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
Retinal Artery Occlusion
work up
Identify risk factors for cardiac sources of emboli: arrhythmia esp a fib, valvular disease
Monitor BP
Look for clues to giant cell arteritis : ≥ 50 yo, HA, scalp tenderness, jaw claudication, malaise, tenderness/thickening or absence of pulse of superficial temporal arteries.
Laboratory Findings
ESR and CRP usually elevated in giant cell arteritis
Screen for DM and hyperlipidemia in all patients.
Consider testing for coagulopathies: antiphospholipid antibodies, lupus anticoagulant, inherited thrombophilia, elevated plasma homocysteine, esp in younger patients.
Imaging
Ultrasonography of carotid arteries, ECG
CT or MR studies for internal carotid artery dissection, if suspected.
Retinal Artery Occlusion
Tx
Ocular massage (intermittent pressure applied to eye). Aqueous outflow is increased with pressure, retinal perfusion should improve once pressure is relieved; may also dislodge the embolism.
Reduction of intraocular pressure by IV mannitol or topical pressure-lowering drops.
Vasodilators to improve ocular blood flow: nitroglycerin.
Carotid endarterectomy/stenting.
In giant cell arteritis with vision loss, treatment is IVsteroids.
Ophthalmology referral to consider thrombolytic therapy or retinal artery embolectomy
Retinal Vein Occlusion
Essentials of Dx
Sudden or blurred vision (varies) monocular loss of vision.
No pain or redness.
Widespread or sectoral retinal hemorrhages.
[Can be non-ischemic (70%) or ischemic]
Central and Branch Retinal Vein Occlusion
general
Common causes of acute vision loss
Branch vein occlusions 4X more common than central vein occlusion
Retinal Vein Occlusion
patho
Reduced venous outflow (stasis), damage to the venous endothelium, hypercoagulable states increase risk for central retinal vein occlusion.
Increased IOP in glaucoma can compromise retinal vein outflow (stasis).
Central retinal artery shares common sheath of adventitia with central retinal vein. Through atherosclerosis, there may be compression of the vein by the artery, inducing central retinal vein occlusion (stasis).
vein occlusion
How does a vein influence ischemia?
Occlusion of central retinal vein leads to backup of blood in retinal venous system and increased resistance to venous blood flow.
Increased resistance causes stagnation of blood and ischemic damage to retina (sounds a bit like HF).
Retinal Vein Occlusion
Risk Factors
Older age
HTN
DM
ASCVD
Smoking
Obesity
Hypercoagulable state
Hyperlipidemia
Glaucoma
Retinal arteriolar abnormalities
Branch Retinal Vein Occlusion
general
Sudden or blurred (varies) loss of vision may occur if fovea is involved.
More gradual visual loss may occur with development of macular edema.
Retinal abnormalities (hemorrhages, microaneurysms, venous dilation and tortuosity, cotton-wool spots) confined to area drained by obstructed vein
Retinal Vein Occlusion
Work Up
Labs
Screening tests for DM, hyperlipidemia, and hyperviscosity
Particularly in younger patients, consider antiphospholipid antibodies, lupus anticoagulant, tests for inherited thrombophilia.
Retinal Vein Occlusion
Tx
Intravitreal injection of VEGF inhibitors benefits patients with macular edema.
Neovascularization
Eyes at risk for neovascular glaucoma following ischemic retinal vein occlusion: treat prophylactically with panretinal laser photocoagulation.
Retinal Vein Occlusion
prognosis
Severity of visual loss initially guides visual outcome.
Initial VA of 20/60 or better indicates good prognosis.
Visual prognosis poor for neovascular glaucoma.
Branch retinal vein occlusion: visual outcome determined by severity of glaucoma and macular damage from hemorrhage, ischemia, or edema.
Temporal Arteritis - Giant cell arteritis GCA
everything
Pathology
Inflammation of large to medium vessels
Remodeling can lead to vessel occlusion
Epidemiology
Age >50, Caucasian / Scandinavian, W>M
Symptoms
HA, scalp tenderness, temporal pain, jaw claudication, fever, amaurosis fugax
Diagnosis
History and exam
ESR >50, CRP less sensitive
Biopsy
Treatment
Prednisone IV or PO, high dose
Immunosuppressive drugs
GCA
general
Systemic inflammatory vasculitis, most common form of systemic vasculitis in adults
Unknown etiology
Classified as large-vessel vasculitisbut also involves medium and small arteries, esp superficial temporal arteries; affects ophthalmic, occipital, vertebral, posterior ciliary, and proximal vertebral arteries.
Histopath: transmural inflammation of intima, media, and adventitia; patchy infiltration by lymphocytes, macrophages, and multinucleated giant cells; can narrow arterial lumen, resulting in distal ischemia.
GCA
vision
Around 50% experience visual symptoms
Initial visual symptoms may be transient and intermittent, typically unilateral visual blurring or vision loss.
Retinal Detachment
Etiology
Nearsightedness and cataract extraction are most common risk factors – penetrating/blunt trauma and prior ocular surgery are also risk factors.
Most cases due to development of ≥ 1 peripheral retinal tears/holes
Most with retinal detachment are > 50. As patients age, vitreous liquefies and contracts, and traction tears develop, detaching retina from posterior wall of the eye.
Once there is a defect, vitreous is able to pass under the retina and progressive detachment results.
Retinal Detachment
Symptoms
Recent onset of, or increase in, floaters (moving spots or strands like cobwebs in the visual field) and photopsias (flashes of light)
Central vision remains intact until the central macula becomes detached.
Retinal Detachment
Shafer’s Sign: “tobacco dust”
Collection of brown pigmented cells in anterior vitreous following a break in retina.
Pigment granules thought to come from shearing force of the break in retinal pigment epithelium
retinal detachment
Red-pigmented cells in vitreous
Red-pigmented cells in vitreous indicate vitreous hemorrhage - 70% correlation with retinal tears.
