See: [eye wiki CRAO](https://eyewiki.aao.org/Retinal_Artery_Occlusion), [Eye and ear guideline CRAO](x-devonthink-item://ECF9A8D1-4A96-4B4F-A91B-5157E809097C) > [!key points] > - transient is *amaurosis fugax* and is essentially an occular [[Stroke|TIA]] > - thrombotic or embolic BRAO = Branch retinal artery occlusion ; a peripheral branch of retinal artery is occluded and so visual compromise confined to that branch. ∴ better outcome # diagnosis > - visual loss is **sudden** over seconds and **unilateral** as well as ==[[Painless loss of vision|painless]]==. > - progresses from outer visual field inwards **Risk factors** - [[Atrial fibrillation|AF]] - IVDU (septic emboli) - atherosclerosis (*carotid atherosclerosis* most common cause) - [[Giant Cell Arteritis|GCA]] → due to *ischaemic optic neuropathy* - or other inflammatory disease/arteritis - thrombophilia/pro-coagulopathy, especially in younger patients (eg antiphospholipid, factor V leiden, protein S and protein C def - [[Sickle Cell Anaemia]] - syphilis (rare) **Exam** - [[Relative afferent pupillary defect|RAPD]] - visual acuity <6/60 - asymmetric [[red reflex]] - pale optic disc - retinal white oedema of infarction (usually takes >24 hours to develop) - cherry red spot of macula due to surrounding oedema ![[Painless loss of vision#Central retinal artery occlusion CRAO vs Central retinal vein occlusion CRVO]] **Investigations** - as for TIA - carotid doppler - ESR and CRP for vasculitis ![[Pasted image 20240328134343.png]] key fundoscopic findings in acute central retinal artery occlusion include general pallor of the retina (except the cherry red spot where the perfused choroid shows through the thinner fovea) and attenuation of retinal arteries (possibly with retinal veins preserved as in the photo above). ![[Pasted image 20240328192815.png| Cherry red spot of the fovea]] # management Retinal artery occlusion is an **eye emergency**. Patients should be referred to the nearest stroke center for further immediate management. need treatment within 90 minutes to prevent permanent retinal damage **Treatment** - digital massage - hypercarbia - diuretics - topical beta blockers - carbonic anhydrase inhibitors (acetazolamide 500mg IV stat) - Digital massage - Hypercarbia - Carbogen 95% O2 + 5% CO2 - Diuretics - Topical beta blockers - Retrobulbar anaesthesia with lignocaine (lidocaine) may relieve vasospasm - Carbonic anhydrase inhibitors - Acetazolamide 500 mg IV stat - Aqueous humor paracentesis if resistant after 30 minutes (after consultation with an ophthalmologist) - Insert a 25 G (or smaller) needle at outer border of iris in a medial direction - Role of anticoagulation / thrombolysis uncertain - a recent randomised trial showed no benefit of local arterial fibrinolysis over conservative treatment > Limited evidence about which (if any) of these interventions may produce benefit ## thrombolysis doesn’t work ==There are no evidence based therapies that have demonstrated efficacy in improving visual outcomes==, and a [meta-study](https://pubmed.ncbi.nlm.nih.gov/26258861/) has suggested that some therapies may be worse than the natural course. Some of these are described below.  Clot busting tissue plasminogen activator (tPA) was evaluated in the [EAGLE study](https://www.ncbi.nlm.nih.gov/pubmed/20609991), which was a randomized controlled trial comparing intra-arterial fibrinolysis to placebo. The study did not recommend intra-arterial tPA for acute CRAO because of significant symptomatic intracranial hemorrhage without evidence of visual benefit. The trial was terminated early due to the adverse effects of tPA.