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NUR 475 – FNP III
HEENT
Normal Vision Changes with Aging: Diagnosis and Management
VISUAL CHANGE
Decrease in visual
acuity
Presbyopia
FUNCTIONAL CORRELATES
Performing all visual tasks
Decrease in contrast
sensitivity
Difficulty seeing under conditions
of poor lighter (e.g., night driving,
church) and poor contrast (e.g.,
reading a newspaper)
Problems with tunnels, movie
theaters, night driving
Decrease in dark
adaptation
Delayed recovery from
glare
Difficulty with near point tasks
Problems with headlights,
decreased visual functioning on
sunny days
MANAGEMENT
Increase illumination
Increase contrast
Corrective eyeglasses
Increase illumination
Filters
Magnification
Illumination
Sunglasses when outdoors
Take a moment to dark/light adapt
before trying to walk
Sunglasses (but not for night driving)
Antireflective lens coating
Hats, visors
Less fluorescent lighting
(Source: Carter, T.L. (September 1994). “Age-related vision changes: A primary care guide. Geriatrics, 49(9), 3745.)
Classifications of Visual Impairment
CLASSIFICATION
Legal blindness
Partially sighted
Functionally visually impaired
DEFINITION
Best visual acuity ≤ 20/200 in the better eye or
Visual filed ≤ 20o
Best visual acuity ≤ 20/70 in the better eye or
Visual filed ≤ 30o
When activities of daily living are affected
Best visual acuity ≤ 20/50
(Source: Carter, T.L. (September 1994). “Age-related vision changes: A primary care guide. Geriatrics, 49(9), 3745.
The four most prevalent age-related ocular diseases and the four leading causes of low vision
in the US are:
 Macular degeneration
 Open-angle glaucoma
 Cataract
 Diabetic retinopathy
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Age-Related Macular Degeneration (AMD)
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Leading cause of irreversible blindness in people 50 years of age or older in the developed world
Prevalence: 30% at age 75+; currently 8 million Americans have AMD
Risk factors: advanced age, white race, heredity, systemic hypertension, and a history of
smoking
Only 10% of individuals with macular degeneration have significant functional visual loss.
Since the macula is the area for central vision and provides the highest degree of visual
resolution, deterioration of this portion of the retina leads to the loss of central vision.
Leads to deficits in form recognition and light sensitivity
Types of macular degeneration:
o Dry (non-exudative) macular degeneration
 Most common (80-90% of cases)
 Manifested by a progressive loss of retinal and pigment epithelium and
gradually increasing central blind spot
 Untreatable
o Wet (exudative, or neovascular) macular degeneration
 Due to accumulation of subretinal blood or exudates (from neovascularization)
 Can have an acute onset with decreased central vision, metamorphopsia
(blurred vision), or a dark spot in the central vision (central scotoma)
 If found early and not yet in fovea, laser phocoagulation therapy is possible
Management (Source: Jager, RD, Mieler, WF, & Miller, JW. (June 12, 2008). NEJM, 358(24), 2606-2617)
o Antioxidant supplementation (Preser-Vision, Bausch & Lomb): Vitamins C & E, beta
carotene, zinc oxide, and cupric oxide.
 NOTE: Not recommended for those with any smoking history due to increased
risk of lung cancer with beta-carotene supplements in current or former
smokers. (Source: Gohel, PS, Mandava, N, Olson, JL, & Durairaj, VK.(April 2008). The
American Journal of Medicine, 121(4), 279-281.)
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Lifestyle and dietary modifications
 Quit smoking
 Decrease dietary intake of fat
 Maintain healthy weight and BP
 Increase dietary intake of antioxidants through foods such as green leafy
vegetables, whole grains, fish, and nuts
o Intravitreal antiangiogenic therapy (injection of antiangiogenic agents directly into the
vitreous)
Visual rehabilitation for macular degeneration
o Self-monitor central vision (Amsler’s chart/Amsler’s grid)
o Magnify the area of central vision
 Hand-held ocular lenses
 Video enlargement
 Microfilm reading systems
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Increase field illumination
Glaucoma
Definition:
 Formerly: increased IOP that leads to blindness
 Now: A group of conditions characterized by eye changes usually associated with increased IOP
 A progressive optic neuropathy involving characteristic structural damage to the optic nerve and
characteristic visual field defects
Changes in IOP:
 Normal IOP: 10-20 mm Hg and IOP difference of less than 3 mm Hg between eyes
 Pressures of 20-30 mm Hg will cause gradual damage over the years due to atrophy of the
retinal ganglion cell layer.
o Damage seen on fundoscopy:
 optic disk shows cupping of the optic nerve head and a decrease in the diameter
of the optic vessels
 as the orange-red area of nerve fiber axons shrinks, the lighter cup in the center
grows and the visual field of the patient becomes smaller
o Changes in the disk are reflected in the patient’s decreased visual acuity
 Pressures of 40-50 mm Hg can cause much more rapid vision loss due to ischemia of the optic
nerve and retinal structures and may even result in vascular occlusion.
 For example of how vision can change with glaucoma:
http://www.ahaf.org/glaucoma/about/understanding/progression-of-glaucoma.html
Incidence:
 5 million people worldwide are blind from glaucoma (World Health Organization)
o People diagnosed with glaucoma in Third World countries are more likely to progress t
blindness due to lack of treatment options
 In US: 2 million diagnosed with glaucoma
 High predominance in:
o African Americans and Asians than Caucasians
o Females more than males
o Between ages 55 and 70
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Conventional pathway for normal flow of aqueous humor: fluid passes from the posterior chamber
through the papillary aperture to the anterior chamber, then to the trabecular meshwork, exiting
through Schlemm’s canal and finally into the episleral veins, which drain into the venous system via the
facial vein.
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Both diagrams taken from: website of National Glaucoma Research, a program of the American Health
Assistance Foundation at http://www.ahaf.org/glaucoma/about/understanding/
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Glaucoma Terminology
(Erwin, EA & Mendelson, M. (July 2005) Acute presentations of glaucoma. Emergency Medicine, 14-21.)
Angle of anterior chamber
Primary glaucoma
Secondary glaucoma
Open-angle glaucoma
Acute angle-closure
glaucoma
Angle created by cornea, iris, and trabecular meshwork
Idiopathic increase in IOP
Increase in IOP from known disease
Insidious increase in IOP that can slowly progress to blindness
Medical emergency marked by abrupt increase in IOP that can rapidly
progress to optic nerve damage and nerve death
A brief note on secondary glaucoma:
 many secondary causes are rare
o exfoliative syndrome and pigment dispersion syndrome
 debris and granules are caught up in the trabecular meshwork and block the
flow of the aqueous humor
o lens-induced glaucoma (lens subluxation or dislocation)
 structures which drain aqueous humor collapse without the lens support
o ocular inflammatory disease (can occur with herpes zoster ophthalmicus)
o intraocular tumors
o ** topical or systemic corticosteroids
Open-Angle Glaucoma
 Most common form of glaucoma
 Primary type
 Slow, usually painless process that occurs over a long period of time
 Diagnosis usually made only after screening of patients in high-risk populations
o > 40 years of age
o Obese patients
o Patients with diabetes, HTN
 Since flow of aqueous humor is a passive process, increased venous pressure
can inhibit the normal removal of aqueous humor.
o History of ocular or severe head trauma
o Family history of glaucoma
 Many elderly patients are being treated for open-angle glaucoma and may present with
adverse effects from their medications.
 Treatment: typically topical medications are used (see next page)
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Class
Cap or label color
Trade (generic) med
names
Beta-adrenergic
blocking agents
Yellow (5%) or light blue
(0.25%)
Betagan (levobunolol)
Timoptic, Betimol
(timolol)
Betoptic (betaxolol)
OptiPranolol
(metipranolol)
carteolol
Local side effects
Alpha-adrenergic
agents
Purple
Alphagan (brimonidine)
Iopidine (apraclonidine)
Carbonic anhydrase
inhibitors
Orange or white
Trusopt (dorzolamide)
Azopt (brinzolamide)
 Redness
 Itching
 Edema
Prostaglandin F2-alpha
analogs
Teal
Xalatan (latanoprost)
Lumigan (bimatoprost)
Travatan (travoprost)
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Miotics
Green
Isopto Carpine, Pilocar
(pilocarpine)
 Minimal transient
ocular discomfort
 Stinging
 Burning
 Irritation
Redness
Stinging
Darkening of the iris
Darkening of
periorbital skin
pigment
 Longer and thicker
eyelashes
 Blurred vision
(especially in younger
patients)
 Tearing
Systemic side effects
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Bradycardia
Impotence
Fatigue
Depression
Exacerbation of
asthma/COPD
Use with caution in
patients with heart
block, heart failure,
asthma, COPD, or
depression
 Dry mouth
 Fatigue
Contraindicated with
MAOIs (or within 14
days of MAOI)
 Minimal transient
bitter taste
Use with caution in
patients with liver
disease, severe renal
disease, adrenocortical
insufficiency, or severe
COPD
Negligible system side
effects
Mechanism of action
Reduces aqueous
humor production
Reduce aqueous humor
production and
increases outflow of
aqueous humor
Decreases aqueous
humor production
Increases the outflow of
aqueous humor
[Note: bimatoprost also
marketed as Latisse, for
eyelash hypotrichosis]
Brow aches
Increases the outflow of
aqueous humor
Compiled from:
Erwin, EA & Mendelson, M. (July 2005). Acute presentations of glaucoma. Emergency Medicine, 14-21. and Kowing, D &
Kester, E., (July 2007). Keep an eye out for glaucoma. The Nurse Practitioner, 18-23.
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If medications are not sufficient to reduce the IOP, laser surgery is the usual next step.
Depending in the type of procedure, laser surgery may be used for open-angle, angle-closure or
neovascular glaucoma. A laser is directed toward the trabecular meshwork, the iris, ciliary body or the
retina and is used in various ways to reduce eye pressure. Laser surgery is performed on an outpatient
basis in an eye doctor’s office or clinic after the eye has been numbed.
There are several types of laser surgeries:
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Trabeculoplasty is often used to treat open-angle glaucoma. In argon laser trabeculoplasty
(ALT), a high-energy laser is aimed at the trabecular meshwork to open areas in these clogged
canals. These openings allow fluid to bypass drainage canals and flow out of the eye. In selective
laser trabeculoplasty (SLT) a low-energy laser treats specific cells in the trabecular meshwork.
Because it affects only certain cells without causing collateral tissue damage, SLT can potentially
be repeated.
Laser peripheral iridotomy (LPI) is frequently used to treat angle-closure glaucoma, in which the
angle between the iris and the cornea is too small and blocks fluid flow out of the eye. In LPI, a
laser creates a small hole in the iris to allow fluid drainage.
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Cyclophotocoagulation is usually used to treat more aggressive or advanced open-angle
glaucoma that has not responded to other therapies. A laser is directed through the sclera or
endoscopically at the eye fluid-producing ciliary body. This helps decrease the production of
fluid and lower eye pressure. Multiple treatments are often required.
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Scatter panretinal photocoagulation is a laser procedure that destroys abnormal blood vessels
in the retina which are associated with neovascular glaucoma.
The most common side effects of laser surgery are temporary eye irritation and blurred vision. There is a
small risk of developing cataracts.
Currently, laser surgery is the most frequently used procedure to treat glaucoma. It normally lowers eye
pressure, but the length of time that pressure remains low depends on many factors, including age of
the patient, the type of glaucoma and other medical conditions that may be present. In many cases,
continued medication is necessary, but potentially in lower amounts.
(Content on laser surgery taken from: http://www.ahaf.org/glaucoma/treatment/common/)
Acute Angle-Closure Glaucoma
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Relatively uncommon cause of glaucoma
Ocular emergency
In patients prone to acute angle-closure glaucoma, the anterior angle of the eye is narrower
than normal, and the conventional route of aqueous humor outflow is more easily blocked by
occlusion of the trabecular meshwork by the iris and the cornea.
IOP can rise to 80 mm Hg, leading to permanent, rapid optic nerve injury or death
Usual chief complaint: headache or eye pain and a significant decrease in visual acuity
o Also: nausea, vomiting, red/painful/swollen eye
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o Systemic effects from vagal nerve stimulation: diffuse abdominal pain, N, V
History: patients may recall episodes of eye pain at night or in dark rooms or theaters, during
periods of emotional upset, or after receiving an anticholinergic or sympathomimetic
medication such as eye drops given prior to an eye exam.
o These episodes may have been relieved with sleep or bright lights, since both cause
miosis, pulling open the anterior chamber angle and allowing aqueous humor to flow
out.
Physical exam
o Mid-dilated fixed pupil (commonly oval-shaped)
o Hazy cornea (can cause patient to see halos around lights)
o Tearing
o Conjunctival injection (red eye)
o Measurement of ocular pressure in both eyes with tonometry
 Schiotz tonometer
 Tono-Pen
o Fundoscopic exam: glaucomatous cupping (ratio of the yellow optic cup to the darker
pigmented optic disk increases), retinal vessel displacement, and splinter or flame
hemorrhages
o Visual acuity testing
Differential diagnosis
o Corneal abrasion or lacteration
o Conjunctivitis
o Iritis
o Uveitis
o Herpes zoster
o Periorbital cellulitis
o Retinal artery occlusion
o Cavernous sinal thrombosis
o Temporal arteritis
o Sinusitis
o Migraine headache
Treatment:
o emergent consultation with an ophthalmologist
o combination of medications used for open-angle glaucoma
o other meds: optic steroids, miotic agents, NSAIDS, hyperosmotic agents
o followed by peripheral irdiotomy or iridectomy
Patient education: warn patient that the other eye is also at risk for an acute angle-closure
glaucoma episode; emphasize seeking immediate care
Cataracts
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An opacity in the normally transparent focusing lens inside the eye that prevents light rays from
being focused clearly on the retina
o Blue light most distorted; may help to use yellow-tinted filters on corrective lenses
One of the most important causes of reversible blindness in elderly persons
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Estimated that number of Americans with cataracts will increase by approximately 50% in the
next 20 years as the population ages
50% of those over age 40 show signs of lens clouding
Leading cause of low vision among whites, blacks, and Hispanics
Causes:
o Aging
o Cumulative UV-B light exposure
o Intraocular diseases (uveitis, intraocular malignancies, retinitis pigmentosa, retinal
detachment)
o Trauma
o Drugs (topical and systemic steroids, phenothiazines, phospholine iodide eyedrops)
o Endocrine/metabolic disorders (diabetes mellitus, hypoparathyroidism, hypothyroidism,
galactosemia)
o Congenital
Treatment: cataract surgery for removal of the cataractous lens and implantation of intraocular
lens
When to have cataract surgery: typically when decreased vision interferes with the patient’s
ability to function in his/her daily living pattern, occupation, lifestyle and desired or required
activities.
o Surgery is not indicated just because a cataract is present, since it may be mild and well
tolerated.
o The surgery may be recommended if the cataract is interfering with diagnosis or
treatment of other ocular diseases such as diabetic retinopathy or potential intraocular
malignancy
o Success rate 80-90%
o Potential complications: wet macular degeneration (usually had early-stage MD lesions
pre-op), posterior capsular opacification (easily correct with laser procedure), retinal
detachment
Diabetic Retinopathy
(Source: Carter, T.L. (September 1994). “Age-related vision changes: A primary care guide. Geriatrics, 49(9), 3745.
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Symptoms: decreased acuity, contrast sensitivity, color perception, and dark/light adaptation,
as well as glare disability and scotomas
Key in preventing visual impairment: early diagnosis and treatment
o All people with diabetes should have a yearly retinal exam through a dilated pupil
Nonproliferative diabetic retinopathy
o Clinical manifestations: dilated retinal veins, microaneurysm, intraretinal hemorrhages,
hard (lipid) exudates, cotton wool spots (microinfarcts) and macular edema
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Patient needs to be monitored for macular edema and proliferative changes every 3-6
months
Proliferative diabetic retinopathy
o Clinical signs: neovascularization, vascular fibrosis and preretinal as well as vitreous
hemorrhages
o Managed with laser photocoagulation
Vision Loss in Older Persons (> age 65)
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Associated with depression, social isolation, falls, and medication errors
Should be screened every 1-2 years with attention to specific disorders such as diabetic
retinopathy, refractive error, cataracts, glaucoma, and age-related macular degeneration
Vision-related adverse effects of commonly used medications, such as amiodarone or
phosphodiesterase inhibitors, should be considered when evaluating vision problems
Prompt recognition and management of sudden vision loss can be vision saving.
Aggressive medical management of diabetes, hypertension, and hyperlipidemia; encouraging
smoking cessation; reducing ultraviolet light exposure; and appropriate response to medication
adverse effects can preserve and protect vision.
Drugs that are Toxic to the Eyes (from publication of The American Academy of Ophthalmology)
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Drugs that cause irreversible damage in recommended doses
o Corticosteroids (cause cataracts)
o Isotretinoin (Accutane) (can cause pseudo-tumor cerebri)
o Hydroxychloroquine (Plaquenil) (causes “bull-s eye” pericentral scotoma)
o Ethambutol (can cause visual loss)
Drugs that cause reversible damage in recommended doses (cause paralysis of accommodation,
so that patients cannot focus on near targets)
o Antipsychotics
o Antihistamines
o Tricyclic antidepressants
o Antispasmodics
o Some centrally-acting drugs for Parkinson’s Disease
Drugs that cause damage only above recommended doses or serum levels
o Digoxin (with dig toxicity, may have yellowish-orange vision; usually returns to normal
with normal serum dig level)
o Phenytoin (Dilantin) can have blurred vision
o Carbamazepine (Tegretol) can have blurred vision
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Eye Pain
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Iritis
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Most common is anterior, confined to the iris
Acute iritis is the more common form seen by primary care providers (vs. chronic)
Occurs in young adults
Causes: ankylosing spondylitis, Reiter’s syndrome, sarcoidosis, collagen diseases (RA, SLE), TB,
syphilis, toxoplasmosis
Manifests as ocular pain, redness, photophobia, and blurred
Tearing may be present, but neither purulent discharge nor a history of trauma or presence of
foreign body is elicited
Exam: pupil tends to be small, may be irregular because the iris has adhered to the anterior lens
Conjunctiva is hyperemic = ciliary flush
Dx: confirmed by presence of inflammatory cells
o The cells, due to the primary inflammation, usually float in the anterior chamber (graded
on a scale of 0 to 4+)
o The inflammatory cells may layer in the anterior chamber
o The inflamed vessels allow protein to leak into the aqueous fluid, making the fluid
appear translucent when viewed with a slit lamp
Treatment: targeted at decreasing inflammation and alleviating pain
o Mydriatic agents (such as phenylephrine) to dilate pupil
o Cycloplegic agents (such as atropine) to ease pain and photophobia
o Corticosteroid drops to suppress the inflammation
Floaters and Flashes
Posterior Vitreous detachment
 The vitreous has the consistency of a dilute gel and is attached to the retina and optic nerve
head
 May sometimes see small specks or clouds moving in the field of vision (floaters)
o Often seen when looking at a plain background, like a blank wall or blue sky
 Floaters are tiny clumps of gel or cells inside the vitreous. What is actually seen are the shadows
they cast on the retina
 When people reach middle age, the vitreous gel may start to thicken or shrink, and pull away
from the back wall of the eye, causing a posterior vitreous detachment.
o More common in people who:
 Are nearsighted
 Have undergone cataract operations
 Have had YAG laser surgery of the eye
 Have had inflammation inside the eye
 Concern: if the vitreous detachment causes a retinal tear, since it can lead to a retinal
detachment. This needs to be corrected to prevent vision loss.
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Also: when the vitreous gel rubs or pulls on the retina, the patient may see what looks like
flashing lights or lightning streaks.
Need ophthalmology to see if:
o Even one new floater appears suddenly
o Sudden flashes of light
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Hearing Problems
Hearing Loss in Normal Aging
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•
•
•
Extremely common in old age
65% of those aged 85 years report some hearing problem
only 16% have a hearing aid or other assistive listening device
only 8% actually use their aid or device
10 dB reduction in hearing sensitivity per decade of life after age 60
Presbycusis (“old man’s hearing”)
•
Decrease in perception of higher frequency tones (consonants are less audible, so words become
only vowels)
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Progresses over time, regardless of amplification
Decreased ability to focus on a desired sound by internally masking competing sounds
(conversation in a restaurant)
To assist patient with presbycusis
•
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•
•
Amplification
eliminate or decrease background nose when direct verbal communication is attempted
Use lowest comfortable tone to speak
Do not shout at the person
Ear Diseases & Hearing Loss
Conductive hearing loss
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AC < BC
Can occur in both the external and middle ear
Cerumen impaction = most common external ear cause of conductive hearing loss
• A frequently overlooked problem in elderly people with hearing impairment
Middle ear conductive hearing loss
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Most common = otosclerosis
Idiopathic stiffening of the bone surrounding the cochlea
Amplification of limited help
Surgical approaches that improve ossicle mobility have resulted in significant improvement.
Sensorineural hearing loss
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Both air and bone conduction are decreased, especially toward higher frequencies
Gradual: neoplasms of brainstem or CN VIII; long-term exposure to high-intensity noise
Sudden: vascular event within inner ear; medication effects
Sudden often accompanied by vestibular sx. of vertigo, dizziness, and nystagmus
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Metabolic causes of hearing impairment can be from toxic medication effects or from endocrine
diseases:
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Thyroid
pancreatic
adrenal
Assessment of Hearing Impairment
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•
•
Obtain thorough history
Examine external ear canal
Remove cerumen impactions
Inspect tympanic membrane
Assess hearing sensitivity
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Whisper testing
Hand-held otoscope /audiometer
Read: “Hearing loss is often undiscovered, but screening is easy” at
http://www.ccjm.org/content/71/3/225.full.pdf+html
 Contains Hearing Handicap Inventory for the Elderly
 Information on hearing aids
Read: “Differential diagnosis and treatment of hearing loss” at
http://www.aafp.org/afp/2003/0915/p1125.pdf
 Includes indicators of hearing loss in infants and young children
 Table on diagnosis of conductive and sensorineural types of hearing loss
Tinnitus: The perception of noises in the ear, head, or both without an external acoustic source.
 Considered a symptom, not a disease
 Frequently associated with hearing loss
 Predictors of tinnitus:
o High-frequency hearing deficit
o Previous loud noise exposure
o Age (more common in age 60-69)
Thorough history and physical examination are very important.
History components:
 HPI for chief complaint of tinnitus
o Location (unilateral or bilateral)
o Duration
o Character (pulsatile, intermittent, constant)
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HTN, DM, smoking, hyperlipidemia, and cerebrovascular disease raise suspicion
of atherosclerosis carotid artery disease, especially in an older patient
presenting with pulsatile tinnitus
 Pulsatile tinnitus causes: carotid stenosis, arteriovenous fistula or
malformations, aneurysms, aberrant carotid artery, intracranial hypertension,
high cardiac output (anemia, hyperthyroidism, drug induced), glomus
typanicum, vascular tumors (glomus jugular)
o Quality (ringing, hissing, roaring)
o Associated vertigo or hearing loss
o Perceptual characteristics (pitch, loudness)
Medical and surgical history
o Noise exposure (occupational, recreational)
o Head trauma
o Medications and ototoxic agents
 Antibiotics, diuretics, chemotherapeutic agents (including mechlorethamine and
vincristine), high doses of aspirin and NSAIDs, quinine, antidepressants
o Dental problems (e.g., TMJ)
o Exacerbating factors (diet, stress, activity level, smoking, alcohol)
o Review of systems
o Prior otologic surgery
Psychosocial history
o Level of annoyance/Impact on quality of life
o Sleep disturbance
o Depression, stress
o Suicidality
Compensation
o Pursuing compensation, disability, or other legal action related to tinnitus
Physical Examination
 HEENT
o Otoscopy
o Tuning fork examination (Weber, Rinne testing)
o Testing of cranial nurses
o Oral cavity examination
o Palpation of temporomandibular joint and inspection of dentition
o Have patient turn head toward the side of the tinnitus (causes compression of the
internal jugular vein)
 With a venous cause, the tinnitus will decrease in intensity or cease
 Turning the head in the other direction will cause an opposite effect
 If the cause is arterial, the maneuver will not have any effect on the tinnitus
 Full cardiovascular assessment, noting BP, murmurs, dysrhythmias
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o
Note any carotid and/or temporal artery bruits
Not to be missed: vestibular schwannoma, Meniere disease, cholesteotoma, glomus jugular tumor, and
temporal bone trauma
Red Flags that should prompt a referral to ENT specialist:
 Unilateral tinnitus
 Pulsatile tinnitus
 Tinnitus associated with:
o Sudden loss of hearing
o Pressure or fullness in one or both ears
o Dizziness or balance problems
o Fluctuating hearing
Diagnostics
 Routine lab testing without a pertinent history is not recommended
 If indicated testing may include
o CBC with diff to R/O anemia or infection
o CMP to determine presence of underlying health conditions such as DM
o ESR to screen for autoimmune process
o FLP to determine possible risk factor for atherosclerosis
o Thyroid function tests
o Vitamin B12 and folate levels might be considered
o Tests for infectious causes such as syphilis, HIV, or Lyme disease may be warranted
based on H & P data
 Tympanometry
 Audiogram (hearing threshold level > 25 decibels is considered abnormal)
NOTE: All patients with unilateral tinnitus or pulsatile tinnitus should be referred to an otolaryngologist
for further evaluation and any radiologic testing.
 If has pulsatile tinnitus and has had recent head trauma or surgery, an urgent referral to an
otolaryngologist is warranted.
o If specialty services are not available, send to emergency department.
Counseling:
 Stress management
 Improvement of sleep patterns
 Avoiding silence by maintaining a safe level of background noise (tapes, white noise generators,
radios)
 Promotion of relaxation and regular exercise
 Examine diet, avoiding excessive use of caffeine, nicotine, alcohol, and salt
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Engagement in meaningful activities and hobbies
Avoid overuse of ASA, NSAIDs, or other potentially ototoxic agents
References:
Newman, C.W., Sandridge, S.A., Scott, M.N., Cherian, K., Cherian, N., Kahn, K.M., & Kaltenbach, J. (May 2011).
Tinnitus: Patients do not have to “just live with it”. Cleveland Clinic Journal of Medicine, 78(5), 312-320.
Ruppert, S.D., & Fay, V.P. (October 2012). Tinnitus evaluation in primary care. The Nurse Practitioner, 37(10), 2026.
Cerumen Impaction
 One of the most common reasons patients seek medical care for ear-related problems
 Cerumen normally expelled from the ear canal by a self-cleaning mechanism assisted by jaw
movement
 Use of hearing aids or earplugs may cause stimulation of cerumen glands, leading to excessive
cerumen production
 Treatment options
o Irrigation
o Manual removal
o Topical preparations
 Considerations
o Narrow ear canal
 may limit visualization and increase risk of trauma from irrigation and manual
removal
 common in persons with Down syndrome, other craniofacial disorders, chronic
external otitis
o Perforated TM: manual removal preferred technique
o Persons with diabetes: cerumen pH higher than normal, may facilitate growth of
pathogens; consider ear drops to acidify the ear canal after irrigation
o Patients with AIDS: tap water irrigation may pose risk for malignant external otitis
o Anticoagulant therapy: higher risk of cutaneous hemorrhage or subcutaneous
hematoma with instrumentation
Reference:
Armstrong, C. (November 1, 2009). Diagnosis and management of cerumen impaction. American Family
Physician, 80(9), 1011-1013.
Allergic rhinitis
 Affects 10-30% of adults and 40% of children in US
 Characterized by one or more of following nasal symptoms
o Congestion
o Rhinorrhea (anterior and posterior)
o Sneezing
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o Itching
May affect a patient’s quality of life through fatigue, headache, cognitive impartment, sleep
disturbance
Types
o Seasonal: caused by seasonal allergens
o Perennial: caused by dust mites, molds, animal allergens, occupational allergens, pollen
Risk factors
o Family history of atopy
o Serum immunoglobulin E (IgE) levels > 100 IU/mL before 6 years of age
o Higher socioeconomic class
o Positive allergy skin prick test
Treatment
o Step 1: allergen avoidance and patient education
o Step 2:
 For mild intermittent symptoms
 Second-generation oral or intranasal antihistamine, as needed
 For mild to moderate persistent symptoms
 Intranasal corticosteroids alone as 1st line treatment
 Consider nasal irrigation or decongestants for nasal congestion
o NOTE: Patients should be instructed to use only sterile, distilled
or previously boiled water for nasal irrigation (To avoid primary
amebic meninogencephalitis that occurred in patients who
irrigated their sinuses with neti pots and contaminated tap
water).
 Consider ipratropium (Atrovent) or intranasal antihistamines for
rhinorrhea
 Consider oral or intranasal antihistamine for persistent nasal ocular
symptoms
 For severe persistent symptoms
 Intranasal corticosteroids PLUS oral or intranasal antihistamine, oral
leukotriene receptor antagonist, or intranasal cromolyn (Nasalcrom)
 If symptoms persist, consider immunotherapy referral or alternative
treatments (e.g., allergen avoidance, nasal irrigation, acupuncture,
probiotics, herbal preparations)
Examples of medications
o Second-generation oral antihistamines
 Zyrtec, Xyzal, Claritin, Clarinex, Allegra
o Intranasal antihistamines
 Astelin, Patanase
o Intranasal corticosteroids
 Beconase, Rhinocort, Omnaris, Veramyst, Flonase, Nasonex, Nasacort
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o
o
Intranasal anticholinergics
 Atrovent
Leukotriene receptor antagonists
 Singulair
References:
Lambert, M. (July 1, 2009). Practice parameters for managing allergic rhinitis. American Family Physician, 80(1),
79-85.
Sur, D.K., & Scandale, S. (June 15, 2010). Treatment of allergic rhinitis. American Family Physician, 81(12), 14401446.
Common viral infections in older adults: Cold vs. Flu…How do you tell the difference?
Fill in the following table based on your readings:
Cold
Symptoms
Onset
Fever
Headache
General aches, Pain
Fatigue, Weakness
Extreme Exhaustion
Stuffy Nose
Sneezing
Sore Throat
Chest Discomfort, Cough
Complications
Prevention
Treatment
Flu (Influenza)
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Dental caries, infections, xerostomia, candidiasis, oral cancer, tongue conditions
Read: “Common Oral Conditions in Older Persons” at http://www.aafp.org/afp/2008/1001/p845.pdf
Read: “Oral Manifestations of Systemic Disease” at http://www.aafp.org/afp/2010/1201/p1381.pdf
Read: “Common Tongue Conditions in Primary Care” at http://www.aafp.org/afp/2010/0301/p627.pdf
Hoarseness: Altered voice quality, pitch, loudness, or vocal effort that impairs communication or
reduces voice-related quality of life.
Causes of Hoarseness
 Inflammatory or irritant
o Allergies and irritants (e.g., alcohol, tobacco)
o Direct trauma (intubation
o Environmental irritants
o Infections (URI, including viral laryngitis)
o Inhaled corticosteroids
o Laryngopharyngeal reflux
o Vocal abuse
 Neoplastic
o Dysplasia
o Laryngeal papillomatosis
o Squamous cell carcinoma
 Neuromuscular and psychiatric
o Multiple sclerosis
o Muscle tension dysphonia
o Myasthenia gravis
o Nerve injury (vagus or recurrent laryngeal nerve)
o Parkinson disease
o Psychogenic (including conversion aphonia)
o Spasmodic dysphonia (laryngeal dystonia)
 Associated system diseases
o Acromegaly
o Amyloidosis
o Hypothyroidism
o Inflammatory arthritis (cricoarytenoid joint involvement
o Sarcoidosis
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Clues that may suggest a serious underlying cause of hoarseness:
 Associated with hemoptysis, dysphagia, odynophagia, otalgia, or airway compromise
 Concomitant discovery of a neck mass
 History of tobacco or alcohol use
 Neurologic symptoms
 Possible aspiration of a foreign body
 Symptoms do not resolve after surgery (intubation or neck surgery)
 Symptoms in a neonate
 Symptoms in a person with an immunocompromising condition
 Symptoms occur after trauma
 Unexplained weight loss
 Worsening symptoms
Diagnosis/Treatment
 When onset of hoarseness is acute, lasting < 2 weeks, with an apparent benign cause (e.g.,
recent vocal abuse, URI, allergy, GERD), and there is nothing to suggest a more serious etiology,
empiric treatment may be instituted with further evaluation
 In patients with recent symptoms of GERD, may try treating with short courses of high-dose PPIs
to see if hoarseness improves
 If systemic condition known to cause hoarseness (hypothyroidism, Parkinson disease) is present,
treat underlying condition. If no improvement in 4 weeks, refer for laryngoscopy
 When hoarseness lasts longer than 2 weeks and does not have an apparent benign cause, direct
evaluation of the larynx by direct or indirect laryngoscopy is indicated
 CT or MRI should not be performed in patients with primary hoarseness before visualizing the
larynx (grade C recommendation)…it is reserved for assessment of specific pathology after the
larynx has been visualized.
 Vocal hygiene
o Humidification of the air
o Avoidance of smoke, dust, and other inhaled irritants
o Avoidance of frequent coughing or throat clearing
o Avoidance of shouting or speaking loudly for prolonged periods
o Increased fluid intake; avoidance of large meals, excessive caffeine and alcohol use, and
spicy foods
 Referral to speech-language pathologist for voice therapy
References:
Feierabend, R.H., & Malik, S.N. (August 15, 2009). Hoarseness in adults. American Family Physician, 80(4), 363370.
Huntzinger, A. (May 15, 2010). Guidelines for the diagnosis and management of hoarseness. American Family
Physician, 81(10), 1292-1296.
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Driving
Requirements for driving include:
 Cognitive capacity, with knowledge of road regulations, how to operate a motor vehicle, and how to
arrive at a certain destination
 Sensory capacity, with visual acuity and hearing ability
 Motor function, with an intact musculoskeletal system and manual dexterity
 Neuromuscular capacity, with strength, coordination, and reaction time
 Skills to integrate the above activities simultaneously in order to drive safely.
Read: “How to assess and counsel the older driver” at http://www.ccjm.org/content/69/3/184.full.pdf+html
Be aware of state law requirements for license renewal, for example in Illinois:

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Drivers age 21 through 80 — licenses are valid for four years and expire on a driver's birthday;
drivers age 81 through 86 — licenses are valid for two years; drivers age 87 and older must
renew their licenses each year.
Vision screening is required for all drivers renewing at a facility.
All persons age 75 and older must take a driving exam.
(http://www.cyberdriveillinois.com/departments/drivers/drivers_license/drlicid.html)
Illinois is one of the few states that does not accept reports from concerned citizens on drivers thought
to be unsafe. The state only accepts reports from law enforcement officers and physicians. If a state
agency finds a complaint reasonable and credible, it may ask the reported driver to submit additional
information, which could be used to help determine if a screening or assessment is justified.
(http://seniordriving.aaa.com/states/illinois)