Otitis externa: Treatment is easy, but a missed diagnosis can be fatal

Otitis externa (OE) is a common ambulatorycare condition. Acute OE manifests from bacterial (90% of cases) or fungal (10% of cases) infections and affects four in 1,000 persons in the United States annually.1 Chronic OE is often the result of dermatologic or allergic etiologies.1-5 The condition is usually confined to the tissues within the external auditory canal (EAC); however, systemic antibiotics are prescribed to treat this problem in 65% of cases.2 Early OE is easily treated with a topical application of an acidifying solution. Untreated infections may progress to a life-threatening condition known as malignant otitis externa (MOE),1,2 especially in patients who are immunocompromised or have diabetes. Thus, the earlier this condition is accurately diagnosed and treated, the less likely the patient is to suffer severe sequelae and the earlier the patient can return to normal activity.

ANATOMY

The EAC is a skin-lined 2.5-cm meatus that includes and extends from the tympanic membrane (TM) to the opening at the external os1 (see Figure 1). The outer third of the canal infrastructure is cartilaginous and covered with a layer of sebaceous and ceruminous glands and hair.1 The inner twothirds of the canal are constructed of an osseous base under a very thin layer of skin that is tightly connected to the underlying periosteum.4 The EAC has specific defenses against offending organisms. A healthy canal is covered with a thin layer of acidic, lysozyme-rich cerumen that prohibits bacterial and fungal growth. Cerumen is also hydrophobic, which prevents the canal from absorbing moisture. Lastly, the migratory pattern of epithelial tissue pushes debris from the TM toward the external os and out of the ear.

PATHOPHYSIOLOGY

Otitis externa results when any one of the above factors fails to protect the EAC. For example, if the canal is stripped of all cerumen through excessive water exposure (water activities, perspiration, and high humidity) or mechanical means (insertion of foreign objects such as cotton swabs, fingers, ear plugs, or hearing aids), then moisture will be allowed into the keratin cells beneath the cerumen.1-4 This creates an ideal pH-elevated environment for bacterial and fungal growth.2,3

Before World War II, fungi were implicated as the primary cause of OE but US military research in the South Pacific proved that bacteria were the most common cause.1 Pseudomonas aeruginosa is the predominant bacterial pathogen, followed closely by Staphylococcus aureus and S epidermidis;1,2,4,6,7 Aspergillus and Candida are the most common fungal organisms.2 Only 5% of OE cases can be attributed to herpes zoster oticus, furunculosis, or bullous myringitis.1

OE can also result from a host of noninfectious conditions classified as eczematous otitis externa, including acne, lupus erythematosus, psoriasis, atopic dermatitis, and seborrheic dermatitis.2 These conditions affect the body as a whole; therefore, systemic treatments will decrease manifestations in the ear canal. Eczematous OE manifests as decreased skin elasticity, atrophy of the ceruminous and sebaceous glands, loss of protective films and secretions, and a pH higher than 6.3 In addition, dryness and atrophy of the glands promote chronic and recurrent OE.3

PATIENT EVALUATION

The early stage of OE occurs within a few days to a week of exposure to a causative agent. Early signs and symptoms are generally mild (minimal discomfort, pruritus, an odorless secretion, modest erythema, decreased hearing, and a feeling of “fullness” in the ear). Beyond the early stage of infection, 1 to 2 weeks after onset, patients will have purulent discharge from the os; marked edema of the EAC; and increased erythema and pain that is exacerbated by chewing, tragal pressure, or movement of the auricle.1 Severe symptoms include profound pain and discharge, complete canal obstruction, and external ear signs, such as preauricular and postauricular lymphadenopathy, parotitis, fever, and auricular cellulitis.1,2

Evaluation begins with a thorough history of the onset and current symptoms. The clinician should ask leading questions regarding precipitating activities, such as the use of finger nails, cotton swabs, or bobby pins in the ear or recent participation in recreational water activities. The history should also take into account significant medical problems that are known to cause OE. Patients with diabetes, a compromised immune system, or local circulatory insufficiency from radiation exposure are particularly vulnerable to rapid progression from mild to severe OE.1,8

Does the patient suffer from any dermatitides such as lupus, atopic dermatitis, or psoriasis? If the answer is Yes, is the patient being treated with a topical or an oral medicine that may help or hinder OE treatment? Accurate answers to these questions will help determine which method of treatment is most expeditious.

PHYSICAL EXAMINATION

A broader, multisystem approach to the physical examination is necessary, including a dermatologic examination that looks for disease-specific skin changes, if the history points toward a systemic cause.1 If there is no history of systemic disease but one is suspected, the appropriate laboratory tests for diagnosis must be ordered. For example, the clinician would order a random blood glucose test if diabetes is suspected. A random glucose or glycosylated hemoglobin test is also appropriate for a patient with known diabetes in order to determine disease control. An ESR or antinuclear antibody test is appropriate if an autoimmune disorder is suspected. However, within the context of OE, these tests should only be ordered when they are strongly indicated, as unnecessary laboratory tests may lead to unnecessary patient expense.

After systemic disorders have been accounted for, a more focused head and neck examination that includes the sinuses, nose, mastoids, temporomandibular joints, mouth, pharynx, ear canal, tympanic membrane, and the auricle should be performed. The local lymph nodes, including the pre- and postauricular and cervical chain lymph nodes must also be included in the examination. The ear canal is examined for otorrhea, which varies widely in appearance.

The characteristics of otorrhea can give clues as to the differential diagnosis of OE (see Table 1). For example, a green, foul-smelling discharge is often the result of a pseudomonal infection.7 The presence of fluffy and white to off-white, black, gray, or bluish green discharge or small black or white conidiophores on white hyphae is associated with Aspergillus infection.2

The EAC is often completely blocked, obscuring direct visualization of the TM. The canal must be cleaned of all debris in order for treatment to be effective. However, flushing the canal must be avoided unless the TM can be fully visualized and is found to be intact.2 Small perforations of the TM are common and often missed on examination. Attempting to flush the EAC when the TM is perforated can result in disruption of the ossicles, which can cause significant cochlearvestibular damage and result in hearing loss, tinnitus, vertigo, and dizziness.2 These complications can lead to the need for surgical intervention.2 Flushing the EAC can also cause damage to the canal itself. Inflammation and maceration make the EAC more susceptible to trauma; therefore, the clinician must also avoid using a cerumen spoon or curette to clean out the canal.2 Lastly, if the EAC cannot be cleared of debris because of swelling, pain, or a lack of equipment, the debris should be left in place. Frequent follow-ups are needed until the secretions clear spontaneously or can be removed with greater ease.2 If the EAC is severely swollen, delivering medication to the place where it is most needed may be mechanically difficult. Therefore, a preformed cellulose wick specifically designed to apply medication within the EAC may be inserted and then left in place to facilitate absorption and delivery of liquid medications to the inner portions of the EAC.1,2

Irrigation of the EAC in patients with OE is very controversial; however, this procedure is still often performed in the primary care setting. No outcome studies have been conducted that would lead to specific guidelines for its use.9 Therefore, the clinician must use extreme caution when proceeding with mechanical debris removal, and all possible adverse outcomes and alternative debris removal options (such as suctioning under direct visualization) should be explained to the patient.1-4

Full visualization of the TM is also essential on initial examination because an obscured view makes differentiating OE from acute otitis media (AOM) difficult.2 Concomitant OE and AOM is not unusual.1,2,10 Tympanometry is used to diagnose AOM if the TM is not obscured and is found to be red.1,10 After confirming the diagnosis of AOM, appropriate oral antibiotic therapy should be given.

TREATMENT

Treatment regimens for OE vary widely and are largely dependent upon clinician specialty and whether the patient is a child or an adult.2,11 However, in cases of mild disease, topical therapy should be attempted first. Topical therapy, first described over 3,000 years ago, is still in use today.1

Before any topical agent is applied, the clinician should safely remove any debris from the EAC. In very mild cases, a combination of 2% acetic acid and 1% hydrocortisone is used at the onset of symptoms.1,2 Some clinicians report more success with a combination of half acetic acid/hydrocortisone and half 90% alcohol.1,12 Warming fluids to body temperature before introducing them into the EAC reduces dizziness,1,2 and gentle tragus manipulation encourages fluid absorption deep into the canal and tissues. Medications are kept within the EAC by placing cotton at the os; using a cellulose wick is recommended if edema reduces the diameter of the EAC by more than 50%. When the swelling goes down—usually in 2 to 3 days—the sponge is no longer needed and can be removed with forceps.1 Most often, the wick falls out on its own.

Moderate to severe cases of OE require antimicrobial ototopical agents, not just an inhibitor such as acetic acid.1 Table 2 lists commonly used ototopical agents. Ototopicals are not more effective than systemic antibiotics, but they can provide localized treatment in concentrations approximately 1,000 times higher than can be provided by systemic antibiotics. In addition, ototopicals are less likely to cause systemic resistance or side effects.1 Oral antibiotics should be used only when OE is persistent, when AOM is present, or when infection has spread locally or systemically.2

An oral antimicrobial should be included when the infection extends to external canal structures (the cervical lymph nodes, parotid glands, or auricle).1 Commonly used antibiotics range from aminoglycosides (neomycin, gentamicin) to fluoroquinolones, with or without concomitant corticosteroids.1 However, aminoglycosides are frequently associated with ototoxicity and allergic dermatitis. In addition, aminoglycosides should never be used in a patient with a perforated TM. Fluoroquinolone preparations allow for better patient adherence because of their ease of use (twice-a-day dosing). Furthermore, these preparations can often be used even when the TM is perforated.1 The risks and benefits of combining corticosteroids with an aminoglycoside or fluoroquinolone should be weighed carefully. Although corticosteroids are known to substantially reduce EAC edema associated with OE, they can also act as a sensitizing agent.1,2

Treatment duration varies somewhat based on severity of disease and speed of resolution. Recommendations are to treat symptoms for 3 days beyond resolution (approximately 5-7 days).2 For more severe disease, a 10- to 14-day treatment course is recommended.2 If symptoms fail to resolve in 5 to 7 days the clinician should consider the possibility of patient sensitivity. For example, perhaps an aminoglycoside allergy is preventing full resolution; or perhaps the patient is sensitive to the preservative (benzalkonium chloride, thimerosal, or propylene glycol) in the agent being used.1

Ten percent of acute OE cases are secondary to a fungal infection. Obvious and uncomplicated fungal infections present with the classic whitish, cottonlike hyphae strands (Candida), with or without interspersed small black or white fungal balls at the tips of the hyphae (Aspergillus).1 Simple fungal infections of the EAC respond to a 2% acetic acid and/or a 90% to 95% alcohol solution. More established infections respond to topical clotrimazole, tolnaftate, or a compounded solution of nystatin 100,000 U/mL otic suspension.1

If typical OE does not respond to standard topical treatment, the clinician must consider the possibility of a fungal superinfection. In cases of a fungal superinfection, a topical antifungal is added to the antibiotic regimen. Recalcitrant cases of fungal infection may require the use of oral itraconazole or fluconazole, 100 mg daily for 10 to 14 days, especially if the TM is perforated. Irrigation should not be used if the TM is perforated, the debris should be removed by suctioning under direct visualization. In addition, the EAC must be kept dry at all times. The patient must be instructed to use a cotton swab with a petroleum jelly when showering to prevent water entering the EAC.

When treating acute OE, the clinician should also take into consideration the possibility of a noninfectious etiology. Underlying disorders such as psoriasis, atopic dermatitis, acne, or seborrhea can be the cause of OE. These diseases need to be optimally treated systemically before full otic benefit can be achieved. Furthermore, simultaneous infectious and autoimmune etiologies are possible.

COMPLICATIONS

All possible reasons for treatment failure must be considered, including the accuracy of the initial diagnosis. Recalcitrant cases of OE often occur in patients with diabetes; patients who are immunocompromised, such as those with HIV infection; and patients who use corticosteroids or receive chemotherapy daily or are undergoing radiation treatment. Coexisting AOM, malnourishment, and chronic illness can also hinder resolution of OE.1,8 Paying close attention to a patient's reaction to treatment can avoid potentially lifethreatening complications. Meticulous cleaning of the EAC, enforcing strict precautions and ear protection for waterrelated activities, identifying potential EAC allergens, and evaluating nutritional and endocrine status are important measures for preventing and managing recalcitrant OE.

Malignant otitis externa MOE results when infection spreads through the canal into the neighboring tissues. MOE involves the mastoid or temporal bone, cartilage, nerves, and blood vessels.13 The organism most often implicated in MOE is Pseudomonas aeruginosa.2,8,13 MOE should be suspected when pain is disproportionate to symptoms; canal skin necrosis or granulation is present; body temperature exceeds 102.2°F (39°C); or in the presence of facial paralysis, vertigo, or meningeal signs.1 MOE is difficult to treat and has a mortality rate of 53% or higher.2 Once MOE is diagnosed, the patient should be referred to a specialist immediately.

Given their superb antipseudomonal activity and excellent GI absorption, fluoroquinolones are the first-line treatment for MOE.2 A combination of beta lactam and aminoglycoside antibiotics is effective for patients who are either allergic to or do not respond to fluoroquinolone therapy.2 A 2-week course of antibiotic therapy is usually necessary. Treatment also includes surgical removal of all infectious and necrotic debris.2

Furuncle This complication is a superficial abscess. A furuncle in the lateral third of the EAC occurs when the apopilosebaceous glands become blocked.2 The treatment for a furuncle includes drainage, hot compress, and topical and systemic antibiotics. The most common organism cultured in this condition is Staphylococcus aureus,1,2 and appropriate antibiotic therapy should be given.

CONCLUSION

OE is a common ambulatory-care condition that can present significant challenges to the clinician if not diagnosed and treated appropriately at its onset. Bacteria are the cause of 90% of cases of OE, the remaining cases are caused by a fungal infection. However, the clinician must always keep in mind the possibility of concurrent endocrine or immune-mediated disease. These conditions are often either the primary cause or a complicating factor in OE. The quicker the causative pathogen is identified, the earlier more focused and appropriate treatment can be rendered, and the less likely the patient will experience complications. Some complications, such as MOE, can be life threatening. Rapid identification of this condition and immediate referral to a specialist can save the patient's life. JAAPA

Richard Handley practices at SCV Quality Care, an urgent care/occupational medicine group in Valencia, California. He has indicated no relationships to disclose relating to the content of this article.

DRUGS MENTIONED

REFERENCES

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