ABSTRACT
Describimos un caso de vasculopatía coroidea polipoidea con líquido subretiniano persistente a pesar de múltiples tratamientos intravítreos con bevacizumab, ranibizumab y aflibercept, así como aflibercept asociado a terapia fotodinámica. El paciente alcanzó la resolución completa después de la inyección intravítrea de brolucizumab, pero experimentó una recurrencia del líquido subretiniano 12 semanas después de la suspensión. Brolucizumab podría ser una opción para tratar el líquido subretiniano después del fracaso de otros agentes anti-VEGF asociados con la terapia fotodinámica. (AU)
We describe one case of polypoidal choroidal vasculopathy with persistent subretinal fluid despite multiple treatment with intravitreal bevacizumab, ranibizumab and aflibercept, as well as aflibercept associated with photodynamic therapy. The patient reached complete resolution after intravitreal brolucizumab injection, but experienced recurrence of subretinal fluid 12 weeks after discontinuation. Brolucizumab might be an option in treating subretinal fluid after failure of other anti-VEGF agents associated with photodynamic therapy. (AU)
Subject(s)
Humans , Female , Middle Aged , Antibodies, Monoclonal, Humanized/administration & dosage , Photochemotherapy , /therapy , Treatment OutcomeABSTRACT
We describe one case of polypoidal choroidal vasculopathy with persistent subretinal fluid despite multiple treatment with intravitreal Bevacizumab, Ranibizumab and Aflibercept, as well as Aflibercept associated with photodynamic therapy. The patient reached complete resolution after intravitreal Brolucizumab injection, but experienced recurrence of subretinal fluid 12 weeks after discontinuation. Brolucizumab might be an option in treating subretinal fluid after failure of other anti-VEGF agents associated with photodynamic therapy.
Subject(s)
Choroid Diseases , Photochemotherapy , Humans , Choroid Diseases/drug therapy , Choroid Diseases/complications , Polypoidal Choroidal VasculopathyABSTRACT
Four patients developed a unilateral tonic pupil following ipsilateral oculomotor nerve palsy. The probable basis for this phenomenon is misdirection of injured oculoparasympathetic fibers in the oculomotor nerve proximal to the ciliary ganglion.
