ObjectiveFovea-involving subretinal haemorrhage is challenging to manage with uncertain visual outcomes. We reviewed outcomes of patients with fovea-involving macular haemorrhage treated with pars plana vitrectomy (PPV) and subretinal tissue plasminogen activator (tPA) with pneumatic displacement.Methods and AnalysisThis is a retrospective interventional case series. All patients with submacular haemorrhage who underwent PPV with subretinal tPA injection were included. Reasons for exclusion encompassed patients who underwent intravitreal tPA injection in the office without surgery, insufficient follow-up or documentation. Primary outcomes of interest were postoperative visual acuity (VA) at month 1 and 3. Secondary outcomes were median VA at month 3 by location of haemorrhage and underlying diagnosis.ResultsThirty-seven total patients were included. The mean age was 68.2 years, with 54.1% (20/37) females. The most common aetiology was exudative macular degeneration (43.2%), followed by undifferentiated choroidal neovascularisation (CNV) (18.9%), polypoidal choroidal vasculopathy (18.9%), traumatic CNV (10.8%), macroaneurysm (5.4%) and proliferative diabetic retinopathy (2.7%). Median preoperative VA was 20/2000, postoperative month 1 was 20/347 (p<0.01), improving to 20/152 (p<0.01) at month 3. Proportion of patients gaining vision 3+ lines in vision was 15/36 (42%). Mean preoperative central subfield thickness on optical coherence tomography was 512.2 µm for sub-retinal pigment epithelium haemorrhage and 648.2 µm for subretinal haemorrhage (p=0.48). Difference in VA by diagnosis was not significant (p=0.60).ConclusionsPPV with subretinal tPA injection and pneumatic displacement of submacular haemorrhage offers modest visual recovery for a diverse group of patients. Location of haemorrhage or specific diagnosis may not predict outcome.
Interruption of the perivascular sympathetic nerves can alleviate CA-induced hypoperfusion and neuronal cell death in the CA1 region of the hippocampus to enhance functional learning and memory.
Purpose
To investigate the benefit of early intra-arterial tissue plasminogen activator (IAT) for treatment of central retinal artery occlusion (CRAO).
Patients and Methods
Fifteen eyes of 15 patients presenting with acute CRAO were included in this retrospective consecutive interventional case series. Patients were excluded if treatment with IAT was not initiated within 12 hours. The diagnosis was confirmed by an ophthalmologist. IAT was performed via a transfemoral arterial approach. Tissue plasminogen activator (tPA) was infused into the ophthalmic artery in aliquots up to 3mg to a maximum of 22mg. Paracentesis was done at the ophthalmologist’s discretion. The primary outcome measure was visual acuity after three weeks. Adverse events were recorded during treatment and follow-up visits.
Results
After treatment with IAT, there was a statistically significant improvement in visual acuity, with a mean change of −0.76 (SD 0.91; range −2.4 to 0.85) logMAR (p=0.006). Vision improved by 3 or more lines in 53%, and of these, the mean Snellen visual acuity improvement was >6 lines. Notably, 4 patients (27%) improved from CF or worse to 20/80 or better. The mean dose of tPA used was 17mg and the mean time to treatment was 8.83 hours (range: 5.5 to 12 hours). There were no statistically significant differences based on time to treatment, dose of tPA, or use of a paracentesis. No major adverse events were recorded.
Conclusion
IAT was safe and showed significant visual improvement in this small uncontrolled study. Larger studies and efforts to decrease time to treatment should be initiated to optimize outcomes.
Background: Some patients with diabetic macular edema (DME) fail to completely respond to anti-vascular endothelial growth factor (VEGF) therapy. These patients have a high treatment burden in the absence of significant improvement. We investigate the role of intravitreal dexamethasone insert (IDI) in eyes with super-refractory DME. Methods: A non-randomized interventional study was performed among eyes with super-refractory DME refractory to anti-VEGF therapy. Eyes were treated with IDI after failing clinical response to anti-VEGF, with a minimum of 15 prior. Failure to respond was defined as failure of vision to improve at least one line on Snellen Acuity chart, central subfield thickness (CST) greater than 320 μm, or failure of CST to improve by 10% or more. Eyes with glaucoma or prior uncontrolled steroid-responsive ocular hypertension were excluded. Patient outcomes were analyzed at weeks 6, 12, 24, and year 1. Results: Six eyes of four patients were identified. All patients had failed aflibercept. The mean number of prior anti-VEGF injections was 34.5. Eyes received an average of 2.92 dexamethasone injections per person-year (PY) and required breakthrough anti-VEGF injection at 1.95/PY. Mean pre-treatment visual acuity was 0.475 LogMAR, improving to 0.342 at week 6, and 0.375 at 1 year. Mean CST pre-injection was 386.5 mm, improving to 315 mm at 1 year. No glaucoma developed. Conclusions: Intravitreal dexamethasone insert appears effective in eyes with super-refractory DME. IDI resulted in excellent anatomic improvement on SD-OCT as well as modest visual improvement. Injection burden was reduced in those who may otherwise receive years of monthly treatments.
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