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14.2.5 Relapsing Polychondritis
In relapsing polychondritis, an autoimmune disease, the body attacks its cartilage
proteoglycans and develops antibodies against the cartilage matrix as well as native
and denatured type II collagen. The average age of onset is in the 50s, and there is
no racial or sexual orientation bias. A hormonal element may trigger the disease, but
the exact cause is unknown.
Joints, the respiratory system (e.g., larynx, trachea, and bronchi), the cardiovascular system (e.g., blood vessels, heart valves), and the head and neck (e.g., ears,
nose, and Eustachian tube) are typical sites of systemic cartilage loss in this disease (1).
Recurrent auricular chondritis can cause long-term damage to the external ear,
which is damaged in up to 88% of cases. In cases of recurrent polychondritis, one
or both auricles may become infected with cellulitis. Because of the lack of cartilage, the earlobes are usually spared. Conductive hearing loss can occur when the
cartilage of the external ear canal is damaged. In contrast, sensorineural hearing
loss, vertigo, or tinnitus can be caused by damage to the anatomy of the inner ear [1].
Arthropathy follows as the second most prevalent symptom of relapsing polychondritis after articular chondritis. Small and large joints are equally affected by
arthropathy, which is nonselective. In addition, the disease is usually seronegative,
asymmetric, and migratory. The presence of rheumatoid factor (RF) can occasionally be detected. However, a concurrent diagnosis of rheumatoid arthritis may be the
reason for this nding.
Nearly 25% of people with recurrent polychondritis go on to develop another
autoimmune disease. These include rheumatoid arthritis, Sjögren’s syndrome,
ulcerative colitis, pernicious anemia, Hashimoto’s autoimmune thyroiditis, myasthenia gravis, and systemic lupus erythematosus [1].
According to a study by Tanaka etal. of 11 patients with ocular inammation
associated with recurrent polychondritis, most individuals had auricular chondritis.
The study included nine cases of scleritis and two cases of anterior uveitis [11].
Laboratory ndings such as mild anemia and a higher erythrocyte sedimentation
rate may support the diagnosis. Detectable antibodies to type II collagen are present
in 30–60% of individuals in the early stages of the disease. Additional tests may be
ordered in cases with clinical suspicion of related disorders, including blood tests
for thyroglobulin antibodies (anti-TG) and microsomal antibodies especially antithyroid peroxidase (anti-TPO), RF, antinuclear antibodies (ANA), and cholinergic
receptor antibodies [1].
Although laboratory tests may be helpful, clinical examination is usually sufcient for diagnosis.
The presence of at least three of the following symptoms or indicators is necessary for a diagnosis, as outlined by the McAdam criterion [1]:
• Bilateral auricular chondritis
• Nasal chondritis
• Nonerosive seronegative inammatory polyarthritis
314
• Ocular inammation
• Respiratory chondritis
• Cochlear or vestibular damage or both
If there is clinical doubt, a cartilage biopsy may be helpful. Hematoxylin and
eosin staining gives the cartilage a very pink color (blue hematoxylin and eosin [H
and E] staining indicates normal cartilage). Neutrophil inltration is the most common histologic nding early in the disease process. Histologic evidence of disease
progression includes neutrophil, eosinophil, and lymphocyte inltration of perichondrial and cartilaginous tissue, cartilage matrix degeneration, and brosis [1].
Two patients had deposition of immunoglobulin C3 complex at the chondrobrous junction as shown by immunouorescence examination of the tissue.
Treatment includes systemic corticosteroid agents, nonsteroidal anti-inammatory
drugs (NSAIDs), or colchicine. In addition to dapsone and methotrexate, other
effective therapies include cyclosporine, cyclophosphamide (CP), mycophenolate
mofetil (MMF), and azathioprine (AZA). Anti-tumor necrosis factor (TNF) agents,
namely iniximab, have been used successfully in the treatment of relapsing polychondritis [12].
M. Kar et al.
14.2.6 Gout
Tophi (deposited uric acid) should be considered as a possible differential diagnosis
in the helix, even if you do not have conventional articular gout. Rarely, histopathologic and crystal studies can distinguish these lesions from malignancy [13]. White
papules on the helix characterize tophi; additional physical examination and history
may help determine whether gout is present.
14.3 Traumatic Disorders
14.3.1 Irritant Contact Dermatitis
There is a dose-dependent reactivity to chemicals in soaps, household cleaners, turpentine, solvents, detergents, and acidic solid and alkaline compounds that can
cause irritant contact dermatitis. These compounds are toxic when they come in
contact with the skin. Soaps, shampoos, and jewelry cleaners contain chemicals that
are more likely to irritate the ears [1].
Primary diagnostic methods include obtaining a patient’s medical history and
visual inspection of the lesions. Irritant contact dermatitis is often characterized by
redness, swelling, small uid-lled lesions called vesicles, and larger blister-like
lesions called bullae. These symptoms are similar to those of allergic contact dermatitis. Keep in mind that allergic contact dermatitis is ve times as common as irritant
contact dermatitis when evaluating lesions. In very rare cases, patch testing may be
helpful in reaching a diagnosis. Patch testing involves applying typical irritants in
14 External Ear Tract Diseases
315
the form of patches to the skin and observing the reaction. But patch testing can
only go so far. Crucially, the level of exposure in the test cannot mimic the actual
level in the clinic. Therefore, the results need to be more accurate [1].
14.3.2 Phototoxic Dermatitis
Phototoxic dermatitis, or Berloque dermatitis, can affect sun-exposed skin on the
face, upper chest, neck, hands, forearms, and legs. This type of dermatitis is not
immune-mediated. The same factors that cause photoallergic dermatitis, whether
ingested or applied topically, also contribute to this condition. However, unlike photoallergy, the agents do not interact with skin proteins. In most cases, UV-Aabsorbing polycyclic compounds are the agents of choice [1].
Ingestion of certain plants and fruits, such as psoralens or furocoumarins, and
certain medications may cause phototoxic dermatitis rather than photoallergy. These
drugs include thiazides, tetracyclines, sulfonamides, phenothiazines, griseofulvin,
chlorothiazines, nalidixic acid, sulfonylureas, and coal tar. The ear is the most typical site of psoralen involvement. Edema in the ears of mice exposed to sunlight is a
side effect of topical quinolones [1].
Post-inammatory hyperpigmentation of the affected areas may help resolve the
lesions, which appear as red streaks. The primary diagnostic techniques for photoallergic dermatitis are history and physical examination. Patch testing may also be
helpful [1].
As part of treatment, it is best to stay out of the sun and away from the offending
substance. If the patient must be in the sun, tell them to wear long sleeves, long
pants, a hat, and sunscreen. Topical corticosteroids and cold compresses may help
relieve symptoms [1].
14.3.3 Phototrauma
Phototrauma, also known as sunburn, is characterized by redness and swelling of
the skin after exposure to ultraviolet light from the sun, tanning beds, or other
sources. The outer layer of the skin absorbs ultraviolet radiation from the sun, primarily UV-B and UV-C.In contrast, UV-A rays from tanning beds can penetrate the
dermis at a concentration ve times higher than natural sunlight. All three types of
ultraviolet light can damage the skin. Sunlight is essential between 11a.m. and
3p.m., even on cloudy days, disproving a common myth. On an overcast day, UV
exposure is reduced by only 20–40% [1].
People with red or blonde hair and fair complexions are most susceptible to photodamage. The severity of sunburn depends on several variables, including the victim’s skin type, the duration and intensity of sun exposure, and other environmental
conditions. Mild skin redness and swelling, blistering (bullae), crusting, and ulceration are all possible lesions. Itchy, irritated, or painful skin may occur. Because of
316
their location on the head, the ears are often the rst to be affected. They are also
often overlooked when applying sunscreen [1].
M. Kar et al.
14.4 Infectious Diseases
14.4.1 Otitis Externa
A condition known as otitis externa (OE) can affect either the EAC, the auricle, or
sometimes both which undergo a process of inammation or infection [14–17]. This
condition affects people of all ages [18].
14.4.1.1 Background
Otitis externa (OE) refers to inammation or infection of the EAC or both the pinna
and EAC [15–17]. It affects people of all ages and is relatively common [18]. Acute
bacterial infections of the epidermis of the external ear canal, most commonly
caused by Staphylococcus aureus or Pseudomonas aeruginosa [19], are the most
common cause of OE.However, viruses, fungi, or other bacteria can also cause this
condition.
Infection with EAC and subsequent OE may be caused by several things, including [20];
• Lack of earwax
• High levels of humidity
• Water trapped in the ear canal
• Elevated temperature
• Local trauma (e.g., traumatic poking with nger, use of cotton swabs, ball-head
pins, pencils, or during the use of hearing aids)
Repeated immersion in water washes away cerumen and dries out the EAC, making aquatic athletes more susceptible to OE.Accumulation of germs and fungi, as
well as skin maceration, can result from water remaining in the ear canal. Summer
is the peak swimming season [18, 20], and OE is more common in tropical regions
[21]. People with allergies such as eczema, allergic rhinitis, or asthma are also more
likely to experience OE [14, 22, 23].
While OE infections rarely cause long-term problems or signicant disability,
they can cause severe pain and short-term health problems (see Presentation).
Although most cases are cured without sequelae with prompt diagnosis including
workup for differential diagnosis and appropriate therapy (see Management), susceptible individuals, such as those with diabetes, compromised immune systems, or
who do not receive treatment, may develop necrotizing (malignant) OE.This infection can be fatal [14, 24].
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14.4.1.2 Anatomy
Elastic cartilage forms the auricle, and the skin covering it is attached to the perichondrium. Hillocks of the auricle begin to form in the sixth week of gestation from
the consolidation of the rst and second branchial arch mesodermal cells. Hill number three is a product of the rst arch, while hills number two, three, and four are all
products of the second arch. By the 20th week of gestation, the auricle takes on an
adult form, although it takes until nine years old to reach full adult size [14, 25].
At eight weeks of gestation, the EAC begins to take shape as the ectoderm lining
the rst pharyngeal cleft thickens and develops toward the middle ear. Beginning at
21weeks of gestation, this central layer of tissue begins to resorb, eventually forming a lled canal by 28weeks. By the time a child reaches nine years of age, the
canal is fully ossied and has grown to adult size. The EAC has anterior, anteroinferior, posterior, and superior connections to the mandibular fossa, parotid gland,
mastoid air cells, and middle cranial fossa, respectively [14].
The EAC is around 2.5cm in length in adults and is lined with squamous epithelium. It shields nearby structures from external inuences and environmental
changes while transmitting sound waves to the middle ear. The superior and posterior thirds of the canal are predominantly cartilaginous, while the inferior and anterior two thirds are bony and covered with thin, tightly adherent skin; neither the
apocrine glands nor the hair follicles are present in this portion of the canal [14].
Around the base of each hair follicle, apo-pilosebaceous units consisting of apocrine and eccrine glands secrete their products through the thicker skin covering the
outer (cartilaginous) portion of the EAC.Sloughed squamous epithelium (cerumen)
and these secretions coat the EAC and keep its pH acidic [4, 5]. As it moves laterally
from the EAC isthmus, this cerumen cover protects the underlying epithelium from
skin breakdown and maceration due to its waxy composition. Individuals produce a
wide range of cerumen [14].
The acidic nature of cerumen has an inhibitory effect on bacterial and fungal
growth. Because the EAC is constantly exposed to water, an excess of cerumen can
create an excellent habitat for bacterial invasion by giving rise to retaining water and
debris, whereas a deciency of cerumen allows bacteria to proliferate. In addition,
bacteria can enter the ear canal directly from localized damage caused by foreign
objects introduced into the ear. When an infection becomes established, it causes
inammation and localized bleeding, resulting in symptoms [14].
14.4.1.3 Classification
The following 14 categories apply to OE:
The two most common types of OE are acute diffuse OE, which is common
among swimmers, and acute localized OE, also called as furunculosis, which is
actually the infection of the hair follicle.
• Prolonged OE (> six weeks)—Similar to acute diffuse OE, but lasts longer.
• Eczematous OE includes a number of dermatologic conditions that can infect the
EAC, including eczemas such as atopic dermatitis or dermatitis associated with
psoriasis or systemic lupus erythematosus.
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M. Kar et al.
• Necrotizing OE, also known as malignant OE, is an aggressive infection that
spreads to deeper tissues adjacent to the EAC.This type of infection is most
common in adults with compromised immune systems, such as diabetics and
AIDS patients.
• Otomycosis, in which a fungus (such as Candida or Aspergillus) infects the
ear canal.
14.4.1.4 Signs andSymptoms
Pain when palpating the tragus (the area just below the ear canal) or pulling on the
auricle is the most obvious physical sign of OE.In addition, patients may experience the following symptoms [14];
• Otalgia—moderate to severe, usually worsens over a few days
• Loss of hearing
• Fullness or pressure in the ear
• Redness, swelling, and narrowing of the external ear canal
• Fever (in some cases)
• Tinnitus
• Itching (particularly with fungal OE or persistent OE)
• Severe, intense, deeper pain—alerting for necrotizing (malignant) OE especially
in immunocompromised patients.
• Otorrhea—initially clear, but quickly transforms into a malodorous purulent
discharge
• Cellulitis of the adjacent soft tissue in face and neck
• Lymphadenopathy in the ipsilateral side of the neck (rare)
• Symptoms on both sides (rare)
• Regular or past experience in or contact with water (such as swimming, surng,
or kayaking)
• History of ear trauma (often involving the use of cotton swabs or other foreign
bodies, or vigorous ear cleaning)
14.4.1.5 Diagnosis
Otoscopy, along with the patient’s history and physical examination, usually provides the clinician with all the information needed to diagnose OE.An otolaryngologist should rule out necrotizing OE in patients with severe ear discomfort who
are diabetic or immunocompromised [14].
Laboratory Testing
If the patient has a weakened immune system, standard treatments are not working,
or a fungal infection is suspected, laboratory tests may be helpful, although they are
not usually necessary. The following may be tested [14]:
• Gram staining and culture of any otorrhea from the affected ear canal.
• Blood glucose level.
• Urine dipstick test analysis.
14 External Ear Tract Diseases
319
Imaging Studies
Most cases of OE do not require imaging. However, radiologic studies may help
rule out mastoiditis or an invasive infection as encountered in necrotizing (malignant) OE.
Imaging studies may include the following [14]
• High-resolution computerized tomography (HRCT) is preferred over routine CT
due to its better ability to depict bony erosion [26]
• Radionuclide bone imaging (also known as bone scintigraphy)
• Gallium scan
• Magnetic resonance imaging (MRI)—Used less than other modalities; may be
needed when soft tissue extension is the primary concern or as a secondary sup-
port to other modalities [27].
14.4.1.6 Management
Most people with OE are treated empirically. First-line treatment includes
• EAC debris removal
• Pain management
• Topical medication administration to control acute inammatory signs such as
edema and suppress infection
• Avoidance of precipitating factors
Pharmacotherapy includes
• Topical medications such as hydrocortisone, acetic acid in aluminum acetate or
acetic acid otic solution,
• Analgesics, such as compounds like acetaminophen or codeine,
• Antibiotics, such as ciprooxacin and antifungals (e.g., clotrimazole solution
1%, nystatin powder) [14, 26].
• Surgical debridement of the ear canal is the gold standard treatment for fungal
infections. It is occasionally required for more severe cases of OE or when there
is a signicant amount of discharge. It is often reserved for necrotizing OE or its
sequelae (e.g., external canal stenosis).
• Abscess incision and drainage [14, 26].
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Auricula Tumors
15
MustafaAltıntaş, NurayBayarMuluk, andRajkoJovic
15.1 Introduction
Approximately “6–10% of all cutaneous malignancies” detected in the head and
neck region are auricular skin tumors [1–3]. The most common cancers found in
this area are basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) of
cutaneous origin. Malignant melanoma, Merkel cell carcinoma, Kaposi’s sarcoma,
and dermatobrosarcoma are some of the rarer histologic types that may be found
[4]. BCC is extremely rare in terms of metastasis. In contrast, SCC tends to metastasize at a relatively high rate and grows inltratively [5]. The most important things
that can cause skin cancer are environmental factors and ultraviolet radiation. Other
risk factors include skin scarring, burns, ulcers, immunosuppression, prior radiation
therapy, exposure to chemical agents, and human papillomavirus infection [6, 7].
The auricle is anatomically distinct and highly structured. It is critical to maintaining facial harmony. In addition, the auricle is part of the H-zone of the face,
also known as the mask area. For this reason, “high-risk” tumors develop on the
auricle [8–10]. In addition, the auricle has a higher risk of invasion and metastasis
for cutaneous malignancies compared to other sun-exposed areas [5]. Surgical and
non-surgical methods are the two primary categories into which many current
treatments for skin cancer fall. Because auricular skin malignancies are very
M. Altıntaş
ENT Department, Antalya Training and Research Hospital, Antalya, Türkiye
N. BayarMuluk (*)
Faculty of Medicine, Department of Otorhinolaryngology, Kirikkale University,
Kirikkale, Türkiye
R. Jovic
Faculty of Medicine, University of Novi Sad, Novi Sad, Republic of Serbia
e-mail: rajkojov@eunet.rs
© 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_15
323