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Acute otitis externa: treatment perspectives.

To understand what happens in patients with acute otitis externa (AOE), we need a firm grasp of what the normal anatomy of the external auditory canal looks like--specifically, the cartilaginous portion and the bony portion (figure 1). The cartilaginous portion contains loosely bound skin with numerous sebaceous and ceruminous glands, while the bony portion has a thin skin that is densely adherent to the underlying periosteum. The subepithelial layer in the bony portion of the external auditory canal is quite minimal.


In the ear with AOE, we see desquamation of the skin into the ear canal and an inflammatory infiltrate (figure 2). We also see hyperplasia of the squamous lining, vasodilation of the underlying capillary bed, and edematous fluid in the subepithelial layers. A massive influx of neutrophils and other acute inflammatory cells rounds out the picture. Rarely are bacteria seen on routine histopathologic staining.


Predisposing factors

The most common risk factors for AOE are prolonged exposure to water (e.g., frequent swimming), certain dermatologic conditions (e.g., psoriasis and eczema), trauma, anatomic abnormalities (e.g., exostoses and narrow canals), some underlying systemic conditions (e.g., diabetes), some concomitant ear diseases (e.g., cholesteatoma), the use of assistive devices (e.g., hearing aids and earplugs), and cancer radiotherapy (figure 3).


Another factor that might well be important to the development of AOE is pH. In 1980, Seyfried and Fraser reported their study of patients who had come to the hospital with AOE. (1) When the history revealed that a patient had been in a swimming pool, the authors tested a sample of the water. They found that in most of these cases, the pH of the water was on the alkaline side.

On average, the normal pH of earwax is 6.9, which is slightly on the acidic side. In diabetics, however, the pH tends to be slightly alkaline. Driscoll et al found that the pH of earwax in diabetics who developed the life-threatening complication of necrotizing otitis externa (skull base osteomyelitis) tended to be near 8, which is clearly on the alkaline side. (2)


It is not always necessary to use an antibiotic to treat AOE. Acidifying solution--such as aluminum acetate, acetic acid/hydrocortisone, boric acid, glycerine-ichthammol, etc.--have been used over the years, certainly in developing countries. These agents are inexpensive and unlikely to cause bacterial resistance.

The use of a topical steroid alone is another option. One randomized, controlled, double-blind study of 39 patients with AOE found that a 2-week course of a topical aminoglycoside/steroid combination was no more effective than a steroid alone in alleviating symptoms. (3)

Nevertheless, the prevailing treatment for AOE is still a topical antibiotic that (1) can be delivered at extremely high concentrations directly to the site of infection, (2) is bactericidal, and (3) can facilitate a rapid clinical and bacteriologic cure, thereby preventing a secondary complication (e.g., cellulitis or middle ear and mastoid involvement). Overall, the inclusion of a steroid with a topical antibiotic appears to modestly improve the clinical time to cure and relief of symptoms compared with topical antibiotic treatment alone. (4)

Unfortunately, some antibiotics can actually cause AOE or a form of it. For example, topical neomycin has been shown to cause contact sensitivity in 5 to 15% of patients. (4) If patch testing is performed, up to 30% of patients may actually demonstrate hypersensitivity to neomycin. (4) This finding was confirmed by Schapowal in an independent study from Switzerland, where 30% of patients who had used neomycin drops exhibited hypersensitivity on patch testing. (5)

Indeed, AOE might be more of an iatrogenic disease than most of us realize. Schapowal also reported that 12.9% of patients with chronic external otitis experienced contact hypersensitivity to commonly used topical treatments. (5) Sometimes the actual treatment of AOE leads to a secondary fungal overgrowth and hence a secondary fungal infection.

Ideally, the ear should be mechanically debrided. However, sometimes the ear canal is so "swollen shut" that it is necessary to use a wick, which acts as a vehicle for the drops and as a hygroscopic to help draw inflammatory fluid from the ear canal.

Finally, if a case of AOE does not resolve over time, do not assume that it is chronic otitis externa. Rare but often-fatal malignancies of the ear canal (e.g., squamous cell carcinoma) have been missed when clinicians failed to consider there might be more to the problem than meets the eye.


Dr. Perry: It is my personal opinion that many patients with recurrent allergic or bacterial otitis externa have a persistent fungal infection. I believe the excoriated skin contains a great deal of fungi--usually Candida albicans, Aspergillus niger, or Aspergillus flavus. So when I see patients with otitis externa, I treat them for a fungal infection for 4 months, because it takes that long for the skin to dry out and disperse the fungal spores.

Fungal infections often follow bacterial infections in patients with otitis externa. Treatment of bacterial infections with an antibiotic will cause the bacterial fungi to deplete the nutrients on the skin, which results in the killing of bacteria. However, the fungus itself will survive and overgrow, which can lead, of course, to persistent infection. So we should be careful in treating otitis externa with an antibacterial over the long term because we might be predisposing our patients to more trouble in the future.

Finally, I tend to think that diffuse AOE is caused by Pseudomonas aeruginosa and that localized otitis externa is usually caused by Staphylococcus aureus.

Dr. Deitmer: In Germany, we call AOE the Q Tip disease because so much of it is caused by microtrauma during manipulation of the ear. Two other common causes that we see are heat and moisture, which lead to what we in Europe call Mediterranean externa. In the Mediterranean area, it is the heat and humidity rather than the quality of the water that makes the skin of the external ear canal open for infection. We see other causes as well, as Dr. Rutka mentioned.

As for therapeutic options, we begin with cleaning, suction, and irrigation. It is very important to clean the canal thoroughly. We can add local antibiotic/steroid drops and perhaps even an antibiotic/steroid ointment applied to cotton gauze. In some cases, we add an oral antibiotic and sometimes even an intravenous antibiotic/steroid combination.

Dr. Perry: An infected external canal will exhibit a spidery dander that we can simply peel off. It's also important to remove excessive material from the stratum corneum and the parakeratotic layer to expose the skin, let it dry, and allow the ototopical agent to be absorbed. Steroids and compression dressings can be used to reduce edema.

Dr. Ovesen: In Scandinavia, external otitis is not a common problem. We don't even see many cases of swimmer's ear in children. But when we do see it, we use a ciprofloxacin/steroid drop instilled directly into the middle ear. We include the steroid regardless of whether the patient's tympanic membrane is perforated. We are very interested in the new ciprofloxacin/dexamethasone eardrop that was approved in the United States last year, and we plan to use it in some trials.

Dr. Barber: AOE is usually very painful, and adequate analgesia is essential. I generally prescribe 75 to 90 mg/kg/ day of acetaminophen 4 times a day. If necessary, I switch to ibuprofen at 20 mg/kg every 8 hours, diclofenac at 2 to 3 mg/kg twice a day, or rofecoxib at 25 to 50 mg/day. In some cases, patients even require hospitalization for more potent analgesia.

Finally, AOE may be part of a more generalized cellulitic condition such as impetigo or erysipelas involving S aureus and Streptococcus pyogenes.


(1.) Seyfried PL, Fraser DJ. Persistence of Pseudomonas aeruginosa in chlorinated swimming pools. Can J Microbiol 1980;26:350-5.

(2.) Driscoll PV, Ramachandrula A, Drezner DA, et al. Characteristics of cerumen in diabetic patients: A key to understanding malignant external otitis? Otolaryngol Head Neck Surg 1993;109:676-9.

(3.) Tsikoudas A, Jasser P, England RJ. Are topical antibiotics necessary in the management of otitis externa? Clin Otolaryngol 2002;27: 260-2.

(4.) Diagnosis and treatment of acute otitis externa. An interdisciplinary update. Ann Otol Rhinol Laryngol Suppl 1999; 176:1-23.

(5.) Schapowal A. Contact dermatitis to antibiotic car drops is due to neomycin but not to ciprofloxacin [abstract]. Allergy 2001;56(suppl 68):148.
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Article Details
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Author:Rutka, John
Publication:Ear, Nose and Throat Journal
Date:Sep 1, 2004
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