Diagnosing retinal artery occlusions
Retinal vascular disease can be difficult to accurately diagnose. There are a myriad of retinal disorders such as retinal phlebitis, retinal arteritis, intraretinal infiltrates, necrotizing retinitis, posterior scleritis, and chorioretinitis that can present with similar findings and complicate the diagnosis.
Retinal vascular disease can be difficult to accurately diagnose. There are a myriad of retinal disorders such as retinal phlebitis, retinal arteritis, intraretinal infiltrates, necrotizing retinitis, posterior scleritis, and chorioretinitis that can present with similar findings and complicate the diagnosis.
Retinal arterial occlusive disease can manifest as several different variations. The most common include central retinal artery occlusion (CRAO), branch retinal artery occlusion (BRAO), and cilioretinal artery occlusion (CLRAO). Almost all cases of retinal arterial occlusions (RAO) are caused by a thrombus, embolus, or thrombo-embolus.
A thrombus is a blood clot that is formed by blood coagulation in hemostasis. An embolus is any detached, traveling intravascular mass (solid, liquid, or gaseous) carried by normal circulation from one part of the body to a distal site.
A thrombo-embolus is a blood clot that detaches from the original site of coagulation and is carried by normal blood circulation to a site distant in the body.1 Other rare documented etiologies of RAOs include migraine, ocular surgery, intravitreal injections, chiropractic care, and infection.2
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Central retinal artery occlusion
The diagnosis of a CRAO in the acute phase is rather straightforward. Patients will often present with a history of sudden and profound vision loss, an afferent pupillary defect, opaque retina, cherry red spot, and retinal arterial attenuation. Less common findings in the acute phase include optic nerve swelling and optic disc pallor.3
A retinal embolus may be detectable in 23 percent of these cases.3 Prior reports indicate that 75 percent of these emboli are composed of cholesterol, 10 percent are calcific, and 15 percent are fibrinous.4
It can be more difficult to make the appropriate diagnosis when a patient presents with an old CRAO. Many patients with a CRAO do not recover vision after the insult and will have a best-corrected visual acuity (BCVA) in the 20/400 to light perception range. The patient will also have signs of arteriolar and venous narrowing, optic atrophy, an absent cherry red spot, and possibly arteriolar sheathing.3
It is important to note that retinal neovascularization is significantly less common with any RAO as compared to a vein occlusion; this is because vascular endothelial growth factor (VEGF) is released by hypoxic retina, not infarcted retina. This is not to say that neovascularization due to CRAO is impossible, however.
A recent study found the prevalence of neovascularization development to be 18 percent in patients with CRAO at an average of 8.5 weeks.5
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