External Ear Inflammatory Diseases 

Updated: Aug 14, 2020
Author: Manali S Amin, MD; Chief Editor: Arlen D Meyers, MD, MBA 


The external ear, namely, the auricle and the external auditory canal, is composed of skin, cartilage, and all associated appendages. The skin and cartilage of the ear are subject to the same insults as similar tissues found elsewhere in the body. Thus, many of the diseases discussed below may be found in greater detail in other Medscape Reference articles.

Inflammation is the body's response to cellular injury. The various etiologies that result in inflammation of the ear are numerous and may be categorized broadly as infectious, traumatic, and immunologic. Infectious diseases of the external ear have been covered in other articles and are not discussed here. Inflammation of the auricle may result from trauma (eg, mechanical pressure from telephones or headbands), radiation exposure,[1] or environmental insults or irritants (eg, chemicals used to clean hearing aids). Immune-mediated inflammation includes atopic and autoimmune disorders. As with many diseases, an etiology is not always apparent. These idiopathic disorders have been grouped into a broad fourth category entitled miscellaneous.


Immunologic and Inflammatory Disorders

Immunologic or inflammatory disorders of the ear may be localized, as in contact dermatitis, or may be a manifestation of a systemic process, such as atopic dermatitis, psoriasis, gout, sarcoidosis, or relapsing polychondritis.[2]

Atopic dermatitis

Atopic dermatitis, also known as eczema, is a systemic disease that manifests as intensely pruritic, erythematous, skin lesions.[3] The disease usually manifests in childhood and is more commonly observed in families with a history of asthma, allergic rhinitis, and other atopic disorders. Recent studies indicate that atopic dermatitis may be the result of an altered immunologic balance in which TH 2 cells (a subtype of helper T lymphocytes) predominate. TH 2 cells synthesize interleukins 4, 5, and 10. In psoriasis, TH 1 cells, which secrete interferon gamma and tumor necrosis factor, predominate.

The lesions are erythematous scaly crusts and/or small (< 0.5 cm), circumscribed, fluid-filled lesions (vesicles), which may become confluent. Linear fissures may also be noted, often in the postauricular region. Although not specific to atopic dermatitis, affected skin exhibits white dermatographism (ie, appearance of a white line when the lesion is stroked). Chronic scratching often results in thickening (lichenification) of the skin and hyperpigmentation. Atopic dermatitis can increase the risk of secondary skin infections. 

Involvement of the external ear is usually part of a more generalized process that involves the face and neck. Lesions are typically found on the face and on extensor surfaces during childhood and on flexural surfaces (eg, antecubital fossa, popliteal fossa), eyelids, ears, hands, and feet in adulthood. Auricular pseudocyst formation has been reported in patients with atopic dermatitis. These cystic lesions vary from 1.5-3.5 cm in size and typically involve the upper, anterior aspect of the pinna. Patients with atopic dermatitis may be more susceptible to pseudocyst formation as a result of trauma from chronic scratching.

Common triggers for the allergic reaction include certain foods, environmental changes, psychological or emotional stress, airborne allergens, and local skin irritants (especially wool). The most common foods that trigger a reaction include eggs, peanuts, milk, fish, soy, and wheat. Although food allergies and atopic dermatitis often coexist, the initial pathophysiology of atopic dermatitis is multifactorial and early skin dysfunction likely plays a vital role in the development of atopic dermatitis.[4]  In women, menstruation and pregnancy may also trigger or exacerbate symptoms.

History and the characteristic distribution and appearance of pruritic lesions help to make the diagnosis. Laboratory tests that may assist in diagnosis include an elevated plasma histamine level, elevated immunoglobulin E (IgE) level, and peripheral eosinophilia. However, these tests are not specific to atopic dermatitis or even to atopic disorders. Histologic examination of the lesions reveals nonspecific intracellular edema with perivascular lymphocytic infiltration.

Patch testing may be performed for identification of the allergen or allergens; it is usually performed on the back or arm and involves application of commercially standardized allergen to the skin. The skin is then observed for an inflammatory reaction. The use test involves the removal of all possible offending agents and a reintroduction of those agents, one at a time, at approximately a 3-day interval, until a reaction is provoked and the allergen is identified. Use testing is often used to identify food allergens. Differential diagnoses include allergic and irritant contact dermatitis, seborrheic dermatitis, neurodermatitis, and psoriasis.

Treatment consists of proper skin care with gentle soaps, moisturizers, topical corticosteroids, topical tacrolimus (a macrolide antibiotic), and topical crisaborole (a phosphodiesterase type 4 inhibitor). Topical tacrolimus has been shown to decrease production of interleukins IL-4, IL-5, and IL-8, as well as IgE. It is an immunosuppressive agent; a burning sensation of the skin is its major side effect. It has relatively poor absorption and, therefore, the side effects often associated with systemic tacrolimus are not seen. In addition to topical medications, oral antihistamines may be administered for relief of pruritus. For skin lesions that are secondarily infected, prescribe saline compresses and topical or oral antibiotics. In severe cases, systemic corticosteroids may be used. Finally, desensitization with immunotherapy is beneficial in patients with moderate to severe disease. 

Allergic contact dermatitis

Allergic contact dermatitis is a true delayed-type hypersensitivity reaction that occurs when a previously sensitized individual comes in contact with the allergen. Contact allergens are formed when a simple chemical of low molecular weight becomes complexed with a skin protein. Upon reexposure, an inflammatory reaction occurs.

In the acute phase, the skin is erythematous, edematous, and pruritic. Small, raised, circumscribed lesions (papules); weeping fluid-filled lesions (vesicles); exudation; and crusting are present. The lesions may become secondarily infected. In the chronic phase, the skin becomes thickened as a result of chronic rubbing or scratching. Thickening of the skin (lichenification), fissuring, and hyperpigmentation may also be observed.

Allergic contact dermatitis of the external ear is most commonly the result of hair products, cosmetics, earrings, hearing aids, topical medications, cell phones, and other objects that contact the pinna. Paraphenylenediamine, parabens, and quaternium-15, which are ingredients often found in shampoos, hair dyes, and hair sprays, commonly affect the conchae and periauricular regions. Hearing aids made of rubber, vinyl plastics, or methylmethacrylates or chemicals used to clean hearing aids may be the offending agents in cases of contact dermatitis of the external canal. Topical preparations, especially those that contain neomycin and related topical aminoglycoside antibiotics (eg, tobramycin, gentamicin) or topical anesthetic agents, such as benzocaine, may also affect the external auditory canal.

Earrings, especially those made of nickel, cobalt, palladium, or white or yellow gold, may cause dermatitis of the lobule.[5] In Europe, a new initiative that calls for a reduction in the amount of nickel in commercial products was adopted following Danish studies that revealed a decrease in nickel allergy after a similar initiative was implemented in Denmark. Finally, lesions on the hemilateral pinna or the preauricular region may be the result of an allergy to chromium, a metal commonly used in cell phones.[6]

In each case, irritated, ulcerated, or inflamed skin appears to increase an individual's likelihood of becoming sensitized to an allergen. When a topical preparation is prescribed, underlying disease is often responsible for irritated inflamed skin within the external auditory canal, along the pinna, or both. Use of hearing aids may occlude the skin within the canal, promoting sensitization of products commonly used to make or to clean hearing aids. In a freshly pierced ear, haptenation is promoted if the dermis comes in contact with a substance such as nickel or gold. Gold sodium thiosulfate, a component of some earrings, has been shown to accumulate in the macrophages of susceptible individuals, resulting in a dense lymphocytic infiltration and pseudolymphoma formation. These pseudolymphomas may present as violaceous, nontender nodules found on ear lobes.

The diagnosis is made with the help of the patient's history and a patch or use test. Patch testing is usually performed on the back or arm and involves subdermal injection of small amounts of allergen. The skin is then observed for an inflammatory reaction. The use test involves the removal of all possible offending agents and the reintroduction of those agents, one at a time, at approximately a 3-day interval, until a reaction is provoked and the allergen is identified. In addition to these 2 tests, a thorough workup includes potassium hydroxide preparation, fungal cultures, Gram stain, and bacterial cultures to exclude a superimposed infection.

In rare instances, a skin biopsy may be performed to identify the lesion. Histopathologic evaluation reveals a dense lymphocytic infiltration with a few eosinophils and plasma cells in the dermis and subcutaneous tissues and lymphoid follicles with germinal centers. T-cell lymphocytic infiltration, especially around blood vessels, is seen in one variant, known as "lymphomatoid contact dermatitis." Clinically and histologically, this can mimic mycosis fungoides and may be considered in the differential diagnosis. Other potential differential diagnoses include irritant contact dermatitis, seborrheic dermatitis, psoriasis, atopic dermatitis, dermatophytosis, infectious eczematoid dermatitis, discoid lupus erythematosus, and angiolymphoid hyperplasia.

Treatment involves avoidance of the offending agent. Silicon hearing aids, which are hypoallergenic, may be substituted in the case of a hearing aid allergy. Using stainless steel earrings until the earring tract has epithelialized adequately may prevent an allergic reaction to earrings. Three weeks is usually appropriate for epithelialization. Cool saline or astringent compresses, topical corticosteroids, aluminum acetate, Burow solution, or Lassar paste can be used for treatment of symptoms. Promptly treat secondary infections with the proper antibiotics. Recent animal studies suggest that blocking IL-18 and IL-12 may be beneficial in the treatment of allergic contact dermatitis.

Photoallergic dermatitis

Photoallergic dermatitis, also known as photodermatosis or solar urticaria, is an inflammatory skin condition that develops when a substance (generally a drug) is altered photochemically so that it haptenates with skin or carrier proteins to form an allergen. The reaction may be elicited when a systemically ingested substance or topically applied substance is altered by blue-violet light (400-500 nm). When the etiologic agent is a topical substance, the dermatitis is considered a true delayed hypersensitivity reaction that requires prior sensitization.

Chemicals that may elicit the reaction include halogenated salicylanilides (found in soaps) and topical phenothiazines and sulfonamides (found in sunscreens). Although chemicals are generally believed to be the causative agents, some evidence suggests that airborne allergens and sunlight may trigger a similar reaction. Often, an etiologic agent cannot be determined.

Photodermatosis of the ears is more common in males. Females tend to have longer hair that covers their ears, preventing sunlight from acting as a catalyst. Lesions may vary in appearance from hives (urticaria) to erythematous, small, raised, circumscribed lesions (papules) and from fluid-filled lesions (vesicles) to scaly, inflammatory, raised lesions (eczematous plaques). Lesions may even be blisterlike in appearance (bullae). Lesions may be pruritic, which usually heal without sequelae. In some individuals, the lesions may persist for months to years.

A diagnosis is made with the help of a history and physical examination. To confirm the diagnosis, a photopatch test may be performed. This consists of the 24-hour application of a standard patch that contains substances such as sulfonamides, phenothiazines, or paraaminobenzoic acid. The patch is then exposed to UV-A light of 5-15 J/m2 and then read again in 48 hours. The patch test is compared with an area of skin that is exposed only to UV-A light and to an area of skin that has been treated with a nonirradiated patch. Differential diagnoses include lupus erythematosus, porphyria, contact and atopic dermatitis, and phototoxic dermatitis.

Primary treatment is avoidance of the etiologic agent and of sunlight. In addition, cold saline compresses or tap water compresses and topical corticosteroids may be applied for relief of symptoms.


Psoriasis (see Psoriasis, Guttate) is a chronic inflammatory skin disorder with 2-5% prevalence. One third of patients who have psoriasis have a family history of the disorder, and evidence suggests that inheritance may be autosomal dominant with incomplete penetrance. The disease has no sexual predilection and the onset is typically in adolescence. Although psoriasis may resolve spontaneously, it is often a lifelong process characterized by exacerbations and remissions.

Lesions are typically pruritic and pink. Erythematous, circumscribed, differentiated lesions (plaques) that are covered with a silvery adherent scale may appear on the body surface. Lesions often coalesce to form larger plaques. An area of paler skin may surround the plaques. If the scale is scratched or removed, pinpoint bleeding may occur, which is called the Auspitz sign, which is not pathognomonic because it may also be observed in seborrheic and actinic keratoses. The disease also exhibits Köbner phenomenon, ie, the development of lesions secondary to mild trauma.

Several variations of psoriasis exist, including guttate, pustular, exfoliative erythrodermic, and inverse. Psoriasis may affect any part of the body, but the knees, elbows, scalp, anogenital region, and nails are most commonly affected. Eighteen percent of patients, especially those with extensive scalp involvement, have external ear involvement at some time during their lives. The periauricular skin, conchae, and external auditory meatus are the regions of the ear most likely to be affected. Ear involvement may be intensely pruritic, and the scaly lesions may accumulate in the external auditory canal, which results in diminished hearing. The ear is affected more often in women, and nearly 50% of ear involvement occurs in individuals aged 10-29 years.

In addition to the classic skin lesions, psoriasis may also manifest as nail and joint involvement. Up to 30% of patients may present with thickening of distal nail plates, separation and pitting of nails, and a white or yellow opacification, commonly referred to as oil spots. Finally, approximately 5% of patients have joint involvement.

Diagnosis is generally made with the help of a history and physical examination. Laboratory examinations usually do not provide any additional information. Occasionally, skin biopsy may be performed. Histologically, psoriasis is characterized by hyperkeratosis, parakeratosis, neutrophilic microabscesses, acanthosis, thinning of the suprapapillary plate, and dilation of superficial dermal vessels with a perivascular infiltration of lymphocytes.

Differential diagnoses include excoriated neurodermatitis, seborrheic dermatitis, and onychomycosis. Although psoriasis and seborrheic dermatitis are often similar in appearance, seborrheic dermatitis is characterized by diffuse, scruffy, greasy-appearing scales and is usually less erythematous than psoriasis. In addition, psoriasis is less likely to affect the face.

Treatment involves high-potency topical corticosteroids with or without occlusion, topical calcipotriene with or without occlusion, a combination of crude coal tar and UV therapy (Goeckerman regimen), topical anthralin, UV therapy with oral psoralens, or topical retinoids. In severe cases, systemic therapy with methotrexate, hydroxyurea, aromatic retinoids such as etretinate, and sulfasalazine (Azulfidine) may be of temporary benefit. Although systemic corticosteroids may be temporarily beneficial, avoid these agents because they aggravate the condition upon withdrawal. Improvements have been reported in diabetic patients who received thiazolidinedione rosiglitazone, including one patient who had complete resolution of plaques over her entire body and ears.[7] However, a recent large-scale, randomized, double-blind, placebo-controlled study showed no benefit from rosiglitazone over placebo.[8]

Relapsing polychondritis

Relapsing polychondritis is an autoimmune disorder in which an individual exhibits a cell-mediated immune response to cartilage proteoglycans and produces antibodies to cartilage matrix and native and denatured type II collagen. Mean age of onset is in the fifth decade of life, and no sexual or racial predilection exists. Although no clear etiology has been identified, a hormonal precipitating factor has been postulated.

Systemic destruction of articular and nonarticular cartilage characterizes the disease, which commonly affects the head and neck (eg, eyes, ears, eustachian tube, nose), respiratory system (eg, larynx, trachea, bronchi), cardiovascular system (eg, heart valves, blood vessels), and joints. Table 1 lists the more common manifestations of relapsing polychondritis and their incidences.

The external ear is affected in up to 88% of cases, and recurrent auricular chondritis can lead to permanent damage. Relapsing polychondritis usually manifests as cellulitis of one or both pinna. Because cartilage is lacking, the earlobes are typically spared. Destruction of external auditory canal cartilage may result in conductive hearing loss, while disruption of inner ear anatomy may result in sensorineural hearing loss, vertigo, or tinnitus.

Table 1. Manifestations of Relapsing Polychondritis [9] (Open Table in a new window)

Organ System


Incidence, %

Additional Information


Auricular chondritis

Hearing loss (sensorineural or conductive), tinnitus, vertigo



Presenting sign in 26% of cases




Presenting sign in 23% of cases


Saddle nose, septal swelling


Presenting sign in 13% of cases


Episcleritis, iritis, conjunctivitis, keratitis





Stridor, choking sensation, laryngeal tenderness




Cardiovascular system

Valvular disease, aneurysms, vasculitis, thrombitis




Derived from Lucente FE, Lawson W, Novick NL: The External Ear. Philadelphia, Pa: W.B. Saunders Co; 1995.

After articular chondritis, arthropathy is the second most common manifestation of relapsing polychondritis. The arthropathy is nonselective and affects both small and large joints with equal frequency. This condition is also typically migratory, asymmetric, and seronegative. Occasionally, a positive rheumatoid factor (RF) is noted. However, this result may be secondary to a concomitant diagnosis of rheumatoid arthritis.

Almost a fourth of individuals diagnosed with relapsing polychondritis develop a second autoimmune disorder. Associated diseases include rheumatoid arthritis, systemic lupus erythematosus, myasthenia gravis, Hashimoto thyroiditis, pernicious anemia, Sjögren syndrome, and ulcerative colitis.

A study by Tanaka et al of 11 patients with ocular inflammation associated with relapsing polychondritis, including nine cases of scleritis and two of anterior uveitis, found that the majority of individuals had auricular chondritis.[10]

Laboratory abnormalities that may support the diagnosis include mild anemia and an elevated erythrocyte sedimentation rate. In the early stages of the disease, 30-60% of patients have detectable levels of antibodies to type II collagen. Additional tests, such as a serum B-12 level, thyroglobulin and microsomal antibodies, RF, antinuclear antibody (ANA), and acetylcholine receptor antibodies, may be obtained based on clinical suspicion for associated diseases.

Diagnosis is generally clinical, although lab tests may be helpful. Diagnosis requires that three of the following symptoms or signs be present (McAdam criteria):

  • Auricular chondritis

  • Nasal chondritis

  • Nonerosive seronegative inflammatory polyarthritis

  • Ocular inflammation

  • Respiratory chondritis

  • Audiovestibular damage

Cartilage biopsy can be useful in cases where clinical uncertainty exists. Staining with hematoxylin and eosin results in a distinctly pink color to the cartilage. (Normal cartilage stains blue with hematoxylin and eosin [H and E] staining.) Early in the disease process, the most common histologic finding is a neutrophilic infiltration. As the disease progresses, histologic findings include infiltration of the cartilage and perichondrial tissues with neutrophils, eosinophils, and lymphocytes, loss of cartilaginous matrix, and, ultimately, fibrosis.

Immunofluorescence studies of the tissue have demonstrated immunoglobulin C3–complex deposition at the chondrofibrous junction in 2 patients. Treatment consists of systemic corticosteroids, NSAIDs, or colchicine. Other treatments that have been tried with success include dapsone, methotrexate, cyclosporine, cyclophosphamide, azathioprine, and mycophenolate mofetil. Anti–tumor necrosis factor (TNF) agents (predominantly infliximab) have also been used successfully in relapsing polychondritis.[11]


Tophi (deposited uric acid), with or without traditional articular gout, can occur at the helix and should be considered in the differential. Rarely, these lesions are miscategorized as a malignancy, but histologic and crystal analysis can make the diagnosis.[12]  White papules within the helix are characteristic of tophi, and further physical examination and history are helpful in evaluating for underlying gout.

Table 2. Differential Diagnoses of Common External Ear Inflammatory Conditions (Open Table in a new window)


Etiology and Epidemiology

Lesion Description

Differential Diagnoses

Atopic dermatitis

Systemic disorder commonly seen in families with history of asthma, allergic rhinitis, or other atopic disorders

Erythematous scaly crusts, fluid-filled lesions, or both

Postauricular fissures may be present

Allergic dermatitis

Contact dermatitis

Seborrheic dermatitis

Neurodermatitis Psoriasis

Allergic contact dermatitis

Delayed-type hypersensitivity when a previously sensitized individual comes in contact with an allergen

Erythematous, edematous, and pruritic

Acute: Circumscribed solid skin elevations, weeping fluid-filled lesions, exudation and crusting may be present

Chronic: Thickening of skin from scratching

Fissuring may be present


Irritant contact dermatitis

Seborrheic dermatitis


Atopic dermatitis


Infectious eczematoid dermatitis

Discoid lupus erythematosus

Angiolymphoid hyperplasia

Psoriasis  TH 1–mediated disease  Characteristic plaque with dominant flexor surface involvement 

Atopic dermatitis 

Nummular eczema

Superficial fungal infections 

Seborrheic dermatitis

Photoallergic dermatitis

Delayed-type hypersensitivity that occurs when an ingested substance reacts with sunlight that results in dermatitis

Variable lesions: hives (urticaria); solid, erythematous, circumscribed, raised skin lesions (papules); small (< 0.5 cm) fluid-filled lesions (vesicles); blisterlike lesions; lesions may be pruritic

Lupus erythematosus


Contact dermatitis

Atopic dermatitis

Phototoxic dermatitis

Relapsing polychondritis

Autoimmune disorder in which antibodies to cartilage matrix and type II collagen are produced

Destruction of articular and nonarticular structures throughout the body

Cellulitis of the ear

Erythema, pain, swelling, and discoloration of pinna

Cellulitis of the pinna

Infectious perichondritis


Insect bite

Overexposure to sunlight and extreme cold

Cogan syndrome

Autoimmune disorders such as lupus





Traumatic Disorders

Irritant contact dermatitis

Irritant contact dermatitis is a dose-dependent reaction to chemicals commonly found in soaps, turpentine, household detergents, solvents, cleaners, and strong alkali and acidic compounds. These chemicals have a direct toxic effect on the skin. Chemicals found in soaps, shampoos, and jewelry cleaners more commonly affect the ears.

History and examination of the lesions are the main diagnostic tools. As in allergic contact dermatitis, erythema and edema, small (< 0.5 cm) fluid-filled lesions (vesicles), and larger blisterlike lesions (bullae) typically characterize irritant contact dermatitis. Lesions are histologically indistinguishable from allergic contact dermatitis. During assessment of the lesions, remember that irritant contact dermatitis is 5 times more common than allergic contact dermatitis. In rare instances, patch testing may assist in making the diagnosis. Patch testing involves placing patches of common irritants on the skin and observing the subsequent reaction. However, a patch test has limitations. Most importantly, test exposure may be less than the actual clinical exposure and, therefore, may fail to elicit the same response.

Differential diagnoses include allergic contact dermatitis, seborrheic dermatitis, atopic dermatitis, and sunburn. Treatment involves avoidance of the offending agent. In severe cases, cool compresses and topical corticosteroids may be used to relieve symptoms.

Phototoxic dermatitis

Phototoxic dermatitis, also known as berloque dermatitis, is a nonimmunologic dermatitis that commonly affects the face, neck, upper chest, hands, forearms, legs, and other sun-exposed skin. Like photoallergic dermatitis, this condition results from a combination of ingested or topical agents and sunlight. Unlike photoallergy, however, the agents do not haptenate with skin proteins. Rather, the agents are usually polycyclic compounds that absorb UV-A radiation.

Phototoxic dermatitis is more common than photoallergy and often results from ingestion of psoralens or furocoumarins found in plants and fruits (eg, limes, parsley, celery, figs) and drugs such as thiazides, tetracycline, sulfonamides, griseofulvin, phenothiazines, chlorothiazides, nalidixic acid, coal tar, and sulfonylureas. Psoralens are most commonly implicated in ear involvement. In mice, topical quinolones have resulted in edema when the ear is exposed to sunlight.

Lesions are streaks of erythema and may resolve with postinflammatory hyperpigmentation of the affected regions. As in photoallergic dermatitis, history and physical examination are usually the main diagnostic tools. Patch testing may also be of assistance.

Treatment involves avoidance of the offending agent and of sunlight. If sun exposure is inevitable, instruct the patient to use protective clothing, a hat, and sunscreen to provide maximum protection. Relief of symptoms may be provided with cool compresses and topical corticosteroids.


Erythema and edema of the skin following exposure to the sun or other sources of UV light (eg, tanning beds) are characteristics of phototrauma, which is more commonly referred to as sunburn. Solar UV light, mostly UV-B and UV-C, is absorbed by the epidermis. By contrast, UV-A, which is 5 times more concentrated in tanning beds than in sunlight, penetrates the dermis. All 3 forms of UV light may damage the skin. Maximum UV exposure occurs between 11:00 am and 3:00 pm and, contrary to popular belief, occurs even on cloudy days. In fact, UV light exposure is reduced by only 20-40% on a cloudy day.

Phototrauma most commonly affects fair-skinned individuals with blond or red hair. A combination of factors, including skin type and length and intensity of sun exposure, affect the degree of damage from sunburn. Lesions may range from mild erythema and edema of the skin to blisterlike lesions (bullae), crusting, and even ulcerations. The skin may be pruritic or tense and painful. The ears are commonly affected because of their position on the head. In addition, they are often overlooked during the application of sunscreen.

Pathophysiologically, UV radiation damages cell membranes and DNA and transiently disturbs protein synthesis. The damage results in elaboration of cytokines and other inflammatory mediators.

Only history and physical examination are needed to help make the diagnosis. However, most patients with sunburn never present to a physician. Therefore, education about prevention is imperative. Many resources regarding sun protection are available, including an instructional course for children. Studies have shown that education is an effective intervention for phototrauma.

Prevention includes use of hats, sunscreens, and protective clothing. Sunscreens are assigned sun protection factor (SPF) ratings. SPF, according to Diffey, is defined as the ratio of the least amount of UV energy required to produce a minimal erythema on skin that is protected by sunscreen to the amount of energy required to produce the same erythema on unprotected skin. Because most individuals apply less sunscreen than required to achieve the SPF, a discussion with the patient about the meaning of SPF is important. Treatment of phototrauma is based on symptoms and includes cool compresses. In severe cases, systemic corticosteroids may be used.

Chondrodermatitis nodularis helicis

Chondrodermatitis nodularis helicis, also known as Winkler disease, is a disease characterized by a small tender nodule on the helix that develops as a result of mechanical or environmental (sun exposure) trauma. Mechanical pressure against the ear may be a result of sleeping on the affected side, excessive telephone or earphone use, and wearing tight headgear. Both men and women are susceptible. Although these lesions generally develop unilaterally and more often on the right side, bilateral lesions have been reported.

Lesions are generally found on the superior portion of the helix in middle-aged and older men and on the lateral rim of the helix and antihelix in women. The lesions may also be noted on the tragus, antitragus, and concha. One report saw an increase in the incidence of such lesions on the antihelix and tragus as a result of an increase in cellular phone usage.[13] To date, one report of a lesion on the posterior aspect of the pinna exists, the result of an unusual sleep position, which further supports mechanical pressure as the etiologic agent.[14] All of these regions of the ear lack the protective benefit of subcutaneous tissue and generally have poor vascular supply.

The characteristic round-to-oval nodules are tender and are usually covered with a scale or crust. Removal of the crust reveals a channel through which necrobiotic substance (ie, degenerated connective tissue) is extruded from the dermis. The lesion may also be ulcerated. It rarely grows larger than 3 mm to 1.5 cm. The primary symptom of patients is pain and tenderness upon manipulation of the lesion.

Differential diagnoses include basal cell carcinoma, squamous cell carcinoma, and premalignant keratoses. To exclude these diagnoses, a biopsy of the lesion may be performed. Histologically, the lesion is a central necrotic area surrounded by a rim of hyperkeratotic and parakeratotic tissue of varying degrees. Hypervascularity from multiple small vessels between the cartilage and the lesion has been noted. In addition, in some cases, a large nerve fiber or multiple small nerve fibers have been noted within the lesion, potentially explaining its painful nature.

Treatment consists of modification of the instigating event (eg, less telephone usage, wearing less constricting headgear) and avoidance of pressure on the affected ear. Other treatment modalities include intralesional corticosteroid injections, topical steroids, cryotherapy, curettage, electrocauterization, intralesional collagen injections, pentoxifylline, and CO2 or argon laser therapy.

Successful treatment of chondrodermatitis nodularis helicis with topical nitroglycerin, in gel or patch form, has been reported.[15] In a prospective study of 11 patients with the disease who were treated with nitroglycerin patches (5 mg; 12 hours per day for 2 months), Garrido Colmenero et al found that 7 patients (63.6%) had a complete response to the therapy.[16, 17]

Surgical excision is another treatment. For larger lesions, a wedge excision of the pinna with a pedicled flap reconstruction, such as the Antia-Buch procedure, may be used.


Currently used in the treatment of malignancies, radiation therapy was once used in the treatment of such benign conditions as acne, hirsutism, eczema, and ringworm. Iatrogenic exposure, whether in the form of x-rays or radiation therapy with cobalt or radium, potentially has many harmful side effects. The external ear, like any other body part, is susceptible to radiation damage. Damage may manifest as radiodermatitis, chondritis, perichondritis, chondronecrosis or osteoradionecrosis (ORN). In addition, some patients may present with a conductive hearing loss secondary to tragal retraction over the external auditory canal or secondary to external auditory canal stenosis.

The ear is commonly affected when it lies in the radiation-treatment field of parotid tumors or of nasopharyngeal carcinoma. External ear injury may also occur following treatment of cutaneous cancers of the pinna and brain malignancies.

Radiodermatitis of the ear can be divided into 2 stages, namely, acute and chronic.

Acute radiodermatitis has a latency period of 6-12 days, and its characteristics are as follows:[18]

  • First degree

    • Erythema followed by spotty hyperpigmentation

    • Transient alopecia

  • Second degree

    • Erythema

    • Edema

    • Vesiculation

    • Exudation

    • Permanent loss of appendages

  • Third degree

    • Primary deep tissue necrosis

    • Acute painful ulcerations

Chronic radiodermatitis has a latency period of 2 years to decades, and its characteristics are as follows:[18]

  • Poikiloderma

  • Roentgen ulcers

  • Roentgen keratoses

  • Roentgen carcinoma

In the acute stage, the ear is erythematous and edematous and the patient typically presents with a raised solid (papular) eruption similar to erythema multiforme. However, the patient may also present with a pruritic hivelike (urticarial) eruption, a thickened skin (lichenoid) eruption, a blisterlike lesion (bullae), or bruise (purpura) on the ear. In rare cases, an exfoliative process with fever and arthralgias may be observed. Other types of dermatitis that may present subsequent to radiotherapy include pemphigus dermatitis, bullous pemphigoid, and morphea. The acute stage generally begins 6-12 days after initial therapy; however, latent periods as long as 3 weeks have been noted.

The chronic stage of radiodermatitis may present as poikiloderma, ulcers, keratoses, carcinoma, or a combination of these conditions. Dry atrophic skin with telangiectasias, mottled hyperpigmentation and hypopigmentation, and loss of appendages characterizes poikiloderma. Sharply defined central ulcers are covered with a necrotic, greasy, yellow eschar. Radiation-related ulcers may also be observed. These ulcers do not heal well. In 20% of patients, a hard infiltrate surrounds the ulcers. This infiltrate is carcinogenic and is referred to as roentgen carcinoma.

Late complications of radiation that affect the external ear are ORN and chondroradionecrosis. Clinically, ORN may manifest as an otitis externa refractory to antibiotic therapy. It often develops months to years following the completion of radiation.

Finally, radiation-related keratoses are precancerous tumors that resemble actinic keratoses. Features of chronic radiodermatitis usually follow second- and third-degree acute radiodermatitis and may not be apparent for years following therapy. Occasionally, deep radiation may sensitize the skin, triggering an acute radiodermatitis upon subsequent x-ray exposure. This phenomenon is rare and occurs only once in every 5000 patients who receive deep radiation.

History and physical examination are the main diagnostic tools. Atrophy of the epidermis, hyalinized and irregularly stained collagen, and telangiectasia of dermal vessels histologically characterize chronic radiodermatitis. In addition, atypical dendritic cells that express antibodies to factor XIIIa are observed in the dermis.

In addition to conductive hearing loss, sensorineural hearing loss is also often seen as a side effect of radiation to the nasopharynx or parotid. The loss may be related to the effects of radiation on the cochlea rather than retrocochlear pathways.

Treatment in the acute stage consists of emollients. In the case of secondary infection, immediately initiate appropriate antibiotic therapy and debride devitalized tissue as necessary. Treatment of ORN or chondroradionecrosis includes systemic antibiotics, debridement of devitalized tissues (including mastoidectomy if temporal bone is involved), and adjunctive hyperbaric oxygen treatment.



Seborrheic dermatitis

Seborrheic dermatitis is the most common skin disorder. It is a chronic inflammatory disorder that affects 3% of the population and has a familial predisposition.[19] Peaks of onset occur in infancy and old age. Although seborrheic dermatitis is not a disorder of sebaceous glands, this condition is most commonly found in the distribution of these glands. The etiologic agents, lipophilic yeasts Pityrosporum ovale and Pityrosporum orbiculare (also known as Malassezia furfur), have an affinity for sebum-rich environments. As a result, conditions characterized by increased oil production, such as Parkinson disease, Down syndrome, and other neurologic conditions, are associated with more severe disease.

Lesions are well-marginated, noncircumscribed, nonelevated regions and appear mildly erythematous in muted shades of pink and orange. Lesions are covered with a characteristic powdery or greasy scale, and the underlying skin may have a serous, crusty quality. The scalp, face, and ears are most commonly affected. Other areas of the body may also be involved.

The ear is usually involved as part of a larger process that involves the scalp, eyelids, forehead, T-zone, and alae nasi. Lesions may affect any part of the ear, including the concha, external meatus, scaphoid fossa, and postauricular regions. Scales may appear branny, diffuse, and flaky. Postauricular thickening, excoriation, and fissuring are often observed. Lesions typically have a symmetric distribution.

The disease is a lifelong process characterized by exacerbations and remissions. Common triggers include physical and emotional stress, eruptions caused by drugs (eg, gold), and diets deficient in vitamin B.

History and physical examination help to make the diagnosis. Potassium hydroxide preparations, fungal cultures, or both may be performed to rule out other causative agents such as tinea. Parakeratosis, follicular spongiosis, and perifollicular lymphocytic infiltration histologically characterize these lesions. Differential diagnoses include psoriasis, neurodermatitis, tinea capitis, tinea faciei, histiocytosis X, favus (infection with Trichophyton schoenleinii) pemphigus, pemphigoid, and Hailey-Hailey disease.

Treatment of ear seborrhea is similar to that of the scalp and includes medicated shampoos that contain zinc pyrithione, coal tar, selenium sulfide, or ketoconazole. A 2% ketoconazole gel (Xolegel) was recently introduced on the market. In addition to its antifungal effects on Malassezia, the gel has antibacterial, anti-inflammatory, sebostatic, and antiproliferative characteristics that make it a particularly promising treatment. Dermatitis may also be treated with warm saline compresses, mild topical corticosteroids, ketoconazole cream, or sulfur ointments. Avoid long-term use of fluorinated corticosteroids because rosacealike acne, atrophy, and telangiectasias may result.

Darier disease

Darier disease is also known as Darier-White disease or keratoses follicularis. This disease is inherited as an autosomal dominant disease with variable penetrance. It typically presents in late childhood or early adulthood and has no race or gender predilection.

Fleshy, circumscribed, solid skin elevations (papules) characterize the disease. These lesions progress to crusty, yellow, or brown papules and later coalesce to form irregular warty papules. The lesions are distributed over the seborrheic areas of the trunk, the hands, and the scalp. Papules are often present on the ears. Papules may also be noted on the mucous membranes of the oral cavity, pharynx, and female genitalia.[20, 21]

The genetic defect has been localized to the ATP2A2 gene on chromosome 12. The sarco/endoplasmic reticulum Ca(2+) ATPase of patients with Darier Disease is altered. This leads to abnormal intracellular Ca(2+) signaling that results in a decrease of cell adhesion and a promotion of cellular apoptosis. Although the ATP2A2 gene is expressed in many types of cells throughout the body, the disease is limited to skin. Electron microscopy evidence suggests that a tonofilament-desmosome complex defect exists. This defect is an important finding because processes that are dependent on Ca(2+) play a role in the interactions of desmosomal cadherins, submembranous plaque proteins, and cytokeratin filaments.

Hormonal factors, steroids, and seasonal factors, especially sun exposure, may trigger or exacerbate symptoms. Individuals with Darier disease have an increased susceptibility to viral and chronic pyogenic infections. Natural history of the disorder is one of chronic relapses.

Differential diagnosis includes diffuse infective otitis externa. Biopsy of the lesion can assist with making a definitive diagnosis. Histologic features include acanthosis, hyperkeratosis, parakeratosis, papillomatosis, suprabasilar clefting, dyskeratosis with corps ronds, and a chronic patchy inflammatory infiltrate in the dermis.

Treatment of Darier disease consists of bland emollients and sunscreens in mild cases and topical or oral aromatic retinoids (eg, etretinate, isotretinoin) in severe cases. Encourage all patients to avoid sun exposure whenever possible. Finally, treat secondary infections with appropriate antibiotics.

Granuloma faciale

Granuloma faciale is a very rare chronic disorder believed to be a variant of lymphocytoblastic vasculitis confined to the skin. The disease most commonly affects middle-aged white men. However, the disease has also been reported in Africans, Asians, and women.

Flesh-colored to brown-red or purple flat discolorations of the skin (macules), small circumscribed elevations (papules), nodules, and plaques characterize the disease. The lesions range from soft to firm in consistency and are sharply demarcated. Surfaces of the lesions may have signs of telangiectasis or scaling. Although the lesions typically do not cause symptoms, some patients may experience burning, itching, or tenderness. The lesions are typically located on the face, especially on the nose, forehead, or cheeks. The lesions may be rarely observed on the ears and in the preauricular region. Sunlight and heat may exacerbate the lesions. The natural course of the disease is slow, progressive growth of the lesions; however, lesions have been noted to involute spontaneously.

History and examination of the characteristic lesions are the main diagnostic tools. Laboratory test results are typically normal and do not assist in the diagnosis. Biopsy and microscopic examination of the lesions help to make a definitive diagnosis. Histopathologic features include a flattened epidermis with a narrow Grenz zone, a dense inflammatory infiltration of the dermis, and leukocytoclastic vasculitis. The infiltrate is typically composed of eosinophils and neutrophils but may also include lymphocytes, histiocytes, plasma cells, and mast cells. Differential diagnoses include sarcoidosis, discoid lupus erythematosus, benign lymphocytic infiltration of the skin, and lymphoma.

Medical treatment modalities include dapsone, clofazimine, antimalarials, and corticosteroids (topical, intralesional, systemic). Surgical options include laser excision (eg, carbon dioxide or argon), surgical excision, dermabrasion, superficial ionizing radiation, cryotherapy with liquid nitrogen, and electrodesiccation. UV light and topical psoralens have also been used with some success. One study has shown that cryotherapy with liquid nitrogen followed immediately with injection of intralesional corticosteroids is the most effective treatment.[22]

Granuloma annulare

Granuloma annulare is an inflammatory disorder of unknown etiology. Solitary or multiple nodules and papules, occasionally in an annular pattern, characterize this skin condition. The disease usually presents in persons older than 40 years and has a 2:1 female-to-male ratio.

Patients typically present with lesions on the dorsum of the hands, wrist, feet, ankles, and knees. The ears may also be affected. The lesions may take any of 3 different forms: (1) a ring of small, circumscribed, solid, skin elevations (papules), which coalesce to form larger differentiated areas (plaques); (2) ring plaques without papules that may have raised, beaded, ringlike (annular) borders; and (3) symmetrical scattered papules in a nonannular pattern. Pruritus is present in more than two thirds of cases.

Sunburns, eruptions caused by drugs, insect bites, tuberculin tests, skin injuries, and viral infections (especially HSV and Epstein-Barr virus [EBV]) may trigger the disease. One account of granuloma annulare was reported to occur after an octopus bite.[23] The disease has been associated with diabetes mellitus or malignancy in 20% of cases. Typically, the lesions resolve spontaneously, usually within 2 years of onset. In some cases, however, the lesions may persist for years. Recurrence is uncommon.

Laboratory abnormalities, although nonspecific, may support the diagnosis. The most common findings are hypercholesterolemia (17%), hypertriglyceridemia (20%), positive antinuclear antibody (ANA; 56%), and elevated immunoglobulin G (IgG) levels (14%).[24] Biopsy of the lesion also can assist in diagnosis. The disease process is specific to the dermis. Lymphohistiocytic granuloma with varying degrees of necrobiosis (degeneration of connective tissue) histologically characterizes the lesion. Epithelioid cells, multinucleated giant cells, and mucin deposits may also be noted.

The differential diagnoses list is extensive and includes granulomatous diseases (eg, sarcoidosis, gout, leprosy, tuberculosis, syphilis) tinea, erythema annulare centrifugum, and rheumatoid nodules. Treatment consists of topical corticosteroids with occlusion or intralesional injection of corticosteroids.

Angiolymphoid hyperplasia with eosinophilia and Kimura disease

Angiolymphoid hyperplasia with eosinophilia (AHE) and Kimura disease are 2 closely related diseases that typically affect the scalp, face, and neck. Angiomatous plaques or nodules that are commonly found in the external auditory meatus, pinna, and retroauricular regions characterize these diseases. Pathogenesis of these diseases is unknown, but a form of benign vascular tumor and an immunologic reaction to injury have been theorized as possible etiologies. These diseases may also develop in response to local arteriovenous shunts or neoplasms. Based on histologic findings, some authors suggest that the two are distinct entities in which Kimura disease is a chronic, allergic inflammatory disease and AHE a benign vascular proliferation.[25]

Kimura disease, first noted in the Japanese population, is a variant of AHE that predominantly affects men (85%) of Asian ethnicity during the second and third decades of life. However, AHE predominantly affects white women (70%) during the fourth to sixth decades of life. The diseases may be associated with pregnancy.

Solitary or multiple vascular nodules and plaques that are dull red or plum-colored characterize the disease. These nodules and plaques are tender, pruritic, and bleed easily. Superficial lesions that affect mostly subcutaneous tissue measure 0.2-1 cm in diameter, while deeper dermal lesions may grow as large as 5-10 cm. Although the lesions are most commonly found around the ear, involvement of the orbit, lacrimal gland, oral mucosa, and parapharyngeal spaces has been reported. Peripheral eosinophilia, more commonly noted in Kimura disease, is a supportive finding but is not essential to making the diagnosis.

A biopsy of the lesion helps to make a definitive diagnosis. Histologic findings consistent with both AHE and Kimura disease include vascular proliferation and perivascular infiltration of lymphocytes, histiocytes, plasma cells, and eosinophils. In Kimura disease, the endothelial cells of the blood vessels are flat. In AHE, the endothelial cell lining of the vascular channels resembles epithelial cells with large nuclei and abundant cytoplasm. Kimura disease is characterized by multiple lymphoid follicles with germinal centers with massive eosinophilic infiltration and even eosinophilic abscesses. By comparison, AHE is characterized by more diffuse lymphoid infiltration and only occasional follicles. Table 3 provides a comparison of the 2 diseases.

Table 3. Kimura Disease Compared With Angiolymphoid Hyperplasia With Eosinophilia (Open Table in a new window)


Kimura Disease




Male predominance (85%)

Second to third decades of life


Female predominance (70%)

Fourth to sixth decades of life


Larger in size

Subcutaneous and deeper tissue involvement

Little or no overlying skin changes

Smaller in size

More superficial

Involvement of overlying epithelium


Frequent finding

Less common

Peripheral eosinophilia

Frequent finding

Less common


Flat endothelial cell lining

Lymphoid follicles with massive eosinophilic infiltration and eosinophilic abscesses

Endothelial cell lining resembles epithelial cells

Diffuse lymphoid infiltration, variable eosinophilic infiltration

Differential diagnoses of the 2 diseases include pyogenic granuloma, follicular mucinosis, atopic dermatitis, persistent reaction to an insect bite, Kaposi sarcoma, pseudolymphoma, eosinophilic granuloma, granuloma faciale, lymphoma, malignant angioendothelioma, and capillary angiomatosis with inflammation.

In rare cases, Kimura disease and AHE may resolve spontaneously. Generally, the lesions progress slowly, with occasional secondary infection. Therapeutic options include radiotherapy, corticosteroids (topical, intralesional, systemic), argon laser ablation, sclerosing injections, cryotherapy, intralesional vinblastine, etretinate, acitretin, and pentoxifylline. The most effective treatment is surgical excision of the tumor or tumors. Although effective, surgical excision is associated with a recurrence rate of 33-50%. Mohs surgery may be a more effective alternative. Recent reports suggest success with topical tacrolimus (an immunosuppressant) as well as with intralesional bleomycin.

Juvenile spring eruption of the ears

Juvenile spring eruption of the ears (JSE), a photodermatosis, primarily affects boys aged 5-12 years. This disorder typically appears in the spring following the first intense sun exposure and may persist through the summer. Often, a history of JSE in other family members, typically fathers and brothers, suggests a familial predisposition. It may affect as many as one in 10 families. Outbreaks of children as well as military personnel have been reported. Although the prevalence is higher in boys, girls also may be affected. However, girls' ears are often protected from the sun by their hair. No association has been found between a predisposition to JSE and skin type, hair color, time spent in the sun or use of protective factors such as sunscreen or a hat.

Triggered by sunlight or a combination of sunlight and cold air, JSE manifests as pruritic, erythematous, circumscribed solid elevations (papules) that progress to small (< 0.5 cm), fluid-filled lesions (vesicles) or even blisterlike lesions (bullae). Within 1-2 weeks, the vesicles crust over and heal with minimal or no scarring.

Lava et al, in reviewing a series of JSE outbreaks, found that symptoms typically involved itching and diffuse erythema of both ears beginning in the evening after a cold, sunny day, with papules or blisters developing within 24-48 hours.[26]

History and physical examination are typically the main diagnostic tools for JSE. Laboratory test results, such as serum, urine, or stool porphyrin levels, and ANA, are normal. Thus far, UV light challenges have proven unsuccessful in reproducing the lesions.

Skin biopsy, although not routinely performed, may be of some assistance in making the diagnosis. Subepidermal vesiculation and a dense, perivascular, and periadnexal lymphohistiocytic infiltration of the dermis are histologic characteristics of the disease. The lymphocytic infiltration is typically composed of CD4+ and CD8+ cells. A purely mononuclear cell infiltrate has also been reported. Histologically and immunohistologically, the lesions are similar to polymorphic light eruption (PLE), suggesting that JSE may actually be a localized variant of PLE.[27] In fact, several accounts of the subsequent development of PLE in individuals who at one time had JSE have been reported. Differential diagnoses include other photodermatosis, erythema multiforme, lupus erythematosus, bullous disorders, hydroa vacciniforme, actinic prurigo, and porphyrias.

Currently, no treatment is recommended for JSE because the disorder is self-limiting. However, treatment with topical steroids and oral antihistamines may be beneficial in patients with extreme pruritus.