Problems of the Eye

7/28/2019 Problems of the Eye

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EXTERNAL AND ACCESSORY STRUCTURES:

The adult eye is a sphere that measures about 1

inch (2.5 cm) in diameter. Only the anterior 1/6 of the eyes surface can

normally be seen.

The accessory structures of the eye include:

Extrinsic eye

Eyelids

Conjunctiva

Lacrimal apparatus


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a. Extr ins ic eye muscles-are attached to the

outer surface of the eye. These muscles

produce gross eye movements and make itpossible for the eyes to follow a moving

object.

Name Action Controlling Cranial

Nerve

Lateral Rectus

Medial Rectus

Superior rectus

Inferior Rectus

Inferior ObliqueSuperior

Oblique

Moves eye laterally

Moves eye medially

Elevates eye

Depresses eye

Elevates eye and turns it laterally

Depresses eye and turns it laterally

VI (abducens)

III (oculomotor)

III (oculomotor)

III (oculomotor)

III (oculomotor)

IV (Trochlear )


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b. Eyelids -anteriorly the eyes are protected by the

eyelids, which meet at the medial and lateral corners

of the eye, the medial and lateral canthusrespectively.

Protecting from the border of the eyelid are the

eyelashes . Modified sebaceous glands associated with the eyelid

edges are the meibomian glands. (these glands

produce an oily secretion that lubricates the eye)

Ciliary glands, modified sweat glands, lie between theeyelashes.


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c. Conjunct iva-a delicate membrane that lines the eyelids

and covers part of the outer surface of the eyeball. It

secretes mucus, which help the eyeball and keep it

moist.

d. Lacrim al apparatus -consist of lacrimal gland and a

number of ducts that drain the lacrimal secretions into the

nasal cavity.


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INTERNALSTRUCTURES: THEEYEBALL

a. SCLERA

Outer most layer of the eyeball/ outer most tunic

Dense fibrous tissue and forms a white opaque

membrane around the eyeball except at the cornea

The transparent window is the corneathrough which

light enters the eye.

Corneais well suplied with nerve endings. Most are pain

fibers, when the cornea is touched, blinking and

increased tearing occur.

Corneais the only tissue in the body that can be

transplanted from one person to another without worry of

rejection.


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b. CHOROID

Middle layer

Highly vascular and pigmented area responsible fornutrient exchange (contains a dark pigment).

Anteriorly the choroid is modified to form two smoothmuscle structures, the ci l iary body-to which thelens is attached, and the i r is.

the pigmented iris has a rounded opening, the pup i lthrough which light passes.

Pupil- regulates the amount of light entering the eyeso that one can see as clearly as possible in theavailable light. In close vision and bright light, the circular muscles contract

and pupil constrict

In distant vision and dark light, the radial fibers contract toenlarge (dilate )


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c. RETINA

Innermost layer of the eyeball

Contains millions of receptor cells

2 specialized receptor (photoreceptors)

Cons daylight vision details and colors of

the objectRods night vision visualization of outline of

objects without revealing color or detail very

sensitive to movement of objects in visual

fields


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LAYERS OF THE EYE


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RETINAASSEENTHROUGHANOPHTHALMOSCOPE


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CAVITIES OF THE EYE

ANTERIOR CAVITY filled with WATERY aqueous humor

Anterior chamber fluid filled space posterior to the cornea and

anterior to the lens and iris

Posterior chamber bounded by iris, lens and ciliary muscles

POSTERIOR CAVITY

Space behind the lens filled with gelatinous vitreous humor


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CAVITIES OF THE EYE


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DEFINITION OF TERMS

VISION Passage of rays of light from an object through the cornea, aqueous

humor, lens and vitreous humor to the retina and its appreciation in thecerebral cortex

IRIS The colored portion of the eye

LENS Crystalline lens, transparent biconvex structure attached to the ciliary

muscle ligament

PUPIL Central opening in the iris responsible for controlling the amount of light

entering the eye by changing its sizeACCOMMODATIONS

Ability of the crystalline lens to vary its refractive power throughrelaxation or contraction of the ciliary muscle, allow clear vision tomaintain when changing vision from distant to near object


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CILIARY MUSCLE

Facilitates light and accommodation reflexes

REFRACTION

Bending the rays of light by contraction and relaxation of the

ciliary muscle causing the lens to change its thickness

Relaxes for distant vision, lens flattened

Contracts for closer vision, increase curvature of the lens.

NEAR POINT

Closest point at which a person can clearly fucos on an object


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LAYERS

10 layers:

Outermost: retinal pigment epithelium (RPE) single layer

Innermost: neuroretina:

- Ganglion cell layer, axons form optic nerve

- Bipolar nerve layer

- Photoreceptors (cons & rods)


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PHOTORECEPTORS

Convert light into electrical

signals

Rods:

For night vision

Do not signal wavelength

information (color)

Cones:

For daylight and color vision

High threshold to light

Concentrated at the fovea


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DIRECTIONOF LIGHT

Light pass through the ganglionand bipolar layers before

reaching the photoreceptors in

all areas of the retina except

the fovea.

In the fovea, the bipolar and

ganglion cell layers are pulled

aside so that light strikes the

photoreceptors directly.

Visual Processing


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ASSESSMENTOF

VISION


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1. Acuity

a. visual acuity test

measure the clients

distance and near

vision.

b. the chart is a

simple tool to record

visual acuity

* Snellen Chart-20/20

vision.


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2. Confrontational test

~ a test performed to examine visualfields or peripheral vision

~ the test assumes that theexaminer has normal peripheralvision

3. Extraocular muscle

Functiona. clients right (lateral position)

b. Upward and right (temporalposition)

c. Down and right

d. Clients left (lateral position)

e. Upward and left (temporalposition)

f. Down and left


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4. Color vision

Ishih ara color plate test-

for color blind people, to

identify the three primary

colors- red, blue and green

5. Pupils~ the pupils are round and equal

size (PERRLA)

6. Sclera and cornea~ normal sclera color is white


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1. Opthalmoscope- usually the pupil has to be

dilated with mydriatics. Changes in the optic

nerve head may indicate IOP.2. Perimeter-for measuring the boundary of the

field of vision. Normal field of vision is 90.

3. Bjerrrums Tangent Screen-to test for centralfield vision.

4. Gonioscopy- angle of the anterior chamber

can be seen.


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DIAGNOSTIC TESTS FORTHE EYE


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1. Sli t lamp exam

(Biomicroscope)-an

instrument used toexamine the anterior

segment of the eye under

great magnification by

means of binocular

microscope with a brilliantbeam of light for

illumination

2. Tonometer-accurate

measurement of IOP:normal: 10- 21 mmHg


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3. Fluorescein angiog raphy

~ detailed imaging and recording ofocularcirculation by a series of

photographs after the administration

of a dye

4. Compu ted tomog raphy

~ a beam of x- rays scans the skulland orbits of the eye

5. Corneal staining

~ a topical dye is instilled into theconjunctival sac outline irregulaties

of the corneal surface that are not

easily visible


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DISORDERSOFTHE

EYE


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A. RISKFACTORSRELATEDTOEYE

DISORDERS

Aging process

Congenital

Diabetesmellitus

Hereditary

Medications

trauma


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B. LEGALLY BLIND

Legal definitions

emphasize visual

acuity and residual

vision.

The best visual acuity

with corrective lenses

in the better eye of 20/

200 or less or visual

acuity of less than 20degrees of the visual

field in the better eye


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WHATARE SOME CAUSESOF

BLINDNESS

AND

LOW

VISION

?

Optical defects

Refraction focusing light as it passes through

different components of the eye Refractive errors are more common and include:

Astigmatism focusing problems whether stimuli are near or

far; usually present at birth; may cause headaches, nausea or

tired eyes

Hyperopia can see better at far distances than close up

Myopia can see better at close range than at distances


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SYMPTOMS OF

RETINAL DISEASES


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MACULARDYSFUNCTION


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MACULAR DYSFUNCTION

Disorder of the central part of the macula (fovea) causes

significant visual impairment, pt. may complain of:

Blurred central vision

Distorted vision (metamorphopsia): micropsia or macropsia,

occur if the photoreceptors become stretched apart or close

together.

Areas of loss of central visual field (scotomata), if part of the

photoreceptor layer becomes covered, e.g. by blood, or if the

photoreceptors are destroyed.


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Blurred central vision

Metamorphopsia

Scotomata


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PERIPHERAL RETINAL DYSFUNCTION

The pt. complains of:

Loss of visual field, detected clinically.

Some diseases may predominantly affect one type of

photoreceptors, ex. Retinitis pigmentosa and night vision.


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ACQUIRED

MACULAR

DISEASES


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AGE-RELATEDMACULARDEGENERATION

(AMD)

The commonest cause of irreversible visual loss in the

developed world.

Associated with increasing age and is typically bilateral

Pathogenesis:

Overtime undigested lipid products deposits in Burchs membrane, seenas yellow lesions called drusen.

Collection of drusen in the macula is termed age related maculopathy

(ARM)

Dry form: the neighboring RPE and photoreceptors show degenerative

changes

Wet/Exudative form: angiogenic factors (ex. VEGF) stimulate new vesselformation from the choroid through Bruchs membrane and RPE into the

sub retinal space forming sub-retinal neovascular membrane.


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Age-related macular degeneration

(AMD)


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(AMD)

Symptoms

Progressive, gradual loss of central vision leading to difficulty

in reading and recognizing distant objects

In the wet form, visual disturbance is sudden

Signs Yellow, well-circumscribed drusen

Areas of hypo/hyperpigmentation

Loss of foveal reflex

In wet, pre-retinal (more occasionally) or subretinalhemorrhage


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(AMD)

Investigations

Diagnosis is based on the appearance of the retina.

In suspected exudative AMD and vision not severely affected

a fluorescein angiogram may be performed to delineate the

position of the sub-retinal neovascular membrane.

Prognosis

Dry AMD: progress very slowly , increasing difficulty in reading

Wet AMD: 75% of pt.s experience marked deterioration invision over 3 years.

A l t d l d ti


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Wet AMD Fluorescein Angiogram of Wet

AMD

Age-related macular degeneration

(AMD)


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(AMD)

Treatment

Active medical intervention remains of limited benefit

Dry AMD:

No treatment

Vision is magnified with low-vision aids (ex. Magnifiers, telescopes) Reassure that peripheral vision will not get affected (navigational vision is

retained)

Wet AMD:

Small proportion of pt.s can benefit

If the sub-retinal Vascular membrane is eccentric to the fovea it may be

possible to obliterate it with argon-laser treatment

Sub foveal vascular membranes can be obliterated by photodynamic

therapy (PDT)

The condition can recur


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(AMD)

Treatment

Recent trials show that drugs that inhibit angiogenesis may be

effective in wet AMD

High dose of antioxidant vitamin and mineral combinationhave limited effect


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MACULARHOLESANDMEMBRANES


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Well-circumscribed hole at the center of

the macule, resulting in major loss ofacuity.

Most are idiopathic in origin but theymay be associated with blunt trauma.

Unlike peripheral retinal holes, macular

holes are not usually associated withretinal detachments.

A pre-retinal glial membrane may formover the macular region, whosecontraction causes puckering of theretina

The early stages of hole formation maybe associated with distortion and mildblurring of vision.

These symptoms may be improved byremoving the membrane withmicrosurgical vitrectomy techniques.


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GASSMACULARHOLESTAGESARE:

Stage 1a: Foveal

detachment. Macular

cyst

Stage 1b: As the fovealretina elevates to the

level of the perifoveal,

the yellow dot of

xanthophyll pigment

changes to a donut

shaped yellow ring.


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Stage 2: This is the first

stage when a full-

thickness break in the

retina exists.

Stage 3: A full-thicknessmacular hole in the retina

exists..

Stage 4: A full-thickness

macular hole exists in the

presence of a completeseparation of the vitreous

from the macula and the

optic disc.


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The appearance of

a macular hole

Macular holes and membranes


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Macular holes and membranes

This is an OCT (optical coherence

tomogram) showing a macular holebefore and after surgery. The defect

in the upper picture is a macular

hole. The lower picture shows the

hole is closed and the retina has

reassumed a more normal

appearance


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MACULAREDEMA


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MACULAREDEMA

Accumulation of fluid within the retina itself

Ophthalmoscopy reveals a loss of the normal foveal reflex

If the diagnosis is in doubt a confirmatory OCT scan or

fluorescein angiogram can be performed.

May be associated with: intraocular surgery;

uveitis;

retinal vascular disease (e.g. diabetic retinopathy);

Rerinitis pigmentosa

Treatment can be difficult and is dependent on the associatedeye disease:

Steroids, macular edema due to uveitis

Acetazolamide, due to retinits pigmentosa or following intraocular surgery


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Retinal Pigment

Epithelium

Macular edema


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Macular edema

OCT scan showing macular eddema


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TOXICMACULOPATHIES


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TOXICMACULOPATHIES

The accumulation of somedrugs in the RPE can cause

macular damage.

These drugs include

chloroquine (more toxic)

and hydroxyxhloroquine

Patients on chloroquine

require regular visual

assessment for

maculopathy

Phenothiazines and

tamoxifen may also cause

maculopathy

Toxic maculopathies


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Toxic maculopathies

Bulls-eye appearance in chloroquine

maculopathy.


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POSTERIOR

VITREOUS

DETACHMENT


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POSTERIORVITREOUS DETACHMENT

The vitreous gel undergoes degenerative changes in patientsin their 50s and 60s (earlier in myopic) causing it to detach

from the retina.

This gives rise to acute symptoms of:

Photopsia (flashing lights).This results from traction on the retina by the

detaching vitreous.

A shower of floaters, representing condensations within the collapsed

vitreous and sometimes may indicate a vitreous hemorrhage when the

detaching vitreous ruptures a small blood vessel.

The symptoms are most marked on bright days when the

small pupil throws a sharper image on the retina. Acute vitreous detachment is an indication for full assessment

of the vitreous and peripheral retina.

POSTERIOR VITREOUS


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POSTERIORVITREOUS

DETACHMENT

Ultrasound picture showing a posterior

vitreous detachment. Note that the vitreous is

still attached at the optic disc and the ora

serrata.


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RETINAL

DETACHMENT


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RETINAL DETACHMENTRetinal detachment occurs

when the layers of the

retina separate because ofthe accumulation of fluid

between them or when

both retinal layers elevate

away from the choroid as aresult tumors

Partial separation becomes

complete if left untreated

When detachmentbecomes complete,

blindness occurs

Retinal detachment1 Cornea

2 Iris

3 Lens

4 Detached retina5 Eyebal


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Pathogenesis:

Rhegmatogenous

ret inal detachment:

most cases, tear in

retina vitreous in

sub-retinal space

Tract ion ret inal

detachment:

contracting fibrous

tissue, ex. DM

Exudative ret inal

detachment:fluids insub-retinal space, ex.

tumors


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A. RHEGMATOGENOUSRETINALDETACHMENT

Retinal separation associated with a break, hole or tear in thesensory retina.

1/1000, increased in:

High myopes patients

Cataract surgery complicated by vitreous loss

Detached retina in the other eye

Recent sever eye trauma

Tears: Most commonly associated with post. vitreous detachment (vitreous

traction)

Lattice degeneration


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RHEGMATOGENOUSRETINALDETACHMENT

Symptoms:

may be preceded by symptoms of a posterior vitreous

detachment

At onset, progressive development of a field defect, often

described as a shadow or curtain. Peripheral field loss (early)

Loss of central vision and marked decrease in visual acuity if

macula is detached

Loss of red reflex, degree depends on area of detachment


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Normal visionRetinal detachment


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Signs

The detached retina is visible on ophthalmoscopy as a

floating, diaphanous membrane.

Bullous retinal detachment: marked accumulation of fluid in

the sub-retinal space A tear in the retina appears reddish pink because of the

underlying choroidal vessels.

Vitreous hemorrhage

Rhegmatogenous retinal


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The clinical appearance of a retinal

detachment; note the retinal tear. The retina has

completely detached.

Rhegmatogenous retinal

detachment


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Management Only by surgery, aim is to close causative break and increase

retinal attachment by inducing inflammation either bycryoprobe or laser.

There are two major surgical techniques for repairing a retinaldetachment: external (conv ent ional approach );relieves vitreous traction,

sclerostomy may be needed first

internal (vitreoret in al su rgery);through pars plana, maintain headposture for several days, avoid air traveling

Check other eye for tears or asymptomatic retinal detachment.

In case of tears without detachment, surgery is doneprophylactically.


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Prognosis

Successful surgery: excellent vision

Macula detached more than 24 hours: acuity not recovered

completely, months to restore part of vision

Complication in surgery: fibrotic changes may occur in the

vitreous (proliferative vitreoretinopathy, PVR). This may cause

traction on the retina and further retinal detachment.


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B. TRACTIONRETINALDETACHMENT

The retina is pulled awayfrom the pigment epitheliumby contracting fibrous tissuewhich has grown on theretinal surface.

Seen in: Proliferative diabetic retinopathy

Proliferative vitreoretinopathy

Vitroretinal surgery

May be in association withrhegmatogenous retinaldetachment


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C. EXUDATIVERETINALDETACHMENT

Detachment of the retina without retinal break, arising frominflammatory disease of choroid, retinal tumors, and retinal

angiomatosis.

Seen in:

Posterior uvitis

Intraocular tumors

Toxemia of pregnancy

Central serous retinopathy affecting the macula

Only macular involvement is symptomatic

May not be detected on direct ophthalmoscope

Foveal detachment results in permanent impairment of visual

acuity


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ASSESSMENT:

Flashes of light

Floaters

Increased in blurred

visionSense of a curtain

being drawn

Loss of a portion


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IMMEDIATEINTERVENTIONS:

Provide bed rest

Cover both eyes with patches to prevent further

detachment

Speak to the client before approaching

Position the clients head as prescribed

Protect the client from injury

Avoid jerky head movements

Minimize eye stress Prepare the client for the surgical procedure as

prescribed


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SURGICALPROCEDURES

Draining fluid from thesubretinal space

Sealing retinal breaks by

cryosurgery

Diathermy

Laser therapy

Scleral buckling

Insertion of gas or silicone

oil


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CATARACT


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Cloudy area in ocular lens

An opacity of the lens thatdistorts the image projected

onto the retina and that canprogress to blindness

Most commonly a result ofdegeneration and othercongenital cause

Partial or total opacity of thenormal transparentcrystalline lens

It is a common cause ofgradual vision loss

The light that enters through

the cornea is blocked by theclouded lens

It affects both eyes, but eachcataract progressesindependently


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CAUSES

AGING PROCESS Senile cataracts chemical changes in lens proteins

Trauma From foreign body injuries of the lens with sufficient force to allow

the aqueous or vitreous humor enter the lens

Congenital Neonates from newborn error of metabolism or from maternal

rubella infection during the first trimester

Congenital anomaly or from genetic causes

Uveitis, glaucoma, retinitis pigmentosa, retinal detachment,DM, hypoparathyroidism or from radiation or infrared rays Complicated cataracts

Intraocular surgery

Steroid therapy, napthalene Toxic cataract


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SIGNS AND SYMPTOMS

OBJECTS APPEAR DISTORTED AND BLURRED Painless gradual vision loss

Annoying glare and poor vision on bright sunlight

Decrease visual acuity

Seeing better in dim light than bright light Pupil changes from black grey to milky white

Optical aberrations

Spots or halos

GlaucomaAbsence of the red reflex


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DIAGNOSTIC TESTS

Visual acuity Confirms the degree of vision loss

Slit lamp exam

Confirms the diagnosis of a lens opacity

Indirect ophthalmoscopy

Reveals dark area


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NURSING INTERVENTION

Surgical removal of the lens, one eye at a time, isperformed

With extracapsu lar extract ionthe lens is lifted out

without removing the lens capsule, the procedure may

be performed by phacoemulsification in which the lens isbroken up by the ultrasonic vibrations and is extracted.

With in tracapsular extract ion th e lensis removed

within its capsule through a small incision

A part ial ir idectomymay be performed with the lens

extraction to prevent acute secondary glaucoma

A lens implantat ionmaybe performed at the time of the

surgical procedure

CATARACT REMOVAL


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CATARACT REMOVAL

Two techniques in removing cataracts

ICCE Intracapsular cataract extraction

The entire lens are removed with cryoprobe

Easier to do

Places the client for risk of retinal detachment

The problem is loss of structure for lens implant

ECCE

Extracapuslar cataract extraction

Primary treatment for congenital and traumatic cataracts

Most common procedure

The anterior capsules, cortex and nucleus are removed leaving the

posterior capsule

Avoids disruption and loss of vitreous humor

Many patients immediately receive lens implant


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COMPLICATIONS

Pupillary block

Corneal decompensation

Loss of vitreous

Hemorrhage

Cystoid macular edema

Lens dislocation

Secondary membrane opacification

Retinal detachment Slip suture line

Increase IOP



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BEFORE SURGERY

Explain the procedure

Instruct the client regarding

the postoperative measures

to prevent or decrease IOP

Advise that the patient willreceive mydriatics or

eyedrops and cycloplegics

to dilate the eye and

facilitate cataract removal,

antibiotics and sedatives

POSTOPERATIVE INTERVENTIONS:


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POSTOPERATIVEINTERVENTIONS:

Elevate the head of the bed 30- 40 degrees Turn the client to the back or unoperative

side

Maintain an eye patch; orient the client to the

environment Position the clients personal belongings to

the unoperative side

Use side rails for safety

Assist with ambulation

AFTER SURGERY


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AFTER SURGERY

INSTRUCT TO NOTIFY THE DOCTOR FOR

SEVERE PAIN, BLEEDING, INCREASEDRAINAGE AND FEVER OCCUR

a. Goal: Reduce stress on the sutures and

prevent hemo rrhage

Activity: ambulate as ordered, usually soon aftersurgery; generally discharged 5-6 hours after

surgery.

Position: flat or low Fowlers; on back or turn to

nonoperative side. Watch out for increase IOP.Keep side rails raised, assist in ambulation and

safety precaution


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Avoid activities that increases IOP: straining at

stool, vomiting, coughing, brushing teeth, brushinghair, shaving, lifting objects over 5 pounds, bending

or stooping.

Provide: mouthwash, hair care, and personal items

within easy reach, step- in slippers.

b. Goal: Promo te psy cho logical wel l being with

elderly, frequent contacts to p revent sensory

depr ivat ion.


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c. Goal: Health Teaching:

If perspective glasses are used (aphakic

glasses), guide through activities withglasses, need to work through centralportion of lens and turn head to side whenlooking to one side to decrease distortion.

Eye care: instillation of eyedrops, eyeshieldat night to prevent injury for 1 month

S/sx of Infection: redness, pain, edema,and drainage, iris prolapsed, hemorrhage

Avoid: heavy lifting and eye trauma

CLIENTEDUCATIONFOLLOWINGCATARACT

SURGERY:


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SURGERY:

Take measures to prevent constipation

Wipe excess drainage or tearing with a sterile wetcotton ball from the inner to the outward canthus

Use an eye shield at bedtime

If a lens implant is not performed, the eye cannot

accommodate and glasses must be worn at alltimes

Cataract glasses act as magnifying glasses and

replace central vision only

Cataract glasses magnify and objects will appearcloser, therefore the client needs to accommodate,

judge distance, and climb stairs carefully


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HOME INSTRUCTION

REPORT sudden eye pain, red and watery eyes,photophobia or sudden visual changes

Instruct about activities that increases IOP for 6 to10 weeks

Follow up is important to monitor and detect anycomplications

Teach to instill eyedrops and ointment and how tochange eye patch

Advise dark glasses to relieve glare

Teach up and down head movements and scanningtechniques

Teach in wearing contact lenses


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GLAUCOMA

GLAUCOMA


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GLAUCOMA

Increased intraocularpressure results frominadequate drainageof aqueous humor

from the Schlemm oroverproduction ofaqueous humor

The conditiondamages the opticnerve and can resultblindness


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TYPES OF GLAUCOMA: OPEN ANGLE

Most common Chronic, simple or wide

angle

Local obstruction of

aqueous humor

between the anterior

chamber and the canal

Blockage or stenosis ofthe channel

Affects about 90% of

glaucoma

Emotional

disturbance

AllergyVasomotor

disturbances

Hereditary

Degenerative

CAUSES:

TYPES OF GLAUCOMA: CLOSED


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TYPES OF GLAUCOMA: CLOSED

ANGLE

Acute or narrowed

Displacement of iris toward the

cornea

Impaired passage of aqueous

humor into the circular canaldue to closure of the angle

between the cornea and the

iris.

Sudden rise of IOP Cause permanent vision loss in

48 to 72 hours

emergency

Trauma

Tumor

Hemorrhage

Iritis

Narrow angle

between the

iris and thecornea

CAUSES


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TYPES OF GLAUCOMA: SECONDARY AND


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TYPES OF GLAUCOMA: SECONDARY AND

CONGENITAL CLOSURE

CAUSES

Trauma

Prolonged corticosteroid

use

Diabetes

Uveitis

Venous occlusion

Neovascularization

surgery

Congenital

malformation and

other anomalies

Secondary Congenital closure


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SIGNS AND SYMPTOMSCHOP


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CLOSED (Closed- HALO)

Dramatic severe eye pain, headache Blurred and cloudy vision

Halos

Hard red eye w/ cloudy cornea

N and V and malaise

OPEN (Open- LOSS OF PERIPHERAL VISION)

Asymptomatic in years

Peripheral vision loss OR tunnel vision

Dark adaptation that is uncorrected by glasses

Blurring of vision Eyes tire easily

Difficulty focusing on near object

Malaise and morning headache

OBJECTIVE DATA:


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OBJECTIVE DATA:

1. Corneal edema

2. Decreased peripheral vision3. Increased cupping of optic disc

4. Tonomtery- pressure is >22 mmHg

5. Pupils: Dilated

6. Redness of the eyes

IFLEFTUNTREATED:


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Rate of secretion of Intraocular fluids

rate of absorption of aqueous humor IOP > 22mmHg

Decreased peripheral

vision & corneal edems

Halos & blurring

of vision

BLINDNESS


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DIAGNOSTIC TEST

TONOMETRY Measures IOP and provides baseline

GONIOSCOPY

Determines the angle of eyes anterior chamber

Slit lamp Allow to see the effects of glaucoma

OPHTHALMOSCOPY

Facilitates visualization of the fundus. Open angle mayhave cupping of the optic disk seen earlier

PERIMETRY OR VISUAL FIELD TEST Determine the extent of tunnel vision,

FUNDUS PHOTOGRAPHY

Monitors and record optic disk changes

NURSING CARE PLAN/ IMPLEMENTATION


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NURSINGCAREPLAN/ IMPLEMENTATION

A. Goal: Reduce Intraocular Pressure

1. activity: Bed rest

2. Position: semi- fowlers

3. Medications as ordered:

a. Mioticsb. Carbonic anhydrase inhibitors

c. Antichlinesterase to facilitate outflow of aqueous

humor

d. Ophthalmic (tomolol) to decrease IOP


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B. Goal : Provide Emotion al Suppo rt

1. Place personal objects within field of vision

2.

Assist with activities3. Encourage verbalization of concerns, fears of

blindness, loss of independence

C. Goal: HEALTH TEACHING:

1 P t i d IOP b idi


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1. Prevent increased IOP by avoiding:

a. anger, excitement and worry

b. constrictive clothing

c. Heavy lifting

d. excessive fluid intake

e. atropine or other mydraitics, which cause dilation

f. straining at stool

f. eye strain

2. Relaxation techniques

3. Prepare for surgical intervention: (if ordered) lasertrabeculoplasty, trabulectomy (filtering)

4. Moderate exercise and safety measures


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TREATMENT

OPEN ANGLE Timolol

Decreases IOP

Admin 1 Drop on affected eye BID

Monitor for cardiac failure

Use cautiously with asthma and bradycardia

May mask sysmptoms of hypoglycemia or thyrotoxicosis

betaxolol


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BURNSOFTHE EYE


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BURNS OF THE EYE

Disrupts integrity of thecornea and causes drying of

the cornea resulting in

chronic conjunctivitis and

corneal ulcerations

Thermal burn s:

Treated in the same way as

burns of skin structures Call opthamologist

ACTINIC TRAUMA


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ACTINIC TRAUMA

Associated with damage to the cornea

from UV rays Damage may be superficial and

resolves in 48 hours

Call opthamologist

Reasure the patient and keep himquiet

Apply patch to both eyes

Instill anesthetic drops as prescribed

Instill mydriatric-cycloplegic drugs asdirected to relax ciliary muscles andiris sphincter spasms

Instill emollient antibiotic ointment asordered

CHEMICAL BURNS Associated with either acid or alkali


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Associated with either acid or alkali

solutions

Both can cause intense pain and

inflammation

Ocular emergency

Irrigations of the eye with water for at

least 25 minutess and repeat procedure

after 15-20 mins until the patient is seenby the optha

Check pH of tears with litmus paper and

continue irrigations until pH is normal

Instill prescribed topical anesthetic forpain and control severe pain thereafter

with systemic analgesics

Measure vision and IOP to determine

status


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ALKALI BURNS

More severe than acid burn May require long term management

Lavage, cycloplegics and collagenous inhibitors

Contact lenses may be used to prevent ulcerations


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CHEMICAL Irrigation of LR or Saline

solutions

Medical emergencies

particularly alkali burns Can lead to severe scarring

and intraocular damage

Avoid touching their eyes

whether their hands areclean or not


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EDUCATION AND PREVENTIVE MEASURES

Eyeglasses and sunglasses should have impact-resistant

lenses

Appropriate glasses should be used for protection against very

bright light, sun, fumes and chemicals sufficient water must be

available

Googles glasses should be worn if there is danger of flying

gravel, wood chips, metals and glass bits

Wear industrial quality safety eyewear in shops and laboratories

Wear protective lenses and goggles in various sports

Warn children about sling shot, bb guns, darts, arrows and etc


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PENETRATINGOBJECTS

An injury that occurs to the

eye in which an object


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eye in which an object

penetrates the eye

Interventions: Never remove the object

because it may be holding

ocular structures in place; the

object must be removed by thephysician

Cover the object with a cup

Do not allow the client to bend

Do not place pressure on the

eye

Client is seen by a physician

immediately


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INFECTIONS ANDINFLAMMATIONS OF THEEYE

SUPERFICIAL LID INFECTIONS


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SUPERFICIAL LID INFECTIONS

Blepharitis Infections of the eyelids with crusting

lids, redness irritation and

mucopurulent secretions

Chronic inflammation of the eyelid May start in childhood and continue

through adulthood

Conditions can sometimes lead to

chalazion or a stye

Onset can be acute resolving withouttreatment within 2-4 weeks


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staphylococcal

allergy

Redness of the eyelids

Flaking skin on the lids

Crusting at the lidmargins, worse onwaking

Cysts at the lid margin(hordeolum)

Red eye Reduce vision

Gritty sensation of theeye

Causes Signs and SymptomsCommon S/Sx

Itching

Irritation

BurningForeign body

sensation

Eye dryness

TREATMENT AND MANAGEMENT


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TREATMENT AND MANAGEMENT

CHLORAMPENICOLOITMENT is given for at

least 4 weeks and up to six

weeks

Topical steroid Ocular antihistamines


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NURSING MANAGEMENT

Assist and educate about topical antibiotic andantihistamine

Administer acetylceisteine supplementation as prescribe

Avoid touching eyes with bare hands

Carefully wipe loose crust away from lashesAvoid touching eyes with bare hands as much as possible

Handwashing

MILD MASSAGE to mechanically empty glands

Meibomian glands Zeis glands

Moll glands


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CONJUNCTIVITIS


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PINK EYE OR MADRAS EYE Inflammation of the

conjunctiva

Most commonly caused by

virus Viral and bacterial are

contagious

CLASSIFICATIONS


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CLASSIFICATIONS

Allergic conjunctivities

Bacterial conjunctivitis

Viral conjunctivits Chemical conjunctivitis

Neonatal conjunctivitis

Blepharoconjunctivits

Keratoconjunctivitis

episcleritis

By Cause By extent of involvement

ALLERGIC


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ALLERGIC BACTERIAL

VIRAL
http://en.wikipedia.org/wiki/File:Swollen_eye_with_conjunctivitis.jpghttp://en.wikipedia.org/wiki/File:01-09-11_0222.jpg


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VIRAL

Associated with URTI,,common cold and sore

throat

Watery discharge

Itchiness Begins with one eye

Pink eye fine and

diffuse

Pyogenic Marked

grittiness/irritation

Stringy, opaque,

grayish or yellowishmucopurulent

discharge that cause

the lids to stick

together Severe crusting

painful

BACTERIAL

TREATMENT(RESOLVES IN 65% OF CASES WITHOUT


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(RESOLVESIN 65% OFCASESWITHOUT

TREATMENT 2 TO 5 DAYS)

ALLERGIC

COOL WATER POURED

OVER THE FACEWITH THE

HEAD inclined downward

constricts capillaries Artificial tears in mild cases

NSAID and antihistamines in

severe cases

Topical steroids drop

Bacterial Viral


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Usually resolveswithout treatment

Antibiotics are onlyneeded if with noimprovement after 3

days No antibiotics

4.8 days

With antibiotics 3.3 days

Delayed antibiotics 3.9 days

No specific treatment

Cold compress

Artificial tears

Avoid touching eyes or

sharing towels andwashcloth

Ban for travel

Bacterial Viral


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UVEITIS

UVEITIS


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UVEITIS

Inflammation of the middle layer of the eye,termed the uvea but in common usage may

refer to any inflammatory process involving

the interior of the eye.

Requires an urgent referral and thoroughexaminations by optha

Urgent treatment to control the

inflammation

Inflammation of the uveal tract Maybe a normal immune response to fight

an infection inside the eye

ANATOMICAL CLASSIFICATION


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ANATOMICAL CLASSIFICATION

ANTERIOR UVEITIS Iridocyclitis

Inflammation of the iris and the anterior chamber

90% of cases

Red eye, pain and decrease vision

Presence of dilated ciliary vessels

Presence of cells and flare in the anterior

chamber

Keratic precipitates on the posterior surface of

the cornea


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INTERMEDIATE UVEITIS Vitritis

Inflammatory cells in the vitreous cavity

Diposition of inflammatory material

POSTERIOR UVEITIS

Chorioretinitis

Inflammation of the retina and the choroid

PAN-UVEITIS

Inflammation of all layers of the uvea


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Herpes simplex

Herpes zoster

Leptospirosis Lyme disease

Histoplasmosis

Syphillis

Toxoplasmosis

TB

Redness of the eye

Blurred vision

Sensitivity to light Dark, floating spots

along the visual fields

Eye pain

Causes Signs and Symptoms

COMPLICATIONS


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COMPLICATIONS

Cataracts Glaucoma

Keratopathy

Retinal edema

Permanent vision loss

MANAGEMENT


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MANAGEMENT

Glucocorticoids (topicaleyedrops or oral)

Rule out first corneal ulcer

Topical cycloplegic (atropine)

PSTTA (posterior subtenon

triamcinolone acetate) Reduces swelling of the eye

Antimetabolite medication(methotrxate)

Given for aggressive cases ofuveitis

NURSING CONSIDERATIONS


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NURSING CONSIDERATIONS

Emphasize goals of care Patient comfort

Preservation of vision

Give specific cycloplegics as

prescribed to relieve discomfort causedby contraction of ciliary muscles

Give prescribed anti-inflammatory

agents to relieve inflammation

Corticosteroids in lowest effective dose

Topical steroids in high doses are

effective in anterioir uveitis


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ENUCLEATIONAND

EXENTERATION

Enucleat ionis removal of the

entire eyeball.


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Exenterat ionis removal of the

eyeball and surroundung tissueThe procedures are performed

for the removal of ocular tumors

After the eye is removed, a ball

implant is inserted to provide a

firm base for socket prosthesis

and to facilitate the best

cosmetic result

Preoperative interventions Postoperative interventions


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Provide emotional

support to the client Encourage the client to

verbalize feelings

related to loss

Monitor vital signs

Assess a pressure

patch or dressing

Report changes in vital

signs or the presence

of bright red drainageon the pressure patch

or dressing


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ORGANDONATION

Donor eyes are obtained

from cadavers


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Donor eyes must be

enucleated soon after deathbecause of rapid endothelial

cell death

Donor eyes must be storedin a preserving solution

Storage, handling, and

coordination of donor tissue

with surgeons is providedby a network of state eye

bank associations across

the country

CARETOTHEDECEASEDCLIENTASA

POTENTIAL EYE DONOR:


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POTENTIALEYEDONOR:

Discuss the option of eye donation withthe physician and family

Raise the head of the bed 30 degrees

Instill antibiotic eye drops as prescribed

Close the eyes and apply a small icepack to closed eyes

PREOPERATIVE CARE TO THE RECIPIENT:


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PREOPERATIVECARETOTHERECIPIENT:

Recipient may be told of the tissue availability onlyseveral hours to 1 day before surgery

Assist in alleviating client anxiety

Assess eye for signs of infection

Report the presence of any redness, watery orpurulent drainage, or edema around the eye to the

physician

Instill antibiotic drops into the eye as prescribed to

reduce the number of microorganisms presentAdminister fluids and medications intravenously as

prescribed

POSTOPERATIVECARETOTHERECIPIENT

Eye is covered with a pressure patch and protective


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ye s co e ed t a p essu e patc a d p otect eshield that is left in place until the next day

Do not remove or change the dressing without aphysicians order

Monitor vital signs

Monitor level of consciousness

Assess dressing

Position the client with the head elevated and thenonoperative side to reduce intraocular pressure

Orient the client frequently

Monitor for complications of bleeding, wound leakage,infection and graft rejection.

Instruct the client how to apply a patch and eye shield Instruct the client to wear the eye shield at night for 1

month and whenever around a small children or pets

GRAFT REJECTION


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GRAFTREJECTION

Rejection can occur atanytime

Inform the client of the signs

of rejection

Signs include redness,swelling, decreased vision,

and pain (RSVP)

Problems of the Eye

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