title: Early treatment of acute submacular haemorrhage secondary to wet AMD using intravitreal tissue plasminogen activator, C3F8, and an anti-VEGF agent.
abstract: PurposeAcute submacular haemorrhage secondary to wet age-related macular degeneration (AMD) has a poor prognosis for which there is currently no 'gold standard' treatment. We evaluated the efficacy of early treatment using intravitreal triple therapy of tissue plasminogen activator (tPA), expansile gas, and an anti-VEGF agent.MethodsThis retrospective case series included eight patients presenting with acute submacular haemorrhage involving the fovea. All patients received treatment with 50 μg (0.05 ml) tPA, 0.3 ml 100% perfluoropropane (C3F8), and an anti-VEGF agent (0.05 mg Ranibizumab or 1.25 mg Bevacizumab in 0.05 ml) administered via intravitreal injection. An anterior chamber paracentesis post injection or vitreous tap was performed before injection to prevent retinal vascular occlusion secondary to raised intra-ocular pressure. Outcomes assessed were visual acuity, change in macular morphology, and complications.ResultsPatients presented promptly with delay between symptom onset and clinic review being 1.9±0.6 days (mean±SD). Treatment was delivered quickly with interval from presentation to treatment being 1.1±1.2 days. Symptom onset to treatment was 3.0±1.0 days. Subfoveal haemorrhage was effectively displaced in all patients. LogMAR visual acuity improved from 1.67±0.47 at presentation to 0.63±0.33 at final follow-up (P<0.0001), a mean of 7.9±4.8 months after treatment. Central retinal thickness improved from 658.1±174.2 μm at presentation to 316.6±142.4 μm at final follow-up (P=0.0028).ConclusionsEarly treatment of submacular haemorrhage using intravitreal tPA, C3F8, and anti-VEGF was effective in significantly improving visual acuity in this series of patients who presented soon after symptom onset. Treatment was well tolerated in this group of elderly and potentially frail patients.
authors.affiliation: Stoke Mandeville Hospital, Buckinghamshire, UK.
authors.forename: S R
authors.initials: SR
authors.lastname: de Silva
authors.affiliation: Stoke Mandeville Hospital, Buckinghamshire, UK.
authors.forename: M S
authors.initials: MS
authors.lastname: Bindra
mesh_terms: D000208:Acute Disease; D000368:Aged; D000369:Aged, 80 and over; D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D000068258:Bevacizumab / Q000627:therapeutic use; D058450:Endotamponade; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D005466:Fluorocarbons / Q000008:administration & dosage*; D006801:Humans; D058449:Intravitreal Injections; D008297:Male; D000069579:Ranibizumab / Q000627:therapeutic use; D012166:Retinal Hemorrhage / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D012189:Retrospective Studies; D055502:Secondary Prevention; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use*; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors; D014792:Visual Acuity / Q000502:physiology; D057135:Wet Macular Degeneration / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology
chemical_list: D020533:Angiogenesis Inhibitors; D005343:Fibrinolytic Agents; D005466:Fluorocarbons; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D000068258:Bevacizumab; C042852:perflutren; D010959:Tissue Plasminogen Activator; D000069579:Ranibizumab