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Chronic external otitis.


Chronic external otitis is probably a disease of mixed etiology; infection and hypersensitivity both play an important role. As such, these two components must be recognized and respected. Steroids are the mainstay of medical management. Antibiotics should be used cautiously and probably on an intermittent basis. The disease appears to be exacerbated by any manipulation of the canal, including aggressive cleansing. Medical therapy will slow the development of fibrosis in some cases, but it does not always prevent it. Once stenosis has progressed to the point that conductive hearing loss develops, surgery will restore hearing and prevent restenosis in at least 80% of cases.


Few conditions encountered by otolaryngologists are as frustrating as chronic external otitis. It is a disease of unknown etiology, its pathophysiology remains sketchy, and even when it responds well to initial management, recurrence is frequent.

The central feature of chronic external otitis is a diffuse low-grade infection of the external auditory canal that can persist for months to years. The disease is characterized clinically by pruritus, scant otorrhea, and a progressive narrowing of the lumen of the canal.


External otitis often arises from the anterior sulcus. The initiating event can be either an episode of acute bacterial external otitis or, not uncommonly, a pre-existing dermatitis that has been present for some time prior to the onset of infection.

In affected patients, the tissue of the external auditory canal is edematous. Histopathologically, the edematous fluid forms principally in the subepithelial layers of the skin, and the edema is usually mild to moderate in intensity (figure 1). A chronic inflammatory cell infiltrate can always be demonstrated. It is often focal. Intensely focal accumulations of inflammatory cells and mucopurulence can actually coalesce to form microabscesses, and over time, areas of calcification develop within these focal areas. In such cases, what begins as mild to moderate subepithelial edema can develop into fibrosis over a period of months to years. Progressive subepithelial fibrosis originates at the medial end of the external auditory canal and often progresses inexorably until it causes postinflammatory medial canal stenosis. [3,4] At various points during the clinical progression of this disease, granulation tissue can be identified in the medial portion of the canal (figure 2). The process by which granulation tissu e forms waxes and wanes in intensity, and the granulation tissue gradually matures into fibrous tissue that concentrically obstructs the medial portions of the external auditory canal (figure 3).

In the final stage of the disease, the end of the external auditory canal becomes a blind, skin-lined sac that terminates a few millimeters lateral to the tympanic membrane (figures 4 and 5). Consequently, there will be a few millimeters of dense fibrous tissue between the blind end of the external auditory canal and the tympanic membrane itself. Ironically, once medial canal fibrosis is complete, the pathologic process ceases. [3,4]

Surprisingly, squamous epithelium rarely becomes trapped between the blind end of the sac and the tympanic membrane, and cholesteatoma formation is uncommon. [1,3] In this respect, acquired stenosis of the external auditory canal arising from chronic external otitis is quite different from acquired canal stenosis arising as a result of trauma. Post-traumatic stenosis of the external auditory canal is frequently complicated by the development of cholesteatoma, which can arise from squamous epithelium trapped in the traumatized portion of the canal.

Clinical presentation

Women are more affected by chronic external otitis than men by a ratio of 2:1. The disease is bilateral in 50% of cases, which suggests that some constitutional or systemic factor predisposes to its development. [3] As might be expected, occlusion of the external auditory canal, usually as a consequence of wearing a hearing aid, exacerbates the condition and hastens its rate of progression. In Slattery and Saadat's series of 24 patients, the mean age at the first visit was 50.5 years; only a single patient was younger than 18 years of age. [3]

A distinguishing feature of chronic external otitis is its painlessness. Patients rarely complain of otalgia. Pruritus, on the other hand, is highly characteristic of this disorder, and it is often intense and persistent. In fact, during the initial stage of the disease, pruritus is the most frequently reported symptom. Otorrhea is usually present, but it is scant, watery or milky, odorless, and generally not very troublesome. Otorrhea is a less common initial complaint than hearing loss. Conductive hearing loss arises as a direct consequence of the narrowing and obstruction of the external auditory canal, and the degree of loss is proportional to the extent of the medial stenos is. As long as even a small lumen (2 to 3 mm) is present, hearing loss is minimal. But as medial fibrosis closes the canal completely, conductive hearing loss rapidly becomes more severe. Maximum hearing loss occurs when the fibrous plug thickens and obliterates the medial end of the external auditory canal. [3-5]

Physical examination

Cerumen is usually absent in chronic external otitis. As mentioned, a watery or milky otorrhea is almost always present, but it is rarely copious. The appearance of the canal varies depending on the level of disease activity. The medial external auditory canal can be shiny, hyperemic, and/or erythematous, and in severe cases it can be covered with granulation tissue. Almost any intermediate stage imaginable can be seen--for example, patchy areas of granulation tissue alternating with areas of shiny skin that are hypervascular or injected. The lateral canal is less severely affected and might even appear to be normal.

As the disease progresses over months or years, the lumen progressively narrows. Prior to a complete medial fibrosis, a narrow lumen usually occupies the center of the external auditory canal. The fibrotic process appears to progress evenly and circumferentially, beginning at the outside of the medial canal and growing inward.

At the end stage of the disease, patients characteristically have a shiny, cerumen-free, blunted canal and no evidence of active infection or ongoing inflammation.


The etiology of chronic external otitis remains unclear. Because the disease is bilateral in 50% of cases, some genetic or constitutional factor might be involved. Moreover, certain environmental factors have been implicated--specifically, high temperature, high humidity, and water exposure. It is possible that the disease might occur only in those individuals who have the right genetic predisposition and the right environment. [1] Among the possible predisposing factors are a history of dermatitis and an allergic diathesis. [1-6]

Bacterial pathogens. While it is clear that there is an infectious component to chronic external otitis, it is equally clear that infection accounts for only a portion of the pathophysiologic process. The bacteria routinely recovered from patients with chronic external otitis are essentially the same as those encountered in acute bacterial external otitis and in chronic suppurative otitis media. [1,3] Most organisms are gram-negative, and Pseudomonas spp. are by far the dominant pathogens, accounting for 30 to 50% of positive cultures. Staphylococcal organisms are seen in 10 to 20% of cultures, and a variety of other gram-negative organisms accounts for the remainder of recovered pathogens. Anaerobic organisms are recovered in many cases, but their pathologic significance remains unclear.

Fungal organisms. Although fungal organisms are not common in acute otitis externa, their role in the chronic form is less well understood. A consensus has emerged that because fungal organisms are much more common in chronic external otitis than in acute disease, they are more likely to be implicated in the pathogenic process. Aspergillus and Candida spp. are the most frequently recovered organisms. Slow-growing fungi might be missed unless special detection techniques are used, such as immunofluorescence microscopy. [6-8]

In rare cases, chronic external otitis is a manifestation of an id reaction. A focus of fungal infection elsewhere in the body can cause a secondary inflammatory process in the external auditory canal. As a result, patients with chronic external otitis must be examined for fungal infections in sites remote from the ear itself. [9,10]

Hypersensitivity. Chrome, nickel, and the material of which ear molds are made are common antigens, and hypersensitivity to them has been implicated in the development of chronic external otitis. Some early reports in the literature also identified substances used in the manufacture of matches as pathophysiologically related to the onset of chronic external otitis among individuals who would use matches to clean or scratch their ears. [11-14]

Unfortunately, the hypersensitivity component in external otitis is frequently iatrogenic. Sensitivity to one or more of the ingredients in ototopical medications appears to be quite common among patients with this disease. Moreover, the incidence of hypersensitivity appears to be rising, especially with respect to the more frequently used antibiotics such as neomycin. The first case of topical sensitization to neomycin ever reported was seen in a patient who had developed an allergic reaction to ototopically administered neomycin. [11] During the 1970s, skin testing in patients with chronic external otitis showed that the incidence of neomycin sensitivity was approximately 8%. [13] Studies conducted in the 1980s showed that this rate had risen to 16%, and in the 1990s, the rate had climbed yet again to 32 to 35%. [12-14]

There is cross-reactivity between neomycin and other aminoglycosides. For example, sensitivity to tobramycin has been identified in countries that have no approved tobramycin-containing topical preparations. Sensitivity to a variety of other ingredients in ototopical medications (including the vehicle itself), topical anesthetics, and topical antihistamines is also quite common in patients with chronic external otitis. To date, no sensitivity to the fluoroquinolone group of antibiotics has been demonstarted. [11-14]

Dermatologic conditions. Pre-existing dermatologic processes are being found with increasing frequency in patients with chronic external otitis. Seborrheic dermatitis is the most common dermatologic condition to affect the external auditory canal. Such patients often have a positive family history and an associated scalp involvement. Other sites that are often involved are the flexor surfaces of the extremities and the retroauricular areas. Psoriasis and neurodermatitis have also been identified as predisposing conditions; in Slattery and Saadat's series, three of their patients had a history of chronic eczema or psoriasis. [1,3,6,7]

In summary, it is generally conceded that chronic external otitis is a multifactorial disorder. Each of the predisposing factors mentioned here might play a greater or lesser role in the development of this disease process in any given individual, and each of the possible etiologic factors must be kept in mind while the disease is being treated.


During the early stages of chronic external otitis, treatment is principally medical. Surgery is generally reserved for patients who have developed medial fibrosis to the point that it results in a clinically significant conductive hearing loss.

Medical treatment. The goals of medical treatment are to arrest the disease completely and to prevent the development of stenosis. Clinicians, however, are frequently disappointed with medical treatment because in some cases it only slows the progression of disease. There are no long-term outcomes data on medical management. [1,3]

Steroids. It is generally conceded that steroids are the most critical component of successful medical management. However, to date only one well-controlled study has been published. [15] Jacobsson et al published the results of a double-blind, placebo-controlled, crossover trial of budesonide. They found that the drug decreased pruritus and otorrhea significantly better than did no treatment. In the context of this very persistent disease, this was a short-term study, and no information about the ultimate development of stenosis or conductive hearing loss was collected. [1,3,4,5]

Steroids can be delivered in a variety of ways, usually as drops and creams. Anecdotally, some otolaryngologists believe that steroid injections into the subepithelial tissues of the external auditory canal are more effective than simple topical applications. It is widely believed that the more potent steroids are more effective than hydrocortisone. The long-term nature of this disease makes the use of systemic steroids impractical.

Antibiotics. Because there is clearly an infectious component to chronic external otitis, antibiotics do play a role. However, they should be used cautiously and probably sparingly. The long periods of time over which this disease progresses make the development of resistant bacterial strains somewhat of a concern, even though the concentrations of medication delivered currently exceed all known minimum inhibitory concentrations for relevant organisms. Moreover, several topically administered antibiotics have been implicated as part of the pathophysiologic process itself. The intermittent use of antibiotic therapy, when possible, can serve to avoid some of these pitfalls.

Antibiotics can be delivered as drops, creams, and powders. Antibiotic powders can be mixed with powdered dexamethasone. Because powders adhere to wet surfaces, they can provide a more consistent level of drug delivery than do topical drops.

Cleansing. Any trauma to the involved medial canal is likely to exacerbate the disease process. Therefore, the cleaning of the external auditory canal should be as atraumatic as possible, and every attempt should be made to provide aural toilet with a "no touch" technique. Although the developing stenosis can tempt the physician to place a wick into the external auditory canal, the presence of a foreign body in contact with the involved tissues appears to be more irritating than helpful.

It is always worth remembering that the foregoing information on the medical management of chronic external otitis is supported only by tradition and opinion and that no long-term outcomes data are available.

Surgical treatment. Once the disease process has progressed to the point that it has produced a significant conductive hearing loss, surgery appears to be the only viable treatment option. The goal of surgical treatment is to remove the stenotic segment of the external auditory canal and to re-create a physiologically functioning tympanic membrane. In Slattery and Saadat's series of 24 patients, the mean preoperative air-bone gap was 25 dB. [3] The air-bone gap diminished to 15 dB at an average of 3.6 years of followup. In Becker and Tos's series of 53 ears (in 47 patients), 33 ears (62%) experienced a closure of the air-bone gap to within 20 dB at late followup ([greater than]2 yr). [4]

If surgical repair of medial canal stenosis is to be successful, all of the involved skin must be removed. Reconstruction, therefore, generally requires relining the external auditory canal. Local flaps can be used for this purpose. Both preconchal and postauricular flaps are well described. The advantages of local flaps as opposed to grafts include less scarring because of increased vascularity. Moreover, the contractural forces that develop during healing tend to pull the canal open. On the other hand, it is often difficult to make a local flap of sufficient length to reach the medial end of the canal. Also, local flaps are bulky and fill a significant portion of the medial external auditory canal. [3,4,16]

Full-thickness grafts are purported to provide greater resistance to trauma, and they can contain glandular elements that provide lubrication. They are also less likely to contract than split-thickness grafts. However, they can also include hair follicles, which can make postoperative management more difficult? [3-5,16,17]

Split-thickness grafts are usually used to line the exposed bone of the external auditory canal after the fibrous plug has been removed. They are easier to obtain than full thickness grafts, but they are harder to place. [3-5]

Selesnick has listed three requirements for the successful surgical repair of medial canal stenosis:

* complete removal of the cicatrix

* performance of a bony canaloplasty

* resurfacing of the bony canal with epithelium

Inexperienced hands, these operations are successful in at least 80% of cases. In Slattery and Saadat's series of 14 surgical procedures, only three patients experienced a recurrence. [3] It is noteworthy, too, that the earliest of these recurrences took place more than 3 years following surgery. Long-term follow-up is required to assess the effectiveness of surgical intervention. In Becker and Tos's series, only 11 of the 47 patients (23%) developed recurrent atresia. [4] In three of these cases, the recurrence appeared within 6 months of surgery and was thought to he attributable to an insufficient removal of fibrous tissue during the primary operation.

From the Division of Pediatric Otology, Children's Medical Center, and the Department of Otolaryngology-Head and Neck Surgery, University of Texas Southwestern Medical Center, Dallas.

Adapted from an educational seminar sponsored by Alcon Laboratories and presented during the annual meeting of the American Academy of Otolaryngology-Head and Neck Surgery, Washington, D.C., Sept. 26, 2000.


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(2.) Lavy JA, Wormald PJ. Pathologic quiz case 1. Benign necrotizing otitis externa (BNOE.). Arch Otolaryngol Head Neck Surg 1997;123:442, 444.

(3.) Slattery WH III, Saadat P. Postinflammatory medial canal fibrosis. Am J Otol 1997;18:294-7.

(4.) Becker BC, Tos M. Postinflammatory acquired atresia of the external auditory canal: Treatment and results of surgery over 27 years. Laryngoscope 1998;108:903-7.

(5.) Selesnick S, Nguyen TP, Eisenman DJ. Surgical treatment of acquired external auditory canal atresia. Am J Otol 1998; 19:123-130.

(6.) Goodman WS, Middleton WC. The management of chronic external otitis. J Otolaryngol 1984;13:183-6.

(7.) Peterkin G. Otitis externa. Presented at the Section of Otology meeting of the Royal Society of Medicine; February 1973.

(8.) Gurr PA, Evans K, Dewey FM, Gurr SJ. Otomycosis: The detection of fungi in ears by immunofluorescence microscopy. Clin Otolaryngol 1997;22:275-83.

(9.) Derebery J, Berliner KI. Foot and ear disease-the dermatophytid reaction in otology. Laryngoscope 1996; 106:181-6.

(10.) Busch RF. Dermatophytid reaction and chronic otitis externa. Otolaryngol Head Neck Surg 1998;11S8420.

(11.) Baer R, Ludwig J. Allergic eczematous sensitization to neomycm. Ann Allergy 1952;10:136-7.

(12.) Fraki JE, Kalimo K, Tuohimac P, Aantaa E. Contact allergy to various components of topical preparations for treatment of external otitis. Acta Otolaryngol 1985;100:414-S.

(13.) Rasmussen PA. Otitis externa and allergic contact dermatitis. Acta Otolaryngol 1974;77:344-7.

(14.) Van Ginkel CJ, Bruintjes TD, Huizing EH. Allergy due to topical medications in chronic otitis externa and chronic otitis media. Clin Otolaryngol 1995;20:326-8.

(15.) Jacobsson S, Karlsson G, Rigner F, et al. Clinical efficacy of budesonide in the treatment of cezematous external otitis. Eur Arch Otorhinolaryngol 1991;245:246-9.

(16.) Adkins WY, Osguthorpe JD. Management of canal stenosis with a transposition flap. Laryngoscope 198l;91:1267-9.

(17.) Harvey SA. Skin grafting in otology. Laryngoscope 1997; 107:1199-202.
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Author:Roland, Peter S.
Publication:Ear, Nose and Throat Journal
Geographic Code:1USA
Date:Jun 1, 2001
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