RESUMEN
PURPOSE: To evaluate ocular hypertension (OHT) after Ozurdex injection to determine the incidence of OHT, therapy for OHT, and any associative factors such as diagnosis, underlying glaucoma and therapy, or sequential Ozurdex injection(s). METHODS: Retrospective consecutive case series with patients receiving one or more intravitreal Ozurdex implantations at a tertiary care academic center. Ocular hypertension was defined as a single measurement of ≥30 mmHg or an increase of ≥10 mmHg from baseline. RESULTS: Ninety-four injections in 52 patients (59 eyes) were reviewed. Forty eyes received a single injection, and 19 eyes received multiple injections. Ocular hypertension developed in 14 patients (26.9%). Thirteen patients (25%) had preexisting glaucoma or suspicion of glaucoma, and 6 of these developed OHT. Glaucoma eye drops were initiated after 13 injections (13.8%). Invasive surgery for glaucoma was required in 3 patients (3.2%): all had glaucoma or suspicion of glaucoma (one case was related to neovascular glaucoma and unlikely related to steroid response after Ozurdex). There was no difference in relative intraocular pressure increase (i.e., difference between final follow-up or subsequent intravitreal injection vs. baseline) between single versus multiple Ozurdex injections (P = 0.883). CONCLUSION: Patients (26.9%) who received Ozurdex developed OHT. Glaucoma or glaucoma-suspicion factors were present in all patients who required invasive surgery for glaucoma. A greater proportion of patients who received multiple injections had an intraocular pressure elevation, but the relative intraocular pressure increase was not significant.
Asunto(s)
Dexametasona/efectos adversos , Presión Intraocular/efectos de los fármacos , Edema Macular/tratamiento farmacológico , Hipertensión Ocular/inducido químicamente , Preparaciones de Acción Retardada , Dexametasona/administración & dosificación , Femenino , Estudios de Seguimiento , Humanos , Inyecciones Intravítreas , Masculino , Persona de Mediana Edad , Hipertensión Ocular/fisiopatología , Pronóstico , Estudios Retrospectivos , Factores de TiempoRESUMEN
PURPOSE: To review the impact of vitrectomy and tube shunts on mean intraocular pressure (IOP) and number of glaucoma medications in pediatric aphakic glaucoma. METHODS: A retrospective review of pediatric patients who underwent combined vitrectomy and glaucoma tube shunt surgery for aphakic glaucoma was conducted. Inclusion criteria were: age 18 years or younger, diagnosis of aphakic glaucoma, preoperative IOP data, and postoperative IOP data for at least 6 months. Mean IOP lowering at 1 year, number of glaucoma medications at 1 year, and surgical complications, including tube occlusion in the postoperative period, were noted. RESULTS: The mean ± standard deviation preoperative IOP was 33.9 ± 10.6 mm Hg (range: 18 to 57 mm Hg) with a mean of three topical IOP-lowering medications. A total of 5 (36%) Ahmed and 9 (64%) Baerveldt tube shunts were placed. One of the Baerveldt tube shunt procedures was combined with revision of a traumatically dislocated tube. The mean IOP at 12 months postoperatively was 16.6 ± 5.8 mm Hg (range: 6 to 28 mm Hg; P < .01, t = 3.74, df = 13) with a mean of 2.3 glaucoma medications. There were no cases of tube occlusion, corneal decompensation, endophthalmitis, or retinal detachment over the 12 months of follow-up. CONCLUSIONS: Combined vitrectomy and placement of a glaucoma tube shunt can be safe and effective in lowering IOP based on mean IOP values and number of glaucoma medications at 1 year. [J Pediatr Ophthalmol Strabismus. 2016;53(6):339-343.].
Asunto(s)
Afaquia Poscatarata/cirugía , Implantes de Drenaje de Glaucoma , Glaucoma/cirugía , Vitrectomía , Adolescente , Afaquia Poscatarata/diagnóstico , Afaquia Poscatarata/fisiopatología , Catarata/congénito , Extracción de Catarata , Niño , Preescolar , Femenino , Glaucoma/diagnóstico , Glaucoma/fisiopatología , Humanos , Lactante , Presión Intraocular/fisiología , Masculino , Estudios Retrospectivos , Agudeza Visual/fisiologíaAsunto(s)
Síndrome de Alagille/diagnóstico , Neovascularización Coroidal/diagnóstico , Distrofias Hereditarias de la Córnea/diagnóstico , Ceguera Nocturna/diagnóstico , Síndrome de Alagille/cirugía , Femenino , Humanos , Fallo Renal Crónico/inducido químicamente , Fallo Renal Crónico/terapia , Trasplante de Hígado , Células Fotorreceptoras de Vertebrados/patología , Diálisis Renal , Epitelio Pigmentado de la Retina/patología , Tacrolimus/toxicidad , Tomografía de Coherencia Óptica , Vitamina A/sangre , Vitamina D/sangre , Adulto JovenAsunto(s)
Infecciones Parasitarias del Ojo/diagnóstico , Miasis/diagnóstico , Retina/patología , Enfermedades de la Retina/diagnóstico , Adolescente , Animales , Diagnóstico Diferencial , Infecciones Parasitarias del Ojo/parasitología , Angiografía con Fluoresceína , Fondo de Ojo , Humanos , Larva , Masculino , Miasis/parasitología , Retina/parasitología , Enfermedades de la Retina/parasitologíaAsunto(s)
Resinas Acrílicas/administración & dosificación , Embolización Terapéutica/métodos , Gelatina/administración & dosificación , Neoplasias Maxilares/irrigación sanguínea , Neoplasias Maxilares/terapia , Arteriolas , Niño , Angiografía con Fluoresceína , Estudios de Seguimiento , Fondo de Ojo , Humanos , Vasos Retinianos , Tomografía de Coherencia ÓpticaRESUMEN
In 1933, famed aviator Wiley Post (1898-1935) was the first pilot to fly around the world solo. In addition, during one of his many stratospheric flights, he discovered the jet stream. What makes his accomplishments even more remarkable is that he did this monocularly, having lost his left eye from traumatic endophthalmitis following an oil rig accident. He underwent a period of self-imposed visual training to maximize his depth perception, and then accomplished what no one had before.
Asunto(s)
Aviación/historia , Percepción de Profundidad , Oftalmología/historia , Trastornos de la Percepción/historia , Adaptación Ocular , Historia del Siglo XIX , Historia del Siglo XX , Humanos , Estados Unidos , Visión MonocularAsunto(s)
Infecciones Oportunistas Relacionadas con el SIDA/diagnóstico , Infecciones Bacterianas del Ojo/diagnóstico , Desprendimiento de Retina/diagnóstico , Vasculitis Retiniana/diagnóstico , Sífilis/diagnóstico , Infecciones Oportunistas Relacionadas con el SIDA/inmunología , Recuento de Linfocito CD4 , Linfocitos T CD4-Positivos/inmunología , Eritema/diagnóstico , Angiografía con Fluoresceína , Mano , Humanos , Masculino , Enfermedades Cutáneas Papuloescamosas/diagnóstico , Serodiagnóstico de la Sífilis , Adulto JovenRESUMEN
Batten disease, or juvenile neuronal ceroid lipofuscinosis (JNCL), results from mutations in the CLN3 gene. This disorder presents clinically around the age of 5 years with visual deficits progressing to include seizures, cognitive impairment, motor deterioration, hallucinations, and premature death by the third to fourth decade of life. The motor deficits include coordination and gait abnormalities, myoclonic jerks, inability to initiate movements, and spasticity. Previous work from our laboratory has identified an early reduction in catechol-O-methyltransferase (COMT), an enzyme responsible for the efficient degradation of dopamine. Alterations in the kinetics of dopamine metabolism could cause the accumulation of undegraded or unsequestered dopamine leading to the formation of toxic dopamine intermediates. We report an imbalance in the catabolism of dopamine in 3 month Cln3(-/-) mice persisting through 9 months of age that may be causal to oxidative damage within the striatum at 9 months of age. Combined with the previously reported inflammatory changes and loss of post-synaptic D1alpha receptors, this could facilitate cell loss in striatal projection regions and underlie a general locomotion deficit that becomes apparent at 12 months of age in Cln3(-/-) mice. This study provides evidence for early changes in the kinetics of COMT in the Cln3(-/-) mouse striatum, affecting the turnover of dopamine, likely leading to neuron loss and motor deficits. These data provide novel insights into the basis of motor deficits in JNCL and how alterations in dopamine catabolism may result in oxidative damage and localized neuronal loss in this disorder.