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especially those with existing hearing losses, should wear
earplugs when exposed to moderately loud noises and specially designed earmuffs when exposed to explosive noises.
Chen XM et al. The role of genetic variants in the susceptibility
of noise-induced hearing loss. Front Cell Neurosci.
2022;16:946206. [PMID: 35903368]
Fischer T et al. Are smartwatches a suitable tool to monitor noise
exposure for public health awareness and otoprotection?
Front Neurol. 2022;13:856219. [PMID: 35432148]
Le Prell CG et al. Noise-induced hearing loss and its prevention:
current issues in mammalian hearing. Curr Opin Physiol.
2020;18:32. [PMID: 32984667]
C. Physical Trauma
Concussive head trauma has effects on the inner ear similar to those of severe acoustic trauma. Some degree of
sensory hearing loss may occur following concussion and
is frequent after lateral skull base fracture.
Bartholomew RA … Kozin ED et al. Labyrinthine concussion:
historic otopathologic antecedents of a challenging diagnosis.
Laryngoscope Investig Otolaryngol. 2020;5:267. [PMID:
32337358]
D. Ototoxicity
Ototoxic substances may affect both the auditory and vestibular systems. The most commonly used ototoxic medications are aminoglycosides; loop diuretics; and several
antineoplastic agents, notably cisplatin. These medications
may cause irreversible hearing loss even when administered
in therapeutic doses. When using these medications, it is
important to identify high-risk patients, such as those with
preexisting hearing losses or kidney disease. Patients
simultaneously receiving multiple ototoxic agents are at
particular risk owing to ototoxic synergy. Useful measures
to reduce the risk of ototoxic injury include serial audiometry, monitoring of serum peak and trough levels, and
substitution of equivalent nonototoxic medications whenever possible.
It is possible for topical agents that enter the middle ear
to be absorbed into the inner ear via the round window.
When the tympanic membrane is perforated, use of potentially ototoxic ear drops (eg, neomycin, gentamicin) is best
avoided.
Correa-Morales JE et al. Prevention and treatment of cisplatin-
induced ototoxicity in adults: a systematic review. Clin
Otolaryngol. 2024;49:1. [PMID: 37818931]
Dillard LK et al. Global burden of ototoxic hearing loss associ-
ated with platinum-based cancer treatment: a systematic
review and meta-analysis. Cancer Epidemiol. 2022;79:102203.
[PMID: 35724557]
Tan WJT et al. Molecular characteristics of cisplatin-induced
ototoxicity and therapeutic interventions. Int J Mol Sci.
2023;24:16545. [PMID: 38003734]
E. Idiopathic Sudden Sensory Hearing Loss
Idiopathic sudden loss of hearing in one ear may occur at
any age, but typically it occurs in persons over age 20 years.
In the setting a normal otologic physical examination,
symptoms may include hearing loss, aural fullness, tinnitus, and dizziness. The cause is unknown; however, idiopathic sudden hearing loss may result from a viral infection
or a sudden vascular occlusion of the internal auditory
artery. Obtaining an MRI is essential after the diagnosis to
rule out retrocochlear pathology (eg, tumors); however,
this should not delay treatment. Prompt treatment with
corticosteroids has been shown to improve the odds of
recovery. Intratympanic administration of corticosteroids
alone or in association with oral corticosteroids has been
associated with an equal or more favorable prognosis.
Because treatment appears to be most effective as close to
the onset of the loss as possible, and appears not to be effective after 6 weeks, a prompt audiogram should be obtained
in all patients who present with sudden hearing loss without
obvious middle ear pathology. Prognosis is mixed, with
many patients living with permanent deafness in the
involved ear, while others have complete recovery.
Chaushu H et al. Spontaneous recovery rate of idiopathic sudden
sensorineural hearing loss: a systematic review and metaanalysis. Clin Otolaryngol. 2023;48:395. [PMID: 36640119]
Chrysouli K et al. The effectiveness of intratympanic steroid
injection in addition to systemic corticosteroids in the treatment of idiopathic sudden sensorineural hearing loss. Am J
Otolaryngol. 2023;44:103872. [PMID: 37060782]
Yoon CY et al. Epidemiology of idiopathic sudden sensorineural
hearing loss in the era of big data. Eur Arch Otorhinolaryngol. 2023;280:2181. [PMID: 36239782]
F. Autoimmune Hearing Loss
Sensorineural hearing loss that occurs in both ears simultaneously may be associated with a wide array of systemic
autoimmune disorders, such as SLE, granulomatosis with
polyangiitis, and Cogan syndrome (hearing loss, keratitis,
aortitis). The loss is most often progressive. The hearing
level often fluctuates, with periods of deterioration alternating with partial or even complete remission. Usually, there
is the gradual evolution of permanent hearing loss, which
often stabilizes with some remaining auditory function but
occasionally proceeds to complete deafness. Vestibular dysfunction, particularly dysequilibrium and postural instability, may accompany the auditory symptoms.
In many cases, the autoimmune pattern of audiovestibular dysfunction presents in the absence of recognized
systemic autoimmune disease. Responsiveness to oral corticosteroid treatment is helpful in making the diagnosis
and constitutes first-line therapy. If stabilization of hearing
becomes dependent on long-term corticosteroid use, steroid-sparing immunosuppressive regimens may become
necessary.
Balouch B et al. Use of biologics for treatment of autoimmune
inner ear disease. Am J Otolaryngol. 2022;43:103576. [PMID:
35963108]
Gordis TM et al. Disease-modifying antirheumatic drugs in the
treatment of autoimmune inner ear disease: a systematic
review and meta-analysis of auditory and vestibular out-
comes. Otol Neurotol. 2023;44:2. [PMID: 36509432]
Yuen E et al. Hearing loss in patients with systemic lupus erythe-
matosus: a systematic review and meta-analysis. Lupus.
2021;30:937. [PMID: 33645314]

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2. Tinnitus
ESSENTIALS OF DIAGNOSIS
»
Phantom noise or sounds.
»
Persistent tinnitus often, although not always,
indicates the presence of hearing loss.
»
Intermittent periods of mild, high-pitched tinnitus
lasting seconds to minutes are common in normal-hearing persons.
» General Considerations
Tinnitus is defined as the sensation of sound in the absence
of an exogenous sound source. Tinnitus can accompany
any form of hearing loss, and its presence provides no diagnostic value in determining the cause of a hearing loss.
Approximately 15% of the general population experiences
some type of tinnitus, with prevalence beyond 20% in
aging populations.
» Clinical Findings
A. Symptoms and Signs
Though tinnitus is commonly associated with hearing loss,
tinnitus severity correlates poorly with the degree of hearing loss. About one in seven tinnitus sufferers experiences
severe annoyance, and 4% are severely disabled. When
severe and persistent, tinnitus may interfere with sleep and
ability to concentrate, resulting in considerable psychological distress.
Pulsatile tinnitus—often described by the patient as
listening to one’s own heartbeat—should be distinguished from tonal tinnitus. Although often ascribed to
conductive hearing loss, pulsatile tinnitus may be far
more serious and may indicate a vascular abnormality,
such as glomus tumor, venous sinus stenosis, carotid
vaso-occlusive disease, arteriovenous malformation, or
aneurysm.
A staccato “clicking” tinnitus may result from middle
ear muscle spasm (middle ear myoclonus) or sometimes
palatal myoclonus. The patient typically perceives a rapid
series of popping noises, lasting seconds to a few minutes,
accompanied by a fluttering feeling in the ear. Specialized
forms of tympanometry may formally diagnose this condition, and it is typically treated surgically.
B. Diagnostic Testing
For routine, nonpulsatile tinnitus, audiometry should be
ordered to rule out an associated hearing loss. For unilateral tinnitus, particularly associated with hearing loss in
the absence of an obvious causative factor (ie, noise
trauma), an MRI should be obtained to rule out a retrocochlear lesion, such as vestibular schwannoma. MRA and
MRV and temporal bone CT should be considered for
patients who have pulsatile tinnitus to exclude a causative
vascular lesion or sigmoid sinus abnormality.
» Treatment
The most important treatment of tinnitus is avoidance of exposure to excessive noise, ototoxic agents, and other factors that
may cause cochlear damage. Masking the tinnitus with music
or through amplification of normal sounds with a hearing
aid may also bring some relief. In addition to masking techniques, habituation techniques, such as tinnitus retraining
therapy and cognitive behavioral therapy, may prove beneficial in those with refractory symptoms. Among patients who
have emotional distress due to tinnitus, numerous antidepressant and antipsychotic medications have been tried.
Unfortunately, these medications do not treat the tinnitus
directly but may allow the patient to cope with it better.
Conlon B et al. Different bimodal neuromodulation settings
reduce tinnitus symptoms in a large randomized trial. Sci
Rep. 2022;12:10845. [PMID: 35773272]
Perrotta MV et al. Bimodal stimulation for the reduction of tin-
nitus using vibration on the skin. Int Tinnitus J. 2023;27:1.
[PMID: 38050877]
3. Hyperacusis
Excessive sensitivity to sound may occur following hearing
loss, such as that due to noise trauma, in patients susceptible to migraines, or for psychological reasons. Patients
with cochlear dysfunction commonly experience “recruitment,” an abnormal sensitivity to loud sounds despite a
reduced sensitivity to softer ones. Fitting hearing aids and
other amplification devices to patients with recruitment
requires use of compression circuitry to avoid uncomfortable overamplification.
Kim EH et al. Exploring the origins of decreased sound tolerance
in tinnitus patients. Front Neurol. 2023;14:1273705. [PMID:
38020634]
Pienkowski M. Loud music and leisure noise is a common cause
of chronic hearing loss, tinnitus and hyperacusis. Int J Environ Res Public Health. 2021;18:4236. [PMID: 33923580]
Ren J et al. Prevalence of hyperacusis in the general and special
populations: a scoping review. Front Neurol. 2021;12:706555.
[PMID: 34539554]
4. Vertigo
ESSENTIALS OF DIAGNOSIS
»
Either a sensation of motion when there is no
motion or an exaggerated sense of motion in
response to movement.
»
Duration of vertigo episodes with associated hearing loss or other neurologic issues are the keys to
diagnosis.
»
Evaluation includes audiogram, electronystagmography (ENG) or videonystagmography (VNG),
and head MRI.

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» General Considerations
Vertigo can be caused by either a peripheral or central etiology, or both (Table 8–2).
» Clinical Findings
A. Symptoms and Signs
Vertigo is the cardinal symptom of vestibular disease. Vertigo is typically experienced as a distinct “spinning”
Table 8–2. Causes of vertigo (listed in alphabetical
order, within categories).
Peripheral causes
Benign paroxysmal positioning vertigo
Ethanol intoxication
Inner ear barotraumas
Ménière disease
Semicircular canal dehiscence
Vestibular neuritis/labyrinthitis
Central causes
Cerebellar ataxia syndromes
Chiari malformation
Multiple sclerosis
Seizure
Wernicke encephalopathy
Mixed central and peripheral causes
Cerebellopontine angle tumors
Vestibular schwannoma
Meningioma
Endocrinopathies
Hypothyroidism
Pendred syndrome
Hyperviscosity syndromes
Waldenström macroglobulinemia
Infections
Lyme disease
Syphilis
Migraine
Stroke and vascular insufficiency
Anterior inferior cerebellar artery stroke
Posterior inferior cerebellar artery stroke
Vasculitides
Behçet disease
Cogan syndrome
Granulomatosis with polyangiitis
Susac syndrome
Vertebral artery insufficiency
Vascular compression
Table 8–3. Common vestibular disorders: differential
diagnosis based on classic presentations.
Duration of
Typical
Vertiginous
Episodes
Seconds Perilymphatic
Hours Ménière disease,
Days Labyrinthitis,
Auditory
Symptoms
Present
fistula
syphilis
autoimmune inner
ear disease,
cerebellopontine
angle tumor,
ototoxicity
Auditory Symptoms
Absent
Benign paroxysmal
positioning vertigo
(cupulolithiasis),
vertebrobasilar
insufficiency,
migraine-associated
vertigo
Migraine-associated
vertigo
Vestibular neuronitis,
migraine-associated
vertigo, multiple
sclerosis, cerebellar
degeneration
sensation or a sense of tumbling or of falling forward or
backward. It should be distinguished from imbalance,
light-headedness, and syncope, all of which are nonvestibular in origin (Table 8–3).
1. Peripheral vestibular disease—Peripheral vestibulopathy may cause vertigo of sudden onset, may be so severe
that the patient is unable to walk or stand, and is frequently
accompanied by nausea and vomiting. Tinnitus and hearing loss may be associated and provide strong support for a
peripheral (ie, otologic) origin.
Critical elements of the history include the duration of
the discrete vertiginous episodes (seconds, minutes to
hours, or days), and associated symptoms (hearing loss).
Triggers should be sought, including diet (eg, increased salt
intake in the case of Ménière disease), stress, fatigue, and
bright lights (eg, migraine-associated dizziness).
The physical examination of the patient with vertigo
includes evaluation of the ears, observation of eye motion
and nystagmus in response to head turning, cranial nerve
examination, and Romberg testing. In acute peripheral
lesions, nystagmus is usually horizontal with a rotatory
component; the fast phase usually beats away from the
diseased side. Visual fixation tends to inhibit nystagmus
except in very acute peripheral lesions or with CNS disease.
In benign paroxysmal positioning vertigo, Dix-Hallpike
testing (quickly lowering the patient to the supine position
with the head extending over the edge and placed 30 degrees
lower than the body, turned either to the left or right) will
elicit a delayed-onset (~10 seconds) fatigable nystagmus.
Nonfatigable nystagmus in this position indicates CNS
disease.
Since visual fixation often suppresses observed nystagmus, many of these maneuvers are performed with Frenzel
goggles, which prevent visual fixation, and often bring out
subtle forms of nystagmus. The Fukuda test can

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demonstrate vestibular asymmetry when the patient steps
in place with eyes closed and consistently rotates in one
direction.
2. Central disease—Vertigo arising from CNS disease
(Table 8–2) tends to develop gradually and then becomes
progressively more severe and debilitating. Nystagmus is
not always present but can occur in any direction, may be
dissociated in the two eyes, and is often non fatigable, vertical rather than horizontal in orientation, without latency,
and unsuppressed by visual fixation. ENG is useful in
documenting these characteristics. Evaluation of audiovestibular dysfunction requires MRI of the brain.
Episodic vertigo can occur in patients with diplopia
from external ophthalmoplegia and is maximal when the
patient looks in the direction where the separation of
images is greatest. Cerebral lesions involving the temporal
cortex may also produce vertigo; it is sometimes the initial
symptom of a seizure. Finally, vertigo may be a feature of a
number of systemic disorders and can occur as a side effect
of certain anticonvulsant, antibiotic, hypnotic, analgesic,
and tranquilizer medications or of alcohol.
Arshad Q et al. What visuospatial perception has taught us about
the pathophysiology of vestibular migraine. Curr Opin
Neurol. 2024;37:32. [PMID: 38018799]
Chari DA et al. Telemedicine algorithm for the management of
dizzy patients. Otolaryngol Head Neck Surg. 2020;163:857.
[PMID: 32600170]
Tarnutzer AA et al. What’s in a name? Chronic vestibular
migraine or persistent postural perceptual dizziness? Brain
Sci. 2023;13:1692. [PMID: 3813714]
B. Vestibular Testing
Vestibular investigations, such as audiologic evaluation,
caloric stimulation, electro- or videonystagmography
(ENG or VNG), vestibular-evoked myogenic potentials
(VEMPs), and MRI, are indicated in patients with persistent vertigo or when CNS disease is suspected. These studies help distinguish between central and peripheral lesions
and identify causes requiring specific therapy. ENG consists of objective recording of the nystagmus induced by
head and body movements, gaze, and caloric stimulation.
It is helpful in quantifying the degree of vestibular
hypofunction.
Grove CR et al. Vestibular perceptual testing from lab to clinic: a
review. Front Neurol. 2023;14:1265889. [PMID: 37859653]
Pastras CJ et al. Vestibular testing- New physiological results for
the optimization of clinical VEMP stimuli. Audiol Res.
2023;13:910. [PMID: 37987337]
» Vertigo Syndromes Due to
Peripheral Lesions
A. Ménière Disease
The cause of Ménière disease is unknown. The classic syndrome consists of episodic vertigo, with discrete vertigo
spells lasting 20 minutes to several hours in association
with fluctuating, often low-frequency, sensorineural hearing loss, tinnitus (usually low-tone and “blowing” in
quality), and a sensation of unilateral aural pressure
(Table 8–3). These symptoms in presence of headaches or
migraines may suggest migraine-associated dizziness. Primary treatment is aimed at decreasing dizzy episodes.
There are no treatments for reduction in hearing loss.
Treatment of Ménière disease typically involves preventive
measures, including low-salt diet and daily diuretics (eg,
acetazolamide). For symptomatic relief of acute vertigo
attacks, lorazepam (0.5–1 mg) or diazepam (2–5 mg) can
be used. Nausea may be treated with oral meclizine
(25 mg). In refractory cases, patients may undergo intratympanic corticosteroid or gentamicin injections, endolymphatic sac decompression, or surgical or vestibular
nerve section. There are increasing reports of imaging,
such as CT or MRI, for evaluation of Ménière disease.
Bächinger D et al. Radiological feature heterogeneity supports
etiological diversity among patient groups in Meniere’s disease.
Sci Rep. 2023;13:10303. [PMID: 37365255]
B. Labyrinthitis
Patients with labyrinthitis suffer from acute onset of continuous, usually severe vertigo lasting several days, accompanied by hearing loss and tinnitus. During a recovery
period that lasts for several weeks, the vertigo gradually
improves. Hearing may return to normal or remain permanently impaired in the involved ear. The cause of labyrinthitis is unknown. Treatment consists of antibiotics, if the
patient is febrile or has symptoms of a bacterial infection,
oral corticosteroids, and supportive care. Vestibular suppressants are useful during the acute phase of the attack
(eg, diazepam) but should be discontinued as soon as feasible to avoid long-term dysequilibrium from inadequate
compensation.
Cohen HS et al. Relationship between clinical measures of
hearing and clinical measures of vestibular function. Am J
Otolaryngol. 2024;45:104052. [PMID: 37801744]
Schoo DP et al. New frontiers in managing the dizzy patient.
Otolaryngol Clin North Am. 2021;54:1069. [PMID: 34294438]
C. Benign Paroxysmal Positioning Vertigo
Patients living with recurrent spells of vertigo, lasting a few
(10–15) seconds per spell, associated with changes in head
position (often provoked by rolling over in bed), usually
have benign paroxysmal positioning vertigo (BPPV). The
term “positioning vertigo” is more accurate than “positional vertigo” because it is provoked by changes in head
position rather than by the maintenance of a particular
posture.
The typical symptoms of BPPV occur in clusters that
persist for several days. There is a brief (10–15 seconds)
latency period following a head movement before symptoms
develop, and the acute vertigo subsides within 10–60 seconds,
although the patient may remain imbalanced for several
hours. Dizziness that lasts for more than a few seconds
(that is several minutes or hours) is not BPPV. Constant
repetition of the positional change leads to habituation.
Since some CNS disorders can mimic BPPV (eg, vertebrobasilar insufficiency), recurrent cases warrant head MRI/MRA.

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In central lesions, there is no latent period, fatigability, or
habituation of the symptoms and signs. Treatment of BPPV
involves physical therapy protocols (eg, the Epley maneuver
or Brandt-Daroff exercises), based on the theory that it
results from cupulolithiasis (free-floating statoconia, also
known as otoconia) within a semicircular canal.
Gurberg J et al. Benign paroxysmal vertigo of childhood. Handb
Clin Neurol. 2023;198:229. [PMID: 38043965]
Saishoji Y et al. Epley manoeuvre’s efficacy for benign paroxys-
mal positional vertigo (BPPV) in primary-care and subspecialty settings: a systematic review and meta-analysis. BMC
Prim Care. 2023;24:262. [PMID: 38042776]
D. Vestibular Neuronitis
In vestibular neuronitis, a paroxysmal, usually single attack
of vertigo occurs without accompanying impairment of
auditory function and will persist for several days before
gradually abating. During the acute phase, examination
reveals nystagmus and absent responses to caloric stimulation on one or both sides. The cause of the disorder is
unclear though presumed to be viral. Treatment consists of
supportive care; vestibular suppressants, such as diazepam
2–5 mg every 6–12 hours during the acute phases of the
vertigo only; oral corticosteroids may potentially be used;
and antiemetics, such as ondansetron and meclizine, followed by vestibular therapy if the patient does not completely compensate.
Farhat R et al. The “Vestibular Eye Sign”- “VES”: a new radio-
logical sign of vestibular neuronitis can help to determine the
affected vestibule and support the diagnosis. J Neurol.
2023;270:4360. [PMID: 37219605]
Lee JY et al. Clinical characteristics of acute vestibular neuritis
according to involvement site. Otol Neurotol. 2020;41:143.
[PMID: 31789808]
E. Traumatic Vertigo
Labyrinthine concussion is the most common cause of
vertigo following head injury. Symptoms generally diminish within several days but may linger for a month or more.
Basilar skull fractures that traverse the inner ear usually
result in severe vertigo lasting several days to a week and
deafness in the involved ear. Chronic posttraumatic vertigo
may result from cupulolithiasis. This occurs when traumatically detached statoconia (otoconia) settle on the
ampulla of the posterior semicircular canal and cause an
excessive degree of cupular deflection in response to head
motion. Clinically, this presents as episodic positioning
vertigo. Treatment consists of supportive care and vestibular suppressant medication (diazepam) during the acute
phase of the attack and vestibular therapy.
Aljabri A et al. The efficacy of vestibular rehabilitation therapy
for mild traumatic brain injury: a systematic review and
meta-analysis. J Head Trauma Rehabil. 2024;39:E59. [PMID:
37335202]
Schlemmer E et al. Vestibular rehabilitation effectiveness for
adults with mild traumatic brain injury/concussion: a
mini-systematic review. Am J Audiol. 2022;31:228. [PMID:
35077655]
F. Perilymphatic Fistula
Leakage of perilymphatic fluid from the inner ear into the
tympanic cavity via the round or oval window is a very rare
cause of vertigo and sensory hearing loss. Most cases result
from physical injury (eg, blunt head trauma, hand slap to
ear); extreme barotrauma during airflight, scuba diving,
etc; or vigorous Valsalva maneuvers (eg, during weight lifting). Treatment may require middle ear exploration and
window sealing with a tissue graft.
Sarna B et al. Perilymphatic fistula: a review of classification,
etiology, diagnosis, and treatment. Front Neurol. 2020;11:1046.
[PMID: 33041986]
Sasaki A et al. Prevalence of perilymphatic fistula in patients
with sudden-onset sensorineural hearing loss as diagnosed by
Cochlin-tomoprotein (CTP) biomarker detection: its association with age, hearing severity, and treatment outcomes. Eur
Arch Otorhinolaryngol. 2024;281:2373. [PMID: 38123733]
G. Cervicogenic Vertigo
Position receptors located in the facets of the cervical spine
are important physiologically in the coordination of head
and eye movements. Cervical proprioceptive dysfunction
is a common cause of vertigo triggered by neck movements. This disturbance often commences after neck
injury, particularly hyperextension; it is also associated
with degenerative cervical spine disease. Although symptoms vary, vertigo may be triggered by assuming a particular head position as opposed to moving to a new head
position (the latter typical of labyrinthine dysfunction).
Cervical vertigo may often be confused with migraineassociated vertigo, which is also associated with head
movement. Management consists of neck movement
exercises to the extent permitted by orthopedic
considerations.
Han E et al. Predictive model for diagnosing central lesions in
emergency department patients with isolated dizziness who
undergo diffusion-weighted magnetic resonance imaging.
Acad Emerg Med. 2022;29:15. [PMID: 34414635]
Piromchai P et al. The efficacy of self-exercise in a patient with
cervicogenic dizziness: a randomized controlled trial. Front
Neurol. 2023;14:1121101. [PMID: 36864911]
Seemungal BM et al. The Bárány Society position on ‘Cervical
Dizziness’. J Vestib Res. 2022;32:487. [PMID: 36404562]
H. Migrainous Vertigo
Episodic vertigo is frequently associated with migraine
headache. Head trauma may also be a precipitating feature.
The vertigo may be temporally related to the headache and
last up to several hours, or it may also occur in the absence
of any headache. Migrainous vertigo may resemble Ménière
disease but without associated hearing loss or tinnitus.
Accompanying symptoms may include head pressure;
visual, motion, or auditory sensitivity; and photosensitivity.
Symptoms typically worsen with lack of sleep and anxiety
or stress. Food triggers include caffeine, chocolate, and
alcohol, among others. There is often a history of motion
intolerance (easily carsick as a child). Migrainous vertigo

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may be familial. Treatment includes dietary and lifestyle
changes (improved sleep pattern, avoidance of stress) and
antimigraine prophylactic medication.
Chu H et al. Prophylactic treatments for vestibular migraine: a
systematic review and network meta-analysis of randomized
clinical trials. Front Pharmacol. 2023;14:1332973. [PMID:
38186654]
Mallampalli MP et al. Care gaps and recommendations in ves-
tibular migraine: an expert panel summit. Front Neurol.
2022;12:812678. [PMID: 35046886]
I. Superior Semicircular Canal Dehiscence
Deficiency in the bony covering of the superior semicircular canal may be associated with vertigo triggered by loud
noise exposure, straining, and an apparent conductive
hearing loss. Autophony is also a common feature. Diagnosis is with coronal HRCT scan and VEMP testing. Surgically resurfacing or plugging the dehiscent canal can
improve symptoms.
Eberhard KE et al. Current trends, controversies, and future
directions in the evaluation and management of superior
canal dehiscence syndrome. Front Neurol. 2021;12:638574.
[PMID: 33889125]
Eberhard KE et al. Transmastoid surgery for superior canal
dehiscence: prospective longitudinal objective and patientreported audiovestibular outcomes. Otol Neurotol. 2024;45:
184. [PMID: 38206067]
» Vertigo Syndromes Due to Central Lesions
CNS causes of vertigo include brainstem vascular disease,
arteriovenous malformations, tumors of the brainstem and
cerebellum, multiple sclerosis, and vertebrobasilar migraine
(Table 8–2). Vertigo of central origin often becomes unremitting and disabling. The associated nystagmus is often
nonfatigable, vertical rather than horizontal in orientation,
without latency, and unsuppressed by visual fixation. ENG
is useful in documenting these characteristics. There are
commonly other signs of brainstem dysfunction (eg, cranial nerve palsies; motor, sensory, or cerebellar deficits in
the limbs) or of increased intracranial pressure. Auditory
function is generally spared. The underlying cause should
be treated.
Bassett A et al. Exploring vestibular assessment in patients with
headache and dizziness. Otolaryngol Clin North Am.
2022;55:549. [PMID: 35490043]
Chari DA et al. The efficient dizziness history and exam. Otolar-
yngol Clin North Am. 2021;54:863. [PMID: 34294439]
Dieterich M et al. Central vestibular networking for sensorimo-
tor control, cognition, and emotion. Curr Opin Neurol.
2024;37:74. [PMID: 38032266]
DISEASES OF THE CENTRAL AUDITORY &
VESTIBULAR SYSTEMS
Lesions of the eighth cranial nerve and central audiovestibular pathways may produce hearing loss and dizziness
(Table 8–3). One characteristic of neural hearing loss is
deterioration of speech discrimination out of proportion to
the decrease in pure-tone thresholds. Another is auditory
adaptation, wherein a steady tone appears to the listener to
decay and eventually disappear. Auditory evoked responses
are useful in distinguishing cochlear from neural losses
and may give insight into the site of lesion within the central pathways.
The evaluation of central audiovestibular disorders usually requires imaging of the internal auditory canal, cerebellopontine angle, and brain with enhanced MRI.
1. Vestibular Schwannoma (Acoustic Neuroma)
Eighth cranial nerve schwannomas are among the most
common intracranial tumors. Most are unilateral, but
about 5% are associated with the hereditary syndrome
neurofibromatosis type 2, in which bilateral eighth nerve
tumors may be accompanied by meningiomas and other
intracranial and spinal tumors. These benign lesions arise
within the internal auditory canal and gradually grow to
involve the cerebellopontine angle, eventually compressing
the pons and resulting in hydrocephalus. Their typical
auditory symptoms are unilateral hearing loss with a
deterioration of speech discrimination exceeding that predicted by the degree of pure-tone loss. Nonclassic presentations, such as sudden unilateral hearing loss, are fairly
common. Any individual with a unilateral or asymmetric
sensorineural hearing loss should be evaluated for an intracranial mass lesion. Vestibular dysfunction more often
takes the form of continuous dysequilibrium than episodic
vertigo. Diagnosis is made by enhanced MRI. Treatment
consists of observation, microsurgical excision, or stereotactic radiotherapy, depending on such factors as patient
age, underlying health, and size of the tumor.
Barrett TF et al. Single-cell multi-omic analysis of the vestibular
schwannoma ecosystem uncovers a nerve injury-like state.
Nat Commun. 2024;15:478. [PMID: 38216553]
Gambacciani C et al. Surgical management of skull base menin-
giomas and vestibular schwannomas. Curr Opin Oncol.
2022;34:713. [PMID: 36093884]
Kalogeridi MA et al. Stereotactic radiosurgery and radiotherapy
for acoustic neuromas. Neurosurg Rev. 2020;43:941. [PMID:
30982152]
2. Vascular Compromise
Vertebrobasilar insufficiency is a common cause of vertigo
in the older adults. It is often triggered by changes in posture or extension of the neck. Reduced flow in the vertebrobasilar system may be demonstrated noninvasively
through MRA. Empiric treatment is with vasodilators and
aspirin.
Clark M et al. A review of carotid and vertebral artery dissection.
Br J Hosp Med (Lond). 2022;83:1. [PMID: 35506728]
3. Multiple Sclerosis
Patients with multiple sclerosis may suffer from episodic
vertigo and chronic imbalance. Hearing loss in this disease
is most commonly unilateral and of rapid onset. Spontaneous recovery may occur.

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Kattah JC et al. Eye movements in demyelinating, autoimmune
and metabolic disorders. Curr Opin Neurol. 2020;33:111.
[PMID: 31770124]
OTOLOGIC MANIFESTATIONS OF AIDS
AIDS may result in many otologic signs and symptoms.
The pinna and external auditory canal may be affected by
Kaposi sarcoma and by persistent and potentially invasive
fungal infections (particularly Aspergillus fumigatus).
Serous otitis media due to eustachian tube dysfunction
may arise from adenoidal hypertrophy (HIV lymphadenopathy), recurrent mucosal viral infections, or an
obstructing nasopharyngeal tumor (eg, lymphoma).
Unfortunately, ventilating tubes are seldom helpful and
may trigger profuse watery otorrhea. Acute otitis media is
usually caused by typical bacterial organisms, including
Proteus, Staphylococcus, and Pseudomonas, and rarely, by
Pneumocystis jirovecii. Sensorineural hearing loss is com-
mon and, in some cases, results from viral CNS infection.
In cases of progressive hearing loss, cryptococcal meningitis and syphilis must be excluded. Acute facial paralysis due
to herpes zoster infection (Ramsay Hunt syndrome)
occurs commonly and follows a clinical course similar to
that in nonimmunocompromised patients. Treatment is
with high-dose acyclovir (see Chapter 34). Corticosteroids
may also be effective as an adjunct.
Dawood G et al. Nature and extent of hearing loss in HIV-
infected children: a scoping review. Int J Pediatr Otorhinolaryngol. 2020;134:110036. [PMID: 32335463]
º
DISEASES OF THE NOSE &
PARANASAL SINUSES
INFECTIONS OF THE NOSE &
PARANASAL SINUSES
Rhinosinusitis may be classified by duration of symptoms.
Rhinosinusitis is called acute rhinosinusitis if less than 4 weeks’
duration or as chronic rhinosinusitis if lasting more than
12 weeks, with or without acute exacerbations. Acute rhinosinusitis may also be classified by presumed etiology, such as
viral rhinosinusitis or acute bacterial rhinosinusitis.
1. Viral Rhinosinusitis (Common Cold)
» Clinical Findings
Due to the numerous serologic types of rhinoviruses, adenoviruses, and other viruses, patients remain susceptible to
the common cold throughout life. These infections, while
generally quite benign and self-limited, have been implicated in the development or exacerbation of more serious
conditions, such as acute bacterial sinusitis and acute otitis
media, asthma, cystic fibrosis, and bronchitis. Nasal congestion, decreased sense of smell, rhinorrhea, and sneezing
accompanied by general malaise, throat discomfort and,
occasionally, headache, are typical in viral infections. Nasal
examination usually shows erythematous, edematous
mucosa and a watery discharge. The presence of purulent
nasal discharge suggests bacterial rhinosinusitis.
Najafloo R et al. Mechanism of anosmia caused by symptoms of
COVID-19 and emerging treatments. ACS Chem Neurosci.
2021;12:3795. [PMID: 34609841]
Vance H et al. Addressing post-COVID symptoms: a guide for
primary care physicians. J Am Board Fam Med. 2021;34:1229.
[PMID: 34772779]
» Treatment
The main treatment for viral rhinitis is supportive care,
including rest, hydration, and use of over-the-counter analgesics and decongestants. There are no effective antiviral
therapies for either the prevention or treatment of most
viral rhinitis despite a common misperception among
patients that antibiotics are helpful. Buffered hypertonic
saline (3–5%) nasal irrigation has been shown to improve
symptoms and reduce the need for NSAIDs. Other supportive measures, such as oral decongestants (pseudoephedrine,
30–60 mg every 4–6 hours or 120 mg twice daily), may
provide some relief of rhinorrhea and nasal obstruction.
Nasal sprays, such as oxymetazoline or phenylephrine,
are rapidly effective but should not be used for more than a
few days to prevent rebound congestion. Withdrawal of the
medication after prolonged use leads to rhinitis medica-
mentosa, an almost addictive need for continuous usage.
Treatment of rhinitis medicamentosa requires mandatory
cessation of the sprays, and this is often extremely frustrating for patients. Topical intranasal corticosteroids (eg, flunisolide, 2 sprays in each nostril twice daily), intranasal
anticholinergic (ipratropium 0.06% nasal spray, 2–3 sprays
every 8 hours as needed), or a short tapering course of oral
prednisone may help during the withdrawal process.
ESSENTIALS OF DIAGNOSIS
»
Associated malaise, headache, and cough.
»
Nasal congestion, facial pressure, rhinorrhea, and
hyposmia.
»
Erythematous, engorged nasal mucosa without
intranasal purulence.
»
Symptoms are self-limited, lasting typically less
than 10 days.
» Complications
Other than mild eustachian tube dysfunction or transient
middle ear effusion, complications of viral rhinitis are
unusual. Secondary acute bacterial rhinosinusitis is a wellaccepted complication of acute viral rhinitis and is suggested by persistence of symptoms beyond 10 days with
purulent green or yellow nasal secretions and unilateral
facial or dental pain.
Dhama K et al. Coronavirus disease 2019-COVID-19. Clin
Microbiol Rev. 2020;33:e00028. [PMID: 32580969]

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CHAPTER 8
2. Bacterial Rhinosinusitis
ESSENTIALS OF DIAGNOSIS
»
Acute onset of symptoms.
»
Purulent yellow-green nasal discharge or
expectoration.
»
Facial pain or pressure over the affected sinus or
sinuses.
»
Nasal obstruction.
»
Associated cough, malaise, fever, and headache.
» General Considerations
Compared with viral rhinitis, acute bacterial rhinosinusitis
infections are uncommon, but they still affect nearly
20 million Americans annually and account for over
2 billion dollars in health care expenditures. Acute bacterial rhinosinusitis is believed to be the result of impaired
mucociliary clearance, inflammation of the nasal cavity
mucosa, and obstruction of the ostiomeatal complex.
Edematous mucosa causes obstruction of the complex,
resulting in the accumulation of mucus in the sinus cavity
that becomes secondarily infected by bacteria. The largest of
these ostiomeatal complexes is deep to the middle turbinate in the middle meatus. This complex is actually a confluence of complexes draining the maxillary, ethmoid, and
frontal sinuses. The sphenoid drains from a separate complex between the septum and superior turbinate.
The typical pathogens of bacterial rhinosinusitis are
S pneumoniae, other streptococci, H influenzae, and less
commonly, S aureus and Moraxella catarrhalis. Pathogens
vary regionally in both prevalence and drug resistance;
about 25% of healthy asymptomatic individuals may, if
sinus aspirates are cultured, harbor such bacteria as well.
» Clinical Findings
A. Symptoms and Signs
There are no agreed-upon criteria for the diagnosis of
acute bacterial rhinosinusitis in adults. Major symptoms
include purulent nasal drainage, nasal obstruction or congestion, facial pain/pressure, altered smell, cough, and
fever. Minor symptoms include headache, otalgia, halitosis, dental pain, and fatigue. Many of the more specific
symptoms and signs relate to the affected sinus(es). Bacterial rhinosinusitis can be distinguished from viral rhinitis
by persistence of symptoms for more than 10 days after
onset or worsening of symptoms within 10 days after initial improvement. Acute rhinosinusitis is defined as lasting less than 4 weeks and subacute rhinosinusitis, as
lasting 4–12 weeks.
Acute maxillary sinusitis is the most common form of
acute bacterial rhinosinusitis because the maxillary is the
largest sinus with a single drainage pathway that is easily
obstructed. Unilateral facial fullness, pressure, and tenderness over the cheek are common symptoms, but may not
always be present. Pain may refer to the upper incisor and
canine teeth via branches of the trigeminal nerve, which
traverse the floor of the sinus. Purulent nasal drainage
should be noted with nasal airway obstruction or facial
pain (pressure). Maxillary sinusitis may result from dental
infection, and teeth that are tender should be carefully
examined for signs of abscess. Drainage of the periapical
abscess or removal of the diseased tooth typically resolves
the sinus infection.
Acute ethmoiditis in adults is often accompanied by
maxillary sinusitis, and symptoms are similar to those
described above. Localized ethmoid sinusitis may present
with pain and pressure over the high lateral wall of the nose
between the eyes that may radiate to the orbit.
Sphenoid sinusitis is usually seen in the setting of pansinusitis or infection of all the paranasal sinuses on at least
one side. The patient may describe a headache “in the
middle of the head” and often point to the vertex.
Acute frontal sinusitis may cause pain and tenderness
of the forehead. This is most easily elicited by palpation of
the orbital roof just below the medial end of the eyebrow.
Hospital-associated sinusitis is a form of acute bacterial rhinosinusitis that may present without the usual
symptoms. Instead, it may be a cause of fever in critically ill
patients. It is often associated with prolonged presence of a
nasogastric or, rarely, nasotracheal tube causing nasal
mucosal inflammation and ostiomeatal complex obstruction. Pansinusitis on the side of the tube is common on
imaging studies.
B. Imaging
The diagnosis of acute bacterial rhinosinusitis can usually
be made on clinical grounds alone. Although more sensitive
than clinical examination, routine radiographs are not costeffective and are not recommended by the Agency for Health
Care Policy and Research or American Association of
Otolaryngology Guidelines. Consensus guidelines recom-
mend imaging when clinical criteria are difficult to evaluate, when the patient does not respond to appropriate
therapy or has been treated repeatedly with antibiotics,
when intracranial involvement or CSF rhinorrhea is
suspected, when complicated dental infection is suspected,
or when symptoms of more serious infection are noted.
When necessary, noncontrast screening coronal CT
scans are more cost-effective and provide more information than conventional sinus films. CT provides a rapid and
effective means to assess all of the paranasal sinuses, identify areas of greater concern (such as bony dehiscence,
periosteal elevation, or maxillary tooth root exposure
within the sinus), and direct appropriate therapy.
CT scans are reasonably sensitive but are not specific.
Swollen soft tissue and fluid may be difficult to distinguish
when opacification of the sinus is due to other conditions,
such as chronic rhinosinusitis, nasal polyposis, or mucus
retention cysts. Sinus abnormalities can be seen in most
patients with an upper respiratory infection, while bacterial
rhinosinusitis develops in only 2%.
If malignancy, intracranial extension, or opportunistic
infection is suspected, MRI with gadolinium should be
ordered instead of, or in addition to, CT. MRI will distinguish

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tumor from fluid, inflammation, and inspissated mucus far
better than CT, and will better delineate tumor extent (eg,
involvement of adjacent structures, such as the orbit, skull
base, and palate). Bone destruction can be demonstrated as
well by MRI as by CT.
» Treatment
All patients with acute bacterial rhinosinusitis should
have careful evaluation of pain. For symptom reduction
in viral rhinitis and bacterial rhinosinusitis without complication, the European Position Paper on Rhinosinusitis
and Nasal Polyps (EPOS) 2012 recommends NSAIDs,
saline nasal sprays, and nasal decongestants (pseudoephedrine, 30–60 mg every 6 hours, up to 240 mg/day;
nasal oxymetazoline, 0.05% or oxymetazoline, 0.05–0.1%,
one or two sprays in each nostril every 6–8 hours for up
to 3 days). In cases of suspected bacterial rhinosinusitis,
intranasal corticosteroids (eg, high-dose mometasone
furoate 200 mcg each nostril twice daily for 21 days) have
demonstrated efficacy in reducing nasal symptoms and
are recommended. Other medications, such as mucolytics,
vitamin C, probiotics, and antihistamines, have not
demonstrated efficacy in the management of acute
rhinosinusitis.
Antibiotic therapy should be reserved for complicated or
protracted acute bacterial rhinosinusitis. Between 40% and
69% of patients with acute bacterial rhinosinusitis improve
symptomatically within 2 weeks without antibiotic therapy. Antibiotic treatment is controversial in uncomplicated cases of clinically diagnosed acute bacterial
rhinosinusitis because only 5% of patients will note a
shorter duration of illness with treatment, and antibiotic
treatment is associated with nearly twice the number of
adverse events compared with placebo. Antibiotics may be
considered when symptoms last more than 10 days or
when symptoms (including fever, facial pain, and swelling
of the face) are severe or when cases are complicated (such
as immunodeficiency). In these patients, administration
of antibiotics does reduce the incidence of clinical failure
by 50% and represents the most cost-effective treatment
strategy.
Selection of antibiotics is usually empiric and based on
a number of factors, including regional patterns of antibiotic resistance, antibiotic allergy, cost, and patient tolerance. For adults younger than 65 years with mild to
moderate acute bacterial rhinosinusitis, the recommended first-line therapy is amoxicillin-clavulanate
(500 mg/125 mg orally three times daily or 875 mg/125 mg
orally twice daily for 5–7 days), or in those with severe
sinusitis, high-dose amoxicillin-clavulanate (2000 mg/125 mg
extended-release orally twice daily for 7–10 days). In
patients with a high risk for penicillin-resistant S pneu-
moniae (age over 65 years, hospitalization in the prior
5 days, antibiotic use in the prior month, immunocompromised status, multiple comorbidities, or severe sinus
infection), the recommended first-line therapy is the
high-dose amoxicillin-clavulanate option (2000 mg/125 mg
extended-release orally twice daily for 7–10 days). For
those with penicillin allergy or hepatic impairment, doxycycline (100 mg orally twice daily or 200 mg orally once
daily for 5–7 days) or clindamycin (150–300 mg every
6 hours) plus a cephalosporin (cefixime 400 mg orally once
daily or cefpodoxime proxetil 200 mg orally twice daily) for
10 days are options. Macrolides, trimethoprimsulfamethoxazole, and second- or third-generation cephalosporins are not recommended for empiric therapy.
Dupilumab, a monoclonal antibody with inhibition of IL-4
and IL-13, is approved for patients with chronic sinusitis
with nasal polyposis.
Hospital-associated infections in critically ill patients
are treated differently from community-acquired infections. Removal of a nasogastric tube and improved nasal
hygiene (nasal saline sprays, humidification of supplemental nasal oxygen, and nasal decongestants) are critical
interventions and often curative in mild cases without
aggressive antibiotic use. Endoscopic or transantral cultures may help direct medical therapy in complicated cases.
In addition, broad-spectrum antibiotic coverage directed at
P aeruginosa, S aureus (including methicillin-resistant
strains), and anaerobes may be required.
» Complications
Local complications of acute bacterial rhinosinusitis
include orbital cellulitis and abscess, osteomyelitis, cavernous sinus thrombosis, and intracranial extension.
Orbital complications typically occur by extension of
ethmoid sinusitis through the lamina papyracea, a thin
layer of bone that comprises the medial orbital wall. Any
change in the ocular examination necessitates immediate
CT imaging. Extension in this area may cause orbital cel-
lulitis leading to proptosis, gaze restriction, and orbital
pain. Select cases are responsive to intravenous antibiotics,
with or without corticosteroids, and should be managed in
close conjunction with an ophthalmologist or otolaryngologist, or both. Extension through the lamina papyracea
can also lead to subperiosteal abscess formation (orbital
abscess). Such abscesses cause marked proptosis, ophthalmoplegia, and pain with medial gaze. While some cases
respond to antibiotics, such findings should prompt an
immediate referral to a specialist for consideration of
decompression and evacuation. Failure to intervene
quickly may lead to permanent visual impairment and a
“frozen globe.”
Osteomyelitis requires prolonged antibiotics as well as
removal of necrotic bone. The frontal sinus is most commonly affected, with bone involvement suggested by a
tender swelling of the forehead (Pott puffy tumor). Following treatment, secondary cosmetic reconstructive procedures may be necessary.
Though rare, intracranial complications of sinusitis can
occur either through hematogenous spread, as in cavernous sinus thrombosis and meningitis, or by direct extension, as in epidural and intraparenchymal brain abscesses.
Cavernous sinus thrombosis is heralded by ophthalmoplegia, chemosis, and visual loss; the diagnosis is most
commonly confirmed by MRI. When identified early, cavernous sinus thrombosis typically responds to intravenous
antibiotics. Frontal epidural and intracranial abscesses are
often clinically silent, but may present with altered mental
status, persistent fever, or severe headache.

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CHAPTER 8
» When to Refer
Failure of acute bacterial rhinosinusitis to resolve after an
adequate course of oral antibiotics necessitates referral to
an otolaryngologist for evaluation. Endoscopic cultures
may direct further treatment choices. Nasal endoscopy and
CT scan are indicated when symptoms persist longer than
4–12 weeks. Any patients with suspected extension of disease outside the sinuses should be evaluated urgently by an
otolaryngologist and imaging should be obtained.
» When to Admit
• Facial swelling and erythema indicative of facial
cellulitis.
• Proptosis.
• Vision change or gaze abnormality indicative of orbital
cellulitis.
• Abscess or cavernous sinus involvement.
• Mental status changes suggestive of intracranial
extension.
• Failure to respond to appropriate first-line treatment or
symptoms persisting longer than 4 weeks.
Hoy SM. Dupilumab: a review in chronic rhinosinusitis with
nasal polyps. Drugs. 2020;80:711. [PMID: 32240527]
Papacharalampous GX et al. Chronic rhinosinusitis with nasal
polyps (CRSwNP) treated with omalizumab, dupilumab, or
mepolizumab: a systematic review of the current knowledge
towards an attempt to compare agents’ efficacy. Int Forum
Allergy Rhinol. 2024;14:96. [PMID: 37394893]
Poto R et al. Imaging of chronic rhinosinusitis with nasal polyps
in the era of biological therapies. Curr Opin Allergy Clin
Immunol. 2024 Jan 11. [Epub ahead of print] [PMID:
38205820]
3. Nasal Vestibulitis & S aureus
Nasal Colonization
Inflammation of the nasal vestibule may result from folliculitis of the hairs that line this orifice and is usually the
result of nasal manipulation or hair trimming. Systemic
antibiotics effective against S aureus (such as dicloxacillin,
250 mg orally four times daily for 7–10 days) are indicated.
Topical mupirocin 2% nasal ointment (applied two or three
times daily) also may be a helpful addition and may prevent future occurrences. If recurrent, the addition of
rifampin (10 mg/kg orally twice daily for the last 4 days of
dicloxacillin treatment) may eliminate the S aureus carrier
state. If a furuncle exists, it should be incised and drained,
preferably intranasally. Adequate treatment of these infections is important to prevent retrograde spread of infection
through valveless veins into the cavernous sinus and intracranial structures.
S aureus is the leading nosocomial pathogen, and nasal
carriage is a well-defined risk factor in the development
and spread of nosocomial infections. Nasal and extranasal
methicillin-resistant S aureus (MRSA) colonizations are
associated with a 30% risk of developing an invasive MRSA
infection during hospital stays. While the vast majority
have no vestibulitis symptoms, screening by nasal swabs
and PCR-based assays has demonstrated a 30% rate of S
aureus colonization in hospital patients and an 11% rate of
MRSA colonization in ICU patients. Elimination of the
carrier state is challenging, but studies of mupirocin 2%
nasal ointment application with chlorhexidine facial washing (40 mg/mL) twice daily for 5 days have demonstrated
decolonization in 39% of patients.
Ontario Health (Quality). Pre-surgical nasal decolonization of
Staphylococcus aureus: a health technology assessment. Ont
Health Technol Assess Ser. 2022;22:1. [PMID: 36160757]
4. Invasive Fungal Sinusitis
Invasive fungal sinusitis is rare and includes both rhinocerebral mucormycosis (Mucor, Absidia, and Rhizopus
spp.) and other invasive fungal infections, such as Aspergillus. The fungus spreads rapidly through vascular channels
and may be lethal if not detected early. Patients with
mucormycosis almost invariably have some degree of
immunocompromise, such as diabetes mellitus, long-term
corticosteroid therapy, neutropenia associated with chemotherapy for hematologic malignancy, or end-stage renal
disease. Occasional cases of sinonasal infection with Asper-
gillus spp. have been reported in patients with untreated
HIV/AIDS. The initial symptoms may be similar to those
of acute bacterial rhinosinusitis, although facial pain is
often more severe. Nasal drainage is typically clear or
straw-colored, rather than purulent, and visual symptoms
may be noted at presentation in the absence of significant
nasal findings. On examination, the classic finding of
mucormycosis is a black eschar on the middle turbinate,
but this finding is not universal and may not be apparent if
the infection is deep or high within the nasal bones. Often
the mucosa appears normal or simply pale and dry. This
may be noted on the hard palate as well. Early diagnosis
requires suspicion of the disease and nasal biopsy with silver stains, revealing broad nonseptate hyphae within tissues and necrosis with vascular occlusion. Imaging, such as
CT or MRI, may initially show only soft tissue changes.
Consequently, biopsy and ultimate debridement should be
based on the clinical setting rather than radiographic demonstration of bony destruction or intracranial changes.
Invasive fungal sinusitis represents a medical and
surgical emergency. Once recognized, voriconazole may
be started by intravenous infusion, and prompt wide surgical debridement is indicated for patients with reversible
immune deficiency (eg, poorly controlled hyperglycemia
in diabetes). Other antifungals, including amphotericin or
the less nephrotoxic lipid-based amphotericin B (Ambisome) and caspofungin, are alternatives to voriconazole
and may be added to voriconazole depending on the fungus. Surgical management, while necessary for any possibility of cure, often results in tremendous disfigurement
and functional deficits (eg, often resulting in the loss of at
least one eye). Even with early diagnosis and immediate
appropriate intervention, the prognosis is guarded. In persons with diabetes, the mortality rate is about 20%. If kidney disease is present or develops, mortality is over 50%;
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