Acute vision loss/Macular degen Flashcards
age related mucular degeneration (AMD)
non-exudative/atrophy (dry)
Most common (90%)
Progression may take decades
Can progress to wet
Bruch membrane thickening -> Drusen proteins accumulates (between RPE and Bruch’s membrane) -> retinal atrophy -> degeneration
AMD
Exudative (wet)
Neo-vascularization
Progression over months, any age
Causes more devastating and sudden vision affects
Accumulated Drusen proteins causes break in Bruch’s membrane -> choroidal neovascularization -> vascular becomes weak and leaks blood and fluid -> scarring within macula
AMD
RF
Increasing age
Family history of AMD
Fair skin/blue eyes
Female
Obesity
Diabetes
Hypertension
High-fat diet / High cholesterol
Long-sighted
*Smoking- accelerates degeneration
Sunlight-accelerates degeneration
AMD
S/Sx
Loss of central vision (slower in dry and more rapid in wet)
Difficulty on tasks that require focusing (driving, reading)
Reduction of night vision
*Distorted lines and shapes
Central vision loss
drusen bodies/proteins with yellow/white deposits
AMD
Tx
Early ARMD requires no intervention (annual assessments important!)
Stop smoking
Vitamin supplementation (Vitamin E, A, Zinc)
Wet -> Laser photocoagulation surgery? Monthly Intravitreal injections?
Improve lighting, large print material, glasses if needed
Goal is to slow progression and keep independence
Amsler grid with AMD
Amaurosis Fugax (AF)
general
Describe vision loss
Transient monocular visual loss (“ocular TIA”)
Visual loss: curtain passing vertically across visual field with complete monocular visual loss lasting a few minutes; similar curtain effect as episode passes (“fleeting blindness”).
Other causes of transient visual loss due to ocular ischemia are giant cell arteritis, hypercoagulable state, severe occlusive carotid disease/ retinal embolus from carotid disease or heart
*Great AF intro video: https://www.youtube.com/watch?v=kSN3_MJ9uH4
Amaurosis Fugax
Tx
If embolism suspected, immediate oralaspirin(at least 81 mg daily) or another antiplatelet drug until cause determined.
Assess carotids
Carotid bruit
Doppler US
Consider urgent carotid endarterectomy or angioplasty with stenting if significant ipsilateral carotid artery stenosis.
“retinal claudication” = severe carotid occlusive disease with dimming of vision in one eye after exposure to bright light
Control HTN.
Retinal embolization due to a fib → anticoagulation based on CHA₂DS₂-VASc.
Retinal Artery Occlusion
Essentials of Dx
Sudden monocular loss of vision.
No pain or redness.
Widespread or sectoral pale retinal swelling
Retinal Artery Occlusion
RF
DM, hyperlipidemia, systemic HTN are common etiologies.
Other causes: giant cell arteritis, hypercoagulable state (including meds that increase coag risk), hyperviscosity, severe occlusive carotid disease.
Consider internal carotid artery dissection if neck pain/recent history of neck trauma.
CentralRetinal Artery Occlusion
general
Sudden profound monocular visual loss.
Visual field may be restricted to an island of vision in temporal field.
Pale swelling of retina with cherry-red spot at fovea.
“Box-car” segmentation of blood in vessels as RBCs separate from serum when blood flow is slowed.
Emboli may be seen in central retinal artery or branches.
Time is retina: irreversible vision loss after 120 minutes
halo around fovea, central artey occlusion
Central retinal artery occlusion
Branch Retinal Artery Occlusion
general
May also present with sudden loss of vision if fovea is involved
Usually sudden loss of discrete area in visual field in one eye
Retinal swelling and cotton-wool spots (nerve fiber infarctions) limited to area of retina supplied by occluded branch