CataractsDefinition: opacity of the lensPathophysiology:

Lens looses water Density increases Lens becomes opaque

Etiology/Genetic Risk (see table 50-2) Congenital Age-related most common, > age of 70 Traumatic Toxic agents Other diseases

PreventionSunglassesEye protection

Clinical Manifestations (see chart 50-6)No pain or eye redness w/ age related

cataractsBlurred visionDouble vision Impaired color perceptionAbsent red reflexCloudy, whitish pupil

InterventionsPhacoemulsion

Extracapsular extraction of lens Intracapsular extraction

Disadvantage: greater risk for retinal detachment, loss of structural support for implanted lens

Corrective vision after implant may be 20/20 for distance, may require reading glasses, may require no glasses at all.

Preop care Outpatient procedure great need for preop teaching Drop instillation technique Medications given: (see chart 50-2 on drug therapy)

Sedative, Acetazolamide, Mitotics, Sympathomimetics, eye paralytics, anesthesia agents

Post op careMeds

Antibiotics, steroids, mild analgesics (AVOID ASA)Dark glassesS/S of trouble:

Pain early after surgery, esp. if assoc. w/ N/V Infection: increasing redness, change in visual acuity,

tears, photophobia, yellow/green drainage Bleeding w/ assoc. vision changes report

immediatelyHome care instructions

Light housework, cooking See table 50-3 avoid these activities See Best Practice for Eyedrop Administration chart

50-5

GlaucomaPathophysiology

Normal IOP = 10-21 mm HgDecreased outflow of aqueous fluidOverproduction of aqueous humorResulting in increased IOPIncreased pressure within eye reduces blood

flow to optic nerve and retina ischemia and death, blindness.

Starts at periphery and works toward center of vision classic sign of tunnel vision.

Painless, loss of vision so insidious as to not be noticable until it’s too late.

Age-relatedOccurs in about 10% of people older than 80

EtiologyPrimary open-angle

Most common Usually bilateral, asymptomatic in early stages Outflow reduction, pressure 22-32mm Hg

Angle-closure Narrow angle, acute glaucoma Sudden onset medical emergency Outflow blockage, pressure 30mmHg or higher

Secondary Results from ocular diseases which cause narrowing

of chamber angle or increased fluid volume within eye

Sudden

InterventionsPrimarily drug therapy

See chart 50-2 Drug Therapy for Eye Problems See Evidence Based Practice: adherence to ocular

drug txSurgical Management – when drugs don’t work

Laser surgery trabeculoplasty

Standard surgical therapy To create new drainage channel Destroy structures that are overproducing aqueous

humor

See Chart 50-10 Nursing Focus on the Older Adult

Diabetic RetinopathyPathophysiology

Complication of diabetes mellitus poor BS control

Background retinopathy Cells of retinal vessels die with leakage of fluid into

eye creating thick yellow-white hard exudates Microaneurysms form leading to hemorrhages in

nerve layer of retina Visual acuity is reduced

Proliferative retinopathy Network of fragile new blood vessels develop, leak

blood and protein into surrounding tissue Leads to reduced visual acuity/blindness

Treatment dependent on severity of retinal damage

Use of laser therapy to seal microaneurysms, decrease bleeding

Vitrectomy performed if frequent bleeding into vitreous occurs and retinal detachment becomes high risk.

Macular DegenerationPathophysiology

Atrophic = age related, dry Gradual blockage of retinal capillaries leading to

ischemia and death of retinal cells blindness Long term dietary intake of antioxidants and lutein and

zeaxanthin may decrease risk of disease or slow progression of disease process

Exudative = wet Sudden decrease in vision after serous detachment of

pigment epithelium in macula Blood collection under macula causes scar formation,

visual distortionTreatment goal

Maximize remaining vision

Review Trauma section in text pg 1105-1106HyphemaContusionForeign bodiesLacerationsSee Best Practice for eye irrigation

Be sure to read Key Points at chapters end

Meniere’s DiseasePathophysiology

TinnitisUnilateral sensorineural hearing lossVertigoAttacks sudden, can last daysCaused by overproduction of or decreased

reabsorption of endolymphatic fluid distortion of inner canal system of the ear

Eventual hearing loss – permanentCause unknown but is associated w/ infections,

allergic reactions, fluid imbalances, long term stress

Age 20-50 yearsWhite malesPrelude to attacks: HA, increasing tinnitus,

feeling of fullness in affected earPeriods of remission early in disease processHearing loss develops with increase in

attacksPatient c/o n/v, rapid eye movements =

nystagmus, severe HA.

Interventions:Drug therapy – primarily for control of

symptoms Diuretics, nicotinic acid, antihistamines,

antiemetics, diazepamSurgical management

Last resort deafness in affected ear Labyrinthectomy Endolymphatic decompression

Inner ear drained and shunt placed Retention of hearing Short term vertigo

Be sure to review Key Points at chapters endYou are also responsible for any general

nursing care that would apply to the disease you have learned about, ie, hearing loss, etc.