Age-related changes

The external auditory canal changes with age. The lateral cartilaginous ear canal weakens with age, reducing structural rigidity, and outgrowths in the medial bony ear canal (e.g., benign exostoses) can further narrow the canal, leading to cerumen impaction and difficulty fitting a hearing aid.[1, 2] Atrophy of the surface epithelium and decreased apocrine gland function of the ear canal predisposes to dryness, scaling, and trauma.

Common pathologies

Cerumen impaction is a frequent consequence of age-related changes in the external auditory canal.[3, 4] Cerumen protects the ear with antimicrobial properties and by capturing foreign particles and is normally eliminated from the ear canal with epithelial migration. In older adults, apocrine glands atrophy, decreasing the watery component of cerumen, producing cerumen that is drier, harder, and less likely to be expelled.[2, 5] Hearing aids and the thicker, fuller tragal hairs associated with normal aging can further impede the canal’s normal “self cleaning” mechanism.[5] Every patient should be regularly evaluated for impaction at clinic visits.[3] Cerumen can be removed with curettage (ideally done with an operative otoscope head, such as a Welch Allyn Operating Otoscope #21700), suction, topical cerumenolytics, or irrigation with warm water. However, irrigation should be avoided in patients who are diabetic, immunocompromised, or those with perforated tympanic membranes due to the risk of precipitating an acute otitis externa or media.[3, 6, 7] Preventive measures include counseling against cotton swab use and encouraging the regular use of emollients like mineral oil or glycerin.[3]

Squamous cell carcinoma, basal cell carcinoma, and actinic keratoses can affect the pinna.[8] With age, skin becomes atrophic due to dermal thinning, disorganized collagen deposition, and decreased elastic tissues and mitotic divisions. Free radicals produced secondary to ultraviolet light exposure promote cross-linking of fibrous proteins and DNA. Risk factors for skin cancer include age, sun exposure, Type I–II skin types on the Fitzpatrick scale, and history of multiple sunburns.[9, 10] Squamous cell carcinoma may present as a red patch, often preceded by actinic keratosis.[9] Basal cell carcinoma presents as an elevated, pink, waxy nodular lesion with a clearly demarcated capillary bed. Maintain a high level of suspicion for malignancy and refer for biopsy when accompanied by persistent otalgia, recurrent otitis externa, bleeding, hearing loss, facial nerve weakness/paralysis, or granulation tissue.[11]

Acute otitis externa (AOE) is a bacterial infection of the external auditory canal often precipitated by a break in the skin secondary to water exposure or manipulation, such as cotton swab use.[12] The setting of a warm, moist ear canal encourages bacterial growth of common pathogens such as Pseudomonas aeruginosa and Staphylococcus aureus. The patient presents with pruritus, purulent discharge, pain, and, at times, conductive hearing loss due to canal narrowing.[12, 13] On physical exam, pulling the pinna elicits significant pain, distinguishing AOE from otitis media.[12] Topical treatment with antiseptic or antibiotic eardrops, with or without steroids, is first-line treatment. Although several meta-analyses of randomized controlled trials have not demonstrated clinically significant differences between topical treatments, ciprofloxacin, and steroid preparation (Cipro HC with hydrocortisone or Ciprodex with dexamethasone) twice a day for 7–10 days is a common, albeit expensive, treatment.[13, 14] Cheaper options include a neomycin, polymyxin, and hydrocortisone preparation (Cortisporin Otic Suspension), which can be given three to four times a day, or antiseptic treatment with acetic acid 2.0%, with or without hydrocortisone 1.0%.[13, 14] If soft tissue swelling limits drug delivery, eardrops may be administered with a wick, along with pain medication and frequent debridement by the physician if needed.[12, 14] Systemic antibiotic treatment, with coverage of Pseudomonas aeruginosa and Staphylococcus aureus, is reserved as adjunctive treatment if the patient is diabetic or immune deficient, if the infection has spread beyond the ear canal, or if topical therapy is unable to be delivered effectively.[14] If significant debris, impaction, or failure of initial antibiotic course occurs, referral to an otolaryngologist is needed.

Malignant otitis externa is a feared complication of AOE and is a rare, potentially lethal infection of the soft tissue and bone of the external auditory canal and skull base by Pseudomonas aeruginosa.[12, 15] Classically, this complication occurs in older, diabetic, and immunocompromised patients. Symptoms include severe otalgia for ≥4 weeks, purulent otorrhea, and, occasionally, cranial neuropathies, particularly facial paralysis.[12] On physical exam, granulation tissue is seen along the ear canal floor. Long-term intravenous antibiotics and correction of immunosuppression (e.g., glucose control in diabetics) are the primary treatment, whereas surgery is reserved for debridement. Suspicion for malignant otitis externa requires emergent referral to an otolaryngologist.

Herpes zoster oticus is a vesicular rash of the external ear canal accompanied by severe pain and hearing loss and, when accompanied by facial paralysis, is called Ramsay Hunt syndrome.[15] Caused by reactivation of latent herpes virus, the incidence increases with age due to the decline of cellular immunity.[16] With a worse prognosis than Bell’s palsy, early treatment with steroids and antiviral medication and an urgent appointment with an otolaryngologist are essential.[17] Treatment for Ramsay Hunt syndrome includes 500 mg famciclovir three times a day for seven days or 800 mg acyclovir five times a day for 7 to 10 days.[18] Oral prednisone of 60 mg daily for 3 to 5 days should also be prescribed.[17] Close monitoring, early audiometric testing, and documentation of the degree of facial paralysis are important in following disease progression and establishing prognosis.

Age-related changes

The middle and inner ear undergo changes with age, including stiffening and thinning of the tympanic membrane and middle ear ossicles, death of inner and outer cochlear hair cells, atherosclerotic changes of inner-ear vessels, and devascularization of the spiral ligament, which impact a patient’s auditory and vestibular systems.[1, 2, 19]

Common pathologies

Although otitis media is a common pediatric problem, it may also occur in older adults, often coinciding with upper respiratory tract infections or allergic rhinitis.[20] Acute otitis media presents with rapid onset of pain and possibly fever, accompanied by fullness and erythema of the tympanic membrane and an effusion. Treatment includes amoxicillin 500 mg three times a day for 7–10 days for uncomplicated otitis media, and amoxicillin/clavulanate 875 mg twice a day or 500 mg three times a day for 10–14 days for diabetic or immunocompromised patients.[21] In complicated cases, myringotomy may be performed in the office by an otolaryngologist to provide immediate symptomatic relief.[20] Referral to an otolaryngologist is needed if middle ear effusions are persistent for ≥8 weeks, particularly if unilateral, to rule out a nasopharyngeal lesion.[22, 23]

In older adults, acquired cholesteatomas may present as a chronically draining ear with purulent otorrhea, hearing loss, tinnitus, vertigo, and/or facial nerve palsy.[24, 25] On otoscopic exam, there can be tympanic membrane retraction, white debris, granulation tissue, and ossicular erosion. Cholesteatomas are due to squamous epithelium in the middle ear, mastoid, or epitympanium. It is unknown how cholesteatomas form, but hypotheses involve epithelial migration or implantation secondary to instrumentation. Cholesteatomas are benign but can lead to significant morbidity secondary to erosive expansion and damage to surrounding structures. A computed tomography (CT) temporal bone scan without contrast and audiogram are essential to early workup and can be ordered before referral to an otolaryngologist. Treatment by an otolaryngologist generally involves surgical removal. Untreated cholesteatomas can lead to serious complications, including CSF otorrhea, labyrinthine fistulas, ossicular erosion, facial nerve paralysis, mastoiditis, and meningitis.

Age-related hearing loss

Treatment of age-related hearing loss generally involves evaluation by an audiologist (a clinician with a master’s or doctoral degree in audiology) or hearing instrument specialist/hearing aid dispenser (a technician licensed by the state to dispense and fit hearing aids). Nearly all insurance programs will cover the cost of audiologic testing by an audiologist with a physician’s referral, but they will not cover hearing aids, which range from $3,000 to $10,000 for bilateral fitting and follow-up care by an audiologist or hearing aid dispenser. Several need-based outreach programs provide access to discount or free hearing aids through an application process that can be coordinated by the referring audiologist. Over-the-counter assistive listening devices (e.g., Pocket Talker, Comfort Duett) and personal sound amplifiers (devices worn on/in the ear similar to a hearing aid but sold as a consumer electronic device not explicitly for the treatment of hearing loss) can also provide amplification and may be a good option, particularly when hearing aids are not possible due to limited time or financial resources.

For older adults with severe to profound hearing loss who no longer obtain significant benefit from hearing aids, cochlear implantation is an option. Cochlear implantation among older adults is a routine outpatient procedure with a safety profile comparable to implantation in younger adults and children and associated with significant gains in speech perception and quality of life.[26, 27] A cochlear implant directly stimulates the cochlear nerve, bypassing the impaired cochlea, and can restore access to sound and language for many adults with severe hearing loss. Cochlear implantation is covered by Medicare and most other private insurance programs. If there is concern for a severe hearing loss, referral to an otolaryngologist who performs cochlear implants, generally at larger academic centers, is warranted.

Sudden sensorineural hearing loss

Sudden sensorineural hearing loss can be distinguished from an acute conductive hearing loss by history, otoscopy, and the Weber and Rinne tests.[28–30] Sudden sensorineural hearing loss involves at least a 30-decibel hearing loss over three contiguous frequencies that generally occurs acutely and less commonly over one to three days.[28, 31] Patients may notice pressure in the affected ear and transient dizziness.[28, 31] A history and physical should include information about trauma, ear pain, drainage, fever, and other associated illnesses to distinguish between an acute otitis media, which simply requires observation or oral antibiotics/ decongestants, and a true sensorineural loss.[28, 32] Sensorineural loss is caused by pathology to the inner ear or auditory nerve from viral infection, tumor, or other etiologies and requires immediate referral to an otolaryngologist for audiologic confirmation, workup, and treatment. Treatment within the first several days is critical for the efficacy of oral corticosteroids (generally 14–21 days of prednisone 1 mg/kg/day with taper) and/or intratympanic steroids (injected directly into the middle ear) in helping to aid hearing recovery.[28]

Tinnitus

Tinnitus is the perception of sound in the absence of external noise.[33] The physical exam and history can differentiate between pulsatile and nonpulsatile tinnitus. Pulsatile tinnitus presents with a rhythmic whooshing sound corresponding to the heartbeat, whereas nonpulsatile tinnitus is described as a ringing or buzzing sound. Persistent pulsatile tinnitus could reflect vascular or other pathologic etiologies (e.g., vascular tumor, benign intracranial hypertension, carotid stenosis) and should be further worked up. Initial workup may include listening for carotid bruits, obtaining a carotid ultrasound, and brain MRI with contrast to evaluate for intracranial masses. Referral to an otolaryngologist is indicated if pulsatile tinnitus is persistent. Nonpulsatile tinnitus is more common and often seen in the setting of hearing loss and can be exacerbated by neck or back strain, stress, or temporomandibular joint problems. If nonpulsatile tinnitus is sporadic and not bothersome, generally no further evaluation is needed. If it is occasionally bothersome, ambient stimulation, which includes using a sound generator when sleeping or having a radio on in the background, is a simple, low-cost approach to decrease attention directed at tinnitus. Tinnitus is commonly associated with hearing loss, and amplification can assist with symptom management. Tinnitus retraining therapies (e.g., neuromonics) are an option for patients whose daily function is severely impacted, but must be used daily for weeks to months with the aim of decreasing loudness and annoyance. If tinnitus worsens, is very bothersome, or is accompanied by vertigo or change in hearing, evaluation by an otolaryngologist is warranted with further referrals for specialized tinnitus management, including tinnitus retraining, biofeedback, and cognitive behavioral therapy.

Age-related changes

Presbytasis is the loss of balance due to aging and is caused by changes in mobility, vision, proprioception, and vestibular function.[2] Balance disorders are worsened by polypharmacy and decreased muscle tone of older adults, which increases the risk of falls and worsens health outcomes.[8]

Common pathologies

Vertigo is the sensation of movement in the absence of movement. Benign paroxysmal positional vertigo (BPPV) is the most common cause of vertigo among older adults and is caused by the displacement of otoconia into the semicircular canals.[34] The displacement leads to brief, episodic vertigo lasting one minute or less precipitated by head movements, most commonly turning over in bed. Performing the Dix-Hallpike maneuver and observing for nystagmus can diagnose posterior semicircular canal BPPV.[34–36] Treatment involves maneuvers that shift the otoconia back into place, such as the Epley manuever.[34, 37] If refractory to treatment, referral to an otolaryngologist is necessary.[35]

Another common peripheral cause of vertigo, Ménière’s disease, is characterized by spontaneous episodes of vertigo accompanied by fluctuating, low-frequency hearing loss, tinnitus, and a sense of aural fullness.[38] The natural history of Ménière’s disease can range from rare episodes to extended periods of vertigo.[34] An individual episode generally lasts for less than one hour.[38] The disorder is thought to originate from excess endolymph within the inner ear that leaks into perilymph, which excites, then inhibits, cranial nerve VIII and basal hair cells.[34, 39] If Ménière’s is suspected, referral to an otolaryngologist is needed. Initial treatment involves a low-salt diet (<1,500 mg of sodium per day) and triameterene/hydrochlorothiazide with intratympanic steroids reserved for more refractory cases.[8, 34, 40]

Migrainous vertigo occurs in roughly 25% of migraine patients and is the second most common cause of episodic vertigo.[34, 38, 41] Vertigo can range from seconds to days and occurs in the absence of or prior to a migraine. Pharmacologic treatment consists of migraine treatment with triptans, calcium channel blockers, and beta blockers. Lifestyle measures such as exercise and cutting back on caffeine, sugar, fat, alcohol, and tobacco are also important.

Age-related changes

Swallowing is a synchronized series of muscle contractions that allows a food bolus to safely enter the stomach.[2, 42] With aging, this process can become problematic due to weakness of masticatory, tongue, and facial muscles. Older patients experience longer swallowing phases that lead to an increased risk of aspiration. This is compounded by the high prevalence of neurologic disorders and polypharmacy in older adults.

Common pathologies

Dysphagia is common in the older population and can be secondary to gastroesophageal reflux disease (GERD), Zenker’s diverticulum, autoimmune disease, and neurologic diseases like cerebrovascular accidents.[8, 42] Further functional tests include the modified barium swallow and flexible endoscopy while swallowing.[2] Referral to a speech-language pathologist is often warranted when dysphagia persists, with further evaluation by an otolaryngologist as needed. Treatment of the underlying pathological process is necessary along with rehabilitation. For instance, Zenker’s diverticulum is commonly treated with surgery by otolaryngologists.[43] Moreover, simple measures like a soft diet and head-of-bed elevation can help tremendously.

Age-related changes

The voice undergoes age-related changes including calcification of the laryngeal cartilage, decreased muscular tone, joint stiffening, and bowing of the vocal folds.[2, 44] These changes are compounded by age-related decreases in secretions, nerve conduction speed, and pulmonary function.

Common pathologies

There are numerous etiologies of voice disorders, including GERD, COPD, vocal cord paralysis, and neurologic disorders.[2, 44] Treating the underlying cause and rehabilitation of the voice often involves a multidisciplinary approach with speech pathologists, otolaryngologists, neurologists, and pulmonologists. Treatment of vocal cord paralysis and presbylaryngis with injectables can be done in an office setting or the operating room. Furthermore, hydration and avoidance of tobacco are essential, and sialogogues may be helpful. Warning signs for neoplasm include progressive hoarseness, dysphagia, and a palpable mass, particularly in a smoker.[44]

Age-related changes

Aging of the nasal cavity and sinuses involves decreased smell and taste secondary to loss of olfactory epithelium.[2, 8] Drugs, radiation, trauma, and infections can compound this loss. Loss of moisture due to atrophy of glandular tissue can lead to excessive nasal dryness and increase the risk of epistaxis.[45] This dryness is exacerbated by common medications prescribed to older adults, especially anticoagulants. Lower mucociliary clearance and immunosenescence increase the risk of infection and inflammation.[45–47]