CRVO with macular oedema in a glaucoma suspect with cardiac history
A 68-year-old man presents with a 5-day history of sudden painless loss of vision in the left eye. He has a 12-year history of type 2 diabetes (HbA1c 9.1%) and hypertension, and takes ramipril and metformin. Left eye: visual acuity 6/60, IOP 17 mmHg, no relative afferent pupillary defect, dilated and tortuous retinal veins in all four quadrants with extensive flame and dot-blot haemorrhages, disc swelling and macular oedema; OCT central subfield thickness is 640 micrometres. Right eye: visual acuity 6/6 with mild non-proliferative changes. He is a glaucoma suspect with crowded discs and IOPs of 20-22 mmHg, and has a family history of glaucoma. He had a myocardial infarction 2 years ago.
1. What is your diagnosis and first-line treatment, and how do his glaucoma and cardiac histories influence your choice?
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Diagnosis: central retinal vein occlusion with macular oedema, in a patient with poorly controlled diabetes and hypertension.
First-line: intravitreal anti-VEGF (ranibizumab or aflibercept) rather than a dexamethasone implant.
Why:
- Anti-VEGF gives comparable or better visual gains with a much lower risk of IOP rise. Dexamethasone carries a 20-30% risk of significant IOP elevation, and he is already a glaucoma suspect with IOPs of 20-22 mmHg and crowded discs.
- His myocardial infarction was 2 years ago. Anti-VEGF has a small systemic thromboembolic signal, but this is not a contraindication and is far smaller than the risk of untreated macular oedema. I would document the discussion and liaise with his cardiologist.
- Baseline: wide-field fluorescein angiography or OCT angiography to assess perfusion, gonioscopy, IOP, and a dilated fundus examination for neovascularisation.
- Treat systemic risk factors: HbA1c 9.1% needs optimisation with his GP, along with blood pressure control.
2. What is your follow-up schedule, and what would prompt you to escalate to panretinal photocoagulation?
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Monitoring:
- Monthly review for 6 months with OCT and visual acuity while on treatment.
- Dilated fundus examination and gonioscopy at every visit to look for neovascularisation of the iris or angle.
- Ask specifically about pain, redness or further visual loss, which could indicate neovascular glaucoma.
Escalate to panretinal photocoagulation if:
- Neovascularisation of the iris or angle develops, particularly with angle involvement or raised IOP.
- He converts to ischaemic CRVO with more than 10 disc areas of non-perfusion and cannot be monitored reliably.
- IOP rises with new vessels.
Note: PRP is not indicated for macular oedema alone and can worsen it; anti-VEGF remains the treatment for the oedema.
3. Six months later, after six anti-VEGF injections, OCT thickness is 280 micrometres but visual acuity remains 6/60, and he develops 2 clock hours of iris neovascularisation with IOP 24 mmHg. What now?
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This is evolving neovascular glaucoma; the poor acuity is probably due to macular ischaemia rather than oedema.
- Check fluorescein angiography or OCT angiography for foveal capillary dropout; if present, further anti-VEGF is unlikely to improve vision.
- Start topical IOP-lowering treatment and arrange urgent panretinal photocoagulation to the ischaemic retina.
- Use anti-VEGF as an adjunct around PRP to reduce the risk of a pressure spike after laser.
- Perform gonioscopy to stage the angle; if there is synechial closure and the IOP remains uncontrolled, consider glaucoma drainage surgery.
- Continue anti-VEGF for the oedema while PRP takes effect, then reassess.
- Explain that visual prognosis is guarded because of ischaemia, and that the priority now is saving the eye and preventing further pressure rise.