Chapter 45: Hearing & Vision Impairment in the Elderly

Sensory impairment affects up to two-thirds of the geriatric population. Identification, evaluation, and treatment of these conditions (Table 45-1) may improve patients’ quality and quantity of life. The impact of sensory impairments is significant. The same objective level of sensory function can result in different levels of disability depending on the needs and expectations of patients. Poor hearing is associated with depression as well as decreased quality of life; poor mental health; and decreased physical, social, and cognitive functioning. Vision impairment increases the risk of death and is associated with an elevated risk of falling and hip fracture, depression, medication errors, and problems with driving.

Research has yet to demonstrate that community-based screening of asymptomatic older people results in improvements in vision or hearing. The US Preventive Services Task Force (USPSTF) and the American Academy of Family Physicians (AAFP) recommend screening for hearing difficulties by questioning elderly adults about hearing impairment and counseling them regarding the availability of treatment when appropriate. In a 2009 update, AAFP and USPSTF concluded that there is inadequate direct evidence that screening for impairment of visual acuity by primary care physicians improves functional outcomes in elderly; yet there is adequate evidence that early treatment of refractive error, cataracts, and age-related macular degeneration (AMD) improves or prevents loss of visual acuity.

PRESBYCUSIS

General Considerations

Presbycusis is the most common form of hearing loss in the elderly, although it often goes unrecognized. It occurs more frequently with advancing age and in patients with a positive family history. This multifactorial disorder is due to a combination of structural and neural degeneration and genetic predisposition. Risk factors for presbycusis include noise exposure, smoking, and medications such as aminoglycoside antibiotics, loop diuretics, and cardiovascular risk factors such as hypertension. Presbycusis is a diagnosis of exclusion.

Prevention

Until the exact pathophysiology of presbycusis is understood, attempts at prevention will be limited. Limitation of noise exposure may reduce the hearing loss. Although several studies have evaluated the role of vitamins, antioxidants, smoking cessation, and diet in preventing presbycusis, there have been no conclusive findings in humans.

Clinical Findings

Patients with this disorder may present with a chief complaint of hearing loss and difficulty understanding speech. However, presbycusis is often diagnosed only after complaints are raised by close patient contacts, or hearing loss is noted on routine screening in a patient without hearing-related complaints. The Hearing Handicap Inventory of the Elderly Screening Version (HHIE-S) is a widely accepted subjective screening tool for hearing disability. Abnormalities of the whisper test are found as the level of hearing loss increases. Results of the Weber tuning-fork test remain normal as long as the hearing loss is symmetric. Results of Rinne testing are normal, because presbycusis is a sensorineural hearing loss and not a conductive one.

An audiogram of a patient with presbycusis typically shows bilaterally symmetric high-frequency hearing loss.

Treatment

The treatment of presbycusis consists of hearing rehabilitation, which often involves fitting for digital and analog types of hearing aids. Patients are more likely to perceive benefit from hearing aids if they view their hearing loss as a problem. Cochlear implantation is reserved for patients with profound hearing loss that is unresponsive to hearing aids. Additional tools include lip-reading classes; television closed captioning; sound-enhancing devices for concerts, church, or other public gatherings; and telephone amplifiers. A combined approach involving the patient, hearing loss specialist, family physician, and close contacts of the patient is likely to produce the best overall treatment plan.

Suggested topics for patient education include patient self-advocation as well as the proper use of hearing aids and other assistive devices.

Prognosis

The expectation of slow progression of this hearing loss should be communicated to the patient. Complete deafness, however, is not typical of presbycusis.

NOISE-INDUCED HEARING LOSS

General Considerations

Noise-induced hearing loss is the second most common sensorineural hearing loss (Table 45-2) after presbycusis. Up to one-third of patients with hearing loss have some component of their deficit that is noise-induced. The degree of hearing loss is related to the level of noise and the duration of exposure. Excessive shear force from loud sounds or long exposure results in cell damage, cell death, and subsequent hearing loss.

Prevention

Hearing protection programs are prevalent in industrial settings and typically include the use of earplugs, intermittent audiograms, and limiting exposure. Patient commitment to the use of hearing protection is critical for the success of prevention programs.

Clinical Findings

Patients may present with tinnitus, decreased speech discrimination, and difficulty hearing when background noise is present. Patients identified through hearing protection programs may be asymptomatic. Results of the whisper test or office-based pure-tone audiometry may be normal or abnormal, depending on the degree of hearing loss.

Audiometric evaluation of noise-induced hearing loss reveals a bilateral notch of sensorineural hearing loss between 3000 and 6000 Hz.

Treatment

When prevention fails, treatment involves hearing rehabilitation, as previously outlined in the treatment of presbycusis. Education about the risks of loud noise exposure should begin when patients are young, because hearing loss can occur from significant recreational noise. The importance of adhering to hearing protection programs should also be emphasized.

Prognosis

Nothing can be done to reverse cell death from noise-induced hearing loss; however, some patients exposed to brief episodes of loud noise exhibit only hair cell injury and may recover hearing over time. These patients are more susceptible to noise-induced hearing loss on reexposure.

Cerumen Impaction

General Considerations

Impaction of wax in the external auditory canal is a common, frequently overlooked problem in the elderly. Removal of cerumen has been shown to significantly improve hearing ability. The incidence of cerumen impactions increases in the elderly population. Chronic skin changes lead to loss of normal migration of skin epithelium leading to exfoliated cell debris accumulation. Cerumen gland atrophy results in drier wax that is more likely to become trapped by the large tragi hairs in the external ear canal. The likelihood of impaction is increased by hearing aid or earplug use.

Prevention

Cerumen impactions may be prevented by the regular use of agents that soften wax. Readily available household agents such as water, mineral oil, cooking oils, hydrogen peroxide, or glycerin may be used. Commercially available ceruminolytic compounds, such as carbamide peroxide, triethanolamine polypeptide, and docusate sodium liquid, are also efficacious, but not more so than less-expensive options.

Clinical Findings

Patients presenting with cerumen impaction may complain of sudden or gradual hearing loss, tinnitus affecting one or both the ears, and interference with hearing aids. Examination of the external canal reveals partial or complete occlusion of the ear canal with cerumen.

Complications

Various removal methods are associated with ear discomfort and potential for ear canal trauma. Canal trauma can result in bleeding, canal swelling, or infection. Warm water should be used for ear irrigation, because cold water can induce vertigo.

Treatment

The management of impactions may be approached in various ways. When the wax is soft, gentle irrigation of the canal with warm water may be sufficient to remove the offending material. In the case of firmer wax, ceruminolytic agents may be applied, followed by irrigation. Any cerumen remaining after these maneuvers may be removed using a curette in combination with an otoscope for direct visualization. The patient may experience an improvement of symptoms even with partial removal of the impaction. Patients should be instructed about ear cleaning techniques and home use of ceruminolytics.

Prognosis

Cerumen impaction has an excellent prognosis, and hearing can be dramatically improved with relatively simple interventions. However, recurrence of impaction is common.

CENTRAL AUDITORY PROCESSING DISORDER

General Considerations

Central auditory processing disorder (CAPD) is the general term for hearing impairment that results from central nervous system (CNS) dysfunction. Any insult to the nervous system such as stroke or dementia can cause CAPD. The disorder is characterized by a loss of speech discrimination that is more profound than the associated loss in hearing.

Prevention

It may be postulated that the protection of the CNS provided by aspirin therapy and hypertension control could reduce the incidence of CAPD.

Clinical Findings

Patients with CAPD have difficulty understanding spoken language but may be able to hear sounds well. A patient may have difficulty following verbal instructions but understand written ones. There are no specific physical findings of CAPD, but patients may have other evidence of neurologic abnormalities.

Treatment

Treatment of CAPD is limited. If CNS dysfunction is caused by a reversible entity, then treatment for the underlying cause should be initiated. Identifying and treating other causes of sensory impairment may improve the patient’s level of disability; however, CAPD may decrease the effectiveness of auditory rehabilitation. Patient education efforts should focus on educating friends and family about the disorder and options for hearing rehabilitation. The prognosis for patients with CAPD is determined by the underlying disorder.

Visual impairment is defined as binocular acuity of 20/40 or worse. Legal blindness is when acuity is worse than 20/200. Older adults with good visual acuity show problems with visual function in real-life situations as testing is usually done in an optimum condition with maximum contrast and illumination with minimal glare. Testing for visual problems with decreased contrast sensitivity, decreased illumination, and increased glare is not practical for primary care providers, and hence it is important that they ask questions routinely to screen for performance under these circumstances. Educating the patient about simple measures to improve the environment may help with their quality of life.

PRESBYOPIA

General Considerations

Presbyopia is an age-associated progressive loss of the focusing power of the lens. Its incidence increases with age. The cause of this disorder is the ongoing increase in the diameter of the lens as a result of continued growth of the lens fibers with aging. This thickened lens accommodates less responsively to the contraction of muscles in the ciliary body, limiting its ability to focus on near objects.

Clinical Findings

Patients presenting with this disorder frequently complain of eye strain or of blurring of their vision when they quickly change from looking at a nearby object to one that is far away. On examination, the only abnormality noted is a decrease in near vision.

Treatment

Because presbyopia is due to normal age-related changes of the eye, there is no proven prevention. In patients with normal distance vision, treatment for this disorder is as simple as purchasing reading glasses. For patients requiring correction of their distance vision, options include spectacle correction with bifocal or trifocal lenses, monovision contact lenses in which one eye is corrected for distance vision and the other eye for near vision, or contact lens correction of distance vision and simple reading glasses for near vision. Surgical treatment of presbyopia is an evolving science, including procedures on the cornea, lens, and sclera.

Prognosis

All patients should be educated to anticipate a decline in near vision with aging. When left uncorrected, problems may occur with reading, driving, or other activities of daily living.

AGE-RELATED MACULAR DEGENERATION

General Considerations

Age-related macular degeneration (AMD/ARMD) is the leading cause of severe vision loss in older Americans. It is characterized by atrophy of cells in the central macular region of the retinal pigment epithelium, resulting in the loss of central vision. Peripheral vision generally remains intact. AMD is typically classified as early and intermediate (usually dry type) or advanced/late AMD, which is divided into atrophic or nonneovascular (dry) or exudative or neovascular (wet) forms. The exudative form occurs in only 10% of patients with AMD, but it is responsible for the majority of severe vision loss related to the disease.

Prevention

Multiple risk factors for this disorder have been studied, including genetic factors, white race, obesity, and cardiovascular disease; only increasing age and tobacco abuse have consistently been associated with AMD. Because smoking has been strongly implicated as a risk factor and continued tobacco use is associated with a worse response to laser photocoagulation, tobacco avoidance and smoking cessation should be highly recommended to all patients. Hypertension has also been linked to a worse response to laser therapy; thus, effective blood pressure control is desirable, as well. Finally, antioxidants play a role in tertiary prevention. Patients with intermediate AMD or unilateral advanced AMD had a ∼25% reduction of their risk for developing advanced AMD if treated with a high-dose combination of vitamin C, vitamin E, β-carotene, and zinc. Patients with early or no AMD did not have the same benefit.

Clinical Findings

A. Symptoms and Signs

Patients may report onset of blurred central vision that is either gradual or acute with difficulty reading in dim light and night driving. Wavy or distorted central vision, known as metamorphopsia; intermittent shimmering lights; and central blind spots, termed scotoma, may all occur. Clinical findings include decreased visual acuity, Amsler grid distortion, and characteristic abnormalities on dilated funduscopic examination. In early disease, the most common findings are drusen: yellowish-colored deposits deep in the retina. In late disease of the atrophic type, areas of depigmentation are seen in the macula. In the exudative form, abnormal vessels (subretinal neovascularization) leak fluid and blood beneath the macula.

B. Special Examinations

Fluorescein angiography may be used by a specialist to confirm the diagnosis and to help determine whether a patient has atrophic or exudative AMD.

Treatment

A. Referral

An ophthalmologist will play a critical role in care of the patient with known or suspected AMD. Urgent referral to an eye specialist should occur if a patient with suspected or known AMD presents with acute visual changes. Treatment of exudative AMD is a rapidly advancing field with many ongoing clinical trials of surgical and pharmaceutical interventions. Current treatment options include laser photocoagulation, photodynamic therapy (Verteporfin), and intravitreal antiangiogenic therapy [antivascular endothelial growth factor (VEGF)]. No effective treatments exist for patient with dry AMD.

Vision rehabilitation is the cornerstone to helping patients maximize their remaining vision and maintain their level of function for as long as possible. Low-vision professionals along with social workers can be of great assistance in recommending optical aids and devices and accessing local, state, and federal resources for the visually impaired. Direct-illumination devices, magnifiers, high-power reading glasses, telescopes, closed-circuit television, large-print publications, and bold-lined paper are some of the many devices that can be employed.

B. Patient Education

Patient education topics include the importance. (Its use is described at http://www.amd.org.)

Prognosis

Many patients with mild dry AMD will not experience significant worsening of their vision. It is difficult to predict which patients will develop advancing disease and further loss of central vision. This condition is generally progressive but is not completely blinding. Peripheral vision should not be affected by AMD.

GLAUCOMA

General Considerations

Glaucoma is the second leading cause of blindness in the United States. Although glaucoma is most often associated with elevated IOP, it is the optic neuropathy that defines the disease. Normal IOP is generally accepted to be between 10 and 21 mmHg. The majority of patients with an IOP of > 21 mmHg will not develop glaucoma, and 30–50% of patients with glaucoma will have an IOP of < 21 mmHg. Despite these facts, it has been clearly shown that as IOP increases, so does the risk of developing glaucoma. Other identified risk factors for glaucoma include family history and advancing age and African-American race. Additional possible risk factors include diabetes mellitus, hypertension, and myopia.

Prevention

The AAFP and the USPTF do not recommend screening for glaucoma, citing insufficient evidence to recommend for or against routine screening by primary care clinicians for elevated IOP or early glaucoma. The American Academy of Ophthalmology recommends screening for glaucoma by an ophthalmologist every 1–2 years after age 65.

Clinical Findings

A. Symptoms and Signs

Patients with acute angle-closure glaucoma typically present with unilateral intense pain and blurred vision. Patients may report seeing halos around light sources and complain of photophobia, headache, nausea, and vomiting. Physical examination shows a middilated pupil, conjunctival injection, and lid edema. Patients generally have markedly elevated IOP, usually between 60 and 80 mmHg.

Primary open-angle glaucoma is a more insidious disease with a long asymptomatic phase. Patients may notice a gradual loss of peripheral vision. Examination may reveal diminished visual fields, elevated IOP, and abnormalities of the optic disk on direct ophthalmoscopy (symmetrically enlarged cup-to-disk ratio, cup-to-disk ratio asymmetry between the two eyes, or a highly asymmetric cup in one eye).

B. Special Tests

Intraocular pressure may be measured using a variety of tools. The most readily available tool is the physician’s hand. Palpation of the globe through a lightly closed lid can reveal asymmetric hardness or bilaterally firm eyeballs and provide a very gross measure of IOP. More accurate tools include the Tono-Pen (a handheld applanation tonometer), Goldmann applanation tonometry, and pneumotonometry (puff test).

Treatment

Patients with significant risk factors or physical findings that raise concern for glaucoma should be referred to an ophthalmologist for further evaluation and confirmation of diagnosis.

A. Acute Angle-Closure Glaucoma

Acute angle-closure glaucoma is a medical emergency that requires immediate referral and treatment.

B. Primary Open-Angle Glaucoma

The treatment of primary open-angle glaucoma consists of pharmacologic and surgical interventions aimed at decreasing the IOP. Although elevated IOP is not required for the diagnosis of glaucoma, it has been shown that reduction of IOP in patients with glaucoma slows the progression of disease. Even patients with normal pressures can benefit from reduction in IOP.

1. Pharmacotherapy

Topical eyedrops or oral medications aimed at decreasing aqueous humor production or increasing outflow are used. Topical agents such as β-blockers and prostaglandin analogs are first-line therapy, and α-adrenergic agents and carbonic anhydrase inhibitors are second-line of therapy. Topical miotics and epinephrine compounds are now infrequently used. Oral medications include carbonic anhydrase inhibitors such as acetazolamide. Topical glaucoma agents have varying degrees of systemic absorption and are capable of producing systemic side effects and drug-drug interactions. Patients should be educated on the importance of routine eye care and of taking medications as prescribed.

2. Surgical intervention

When medical management is unsuccessful, surgical intervention is considered. Laser trabeculoplasty and laser or conventional trabeculectomy are the most commonly performed procedures.

Prognosis

Untreated glaucoma can result in blindness. Rapid treatment of acute angle-closure glaucoma may preserve vision. Treatment of primary open-angle glaucoma can prevent further loss of vision, but typically does not restore lost vision.

CATARACTS

General Considerations

Any opacification of the lens is termed a cataract. Cataract disease is the most common cause of blindness worldwide and the most common eye abnormality in the elderly. Risk factors for cataracts include advancing age, exposure to ultraviolet (UV) B light, glaucoma, smoking, alcohol abuse, diabetes, and chronic steroid use. Diet and vitamins do not play a role in development or progression of the disease. Because cataracts tend to develop slowly, the patient may not be fully aware of the degree of vision impairment.

Prevention

Prevention of cataracts is aimed at the modifiable risk factors. Physicians should use steroids at as low a dose as is therapeutic and discontinue them when possible. Patients should be advised on how to minimize UV light exposure as well as the benefits of smoking cessation and control of chronic diseases.

Clinical Findings

Patients may report blurring of vision, “ghosting” of images, difficulty seeing in oncoming lights (glare) and difficulty with night driving, and monocular diplopia. The patient may also complain of a decrease in color perception and even note “second sight,” which is an improvement in near vision with a nuclear cataract. Examination of the eye reveals opacification of the lens. Cataracts may be easier to see with dilation of the eye and a direct ophthalmoscope at +5D (diopters) setting held 6 inches from the patient’s eye.

Treatment

The treatment of cataracts is predominantly surgical. Although small cataracts may be treated by an updated eyeglass prescription, most patients with significant symptoms from a cataract benefit from surgical removal and replacement of the lens. Factors influencing the timing of surgery include life expectancy, current level of disability, status of other medical illnesses, family and social situations, and patient expectations.

Family physicians may aid patients in understanding the surgery and assisting with preoperative management. Cataract surgery is a low-risk procedure. Routine use of laboratory testing and electrocardiogram screening has not improved surgical outcome. Individuals should receive a history and physical examination prior to undergoing surgery. Additional testing is recommended only if findings are abnormal. Cataract surgery is often accomplished under local anesthesia with minimally invasive techniques. In this case, there is no need to discontinue anticoagulation for the procedure. Surgeons should be made aware if patients are taking α-blockers as this is associated with a complication called intraoperative floppy iris syndrome.

Prognosis

Cataracts do not resolve and may progress without treatment. The prognosis with surgical treatment is excellent, and ≤95% of patients obtain improved vision after surgery.

DIABETIC RETINOPATHY

General Considerations

Diabetic retinopathy (DR) is the leading cause of blindness in adults in the United States. It is important to consider diabetic retinopathy as a disease of the aging eye because prevalence increases with duration of diabetes mellitus. The risk of blindness attributable to this disorder is greatest after 30 years of illness. DR is divided into two major forms: nonproliferative (NPDR) and proliferative (PDR), named for the absence or presence of abnormal new blood vessels emanating from the retina, respectively. NPDR can be further classified into mild, moderate, severe, and very severe categories depending on the extent of nerve fiber layer infarcts (cotton-wool spots), intraretinal hemorrhages, hard exudates, and microvascular abnormalities. The severity of proliferative retinopathy can be classified as early, high-risk, and severe depending on the severity and extent of neovascularization.

Prevention

Patients with diabetes mellitus type 2 should have a comprehensive eye examination by an ophthalmologist shortly after diagnosis to screen for signs of retinopathy. Meticulous glycemic control decreases the risk of development and progression of retinopathy in all patients with diabetes. In addition, tight control of blood pressure also significantly reduces a patient’s risk of developing retinopathy.

Clinical Findings

Many patients presenting with diabetic retinopathy are free of symptoms; even those with the severe proliferative form may have 20/20 visual acuity. Others may report decreased vision that has occurred slowly or suddenly, unilaterally or bilaterally. Scotomata or floaters may also be reported. Funduscopic examination reveals any or all of the following: microaneurysms, dot and blot intraretinal hemorrhages, hard exudates, cotton-wool spots, boat-shaped preretinal hemorrhages, neovascularization, venous beading, and macular edema.

Fluorescein angiography may be performed by an ophthalmologist to further assess the degree of disease.

Treatment

Untreated proliferative retinopathy is relentlessly progressive, leading to significant vision impairment and blindness. In addition to maximizing glucose and blood pressure control, focal and pan-retinal laser photocoagulation surgery or vitrectomy is the mainstay of acute and chronic treatment and may preserve vision in certain patients. There is emerging evidence that intravitreal anti-VEGF treatment can be used in the management of retinopathy. When vision loss has occurred, vision rehabilitation should be initiated, as described earlier in the discussion of AMD. Topics to review with patients include the importance of an annual, comprehensive eye examination, glycemic control, and hypertension management.

Prognosis

Early diagnosis and treatment, as well as tight glycemic and blood pressure control, improve prognosis and prevents blindness.