Shaun C. Desai, Nsangou Ghogomu, Jeffrey Sharon, and M. Allison Ogden
Cerumen Impaction
GENERAL PRINCIPLES
· Cerumen is composed of desquamated skin and adnexal gland lipid secretions (sebaceous and apocrine sweat glands) in the external auditory canal (EAC). It functions to clean, protect, and lubricate the EAC.
· Risk factors for cerumen accumulation/impaction include age >60 years, cognitive impairment, obstruction of the EAC by hair proliferation or narrowing (e.g., scarring from chronic infection or in Down syndrome), foreign bodies (e.g., hearing aids or earplugs), the use of cotton-tipped swabs, skin conditions that affect the EAC, genetic factors, and impairment of self-migration of cerumen out of the EAC.
· Cerumen impaction may cause hearing loss, otalgia, fullness, itching, tinnitus, and cough, but it is mostly asymptomatic.
DIAGNOSIS
Diagnosis is made by direct visualization during otoscopy of cerumen, which ranges widely in texture (soft and liquid to hard and dry) and color.
TREATMENT
· The bony portion of the EAC can be quite sensitive and is easily abraded or lacerated.
· Home use of cotton swabs, aural jet irrigators, and ear candling is strongly discouraged.1
· Removal of cerumen is recommended when accumulation/impaction causes symptoms or prevents adequate and necessary examination.1
· Cerumen disimpaction may be achieved via irrigation, cerumenolytics, or manual removal other than irrigation.1
· Irrigation
o This consists of flushing cerumen from the ear canal with a large syringe of water, hydrogen peroxide, or 50% solution of white vinegar with the patient sitting up.
o The irrigant should be approximately body temperature and directed toward the superior wall of the EAC (rather than at the tympanic membrane [TM]) until the cerumen is extruded.
o Irrigation is contraindicated when a history of perforation exists, infection is present, or the patient has had a prior ear surgery/mastoidectomy.
o Excessive force induces pain and may result in EAC lacerations or TM perforation, but the latter is a rare complication.
o Irrigation with plain tap water may be associated with otitis externa (OE) in diabetics. Otorrhea and/or otalgia should be reported promptly to the physician.
· Cerumenolytics
o This entails instilling substances into the EAC, resulting in thinning or lubrication of the cerumen and promoting its egress from the EAC.
o There are three types of topical agents used as cerumenolytics.
§ Water based, such as plain water/saline, 3% hydrogen peroxide, 2% acetic acid (Acetasol), docusate 1% liquid (Colace), 10% sodium bicarbonate, and 10% triethanolamine polypeptide oleate condensate (Cerumenex, no longer available in the US due to ototoxicity concerns).
§ Oil based, including olive oil, almond oil, mineral oil, and arachis (peanut) oil.
§ Non–water, non–oil-based product available in the US is 6.5% carbamide peroxide (urea hydrogen peroxide) (Debrox, Murine).
o Cerumenolytics are superior to no treatment for clearing cerumen and avoiding irrigation, but no particular agent has been found to be consistently better than the others or saline.2,3
o The effectiveness of cerumenolytics increases with the number of days they are used.
o All cerumenolytics may also be used prior to irrigation to increase the chance of success.
o Use of cerumenolytics is contraindicated in patients with OE, otitis media (OM), and TM perforation.
· Manual removal other than irrigation
o Manual removal requires clinician skill, adequate illumination, and the proper equipment.
o Typically, a metal or plastic loop or spoon is used with direct visualization through a handheld otoscope.
o Potential harms include pain, laceration of the EAC, perforation of the TM, and infection.
· Referral to an otolaryngologist is appropriate for use of a binocular microscope and otologic instruments when the cerumen is severely impacted or when other attempts have failed.
· Other factors that make referral appropriate include TM perforation, a history of TM or mastoid surgery, radiation to the EAC, EAC stenosis, or pain with other attempts at removal.
Otitis Externa
GENERAL PRINCIPLES
· OE is defined as inflammation of the EAC, which can be acute or chronic, bacterial or fungal, and limited to the EAC or extending to the surrounding skin, the auricle, or the skull base.
· Bacteria account for 98% of acute otitis externa (AOE), and cultures of purulent secretions typically reveal Pseudomonas aeruginosa and Staphylococcus aureus.
· Otomycosis is a superficial infection of the EAC caused by fungi such as Aspergillus niger and Candida albicans. Risk factors include recent antibiotic or steroid ear drops.
· Necrotizing (malignant) OE is a severe complication of AOE seen most commonly in the elderly, diabetics, and the immunocompromised. Infection aggressively spreads to the surrounding tissue including cartilage, temporal bone, and skull base; it can be viewed as an osteomyelitis of the temporal bone. It is most often caused by P. aeruginosa.
DIAGNOSIS
· Symptoms include unilateral itching or pain (which can be severe), hearing loss, and/or fetid drainage.
· Risk factors include water exposure such as swimming (swimmer’s ear), local trauma with a foreign body, excess cleaning/scratching of the EAC, high humidity (tropical ear), warm temperatures, and hearing aid/ear plug use.
· Physical examination of an ear with AOE reveals a normal auricle but tenderness with tragal manipulation. The EAC skin is erythematous and edematous, with the lumen (which can occlude from the edema) containing moist desquamated debris, serum, or seropurulent secretions. In severe cases, the infection can extend beyond the EAC to the surrounding tissue, producing cellulitis of the periauricular skin and perichondritis of the auricle.
· The differential diagnosis of OE is presented in Table 40-1.
· The symptoms of otomycosis are similar to bacterial OE, but there is usually more itching and less pain. Exam shows a swollen and erythematous EAC with white, yellow, or black fluffy, spore-like fungal elements.
· Exam findings of necrotizing OE include pain out of proportion to exam, granulation tissue at the bony-cartilaginous junction, high fever, significant otorrhea, and cranial nerve palsies (most commonly facial nerve). CT, MRI, bone scanning, and erythrocyte sedimentation rate (ESR) can help confirm this diagnosis.
TABLE 40-1 Differential Diagnosis of Otitis Externa
EAC, external auditory canal; OM, otitis media; TM, tympanic membrane.
TREATMENT
· The EAC should be carefully cleaned by flushing out excess cerumen, desquamated skin, purulent material, and any foreign body, thereby allowing topical treatments to reach the affected skin.
· In advanced cases, proper cleansing may require referral to an otolaryngologist for the use of a binocular microscope and otologic instruments.
· There are a large number of topical otic preparations for treatment: acidifying agents, antiseptics, antibiotics, and corticosteroids, individually or in combination. All appear to have similar efficacy, but antibiotics with or without steroids are most commonly used.4,5
· The most common topical otic antibiotics
o Polymyxin B and neomycin (with 1% hydrocortisone, previously sold under the brand name Cortisporin Otic, now generic, dosed tid to qid). With prolonged use, neomycin may actually cause chronic OE secondary to allergic dermatitis.
o Ciprofloxacin 0.2% (with 1% hydrocortisone, Cipro HC Otic, dosed bid) and 0.3% (with 0.1% dexamethasone, Ciprodex Otic, dosed bid).
o Ofloxacin 0.3% (Floxin Otic, dosed bid).
· Initial duration of therapy is 7 to 10 days, but that can be extended if the infection is not resolved. To deliver drops, another person should fill the EAC with drops while the patient lies with the infected ear up, and some gentle tragal manipulation can help the drops disperse throughout the EAC.
· Antibiotics are clearly better than placebo, and no single antibiotic has been clearly shown to be superior to any other. However, those treated with a quinolone may improve somewhat faster than those treated with a nonquinolone.4,5
· The addition of oral antibiotics is usually unnecessary except in patients with diabetes, immunodeficiency, or infection beyond the EAC.
· The addition of topical steroids to topical antibiotics does not seem to substantially improve clinical cure rates, though they may speed pain relief.
· When there is a suspected or known TM rupture, ototoxic agents (alcohol, acidifiers, Cortisporin, and aminoglycosides) should not be used. Ofloxacin and ciprofloxacin/dexamethasone are approved for middle ear use.4
· If the EAC is significantly narrowed because of edema, topical therapy may be difficult to deliver and a wick (Otowick, Merocel, or ribbon gauze) should be placed. The wick should be gently inserted into the EAC to provide a conduit for the antibiotic drops. As the edema recedes, the wick can be removed, usually after 24 to 72 hours.
· Otomycosis treatment is with acidifying drops such as 50% white vinegar solution, aluminum sulfate-calcium acetate (Domeboro), or antifungals solutions (clotrimazole, Lotrimin).
· Necrotizing OE requires hospital admission with otolaryngology consultation, topical and intravenous high-dose antipseudomonal antibiotic therapy, and ear cleaning, and occasionally, surgical debridement is required.
Otitis Media
GENERAL PRINCIPLES
· OM is inflammation of the middle ear.
· Acute otitis media (AOM) is defined by the presence of middle ear effusion with acute symptoms and signs of illness and middle ear inflammation.6 It is an infectious process caused by viruses or bacteria and is far more common in young children than adults, but it does occur in adults.
o The most common viruses are rhinoviruses, influenza viruses, adenoviruses, and respiratory syncytial virus.
o The most common bacteria are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.7
o AOM is generally thought to be preceded by inflammation of the upper respiratory tract (e.g., a viral infection or allergic) resulting in obstruction of the isthmus of the eustachian tube (ET). Fluid accumulates in the middle ear due to negative pressure, with subsequent growth of microorganisms.
· Otitis media with effusion (OME, otherwise known as serous otitis) is a chronic form of middle ear inflammation with a persistent effusion without acute signs of infection.
· The ET, which is responsible for ventilation of the middle ear, is normally closed at rest, but opens during swallowing or autoinsufflation (Valsalva maneuver). Apart from AOM and OME, difficulty opening the ET, termed eustachian tube dysfunction (ETD), can result in long-term negative middle ear pressure, causing thinning and inward collapse (atelectasis) of the TM, hearing impairment, difficulty with pressure changes (flying or scuba diving), and potentially cholesteatoma.8 Causes and risk factors for ETD are presented in Table 40-2.
TABLE 40-2 Causes and Risk Factors for Eustachian Tube Dysfunction
URI, upper respiratory infection; XRT, radiation therapy.
DIAGNOSIS
· The most common symptoms of AOM are abrupt onset of otalgia, hearing loss, and occasionally fever.
· OME typically presents with ear fullness and hearing loss. Symptoms of acute infection like pain are absent.
· Otorrhea may develop if there is a TM perforation, which can be caused by excessive middle ear pressure.
· Otoscopy during AOM will show a bulging, sometimes erythematous, opaque TM with decreased mobility on pneumatic otoscopy. Normal middle ear landmarks, like the incudostapedial joint, will be obscured. Yellow purulent fluid is present behind the TM. Viral infection can display vesicles or bullae on the TM (bullous myringitis).
· Otoscopy during OME will show an opaque TM with decreased mobility, loss of middle ear landmarks, possibly air-fluid level or bubbles, or a TM with a radially injected vascular pattern. A clear effusion in the middle ear can be harder to visualize than a colored effusion (typically amber).
TREATMENT
· Acute otitis media
o There are no evidence-based treatment recommendations specifically for adults with AOM. The recommendations here are based on those for pediatric patients.6
o Observation of otherwise healthy patients with mild-to-moderate uncomplicated AOM for 2 to 3 days is appropriate.6
o Antibiotic therapy may be helpful for those who are initially severely symptomatic or for those with persistent symptoms after 2 to 3 days.
o Amoxicillin 500 mg tid for 5 to 10 days is a reasonable first-line choice for the majority of patients.6
o Alternative first-line antibiotics include trimethoprim-sulfamethoxazole DS, 1 bid; azithromycin, 500 mg qd; or clarithromycin, 500 mg bid.
o When patients fail to respond to first-line treatment or when there are significant concerns regarding resistance, amoxicillin-clavulanate, 875 mg bid, or cefuroxime axetil, 500 mg bid, may be used.
o Tympanocentesis, performed by an otolaryngologist, for culture is rarely necessary but may be helpful in immunocompromised patients, patients whose symptoms fail to respond, or patients in whom complications of AOM, such as intracranial infection, develop.
· Otitis media with effusion
o Because OME is not itself an infectious process, antibiotic therapy is usually not indicated.
o Autoinsufflation (Valsalva maneuver), where air is forced up the ET by exhaling against a closed mouth and pinched nostrils, may be beneficial.9
o Watchful waiting is a reasonable approach in the majority of adults. Referral to an otolaryngologist if persistent effusion after 2 to 3 months is reasonable for examination of the nasopharynx for an anatomic obstruction, like a tumor, and to consider ear tube placement.
o Antihistamines, decongestants, and nasal corticosteroids are of uncertain efficacy with regard to OME.10,11
· The treatment of ETD most often involves treatment of the underlying cause (Table 40-2), including decongestants and antihistamines.8 There is no evidence in humans that systemic steroids are effective; however, topical nasal steroids would be appropriate for ETD thought due to allergic rhinitis. Surgical treatments are possible but uncommonly used.
Tinnitus
GENERAL PRINCIPLES
· Tinnitus is a very common and oftentimes very bothersome complaint and is defined as the perception of sound that is not related to any external source. It can affect one or both ears and can be intermittent or continuous.
· Objective tinnitus refers to sounds arising from within the body that an examiner can also perceive. It is usually secondary to turbulent blood flow through vessels near the ear and is often pulsatile. Rarely, it can be caused by myoclonus of palatal or middle ear muscles, producing a clicking sound.
· Subjective tinnitus, on the other hand, is the perception of sound in the absence of an actual acoustic stimulus (internal or external). Subjective tinnitus is much more common than objective tinnitus.
· Prevalence of tinnitus increases with age. Tinnitus is often associated with hearing loss.
· There are many potential etiologies, some of them quite serious, but the cause is benign in the overwhelming majority of patients (Table 40-3).12
TABLE 40-3 Causes of Tinnitus
AOM, acute otitis media; AVF, arteriovenous fistula; AVM, arteriovenous malformation; ETD, eustachian tube dysfunction; HIV, human immunodeficiency virus; NSAID, nonsteroidal anti-inflammatory drug; OE, otitis externa; OME, otitis media with effusion; TM, tympanic membrane.
Data from Lockwood AH, Salvi RJ, Burkard RF. Tinnitus. N Engl J Med 2002;347:904–10.
DIAGNOSIS
· Tinnitus may be described by patients in many ways including pulsing, humming, rushing, whooshing, clicking, cricket-like ringing, buzzing, hissing, whining, whistling, and high or low pitched.
· Particular attention should be paid to the otologic history including hearing loss, noise exposure, history of ear infections or ear surgery, cerumen impaction, vertigo, focal neurologic deficits, and exposure to ototoxins.
· Some patients with bothersome tinnitus have significant quality of life impairment, including sleep disturbance, impaired concentration, and mood alterations; they may require more aggressive treatment.
· Perform a head and neck exam, including otoscopy, neurologic exam including the cranial nerves, auscultation around the ear and of the carotid artery, and cardiac auscultation. Glomus tumors, which can cause pulsatile tinnitus, can be seen as reddish masses present inferiorly in the middle ear space.
· Audiometry will be indicated for most patients.
· In patients with a straightforward cause for the tinnitus (e.g., symmetric high-frequency hearing loss in a patient with noise exposure), no further workup is required. Referral to an otolaryngologist is appropriate when other abnormalities are seen on audiogram or there is evidence of objective tinnitus not clearly due to carotid stenosis, heart murmur, or a high flow state.
· Imaging of the brain should be undertaken in patients with focal neurologic signs.
TREATMENT
· Objective tinnitus, while much less common, may be amenable to specific therapies, such as surgery, to correct the underlying cause.
· Competing environmental sounds can mask the tinnitus. Common choices for masking include background noise including music, television, or a room fan. This strategy is especially useful for patients with difficulty sleeping.
· Masking devices are sometimes used to provide relief from intractable tinnitus. These are essentially sound generators worn like a hearing aid that produce low-level broadband noise and are available from audiologists. There are limited data on their effectiveness.13
· Drugs that are known to cause tinnitus, such as aspirin, nonsteroidal antiinflammatory drugs (NSAIDs), aminoglycosides, and heterocyclic antidepressants, should be discontinued, if possible. In addition, stimulants like caffeine, nicotine, and decongestants should be avoided.
· Many medications have been studied as treatments for tinnitus, including benzodiazepines, gabapentin, melatonin, and antidepressants.14–16 While none have been clearly shown to be effective in eliminating tinnitus, in some patients, they do provide some benefit. Of those, melatonin has minimal side effects and is a reasonable option for patients with sleep disturbance from tinnitus.
· Tinnitus retraining therapy, which includes counseling and sound therapy several hours a day, may be helpful. The goal is to habituate the patient to the sound and to decrease its negative associations.17
· Cognitive-behavioral therapy may be helpful as well, especially in patients with underlying psychiatric disease.18
Vertigo
GENERAL PRINCIPLES
· Dizziness is a nonspecific term, and further characterization as vertigo, presyncope, or disequilibrium is helpful.
· Characteristics of vertigo help distinguish between central or peripheral causes.
· The most common peripheral causes of vertigo include benign paroxysmal positional vertigo (BPPV), Ménière disease, and vestibular neuritis.
o BPPV is caused by loose particles (otoliths) in the semicircular canals (usually posterior canal).
o Ménière disease is thought to be caused by elevated fluid pressures in the inner ear (endolymphatic hydrops).
o Vestibular neuritis is thought to be caused by inflammation of the vestibular nerve.
DIAGNOSIS
Clinical Presentation
History
· Try to determine whether the dizziness is vertigo (the illusion of movement of self or environment), disequilibrium (general imbalance), or presyncope (patient feeling like he or she is going to pass out).
· If the patient has vertigo, ask about onset, triggers, duration of each episode, frequency of episodes, and associated symptoms (headaches, hearing loss, tinnitus, ear fullness, otalgia, postural instability).
· Look for red flags such as focal neurologic signs that may suggest stroke or brain lesion.
· Table 40-4 lists causes of vertigo, and Table 40-5 lists characteristics of each.19
o BPPV: Sudden, intense vertigo lasting for seconds triggered by laying head back to one side or looking up.20
o Ménière disease: Intermittent vertigo lasting minutes to hours, without a clear trigger, typically associated with unilateral aural fullness, tinnitus, and fluctuating hearing loss.
o Vestibular neuritis: Severe sudden vertigo lasting for days associated with nausea and vomiting. If this is accompanied by sudden hearing loss, it is classified as labyrinthitis.
TABLE 40-4 Causes of Dizziness and Vertigo
TABLE 40-5 Clinical Features of Common Causes of Vertigo
Physical Examination
· The goal of the exam is to determine whether the vertigo is peripheral (inner ear) or central (brain) (Table 40-6). The exam should include a full cranial nerve exam, otoscopy, and careful evaluation of the eyes for nystagmus in the following situations: looking straight ahead, gazing 30 degrees left and right, and while performing the Dix-Hallpike maneuver (Fig. 40-1).20
· In BPPV, rotary nystagmus may be observed with the head turned toward the affected side during the Dix-Hallpike maneuver.
· In Ménière disease, the physical exam is often normal with the exception of possible hearing loss.
· In vestibular neuritis, there is a mostly horizontal nystagmus that beats away from the affected ear.
· Table 40-5 provides additional details along with findings seen with stroke and migraine.19
Figure 40-1 Dix-Hallpike maneuver. (From Furman JM, Cass SP. Benign paroxysmal positional vertigo. N Engl J Med 1999;341:1590–1596, with permission.)
TABLE 40-6 Distinguishing Peripheral and Central Vertigo
aBenign paroxysmal positional vertigo (BPPV), Ménière disease, and migraine-associated vertigo.
bVestibular neuritis, labyrinthitis.
cLabyrinthitis, Ménière disease.
Modified from Goebel JA. Practical Management of the Dizzy Patient, 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008.
Diagnostic Testing
· Audiometry is indicated for patients with auditory symptoms.
· Brain CT scan or MRI may be helpful in workup of central vertigo.
· Vestibular testing is usually not indicated in the workup of peripheral vertigo.
TREATMENT
· Benign paroxysmal positional vertigo: Otolith repositioning with the Epley maneuver is successful in the vast majority of patients (Fig. 40-2).20 Referral to an otolaryngologist for possible surgical intervention (e.g., canal plugging) is indicated for refractory cases.
· Vestibular neuritis: Vestibular suppressants (meclizine, benzodiazepines) and antinausea medications (promethazine) should be used to treat symptoms. Vestibular suppressants should not be used for more than a few days. A short course of high-dose steroids is widely prescribed, though a recent meta-analysis did not support its use.21
· Ménière disease: Acutely, vestibular suppressants and antiemetics are recommended. Chronically, diet modification (avoidance of salt, caffeine, and alcohol), trigger avoidance (nicotine, stress, fatigue, allergy), and diuretics.22Refractory cases may benefit from intratympanic gentamicin, intratympanic steroids, or surgery.
Figure 40-2 Epley maneuver. (From Furman JM, Cass SP. Benign paroxysmal positional vertigo. N Engl J Med 1999;341:1590–1596, with permission.)
Hearing Loss
GENERAL PRINCIPLES
· Conductive hearing loss (CHL) is caused by impaired sound transmission through external and middle ears. Examples include cerumen impaction, middle ear effusion, otosclerosis, and cholesteatoma.
· Sensorineural hearing loss (SNHL) is caused by dysfunction at the level of the inner ear, auditory nerve, or brain. Examples include presbycusis, noise-induced hearing loss, vestibular schwannoma (formerly known as acoustic neuroma), and Ménière disease.
· Sudden sensorineural hearing loss is an emergency that requires immediate treatment.
DIAGNOSIS
Clinical Presentation
· Table 40-7 includes a list of causes of hearing loss.23,24 It is important to note side, age at onset, course of hearing loss (e.g., sudden, progressive, or fluctuating), associated symptoms (tinnitus, vertigo, aural fullness, otalgia, or otorrhea), and history of ear disease.
· Check for risk factors such as meningitis, head trauma, noise exposure, and ototoxic medications (chemotherapy, aminoglycosides).
· Check EAC for obstruction (e.g., cerumen, foreign body, infection, lesions). Look at the tympanic membrane for perforation, scarring, or retraction. Look for middle ear fluid or masses.
· Perform a tuning fork test (512 Hz):
o The Weber test: Place the vibrating tuning fork on the midline forehead between the eyebrows or one of the maxillary incisor teeth. The sound is perceived as louder in the ear with conductive loss or in the better-hearing ear with SNHL.
o The Rinne test: Place the vibrating tuning fork on the mastoid process and then over but not touching the EAC. The sound is louder with the fork on the mastoid with CHL and louder over the EAC when conductive loss is not present.
TABLE 40-7 Causes of Hearing Loss
EAC, external auditory canal.
Diagnostic Testing
· Pure tone audiometry allows for classification as conductive, sensorineural, or mixed. Other aspects of the audiogram provide useful information: speech discrimination suggests abnormalities in cochlear nerve; tympanometry is used to evaluate middle ear status.
· Temporal bone CT and MRI are used in select cases.
· Lab testing is rarely useful but can evaluate syphilis and autoimmune hearing loss.
TREATMENT
· Sudden SNHL: After confirmation by immediate audiogram, typical treatment is prednisone, 1 mg/kg/day up to 60 mg/day × 1 week, and then tapered over 14 days, with repeat audiometry 2 weeks into treatment. Intratympanic steroid injections are also commonly used. Treatment should ideally be started within 48 hours of onset. It is important to note that studies on this point have come to contradictory conclusions.25–27 Urgent ENT consultation is recommended for workup and treatment.
· Ménière disease: Refer to vertigo section for treatment. Hearing loss is addressed with amplification.
· Vestibular schwannoma: Benign cranial nerve VIII tumor that is associated with unilateral SNHL, tinnitus. Treatment includes observation, surgery, or stereotactic radiation.
· Autoimmune inner ear disease: Bilateral, symmetric, rapidly progressive or fluctuating SNHL. Treatment consists of prednisone (1 mg/kg/day to a maximum of 60 mg/day) for 4 weeks, followed by a repeat audiogram. Responders are continued until recovery plateaus and then are decreased to 10 mg/day for 6 months. Nonresponders are tapered off prednisone over 14 days.24
· Presbycusis: Bilateral, symmetric, slowly progressive SNHL associated with aging and noise exposure. Treatment is ear protection in noise, hearing amplification, and cochlear implantation.
· Otosclerosis: Autosomal dominant inherited unilateral or asymmetric CHL or mixed hearing loss is seen in younger adults and more frequently in women. Otosclerosis is due to fixation of the stapes footplate. Treatment is hearing amplification or surgery.
· Cholesteatoma: Keratin cyst of the middle ear and/or mastoid. Recurrent infection and otorrhea is common. The cholesteatoma can erode bony structures of the middle ear, including the ossicles. Treatment is surgical resection with reconstruction of the ossicular chain when indicated.
· Noise-induced hearing loss: Prevention is by hearing protection. Occupational Safety and Health Administration (OSHA) publishes guidelines for maximum noise level and duration of noise exposure.
Epistaxis
GENERAL PRINCIPLES
· The location of epistaxis is anterior and thus easily visible in the front of the nasal cavity >80% of the time. This usually involves an area of the anterior nasal septum known as Kiesselbach plexus, where multiple vessels anastomose.
· In posterior epistaxis, the source of bleeding cannot be seen on anterior rhinoscopy and is more difficult to control.
· Dry nasal mucosa is a factor in many cases of epistaxis and occurs with increased frequency in winter months.
· The location and severity of the bleed will determine the algorithm for management.
DIAGNOSIS
· Refer to Table 40-8 for causes of epistaxis. Relevant history includes triggers (including trauma, manual manipulation), severity, location, duration, and frequency of bleeding.
· Consider predisposing medical conditions (hypertension, liver disease, kidney disease, coagulopathy, thrombocytopenia), medications (anticoagulants, NSAIDs, steroid nasal sprays), intranasal cocaine use, and nasal cannula and nonhumidified continuous positive-airway pressure (CPAP) use.
· Hypertension itself typically is not the immediate cause of epistaxis. On the other hand, patients with significant epistaxis are frequently quite anxious and, therefore, likely to be hypertensive to some degree.
· Symptoms suggestive of underlying malignancy include unilateral nasal obstruction, severe unilateral bleeding, cheek numbness, and visual changes.
· Check for family history of epistaxis.
· Evaluate for risk factors, such as hypertension, and degree of blood loss as evidenced by hypotension and tachycardia. Anterior rhinoscopy involves use of a nasal speculum and headlight to visualize the anterior portion of the nose, mainly the Kiesselbach plexus. This area can also be visualized with an otoscope inside the nasal cavity. Look for predisposing conditions on exam such as deviated septum, septal perforation, and telangiectasias (suggestive of Osler-Weber-Rendu disease). For further evaluation, refer to otolaryngology for nasal fiberoptic endoscopy.
· Laboratory testing is appropriate to assess the severity of blood loss or coagulopathy.
· CT or MRI may be indicated to evaluate for neoplasms.
TABLE 40-8 Causes of Epistaxis
HHT, hereditary hemorrhagic telangiectasia; NSAID, nonsteroidal anti-inflammatory drug; URI, upper respiratory infection.
TREATMENT
· All epistaxis: Begin with fluid resuscitation and stabilization. Patient should lean forward to have blood run out of the nose rather than down the throat. Systemic coagulopathies should be reversed. Hypertension should be controlled, but precipitous drops in blood pressure are not necessary and may be injurious.
· Anterior epistaxis: Start by spraying nasal decongestant spray (oxymetazoline or phenylephrine) followed by pinching nose shut against the nasal septum using index and thumb for 15 continuous minutes. If the bleeding persists, spray again followed by another 15 minutes of continuous pressure. If the bleeding continues to be refractory, the patient may require nasal cauterization (typically with localized silver nitrate), nasal packing, or other maneuvers to control the bleeding. In these circumstances, emergency department evaluation may be warranted.
· Posterior epistaxis: Nasal packing is usually required using commercially available nasal packing. Nasal packing may require hospital admission for pain control and to monitor for persistent bleeding and reflex bradycardia. If packing fails to control the treatment, the patient will require either endoscopic surgery (cautery, arterial ligation) or neurointerventional arterial embolization via transfemoral catheter.
· Posttreatment: Nasal packs are usually kept in place for 3 to 5 days, and patients are given cephalexin (or other anti-Staphylococcus antibiotics) for toxic shock syndrome prophylaxis. All patients must use saline nasal spray and humidifier to decrease risk of recurrence. Nasal decongestant sprays can be used in cases of slight oozing but should not be used for more than 3 consecutive days due to rebound congestion. Finally, patients should avoid nose blowing, nose picking, straining, and anticoagulants, if possible. Predisposing conditions should be managed as indicated.
· Recurrent epistaxis should be referred to an otolaryngologist to rule out underlying pathology and to evaluate for possible surgical intervention.
Hoarseness
GENERAL PRINCIPLES
· Normal voice depends on passive vibration of the vocal cords in the adducted position during exhalation. Hoarseness (dysphonia) is a symptom of abnormal voice due to vocal cord pathology.
· Risk factors for hoarseness include smoking, voice abuse, laryngopharyngeal reflux (LPR), and impaired vocal cord motion.28,29
· See Table 40-9 for list of causes of hoarseness.
TABLE 40-9 Causes of Hoarseness
DIAGNOSIS
· Check for history of vocal overuse, smoking, alcohol use, gastroesophageal reflux, cough, neurologic disorders, neck trauma, postnasal drip, neck or chest surgery (which can cause recurrent laryngeal nerve injury resulting in vocal cord paralysis), and radiation. Worrisome symptoms include progressive disease, stridor, pain, hemoptysis, weight loss, and aspiration.
· This should include a thorough head and neck exam with particular attention paid to cranial nerves, oral cavity, oropharynx, and neck.
· Referral to ENT for transnasal flexible fiberoptic exam or transoral mirror exam to assess for vocal cord pathology is usually necessary for hoarseness that persists beyond 3 weeks. Further evaluations may be warranted, including imaging or biopsy. Stridor is an indication for urgent referral to ENT.
· A video laryngoscopic exam performed by a speech pathologist uses high-resolution video and strobe light to evaluate the mucosal wave of the vocal cords, which is necessary for the normal production of voice.
· If reflux is suspected, pH probe testing can be used to evaluate for LPR, but, most commonly, clinical response to a trial of proton pump inhibitors is used to confirm diagnosis.
TREATMENT
· Acute laryngitis: The most common cause of acute hoarseness, due to viral upper respiratory infection (URI). Typically resolves within 2 weeks. Treatment is hydration, humidification, and voice rest. Antibiotics are rarely indicated in adults.
· Chronic laryngitis: Often due to smoking, reflux, or postnasal drip. Treatment is hydration and elimination of the source of irritation.29
· Vocal cord nodules: Bilateral calluses on the vocal cords due to excessive or harsh voice use. Speech therapy helps the patient eliminate abusive voice patterns. If refractory, surgery can remove the nodules.
· Vocal cord polyps: Due to voice abuse or smoking. Smoking cessation and voice therapy are the mainstay of therapy. If persistent, transoral microsurgery can excise the polyps.
· Laryngeal papilloma: Due to human papillomavirus (HPV) type 6 or 11. Treatment is designed to decrease symptoms by excision of papillomata using a transoral approach. Papillomas frequently recur, and close surveillance is necessary.
· Malignancy: Usually seen in chronic smokers and drinkers. Tracheostomy may be required if the airway is obstructed. Treatment depends on histology, stage, and exact location. Uni- or multimodality treatment including surgery, radiation, and chemotherapy is used.
· Vocal cord paralysis: Paralysis can be unilateral or bilateral and is thought to be due to injury or inflammation of the vagus nerve or its recurrent laryngeal nerve branch, from iatrogenic (neck or chest surgery) injury, trauma, stroke, neoplasm, or idiopathic. In addition to hoarseness, vocal cord paralysis can lead to aspiration, due to inability to protect the airway during swallow or from oral secretions. Surgery to medialize the vocal cord, temporarily or long term, can address both problems. Bilateral vocal cord paralysis can cause airway obstruction and may need to urgently be addressed.
· Vocal cord bowing (presbylarynx): Due to vocalis muscle atrophy, which is more pronounced with advanced age. Patients tend to be soft spoken and have difficulty projecting voice. Speech therapy may be beneficial. In more severe cases, surgery can be considered to augment the vocal cords.
· Spasmodic dysphonia: A focal dystonia affecting either abductors or adductors of the vocal cords resulting in sudden choked-off speech or sudden breathy gaps in speech. Speech therapy is the treatment of choice. Botox may be used in refractory cases.
Sialolithiasis
GENERAL PRINCIPLES
· There are three pairs of major salivary glands: parotid, submandibular, and sublingual. Salivary gland duct stones (sialolithiasis) can result in blockage of the gland’s secretions resulting in subsequent inflammation and, possibly, secondary bacterial infection (acute sialadenitis).30
· The Wharton duct, which drains the submandibular gland into the anterior floor of mouth, is the most common site for sialolithiasis.
· The pathophysiology of stone formation is not well understood, although relative stagnation of saliva in the setting of obstruction is thought to be contributory.
· Risk factors for the development of sialolithiasis include dehydration, medications causing dry mouth (anticholinergics, diuretics), trauma, gout, and smoking. Systemic hypercalcemia is not thought to be related.
DIAGNOSIS
· Although some salivary stones are asymptomatic, patients most often present with pain and swelling of the involved gland. Symptoms usually involve one gland at a time, although multiple stones can be present. Swelling can be episodic or persistent, oftentimes aggravated by eating.
· Physical exam findings will include swelling and tenderness of the involved gland, and purulent saliva may be expressed out of the papilla of the Wharton duct (anterior floor of mouth) or the Stensen duct (buccal mucosa opposite second maxillary molar). A stone may be palpable in the floor of the mouth.
· Long-term obstruction can result in a firm, chronically inflamed gland.
· The differential diagnosis of symptomatic sialolithiasis includes viral sialadenitis (e.g., mumps, HIV, coxsackievirus, influenza, parainfluenza, herpes), bacterial sialadenitis (which can occur in the absence of stones), salivary gland tumors (benign or malignant), Sjögren syndrome, sarcoidosis, malnutrition/alcoholism, or radiation.
· CT scans can usually identify stones but also demonstrate abscess formation or underlying neoplastic process. Ultrasound can also detect up to 90% of stones >2 mm.31 MRI and sialography are rarely indicated for diagnosis of sialolithiasis.32
TREATMENT
· In general, treatment is conservative and includes aggressive hydration, sialogogues (sour candy or lemon wedges), massaging the gland/duct, warm compresses, and eliminating any drugs that cause dry mouth. Most stones smaller than 2 mm will pass without any interventional procedure.
· Bacterial sialadenitis is treated with dicloxacillin or cephalexin for 7 to 10 days. S. aureus is the most common pathogen. When there is surrounding cellulitis or concern for local abscess formation, inpatient admission for IV antibiotics should be considered.
· Persistent, severe, and recurrent symptoms as well as a persistent mass despite antibiotic therapy should prompt referral to an otolaryngologist.
· Interventional procedures are usually avoided in the acute infectious period but may be pursued for persistent or recurrent symptoms. Stones may be amenable to removal with wire basket under fluoroscopic guidance or sialendoscopic visualization or through intraoral approach. Parotidectomy or submandibular gland excision may be required if gland-preserving approaches are not successful.
Neck Mass
GENERAL PRINCIPLES
· The neck can be divided into lateral and central compartments. The lateral compartment is further divided by the sternocleidomastoid muscle into anterior and posterior triangles.
· Age of the patient often is helpful in guiding workup and management. Masses in patients <40 years old are more likely to be benign and congenital in origin. A persistent neck mass in an adult >40 should be considered neoplastic until proven otherwise.
· The most common malignant neck mass in an adult is metastatic squamous cell carcinoma from the upper aerodigestive tract. Risk factors include smoking and drinking history.
DIAGNOSIS
Clinical Presentation
· A thorough history including duration of symptoms, growth pattern, and presence of pain should be obtained. Other important symptoms include unintentional weight loss, dysphagia, hoarseness, otalgia (oropharyngeal and laryngeal tumors often present with referred pain to the ear), or shortness of breath.
· A detailed physical exam is essential in establishing a proper diagnosis. Characteristics of the neck mass including the location, size, shape, mobility, and tenderness all give important clues. Physical exam should also include a very thorough head and neck exam including examining the overlying skin for any lesions, exam of the cranial nerves, palpation of the thyroid gland, otoscopic exam, nasal exam, and a thorough exam of the oral cavity and oropharynx with special attention paid to any asymmetry of the tissues.
· Reactive lymphadenitis (e.g., from a recent URI or skin infection) is usually tender, mobile, and rubbery firm but not distinctly hard.
· Congenital neck masses (e.g., branchial cleft cysts, thyroglossal duct cysts) are usually softer, compressible, mobile, and not tender unless acutely infected. A midline neck mass that elevates with swallowing should raise suspicion of thyroglossal duct cyst.
· Malignant tumors (e.g., metastatic squamous cell carcinoma) are usually nontender and hard and can be fixed to underlying structures. Some tumors, like lymphoma, can grow rapidly.
Diagnostic Testing
· Further workup should be obtained in patients who have a neck mass lasting longer than 3 weeks despite a trial of antibiotic therapy.
· Laboratory testing can be helpful if there has been exposure to tuberculosis, brucellosis, Bartonella, or Toxoplasma. In patients with diffuse adenopathy, consider Epstein-Barr virus (EBV), cytomegalovirus (CMV), HIV, erythrocyte sedimentation rate (ESR), and/or C-reactive protein (CRP) testing.
· Initial imaging of a newly diagnosed neck mass should be CT of the neck with contrast, unless a thyroid mass is suspected, in which case ultrasound is recommended. MRI and PET scans are not indicated for first-line evaluation of a new neck mass.
· Fine-needle aspiration and/or core biopsy is the procedure of choice for obtaining tissue diagnosis, unless imaging suggests a highly vascular lesion. Incisional and excisional biopsies are rarely indicated for initial diagnosis since they can impair surgical treatment of malignant tumors.
TREATMENT
Treatment depends on the underlying cause. Patients with persistent neck mass longer than 3 weeks require referral to an otolaryngologist for further evaluation and treatment.
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