Current Geriatric Diagnosis & Treatment, 1st Edition

Section III - Common Disorders in the Elderly

16. Visual & Hearing Impairment

Timothy Lewis MD

Gregg Warshaw MD


General Considerations

Visual impairment, defined as best corrected visual acuity worse than 20/40 and better than 20/200 in the better seeing eye, increases rapidly with age, especially after age 75. Visual impairment often limits functional independence among older adults and correlates with physical disability, falls, social isolation, and depression. Blindness carries a range of definitions, from no vision at all to best corrected visual acuity < 20/200 in the better seeing eye.

The predominant age-related eye diseases causing visual impairment and blindness include age-related macular degeneration, cataract, diabetic retinopathy, and glaucoma. Whites most often have impairment or blindness from age-related macular degeneration, whereas blacks have higher rates of impairment and blindness from cataract, glaucoma, and diabetic retinopathy. Uncorrected refractive error is another prevalent cause of visual impairment that affects all age groups. Nearsightedness (myopia) is generally less frequent with age, whereas farsightedness (hyperopia) generally increases with age. About 33% of older individuals with acuity worse than 20/40 improve to 20/40 or better with correction of refractive error.

Clinical Findings


Age-related eye changes include functional alterations in accommodation, acuity, refractive power, visual fields, contrast sensitivity, corneal sensation, dark adaptation, and tear production as well multiple structural changes (Table 16-1). Presbyopia, the progressive loss of lens accommodation for near vision, usually becomes apparent by 45 years of age. Individuals with presbyopia find it increasingly difficult to focus on near objects that appear blurred without use of convex lens.


Visual acuity should be measured in each eye separately using a standard Snellen chart at 20 feet and a hand-held chart for checking near vision. The testing room should be adequately lighted, and glasses should be clean and properly aligned to optimize testing conditions. Evaluation should include inspection of the optic disk for cupping, color, and sharpness of margins. Evidence of arteriolar narrowing, hemorrhages, and exudates should also be noted during the retinal examination. Examination of the macula for pigmentary abnormalities suggestive of macular degeneration is also recommended. The nonophthalmologist's eye examination should also include inspection of the lids for entropion, ectropion, and blepharitis as well as penlight examination for corneal clarity, conjunctival redness, eyelash crusting, and pupillary reaction. Additionally, pupillary testing with the swinging flashlight test is recommended to rule out an afferent pupillary defect.



  • A lens opacity that can be observed through a well-dilated pupil with an ophthalmoscope or slit lamp.
  • Symptoms may include blurred vision, increased glare, multiple images, alterations in color, and streaking of lights at night.
  • The 3 main types of cataract are nuclear, cortical, and posterior subcapsular.

General Considerations

Cataracts are usually age related and are the leading cause of blindness in the world. Cataracts affect whites more frequently than other races, especially with increasing age. Severe contrast sensitivity impairment resulting from cataract disease increases at-fault automobile crash risk, even when affecting only 1 eye.


The pathogenesis of cataract formation is unknown, but its risk factors include advancing age, excessive exposure


to sunlight, and smoking. Cataracts may also arise in the setting of eye trauma, toxic substance exposure, steroid medications, or systemic diseases such as diabetes.

Table 16-1. Age-related eye changes.

   Decreased refractive power
   Decreased dark adaptation
   Decreased contrast sensitivity
   Visual field constriction
   Decreased tear production, resulting in dry eyes
   Increased difficulty with upward gaze, convergence
   Lens enlargement, resulting in narrowing of the anterior chamber angle
   Decreased lens translucency resulting in decreased retinal illumination
   Increased lens stiffness and decreased curvature
   Rod cell loss
   Liquefaction of vitreous gel
   Loss of eyelid tone, resulting in entropion or ectropion
   Rising intraocular pressure


High-dose supplementation with antioxidant vitamins does not prevent the development or progression of age-related cataracts. The use of sunglasses and hats to block ultraviolet light (UV-B) and smoking cessation are recommended for cataract prevention. Most traumatic cataracts are preventable through the use of protective safety goggles.

Clinical Findings


Symptoms include glare-related vision loss, difficulty with contrast sensitivity, and reduction of visual acuity. Color perception may be altered because of yellowish discoloration of the lens. A cataract produces characteristic alterations in the red reflex. A cortical cataract usually appears as peripheral dark opacities, some of which are commonly oriented radially against the red reflex. A posterior subcapsular cataract typically appears as a central area of irregular darkening of the red reflex. A dense nuclear sclerotic cataract appears as a dull gold reflection of light from the lens when the dilated pupil is viewed with a flashlight.


The best method to identify older persons with clinically significant cataract is to obtain a history and perform a routine ophthalmological examination, including a visual acuity check. Individuals with abnormal visual acuity that does not correct with refraction need referral to an ophthalmologist for further evaluation. It is not beneficial to screen asymptomatic persons for cataracts because their detection at a preimpairment stage does not confer a more favorable prognosis.

Differential Diagnosis

The differential diagnosis of age-related cataracts includes other disorders that reduce vision and are associated with an altered red reflex. Principal among these is blood in the vitreous. Traumatic cataract is usually associated with a well-documented history of severe ocular injury, frequently an open globe injury. Intraocular diseases such as chronic uveitis, glaucoma, and retinal detachment are also associated with cataract development.


Glaucoma and lens-induced uveitis are unusual complications of cataract. Lens-induced uveitis requires extraction of the lens. Cataracts are associated with visual hallucinations in persons with Alzheimer's disease, although the role of cataract treatment as an adjunct to antipsychotic therapy in persons with dementia is unknown.



Most individuals are acceptable candidates for cataract surgery, provided the intervention appears likely to restore vision to a satisfactory level. Acceptable candidates must be able to lie supine for 30 min or more and be free of unstable, life-threatening medical disorders. With current methods of clear cornea incision and topical anesthesia, even patients undergoing anticoagulation with coumadin are generally considered reasonable candidates. Cataract surgery is usually done in the outpatient setting and can be performed with minimal systemic medications.

Phacoemulsification (ultrasonic emulsification of the nucleus) is currently the procedure of choice for all routine cataract surgery. Visual rehabilitation takes about 1-3 weeks after phacoemulsification compared with 2-4 mo required for extracapsular cataract extraction. More than 90% of patients achieve a postoperative visual acuity of 20/40 or better.


Surgery is indicated if improved vision is considered attainable and would lead to improved functioning.


Surgery is unnecessary if the patient has sufficient vision to perform all important activities. When cataract surgery is indicated, visual acuity is usually 20/50 or worse. However, cataract surgery is sometimes indicated in the setting of lesser visual acuity loss when certain lens-induced diseases are present (eg, certain types of glaucoma or uveitis). Surgery may also be indicated if there is concomitant ocular disease (eg, diabetic retinopathy) that requires clear media to permit access to the retina for diagnosis or treatment.

Some patients may not benefit from cataract surgery because of preexisting cognitive problems. The decision whether to perform cataract surgery in patients with dementia should be guided by the expected impact on the individual's function and quality of life. If the demented patient is no longer reading or watching television because of cognitive impairment, improved vision is likely unnecessary. One should also consider whether cataract surgery would lessen disorientation, ambulatory fall risk, or troublesome visual hallucinations.


Preoperative care should include a history and physical examination to assess the patient's perioperative medical needs. The recognition of unstable life-threatening medical conditions and factors that would preclude supine positioning for ≥ 30 min (ie, severe kyphoscoliosis or decompensated congestive heart failure) is critical. Routine preoperative tests (eg, 12-lead electrocardiogram, complete cell count, electrolytes, urea nitrogen, and creatinine) are generally unnecessary before cataract surgery and do not appear to reduce perioperative morbidity and mortality.


Prompt recognition of complications that may occur after cataract surgery is essential. The incidence of endophthalmitis is about ≤ 0.2% and may present with eye pain, conjunctival injection, or vision loss. Retinal detachment, occurring in ~0.1% of surgeries, may be heralded by photopsia (reported as sparks or flashes) and floaters. Both complications require immediate consultation with an eye surgeon. Opacification of the posterior lens capsule is a less serious complication that is easily treated with laser capsulotomy.


Age-related cataracts usually progress slowly over a period of years, and patients should be offered reassurance that they may never require surgery.

Age-Related Eye Disease Study Research Group: A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E and beta carotene for age-related cataract and vision loss: AREDS report no. 9. Arch Ophthalmol 2001;119:1439. [PMID: 11594943] (A lack of a protective effect of antioxidant vitamins on prevention of cataracts was demonstrated.)

Owsley C et al: Visual risk factors for crash involvement in older drivers with cataract. Arch Ophthalmol 2001;119:881. [PMID: 11405840] (Analysis of elevated crash risk among older drivers with cataract.)

Schein OD et al: The value of routine preoperative medical testing before cataract surgery. N Engl J Med 2000;342:168. [PMID: 10639542] (Routine medical testing before cataract surgery did not measurably increase safety.)



  • Characterized by degeneration of the macular retina, leading to symptoms of central vision loss or distortion.
  • Often the first sign of the disease is the appearance of drusen, or yellow-white deposits apparent under the retina during the dilated eye exam.

General Considerations

Age-related macular degeneration (AMD) damages central vision and is the leading cause of irreversible blindness in older adults. The cause is unknown, and the prevalence of AMD and its associated blindness more than triples by decade after age 70. The Age-Related Eye Disease Study Research Group confirmed other associations besides age, including race (usually white), gender (slight female predominance), family history, and history of smoking and hypertension. The disease is classified into 2 groups: atrophic (nonexudative/“dry”) and neovascular (exudative/“wet”). The more severe neovascular form is responsible for ~90% of the legal blindness cases attributable to AMD.


Smoking cessation and adequate hypertension control are recommended preventive measures for AMD. Supplementation with zinc plus antioxidants (vitamin C, vitamin E, and beta carotene) may provide a limited delay in the progression of AMD and in vision loss among patients with newly diagnosed AMD. Patients


with well-established AMD featuring geographic atrophy or hemorrhagic-exudative lesions do not appear to benefit from such therapy. The risk of visual acuity loss in some persons with the neovascular form of AMD is reduced by laser photocoagulation and photodynamic therapy.

Clinical Findings


AMD results in the inability to read, drive, identify faces, or perceive details because of the loss of central macular vision. Individuals with AMD may be able to see seemingly small objects in their peripheral vision, even though they possess extensive central visual field loss. Patients can be reassured that AMD does not usually lead to total blindness because peripheral vision is usually spared. Eye involvement is usually bilateral but is frequently asymmetric. Symptoms include impaired color vision, darkened or empty areas in the visual fields (scotomas), and distortion of straight lines.


The primary retinal findings in AMD are yellow globular spots of proteinaceous material (drusen) that appear under the macular retina during dilated eye exam. As the disease progresses, chorioretinal atrophy occurs. In the neovascular form of the disease, abnormal vessels proliferate and leak fluid or blood. Fluorescence angiography may reveal the neovascular network responsible for the bleeding or exudation and provide information essential for treatment recommendations and prognostication.


Visual distortion and profound loss of central vision are the main complications of AMD. Patients should be instructed to obtain prompt ophthalmological evaluation when any visual changes occur. Patients with drusen are often instructed to look daily at an Amsler grid. This grid features a central dot on which the patient focuses separately with each eye. In the normal eye, no grid distortion appears. Perceived distortion or absence of grid lines (scotoma) may indicate fluid leakage beneath the macular retina from a choroidal neovascular membrane.


There is no effective therapy for most patients with AMD. However, selected patients with neovascular AMD may benefit from focal photocoagulation or photodynamic therapy. Laser surgery is the main treatment for neovascular AMD but is feasible only when the neovascular lesions are located a safe distance away from the center of the macula. The laser destroys the portion of the retina overlying the targeted vessels, leaving a permanent scotoma. The goal of laser photocoagulation therapy is to stabilize vision, although a significant proportion of patients who undergo laser therapy experience recurrent neovascularization. Patients with central vision loss affecting both eyes may benefit from referral for low-vision rehabilitation.


Most patients with macular drusen never experience significant central vision loss. Although regular ophthalmic examinations are generally recommended, there is no evidence that such practice is any better in terms of visual outcomes than that of having patients return promptly if they notice new visual symptoms. The natural course of neovascular AMD is toward permanent loss of central vision over a variable time period.


  • The risk of visual acuity loss in small, highly selected subgroups of persons with newly detected neovascular AMD with an exudative-hemorrhagic macular lesion appears to be reduced by laser photocoagulation and photodynamic therapy.
  • Prompt ophthalmic evaluation is necessary to assess the need for laser therapy whenever a patient with AMD experiences sudden vision loss.
  • Hypertension and smoking are currently the only known modifiable risk factors for AMD development.

Age-Related Eye Disease Study Research Group: A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8. Arch Ophthalmol 2001;119:1417. [PMID: 11594942] (Recommends supplement of antioxidants plus zinc for select population of patients with AMD.)

Age-Related Eye Disease Study Research Group: Risk factors associated with age-related macular degeneration. A case-control study in the age-related eye disease study: Age-related eye disease study report number 3. Ophthalmology 2000;107:2224. [PMID: 11097601] (Reviews risk factors for AMD and suggests avoidance of smoking and control of hypertension to reduce risk for AMD.)





  • Dilating the pupils is important when screening for the presence of diabetic retinopathy.
  • Nonproliferative diabetic retinopathy is characterized by microaneurysms, intraretinal hemorrhages, hard exudates, macular edema, and cotton wool spots (retinal infarcts).
  • Proliferative diabetic retinopathy is typified by neovascularization of the optic disk and retina, preretinal and vitreous hemorrhages, and development of fibrotic vitreoretinal bands, which lead to retinal wrinkling and tractional retinal detachment.

General Considerations

Diabetic retinopathy is the third leading cause of adult blindness. The longer an individual has diabetes, the greater is the risk for diabetic retinopathy. Generally, patients who experience diabetic retinopathy have had diabetes for ≥ 20 years. Background diabetic retinopathy (BDR), also called nonproliferative diabetic retinopathy, is the initial stage. It involves loss of pericytes, capillary dilatation and associated microaneurysms, and capillary leakage, causing exudate and macular edema. The later stage, proliferative diabetic retinopathy (PDR), involves neovascularization accompanied by preretinal hemorrhage and contraction of the fibrovascular tissue.


Diabetic retinopathy is a progressive microangiopathy with characteristic small vessel damage and occlusion. The cause of the disease is not known, but it appears to involve hyperpermeability of involved vessels. In PDR, progressive retinal ischemia stimulates the formation of delicate new vessels that leak serum proteins.



It has been proven that better glycemic control improved retinopathy outcomes in type 1 diabetics. In addition, the incidence of diabetic retinopathy among type 2 diabetics is strongly associated with glycemic and blood pressure control. Intensive insulin therapy in type 2 diabetics may reduce the relative risk of progressive retinopathy and result in a cost savings because of its beneficial effects on diabetic complications.


Detection and appropriate laser photocoagulation treatment of PDR have the potential to reduce visual loss in elderly patients with diabetes. Often-cited guidelines for diabetes care prescribe annual funduscopic examinations to screen for PDR and macular edema. However, the optimal screening interval for patients at low risk for diabetic eye complications has not been adequately determined. Patients with poor glycemic control (ie, hemoglobin A1C > 10.0%) are at the highest risk for diabetic retinopathy and benefit the most from aggressive annual screening. In lower risk patients (ie, those with good glycemic control, older age, and no retinopathy at baseline exam), simulation studies suggest that annual retinal screening produces little benefit that cannot be achieved with screening every 2-3 years.

Clinical Findings


Symptoms of diabetic retinopathy include a decrease in visual acuity, contrast sensitivity, dark adaptation, and blue-yellow color perception. Visual field testing may show scotomas corresponding to areas of retinal edema and nonperfusion.


Diabetic retinopathy demonstrates significant variability over time; therefore, special retinal cameras are used to document details of the fundus for future comparisons. Fluorescein angiography assists in the evaluation of all forms of diabetic retinopathy and guides planning of laser treatment.

Differential Diagnosis

The differential diagnosis of diabetic retinopathy is quite extensive, including hypertensive retinopathy, branch and retinal vein occlusions, various inflammatory and autoimmune retinopathies, and even some toxicities to systemic medications. Hypertensive retinopathy is the main consideration. Accelerated hypertension can cause extensive retinopathy with hemorrhages and cotton wool spots similar to those seen in diabetic retinopathy.



In PDR fragile new blood vessels proliferate onto the posterior surface of the vitreous. When the vitreous


starts to contract away from the retina, these blood vessels can bleed, causing massive vitreous hemorrhage, which may lead to sudden vision loss.


This complication severely compromises visual acuity. It can occur at any level of background retinopathy or PDR. The macular retina becomes thickened (edematous), and hard exudates accumulate in the retina.


Treatments for diabetic retinopathy vary depending on whether the patient has BDR, PDR, or both. BDR associated with macular edema in the presence of apparent or threatened visual impairment is currently treated with focal laser photocoagulation to intraretinal leak sites identified by fluorescein angiography. This treatment offers improved visual acuity in many cases. Once diagnosed with non-PDR, patients should be examined by an ophthalmologist for proliferative changes every 3-6 mo.

Moderate to severe PDR with mild to moderate vitreous hemorrhage, but without extensive vitreoretinal fibrosis or tractional retinal detachment, is currently treated by peripheral panretinal photocoagulation. This treatment induces regression of neovascularization of the optic disk and retina, which reduces the risk of severe vision loss. However, there is no compelling evidence that such treatment is beneficial in patients with mild PDR. Profound PDR with extensive vitreoretinal fibrosis, tractional retinal detachment, or dense recurring vitreous hemorrhage usually requires a surgical procedure known as posterior vitrectomy. In this procedure, intravitreal blood and vitreoretinal fibrous membranes are removed surgically.

Some patients have both BDR with clinically significant macular edema and moderate to severe PDR. Current evidence indicates that the BDR should be addressed initially and that treatment of the PDR should follow. This seems to provide a better visual outcome than treating both components simultaneously or performing panretinal photocoagulation first and focal laser treatment for macular edema second.


Most persons with type 1 diabetes eventually experience diabetic retinopathy. In the UKPDS trial of type 2 diabetic patients, the incidence of retinopathy after 6 years in patients with no retinopathy at baseline was about 1 in 5. In the same study, nearly 33% of patients with retinopathy at baseline experienced progressively greater retinopathy over 6 years.


  • Good glycemic control and aggressive treatment of hypertension in patients with diabetes help minimize the development and progression of diabetic retinopathy.
  • The risk of developing severe visual loss from PDR and macular edema can be reduced significantly by the use of laser photocoagulation.
  • It is cost-effective to perform periodic screening retinal exams in all patients with diabetes, and annual examinations are recommended, especially in those at increased risk for diabetic ocular disease (ie, hemoglobin A1C> 10%).

Stratton IM et al: UKPDS 50: Risk factors for incidence and progression of retinopathy in type II diabetes over 6 years from diagnosis. Diabetologia 2001;44:156. [PMID: 11270671] (Provides data emphasizing the need for good glycemic and blood pressure control to minimize diabetic retinopathy.)

United Kingdom Prospective Diabetes Study Group: Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38. BMJ 1998;12;317:703. [PMID: 9732337] (Tight blood pressure control minimizes microvascular complications in type 2 diabetes.)

Vijan S et al: Cost-utility analysis of screening intervals for diabetic retinopathy in patients with type 2 diabetes mellitus. JAMA 2000;283:889. [PMID: 10685713] (Analysis of the cost-utility of annual vs. less frequent screening intervals for diabetic retinopathy.)

Wake N et al: Cost-effectiveness of intensive insulin therapy for type 2 diabetes: A 10-year follow-up of the Kumamoto study. Diabetes Res Clin Pract 2000;48:201. [PMID: 10802159] (Prospective cost-effectiveness analysis of intensive insulin therapy regarding diabetic microvascular complications.)



  • Diagnosis is based on optic disk examination, intraocular pressure, and visual field measurement.
  • Diagnosis is made on the basis of routine periodic ophthalmoscopy and tonometry.



General Considerations

Glaucoma is a group of diseases traditionally defined by a triad of signs, including at least 2 of the following: elevated intraocular pressure (IOP), optic disk cupping, and visual field loss. Secondary and congenital forms of glaucoma exist; however, primary glaucomas (open angle and closed angle) are the more prevalent forms in older populations. Primary open-angle glaucoma (POAG) is a chronic disease that accounts for > 90% of all cases, whereas primary closed-angle glaucoma accounts for < 10%.

The prevalence of POAG is greatest in black and Hispanic populations. Individuals with a positive family history of glaucoma have an estimated 3-fold increased risk.


Vision loss resulting from glaucoma cannot be reversed, but its progression can be prevented by early diagnosis and treatment. Periodic glaucoma screening is critical for high-risk groups such as blacks, Hispanics, and those with a family history of glaucoma. The American Academy of Ophthalmology recommends periodic eye examinations to identify patients at risk for glaucoma. Current guidelines recommend screening every 2-4 years for patients aged 40-64 years and every 1-2 years for those ≥ 65 years.

Clinical Findings


The loss of vision is unnoticeable until a significant amount of nerve damage has occurred. In POAG symptoms may be subtle, consisting of blurred vision, halos around lights, and impaired dark adaptation. Classically, vision loss starts in the nasal field (temporal retina). In contrast, patients with acute primary closed-angle glaucoma may have blurred vision, severe headache, nausea, vomiting, corneal edema, and a mid-dilated pupil.

  2. Tonometry—Elevated IOP alone is neither sufficient nor necessary as a diagnostic criterion for glaucoma. In the normal eye, IOP ranges from 10-21 mm Hg. POAG can exist in individuals who have a normal IOP during 1 or more measurements. A patient identified as having isolated intraocular hypertension does not necessarily have POAG; however, such a patient should be monitored for POAG periodically.
  3. Optic disk assessment & gonioscopy—Glaucomatous optic atrophy leads to enlargement of the optic disk cup and associated disk pallor. Optic disk cupping is also associated with nasal displacement of the retinal vessels on the disk. Asymmetry of the optic disks in size and shape, or a cup-disk ratio > 0.5 in the setting of elevated IOP is highly suggestive of glaucomatous atrophy.

Gonioscopy measures the anatomic configuration of the anterior chamber angle and determines whether the eye has an open angle or a closed angle.

  1. Visual field examination—Periodic visual field examination is essential to the diagnosis and follow-up of glaucoma. The field loss pattern, progression, and correlation with optic disk changes aid in monitoring disease progression.

Differential Diagnosis

Acute primary angle closure glaucoma must be differentiated from other disorders that cause acute painful unilateral visual loss. Relevant conditions include inflammation of the iris, the ciliary body, and the anterior uveal tract, all of which cause mildly decreased vision, which is often associated with photophobia. All are diagnosed clinically with a slit-lamp examination. Acute conjunctivitis is also a diagnostic possibility, but, unlike closed-angle glaucoma, it manifests little or no pain and no vision loss.


If uncontrolled, glaucoma usually results in progressive visual loss. The rate and extent of visual loss depend greatly on the type of glaucoma and individual characteristics of the patient. In chronic POAG there appears to be 2 distinct groups of patients: (1) those who seem not to lose vision progressively or who lose vision slowly and to a limited extent over long periods of time if untreated or inadequately treated and (2) those who seem to worsen progressively even if appropriate treatment is provided in a timely manner.


Treatments for glaucoma focus on lowering IOP. Several modern analyses have demonstrated the importance of IOP control in the reduction of visual field deterioration in open-angle glaucoma. The treatment goal is to stabilize visual field loss and optic nerve damage. Both medical and surgical therapies help to achieve this goal.


The majority of topically applied glaucoma medicines lower IOP through a reduction in aqueous production or resistance to outflow. Topically applied β-adrenergic antagonists have been a mainstay in the initial treatment of chronic POAG. The other major drug classes


include α-adrenergic agonists, muscarinic agonists (ie, pilocarpine), and carbonic anhydrase inhibitors (topical or oral). In recent years, several new ocular hypotensive medications have become available, including prostaglandin analogs, carbonic anhydrase inhibitors, and combination drugs.

All the medications used to treat glaucoma can have clinically important local and systemic adverse effects in elderly patients (Table 16-2). It is, therefore, prudent to include ophthalmic medications in the routine medication review for all older adults. Nasolacrimal occlusion, a technique aimed at reducing the risk of adverse systemic effects from topical eye medications, is difficult for older patients possessing limited dexterity.


Surgery may be used to lower IOP in patients refractory to medical therapy. The most common surgical procedure for this purpose is laser trabeculoplasty. Additional measures may be necessary, including continued topical medications or filtering operations such as iridectomy or trabeculectomy.

Table 16-2. Topical ophthalmic agents used for glaucoma.



Usual dosagea

Adverse effects

Beta-adrenergic antagonists

Betaxolol (Betoptic)
Levobunolol (Betagan)
Timolol (Timoptic, Betimol)b

0.5%, 1 drop twice daily
0.5%, 1 drop once or twice daily
0.25% and 0.5% solution, 1 drop once or twice daily

Bronchospasm, congestive heart failure, bradycardia, depression, impotence


Dipivefrin (various)
Epinephine (various)

0.1%, 1 drop twice daily
0.25-2.0%, 1-2 drops once or twice daily

Tachyarrhythmias, increased blood pressure, anxiety, headache, tremor, eye discomfort, papillary dilatation, allergic conjunctivitis

Cholinergic miotics

Carbachol (various)
Pilocarpine (various)

0.01-3.0%, 1-2 drops up to 3 times per day
1-10%, 1 drop three to four times daily

Miosis, eye or brow pain, blurred vision, myopia, bronchospasm, pulmonary Pilocarpine edema

Carbonic anhydrase inhibitors

Brinzolamide (Azopt)
Dorzolamide (Trusopt)

1%, 1 drop three times daily
2%, 1 drop three times daily

Stinging, blurred vision, blepharitis, bitter taste, alopecia, dry mouth

Prostaglandin analogs

Bimatroprost (Lumigan)
Latanoprost (Xalaten)
Travoprost (Travatan)
Unoprostone isopropyl (Rescula)

0.03%, 1 drop once daily
0.005%, 1 drop once or twice daily in the evening
0.004%, 1 drop once daily
0.15%, 1 drop twice daily

Increased iris pigmentation, conjunctival hyperemia, ocular irritation, infection (upper respiratory tract infections), headache, abnormal liver function tests, and hirsutism

aConcentration and dosage of medications must be adjusted to the response of the patient.
bVerapamil should be used with extreme caution in patients taking ophthalmic timolol because of the potential for additive effects on prolonging atrioventricular conduction, and causing hypotension and left ventricular failure.
From American Society of Health-System Pharmacists: Drug Information. American Society of Health-System Pharmacists, 2002. Used with permission.


Without treatment open-angle glaucoma may progress insidiously to complete blindness. Patients with medically controlled IOP that is achieved before the occurrence of extensive glaucomatous damage have a good prognosis.

Kwon YH et al: Rate of visual field loss and long-term visual outcome in primary open-angle glaucoma. Am J Ophthalmol 2001;132:47. [PMID: 11438053] (Lower IOP proved to be associated with slower visual field decline.)

Weih LM et al: Prevalence and predictors of open-angle glaucoma: Results from the visual impairment project. Ophthalmology 2001;108:1966. [PMID: 11713063] (Strongest risk factor for glaucoma was a positive family history, after adjusting for age.)




Vascular diseases such as retinal vascular occlusions and anterior ischemic optic neuropathy associated with temporal arteritis increase in frequency and severity in old age. These disorders can lead to catastrophic vision loss. Patients with giant cell (temporal) arteritis usually have systemic symptoms and signs. Occult giant cell arteritis initially presents with visual symptoms and ocular signs without any systemic symptoms or signs. Giant cell arteritis should be suspected in a patient with visual loss and clinical findings of arteritic anterior ischemic optic neuropathy, central retinal artery occlusion, or posterior ischemic optic neuropathy. Urgent corticosteroid administration is begun, followed by a diagnostic evaluation. The evaluation should include measurement of the sedimentation rate and C-reactive protein and biopsy of the temporal artery.


Interventions for low vision can improve the outlook for many visually impaired older adults and reduce their sense of isolation. A low-vision evaluation by a professional is recommended. Numerous agencies serving the visually impaired (private or state supported) and organizations such as the American Academy of Ophthalmology, American Optometric Association, National Eye Institute, and Lighthouse International offer additional resources.

Low-vision aids and rehabilitation strategies are designed to enhance quality of life for the low-vision patient. Optical devices such as stand magnifiers, high-powered spectacles, hand magnifiers, and closed-circuit magnification systems enhance visual acuity by enlarging the retinal image. Nonoptical devices include large-print reading material, “talking books,” and writing guides. The U.S. Library of Congress administers a free library program of braille and audio materials circulated to eligible borrowers by postage-free mail and publishes a directory of publishers and distributors of large-type books and periodicals. Reading devices such as the Kurzweil machine are available in some public institutions such as libraries. This machine reads typed print out loud in a synthesized voice to permit increased independence for visually impaired persons. In some cities, closed-circuit radio reading services offer daily newspapers, magazines, and books. Rehabilitation programs exist that provide mobility training and training for activities of daily living tailored to the visually impaired.

Sometimes the simple act of making patients aware of low-vision services opens opportunities that ultimately improve quality of life.


American Academy of Ophthalmology: (Provides informational pamphlets and resource list.)

Macular Degeneration International: (Scientifically reviewed web site offering information and support for patients with AMD and their families; it includes information on low-vision aids.)

Lighthouse International: (Features services such as a catalog of nonoptical devices and a guidebook for visually impaired older adults.)

National Eye Institute: (Lists helpful resources and provides information to low-vision individuals and their families and includes information on outreach programs aimed at health care professionals to increase awareness of low-vision issues and resources.)

National Eye Institute: Vision Problems in the U.S.—Prevalence of Adult Vision Impairment and Age-Related Eye Diseases in America: (Detailed report on U.S. prevalence data regarding the 4 main eye diseases.)


General Considerations

More than 33% of individuals ≥ 65 years have hearing loss. The incidence of hearing loss is estimated to double per decade, beginning with 16% at 60 years of age and proceeding to 32% at 70 years and 64% at 80 years. When matched for age, males tend to have worse hearing than females.


The most common pattern of hearing loss in older adults is presbycusis, a bilateral high-frequency sensorineural hearing loss that occurs with advancing age. Pure-tone threshold sensitivity diminishes with aging. Hearing declines gradually in the majority (97%) of the population; those older than 55 years lose hearing at a rate of 9 dB/decade. Hearing loss is also compounded by complex central auditory disability. This phenomenon appears at a mean age of 60 years but has great individual variation in its progression thereafter.


Speech discrimination is also reduced with aging. Older persons generally have more difficulty understanding speech when there is any element of speech degradation or unfavorable signal-to-noise ratio, such as degraded pronunciation or transmission, rapid speech, or speech


heard against a backdrop of other conversations. Speech recognition with simultaneous sentence competition begins to deteriorate slowly starting in the fourth decade of life, a decline that accelerates after the seventh decade.


Patients should be screened for a history of excessive noise exposure and educated about the importance of noise avoidance and the use of hearing protective devices. Noise-induced hearing loss is permanent but largely preventable. It begins at the higher frequencies (3000-6000 Hz) and develops gradually as a consequence of cumulative exposure to excessive sound levels. Patients should be warned about work or recreational activities that generate excessive noise exposure such as lawn mowing (90 dB), stereo headphone use (100 dB), or firearm use (140-170 dB). Hearing loss can develop after chronic exposures equal to an average decibel level of 85 dB or higher for an 8-h period.

Hearing loss secondary to ototoxic drugs can be minimized by careful attention to proper drug dosing, patient risk profiles, and early recognition of ototoxicity. Common classes of ototoxic drugs are listed in Table 16-3. Sensorineural hearing loss associated with aminoglycosides or chemotherapeutic agents is permanent.

Clinical Findings


Hearing loss is often heralded by its functional consequences, including diminished speech understanding, social isolation, mood alteration, and apparent decline in cognitive performance. The clinical signs and symptoms may occur insidiously. Therefore, identification of hearing impairment sometimes requires direct questioning under challenging listening conditions. The patient should be asked about difficulty hearing speech in large groups, soft voices, or telephone conversations. Collateral history from a spouse or other individuals familiar with the patient's hearing performance may be useful. Some patients deny hearing difficulty, fearing stigmatization associated with wearing a hearing aid. If symptoms are not acknowledged, diagnosis and treatment of hearing loss may be delayed until the impairment is well advanced.

Table 16-3. Ototoxic medications.

   Nitrogen mustard
   Loop diureticsa

aHearing loss and tinnitus are reversible with these agents.


No single screening procedure is ideal. Screening tests such as the whispered voice, the finger rub, and the tuning fork test have been studied with relatively few patients and examiners, and inadequate data exist regarding interobserver reliability and observer repeatability.

The Hearing Handicap Inventory for the Elderly- Screening Version (HHIE-S; Table 16-4) is a reliable and valid self-assessment inventory for identifying disabling hearing impairment among elderly patients in the ambulatory setting. The HHIE-S was found to have a


sensitivity of 76% and a specificity of 71% for scores of > 8 compared with the gold standard of pure-tone audiometry. The HHIE-S is easy to use in general practice, and the resulting interventions reduce hearing handicap. Self-assessment inventories appear to have an advantage over pure-tone audiometry in identifying patients who are willing to accept further evaluation and treatment.

Table 16-4. The hearing handicap inventory for the elderly-screening.

Does a hearing problem cause you to feel embarrassed when you meet new people?
Does a hearing problem cause you to feel frustrated when talking to a member of your family?
Do you have difficult hearing when someone speaks in a whisper?
Do you feel handicapped by a hearing problem?
Does a hearing problem cause you difficulty when visiting friends, relatives, or neighbors?
Does a hearing problem cause you to attend religious services less often than you would like?
Does a hearing problem cause you to have arguments with family members?
Does a hearing problem cause you difficulty when listening to television or radio?
Do you feel that any difficulty with your hearing limits/hampers your personal or social life?
Does a hearing problem cause you difficulty when in a restaurant with relatives or friends?

Answers are scored as yes (4), sometimes (2), and no (0). Total point range, 0-40; 0-8, no self-perceived handicap; 10-22, mild to moderate handicap; 24-40, significant handicap. Adapted with permission from Ventry IM, Weinstein BE:Identification of elderly people with hearing problems. ASHA 1983;25:37. Used with permission.

A more reliable, practical, and accurate screening method uses a portable audiometer housed within an otoscope or connected to earphones. The audiometer presents pure tones at 500, 1000, 2000, and 4000 Hz. Using a 40-dB definition of hearing impairment as the gold standard, one such device (Audioscope; Welch Allyn, Inc.) has a sensitivity ranging from 87-96% and a specificity ranging from 70-90%.


An important focus of the routine otological examination is the identification of reversible causes of conductive hearing loss. These include otitis externa, cerumen impaction, foreign objects obstructing the external auditory canal, and osteoma. Assessment of the integrity and mobility of the tympanic membrane is also indicated. Tuning fork tests such as the Rinne and the Weber tests allow differentiation of conductive and sensorineural hearing loss.


If office-based screening suggests hearing impairment, the patient should be referred to an audiologist for formal evaluation. An audiologist will perform an audiogram to answer the following 3 questions:

  1. Is a sensorineural, conductive, or mixed hearing loss present?
  2. Is the loss unilateral or bilateral?
  3. At what frequencies (testing for octave frequencies of 250-8000 Hz) does the loss occur?

The vertical axis of the audiogram shows hearing level (HL) measured in decibels ranging from very soft 10 dB to a very loud 110 dB. The 0-dB pure-tone HL represents the average hearing sensitivity threshold for young adults. The horizontal axis specifies the frequencies of the presented pure tones. The most critical frequencies for speech reception and understanding are 500, 1000, 2000, and 3000 Hz.

The audiogram measures hearing levels for air conduction and bone conduction of pure tones at the specified frequencies in each ear separately. Air conduction testing measures the function of the entire auditory system from the ear canal through the middle ear to the cochlea and its afferent neural pathways to the brain. Therefore, loss in air conduction can be due to a disorder anywhere in the auditory system. To better locate the anatomic site of the hearing disorder, pure-tone bone conduction is also performed. Sound transmitted via bone conduction bypasses the outer ear and middle ear. When hearing loss is identified by air conduction and bone conduction, a sensorineural hearing loss is present (Figure 16-1). When air conduction results suggest hearing loss but bone conduction results are normal, a conductive hearing loss is present.

A complete audiological assessment also measures speech sensitivity and speech discrimination. Assessment of the speech reception threshold (SRT) involves presenting 2-syllable words to 1 ear at a time and measuring the softest level at which 50% of the words can be identified. The SRT should be within 10 dB of the pure-tone average (PTA) thresholds of 500, 1000, and 2000 Hz and thus serves to verify the reliability of the pure-tone threshold levels. Speech discrimination is evaluated by presenting a list of monosyllabic words to each ear at a comfortable loudness (typically 40 dB above the PTA) and recording the percentage of correct responses. On a scale ranging from 0-100%, speech discrimination scores of 90-100% are considered normal. Better speech discrimination scores correlate with better prognosis for hearing aid success.

Pure-tone air conduction, bone conduction, SRT, and speech discrimination assessment constitute the essential


audiological testing for patients with hearing loss. Audiological procedures such as brainstem auditory evoked potentials, electrocochleography, and acoustic reflex testing are available for more specialized site-of-lesion testing. These specialized tests may be used when evaluating asymmetric sensorineural hearing loss, a suspected eighth nerve lesion, or a central auditory disorder.


Figure 16-1. Audiogram illustrating sensorineural hearing loss. This pattern is typical of age-related hearing loss; the hearing level is normal for low frequencies but impaired for higher frequencies to a similar degree for air and bone conduction.

Cochlear and eighth nerve lesions can be distinguished by immitance-based evaluation of the stapedius reflex. Brainstem auditory evoked potentials are used in the diagnosis of acoustic tumors. Referral to an otolaryngologist is recommended when a patient has a hearing impairment that is inconsistent with presbycusis, experiences acute or unilateral hearing loss, or has a speech discrimination impairment that is disproportionate to the degree of hearing loss.

Differential Diagnosis

Presbycusis is the predominant cause for hearing loss among older individuals. The other causes fall into 3 categories: sensorineural, conductive, and mixed loss. Mixed loss refers to a combination of conductive and sensorineural hearing loss. A variety of diseases cause hearing loss of each type (Table 16-5). Disorders of the outer ear and middle ear cause conductive hearing loss by disrupting the process of sound transmission via the external canal, tympanic membrane, and ossicular chain. Disorders of the inner ear cause sensorineural hearing loss by damaging the cochlea, eighth cranial nerve, or internal auditory canal.

  2. Infection—Infection of the external auditory canal (EAC) causes conductive hearing loss when there is resultant blockage of the external auditory canal. Typically, such blockage occurs as a result of inflammation and edema of the canal. Otitis externa causes ear pain and canal edema.
  3. Tumors—Certain tumors can cause occlusion of the EAC, leading to conductive hearing loss. Canal tumors such as squamous carcinoma can be mistaken for otitis externa; the diagnosis is provided by biopsy.
  5. Infection—Otitis media, although more common in children, also causes conductive hearing loss in adults. The fluid that accumulates in the middle ear interferes with normal tympanic membrane vibration during sound transmission.
  6. Tumors—Tumors of the middle ear (eg, squamous cell carcinoma) are rare compared with benign growths such as cholesteatoma. Management is surgical.

Table 16-5. Causes of hearing loss.

   Outer ear causes
      External otitis
      Squamous cell carcinoma
   Middle ear causes
      Otitis media
      Tympanic membrane perforation
      Glomus tumors
      Temporal bone trauma
      Paget's disease
   Inner ear causes
      Noise exposure
      Ménière's disease
      Ototoxic drugs
      Viral cochleitis
      Acoustic neuroma
      Multiple sclerosis
      Vascular Disease

  1. Cholesteatoma—Symptoms such as hearing loss and recurrent ear drainage should prompt investigation for a cholesteatoma. By definition, a cholesteatoma is a growth of desquamated stratified squamous epithelium that originates on the surface of the eardrum and often becomes cystic as it grows within the middle ear. Its formation is associated with tympanic membrane trauma or abnormal retraction resulting from impaired eustachian tube function. Cholesteatoma can cause erosion of the ossicular chain and mastoid; subsequent complications include hearing loss, brain abscess, vertigo, and facial nerve paralysis. Management requires referral to an otolaryngologist for surgical treatment.
  2. Otosclerosis—Otosclerosis refers to bony overgrowth affecting the footplate of the stapes, leading to its fixation and subsequent conductive hearing loss. Treatment involves either hearing amplification or stapedectomy. Systemic bone diseases such as Paget's disease and immunological diseases such as rheumatoid arthritis can also lead to conductive hearing loss.



  1. Tympanic membrane perforation—A perforation of the tympanic membrane arises commonly from trauma or infection. The degree of conductive hearing loss depends on the location and size of the perforation. An audiogram is needed to measure hearing function. An inspection of the tympanic membrane is useful to identify skin that has become trapped on the undersurface of the tympanic membrane and could result in cholesteatoma formation.
  2. Vascular—Benign paragangliomas such as glomus tympanicum or jugulare tumors arising in the middle ear can cause conductive hearing loss. On pneumoscopy, they often appear as a red, blanchable mass behind the tympanic membrane. In addition to hearing loss, they can cause bone erosion and damage to cranial nerves 7-12.
  1. Presbycusis—Presbycusis is the most common type of hearing loss among the aged. Hearing loss that deviates from its characteristic pattern (bilateral, symmetric, high-frequency hearing loss) should prompt further otological evaluation.
  2. Noise—Noise is the second most common cause of sensorineural hearing loss after presbycusis. Noise-induced hearing loss characteristically features a notched pattern of sensory threshold shift on the audiogram.
  3. Infection—Both viral cochleitis and bacterial meningitis are causes of sensorineural hearing loss. Infection can cause profound hearing loss by destroying the cochlear inner hair cells, which are unable to regenerate in mammals. Treatment is sometimes possible with a cochlear implant. Viral cochleitis usually presents as sudden sensorineural hearing loss. Other causes of sudden hearing loss that should be considered include vascular ischemic events, acoustic neuroma, Ménière's disease, multiple sclerosis, and perilymph fistulas.
  4. Ménière's disease—Ménière's disease causes hearing loss that is almost always low frequency and is typically episodic with periods of vertigo, hearing loss, tinnitus, and aural fullness. The associated hearing loss may become permanent over time and involve other frequencies.
  5. Trauma—Trauma in the form of blunt head injury or barotrauma can cause inner ear as well as middle ear damage, leading to hearing loss. Transverse temporal bone fractures cause a fracture through the inner ear and result in a dead ear.
  6. Tumors—Tumors of the inner ear are usually benign. Acoustic neuroma, the most common benign tumor in this region, originates from the eighth cranial nerve. Patients with an acoustic neuroma are most commonly either asymptomatic or complain of unilateral sensorineural hearing loss, although they can also have other symptoms such as unilateral tinnitus, dizziness, or headaches. Other tumors causing sensorineural hearing loss include meningioma and lipoma.
  7. Endocrine & systemic—Metabolic abnormalities can cause sensorineural hearing loss. Diabetes, with its attendant small vessel disease, can cause cochlear ischemia. Other causes include hyperthyroidism and hypothyroidism and systemic illnesses such as syphilis.
  8. Iatrogenic—The potential ototoxicity of medications assumes greater importance in older patients who receive a disproportionately high percentage of all prescription drugs. The aminoglycosides are the best known ototoxic drugs. Tobramycin and amikacin are more cochleotoxic, whereas gentamicin and streptomycin are more vestibulotoxic. Hearing levels should be monitored whenever ototoxic medications are administered.
  9. Neurogenic—Stroke, transient ischemic attacks, multiple sclerosis, and Arnold-Chiari malformations are neurogenic causes of sensorineural hearing loss.


The complications of hearing impairment affect functional, emotional, social, and cognitive domains. Predisposed to social isolation and communication difficulties, individuals with hearing loss may experience depression or other mood disorders. A hearing-impaired individual can be mistaken to have dementia.


Successful rehabilitation of elderly patients with hearing loss is a complex process performed by clinical audiologists. A holistic approach to this process involves consideration of patients' status in at least 4 domains: communication (auditory and audiovisual speech reception, hearing disability, and conversational fluency), physical (manual dexterity, general health, and visual status), psychological (attitude, depression, mental status, and motivation), and social (physical and social environments). The most important strategy for rehabilitation of hearing loss among the elderly is the hearing aid. Additional approaches include education in speech reading, auditory training, and use of assistive listening devices.

  2. Efficacy—Hearing aids significantly improve the quality of life (eg, increase in social and emotional function and communication function and decrease in depression) of patients with sensorineural hearing loss.


Patients should be advised that acclimatization to hearing aids, and their full benefits, typically occurs after ≥ 1 mo.

  1. Candidacy & audiology referral—The amount of hearing loss is less crucial than patient awareness and acceptance of hearing loss, communication difficulties, and motivation to try amplification. Patients with hearing loss not amenable to medical or surgical treatment (ie, presbycusis) should be referred to a clinical audiologist. The audiologist should recommend a type of hearing aid or aids based on the patient's hearing needs and goals, provide training in the use of amplification and other selected rehabilitative approaches, review the advantages and limitations of hearing aids, and provide supportive follow-up.
  2. Selection & fitting—Selection and fitting procedures for hearing aids have become increasingly complex with the development of “high-tech” hearing aid features, including miniaturized styles, programmability, multimicrophone technology, and digital signal processing capabilities. With symmetric hearing loss, binaural hearing aid fitting provides the most benefit. Hearing aids come in several basic types, but all are designed to increase the intensity of sound and deliver it to the ear with maximal fidelity. Body hearing aids, now somewhat outdated, are the largest in size. They were traditionally used by persons with severe-profound hearing loss or those who lacked the dexterity to manipulate smaller hearing aids. Behind-the-ear (BTE) hearing aids have a case that fits behind the ear and conduct sound through a tube to an ear mold in the ear canal. Modern BTE hearing aids have greater amplification than the traditional body hearing aids.

In-the-ear (ITE) hearing aids are self-contained, fitting into the external ear, and are preferred by many patients because of their cosmetic appeal and ease of insertion and adjustment. In-the-canal hearing aids fit entirely into the outer portion of the ear canal and are even less visible. They provide sound amplification similar to most BTE and ITE hearing aids. However, they pose a problem for patients with dexterity problems because their tiny size hampers insertion and adjustment. Completely-in-the-canal hearing aids are the smallest and most expensive aids and fit entirely within the ear canal. They are suitable for patients with mild to moderate hearing impairment, good manual dexterity, and an ear canal free of adverse medical conditions.

Semi-implantable hearing aids were introduced in the late 1990s. These devices may eventually offer a reliable option for hearing-impaired patients who cannot wear an occlusive ear mold (eg, because of severe external otitis). A prototype model has a transducer that is attached directly to the ossicular chain and linked by telemetry to an externally worn audioprocessor.

Hearing aids also differ in their internal features and electronic circuitry and are classified as nonprogrammable, programmable analog, or digital. Terms used in the discussion of hearing aids, including circuitry options, are summarized in Table 16-6. Programmable hearing aids with a directional microphone have been found to be the most effective. However, the cost-effectiveness of hearing aids with advanced electronic features needs to be determined.

  1. Cost—Audiology evaluations are covered by Medicare, but hearing aids are not. In many states, Medicaid will pay for hearing aids. The cost of hearing aids ranges from about $500-$3000. Digital hearing aids cost 2-3 times that of high-quality conventional analog aids. Programmable digital aids may be programmed to meet individual needs and adjust automatically to changing levels of environmental sound, but a midrange model costs about $1400.

Cochlear implants have become widely accepted as a means of hearing rehabilitation in people with advanced sensorineural hearing loss who are unable to gain effective speech recognition with hearing aids. In appropriately selected patients, cochlear implantation improves communication ability and leads to positive psychological and social benefits; furthermore, the surgery appears to be safe and well tolerated in geriatric patients. Multichannel cochlear implants have been found to improve hearing-related quality of life and compare favorably with other accepted medical interventions in terms of cost-effectiveness (~$15,000 per quality-adjusted-life-year).


In difficult listening situations, such as noisy public places, a variety of assistive listening devices (ALDs) are available to provide further benefit to hearing-impaired individuals. ALDs usually consist of a microphone placed close to the desired sound and a means by which sound is transmitted directly to the listener. Examples of ALDs include infrared or FM radio listening systems for televisions, stereos, concerts, and church sermons.

Some additional devices currently available to aid hearing-impaired individuals include amplified telephones that are hearing-aid compatible, portable telephone amplifiers, text telephones, signaling systems that make lamps flash on and off when the telephone or doorbell rings, vibrating alarm clocks, televisions with closed captioning, and flashing smoke detectors.


Individuals with hearing impairment can learn techniques that improve communication effectiveness, including speech reading. Speech reading uses interpretation


of lip movements, facial expressions, body movements, and gestures to enhance understanding of speech. Speech reading is usually taught together with hearing aid orientation by audiologists. Communication with hearing-impaired elderly persons is also facilitated when the speaker's face is in full view of the listener (within 2-3 ft), background noise is reduced, and speech is delivered with adequate pauses between sentences. One should avoid shouting and attempt to speak clearly at a slightly louder than normal intensity. When repetition is necessary, it is often most effective to paraphrase the message or write key words.

Table 16-6. Hearing aid terminology.



Nonprogrammable hearing aid

Offers good sound quality at a reasonable price; limited flexibility in adjustments.

Programmable analog hearing aid

Digital/analog hybrid. Sound is converted to voltage waveform; the filtering process is programmable.

Digital hearing aid

Sound is converted to digital computer code, which undergoes processing via a digital signal processor.


Circuitry that helps people talk on telephone by converting eletromagnetic signal from telephone to amplified sound.


Circuitry that keeps loud sounds from being overamplified while dynamically increasing the volume of soft sounds.


Refers to the number of frequency bands into which the incoming signal is divided.
   Programmable aids with multiple channels can reduce the intensity of a loud low-pitched sound, with minimal effect on an incoming high-frequency channel.


Aids with multiple memories have several different signal processing schemes that are stored and can be selected by the user to suit differing listening situations (ie, quiet room vs. a situation with background noise).

Remote control

Allows remote adjustment of many hearing aid functions, such as on/off, volume, memories, telecoil.

Omnidirectional microphone

Picks up sounds form all directions (the standard microphone).

Directional microphone

Incorporates noise cancellation circuitry for improved speech understanding in noisy environments.

From Klein AJ, Weber PC: Hearing aids. Med Clin North Am 1999;83:139. Used with permission.


  • Hearing aids significantly improve the quality of life of patients with sensorineural hearing loss. Programmable hearing aids with directional microphones outperform less expensive nonprogrammable models.
  • Cochlear implantation is a cost-effective means of auditory rehabilitation for individuals with advanced sensorineural hearing loss that cannot be adequately treated with hearing aids.


National Institute on Deafness and Other Communication Disorders: (This site provides a wealth of information on hearing disorders and is useful for laypersons and professionals. It also includes links to > 140 hearing-related organizations.)



Munoz B et al: Causes of blindness and visual impairment in a population of older Americans: The Salisbury Eye Evaluation Study. Arch Ophthalmol 2000;118:819. [PMID: 10865321] (Current epidemiology of blindness and visual impairment in the United States.)

Rodriguez J et al: Causes of blindness and visual impairment in a population-based sample of U.S. Hispanics. Ophthalmology 2002;109:737. [PMID: 11927431] (Presents important epidemiology data on visual impairment in this growing ethnic population.)

Shingleton BJ et al: Blurred vision. N Engl J Med 2000;343:556. [PMID: 10954765] (Excellent review of blurred vision for the nonophthalmologist/primary care physician.)


Buchman CA et al: Cochlear implants in the geriatric population: Benefits outweigh risks. Ear Nose Throat J 1999;78:489. [PMID: 11318481] (Review of cochlear implants' role in hearing rehabilitation.)



Hands S: Hearing loss in over-65s: Is routine questionnaire screening worthwhile? J Laryngol Otol 2000;114:661. [PMID: 11091826] (Prospective study of a practical hearing loss screening tool.)

Jennings CR, Jones NS: Presbycusis. J Laryngol Otol 2001;115: 171. [PMID: 11244520] (Review of presbycusis and epidemiology of hearing loss.)

Johnson CE et al: A holistic model for matching high-tech hearing aid features to elderly patients. Am J Audio 2000;9:112. [PMID: 11200187] (Review of methods for matching hearing aid features to older patients based on a holistic model.)

Klein AJ, Weber PC: Hearing aids. Med Clin North Am 1999; 83:139. [PMID: 9927966] (Review of modern hearing aid assessment and technologies.)

Mulrow CD, Lichtenstein MJ: Screening for hearing impairment in the elderly: Rationale and strategy. J Gen Intern Med 1991;6:249. [PMID: 2066832] (Classic evidence-based review of screening tests for hearing impairment.)

Palmer CS et al: A prospective study of the cost-utility of the multichannel cochlear implant. Arch Otolaryngol Head Neck Surg 1999;125:1221. [PMID: 10555693] (Cost-utility analysis of cochlear implantation.)

Rabinowitz PM: Noise-induced hearing loss. Am Fam Physician 2000;61:2749. [PMID: 10821155] (Review of noise-induced hearing loss for the primary care physician.)

Ventry IM, Weinstein BE: Identification of elderly people with hearing problems. ASHA 1983;25:37. [PMID: 6626295] (Original presentation of the classic screening questionnaire, The Hearing Handicap Inventory for the Elderly-Screening Version.)

Welsh LW et al: Function of a hearing aid under stressful conditions. Ann Otol Rhinol Laryngol 2000;109:929. [PMID: 11051433] (Review of the aging auditory system and comparison of auditory function of normal persons to hearing-aided patients.)

Yueh B et al: Randomized trial of amplification strategies. Arch Otolaryngol Head Neck Surg 2001;127:1197. [PMID: 11587599] (Addresses the issue of whether technologies such as programmable circuits and directional microphones are worth the added expense.)