eyes and vision problems

myopia

nearsightedness

hyperopia

farsightedness

astigmatism

problems with focus

persbyopia

lens loses elasticity (reading glasses)

Arcus senilis (aging)

harmless opaque, bluish-white ring/outer edge of cornea

Cataracts

OPACITY (clouding) of lens

With aging starting at 50~ lens gradually loses water, ↑ density

◼ Painless/ no redness loss of transparency, blurring of vision

• other reasons my include: trama, toxin (steroids), DM, down syndrome

◼ Can occur in both eyes, at different rates

complication are glaucoma, retinal detachment, retinitis pigmentosa

diagnose cataracts

Impaired sensory perception

◼ Retinal/ophthalmoscopic exam after pupil dilation

Snellen Chart

cataracts trx.

surgery → full vision improvements in 4-6 weeks

surgry is done when ADLs are affected

Phacoemulsification: High-frequency sound waves break up lens

pieces, removed by suction, capsule intact

cataracts pre op and teaching

assess ability to instill eye drops several X/day

◼ Ask about meds affecting clotting (ASA, warfarin, clopidigrel)

◼ Teaching re: complications to monitor

Increased intraocular pressure (IOP) & infection

cataracts post op

• eye drop regimen at home ( schedule, eye drop guide, timer)

• avd activities that inc intraocular pressure

• protective eye shields at night, new driving avoid bright light so wear dark glasses

normal cataract post op expectation

slightly swollen, bloodshot, mild discomfort, itching

cataracts post op complications

Report S/S acute rise in IOP or hemorrhage ~ EMERGENCY

Sudden sharp unrelieved PAIN with N & V

◼ Bleeding, ↑ discharge from eye

◼ Report S/S infection

◼ Yellow/green thick drainage

Glaucoma

Increased intraocular pressure (↑ IOP)

Fluid pressure within eye (aqueous humor [AH])

◼ Optic nerve atrophy

◼ Visual field loss

If too high ~ compression of retinal blood vessels

& photoreceptors/nerve fibers…ischemia/death

◼ If too many affected ~ permanent blindness

no known way to prevent

Primary Open-angle (POAG) ~ more common

◼ Affects both eyes, develops gradually/unnoticed

◼ NO S/S early ~ “thief in the night”

◼ Vision foggy, headaches later ~ halos late

Primary Angle-Closure Glaucoma (PACG)

◼ ACUTE, less common, ONE eye only/blockage

◼ Sudden onset ~ EMERGENCY

s/s of POAG

gradual loss of visual field, painless

s/s of PACG

acute, sudden severe pain, rainbow halos/lights

While glaucoma _____ _____ ______,

blindness from glaucoma CAN be

prevented with _____ _____, lifelong

treatment & close monitoring.

Since majority of cases are POAG &

have no early S/S…

____ ____ ____ are a must!

• cannot be prevented

• early detection

• Regular eye exams

glaucoma med goals

does not improve vision already lost it just prevents futer damage damage by ↓ IOP.

lifelong trx schedule so adherence is key

Standard tx for POAG and teaching

Eye gtt regimen

• main goal to lower IOP

• 2-4 X/day, usually 2-3 different drops

  ◼ Must wait 5-10 min between drugs to prevent wash out so teach about adherence, good hand washing and maintaining a good schedule, avd touching eye with tip

comp: Punctal Occlusion: Pressure at corner of eye near nose immediately after to prevent systemic absorption

Glaucoma drug therapy first line agents beta blockers- timolol (Timoptic)

precautions: systemic infection, bradycardia so check pulse at home 2x/day, bronchoconstriction

Glaucoma drug therapy first line agents Prostaglandin Analogs- Latanoprost (Xalatan)

Can ↑ brown pigmentation of iris/eyelid & growth of eyelashes but can cause Engorgement ocular blood vessels

Glaucoma drug therapy first line agents Alpha2-Adrenergic Agonists - brimonidine (Alphagan)

• L-T use

• ↓ AH formation & ↑ outflow

• dry mouth, headache, blurred vision

Precautions: Wait 15 mins before putting contact lenses

Glaucoma 2nd Line Agents Pilocarpine

• Short-acting (4 X/day)

• Emergency tx of acute angle-closure form

TYPICAL APPROACH to TX

Start with timolol, brimonidine, or latanoprost…monitor

Glaucoma ~ Care Coordination

Teaching ~ Proper Instillation/schedule of gtts

◼ Lifelong…..ADHERENCE is key

• Handwashing, return demonstration

• timer/reminder system

Regular medical F/U & monitoring S/S infection, inc IOP

Macular Degeneration

Deterioration of the macula → Central vision deficits

age related AMD

Drusen ~ yellow deposits under the retina; ↑ risk

◼ Progressive deterioration over time

Dry AMD (non-exudative)

gradual blockage of retinal capillaries become ischemic, necrotic where Distortion at 1st, then bilateral central vision decline

Dry AMD (non-exudative) risk factors

55+, being White, family history

◼ DM, HTN, high cholesterol

NO cure; only mgmt to slow progression

• risk decreases with vitamin C,E, zinc

Wet AMD (exudative)

Sudden & more severe, any age

central vision loss

DRY form can develop WET

Once vision lost, cannot be regained

◼ Classic S/S ~ metamorphopsia (blurred lines)

Macular Degeneration DIAGNOSIS

Visual acuity test

◼ Dilated eye exam (drusen present?)

AMSLER GRID ~ metamorphopsia

◼ Checkerboard layout of lines to detect worsening AMD to wet form

Annual eye exams are important

trx for dry

High dose antioxidants (special formulation ~

vitamins A, C, E, beta-carotene & zinc) prevent

conversion to WET

trx for wet ( more serious form)

Meds very effective in preventing vision loss

◼ Vascular endothelial growth factor inhibitors

(VEGFIs) ~ angiogenesis inhibitors

what do VEGFIs do for macular degeneration

Intravitreal injections every 1-3 months ~ painless that induces angiogenesis, inc vascular permeability & promotes inflammation

AE for VEGFIs

Endophthalmitis (inflammation inside eye)

Macular Degeneration NC and teachings

Regular eye exams

◼ Dietary Salmon, carrots, sweet potato, broccoli, eggs

• High-dose vitamin/antioxidants (dry form): Oculite PreserVision

• wear sunglasses and dont smoke

• Use of Amsler grid at home to detect Dry → Wet