title: Submacular hemorrhage in neovascular age-related macular degeneration: A synthesis of the literature.
abstract: Large submacular hemorrhage, an uncommon manifestation of neovascular age-related macular degeneration, may also occur with idiopathic polypoidal choroidal vasculopathy. Submacular hemorrhage damages photoreceptors owing to iron toxicity, fibrin meshwork contraction, and reduced nutrient flux, with subsequent macular scarring. Clinical and experimental studies support prompt treatment, as tissue damage can occur within 24 hours. Without treatment the natural history is poor, with a mean final visual acuity (VA) of 20/1600. Reported treatments include retinal pigment epithelial patch, macular translocation, pneumatic displacement, intravitreal or subretinal tissue plasminogen activator, intravitreal anti-vascular endothelial growth factor (VEGF) drugs, and combinations thereof. In the absence of comparative studies, we combined eligible studies to assess the VA change before and after each treatment option. The greatest improvement occurred after combined pars plana vitrectomy, subretinal tissue plasminogen activator, intravitreal gas, and anti-vascular endothelial growth factor treatment, with VA improving from 20/1000 to 20/400. The best final VA occurred using combined intravitreal tissue plasminogen activator, gas, and anti-vascular endothelial growth factor therapy, with VA improving from 20/200 to 20/100. Both treatments had an acceptable safety profile, but most studies were small, and larger randomized controlled trials are needed to determine both safety and efficacy.
authors.affiliation: Centre Nord Exploration Ophtalmologique, Lille, France.
authors.forename: Dinu
authors.initials: D
authors.lastname: Stanescu-Segall
authors.affiliation: Bucharest Eye Hospital and Clinic, Bucharest, Romania.
authors.forename: Florian
authors.initials: F
authors.lastname: Balta
authors.affiliation: Department of Ophthalmology, School of Medicine, King's College London, London, UK. Electronic address: t.jackson1@nhs.net.
authors.forename: Timothy L
authors.initials: TL
authors.lastname: Jackson
mesh_terms: D000399:Air Pressure; D020533:Angiogenesis Inhibitors / Q000627:therapeutic use; D000068258:Bevacizumab / Q000627:therapeutic use; D058450:Endotamponade; D006801:Humans; D000069579:Ranibizumab / Q000627:therapeutic use; D012166:Retinal Hemorrhage / Q000150:complications* / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors; D014821:Vitrectomy; D057135:Wet Macular Degeneration / Q000150:complications* / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy
chemical_list: D020533:Angiogenesis Inhibitors; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D000068258:Bevacizumab; D010959:Tissue Plasminogen Activator; D000069579:Ranibizumab
keywords: anti-vascular endothelial growth factor; bevacizumab; gas; macular translocation; neovascular age-related macular degeneration; pneumatic displacement; ranibizumab; subretinal hemorrhage; tissue plasminogen activator; vitrectomy