Interferences to Safety Needs Due to Sensory Deprivation and Aging
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Transcript Interferences to Safety Needs Due to Sensory Deprivation and Aging
Cataracts
Definition: opacity of the lens
Pathophysiology:
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
Prevention
Sunglasses
Eye protection
Clinical Manifestations (see chart 50-6)
No pain or eye redness w/ age related cataracts
Blurred vision
Double vision
Impaired color perception
Absent red reflex
Cloudy, whitish pupil
Interventions
Phacoemulsion
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 care
Meds
Antibiotics, steroids, mild analgesics (AVOID ASA)
Dark glasses
S/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 immediately
Home care instructions
Light housework, cooking
See table 50-3 avoid these activities
See Best Practice for Eyedrop Administration chart 50-5
Glaucoma
Pathophysiology
Normal IOP = 10-21 mm Hg
Decreased outflow of aqueous fluid
Overproduction of aqueous humor
Resulting in increased IOP
Increased 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-related
Occurs in about 10% of people older than 80
Etiology
Primary 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
Interventions
Primarily drug therapy
See chart 50-2 Drug Therapy for Eye Problems
See Evidence Based Practice: adherence to ocular drug tx
Surgical 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 Retinopathy
Pathophysiology
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 Degeneration
Pathophysiology
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
distortion
Treatment goal
Maximize remaining vision
Review Trauma section in text pg 1105-1106
Hyphema
Contusion
Foreign bodies
Lacerations
See Best Practice for eye irrigation
Be sure to read Key Points at chapters end
Meniere’s Disease
Pathophysiology
Tinnitis
Unilateral sensorineural hearing loss
Vertigo
Attacks sudden, can last days
Caused by overproduction of or decreased reabsorption
of endolymphatic fluid distortion of inner canal
system of the ear
Eventual hearing loss – permanent
Cause unknown but is associated w/ infections, allergic
reactions, fluid imbalances, long term stress
Age 20-50 years
White males
Prelude to attacks: HA, increasing tinnitus, feeling of
fullness in affected ear
Periods of remission early in disease process
Hearing loss develops with increase in attacks
Patient c/o n/v, rapid eye movements = nystagmus,
severe HA.
Interventions:
Drug therapy – primarily for control of symptoms
Diuretics, nicotinic acid, antihistamines, antiemetics,
diazepam
Surgical 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 end
You are also responsible for any general nursing care
that would apply to the disease you have learned
about, ie, hearing loss, etc.