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External Ear Tract Diseases
14
MuratKar, CemalCingi, andEleftheriosFerekidis
14.1 Introduction
The external ear, which includes the auricle laterally and external auditory canal
(EAC) medially, is composed of skin with its attached appendages and cartilage.
Like any other analogous tissue, the skin and cartilage of the ear can take a beating.
Therefore, other Medscape reference articles [1] describe some of the conditions
mentioned here in more detail.
The immune system responds to cell damage by causing inammation. Many
different things can cause inammation in the ear, but the most common fall into
three main categories: traumatic, immunologic, and viral. Infectious diseases of the
external ear are not discussed here as they are covered in other topics. Radiation
exposure [2], mechanical pressure from a telephone or headband, environmental
insults, or irritants such as chemical agents used to disinfect hearing aids can all
cause auricle inammation. Atopic and autoimmune diseases are examples of
immune-mediated inammation. For many conditions, the etiology may not be
obvious. Idiopathic conditions are included under the umbrella term “miscellaneous” [1].
M. Kar
Department of Otorhinolaryngology, Alanya Training and Research Hospital, Alaaddin
Keykubat University, Alanya, Türkiye
C. Cingi (*)
Faculty of Medicine, Department of Otorhinolaryngology, Eskisehir Osmangazi University,
Eskisehir, Türkiye
E. Ferekidis
Eugenidion Hospital, National University of Athens, Athens, Greece
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2024
M. T. Kalcioglu et al. (eds.), Otology Updates, Comprehensive ENT,
https://doi.org/10.1007/978-3-031-76173-7_14
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14.2 Immunologic andInflammatory Disorders
Inammatory or immunologic conditions affecting the ears may be localized, such
as contact dermatitis, or systemic, such as atopic dermatitis, psoriasis, relapsing
polychondritis, gout, or sarcoidosis [3].
14.2.1 Atopic Dermatitis
Intensely itchy, red skin lesions are the outward sign of a systemic disease called
atopic dermatitis or eczema [4]. Asthma, allergic rhinitis, and other atopic diseases
tend to run in families, and the condition typically appears in children. Recent
research suggests that an imbalance in the immune system, namely the dominance
of TH 2 cells (a subtype of helper T lymphocytes), may be the root of atopic dermatitis. Levels 4, 5, and 10 of interleukins are produced by TH2 cells. Th1 cells, the
primary immune cells in psoriasis, produce IFN-gamma and TNF-alpha.
Lesions may be red, scaly crusts or tiny, uid-lled vesicles that are outlined and
may coalesce into a large lesion. Also look for linear ssures, most commonly
around the ear. Although not exclusive to atopic dermatitis, white dermatographism
(the appearance of a white line after the area of skin lesion is lightly scratched) is a
hallmark of affected skin. Thickening and darkening of the skin are common results
of chronic scratching. Atopic dermatitis increases the likelihood of developing subsequent skin infections [1].
The external ear is typically affected as a subset of a larger facial and cervical
area. In children, lesions tend to appear on the face and other extensor surfaces; in
adults, they manifest on exural surfaces (such as the antecubital and popliteal fossae), eyelids, ears, hands, and feet. Some people with atopic dermatitis develop
auricular pseudocysts. These cystic lesions range in size from 1.5 to 3.5cm and
usually involve the anterior surface of the auricular pinna. Pseudocyst formation
may be accelerated in patients with atopic dermatitis due to stress caused by persistent scratching [1].
Certain foods in the diet, mental or emotional stress, changes in the environmental conditions, airborne allergens, and local skin irritants (some natural bers especially wool as well as synthetic bers) are common allergen triggers. In terms of
frequency of reaction, the most common culprits are wheat, eggs, peanuts, milk,
sh, and soy. Although atopic dermatitis and food allergies often occur together,
many factors contribute to the pathophysiology of atopic dermatitis in its early
stages, and skin dysfunction is likely to have a signicant impact [5]. In women,
symptoms may be triggered or worsened during menstruation and pregnancy [1].
The patient’s medical history and the specic location and appearance of the
pruritic lesions aid in the diagnosis. Elevated plasma histamine levels, elevated
immunoglobulin E (IgE) levels, and peripheral eosinophilia are all possible laboratory tests that may aid in the diagnosis. However, these tests can detect any atopic
disorder not just atopic dermatitis. Histologically, lesions show perivascular lymphocytic inltration and nonspecic intracellular edema [1].
14 External Ear Tract Diseases
309
A patch test can be performed to determine which allergens are present. This test
typically involves applying a commercially standardized allergen to a specic area
of skin, such as the back or arm. The next step is to look for signs of inammation
on the skin. In challenge testing, potential allergens are eliminated one at a time and
then reintroduced at 3-day intervals until an allergic reaction is induced, and the
allergen is identied. Challenge testing is the standard way to nd out what foods
people are allergic to. Psoriasis, neurodermatitis, seborrheic dermatitis, allergic and
irritant contact dermatitis, and others are among the possible differential diagnoses [1].
Topical corticosteroids, a phosphodiesterase type 4 inhibitor called crisaborole,
a macrolide antibiotic called tacrolimus, mild cleansers, and moisturizers are all
part of the treatment plan. There is evidence that topical tacrolimus reduces IgE and
interleukins (IL)-4, IL-5, and IL-8. As an immunosuppressive agent, the most common side effect is blistering of the skin. The adverse effects commonly associated
with systemic tacrolimus do not manifest because of its comparatively limited
absorption. Oral antihistamines are another option for treating pruritus in addition
to topical medications. Saline compresses and antibiotics, either topical or oral,
should be prescribed for secondarily infected skin lesions. In extreme cases, systemic corticosteroids can be administered. Lastly, people with moderate to severe
disease may benet from immunotherapy desensitization [1].
14.2.2 Allergic Contact Dermatitis
The delayed-type hypersensitivity reaction known as allergic contact dermatitis
occurs when an allergic person who has been previously sensitized is exposed to the
allergen. A contact allergen is formed when a skin protein forms a compound with
a simple, low-molecular-weight molecule. Re-exposure triggers an inammatory
response.
During the acute phase, the skin becomes red, swollen, and itchy. It shows signs
of exudation, crusting, small, raised, circumscribed lesions (papules), and blisters
that are lled with uid and leak. Secondary infection of the lesions may occur. The
chronic phase is characterized by thickening of the skin due to persistent rubbing or
scratching. Possible side effects include skin thickening (lichenication), ssuring,
and hyperpigmentation [1].
Many things that come in contact with the pinna, such as hair accessories, cosmetics, earrings, hearing aids, topical treatments, and cell phones can cause allergic
contact dermatitis of the external ear. Shampoos, hair dyes, and hair sprays typically
contain paraphenylenediamine, parabens, and quaternion-15, which can irritate the
conchae and periauricular areas. External canal contact dermatitis may be caused by
hearing aids made of rubber, vinyl plastic, or methyl methacrylate, as well as chemicals used to clean them. Topical aminoglycoside antibiotics (neomycin and related
preparations such as tobramycin or gentamicin) and topical anesthetics (e.g., benzocaine) are two examples of topical preparations that can potentially affect the
EAC [1].
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Nickel, cobalt, palladium, white gold, and yellow gold earrings are most likely to
cause lobule dermatitis [6]. Research from Denmark found a decrease in nickel
allergies after a similar program was implemented, leading to a new push in Europe
to reduce the amount of nickel in consumer products. The nal possible explanation
for preauricular or hemilateral auricular lesions is a chromium allergy, as chromium
is a metal commonly used for plating cell phones [7].
Allergen sensitization is more common in individuals with skin conditions such
as irritated, ulcerated, or inammatory skin. It is common for sore and inamed skin
in the external auditory canal, along the auricle, or both to be the result of an underlying medical condition when topical medications are recommended. Skin in the
canal may become more sensitive to materials used to make or clean hearing instruments with prolonged wear. Contact of the dermis with substances such as nickel or
gold promotes hyphenation in a newly pierced ear. Gold sodium thiosulfate earrings
may induce macrophage accumulation leading to extensive lymphocytic inltration
and development of pseudolymphoma in susceptible individuals. A violaceous,
non-tender lump on the earlobe may be a pseudolymphoma [1].
The patient’s medical history and the results of a patch or application test are
used to make the diagnosis. A small amount of an allergen is injected subcutaneously into a specic area, most often the back or arm, to perform a patch test. The
next step is to look for signs of inammation on the skin. To identify an allergen, the
patch test involves eliminating all potential triggers and reintroducing them one at a
time, about 3days apart, until an adverse reaction occurs. To rule out superimposed
infection, a complete workup includes these tests with Gram stain, bacterial cultures, potassium hydroxide preparation, and fungal cultures [1].
In highly unusual cases, a skin biopsy may be obtained to conrm the diagnosis
of the lesion. Histopathologic examination reveals a dense inltration of lymphocytic cells, small numbers of eosinophils, plasma cells, lymphoid follicles with germinal centers, and subcutaneous tissue and dermis. A variant called “lymphomatoid
contact dermatitis” is characterized by T-cell lymphocytic inltration, particularly
around blood vessels. This condition may be histologically and clinically similar to
mycosis fungoides and should be considered in the differential diagnosis. Infectious
eczematoid dermatitis, discoid lupus erythematosus, psoriasis, irritant contact dermatitis, seborrheic dermatitis, dermatophytosis, and angiolymphoid hyperplasia are
other possible differential diagnoses [1].
As a form of treatment, avoidance of the offending agent is essential. If a person
is allergic to hearing aids, they can be replaced with hypoallergenic silicone hearing
aids. To prevent an allergic reaction to earrings, it is recommended that stainless
steel earrings be worn until the ear canal is fully epithelialized. Epithelialization
typically takes three weeks. Lassar’s paste, aluminum acetate, Burow’s solution,
topical corticosteroids, cold saline or astringent compresses, etc., may be used to
relieve discomfort. Appropriate medications should be used promptly to treat secondary infections. Recent animal research has shown that allergic contact dermatitis
may be better treated by inhibiting IL-18 and IL-12 [1].
14 External Ear Tract Diseases
311
14.2.3 Photoallergic Dermatitis
Inammatory skin conditions such as photoallergic dermatitis, photodermatosis, or
solar urticaria can occur when a substance, often a drug, is photochemically
changed. It then behaves as a hapten and binds with skin or carrier proteins to produce an allergen. When a chemical is applied topically or taken orally, blue-violet
light (400–500nm) can change the material and trigger the reaction. Dermatitis is a
delayed or type IV hypersensitivity reaction which occurs after an essential sensitization phase priorly when the etiologic agent is a topical chemical [1].
Topical phenothiazines, sulfonamides, and halogenated salicylanilides (found in
soaps) are among the chemicals that can trigger the reaction. Although chemicals
are usually thought to be the culprits, there is some evidential data suggesting that
airborne allergens and sunlight can cause a similar reaction. It is not uncommon for
the etiologic agent to remain unknown [1].
Men are more likely to have photodermatosis of the ears. Most women wear long
hair to protect their ears from the sun’s rays. Lesions can take several forms, including scaly, inamed, raised lesions (eczematous plaques), uid-lled vesicles, and
erythematous, small, raised, localized lesions (papules). Lesions may resemble blisters (bullae). Itchy lesions usually go away on their own. In some people, the lesions
may persist for a long time, even years [1].
A diagnosis is made based on the patient’s history and physical examination
ndings. A photopatch test may be performed to conrm the diagnosis.
Sulfonamides, phenothiazines, or para-aminobenzoic acid are compounds in the
conventional patch that is applied for 24hours. The patch is then exposed to 5–15J/
m2 of UV-A light and measured again after 48hours. An area of skin treated with
a non- irradiated patch and another area exposed to UV-A light are used to compare
the patch test. Other possible diagnoses include porphyria, phototoxic dermatitis,
atopic dermatitis, contact dermatitis, and lupus erythematosus [1].
The mainstay of treatment is to stay out of the sun and away from the etiologic
agent. For additional symptom relief, topical corticosteroids or cold saline compresses with tap water may be tried [1].
14.2.4 Psoriasis
Psoriasis is an autoimmune chronic inammatory skin disease affecting 2–5% of
the population. There is evidence that psoriasis may be inherited with an autosomaldominant trait with partial penetrance; one third of patients with the disease have a
family history. The disease typically manifests in adolescence and shows no sexual
preference. Psoriasis is a chronic skin condition that can are up and go into remission. However, it can sometimes clear up on its own [1].
Pink, itchy lesions are common. A silvery, adherent scale may surround erythematous, circumscribed, differentiated lesions (plaques) that appear on the skin.
Lesions often tend to present in groups and coalesce to form larger sized plaques.
The skin surrounding the plaques may be paler. Because it is also seen in seborrheic
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and actinic keratoses, Auspitz sign, or punctate bleeding that may occur when the
scale is scratched or removed, is not pathognomonic. The condition also presents
with Köbner’s phenomenon, which is the formation of lesions due to minor trauma.
Different types of psoriasis can manifest in different ways; some examples are
guttate, pustular, exfoliative erythrodermic, and inverse. The elbows, knees, scalp,
anogenital area, and nails are the most typical areas affected by psoriasis, but it can
manifest anywhere on the body. At least one external ear involvement occurs in 18%
of individuals, disproportionately affecting those with signicant scalp involvement. The most commonly affected areas of the ear include the periauricular skin,
the auricular conchae, and the external auditory meatus. In addition to the potential
for very itchy ears, the accumulation of scaly lesions in the EAC can reduce hearing
ability. Women are more likely than men to have ear involvement, and people
between the ages of 10 and 29 account for about half of all cases [1].
Psoriasis can present in a variety of ways, including typical skin, nail, and joint
lesions. Thickened distal nail plates, nail separation and pitting, and yellow or white
opacities (oil spots) may be seen in up to 30% of patients. Finally, joint involvement
occurs in approximately 5% of cases.
In a prospective study carried out at two university hospitals in Spain, 188
(18.8%) of 1000 patients with psoriasis of the EAC were reported by Galache etal.
According to the researchers, involvement of the scalp, nails, and genitalia, inverse
psoriasis and severe psoriasis was associated with this disease manifestation.
Neither obesity nor psoriatic arthritis was found to be associated [8].
A patient’s history and physical examination are the primary tools for diagnosing
psoriasis. Laboratory tests usually do not provide further information. In rare cases,
a skin biopsy may be necessary. Histologically, psoriasis manifests as hyperkeratosis, parakeratosis, acanthosis, neutrophilic microabscesses (Munro’s microabscesses), thinning of the epidermis overlying the dermal papillae which is the layer
called as suprapapillary plate, and dilated and tortuous supercial dermal arteries
with supercial lymphocytic perivascular inltration [1].
The differential diagnosis includes onychomycosis, excoriated neurodermatitis,
and seborrheic dermatitis. While psoriasis and seborrheic dermatitis may appear
similar, the latter is typically less erythematous and has oily and disorganized scales.
The face is a less common site for psoriasis [1].
Various treatments are available, including non-occlusive topical corticosteroids,
calcipotriene, topical anthralin, oral psoralens and ultraviolet therapy, topical retinoids, and a combination of coal tar and ultraviolet therapy (the Goeckerman regimen). Methotrexate, hydroxyurea, cyclosporin, aromatic retinoids (e.g., etretinate),
and sulfasalazine may provide short-term relief in extreme cases when administered
systemically. Systemic corticosteroids may help for a while, but you should stay
away from them because they make the situation worse after the patient stops taking
them. Patients with diabetes who took thiazolidinedione rosiglitazone showed
improvements, with one patient reporting the complete disappearance of plaques
from her ears and body [9]. A new large study of rosiglitazone and placebo found no
difference in efcacy [10].