffold that fosters proliferative vitreoretinopathy. On the other hand, late vitrectomy is less challenging as there is a lower risk of bleeding and posterior vitreous detachment induction is easier. The purpose of this work is to report the functional and anatomical outcomes following ocular traumatic injuries in a United States-based cohort, emphasizing the time of intervention.Methods: This was a retrospective case series of 110 patients with traumatic ocular injuries who underwent PPV between 2008 to 2020. Patients were grouped into four timing categories: same day (0 days), early (1–7 days), delayed (8–14 days), and late (> 14 days). Multivariable regression models controlling for confounding were implemented to assess the impact of vitrectomy timing on anatomical and functional outcomes. Visual acuity (VA) at baseline and after surgery, proliferative vitreoretinopathy (PVR), and enucleation for each vitrectomy timing category were recorded.Results: Patient demographics and severity of ocular trauma were comparable across timing categories. Final VA in LogMAR was found to have a stepwise worsening as the time of ocular trauma to vitrectomy was increased (p < 0.05). For every one-step increase in the vitrectomy timing category, there was an adjusted 0.24 (CI 0.04–0.44) increase in final VA. No patient in the same day vitrectomy group had an enucleation or PVR, while patients who had late vitrectomies had the largest number of both enucleations and PVR (44.4% and 52.0%, respectively). In adjusted analysis, there was 3.11 increased odds (CI 1.03–9.42) of developing PVR for a one-step increase in vitrectomy timing (p < 0.05).Conclusion: Vitrectomy on the same day of injury has the best final VA, and the lowest incidence rates of PVR and enucleation in comparison to other timing categories, regardless of etiology.

Crystalline deposits and neurosensory retinal cavitary changes can develop in both tamoxifen retinopathy and nonproliferative idiopathic macular telangiectasia type 2 (MacTel2). MacTel2 is typically differentiated from tamoxifen retinopathy based on the presence of late leakage and mid-phase telangiectatic vessels on fluorescein angiography (FA) and the presence of hyperautofluorescence. Unlike MacTel2, tamoxifen retinopathy is known to be a progressive disease and the cessation of tamoxifen results in resolution of retinopathy. We report a unique case of nonproliferative MacTel2 in a 36-year-old Hispanic woman with tamoxifen use and the vision outcome 30 months after cessation of tamoxifen. The FA and optical coherence tomography angiography findings of this patient support the diagnosis of MacTel2, but her cessation of tamoxifen led to partial reversal of the topographic findings and improvement in visual acuity. This patient is also unique in the unusually young age of presentation for MacTel2. Our case supports that there are common pathways in the pathogenesis of tamoxifen retinopathy and MacTel2, and tamoxifen use could potentially accelerate foveal atrophy in patients with MacTel2.

To present a case of unilateral IMPG2-associated adult onset vitelliform macular dystrophy (AVMD). A 68 year-old female presented with best corrected visual acuity (BCVA) of 20/20 and 20/40 for the right and left eye respectively. The patient had a left subfoveal yellow lesion on dilated fundus examination. Optical coherence tomography showed hyper-reflective material accumulation below the fovea in the left eye only. The patient was followed for 10 years with stable BCVA, and evolution of the subretinal vitelliform lesion to a “vitelliruptive” stage. The right eye did not develop vitelliform lesion. Genetic testing identified a heterozygous likely disease-causing variant in IMPG2; c.3423–7_3423-4del. This is the first report of unilateral AVMD associated with IMPG2, expanding the phenotypic spectrum of IMPG2 retinopathy. We provide further evidence that IMPG2 variants can cause both autosomal recessive rod-cone dystrophy and autosomal dominant AVMD, with implications for patient counselling.

To report a series of three patients with von Hippel-Lindau (VHL) disease who demonstrated regression of their retinal hemangioblastomas (RH) using belzutifan in conjunction with photocoagulation therapy. Patient 1, a 23-year-old female, presented with multiple RHs in her right eye (OD) that were lasered. Her left eye (OS) revealed a large inferotemporal RH that measured approximately 2.1 mm². Systemic belzutifan was administered. Four months after initiation of treatment, the lesion regressed to 1.4 mm², but belzutifan was not well-tolerated and was discontinued due to side effects. At the date of belzutifan discontinuation, the lesion measured about 1.1 mm². Focal laser photocoagulation was applied. The lesion regressed to around 0.6 mm². Two additional laser treatments were applied one month later. On the most recent follow-up, the lesion was completely fibrosed.Patient 2, a 32-year-old male, presented with one RH OD and two RHs OS. Belzutifan was administered for one month before the patient began experiencing side effects of the medication. Consequently, the dose of belzutifan was decreased. After one month with the lowered dose, laser coagulation was applied to OS. In the most recent follow-up, five months after the initial presentation, the lesions remain less vascularized and reduced in size.Patient 3, is a 44-year-old male with a large RH OD. Following seven months of belzutifan daily, there was a significant reduction in the RH size. Belzutifan, a hypoxia-inducible factor inhibitor, is an FDA-approved medication for VHL disease associated with renal cell carcinoma, central nervous system hemangioblastomas, or pancreatic neuroendocrine tumors that do not require immediate surgical resection. Because of the high incidence of VHL-associated RHs, adjuvant laser photocoagulation therapy when belzutifan is suspended or withheld can allow for the regression of large lesions. In this case series, we also propose a reproducible and technically simple method to measure RH lesions size, using Optos fundus imaging.