ABSTRACT
INTRODUCTION: Unexplained visual loss after removal of silicone oil from the eye has been described. The purpose of this study is to determine the incidence of unexplained loss of visual acuity after SO removal and to provide possible explanations for this phenomenon. METHODS: This retrospective study included patients that underwent vitreoretinal surgery, at Centro Hospitalar São João, between January of 2012 and October of 2018. Inclusion criterion was vitreoretinal surgery in which the chosen endotamponade was SO, followed by removal of SO and exchange with balanced salt solution (BSS) or air. After SO removal, patients with documented loss of best corrected visual acuity (BCVA) on two or more Snellen lines were analyzed and patients in which the cause of the visual loss was identified, namely OHT (intraocular pressure > 21 mmHg), retinal re-detachment, glaucoma, retinal proliferative membrane formation, or corneal decompensation, were excluded. All patients with unexplained visual loss underwent spectral domain optical coherence tomography (SD-OCT) to exclude causes of visual reduction such as cystoid macular edema, epiretinal membrane, or ellipsoid/interdigitation zone disruption. A p value less than 0.05 was considered statistically significant. RESULTS: A total of 46 eyes underwent SO tamponade and SO removal during the study period. In 34.8% of the cases (n = 16) there was visual acuity loss in at least two Snellen lines. Of 46 eyes, 23.9% (n = 11) showed vision loss due to known secondary causes. Unexplained loss of visual acuity after SO removal occurred in 10.9% of cases. OHT during silicone endotamponade (p = 0.046) and silicone emulsification (p = 0.001) were identified as factors associated with unexplained visual loss after SO removal. CONCLUSION: Unexplained loss of visual acuity after SO removal occurred in 10.9% of cases. OHT during silicone endotamponade and SO emulsification were identified as important factors in the ethology of this phenomenon.
ABSTRACT
PURPOSE: To report the clinical (anatomic and functional) and genetic findings of Wagner Syndrome (WS) in a Portuguese family. METHODS: Nine members of the family agreed to be examined. All had complete clinical eye examinations. The proband and selected patients underwent color fundus photography, spectral domain optical coherence tomography (SD-OCT), automatic static white-on-white computerized perimetry, and electrophysiology assessment (flash ERG, multifocal(mf) ERG and dark adaptometry). A pedigree was constructed based on interviews with known affected subjects. Genomic DNA samples derived from venous blood were collected from all affected family members examined. RESULTS: Twenty-eight family members are affected. This family has the typical features of Wagner Syndrome, namely an empty vitreous cavity with veils, mild myopia and cataract. Four examined patients underwent vitreoretinal surgery due to abnormal peripheral vitreoretinal adhesions with peripheral retinal traction (n = 3). Retinal detachment was observed in 5 of the examined subjects. Four of them occurred between the ages of 5 and 15 years. Chorioretinal atrophy is also a frequent finding which results in moderate to severe visual field and advanced rod-cone dystrophy from younger ages, also confirmed by absence of scotopic function on dark adaptation. The macular dysfunction on mfERG was profound and of early onset. A heterozygous mutation in intron 7 of the VCAN gene (c.4004-1G > A) was found. CONCLUSIONS: We described a rare autosomal dominant vitreoretinopathy with near complete penetrance in a Portuguese family. Abnormal peripheral vitreoretinal adhesions, retinal detachment and chorioretinal atrophy are present in most of the examined individuals at young ages. Early onset of advanced visual field and electrophysiologic abnormalities were observed in this family. We also added relevant information to the literature by reporting our experience in surgical management of Wagner Syndrome patients with, and at risk of, retinal detachment.
Subject(s)
DNA/genetics , Dark Adaptation/physiology , Mutation , Retinal Degeneration/diagnosis , Tomography, Optical Coherence/methods , Versicans/deficiency , Visual Fields/physiology , Adolescent , Adult , Child , Child, Preschool , DNA Mutational Analysis , Electroretinography , Female , Humans , Male , Pedigree , Portugal , Retina/pathology , Retina/physiopathology , Retinal Degeneration/genetics , Retinal Degeneration/physiopathology , Versicans/genetics , Versicans/metabolism , Visual Acuity , Visual Field Tests , Young AdultABSTRACT
PURPOSE: To report the safety and efficacy of intravitreal recombinant tissue plasminogen activator (rtPA) with gas for managing submacular hemorrhage. METHODS: Patients with submacular hemorrhage centered in or close to the fovea underwent hemorrhage displacement with intravitreal injection of rtPA (50 µg/0.05 mL) followed by gas injection (0.3 mL SF6). Anatomic and visual outcomes are described. RESULTS: Exudative age-related macular degeneration (AMD) (n = 4) and blunt trauma (n = 2) were the etiologies of submacular hemorrhage in this sample. Intravitreal injection of rtPA decreased the extent of submacular hemorrhage in all eyes, with complete hemorrhage displacement in 2 and partial displacement in 4. Visual acuity remained stable (n = 4) or improved (n = 2) after the procedure. Improvements in anatomic and visual outcomes were less evident in exudative AMD cases, which also had longer hemorrhage duration. Recurrence occurred only in 1 eye. No evident rtPA-associated retinal toxicity was observed. CONCLUSIONS: Untreated submacular hemorrhage has poor visual prognosis. Our results suggest that rtPA injection is a minimally invasive, simple, inexpensive procedure with few related complications. Cost-benefit of this injection seems acceptable.
