From the Guidelines
Central retinal artery occlusion (CRAO) is a medical emergency that requires immediate attention, ideally within 4-6 hours of symptom onset, to prevent permanent vision loss, as recommended by the American Heart Association 1. The central retinal artery is the main blood vessel that supplies oxygen and nutrients to the retina of the eye, and its blockage can cause sudden, painless vision loss in the affected eye.
- The central retinal artery enters the eye through the optic nerve and branches into smaller vessels that nourish the inner retinal layers.
- It is a branch of the ophthalmic artery, which itself originates from the internal carotid artery.
- CRAO is considered an ocular emergency that can cause severe visual loss and is a harbinger of further cerebrovascular and cardiovascular events, as stated in the scientific statement from the American Heart Association 1.
- Treatment approaches may include ocular massage, anterior chamber paracentesis, breathing a mixture of 95% oxygen and 5% carbon dioxide, or medications to lower intraocular pressure.
- The central retinal artery is particularly vulnerable to emboli, thrombosis, and inflammatory conditions, which is why patients with CRAO should undergo cardiovascular evaluation to identify underlying systemic conditions like carotid artery disease, cardiac valvular disease, or hypercoagulable states that may have contributed to the occlusion, as highlighted in the Preferred Practice Pattern (PPP) by the Ophthalmology journal 1.
- Risk factors for CRAO include cigarette smoking, hypertension, high serum lipid levels, coagulopathy, body mass index, diabetes, and cardiac disease, including atrial fibrillation, which are all important modifiable risk factors associated with retinal emboli 1.
From the Research
Central Retinal Artery Occlusion
- Central retinal artery occlusion (CRAO) is a sudden, frequently irreversible, monocular vision loss, analogous to acute cerebral ischemia 2.
- The individual etiology of CRAO remains unclear in many cases, with potential pathomechanisms including embolism, vasoobliteration, and vascular compression 3.
- Emboli, which can be calcified, thrombotic, myxomatous, bacterial, or cholesterol, are often of carotid or cardiac origin 3.
- Atherosclerotic plaques, giant-cell arteritis, and other types of vasculitis may cause vasoobliteration, while a retrobulbar mass can lead to optic nerve and central retinal artery compression 3.
Symptoms and Diagnosis
- CRAO leads to a unilateral acute painless loss of vision 3.
- Funduscopic signs of CRAO are described, and late development of iris neovascularization and neovascular secondary glaucoma may occur in up to 15% of cases 3.
- The prognosis of CRAO has been poor, with spontaneous remission and recovery of visual function being rare 3.
Treatment
- Initial treatment should include immediate paracentesis of the anterior chamber, digital massage of the globe, and intravenous administration of azetazolamide to stimulate retinal reperfusion by lowering intraocular pressure 3.
- Selective intra-arterial fibrinolysis with Urokinase or recombinant plasminogen activator (rtPA) has shown promising success rates 3.
- However, a multicenter randomized trial found that local intra-arterial fibrinolysis (LIF) using rtPA did not improve visual outcomes compared to conservative standard treatment (CST) and had a higher rate of adverse reactions 4.
- Management of CRAO should be focused on secondary prevention of vascular events, such as cerebral ischemia, myocardial infarction, and cardiovascular death 5.
Timing and Mode of Presentation
- The mean time from onset of vision loss to presentation is around 31 hours, with 58% of patients presenting within 20 hours of vision loss 2.
- The majority of patients present first to a general practitioner, and the mean delay from referral to assessment by an in-hospital ophthalmologist is around 5 hours 2.