Sensory Disorders Topics Sensory and The Effects of Aging Eyes and Vision Ears and Hearing Sensory other We will primarily discuss vision and hearing The other senses taste smell and touch will be discussed briefly in much less detail ID: 775270
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Slide1
Sensory Disorders
Fall 2009
Slide2Sensory Disorders: Topics
Sensory and The Effects of AgingEyes and Vision Ears and HearingSensory (other) We will primarily discuss vision and hearing.The other senses, taste, smell and touch will be discussed briefly, in much less detail
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Slide3Structure of the Eye
Eyeball has three layers: Sclera (the external white of the eye)Uvea (the middle layer, includes the choroid, ciliary body, and iris)Retina (inner layer, includes photoreceptors [rods and cones]
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Slide4Anatomy of the globe (eyeball)
The eyeball has several coverings:1.Conjunctiva thin, single cell transparent layer that covers the eyeball and is continuous with the eyelids2.Cornea is the outermost fibrous layer, covers the iris, transparent and avascular. Helps to focus light as it is curved. Most frequently transplanted tissue. The avascularity prevents circulating antibodies from attacking the transplant. Has pain fibers – response tears.
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Slide5Anatomy con’t
3.Sclera “hard” is the white part of the eye. Firm covering that maintains the shape of the globe; provides some protection to inner structures4.Uvea is the middle, vascular layerIris the color portion of the uvea; contains circular (parasympathetic) muscles to constrict the pupil and radial (sympathetic) muscles to open the pupil. Legal & illegal drugs mimic the parasympathetic systemIris acts like the shutter of a cameraParasympathomimetics – Narcotics, adrenalize, pilocarpine – used in gluacoma to constrict the pupil.
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Slide6Anatomy con’t
Ciliary body (2nd most vascular)consists of ciliary muscles to change the shape of the lens and ciliary processes to secrete fluid that fills the eye.5. Choroid provides vascular supply to retina6. Retina inner (nervous) layer at back of eye; beginning of perception of light.Optic disc contains the blind spot, a single artery & single vein and is the egress for this retinal artery, vein, and Optic Nerve (CN II)
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Slide7Anatomy con’t
Retina con’t;Contains 120 million rods, for photoreception; can see shades of gray, black & white, perceive movement and shapes; increase in number as one moves eye peripherally. Therefore, best vision in darkness is peripheral vision; a survival advantage against predators
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Slide8Anatomy con’t
Retina con’tRetina also has 6 million cone-shaped photoreceptors; the color receptors; allow for color vision in bright light conditions; no colors are seen in dim light (night vision) because the cones do not function in dark conditions7. Maculae lutea (yellow spot) the direct center of the retina. Provides the clearest vision
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Slide9Anatomy con’t
Eyeball has 3 chambersAnterior – between cornea and iris. Aqueous humor nourishes the lens. Canal of Schlemn regulates inraocular pressure. Glaucoma results when pressure builds up in the eyball either from overproduction of aqueous humor or failure of the canal of Schlemn.Posterior between the iris and the lensVitreous between the lens and retina – filled with vitreous, a jelly-like substance
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Slide10Anatomy con’t
The eye is a hollow organ. For the eye to function properly, the gel in the posterior segment (vitreous humor) and the fluid in the anterior segment (aqueous humor) must be present in set amounts that apply pressure inside the eye to keep it ball-shaped.Once eye growth is complete, the gel (vitreous) does not change in volume, however the aqueous humor is continuously made from blood plamsa.
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Slide11Anatomy con’t
The eye has the following accessories:Palpebrae (pal-pee-bry) are the eyelids which spread tears and protect eye from traumaEyelashes filter dust and debris and signal their approachLacrimal glands and lacrimal ducts. The glands produce 1 ml of fluid/day, which drains into nose (why your nose runs when you cry)
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Slide12Anatomy con’t
Six extrinsic eye musclesLateral and medial rectus muscles control lateral (outside) and medial (toward midline) movements.Inferior and superior obliques control rotational, upward and downward movement. Eyes rotate slightly to keep perception on the horizon relatively flatSuperior and inferior rectus for upward and dwonward movementControlled by CN III, IV, VI; provide finest motor control in bodyTo supress blurring, the brain directs the eyes to pick a fixed point in a moving landscape, follow it until it disappears, then pick another point. (like watching a speeding train go by). This is called nystagmus (quick-skip-quick-skip).Abnormal nystagmus can indicate brain damage.
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Slide13Structure of the Eye
Cornea - the clear, dome-shaped tissue covering the front of the eye. Iris - the colored part of the eye - it controls the amount of light that enters the eye by changing the size of the pupil Lens - a crystalline structure located just behind the iris - it focuses light onto the retina Optic nerve - the nerve that transmits electrical impulses from the retina to the brain
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Slide14Structure of the Eye
Pupil - the opening in the center of the iris- it changes size as the amount of light changes (the more light, the smaller the hole)Vitreous - a thick, transparent liquid that fills the center of the eye - it is mostly water and gives the eye its form and shape (also called the vitreous humor or aqueous humor)
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Slide15Physiology of light & vision
Retina - sensory tissue that lines the back of the eye. It contains millions of photoreceptors (rods and cones) that convert light rays into electrical impulses that are relayed to the brain via the optic nerveShape, movement, size, color & orientation in space is organized by the visual center.
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Slide16Cont from prior page
Light strikes the retina, stimulating the rods and conesPhotoreceptors convert light energy into chemical energy (photons)Chemical energy is converted into nerve conductionChemical action is Vitamin A dependent for renewalThe signal finally reaches the neurons in the optic nerve (CN II) to the brainThe rods tend to converge into one nerve cell and thus offer better vision in dim light (movement) at the cost of blurring shapesThe cones tend to have one nerve each and therefore, give sharper images (resolution) in color while sacrificing sensitivity.
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Slide17Eye Function
Eye function consists ofRefractionPupil constrictionAccommodationConvergencePortion of the trigeminal nerve (CN V) stimulates blinking when the cornea is touchedCN VII (facial nerve) innervates tear glands and the muscles associated with closing the eyelid
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Slide18Refraction
Refraction (the bending of light to focus images on the retina)Hyperopia (farsightedness) Inability of the eye to adequately refract (break-up) light Eyeball may be too short or the cornea have too little curvature Objects at a distance are seen clearly; close objects are blurred Myopia (nearsightedness) Astigmatism
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Slide19Refraction
Myopia (nearsightedness) Objects at a distance are blurred; close objects are seen clearlyEyeball may be too long or the cornea have too much curvatureLight coming into the eye does not focus correctly creating a blurred image of distant objectsAstigmatism Uneven surface on, or in the eye (esp the cornea) which distorts vision
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Slide20Pupil Constriction
Constriction and dilation control the amount of light that enters the eye.If the level of light to one or both eyes is increased, both pupils constrict.The amount of constriction depends on how much light is available and how well the retina can adapt to light changesConstriction (miosis); dilation (mydriasis)
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Slide21Accommodation
Allows the healthy eye to focus images sharply on the retina whether the image is close or far awayThe process of maintaining a clear visual image when gaze is shifted from distant to near object is known as accommodation.The eye can adjust its focus by changing the shape of the lens
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Slide22Convergence
Ability to turn both eyes inward toward the nose to ensure only a single image of close objects is seen.
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Slide23Treatment of Common Refractory Errors
Corrective glasses Contact lensesRefractory surgery - Photorefractive keratectomy (PRK) - Laser-in-situ keratomileusis (LASIK)
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Slide24Structural Changes of the EyeRelated to Aging
Appearance of the eyeArcus senilis (a product of hyperlipidemia; bluish white ring around the cornea); does not affect visionSclera takes on a yellowish (r/t fat deposits) or bluish hue (do not confuse w/jaundice in elderly – look for other S&S of jaundice such as skin, liver enzymes)CorneaWith aging, flattens. Result is blurred and distorted vision
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Slide25Structural Changes of the EyeRelated to Aging
Ocular musclesStrength decreases – pt must refocus to maintain a single imageLensHardens and becomes compact (Cataracts) – wear corrective lenses Iris Decreased ability to dilate – need better lightingSmaller pupilPoor adaptation to darkness
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Slide26Structural Changes of the EyeRelated to Aging
PupilSize is smaller; Reduced ability to see in dim lightColor VisionAbility to differentiate between colors of short wavelength (green, blue, violet) decreasesTearsDiminished tearingDry eyesRisk for infectionDiscomfort
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Slide27Structural Changes of the EyeRelated to Aging
PresbyopiaLens yellows with age, aging lens hardens, shrinks and loses elasticity. Loss of elasticity results in loss of accommodation-must hold objects away to focus; narrow field of visionReading glasses!
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Slide28Assessment of the Eyes:Overview
HistoryObtain subjective data Demographic dataAge is a biggie! Why?Family history and genetic riskSometimes relevant Personal historyAny systemic problems that can be r/t eye/vision problem?Taking decongestants and antihistamines? (May dry eyes and increase IOP)
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Slide29Considerations for the Elderly
Health historyChronic conditions may have an adverse effect on visionExamples: diabetes; cataracts; others?MedicationsAntihistamines and decongestants (dry eyes)Blurred or double vision (diplopia)
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Slide30Considerations for the Elderly (and others)
Tear secretion - Anticholinergics - Antihistamines - Beta-blockers Myopia (nearsightedness) and blurred vision - Diuretics - Sulfonamides
Diplopia (double vision) - Carbamazepine (anti-convulsant / mood stabilizer) TegretolRetina - Tamoxifen - Digoxin (retinal toxicity / disturbance of color vision)
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Slide31Assessment of the Eyes: Overview
Current health problemsSudden change in vision is a medical emergencyInspectionSymmetry of eyesEyelids and eyebrows Measurement of visionAcuityNear-vision and far-vision testingVisual fields and EOMColor visionPsychosocialHow is your patient coping?
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Slide32Considerations for the Elderly
Again, remember that… Vision fails as the lens becomes harder and denser Loss of elasticity reduces ability of the lens to change shape when focusing on objectsDecrease in the diameter of the pupil decreases the amount of light reaching retina thus reduces the ability to see in dimmed light (Zagaria, 2007)
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Slide33Considerations for the Elderly
Look for… - Sclera and lens color changes - Decreased tear secretion - Slower accommodation - Atherosclerotic changes in retinal vasculature - Dryness of eyes - Decreased color perception
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Slide34Nursing Considerations
Safe and effective care environmentHealth promotion and maintenancePsychosocial IntegrityPartial or complete vision lossUse of support groups and local resourcesDiagnostic procedures and follow up carePhysiologic Integrity
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Slide35Assessment of the Eye
Assess if patient has problems with eyes/visionAcuityMeasures distance and near visionSnellen chart used to measure distance (20 feet from chart)Rosenbaum pocket vision tests near vision (use in patients over 40 years of age-hold card @14ft)Why?Confrontational Test Tests peripheral vision
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Slide36Assessment of the Eye
Extraocular movement (CNs III, IV, VI)3 testsCorneal light reflex (tests alignment)Six cardinal positions of gaze (tests muscle function) Cover-uncover test (also tests muscle function r/t ability to focus)Monitor for symmetric eye movementWhy?
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Slide37Assessment of the Eye
Culture and smear of corneal or conjunctival swaps to Dx infectionOphthalmoscopy (Permits viewing of external and internal eye structuresSlit lamp microscopy (Uses microscopic technology to examine anterior ocular structures)Tonometry (Tool used to measure IOP. Normal IOP: 10 to 21 mm Hg) When might IOP be higher during the day?Corneal staining (Used as evaluation tool in cases of trauma; foreign bodies; ulcers; abrasions) CT scan (useful in examining the EOMs; bony structures and eye itself, can detect tumor)MRI (replaced CT for examining optic nerve and orbit)
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Slide38Assessment of the Eye –Common Abnormalities
Hordeolum “stye”Inflammation of glandCaused by bacterial infection (staph and strep)Tx w/ warm compresses and antibacterial ointmentChalazionSwollen sebaceous gland of eyelid r/t block in gland’s ductTx w/ warm compress, antibacterial ointment, surgeryBlepharitisInflammation of the eyelidsCan be associated with having dandruff of the scalp Tx w/ anti-tear shampoo, warm compress
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Slide39Assessment of the Eye –Common Abnormalities
Ptosis Drooping of the upper eyelidCan be r/t disorder of oculomotor nerve (CN III) Hemorrhage – traumatized blood vessel, usually well defined bright red area in conjunctiva. Resolves on ownConjunctivitis – (pink eye)Inflammation of conjunctiva – edema, burning, itching, tearsViral or bacterial – easily transmitted from person to personStaph, H.Influenza, PseudomonasTx with topical antibiotics, handwashingCaused by allergy (pollen; animal dander; dust)
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Slide40Assessment of the Eye –Common Abnormalities
JaundiceHepatitisYellowish color is a normal variant in elderlyArcus senilusGrayish line (ring-like) in the periphery of cornea Common in elderly (fatty deposits)Abnormal finding in younger individuals (hyperlipidemia) ExophthalmosProtrusion of eyeballsAssociated with hyperthyroidism
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Slide41Assessment of the Eye –Common Abnormalities
HeterochromiaDifferent eye colorCongenital or r/t inflammation; tumor of iris Strabismus Abnormal alignment of the eyesWhat else to know…Legal blindness is defined as a visual acuity of 20/200 or less in the better eye with the best correction possible
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Slide42Assessment of the Eye –Common Abnormalities
Amblyopia “Lazy-eye” one eye is not used enough for the visual system in the brain to develop properly.Poor eyesight not due to any detectable cause Corneal abrasion and scarring Painful scrape or scratch of the corneaAssociated with traumaPain,Tearing,Blurred visionTx w/antibiotics, antifungals, &Antivirals, steroids
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Slide43Assessment of the Eye
Xanthelasma
Jaundice (icterus)
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Slide44Colorblindness
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Slide45Colorblindness
(Shown again)Individuals who are NOT colorblind should have been able to see a circle, star and a square in the previous picture
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Slide46Colorblindness
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Slide47Colorblindness
(Shown again)Individuals who are NOT colorblind should have been able to see a yellow square and a faint brown circle in the previous picture
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Slide48Colorblindness
Which object do you see?
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Slide49Colorblindness
Individuals who are colorblind will see nothing
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Slide50Eye Trauma
Etiology - Traumatic hyphema (bleeding in the eye) - Penetrating injury - Chemical (acidic pH< 4; alkaline pH > 10) exploded car batteries - Thermal (destroys rods and cones) - Enucleation Treatment - Corneal transplant (for clouding; scarring)
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Slide51Cataracts
An opacity or clouding of the crystalline lens that blocks the passage of light needed for vision, distorts image projected onto retina Is the 3rd leading cause of blindness in the US Etiology - Aging - Congenital - Traumatic - Secondary to UV exposure, steroids, DM The lens will enlarge causing increased IOP resulting in Glaucoma
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Slide52Cataracts
Cloudy white lens over the pupil (characteristic of a cataract) Children may have congenital cataracts
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Slide53Cataracts - Assessment
Opacity or cloudy white pupilDecreased visionGlareObliteration of parts of imagesDecreased perception of colorDistorted imagesPhotophobia (sensitivity to light)
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Slide54Cataracts - Treatment
Non-surgicalReading glassesIncreased lightingSurgical - outpatientRemoval of cataract (extracapsular extraction) with implantation of intraocular lens (IOL)
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Slide55Cataracts – Post-opPatient Education
Elevate HOB 30-45 degrees immediately post-op; Eye drops (antibiotics, steroids, analgesic) several times/day for 2-4 weeksADLs are resumed as the patient feels ableInstruct on methods to prevent increased IOPDo not sleep on operated side for 3-4 weeksAvoid rubbing; protect the eyes with patch/sunglassesDo not bend over below waistlineAvoid heavy physical activity x6 weeksAvoid sneezing, coughing, straining, vomitingAssess appearance of eye
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Slide56Cataracts – Post-opPatient Education
Notify if…Redness of the eye increases or eye pain is severeIf discharge from eye increases or changes color (to greenish)Vision decreasesAlert patient that vision may not be “normal” immediately after surgery
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Slide57Glaucoma
Second leading cause of blindnessMay damage the eye without the person being aware of itCharacterized by increased IOP (NL 10-21 mm Hg) associated with progressive loss of peripheral visionCupping of the optic disc and optic nerve destructionProgressively destroys the optic nerve
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Slide58Glaucoma
Optic nerve fibers carry impulses of sight from the retina to the brainIncreased IOP and loss of blood flow to optic nerve results in nerve fiber deathThe cup enlarges as compared to the disk
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Slide59Types of Glaucoma
Primary/Chronic Open Angle (90%)Caused by a reduction in the outflow of aqueous humor due to obstruction in trabecular meshworkDevelops slowly; no symptomsPrimary/Chronic Closed AngleOutflow of aqueous humor is impaired due to narrowing of the angle between the iris and corneaAcute Closed AngleSudden onset, severe eye pain; nausea and vomiting; colored halos; blurred vision; ocular redness. MEDICAL EMERGENCY
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Slide60Primary/Chronic Open-Angle Glaucoma
SymptomsFrequent change in eye glasses without any improvement in visionInability of eyes to adjust to darkened roomsLoss of peripheral visionRainbow colored rings around lightsPersistent dull eye painHeadaches
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Slide61Primary/Chronic Open-Angle Glaucoma
DiagnosisTonometryNormal pressure 10-21 mmHgFor glaucoma 22-32 mmHgExam with Ophthalmoscope Evaluation of color and configuration of optic diskPerimetry-measurement of the central field of visionCupping of the optic disk is the most reliable sign in chronic simple glaucoma
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Slide62Treatment for Primary/Chronic Open-Angle Glaucoma
Medical (Important)Beta-adrenergic blockers (Timoptic) decreases aqueous humor production (used in the treatment of glaucoma)Carbonic anhydrase inhibitors (Diamox) Decreases aqeous humor production. Watch for signs of potassium depletion (used in the treatment of glaucoma; epileptic seizures)Miotic eye drops (pilocarpine) constrict pupils and contract the ciliary muscle, increasing the outflow of aqueous humor. Decreases visual acuity, particularly when poorly illuminated
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Slide63Primary/Chronic Open-Angle Glaucoma Surgical Treatment
Indicated when conservative treatment measures failTrabeculoplasty – applications of laser beam on trabecular meshwork; changes the configuration and leads to increased outflow of aqueous humorTrabeculectomy – an opening is made under a partial thickness scleral flap allowing aqueous humor to flow
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Slide64Acute Closed-Angle Glaucoma
A medical emergency!SymptomsSevere painDecreased visionPupil enlarged and fixedColored rings (halos) around lightsEye is redSteamy corneaIOP 50 mmHg or higherWhat happensA blockage of the trabecular meshwork at the point of fluid outflow. IOP increases and may cause damage to the optic nerve. (Optic nerve transmits images from the eye to the brain)
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Slide65Treatment for Acute Closed-Angle Glaucoma
MedicalOsmotic diuretics (Mannitol) potent diuretic; rapidly reduces the production of aqueous humor in the eye; decreases IOPPrimarily used to treat acute attacks or in preparation for surgery. Not for chronic useCarbonic anhydrase inhibitors (Diamox) Decreases aqeous humor production. Watch for signs of potassium depletion (used in the treatment of glaucoma; epileptic seizures)Miotic eye drops (pilocarpine) constrict pupils and contract the ciliary muscle, increasing the outflow of aqueous humor. Decreases visual acuity, particularly in poor illumination
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Slide66Surgical Treatment for Acute Closed-Angle Glaucoma
Laser iridotomyAttempts to lower IOP by directly damaging the ciliary bodies (permanently)Procedure frequently needs to be repeated Patients are at risk for severe inflammation; retinal detachment and hemorrhagingPeripheral iridectomyPerformed to form a permanent connection between the anterior and posterior chambersPrevents the iris from occluding the anterior chamberPerformed when laser treatment is unsuccessful
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Slide67Preventative Measures for Individuals with Glaucoma
Keep a reserve bottle of eye dropsCarry eye drops when away from homeCarry ID for glaucoma and eye dropsBe aware of the location of the closest 24-hour drug storeMedications are required for a lifetimeKnow the name, dosage, frequency, and side effects of medications
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Slide68Preventative Measures for Individuals with Glaucoma
Know the signs/symptoms that should be reported immediatelyAcute eye pain deep in the eyeSudden change in visionHalos around lightsVital sign changes
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Slide69Detached Retina
What is retinal detachment?Retinal detachments often develop in eyes with retinas weakened by a hole or tearFluid seeps underneath weakening the attachmentRetina detaches(Like wallpaper peeling off a wall)When detached, the retina cannot compose a clear image from incoming light and vision is blurred and dim
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Slide70Detached Retina
Occurs when the two retinal layers separate as a result of a full-thickness break in the sensory retinaResults in liquefied vitreous humor passing through into the subretinal spaceAs the detachment extends, blindness can occur because of macula detachment
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Slide71Detached Retina
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Slide72Detached Retina(Causes)
TraumaMyopic degeneration TumorsHemorrhageMay follow sudden severe physical exertion in a debilitated individualMay occur suddenly or develop over time
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Slide73Detached Retina – Symptoms
Usually sudden and painless (no pain fibers)Floaters and flashers (photopsia)Floating spots or opacities before the eyes (blood and cells freed at time of tear)Flashes of light (vitreous traction on the retina)Progressive loss of vision in one area (curtain-drawn before eyes)
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Slide74Detached Retina – Diagnosing
Based on ophthalmoscopic exam of retinaPrevention is based upon early detectionHigh risk individualsDiabetic retinopathy (damage to blood vessels of the retina)High degree of myopia (distant objects are blurred)
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Slide75Surgical Treatment ofDetached Retina
Goal is to seal off areas of tearsScleral BucklingSclera and choroid are indented toward area of breakPhotocoagulationProduces inflammatory reaction at the site of the tear that causes chorioretinal adhesionsCryopexySubfreezing temperatures used to produce inflammatory reactionPneumatic retinopexyIntraocular injection of air or gas to tamponade the tear
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Slide76Diabetic RetinopathyPathophysiology
A disorder of the blood vessels of the retina which usually appears about 10 years after the onset of DMCan be detected in 65% of individuals with Type I diabetes for 15 years and in 60% of individuals with Type II diabetesResponsible for 10% of newly reported cases of blindness each year
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Slide77Diabetic RetinopathyPathophysiology
Retinal blood flow is poor; hypoxia develops; retinal cells secrete a “growth factor” – stimulates new vessel formation. Vessels are fragile, thin, week and bleedLead to hemorrhage and vision lossTiny microaneurysms develop in the retinal capillary wallsRetinal veins widen and become tortuous; small hemorrhages develop leaving small scars in those areasProtein leaks causing retinal edema, especially in the area of the macula Linked to fasting BG levels >129 mg/dl. HTN icreases rate of development too – Glycemic control is imperative to keep at near normal BG levels
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Slide78Diabetic Retinopathy
Tortuous vesselsMicro-aneurysms“Fluffy wool” exudates on the retinaNew vessel formationAs the disease progresses, multiple spots or “floaters” Increasing loss of vision
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Slide79Diabetic Retinopathy
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Slide80Diabetic Retinopathy -Diagnosis
OphthalmoscopyFluorescein angiography Retinal dye injection is used to determine if there is proper circulation in the retinal vessels in the eye. When dye is injected in a vein in the arm, a rapid series of photographs are taken. Among other things this test can detect problems such as blockages and tumors
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Slide81Diabetic Retinopathy - Prevention
Type I DM See ophthalmologist within three years of diagnosis; then yearlyType II DM At diagnosis and yearlyWomen who are pregnant should be examined each trimester ComplicationsMay lead to massive retinal hemorrhage and retinal detachment
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Slide82Diabetic RetinopathyManagement
PhotocoagulationLaser is directed on the retina, damaging and scarring the peripheral retina in order to decrease the ischemia (temporary deficiency of blood flow) which induces neurovascularization Vitrectomy Surgeon removes the opaque bloody fluid and debris, and scar tissue to alleviate traction on the retina
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Slide83Diabetic Retinopathy –Nursing Considerations
Patient teaching regarding:DM – Tight glycemic controlImportance of regular eye exams Assess ability to administer insulin if vision is impaired
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Slide84Age-Related Macular Degeneration
Macular degeneration is a medical condition predominantly found in elderly adults in which the center of the inner lining of the eye, known as the macula area of the retina, suffers thinning, atrophy, and in some cases bleeding. This an result in loss of central vision and thus inability to see fine details; to read; or to recognize faces.
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Slide85Age-RelatedMacular Degeneration
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Slide86Age-Related Macular Degeneration
A disease of the aging retina; cause is unknownCigarette smokers are at a significantly higher riskResults from degenerative changes to the choriocapillaries or the retinal pigment epithelium
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Slide87Age-Related Macular Degeneration with Hemorrhage
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Slide88Macular DegenerationTypes
Exudative (wet) typeCharacterized by sudden growth of new vessels in the macular regionVessels are fragile and leak blood and fluid that damages the macula by interfering with the blood supplyNon-exudative (dry) typeMost common type (90%)Caused by degeneration of the light sensitive cells of the maculaScattered round spots (drusen) appears in the macular region
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Slide89Macular Degeneration
Central vision loss in one or both eyesDecreased ability to distinguish colorsClassic: “Drusen” Tiny yellow or white extracellular accumulations that may or may not be an early sign of macular degeneration (a small number are expected with aging)
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Slide90Diagnosing Macular Degeneration
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Ophthalmoscopy
Amsler
grid-distorted or wavy lines, spots or areas totally missing, center is dark.
Slide91Management of Age-RelatedMacular Degeneration
No acceptable treatment for the dry-typeLaser – damages remaining vessels in the center of the maculaPhotodynamic therapy (PDT) – destroys abnormal blood vessels without permanent retinal damageLucentis – injection to prevent new vessel growthHigh doses of vitaminsVitamin C 500 mgVitamin E 400 UBeta-Carotene 15 mgZinc, as zinc oxide 80 mgCopper, as cupric oxide 2 mg
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Slide92Retinitis Pigmentosa
Group of inherited disorders that slowly leads to degeneration of part of the retina, primarily photoreceptors, that over time leads to blindnessFirst loss is night vision; then peripheral vision, resulting in tunnel vision; then color vision; then blindnessHereditary; can begin in childhoodNo cure – high dose vitamin-A may slow progression. Research on retinal microchip implantation and stem cell therapy
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Slide93Differentiating Loss of Vision
Normal visionDiabetic retinopathy In diabetic retinopathy, the blood vessels in the back of the eye (retina) may rupture and leak. This causes parts of the retina to die and results in a loss of vision where the leaking occurred
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Slide94Differentiating Loss of Vision
Age-relatedMacularDegenerationIn age-related macular degeneration, the center part of the eye and retina (macula) dies-off, leaving a black hole or "scotoma" right where you're looking - in this case the teenager's nose. Because people with age-related macular degeneration have to rely on side vision to read, visual acuity is greatly reduced and if both eyes are affected the person would have to give-up driving a car
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Slide95Differentiating Loss of Vision
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Cataract:
Clouding of the lens of the eye and light that passes through the lens to the retina is scattered. The scattered light causes images to be blurred and visual acuity is reduced.
Glaucoma and Retinitis Pigmentosa:
Although very different diseases, both glaucoma and retinitis pigmentosa (RP) cause a loss of side vision leading to “tunnel vision.” Individuals with glaucoma or RP often become legally blind because of severe loss of side vision
Slide96Cyotomegalvirus (CMV) Retinitis
Member of the herpes group of viruses Direct viral invasion of retinal cellsCMV infection is present in many individuals and problematic when disease is evident Most common site for CMV is in the individual with HIV
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Slide97Symptoms of Cytomegalvirus(CMV) Retinitis
Blurred visionDecreased visionFloatersMay lead to blindness (causes chorioretinitis, an exudative inflammatory process that involves retinal vessels)
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Slide98Diagnosis of Cytomegalvirus (CMV) Retinitis
Patient historyImmunocompromised patientFundoscopic exam (one or many small white lesions, or “cotton wool spots” along vessels can be associated)
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Slide99Management of Cytomegalvirus (CMV) Retinitis
Gancyclovir (IV or PO)AnemiaPhlebitis Foscarnet (IV)Renal failureAnemia Gancyclovir implants or intra-orbitally
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Slide100Carcinoma of the Eye
Choroidal melanoma Iris melanomaRetinoblastoma
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Choroidal melanoma (left)
Iris melanoma (above)
Slide101Common Nursing Diagnosesfor Eye Problems
Disturbed sensory perception r/t visual deficitRisk for injury r/t visual impairmentSelf-care deficit r/t visual impairmentAnticipatory grieving r/t loss of functional vision lossAcute pain r/t pathophysiologic process and/or surgical correctionNoncompliance r/t inconvenience of lifelong meds
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Slide102Question
Which of the following would be a sign of a post-operative cataract complication?Change in color visionSudden loss of visionHallucinations; headache; changes in color vision; flashes of lightFlashes of light; floaters; increased tearing
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Slide103Question
Which of the following would be a sign of a post-operative cataract complication? Answer: Flashes of light; floaters; increased tearing
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Slide104Question
A 37-year-old Type I diabetic is admitted with a hyperglycemic episode. The patient describes frequent episodes of blurred vision. An examination of the eye fundus by opthalmoscopy revealsNarrowing of retinal arteries and hemianopsis Scattered round white spots in the macular regionTortuous vessels, fluffy wool exudates, new vessel growthCupping of the optic disc
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Slide105Question
A 37-year-old Type I diabetic is admitted with a hyperglycemic episode. The patient describes frequent episodes of blurred vision. An examination of the eye fundus by opthalmoscopy revealsAnswer: Tortuous vessels, fluffy wool exudates, new vessel growth
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Slide106Which Med for Which Condition?
Midriatic (pupil dilates, example is Atropine)Miotic (constricts pupil and contracts the ciliary muscle allowing for enhanced circulation of aqueous humor)Osmotic (draws fluid into intravascular space to lower IOP)Anti-inflammatory
Acute closed-angle glaucomaChronic closed-angle glaucomaCorneal abrasionConjunctivitis Ophthalmoscopy
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Slide107Which Meds for Which Condition (Answers)
Midriatic (pupil dilates, example is Atropine)Miotic (constricts pupil and contracts the ciliary muscle allowing for enhanced circulation of aqueous humor)Osmotic (draws fluid into intravascular space to lower IOP)Anti-inflammatory
Acute closed-angle glaucomaChronic closed-angle glaucomaCorneal abrasionConjunctivitis Ophthalmoscopy
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Slide108Ears
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Slide109Ears
Ear has three partsExternal earMiddle earInner ear
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Slide110Ears and Hearing:Assessment
Obtain a thorough history DemographicsGender (some hearing disorders more common men than in women and vice versa) Age (elderly) Family history and Genetic risk70% of people with Down syndrome develop hearing loss in adulthood
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Slide111Ears and Hearing:Assessment
Personal historyAsk about past and present problems with pain, vertigo tinnitus, loss of hearing, difficulty understanding people who are talkingSocioeconomic statusAvailability of healthcareCurrent health problems Dizziness or vertigoPhysical assessment
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Slide112Assessment of the Ear
Otoscopic examinationAuditory assessmentAir versus bone conduction soundTransmissionConductive, sensorineural or mixedVestibular assessment
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Slide113Diagnostic Testing and the Ear
CTAudiometryPure tone (tests hearing threshold levels) SpeechElectronystagmographyArtificial stimulation of the vestibular apparatusInvolves induced nystagmus (rapid involuntary movement of the eye)Can suggest etiology of vertigoPurpose is in determining if there is something wrong with the vestibular portion of the inner ear. If dizziness is not caused by the inner ear, it might be caused by disorders of the brain, or by medical disorders (low blood pressure)
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Slide114Classification of Hearing Loss
Conductive hearing lossi.e., problem conducting sound wavesObstructionOtosclerosis (overgrowth of bone in the inner ear)Sensorineural hearing lossRoot cause sometimes found in CN VIII, (Vestibulocochlear nerve)Resulting from exposure to loud noisesDiabetesDamage to inner earMeniere’s Disease Mixed hearing lossCombination of conductive hearing loss and sensorineural hearing loss
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Slide115The Outer Ear
InfectionsExternal otitis PAINItching or ear canalInflammationCerumenForeign bodyProblems of Tympanic membrane Chronic otitis media (middle ear infection) is a common cause of hearing loss; trauma
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Slide116Some Acute Perforations Will Heal Spontaneously
MyringoplastyPerformed if the perforation if only the membrane with no other accompanying damageTympanoplastyPerformed if the middle ear is involvedPost-opDo not blow nose; sneeze or cough with mouth openAvoid physical activity for one weekKeep ear dry for six weeksDo not shampoo hair for one weekAvoid airplane travel for one week
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Slide117Middle Ear
InfectionsOtitis media Throbbing pain, drainage, fever, bulging tympanic membrane with possible perforationOtosclerosisHardening of the ear (stapes); normal canal and ear drum; progressive conductive hearing lossTraumaTo the tympanic membrane from a blast or blunt injuryCan cause a fracture or dislocation of the ossicleFacial nerve is also vulnerableEustachian tube disordersMost common blockage due to enlarged adenoid tissue
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Slide118Inner Ear
InfectionsLabyrinthitis; can be viral or bacterial TumorsAcoustic neuroma of CN VIII; most common benign tumorBalance DisordersMeniere’s disease, a triad of symptoms – vertigo, dizziness, tinnitus, and hearing loss. Affects CN VIII Tinnitus Ringing noiseVertigoWhen eyes are open, world seems to be spinning
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Slide119Meniere’s Disease
AssessmentHistory of fallsDisability in relation to ADLsFears Hearing acuity fluctuationsSense of fullness of the hearAutonomic response: Pallor; sweating; N/VProgressive, permanent hearing loss
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Slide120Meniere’s Disease:Diagnosis
Audiometric testingTests amount of hearing lossMRIUsed to identify presence of tumors or masses
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Slide121Meniere’s DiseaseTreatment
Bed rest during attackAvoid sudden movementMedicationsDimenhydrinate (Dramamine)Cyclizine hydrochloride (Marezine)Meclizine (Bonine; Antivert; sedatives and hypnotics)
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Slide122Nursing Diagnosis
Risk for injury fallsFear: Uncertainty of attacksAnxiety: Vertigo as threat to self-conceptFluid volume deficit: Nausea and vomitingKnowledge deficit r/t lack of exposure to informationTo move slowly; not turn head quickly
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Slide123Noise Induced Hearing Loss
Major portion of hearing impairment among individuals 35 – 65 years of ageCan be traumaticSudden loud noise; i.e., blast)Over time from repeated injury from noiseMajor causesIndividual noiseFirearms (second)Loss of higher frequencies
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Slide124Presbycusis
Hearing loss related to agingMore common after age 50Hearing loss of higher frequenciesAccompanied by tinnitis
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Slide125Hearing Aids
All hearing aids consist ofMicrophoneAmplifierBatteryReceiver In the ear for hearing loss of 25 – 65 dB; worn in ear concha (pinna)In the canal for hearing loss of 25 – 50 dB; worn in ear canalPostauricular – for hearing loss of 25 -80 dB; worn behind ear
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Slide126Care of Hearing Aids
Turn off when not usingOpen battery compartment at night to avoid draining the batteryKeep extra batteries available at all timesWash earmold frequently with mild soap and water with the use of pipe cleaner to cleanse the cannulaDo not wear if ear infection
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Slide127Sense of Taste
Taste (gustation) serves as a protector from rotten or putrid food and provides delightful sensations of creamy , chocolate, crunchy chips, chew taffy and fruitful piesTaste sensors ara most efficient at room temp and respond only to substances in solutionTaste buds are locate in four areas of the tongue that sense sweet, salt, bitter & sour.Tongue also aids in swallowing and speech
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Slide128Taste con’t
Motor movement controlled by CN XII; temp and position controlled by CN V and IXSensation is altered secondary to neuro disorders & trauma. Evaluate for possible causes including diet, medication, smoking, caffeine and olfactory disturbancesWorks closely with CN1 to identify tastes
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Slide129Sense of Smell
Sense of smell (olfaction) serves as guardian from danger. Warns of impending danger from gas leaks, smoke, fires, rancid meat/fish, sour dairy productsDisorders often undetectedEmotional changes assoc with loss of smellNew research may offer clues to alterations in diet habits, wt loss or gain, anorexia, malnourishment, even ADL such as bathing and brushing teeth.
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Slide130Sense of Touch
Sense of touch (tactile) includes sensations pertaining to the skinTactile receptors located thru-out skinCutaneous sensations of touch, pressure, vibration, cold, heat and painPts unable to sense temp variations need interventions regarding heat and cold therapies, bath water, cooking and exposureImmobility, skin integrity big issues for nurses
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Slide131The End!
Sensory