Chronic Vision Loss Flashcards
Causes of chronic vision loss
Progressive vision loss: Cataract, AMD, Glaucoma, Amblyopia
Acute/chronic: Diabetic retinopathy
Misc: Refractive error, dry eye, cornea
Cataract
Lens clouding
33% of all blindness
Prevalence increases w/ age (typically 60s-80s)
Cataract Sx
Progressively blurry vision (typically over years)
Halos, Glare
Sx tend to be worse @ night (increasingly worse night driving)
Nuclear sclerosis cataract
Center of lens progressively clouds w/ age
Possible associations: UV, diet, systemic disease, free radicals
Myopic shift can occur d/t cataract
Posterior subcapsular cataract
Clouding of posterior lens aspect
Usually small/thin but greatly affects vision
Ass w/ dibetes, steroid usage
Can develop quickly
Cortical cataract
Cortex changes
Usually spoke-like
Rarely affect vision unless in visual axis (as they become more progressed)
May cause more glare
Miscellaneous cataracts
Traumatic (post-surgical or other)
Congenital (e.g. metabolic disorder)
Cataract Tx
Extraction (If functionally significant)
Generally, when vision < 20/40, glare, halos (difficult to drive, read, etc.)
Do the benefits of extraction outweigh risks? If not, don’t perform
Cataract Extraction
Small incision @ edge of cornea
Break cataract w/ phacoemulsification & suction out
Leave edge of capsule to attach new IOC lens
Feel grittiness in eye at first, goes away in a couple days
Typically under conscious sedation, occasionally paralyze EOM, rarely under full anesthesia
Age-related macular degeneration (AMD)
Blurred/no vision in center of visual field
1.75 million in US
LEADING CAUSE OF IRREVERSIBLE BLINDNESS IN DEVELOPED COUNTRIES
Ass w/ family hx, caucasian, smoking, age
Dry/non-neovascular AMD
80-90%
Drusen (yellow deposits) formation
Loss of retinal pigment epithelium –> atrophy of photoreceptors (geographic atrophy)
Wet/neovascular AMD
10-20%
Neovascular membranes form under retina
New vessels leak, fluid accumulates in retina
AMD Sx
Blurry vision centrally
Peripheral vision spared
May be distorted (Amsler grid)
AMD Dx
Fluorescein angiography (ID leaky vessels, wet vs. dry) Optical coherence tomography/OCT (Cross section of macula, ID fluid under retina)
AMD Tx
Prevention - Don’t smoke, AREDS2 vitamins for dry AMD (Vitamin C, Vitamin E, Lutein, Zeaxanthin, Zinc) reduce pt. going from dry –> wet by 25%
Neovascularization Tx: Anti-VEGF injections to prevent new vessel growth. Monthy-ish
Glaucoma
Death of retinal ganglion cells High IOP does NOT = glaucoma Loss of peripheral vision, slow development of tunnel vision (Rarely blinds) SLOW 6-8x more common in Blacks Ass. w/ advanced age, family hx
Glaucoma Pathophysiology
Unknown.
Damage to cell bodies or axons primarily?
Ocular hypertension, low tension glaucoma
Types of Glaucoma
Primary open angle
Acute angle closure
Chronic angle closure
Secondary
Primary open angle glaucoma
Trebecular meshwork open and functioning
Fluid not draining fast enough (increased humor production) and pressure increased
Acute angle closure glaucoma
Trebecular meshwork closed off
Iris too close to cornea/closes off
Patient ed. w/ glaucoma tx
Pt. quit glaucoma meds and say they feel great, glaucoma isn’t getting worse.
BUT –> only advanced visual field defects are noticeable
SO –> meds are preventing or slowing worsening of glaucoma, even if “not noticeable”
AND –> if you stop meds, glaucoma will slowly get worse
Glaucoma Exam
Increased cup:disc ratio often seen (but not always)
Glaucoma Dx
Increased IOP, cup/disc ratios
Decreased visual fields, retinal nerve fiber layer on OCT
Glaucoma Tx
Drops! Prostaglanding, beta-blocker, alpha agonist, carbonic anhydrase inhibitor
Laser directly into trabecular meshwork (decreases pressure and opens drainage); Similar to adding a drop
Surgery: (Trabeculectomy, Tube (possibly valved), Mini-shunt) - allows drainage, works well, but can fall out, needs lots of follow-u and may still need drops
