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Objectives
During this session we will:
1.Review the anatomy and physiology of the eye;
2.Discuss assessment of the eye;
3.Discuss common conditions of the eye; and
4.Discuss the management of patients presenting with
these conditions.
Diagnostic Evaluation
Ophthalmoscopy
Direct and indirect
Examines the cornea, lens and retina
Slit-lamp examination
Color vision testing
Amsler grid
Ultrasonography
Diagnostic Evaluation
Tonometry
Measures intraocular pressure
Gonioscopy
Visualizes the angle of the anterior chamber
Perimetry testing
Evaluates field of vision
Scotomas: blind areas in the visual field
Impaired Vision
Refractive errors
Can be corrected by lenses which focus light rays on
the retina
Emmetropia: normal vision
Myopia: nearsighted
Hyperopia: farsighted
Astigmatism: distortion due to irregularity of the cornea
Glaucoma
A group of ocular conditions in which damage to the optic
nerve is related to increased intraocular pressure (IOP)
caused by congestion of the aqueous humor
The leading cause of blindness in adults in the U.S.
Incidence increases with age
Eatiology
Primary glaucoma
No evidence of preexisting ocular or systemic disease
Secondary glaucoma
Occur from inflammatory processes that affect the
eye
Tumours
Trauma resulting in haemmorhage (cells obstruct out
flow of aquous humor)
Glaucoma
Risk factors
Others
Family history
Older age
Diabetes
Cardiovascular disease
Hypertension
African American
Myopia
Eye trauma
Prolonged use of
systemic
corticosteroids
Pathophysiology of Glaucoma
Normal IOP is 10-21mm Hg
In glaucoma, aqueous production and
drainage are not in balance.
When aqueous outflow is blocked, pressure
builds up in the eye.
Increased IOP causes irreversible
mechanical and/or ischemic damage.
Classification/Types of Glaucoma
Open-angle
Chronic open angle glaucoma
Normal tension glaucoma
Ocular hypertension
Close angle (Angle-closure- pupillary block) glaucoma
Acute angle-closure
Subacute angle-closure
Chronic angle-closure
Congenital glaucomas and glaucoma secondary to other
conditions
Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins
Classification/Types Contd.
Close angle (narrow angle)- accounts for 5-10%
of cases
Occurs as a result of an inherited anatomical defect
Causes a shallow/narrow anterior chamber
Outflow becomes impaired when iris thickens as a
result of pupillary dilation
Blocks circulation between anterior and posterior
chambers
Eliminates or reduce angel where aquos reabsorbtion
occurs
Closed Angle
Symptoms are related to a sudden increase in IOP:
occular pain
Blurred vision
Pupil may be enlarged
Symptoms relieved by sleep. If prolonged
Eye becomes reddened with corneal oedema (eye has
hazy appearance)
Headache
Nausea and vomiting may occur
Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins
Open angle
Most common form of glaucoma
Manifests after 35 yrs. of age and incidence of .5 to 2%
in persons 40yrs. and older.
Increased IOP occurs in the absence of obstruction at the
iridocorneal angle
Occurs as a result of an abnormality in the trabecular
meshwork that controls the flow of aquos humor in the
canal of schelmm
Usually asymptomatic
Clinical Manifestations
Asymptomatic
unaware of the condition until there is significant
vision loss
peripheral vision loss, blurring, halos, difficulty
focusing, difficulty adjusting eyes to low lighting
May also have aching or discomfort around eyes
Headache
Diagnostic Findings
Tonometry to assess IOP
Opthalmoscopy to inspect optic nerve
Gonioscopy to assess the angle of the
anterior chamber
Perimetry to assess visual fields
Progression of visual field defects
Optic nerve damage presents with
Pallor and cupping of optic nerve
Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins
Managment
Medical Management
Prevention of optic nerve damage
Life long therapy required
Pharmacotherapy
Aim to increase outflow of fluid
Miotics eg pilocarpine
Adrenagic agonists eg epinephrine
Increases production of aquos out flow
Pharmacologic therapy
Decreases aquos humor production
Beta blockers eg. timoxin
Carbonic anhydrase inhibitors eg. Methazolamide
Alphaadrenagic agonists eg. brimomidine
Prostaglandin analogs
Increases uveosceral outflow
Glaucoma
Surgical
Depends on cause of increase in IOP
Trabeculoplasty: opens intratrabecular spaces & the
canal of schelm
Iridotomy: opening in iris to correct papillary block
Filtering procedures drain aqeous humour into
subconjuctival space
Tribeculectomy: removal of part of the trabecular mesh
work
Drainage implant or shunts
Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins
Complications
Burns to cornea, retina or lens
Uveitis
Closure of iridotomy
Transient increase in IOP
Hemorhage
Cataract formation
Nursing Management
Patient education.
Adherence to therapy and continued care to prevent
further vision loss
Provide education regarding use and effects of
medications.
Medications used for glaucoma may cause vision
alterations and other side effects
Provide support and interventions to aid the patient in
adjusting to vision loss/potential vision loss.
Discharge Planning
Lifelong therapuetic regime for chronic
condition
Ensure pt. and family understands the
disease and how it progresses
Use of medication
Effect of medication
Follow up treatment
Infectious/Inflammatory Disorders
Conjuctivitis
Clinical manifestations:
Foreign body sensation
Scratching or burning sensation
Itching
Photophobia
Discharge, papillary formation, follicles
Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins
Conjuctivitis
Bacterial
Acute or chronic
Causative agents is strep pneumoniae, haemophilus,
influenza and staph. Aureus.
Onset is acute
Purulent discharge
Viral conjuctivitis
Adeno virus, herpes symplex
Acute or chronic
Watery discharge
Follicles prominent
pseudomembranes
Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins
Conjunctivitis
Assessment & Diagnostic findings
Appearance
Lymphadenopathy
Presence of pseudo or true membranes
Eye swab
Management
Depends on type
Antibiotic therapy (bacterial)
Corticosteroids and antihistamines (allergic)
Education to prevent spread (58:9)
Inflammatory Conditions
Cataracts
An opacity or cloudiness of the lens that interferes with
light transmission to the retina.
Most common cause of age related vision loss
Increased incidence with aging
Occur in 50% of persons 65 to 74 yrs. And in 70% of
persons 75yrs. and older
Cataracts
Etiology
Injury to lens
Aging process, diabetes
Prolong exposure to ultra violet light
Radiation
Drugs (corticosteroids)
Risk Factors
Aging
Other occula conditions (infections)
Toxic factors (corticosteroids, smoking)
Nutrition (poor)
Physical (trauma, ultraviolet radiation)
Diseases (diabetes, renal disorders)
Pathophysiology
May be unilateral or bilateral
Can develop in years or in months
With normal aging the nucleus and cortex of the lens
enlarge when new fibres are formed in cortical zone of
lens
Lens protein become more insoluble
Concentrations of calcium, sodium, potassium and
phosophate increases
Leads to loss of lens transparency
Cataracts
Types
Congenital
Traumatic/ secondary to disease
Further categorized by the part of lens that is affected:
Nuclear cataract formation
Cortical cataract formation
Posterior subcapsular cataract
Clinical Manifestations
Painless, blurry vision
Sensitivity to glare
Reduced visual acuity
Other effects include myopic shift
Astigmatism, diplopia (double vision),
color shifts including brunescens (color value shift to
yellow-brown)
Nursing Management
Preoperative care
Usual preoperative care for ambulatory surgery
Dilating eye drops or other medications as ordered
Antibiotic drops
Mydriatics
Enema to prevent constipation & straining post surgery
Facial scrub morning of surgery
Place personal items on bedside of unoperated eye
Educate on preventing stress on suture
Rubbing eye,
coughing, sneezing,
Copyright 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins