Sudden Visual Loss in a Patient on Anticoagulation
A 68-year-old man presents to the emergency eye clinic with painless profound loss of vision in the right eye, noted on waking 6 hours ago. He reports a 'curtain' descending over the right visual field. Best-corrected acuity is counting fingers right eye and 6/9 left eye. There is a right relative afferent pupillary defect. Fundoscopy of the right eye shows a pale, milky retina with a cherry-red spot at the macula; the left fundus is normal. He has atrial fibrillation and takes warfarin, INR 2.4 today. Blood pressure is 168/94 mmHg. He had a transient episode of right eye visual loss lasting 4 minutes three weeks ago that fully resolved. He asks whether the vision will come back and whether he needs any tests.
1. What is the most likely diagnosis, and what does the history of the previous transient episode tell you about the mechanism?
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The picture is a central retinal artery occlusion (CRAO) of the right eye: sudden painless monocular loss, RAPD, and the classic pale retina with a cherry-red spot (the macula is spared because its blood supply is choroidal).
The preceding 4-minute episode of transient monocular visual loss was an amaurosis fugax - a retinal TIA. This is the key diagnostic clue: it establishes an embolic/atheromatous or cardioembolic mechanism rather than arteritis or a purely local retinal problem. In a patient with atrial fibrillation, cardioembolism is the leading candidate, but ipsilateral carotid atheroma must also be considered. The mechanism matters because it directs the work-up (carotid imaging, cardiac evaluation) and secondary prevention, not just the eye.
2. Should he be referred urgently for thrombolysis or other acute intervention? Justify your reasoning.
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He is well outside the window in which any retinal salvage is realistic - presentation is at 6 hours, and the retinal tolerance to ischaemia is short (animal data suggest irreversible damage within roughly 90–100 minutes; human outcomes with intra-arterial or intravenous thrombolysis are unproven and carry systemic risk, particularly with an INR of 2.4 on warfarin).
So the judgement is: do not chase heroic ocular reperfusion. The priority shifts to (a) confirming the mechanism and (b) preventing the far more consequential event this heralds - a stroke. CRAO is now recognised as a form of acute ischaemic stroke with a high short-term stroke risk. He needs same-day/urgent stroke or TIA assessment, not reassurance and an outpatient eye review. The visual prognosis for the right eye should be given honestly: poor, with most patients retaining only peripheral light perception or worse, and a small chance of some recovery.
3. List the investigations you would arrange and explain how each changes management.
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- Urgent ESR/CRP and full blood count: to exclude giant cell arteritis, which would mandate high-dose steroids and is a sight-threatening (and fellow-eye-threatening) diagnosis - even though his age and the embolic prodrome make it less likely, it must not be missed.
- Carotid duplex / CT angiography of the neck: to identify ipsilateral carotid stenosis, which could make him a candidate for carotid endarterectomy/revascularisation and changes antiplatelet strategy.
- ECG and cardiac rhythm assessment (e.g. ambulatory monitoring): to confirm/characterise atrial fibrillation and guide anticoagulation quality.
- Echocardiography: to look for a cardioembolic source (valve disease, thrombus, patent foramen ovale).
- Blood pressure review, HbA1c, lipids: vascular risk factor optimisation.
- Review of anticoagulation control (INR history/time in therapeutic range): a subtherapeutic INR would support cardioembolism and prompt a conversation about anticoagulant choice.
Each test is chosen because it changes a decision - steroids, surgery, or anticoagulant/antiplatelet strategy - rather than for completeness.