RESUMEN
CLINICAL CASE: Forteen year old patient presenting progressive decrease in visual acuity of the left eye after 3 months of evolution. On examination he presents bilateral drusen of papilla, associated with juxtapapillary neovascular membrane, which seriously compromises the vision and visual field of the left eye. RESULT: Treatment with 3 consecutive injections of intravitreal ranibizumab resulted in the inactivation of the neovascular membrane with reabsorption of subretinal fluid and improvement of the best corrected visual acuity of the left eye. After 9 months of follow-up, it was 20/20 and stable. CONCLUSION: Although optic nerve head drusen are considered benign, neovascular membranes can be a complication. Anti-VEGFs are an effective alternative for treatment.
Asunto(s)
Inhibidores de la Angiogénesis/uso terapéutico , Neovascularización Coroidal/tratamiento farmacológico , Drusas del Disco Óptico/tratamiento farmacológico , Ranibizumab/uso terapéutico , Adolescente , Neovascularización Coroidal/complicaciones , Femenino , Humanos , Drusas del Disco Óptico/etiologíaRESUMEN
We present a case of Retinitis Pigmentosa with atypical aspect of fundus (Punctata Albescens), associated with Cystoid Macular Oedema and Optic Disc Drusen.
Asunto(s)
Edema Macular/diagnóstico , Drusas del Disco Óptico/diagnóstico , Retinitis Pigmentosa/diagnóstico , Adulto , Antioxidantes/uso terapéutico , Inhibidores de Anhidrasa Carbónica/uso terapéutico , Diagnóstico Diferencial , Progresión de la Enfermedad , Quimioterapia Combinada , Electrorretinografía/métodos , Femenino , Humanos , Edema Macular/complicaciones , Edema Macular/tratamiento farmacológico , Drusas del Disco Óptico/complicaciones , Drusas del Disco Óptico/tratamiento farmacológico , Retinitis Pigmentosa/complicaciones , Retinitis Pigmentosa/tratamiento farmacológico , Índice de Severidad de la Enfermedad , Tomografía de Coherencia Óptica , Resultado del Tratamiento , Ultrasonografía , Pruebas del Campo VisualRESUMEN
UNLABELLED: In the case report, bilateral cystoid macular edema with optic disc edema on the left side in young man is described. As etiology out of the systemic diseases, we considered the hypertension. The results of the neurological examination, including the brain CT examination were physiological. The patient was examined by the internal specialist, the hypertension was treated - and it was the presumed etiology of the ophthalmologic findings. Due to the repeated worsening of the ophthalmologic findings, we searched for other etiology. Bilateral buried optic disc drusen were found by means of ultrasound. Bilateral cystoid macular edema and optic disc edema were evaluated as signs of circulatory disturbance of the posterior ciliary arteries and macular choroid caused by optic disc drusen. The antiglaucomatic treatment was started with - alpha 2 adrenergic receptors agonist - brimonidine - which increases the blood supply of the optic nerve and decreases the intraocular pressure with presumed delay of axons dysfunction. KEY WORDS: macular edema, optic disc drusen, intraocular pressure, visual field, ultrasound.
Asunto(s)
Edema Macular/etiología , Drusas del Disco Óptico/complicaciones , Agonistas de Receptores Adrenérgicos alfa 2/uso terapéutico , Tartrato de Brimonidina/uso terapéutico , Diagnóstico Diferencial , Humanos , Presión Intraocular/fisiología , Edema Macular/diagnóstico , Edema Macular/tratamiento farmacológico , Masculino , Drusas del Disco Óptico/diagnóstico , Drusas del Disco Óptico/tratamiento farmacológico , Papiledema/diagnóstico , Papiledema/tratamiento farmacológico , Papiledema/etiología , Tonometría Ocular , Campos Visuales/fisiologíaRESUMEN
PURPOSE: Mutations in the MFRP (membrane-type frizzled-related protein) gene leads to an entity characterized by retinitis pigmentosa, nanophthalmos, optic disk drusen, and macular changes, originally described as foveoschisis. Despite the association of MFRP gene mutation and increase in macular thickness, no treatment modality has been described for cystoid macular edema related to this particular entity so far. METHODS: In this case report, a 52-year-old woman presented with nanophthalmos, optic disk drusen, retinitis pigmentosa, and increase in macular thickness. Genetic analysis revealed an MFRP gene mutation. The patient was treated with topical carbonic anhydrase inhibitors. RESULTS: A progressive decrease in macular thickness and cystic changes was observed during the 2-month course of topical carbonic anhydrase inhibitor treatment, and best-corrected visual acuity improved from 20/100 to 20/50. Macular thickness remained stable after 6 months of follow-up. CONCLUSION: Cystoid macular edema is part of the macular changes noted in the MFRP mutation-related nanophthalmos-retinitis pigmentosa-foveoschisis-optic disk drusen, syndrome. Taking into account that resolution of cystoid macular edema in patients with retinitis pigmentosa may delay an irreversible decrease in visual acuity, treatment should be considered when cystic changes are suspected. Topical carbonic anhydrase inhibitor was effective in decreasing macular thickness and cystic changes in the patient reported.
Asunto(s)
Inhibidores de Anhidrasa Carbónica/administración & dosificación , Proteínas de la Membrana/genética , Microftalmía/tratamiento farmacológico , Drusas del Disco Óptico/tratamiento farmacológico , Retinitis Pigmentosa/tratamiento farmacológico , Sulfonamidas/administración & dosificación , Tiofenos/administración & dosificación , Administración Tópica , Femenino , Mutación del Sistema de Lectura , Humanos , Edema Macular/tratamiento farmacológico , Persona de Mediana Edad , Síndrome , Resultado del TratamientoRESUMEN
We report two cases of atypical temporal arteritis. A 73-year-old woman with typical internal (diabetes, hypertony, hypercholesterinemia) and ophthomological (optic disc drusen) risk factors for N-AION reported with an acute unilateral decrease in vision. General symptoms, laboratory analysis and biopsy led to the diagnosis of temporal arteritis and iv steroids were administered. An 83-year-old male patient reported with a sudden unilateral decrease in vision, but did not complain about general symptoms. Laboratory analysis revealed no signs for temporal arteritis, therefore the patient was referred to his internal specialist for evaluation of internal risk factors for N-AION. A few days later the patient reported with a unilateral decrease in vision of the partner eye. This time blood analysis was suggestive of temporal arteritis although no general symptoms were reported. Diagnosis was supported by a biopsy of the temporal artery and steroids were administered. These two cases teach us how dangerously easy temporal arteritis can be overlooked and that we have to take even the slightest hint for temporal arteritis seriously and initiate treatment as early as possible.