Medley O. Gatewood
OTOLOGIC EMERGENCIES
OTALGIA
Primary otalgia, caused by auricular and periauricular disease, may occur from trauma, infection, foreign body, cerumen impaction, cholesteatoma, and neoplasm.
Referred otalgia may occur with dental disease, oropharyngeal and retropharyngeal processes, nasal cavity pathology, and disorders of the throat and neck.
Ascertaining the cause of otalgia requires careful history and physical examination, with further management and treatment guided by the diagnosis.
TINNITUS
Tinnitus is the perception of sound without external stimuli. It may be constant, pulsatile, high or low pitched, hissing, clicking, or ringing in nature.
Objective tinnitus can be heard by the examiner, whereas the more common subjective tinnitus cannot.
Causes of tinnitus include sensorineural hearing loss, hypertension, conductive hearing loss, head trauma, medications, temporomandibular joint disorders, depression, acoustic neuromas, multiple sclerosis, benign intracranial hypertension, Ménière’s disease, Cogan’s syndrome, arteriovenous malformations, arterial bruits, enlarged eustachian tube, palato-myoclonus, and stapedial muscle spasm.
Common medications resulting in tinnitus include aspirin, nonsteroidal anti-inflammatory drugs, aminoglycosides, loop diuretics, and chemotherapeutics.
Pharmacologic treatment with antidepressant medications may alleviate tinnitus in which no correctable cause can be found.
SUDDEN HEARING LOSS
Causes of sudden hearing loss are varied and may be idiopathic (most common), infectious (mumps, Epstein-Barr virus, herpes, cytomegalovirus (CMV), syphilis, and labyrinthitis), vascular/hematologic (leukemia, sickle-cell disease, polycythemia, Berger’s disease, and cerebral aneurysm), metabolic (diabetes, hyperlipidemia), rheumatologic (temporal arteritis, Wegener’s granulomatosis), conductive causes (otitis externa, otitis media [OM], ruptured tympanic membrane [TM], neoplasm, and osteonecrosis), Ménière’s disease, Cogan’s syndrome, acoustic neuroma, coch-lear rupture, and ototoxic medications.
Indictors of poor prognosis include severe hearing loss on presentation and the presence of vertigo.
If the cause is not readily determined by history and physical examination, otolaryngologic consultation is necessary.
OTITIS EXTERNA
PATHOPHYSIOLOGY
The most common organisms implicated in otitis externa are Pseudomonas aeruginosa, Enterobacteriaceae, and Proteus species, and Staphylococcus aureus, with P. aeruginosa being the most common organism causing malignant otitis externa.
Otomycosis (fungal otitis externa) is found in tropical climates and the immunocompromised or subsequent to long-term antibiotic therapy.
Aspergillus and Candida are the most common fungal pathogens.
Risk factors for the development of otitis externa include swimming, trauma of the external canal, and any process that elevates the pH of the canal.
CLINICAL FEATURES
Otitis externa is characterized by pruritus, pain, and tenderness of the external ear.
Erythema and edema of the external auditory canal (EAC), otorrhea, crusting, and hearing impairment may also be present.
Pain is elicited with movement of the pinna or tragus.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
The treatment of otitis externa includes analgesics, cleaning the EAC, acidifying agents, topical antimicrobials, and occasionally topical steroid preparations.
Ofloxacin otic five drops twice daily, acetic acid/hydrocortisone otic five drops 3 times daily (do not use with perforated TM), and ciprofloxacin/hydrocor-tisone otic three drops twice daily are commonly used for 7 days to treat otitis externa.
If significant swelling of the external canal is present, a wick or piece of gauze may be inserted into the canal to allow passage of topical medications.
MALIGNANT OTITIS EXTERNA
Malignant otitis externa is a potentially life-threatening infection of the EAC with variable extension to the skull base.
In greater than 90% of cases, it is caused by P. aeruginosa.
Elderly, diabetic, and immunocompromised patients are most commonly affected.
Diagnosis of malignant otitis externa requires a high index of suspicion.
Computed tomography (CT) is necessary to determine the extent and stage of the disease.
Emergent otolaryngologic (ENT) consultation, tobramycin 2 milligrams/kg IV and piperacillin 3 to 4 grams IV, or ceftriaxone 1 gram IV, or ciprofloxacin 400 milligrams IV, and admission to the hospital are mandatory.
OTITIS MEDIA
EPIDEMIOLOGY
Although adults may present with OM, its incidence and prevalence peak in the preschool years and then decrease with increasing age.
PATHOPHYSIOLOGY
The most common bacterial pathogens in acute OM are Streptococcus pneumoniae, Haemophilus influen-zae, and Moraxella catarrhalis.
The predominant organisms involved in chronic OM are S. aureus, P. aeruginosa, and anaerobic bacteria.
CLINICAL FEATURES
Patients with OM present with otalgia, with or without fever; occasionally, hearing loss and otorrhea are present.
The TM may be retracted or bulging and will have impaired mobility on pneumatic otoscopy.
The TM may appear red as a result of inflammation or may be yellow or white due to middle ear secretions.
Complications of OM include TM perforation, conductive hearing loss, acute serous labyrinthitis, facial nerve paralysis, acute mastoiditis, lateral sinus thrombosis, cholesteatoma, and intracranial complications (meningitis, brain abscess, extradural abscess, and subdural empyema).
EMERGENCY DEPARTMENT CARE AND DISPOSITION
A 10-day course of amoxicillin 250 to 500 milligrams PO 3 times daily for 7 to 10 days is the preferred initial treatment for OM. Alternative agents include azithromycin 500 milligrams PO daily for 1 day and then 250 milligrams PO daily for 4 days, or cefuro-xime 500 milligrams PO twice daily for 10 days.
Cefuroxime or amoxicillin/clavulanate may be given for OM unresponsive to first-line therapy after 72 hours.
Antibiotic coverage should be extended to 3 weeks for patients with OM with effusion.
TM perforation and conductive hearing loss are most often self-limiting and often require no specific intervention.
ACUTE MASTOIDITIS
Acute mastoiditis occurs as infection spreads from the middle ear to the mastoid air cells.
Patients present with otalgia, fever, and postauricular erythema, swelling, and tenderness.
Protrusion of the auricle with obliteration of the pos-tauricular crease may be present.
CT will delineate the extent of bony involvement.
Emergent ENT consultation, vancomycin 1 to 2 grams IV or ceftriaxone 1 gram IV, and admission to the hospital are necessary. Surgical drainage ultimately may be required.
LATERAL SINUS THROMBOSIS
This condition arises from extension of infection and inflammation into the lateral and sigmoid sinuses.
Headache is common, and papilledema, sixth nerve palsy, and vertigo may be present.
Diagnosis may be made with CT, although magnetic resonance imaging or angiography may be necessary.
Therapy consists of emergent ENT consultation, combination therapy with nafcillin 2 grams IV, ceftriaxone 1 gram IV, and metronidazole 500 milligrams IV, and hospital admission.
BULLOUS MYRINGITIS
Bullous myringitis is a painful condition of the ear characterized by bulla on the TM and deep EAC.
Numerous pathogens have been implicated including viruses, Mycoplasma pneumoniae, and Chlamydia psittaci.
The diagnosis is made by clinical examination.
The treatment consists of pain control and warm compresses. Antibiotics can be given for concomitant OM.
TRAUMA TO THE EAR
A hematoma can develop from any type of trauma to the ear.
Improper treatment of ear hematomas can result in stimulation of the perichondrium and development of asymmetric cartilage formation. The resultant deformed auricle has been termed cauliflower ear.
Immediate incision and drainage of the hematoma with a compressive dressing is necessary to prevent reaccumulation of the hematoma.
Thermal injury to the auricle may be caused by excessive heat or cold.
Superficial injury of either type is treated with cleaning, topical non-sulfa-containing antibiotic ointment, and a light dressing.
Frostbite is treated with rapid rewarming by using saline-soaked gauze at 38°C to 40°C.
The rewarming process may be very painful and analgesics will be necessary.
Any second- or third-degree burn requires immediate ENT or burn center consultation.
FOREIGN BODIES IN THE EAR
Signs of infection or TM perforation should be sought on examination.
Live insects should be immobilized with 2 % lidocaine solution distilled into the ear canal before removal.
Foreign bodies may be removed with forceps and direct visualization or with the aid of a hooked probe or suction catheter.
Irrigation is often useful for small objects; however, organic material may absorb water and swell.
ENT consultation is required for cases of foreign body with TM perforation or if the object cannot be safely removed.
TYMPANIC MEMBRANE PERFORATION
TM perforations can result from middle ear infections, barotrauma, blunt/penetrating/acoustic trauma, or (rarely) lightning strikes.
Acute pain and hearing loss are usually noted, with or without bloody otorrhea. Vertigo and tinnitus, when present, are usually transient.
As most TM perforations heal spontaneously, antibiotics are not necessary unless there is persistent foreign material in the canal or middle ear.
NASAL EMERGENCIES AND SINUSITIS
EPISTAXIS
Epistaxis is classified as anterior or posterior.
Posterior epistaxis is suggested if an anterior source is not visualized, if bleeding occurs from both nares, or if blood is seen draining into the posterior pharynx after anterior sources have been controlled.
Have patients blow their nose to dislodge any clots. Instill 0.05% oxymetazoline two sprays/nostril or 0.25% phenylephrine two sprays/nostril. Apply direct external pressure for 15 minutes while leaning forward in the “sniffing” position. Repeat if necessary.
If this approach fails, and an anterior source of bleeding is visualized, proceed to chemical cautery with silver nitrate after hemostasis is achieved with cotton swabs or pledgets soaked in a 1:1 mixture of a 4% lidocaine and 0.05% oxymetazoline inserted into the nasal cavity. If no source is identified, proceed to packing.
Anterior nasal packing may be performed with dehydrated nasal sponges, anterior epistaxis balloons (Fig. 153-1), thrombogenic foams and gels, or gauze. If packing or local cautery fails to control anterior bleeding, ENT consultation is necessary.
Posterior epistaxis may be treated with a dehydrated posterior sponge pack or an inflatable balloon posterior tamponade device. All patients with posterior packs require ENT consultation for hospital admission.
All patients with nasal packs should be started on antibiotic prophylaxis with amoxicillin/clavulanate 500/125 milligrams PO three times daily to prevent toxic shock syndrome.
Treatment of elevated blood pressure during an acute episode of epistaxis is generally not advised except in consultation with an otolaryngologist for cases of persistent epistaxis not uncontrolled by the above measures.
FIG. 153-1. Anterior and posterior packing. Overinflation of the posterior balloon can result in pressure necrosis.
NASAL FRACTURES
Nasal fractures are the most common facial fracture.
Nasal fracture is a clinical diagnosis suggested by the injury mechanism, swelling, tenderness, crepitance, gross deformity, and periorbital ecchymosis.
Radiographic diagnosis usually is not necessary in the ED; ultrasound is an alternative to plain radiography (Fig. 153-2).
Intermittent ice application, analgesics, and over-the-counter decongestants are the normal treatment.
ENT follow-up within 6 to 10 days for reexamination and possible fracture reduction is prudent.
The nose should be examined for a septal hematoma. If left untreated, a septal hematoma may result in abscess formation or necrosis of the nasal septum.
The treatment of septal hematoma is local incision and drainage with subsequent placement of an anterior nasal pack.
A fracture of the cribriform plate may violate the subarachnoid space and cause cerebrospinal fluid rhinorrhea. Symptoms may be delayed for several weeks.
If a cribriform plate injury is suspected, CT and immediate neurosurgical consultation should be obtained.
FIG. 153-2. US still image of nasal fracture demonstrating cortical disruption. A large gap is seen between bone fragments. (Reproduced with permission from Ma OJ, Mateer JR, Blaivas M: Emergency Ultrasound, 2nd ed. © 2008, McGraw-Hill, New York.)
NASAL FOREIGN BODIES
Nasal foreign bodies should be suspected in patients with unilateral nasal obstruction, foul rhinorrhea, or persistent unilateral epistaxis.
After topical vasoconstriction with 0.05% oxymeta-zoline and possibly local anesthesia with 4% nebulized lidocaine, the foreign body should be removed under direct visualization.
Tools for removal include forceps, suction catheters, hooked probes, and balloon-tipped catheters. ENT consultation is required for any unsuccessful removal.
SINUSITIS AND RHINOSINUSITIS
EPIDEMIOLOGY
Rhinosinusitis affects one in seven adults in the United States, resulting in approximately 31 million patients being diagnosed annually.
The primary cause is viral illness; bacterial infections account for only 2% to 10% of acute rhinosinusitis cases.
PATHOPHYSIOLOGY
Sinusitis is inflammation of the mucosal lining of the paranasal sinuses (maxillary, frontal, ethmoid, and frontal).
Rhinosinusitis is sinusitis also involving the nasal cavity, almost always involves rhinitis, and is extremely common. It can be classified as acute, subacute, or chronic.
CLINICAL FEATURES
Symptoms include nasal congestion or blockage, facial pain or pressure, hyposmia, nasal discharge, tooth pain, fever, and sinus pressure with head/body movement.
There may be pain and tenderness with sinus percussion, mucosal swelling, facial swelling, and redness.
DIAGNOSIS AND DIFFERENTIAL
The diagnosis of uncomplicated acute rhinosinusitis is clinical, and imaging is not necessary in nontoxic, uncomplicated rhinosinusitis patients.
In 2012 the Infectious Disease Society of America recommend using the following criteria to diagnose bacterial sinusitis: bacterial rather than viral rhinosinusitis should be diagnosed when any of the following three criteria are met: (1) persistent symptoms lasting at least 10 days, without improvement; (2) severe symptoms or high fever and purulent nasal discharge or facial pain for 3 to 4 days at illness onset; or (3) acutely worsening symptoms after 5 to 6 days of a previously improving upper respiratory infection.
CT scans are helpful in evaluating toxic patients and possible intracranial extension. Patients with chronic rhinosinusitis or recurrent acute rhinosinusitis warrant bacterial cultures and a sinus CT, preferably as an outpatient.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Treatment for acute uncomplicated disease is generally supportive.
Nasal irrigation with or without nasal decongestants (0.05% oxymetazoline two sprays/nostril twice daily or 0.25% phenylephrine two sprays/nostril four times daily) is first-line therapy. Decongestants’ use is to be limited to ≤3 days.
Empirical antibiotic therapy should be started as soon as acute bacterial rhinosinusitis is diagnosed clinically; amoxicillin-clavulanate orally, 22.5 milligrams/kg/dose up to 850 milligrams, twice daily, is recommended for both children and adults. Amoxicillin alone, macrolides, and trimethoprim-sulfamethoxazole are not recommended.
Doxycycline (2.2 milligrams/kg/dose up to 100 milligrams, twice daily) is an alternative. Levofloxacin and gatifloxacin are alternatives.
Complications include meningitis, cavernous sinus thrombosis, intracranial abscess and empyema, orbital cellulitis, and osteomyelitis. Patients with these deeper complications usually appear systemi-cally ill or have focal neurologic findings.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 237, “Common Disorders of the External, Middle, and Inner Ear,” by Mark Silverberg and Michael Lucchesi, and Chapter 239, “Epistaxis, Nasal Fractures, and Rhinosinusitis,” by Shane M Summers and Ta reg Bey.