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DISORDERS OF THE EYES & LIDS
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Table 7–3. Adverse ophthalmic effects of systemic drugs (selected list).
Medications Possible Ophthalmic Side Effects
Vitamins
Vitamin A Papilledema
Vitamin D Band-shaped keratopathy
Rheumatologic agents
Chloroquine, hydroxychloroquine Retinal degeneration principally involving the macula, vortex keratopathy
Gold salts Deposits in the cornea, conjunctiva, and lens
NSAIDs (eg, ibuprofen, naproxen, indomethacin) Vortex keratopathy (ibuprofen, naproxen), corneal deposits (indomethacin),
Penicillamine Ocular pemphigoid, optic neuropathy, extraocular muscle palsy (myasthenic
Salicylates Subconjunctival and retinal hemorrhages, nystagmus
Dermatologic agents
Dupilumab Conjunctivitis
Retinoids (eg, isotretinoin, tretinoin, acitretin, and
etretinate)
Bisphosphonates
Alendronate, pamidronate Scleritis, episcleritis, uveitis
If no baseline abnormalities are present, screening should
be repeated annually beginning after 5 years. More fre-
retinal degeneration principally involving the macula (indomethacin)
syndrome)
Papilledema, blepharoconjunctivitis, corneal opacities, decreased contact lens
tolerance, decreased dark adaptation, teratogenic ocular abnormalities,
idiopathic intracranial hypertension, optic neuritis
before alpha-adrenoreceptor antagonist treatment is
started, if possible.
quent screening is necessary in patients treated with doses
greater than 5.0 mg per kg measured body weight per day
of hydroxychloroquine or greater than 2.3 mg/kg/day of
chloroquine, in patients with kidney or macular disease, or
in those taking tamoxifen.
Patients receiving long-term systemic corticosteroids
are at increased risk for several ocular complications,
ocular complications including serous retinal detachment,
cystoid macular edema, and retinal vein occlusion. Patients
receiving MEK inhibitors should have a complete eye exami-
nation at baseline before the initiation of these medications
and should be referred for an eye examination if blurred or
reduced vision develops while taking MEK inhibitors.
(continued)
The chemotherapeutic MEK inhibitors are associated with
including glaucoma, cataract, and central serous retinopathy. They should be referred to an eye care professional for
an eye examination at baseline before starting corticosteroids and at any time if reduced or blurry vision develops.
An ophthalmologist should be informed whether a
patient is taking or has ever taken alpha-adrenoreceptor
antagonists (such as tamsulosin) before cataract surgery
because these medications increase the risk of intraoperative floppy iris syndrome, which can make cataract surgery
more challenging. Cataract surgery should be completed
Arora S et al. Retinal toxicities of systemic anticancer drugs.
Surv Ophthalmol. 2022;67:97. [PMID: 34048859]
Park SSE et al. Dealing with floppy iris syndrome. Curr Opin
Ophthalmol. 2022;33:3. [PMID: 34711714]
Somisetty S et al. The impact of systemic medications on retinal
function. Asia Pac J Ophthalmol (Phila). 2023;12:115. [PMID:
36971705]
Yusuf I et al. Hydroxychloroquine-induced retinal toxicity. Front
Pharmacol. 2023;14:1196783. [PMID: 37324471]
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8
Otolaryngology Disorders
Elliott D. Kozin, MD
Rosh Sethi, MD
Lawrence R. Lustig, MD
º
DISEASES OF THE EAR
HEARING LOSS
ESSENTIALS OF DIAGNOSIS
»
Hearing loss is generally categorized as either
conductive or sensorineural.
»
Diagnostic evaluation routinely includes
audiologic testing.
» Classification & Epidemiology
Table 8–1 categorizes hearing loss as normal, mild, moderate, severe, or profound and outlines the vocal equivalent as
well as the decibel range.
A. Conductive Hearing Loss
Conductive hearing loss results from a mechanical disruption of the external auditory canal or middle ear. Several
mechanisms may result in impairment of the passage of
sound vibrations to the inner ear, such as obstruction (eg,
cerumen impaction), mass loading (eg, middle ear effusion), stiffness (eg, otosclerosis), and discontinuity (eg,
ossicular disruption). Conductive losses in adults are most
commonly due to cerumen impaction or transient eustachian tube dysfunction from upper respiratory tract infection. Persistent conductive losses usually result from
chronic ear infection, trauma, or otosclerosis. Perforations
of the tympanic membrane may also result in a conductive
hearing loss. Conductive hearing loss is often correctable
with medical (eg, use of a hearing aid) or surgical (eg,
repair of tympanic membrane and ossicular chain) therapy,
or both. CT of the temporal bone may be used as an
adjunct to physical examination to determine the potential
cause of conductive hearing loss.
B. Sensorineural Hearing Loss
Sensorineural hearing losses are common in adults and
generally result from deficits of the inner ear or central
(brain) auditory pathway. Sensory hearing loss results from
deterioration of the cochlea, usually due to loss of sensory
hair cells within the organ of Corti. The most common
form of sensorineural hearing loss is age-related hearing
loss that manifests as a gradually progressive, predominantly high-frequency hearing loss. Other causes of sensorineural hearing loss include excessive noise exposure;
head trauma; ototoxic medications, such as cisplatin-based
chemotherapy; and systemic diseases.
While most types of sensorineural hearing loss are
gradual, sensorineural hearing loss may be sudden. Sud-
den sensorineural hearing loss, often called idiopathic
sudden sensorineural hearing loss, is considered an
otologic emergency and may be treatable with oral or
intratympanic corticosteroids if delivered within several
weeks of onset. Long-term severe to profound sensorineu-
ral hearing loss due to deficits at the level of the inner ear
may be correctable with surgery, such as cochlear implantation. Sensorineural hearing loss may also be due to deficits at the level of the central auditory pathway, including
lesions involving the eighth cranial nerve, auditory nuclei,
ascending tracts, or auditory cortex. Examples of central
causes of hearing loss include acoustic neuroma, multiple
sclerosis, and auditory neuropathy. Treatment of hearing
loss due to central causes are usually aimed at addressing
the underlying pathology.
US Preventive Services Task Force; Krist AH et al. Screening for
hearing loss in older adults: US Preventive Services Task
Force recommendation statement. JAMA. 2021;325:1196.
[PMID: 33755083]
Table 8–1. Hearing loss classification.
Classification Vocal Equivalent Decibel (dB) Range
Normal Soft whisper 0–20 dB
Mild Soft spoken voice 20–40 dB
Moderate Normal spoken voice 40–60 dB
Severe Loud spoken voice 60–80 dB
Profound Shout > 80 dB
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» Evaluation of Hearing (Audiology)
In a quiet room, the hearing level may be estimated by having the patient repeat aloud words presented in a soft
whisper, a normal spoken voice, or a shout. Normal spoken
voice is about 60 decibels. A 512-Hz tuning fork is useful in
differentiating conductive from sensorineural hearing loss.
In the Weber test, the tuning fork is placed directly on the
forehead or front teeth. In conductive losses, the sound is
heard as louder in the ear with poorer hearing; however, in
sensorineural losses, the sound radiates to the ear that
hears better than the other ear. In the Rinne test, the tuning
fork is placed alternately on the mastoid bone (bone conduction) and in front of the ear canal (air conduction). In
conductive losses greater than 25 dB, bone conduction
sounds louder than air conduction.
Formal audiometric studies are performed in a soundproofed room. Pure-tone thresholds in decibels (dB) are
obtained over the range of 250–8000 Hz. Conductive losses
create a “gap” between the air and bone thresholds, whereas
in sensorineural losses, both air and bone thresholds are
equally diminished. Speech discrimination measures the
clarity of hearing, reported as percentage correct (90–100%
is normal). Auditory brainstem-evoked response screening
method is most commonly used in newborn screening and
may determine the approximate location of the lesion (eg,
cochlea or brain). MRI scanning is the most sensitive and
specific test to determine the possible location of a defect
resulting in sensorineural hearing loss.
Every patient who reports hearing loss should be referred
for audiologic evaluation unless the cause is easily remediable (eg, cerumen impaction, otitis media). Immediate audio-
metric referral is indicated for patients with idiopathic
sudden sensorineural hearing loss because it requires treatment (corticosteroids) within a limited several-week time
period.
Feltner C et al. Screening for hearing loss in older adults:
updated evidence report and systematic review for the US
Preventive Services Task Force. JAMA. 2021;325:1202.
[PMID: 33755082]
Irace AL et al. Longitudinal associations of subclinical hearing
loss with cognitive decline. J Gerontol A Biol Sci Med Sci.
2022;77:623. [PMID: 34516645]
Sharma RK et al. Age-related hearing loss and the development
of cognitive impairment and late-life depression: a scoping
overview. Semin Hear. 2021;42:10. [PMID: 33883788]
the cochlear implant—an electronic device that is surgi-
cally implanted into the cochlea to stimulate the auditory
nerve—offers socially beneficial auditory rehabilitation.
Buchman CA et al. Unilateral cochlear implants for severe, pro-
found, or moderate sloping to profound bilateral sensorineural hearing loss: a systematic review and consensus statements.
JAMA Otolaryngol Head Neck Surg. 2020;146:942. [PMID:
32857157]
Dixon PR et al. Health-related quality of life changes associated
with hearing loss. JAMA Otolaryngol Head Neck Surg.
2020;146:630. [PMID: 32407468]
Lindquist NR et al. Cochlear implants for single-sided deafness:
quality of life, daily usage, and duration of deafness. Laryngoscope. 2023;133:2362. [PMID: 36254870]
Zeitler DM et al. American Cochlear Implant Alliance Task
Force: Recommendations for determining cochlear implant
candidacy in adults. Laryngoscope. 2024;134 (Suppl 3):S1.
[PMID: 37435829]
DISEASES OF THE AURICLE
Disorders of the auricle include skin cancers due to sun
exposure. Traumatic auricular hematoma must be drained
to prevent significant cosmetic deformity “cauliflower ear”
or canal blockage resulting from dissolution of supporting
cartilage. Similarly, cellulitis of the auricle must be treated
promptly to prevent perichondritis and resultant deformity. Relapsing polychondritis is characterized by recurrent, frequently bilateral, painful episodes of auricular
erythema and edema and sometimes progressive involvement of the cartilaginous tracheobronchial tree. Treatment
with corticosteroids may help forestall cartilage dissolution. Polychondritis and perichondritis may be differentiated from cellulitis by sparing of involvement of the lobule,
which does not contain cartilage.
Akdoğan Ö et al. Sudden sensorineural hearing and vestibular
loss in a case of relapsing polychondritis. Ann Otol Rhinol
Laryngol. 2021;130:1412. [PMID: 33813869]
Dalal PJ et al. Risk factors for auricular hematoma and
recurrence after drainage. Laryngoscope. 2020;130:628.
[PMID: 31621925]
Mertz P et al. Relapsing polychondritis: Best Practice & Clinical
Rheumatology. Best Pract Res Clin Rheumatol. 2023;37:
101867. [PMID: 37839908]
DISEASES OF THE EAR CANAL
» Hearing Amplification
Patients with hearing loss not correctable by medical
therapy may benefit from hearing amplification. Contemporary hearing aids are comparatively free of distortion
and have been miniaturized to the point where they often
may be contained entirely within the ear canal or lie inconspicuously behind the ear.
For patients with conductive loss or unilateral profound
sensorineural loss, bone-conducting hearing aids directly
stimulate the ipsilateral cochlea (for conductive losses) or
contralateral ear (profound unilateral sensorineural loss).
In most adults with severe to profound sensory hearing loss,
1. Cerumen Impaction
Cerumen is a protective secretion produced by the outer
portion of the ear canal. In most persons, the ear canal is self-
cleansing and no hygiene measures are recommended. Cerumen impaction is most often self-induced through ill-advised
cleansing attempts by entering the canal itself, eg, digital
trauma or use of a cotton-tip applicator. It may be relieved by
the patient using detergent ear drops (eg, 3% hydrogen peroxide; 6.5% carbamide peroxide) and irrigation, or by the
clinician using mechanical removal, suction, or irrigation.
Irrigation is performed with water at body temperature to
avoid a vestibular caloric response. The stream should be
directed at the posterior ear canal wall adjacent to the
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cerumen plug. Irrigation should be performed only when
the tympanic membrane is known to be intact.
Use of jet irrigators (eg, WaterPik) should be avoided
since they may result in tympanic membrane perforations.
Following irrigation, the ear canal should be thoroughly
dried (eg, by the patient using a hair blow-dryer on lowpower setting or by the clinician instilling isopropyl alcohol) to reduce the likelihood of otitis externa. Specialty
referral is indicated if impaction is frequently recurrent, if
it has not responded to routine measures, or if there is
tympanic membrane perforation or chronic otitis media.
Horton GA et al. Cerumen management: an updated clinical review
and evidence-based approach for primary care physicians.
J Prim Care Community Health. 2020;11:2150132720904181.
[PMID: 31994443]
2. Foreign Bodies
Foreign bodies in the ear canal are more frequent in children than in adults. Firm materials may be removed with a
loop or a hook, taking care not to displace the object medially toward the tympanic membrane; microscopic guidance is helpful. Aqueous irrigation should not be performed
for organic foreign bodies (eg, beans, insects), because
water may cause them to swell. Living insects are best
immobilized before removal by filling the ear canal with
lidocaine or mineral oil. Lidocaine should never be used in
a patient with a possible tympanic membrane perforation
as this may result in a profound vestibular response.
begins in the floor of the ear canal and may extend into the
middle fossa floor, the clivus, and even the contralateral
skull base.
» Clinical Findings
Examination reveals erythema and edema of the ear canal
skin, often with a purulent exudate (Figure 8–1), as well as
surrounding periauricular cellulitis. Manipulation of the
auricle elicits pain. The lateral surface of the tympanic membrane is often erythematous. When the canal skin is very
edematous, it may be impossible to visualize the tympanic
membrane. In immunocompromised patients, such as those
with diabetes, malignant otitis externa typically presents
with persistent otorrhea; granulation tissue in the ear canal;
deep otalgia; and in advanced cases, progressive palsies of
cranial nerves, such as cranial nerve VI, VII, IX, X, XI,
or XII. Diagnosis of malignant otitis externa is confirmed by
the demonstration of osseous erosion on CT scanning and
laboratory testing showing high inflammatory markers, such
as ESR and CRP. MRI scanning is often important to rule out
abscesses that may result from malignant otitis externa.
» Treatment
Treatment of otitis externa involves protection of the ear
from additional moisture and avoidance of further
Kim KH et al. Clinical characteristics of external auditory canal
foreign bodies in children and adolescents. Ear Nose Throat
J. 2020;99:648. [PMID: 31814447]
3. Otitis Externa
ESSENTIALS OF DIAGNOSIS
»
Otalgia.
»
Erythema, edema, and purulence of the external
auditory canal skin.
»
Patients who are immunocompromised or have
diabetes are at risk for “malignant” otitis externa
(osteomyelitis of the skull base).
» General Considerations
Otitis externa, often called “swimmer’s ear,” presents with
otalgia with associated external auditory canal edema and
purulent discharge. There is often a history of recent water
exposure or mechanical trauma (eg, scratching, cotton
applicators). Otitis externa is usually caused by gramnegative rods (eg, Pseudomonas, Proteus) or fungi (eg,
Aspergillus), which grow in the presence of excessive moisture. In patients who are immunocompromised or have
diabetes, persistent otitis externa may evolve into osteomyelitis of the skull base (so-called malignant otitis externa).
Usually caused by Pseudomonas aeruginosa, osteomyelitis
▲
Figure 8–1. Malignant otitis externa in a 40-year-old
woman with diabetes mellitus, with typical swelling and
honey-colored crusting of the pinna. Both the external
auditory canal and temporal bone were involved in the
pseudomonal infection. (Used, with permission, from E.J.
Mayeaux Jr, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr,
Chumley H. The Color Atlas of Family Medicine, 2nd ed.
McGraw-Hill, 2013.)
OTOLARYNGOLOGY DISORDERS
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mechanical injury by scratching. In cases of moisture in the
ear (eg, swimmer’s ear), acidification with a drying agent
(ie, a 50/50 mixture of isopropyl alcohol/white vinegar) is
often helpful. When infected, an otic antibiotic solution or
suspension of an aminoglycoside (eg, neomycin/polymyxin B)
or fluoroquinolone (eg, ciprofloxacin), with or without a
corticosteroid (eg, hydrocortisone), is usually effective.
Purulent debris filling the ear canal should be gently
removed to permit entry of the topical medication. Drops
should be used abundantly (five or more drops three or four
times a day) to penetrate the depths of the canal. When
substantial edema of the canal wall prevents entry of drops
into the ear canal, a wick is placed to facilitate their entry. In
recalcitrant cases—particularly when cellulitis of the periauricular tissue has developed—oral fluoroquinolones (eg,
ciprofloxacin, 500 mg twice daily for 1 week) are used
because of their effectiveness against Pseudomonas. Newer
medications that are ciprofloxacin suspensions hold promise to improve otitis externa outcomes. Any case of persistent
otitis externa in patients who are immunocompromised or
have diabetes must be referred for specialty evaluation.
Treatment of malignant otitis externa requires prolonged antipseudomonal antibiotic administration, often
for several months. Although intravenous therapy is often
required initially (eg, ciprofloxacin 200–400 mg every
12 hours), selected patients may be graduated to oral ciprofloxacin (500–1000 mg twice daily). To avoid relapse, antibiotic therapy should be continued, even in the
asymptomatic patient, until gallium scanning indicates
marked reduction or resolution of the inflammation. Surgical debridement of infected bone is reserved for cases of
deterioration despite medical therapy.
obscuring the tympanic membrane to a variable degree.
Solitary osteomas are of no significance as long as they do
not cause obstruction or infection. Multiple exostoses,
which are generally acquired from repeated exposure to
cold water (eg, “surfer’s ear”), may progress and require
surgical removal if completely occluding the external
auditory canal or resulting in frequent infections.
Wille AE et al. Prevention of external auditory canal exostosis in
the Colorado whitewater community. J Osteopath Med.
2022;122:431. [PMID: 35355493]
6. Neoplasia
The most common neoplasm of the ear canal is squamous
cell carcinoma. When an apparent otitis externa does not
resolve on therapy, a malignancy should be suspected and
biopsy performed. This disease carries a very high 5-year
mortality rate because the tumor tends to invade the lymphatics of the cranial base and must be treated with wide
surgical resection and radiation therapy. Adenomatous
tumors, originating from the ceruminous glands, generally
follow a more indolent course.
Komune N et al. Prognostic impact of tumor extension in
patients with advanced temporal bone squamous cell
carcinoma. Front Oncol. 2020;10:1229. [PMID: 32850367]
Piras G et al. Management of squamous cell carcinoma of the
temporal bone: long-term results and factors influencing
outcomes. Eur Arch Otorhinolaryngol. 2021;278:3193.
[PMID: 32979119]
Seligman KL et al. Temporal bone carcinoma: treatment patterns
and survival. Laryngoscope. 2020;130:E11. [PMID: 30874314]
Jackson EA et al. Acute otitis externa: rapid evidence review. Am
Fam Physician. 2023;107:145. [PMID: 36791445]
Plum AW et al. An overview of acute otitis externa. Otolaryngol
Clin North Am. 2023;56:891. [PMID: 37516653]
Smith ME et al; INTEGRATE (The UK ENT Trainee Research
Network). Acute otitis externa: consensus definition,
diagnostic criteria and core outcome set development. PLoS
One. 2021;16:e0251395. [PMID: 33989313]
4. Pruritus
Pruritus of the external auditory canal, particularly at the
meatus, is common. While it may be associated with otitis
externa or with seborrheic dermatitis or psoriasis, most
cases are self-induced from excoriation or overly zealous
ear cleaning. To permit regeneration of the protective cerumen blanket, patients should be instructed to avoid use of
soap and water or cotton swabs in the ear canal and avoid
any scratching. Patients with excessively dry canal skin
may benefit from application of mineral oil, which helps
counteract dryness and repel moisture. When an inflammatory component is present, topical application of a corticosteroid (eg, 0.1% triamcinolone) may be beneficial.
5. Exostoses & Osteomas
Bony overgrowths of the ear canal are a frequent incidental
finding and rarely have clinical significance. They present
as skin-covered bony mounds in the medial ear canal
DISEASES OF THE EUSTACHIAN TUBE
1. Eustachian Tube Dysfunction
ESSENTIALS OF DIAGNOSIS
»
Aural fullness.
»
Discomfort with barometric pressure change.
»
Retracted eardrum.
The tube that connects the middle ear to the
nasopharynx—the eustachian tube—provides ventilation
and drainage for the middle ear. It is normally closed,
opening only during swallowing or yawning. When eustachian tube function is compromised, air trapped within the
middle ear becomes absorbed and negative pressure results.
The most common causes of eustachian tube dysfunction
are diseases associated with edema of the tubal lining, such
as viral upper respiratory tract infections and seasonal
allergies. The patient usually reports a sense of fullness in
the ear and mild to moderate impairment of hearing.
When the tube is only partially blocked, swallowing or
yawning may elicit a popping or crackling sound. Examination may reveal retraction of the tympanic membrane
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and decreased mobility on pneumatic otoscopy. Following a
viral illness, this disorder is usually transient, lasting days to
weeks. Treatment with systemic and intranasal decongestants (eg, pseudoephedrine, 60 mg orally every 4–6 hours;
oxymetazoline, 0.05% spray every 8–12 hours), combined
with autoinsufflation by forced exhalation against closed
nostrils, may hasten relief. Autoinsufflation should not be recommended to patients with active intranasal infection since
this maneuver may precipitate middle ear infection. Allergic
patients may also benefit from intranasal corticosteroids (eg,
beclomethasone dipropionate, two sprays in each nostril
twice daily for 2–6 weeks). Air travel, rapid altitudinal change,
and underwater diving should be avoided until resolution.
An overly patent eustachian tube (“patulous eusta-
chian tube”) is a relatively uncommon, although quite
distressing problem. Patients typically describe fullness in
the ear and autophony (an exaggerated ability to hear oneself breathe and speak). A patulous eustachian tube may
develop during rapid weight loss, such as following pregnancy, or it may be idiopathic. In contrast to eustachian
tube dysfunction, the aural pressure is often made worse by
exertion and may diminish during an upper respiratory
tract infection. Although physical examination is usually
normal, respiratory excursions of the tympanic membrane
may occasionally be detected during vigorous breathing.
Treatment includes avoidance of decongestant products
and rarely surgery on the eustachian tube itself.
Froehlich MH et al. Eustachian tube balloon dilation: a system-
atic review and meta-analysis of treatment outcomes. Otolar-
yngol Head Neck Surg. 2020;163:870. [PMID: 32482125]
Kaderbay A et al. Balloon dilation for persistent unilateral
chronic obstructive Eustachian tube dysfunction is effective:
a prospective multicentre study. Eur Arch Otorhinolaryngol.
2023;280:1101. [PMID: 35932313]
Kjær Krogshede S et al. Balloon dilation of the Eustachian tube:
a randomized controlled trial with 6 months follow-up. J Int
Adv Otol. 2022;18:501. [PMID: 36349672]
Yang HH et al. Clinical predictors of symptom improvement
following eustachian tube balloon dilation. Ann Otol Rhinol
Laryngol. 2023;132:1032. [PMID: 36226334]
2. Serous Otitis Media
ESSENTIALS OF DIAGNOSIS
»
Negative pressure from eustachian tube obstruction causes transudation of fluid into the middle
ear and stasis.
»
Dull and hypomobile tympanic membrane.
Prolonged eustachian tube dysfunction with resultant
negative middle ear pressure may cause a transudation of
fluid. In adults, serous otitis media usually occurs with an
upper respiratory tract infection, with barotrauma, or with
chronic allergic rhinitis, but when persistent and unilateral,
nasopharyngeal carcinoma must be excluded. The tympanic membrane is dull and hypomobile, occasionally
accompanied by air bubbles in the middle ear and
conductive hearing loss. The treatment of serous otitis
media is similar to that for eustachian tube dysfunction. A
short course of oral corticosteroids (eg, prednisone, 40 mg/
day for 7 days) has been advocated by some clinicians, as
have oral antibiotics (eg, amoxicillin, 250 mg three times
daily for 7 days)—or even a combination of the two. The
role of these regimens remains controversial, but they are
probably of little lasting benefit. When medication fails to
bring relief after several months, a ventilating tube placed
through the tympanic membrane may restore hearing and
alleviate the sense of aural fullness.
Mulvaney CA et al. Antibiotics for otitis media with effusion
(OME) in children. Cochrane Database Syst Rev. 2023;10:
CD015254. [PMID: 37870130]
Otteson T. Otitis media and tympanostomy tubes. Pediatr Clin
North Am. 2022;69:203. [PMID: 35337534]
3. Barotrauma
Persons with poor eustachian tube function (eg, congenital
narrowness or acquired mucosal edema) may be unable to
equalize the barometric stress exerted on the middle ear by
air travel, rapid altitudinal change, or underwater diving.
The problem is generally most acute during airplane descent,
since the negative middle ear pressure tends to collapse and
block the eustachian tube, causing pain. Several measures
are useful to enhance eustachian tube function and avoid
otic barotrauma. The patient should be advised to swallow,
yawn, and autoinsufflate frequently during descent. Oral
decongestants (eg, pseudoephedrine, 60–120 mg) should be
taken several hours before anticipated arrival time so that
they will be maximally effective during descent. Topical
decongestants, such as 1% phenylephrine or oxymetazoline
nasal spray, should be administered 1 hour before arrival.
For acute negative middle ear pressure that persists on
the ground, treatment includes decongestants and attempts
at autoinsufflation. Myringotomy with or without placement of a tympanostomy tube provides immediate relief
and is appropriate for severe otalgia and hearing loss.
Underwater diving may represent an even greater barometric stress to the ear than flying. Patients should be
warned to avoid diving when they have an upper respiratory infection or episode of nasal allergy. During the
descent phase of the dive, if inflation of the middle ear via
the eustachian tube has not occurred, pain will develop
within the first 15 feet; the dive must be aborted. In all
cases, divers must descend slowly and equilibrate in stages
to avoid the development of severely negative pressures in
the tympanum that may result in hemorrhage (hemotympanum) or in perilymphatic fistula. In the latter, the oval or
round window ruptures, resulting in sensory hearing loss
and acute vertigo. During the ascent phase of a saturation
dive, sensory hearing loss or vertigo may develop as the
first (or only) symptom of decompression sickness. Immediate recompression will return intravascular gas bubbles
to solution and restore the inner ear microcirculation.
Tympanic membrane perforation is an absolute contraindication to diving, as the patient will experience an unbal-
anced thermal stimulus to the semicircular canals and may
experience vertigo, disorientation, and even emesis.
OTOLARYNGOLOGY DISORDERS
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Millan SB et al. Prevention of middle ear barotrauma with
oxymetazoline/fluticasone treatment. Undersea Hyperb Med.
2021;48:149. [PMID: 33975404]
Scarpa A et al. Inner ear disorders in SCUBA divers: a review.
J Int Adv Otol. 2021;17:260. [PMID: 34100753]
DISEASES OF THE MIDDLE EAR
1. Acute Otitis Media
ESSENTIALS OF DIAGNOSIS
»
Otalgia.
»
Purulent fluid of the middle ear.
»
Erythema and hypomobility of tympanic
membrane.
» General Considerations
Acute otitis media is a bacterial infection of the mucosally
lined, air-containing spaces of the middle ear. Purulent
material may extend to pneumatized mastoid air cells and
petrous apex of the lateral skull base. Acute otitis media is
usually precipitated by a viral upper respiratory tract
infection that causes eustachian tube obstruction. This
results in accumulation of fluid and mucus, which becomes
secondarily infected by bacteria. The most common pathogens are Streptococcus pneumoniae, Haemophilus influen-
zae, and Streptococcus pyogenes.
» Clinical Findings
Acute otitis media may occur at any age. Presenting symptoms and signs include otalgia, aural pressure, decreased
hearing, and often fever. The typical physical findings are
erythema and decreased mobility of the tympanic membrane (Figure 8–2). Occasionally, bullae will appear on the
tympanic membrane.
Rarely, when middle ear empyema is severe, the tympanic membrane bulges outward. In such cases, tympanic
membrane rupture is imminent. Rupture is accompanied
by a sudden decrease in pain, followed by the onset of otorrhea. With appropriate therapy, spontaneous healing of the
tympanic membrane occurs in most cases. Acute mastoiditis results from an infection extending from the middle ear
to the mastoid air cells. It is diagnosed by pain, postauricular erythema, and occasionally proptosis of the auricle.
Frank swelling over the mastoid bone or the association of
cranial neuropathies or central findings indicates severe
disease requiring urgent care. Evaluation includes imaging,
such as CT, to determine presence of “coalescence” of air
cells and associated soft-tissue abscess.
» Treatment
The treatment of acute otitis media is specific antibiotic
therapy, often combined with nasal decongestants. The
first-choice antibiotic is amoxicillin 1 g orally every 8 hours
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▲
Figure 8–2. Acute otitis media with effusion of right
205
ear, with multiple air-fluid levels visible through a
translucent, slightly retracted, nonerythematous
tympanic membrane. (Used, with permission, from Frank
Miller, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr,
Chumley H. The Color Atlas of Family Medicine, 2nd ed.
McGraw-Hill, 2013.)
for 5–7 days. Alternatives (useful in resistant cases) are
amoxicillin-clavulanate 875/125 mg or 2 g/125 mg ER
every 12 hours for 5–10 days; or cefuroxime 500 mg or
cefpodoxime 200 mg orally every 12 hours for 5–7 days.
Recurrent acute otitis media may be managed with longterm antibiotic prophylaxis. Single daily oral doses of sulfamethoxazole (500 mg) or amoxicillin (250 or 500 mg) are
given over a period of 1–3 months. Failure of this regimen
to control infection is an indication for insertion of ventilating tubes.
Surgical drainage of the middle ear (myringotomy),
debridement of the mastoid (mastoidectomy), or both are
reserved for patients with severe otalgia or when complications of otitis (eg, mastoiditis, meningitis) have occurred.
Hoberman A et al. Tympanostomy tubes or medical manage-
ment for recurrent acute otitis media. N Engl J Med.
2021;384:1789. [PMID: 33979487]
Venekamp RP et al. Antibiotics for acute otitis media in children.
Cochrane Database Syst Rev. 2023;11:CD000219. [PMID:
37965923]
2. Chronic Otitis Media
ESSENTIALS OF DIAGNOSIS
»
Chronic otorrhea with or without otalgia.
»
Tympanic membrane perforation with conductive
hearing loss.
»
Often amenable to surgical correction.
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» General Considerations
Chronic infection of the middle ear and mastoid generally
develops as a consequence of recurrent acute otitis media,
although it may follow other diseases and trauma. Perforation or retraction of the tympanic membrane may be present. The bacteriology of chronic otitis media differs from
that of acute otitis media. Common organisms include
P aeruginosa, Proteus species, Staphylococcus aureus, and
mixed anaerobic infections.
» Clinical Findings
The clinical hallmark of chronic otitis media is purulent
aural discharge. Drainage may be continuous or intermit-
tent, with increased severity during upper respiratory tract
infection or following water exposure. Pain is uncommon
except during acute exacerbations. Conductive hearing loss
results from destruction of the tympanic membrane or
ossicular chain, or both.
» Treatment
The medical treatment of chronic otitis media includes
regular removal of infected debris, use of earplugs to protect against water exposure, and topical antibiotic drops
(ofloxacin 0.3% or ciprofloxacin with dexamethasone) for
exacerbations. Oral ciprofloxacin, active against Pseudo-
monas, 500 mg twice a day for 1–6 weeks, may help dry a
chronically discharging ear.
In most cases, surgery is the definitive management of
tympanic membrane perforations with or without association of ossicular disruption. Successful reconstruction of
the tympanic membrane may be achieved with autologous
tissue, such as temporalis fascia, in about 90% of cases,
often with improvement in conductive hearing.
▲
Figure 8–3. Cholesteatoma. (Used, with permission,
from Vladimir Zlinsky, MD, in Roy F. Sullivan, PhD:
Audiology Forum: Video Otoscopy, www.RCSullivan.com;
from Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. The
Color Atlas of Family Medicine, 2nd ed. McGraw-Hill, 2013.)
of cholesteatoma is surgical, including marsupialization of
the sac or its complete removal. This may require the creation of a “mastoid bowl” in which the ear canal and mastoid are joined into a large common cavity that must be
periodically cleaned.
Basonbul RA et al. Systematic review of endoscopic ear surgery
outcomes for pediatric cholesteatoma. Otol Neurotol.
2021;42:108. [PMID: 33165162]
Manzoor NF et al. Comparative analysis of recidivism after
endoscopic and microscopic-based cholesteatoma resection.
Otol Neurotol. 2022;43:466. [PMID: 35287152]
Roychowdhury P…Kozin ED et al. In-office repair of tympanic
membrane perforation. Otol Neurotol. 2021;42:e1636.
[PMID: 34420025]
Sainsbury E et al. Tissue engineering and regenerative medicine
strategies for the repair of tympanic membrane perforations.
Biomater Biosyst. 2022;6:100046. [PMID: 36824158]
» Complications of Otitis Media
A. Cholesteatoma
Cholesteatoma is a special variety of chronic otitis media
(Figure 8–3). The most common cause is prolonged eustachian tube dysfunction, with inward migration of the
upper flaccid portion of the tympanic membrane. This
creates a squamous epithelium-lined sac, which—when its
neck becomes obstructed—may fill with desquamated
keratin and become chronically infected. Cholesteatomas
typically erode bone, including the ossicular chain with
extension into the mastoid. Over time, cholesteatoma may
erode into the inner ear, involve the facial nerve and, on
rare occasions, spread intracranially. Otoscopic examination may reveal a retraction pocket of the tympanic membrane or a marginal tympanic membrane perforation that
exudes keratin debris or granulation tissue. The treatment
B. Mastoiditis
Acute suppurative mastoiditis usually evolves following
several weeks of inadequately treated acute otitis media. It
is characterized by pain and postauricular cellulitis accompanied by a spiking fever. CT scan reveals coalescence of
the mastoid air cells due to destruction of their bony septa.
Initial treatment consists of intravenous antibiotics (eg,
cefazolin 0.5–1.5 g every 6–8 hours) directed against the
most common offending organisms (S pneumoniae,
H influenzae, and S pyogenes), and myringotomy for
culture and drainage. Failure of medical therapy indicates
the need for surgical drainage, such as a mastoidectomy.
C. Petrous Apicitis
The medial portion of the petrous bone between the
inner ear and clivus may become a site of persistent infection when the drainage of its pneumatic cell tracts
becomes blocked. This may cause foul discharge, deep ear
and retro-orbital pain, and sixth nerve palsy (Gradenigo
syndrome); meningitis may be a complication. Treatment
is with prolonged antibiotic therapy (based on culture
results) or surgical drainage via petrous apicectomy or
both.
OTOLARYNGOLOGY DISORDERS
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207
Isaac H et al. Transmastoid and transtemporal drainage of
petrous apicitis with otitis media. Ann Otol Rhinol Laryngol.
2021;130:314. [PMID: 32772562]
D. Facial Paralysis
Facial palsy may be associated with either acute or chronic
otitis media. In the acute setting, it results from inflammation of the seventh nerve in its middle ear segment. Treatment consists of myringotomy for drainage and culture,
followed by intravenous antibiotics (based on culture
results). The use of corticosteroids is controversial. The
prognosis is excellent, with complete recovery in most cases.
Facial palsy associated with chronic otitis media usually
evolves slowly due to chronic pressure on the seventh nerve
in the middle ear or mastoid by cholesteatoma. Treatment
requires surgical correction of the underlying disease. The
prognosis is less favorable than for facial palsy associated
with acute otitis media.
Fichera P et al. Acute otitis media and facial paralysis in chil-
dren: A systemic review and proposal of an operative algo-
rithm. Audiol Res. 2023;13:889. [PMID: 37987335]
Mohan S et al. Considerations in management of acute otitis
media in the COVID-19 era. Ann Otol Rhinol Laryngol.
2021;130:520. [PMID: 32911957]
E. Sigmoid Sinus Thrombosis
Trapped infection within the mastoid air cells adjacent to
the sigmoid sinus may cause septic thrombophlebitis. This
is heralded by signs of systemic sepsis (spiking fevers,
chills), at times accompanied by signs of increased intracranial pressure (headache, lethargy, nausea and vomiting,
papilledema). Diagnosis can be made noninvasively by
magnetic resonance venography (MRV). Primary treatment is with intravenous antibiotics (based on culture
results). Additional treatment, such as anticoagulation,
surgical drainage, ligation of the internal jugular vein, or
some combination thereof, may be indicated when embolization is suspected.
thrombophlebitis adjacent to an epidural abscess. The predominant causative organisms are S aureus, S pyogenes, and
S pneumoniae. Rupture into the subarachnoid space results
in meningitis and often death. (See Chapter 32.)
Botti C et al. Pneumolabyrinth: a systematic review. Eur Arch
Otorhinolaryngol. 2021;278:4619. [PMID: 33881577]
3. Otosclerosis
Otosclerosis is a progressive disease with a marked familial
tendency that affects the bony otic capsule. Lesions involving the footplate of the stapes result in increased impedance to the passage of sound through the ossicular chain,
producing conductive hearing loss. This may be treated
either through the use of a hearing aid or surgical replacement of the stapes with a prosthesis (stapedectomy). When
otosclerotic lesions involve the cochlea (“cochlear otosclerosis”), permanent sensory hearing loss may occur.
Gillard DM et al. Cost-effectiveness of stapedectomy vs hearing
aids in the treatment of otosclerosis. JAMA Otolaryngol Head
Neck Surg. 2020;146:42. [PMID: 31697352]
Patel S et al. A systematic review of the effectiveness of bisphos-
phonates for otosclerosis. Otol Neurotol. 2022;43:530. [PMID:
35213475]
Teaima AA et al. Comparison of the efficacy of cochlear implan-
tation and stapes surgery in far advanced otosclerosis: a metaanalysis study. Eur Arch Otorhinolaryngol. 2023;280:77.
[PMID: 35687184]
4. Trauma to the Middle Ear
Tympanic membrane perforation may result from impact
injury or explosive acoustic trauma (Figure 8–4). Spontaneous healing occurs in most cases. Persistent perforation
may result from secondary infection brought on by exposure to water. During the healing period, patients should be
advised to wear earplugs while swimming or bathing.
Ziv O et al. Post-operative clinical course in children undergoing
mastoidectomy due to complicated acute mastoiditis. Eur
Arch Otorhinolaryngol. 2022;279:3891. [PMID: 34714371]
F. Central Nervous System Infection
Otogenic meningitis is the most common intracranial
complication of ear infection. In the setting of acute suppurative otitis media, it arises from hematogenous spread
of bacteria, most commonly H influenzae and S pneu-
moniae. In chronic otitis media, it results either from passage of infection along preformed pathways, such as the
petrosquamous suture line, or from direct extension of
disease through the dural plates of the petrous pyramid.
Epidural abscesses arise from direct extension of disease
in the setting of chronic infection. They are usually
asymptomatic but may present with deep local pain,
headache, and low-grade fever. They are often discovered
as an incidental finding at surgery. Brain abscess may arise
in the temporal lobe or cerebellum as a result of septic
▲
Figure 8–4. Traumatic perforation of the left
tympanic membrane. (Used, with permission, from
William Clark, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr,
Chumley H. The Color Atlas of Family Medicine, 2nd ed.
McGraw-Hill, 2013.)
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Hemorrhage behind an intact tympanic membrane (hemotympanum) may follow blunt trauma or extreme barotrauma. Spontaneous resolution over several weeks is the
usual course. When a conductive hearing loss greater than
30 dB persists for more than 3 months following trauma,
disruption of the ossicular chain should be suspected.
Middle ear exploration with reconstruction of the ossicular
chain, combined with repair of the tympanic membrane
when required, will usually restore hearing.
Simani L et al. Paper patching versus watchful waiting of trau-
matic tympanic membrane perforations: a meta-analysis.
Laryngoscope. 2021;131:2091. [PMID: 33881175]
Straughan AJ et al. Feel the burn! Fireworks-related otolaryngo-
logic trauma. Ann Otol Rhinol Laryngol. 2021;130:1369.
[PMID: 33834893]
Zhao X et al. The latest progress of tympanic membrane repair
materials. Am J Otolaryngol. 2022;43:103408. [PMID:
36031699]
5. Middle Ear Neoplasia
Primary middle ear tumors are rare. Glomus tumors arise
either in the middle ear (glomus tympanicum) or in the
jugular bulb with upward erosion into the hypotympanum
(glomus jugulare). They present clinically with pulsatile
tinnitus and hearing loss. A vascular mass may be visible
behind an intact tympanic membrane. Large glomus jugulare tumors are often associated with multiple cranial neuropathies, especially involving nerves VII, IX, X, XI, and XII.
Treatment usually requires surgery, radiotherapy, or both.
Pulsatile tinnitus thus warrants magnetic resonance angiography (MRA) and MRV to rule out a vascular mass.
Dharnipragada R et al. Modern management of complex tympa-
nojugular paragangliomas: a systematic review and metaanalysis. World Neurosurg. 2023;170:149. [PMID: 36400356]
Taïeb D et al. Clinical consensus guideline on the management
of phaeochromocytoma and paraganglioma in patients harbouring germline SDHD pathogenic variants. Lancet Diabetes Endocrinol. 2023;11:345. [PMID: 37011647]
EARACHE
Earache can be caused by a variety of otologic problems,
but otitis externa and acute otitis media are the most common. Otitis externa and acute otitis media may be differentiated using history and physical examination, including
pneumatic otoscopy. Pain out of proportion to the physical
findings may be due to herpes zoster oticus, especially
when vesicles appear in the ear canal or concha. Persistent
pain and discharge from the ear suggest osteomyelitis of
the skull base or cancer, and patients with these symptoms
should be referred for specialty evaluation.
Nonotologic causes of otalgia are numerous. The sensory innervation of the ear is derived from the trigeminal,
facial, glossopharyngeal, vagal, and upper cervical nerves.
Because of this rich innervation, referred otalgia is quite
frequent. Temporomandibular joint dysfunction is a common cause of referred ear pain. Pain is exacerbated by
chewing or psychogenic grinding of the teeth (bruxism)
and may be associated with dental malocclusion. Repeated
episodes of severe lancinating otalgia may occur in glossopharyngeal neuralgia. Infections and neoplasia that
involve the oropharynx, hypopharynx, and larynx frequently cause otalgia. Persistent earache demands specialty
referral to exclude cancer of the upper aerodigestive tract.
Norris CD et al. Secondary otalgia: referred pain pathways and
pathologies. AJNR Am J Neuroradiol. 2020;41:2188. [PMID:
33093134]
DISEASES OF THE INNER EAR
1. Sensorineural Hearing Loss
Diseases of the cochlea and central auditory pathway result
in hearing loss, a condition that is usually irreversible. The
primary goals in the management of sensory hearing loss
are prevention of further losses and functional improvement with auditory rehabilitation, such as with a hearing
aid or cochlear implant.
A. Presbycusis
Presbycusis, or age-related hearing loss, is the most frequent cause of sensory hearing loss and is progressive,
predominantly high-frequency, and symmetrical. Various
etiologic factors (eg, prior noise trauma, drug exposure,
genetic predisposition) may contribute to presbycusis.
Most patients notice a loss of speech discrimination that is
especially pronounced in noisy environments. About 25%
of people between the ages of 65 and 75 years and almost
50% of those over 75 experience hearing difficulties. There is
emerging evidence that conventional audiometry may not
fully capture hearing loss (known as “hidden hearing
loss”). Many patients may have subclinical hearing loss.
New testing modalities are being devised to detect hearing
loss in the setting of normal audiograms.
Choi JY et al. The impact of hearing loss on clinical dementia
and preclinical cognitive impairment in later life. J Alzheimers Dis. 2021;81:963. [PMID: 33867361]
Drennan WR. Identifying subclinical hearing loss: extended
audiometry and word recognition in noise. Audiol Neurootol.
2022;27:217. [PMID: 34727540]
Yeo BSY et al. Association of hearing aids and cochlear implants
with cognitive decline and dementia: a systematic review and
meta-analysis. JAMA Neurol. 2023;80:134. [PMID: 36469314]
B. Noise Trauma
Noise trauma is the second most common cause of sensorineural hearing loss. Sounds exceeding 85 dB for 8 hours
or more are potentially injurious to the cochlea. The loss
typically begins in the high frequencies (especially 4000 Hz)
and, with continuing exposure, progresses to involve the
speech frequencies. Among the more common sources of
injurious noise are industrial machinery, weapons, and
excessively loud music. Monitoring noise levels in the
workplace by regulatory agencies has led to preventive
programs that have reduced the frequency of occupational
losses. Smartwatches have also recently gained capacity to
measure environmental noise levels. Individuals of all ages,
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