Chapter 151. Ear, Nose, and Sinus Emergencies

Otitis Externa

Otitis externa, or “swimmer's ear,” is characterized by pruritus, pain, and tenderness of the external ear. Erythema and edema of the external auditory canal, otorrhea, crusting, and hearing impairment may also be present. Pain is elicited with movement of the pinna or tragus. Risk factors for development of otitis externa include swimming, trauma of the external canal, and any process that elevates the pH of the canal.

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, or fungal otitis externa, is found in tropical climates and in the immunocompromised or subsequent to long-term antibiotic therapy. Aspergillus and Candida are the most common fungal pathogens.

The treatment of otitis externa includes analgesics, cleaning the external auditory canal, acidifying agents, topical antimicrobials, and occasionally topical steroid preparations. Ofloxacin otic 5 drops 2 times daily, acetic acid/hydrocortisone otic 5 drops 3 times daily (do not use with perforated TM), and ciprofloxacin/hydrocortisone otic 3 drops 2 times 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 is a potentially life-threatening infection of the external auditory canal with variable extension to the skull base. In greater than 90% of cases, it is caused by Pseudomonas 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/kilogram IV and piperacillin 3.375 to 4.5 grams IV, or ceftriaxone 1 gram IV, or ciprofloxacin 400 milligrams IV, and admission to the hospital are mandatory.

Otitis Media

The incidence and prevalence of otitis media (OM) peak in the preschool years and decline with advancing age. The most common bacterial pathogens in acute OM are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. The predominant organisms involved in chronic OM are S aureus, P aeruginosa, and anaerobic bacteria.

Patients with OM present with otalgia, with or without fever; occasionally, hearing loss and otorrhea are present. The tympanic membrane (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.

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 then 250 milligrams PO daily for 4 days, or cefuroxime 500 milligrams PO 2 times 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. Analgesics should be prescribed for patients with any degree of pain. Patients should follow-up with a primary care physician for reexamination and to assess the effectiveness of therapy.

Complications of OM include TM perforation, conductive hearing loss, acute serous labyrinthitis, facial nerve paralysis, acute mastoiditis, lateral sinus thrombosis, cholesteatoma, and intracranial complications. TM perforation and conductive hearing loss are most often self-limiting and often require no specific intervention. Facial nerve paralysis is uncommon but requires emergent ENT consultation.

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 postauricular 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 nonsulfa-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

On examination, the foreign body is usually visualized and signs of infection or TM perforation should be sought. 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. Patients with perforations from isolated blunt or noise trauma can be discharged with expedited specialty referral and should be instructed not to allow water to enter the ear canal.

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 vascular, mechanical, neurologic, Ménière disease, and other causes. Common medications resulting in tinnitus include aspirin, nonsteroidal anti-inflammatory drugs, aminoglycosides, loop diuretics, and chemotherapeutics; if the patient's condition allows, potentially offending drugs should be stopped. Accurate diagnosis usually requires referral to an otolaryngologist. Pharmacologic treatment with antidepressant medications may alleviate tinnitus in which no correctable cause can be found.

Hearing Loss

Causes of sudden hearing loss are varied and may be idiopathic (most common), infectious, vascular or hematologic, metabolic, rheumatologic, or conductive. Other causes include Ménière disease, Cogan syndrome, acoustic neuroma, cochlear 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.

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.

1. A quick history should determine the duration and severity of the hemorrhage and the contributing factors (trauma, anticoagulant use, infection, bleeding diathesis, etc).

2. The patient should blow their nose to dislodge any clots. Instill 0.05% oxymetazoline 2 sprays/nostril or 0.25% phenylephrine 2 sprays/nostril.

3. Inspect for anterior bleeding using a good light source, a nasal speculum and a suction catheter.

4. Direct external pressure is then applied for 15 min while leaning forward in the “sniffing” position. Reexamine. Repeat once if necessary.

5. If this approach fails, and an anterior source of bleeding is visualized, proceed to chemical cautery. If no source is identified, proceed to packing.

6. Chemical cautery with silver nitrate is the standard of care for emergency department (ED) cautery of anterior epistaxis. Insert cotton swabs or pledgets soaked in a 1:1 mixture of a 4% lidocaine and 0.05% oxymetazoline into the nasal cavity with bayonet forceps. After hemostasis is achieved, the mucosa is cauterized by firmly rolling the tip of a silver nitrate applicator over the area until it turns silvery-black. A small surrounding area also should be cauterized to control local arterioles. Overzealous use of cautery and bilateral septal cautery are discouraged because they may cause septal perforation and unintended local tissue necrosis.

7. Anterior nasal packing may be performed with thrombogenic foams and gels, commercial devices, or gauze. Dehydrated nasal sponges are available in several lengths to control anterior and posterior epistaxes. A film of antibiotic ointment is applied, then the sponge is rapidly inserted along the floor of the nasal cavity where it expands upon contact with blood or secretions. Expansion can be hastened by rehydrating the sponge with sterile water from a catheter-tipped syringe. The longer sponges used to control posterior hemorrhages have been associated with some morbidity and should be used only for posterior epistaxis. Inflatable epistaxis tamponade balloons can also be used to control anterior and/or posterior hemorrhage, are easy to use and are generally more comfortable than nasal sponges. Thrombogenic foams and gels are bioabsorbable, do not require removal, and are generally well tolerated. All nonabsorbable nasal packs should be removed in 2 to 3 days by an ENT physician. If packing or local cautery fails to control anterior bleeding, ENT consultation is necessary.

8. Posterior epistaxis may be treated with a dehydrated posterior sponge pack, as outlined above, or an inflatable balloon tamponade device. The balloon devices use independently inflatable anterior and posterior balloons to quickly control refractory epistaxis at these sites; the instructions for insertion are included in the balloon kit. To protect against potentially serious complications, all patients with posterior packs require ENT consultation for possible hospital admission. Posterior packs are removed 2 to 3 days after placement.

9. All patients with nasal packs should be started on antibiotic prophylaxis with amoxicillin/clavulanate 500/125 milligrams PO 3 times daily.

Complications of nasal packing include dislodgment of the pack, recurrent bleeding, sinusitis, and 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.

Nasal Fractures

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. 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 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.

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% oxymetazoline 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 & Rhinosinusitis

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.

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.

Complications include meningitis, cavernous sinus thrombosis, intracranial abscess and empyema, orbital cellulitis, and osteomyelitis. Patients with these deeper complications usually appear systemically ill or have focal neurologic findings.

The diagnosis of uncomplicated acute rhinosinusitis is clinical, and imaging is not necessary. 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.

Treatment for acute uncomplicated disease is generally supportive. Nasal irrigation with or without nasal decongestants (0.05% oxymetazoline 2 sprays/nostril 2 times daily or 0.25% phenylephrine 2 sprays/nostril 4 times daily) is first-line therapy. Decongestants use is to be limited to ≤ 3 days. Oral antibiotic should be reserved for patients with purulent nasal secretions and severe symptoms ≥ 7 days. If prescribed, choices for a 10-day antibiotic regimen include amoxicillin 1 gram PO 3 times daily (first-line), trimethoprim/sulfamethoxazole 160/800 milligrams 2 times daily or erythromycin 250 to 500 milligrams 2 times daily, (if penicillin allergic), and levofloxacin 500 milligrams daily (if antibiotics in prior 6 weeks).