Figure 12-1
Ophthalmic artery vascular anatomy
OA passes into orbit through optic canal where it travels with the optic nerve
Gives off central retinal artery (first branch) and posterior ciliary arteries near the orbital apex
Central Retinal Artery: main artery supplying the retina; gives off terminal branches (end arteries) that can be visualized by ophthalmoscopy
Posterior Ciliary Arteries: pierce the sclera and supply the uvea, optic nerve
Transient Monocular Blindness (TMB)
Transient retinal ischemia
Partial/complete dimming or obscuration of vision, lasting seconds to minutes, followed by total recovery
Commonly due to carotid disease
Retinal emboli
Thromboembolism (artery to artery or cardioembolic): pale white platelet plugs
Cholesterol (bright Hollenhorst plaques seen in central retinal artery)
Hypoperfusion – due to severe stenosis or occlusive disease leading to low retinal arterial pressure
Symptom onset is less rapid, and duration is longer than embolic TMB
Vision loss induced by situations that increase retinal oxygen demand (exposure to bright light)
Contrast acuity altered: bright objects appear brighter; darker objects more difficult to see
Symptoms more likely to recur
Provoked by systemic hypotension, venous hypertension , extracerebral steal
Either mechanism can lead to complete or partial vision loss of the ipsilateral eye
Associated with lower risk of future ipsilateral stroke than hemispheric TIA
Ophthalmic artery occlusion
Similar pathogenesis to ICA occlusion
Vision loss severe or permanent, with most patients having only residual trace light perception
Proximal OA occlusion may be asymptomatic due to ECA collateral flow
Clinical signs: opacified retina, faint or absent cherry red spot due to infarction of choroid, eye pain, pupillary dilation (concurrent ischemia to ciliary ganglion or iris sphincter), with chronic changes of optic atrophy and arterial attenuation
Central retinal artery occlusion (Fig. 12-2)
Figure 12-2
Central retinal artery occlusion (left). Note the pale retina and cherry red spot. Hollenhorst plaque (right) in a patient with acute monocular vision loss and hyperlipidemia
Due to occlusion of central retinal artery from embolic obstruction, thrombosis or hemorrhage, inflammatory (GCA, PAN, Buergers), angiospasm, hypotension, glaucoma, APLS
Most common emboli are cholesterol, platelet-fibrin, and calcium
Clinical signs: nonreactive pupil to direct light, preserved consensual response, cherry red spot on macula, white ground glass appearance of retina, absent temporal artery pulse in GCA
Treatment: lie patient flat, digital globe massage +/− anterior paracentesis by ophthalmology, consider tPA , Diamox or mannitol to reduce intraocular pressure
Branch retinal artery occlusion: embolism lodges at arterial bifurcation of CRA branch
Sudden loss of a visual field section
Clinical signs: visible retinal embolus
Treatment: same as CRAO
Ischemic optic neuropathy (ION): infarct of optic nerveGet Clinical Tree app for offline access
Ophthalmic artery provides blood supply to ON via two or more posterior ciliary arteries
Clinical signs: APD, loss of visual acuity
Etiologies
Nonarteritic (noninflammatory) occlusive disease: DM , HTN
Arteritic: inflammatory (GCA)
Embolic obstruction
Subtypes
Anterior (AION): swelling of optic disc, peripapillary hemorrhage
Visible optic disc pathology
Far more common than PION
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