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Current Otolaryngology > XII. External & Middle Ear > Chapter 47. Diseases of the External Ear >
| Diseases of the External Ear: Introduction Anatomy Morphology The pinnae of the external ear are bilaterally symmetric elastic cartilaginous frames that aid in focusing and localizing sound. Each pinna is anchored to the cranium by skin, cartilage, the auricular muscles , and extrinsic ligaments. The anatomy of the pinna is illustrated in Figure 471. The external auditory canal (EAC) is typically 24 mm in length with a volume of 12 mL. The lateral third of the canal is made of fibrocartilage, whereas the medial two thirds are osseous. During early childhood, the canal is straight, but takes on an "S" shape by the age of 9. The EAC has an important relationship with the mastoid segment of the facial nerve , which lies posterior to the EAC as it descends toward the stylomastoid foramen. The temporomandibular joint is anterior to the EAC, and disease processes affecting this joint may lead to otalgia. Skin The EAC is lined by stratified squamous epithelium that is continuous with the skin of the pinna and the epithelial covering of the tympanic membrane . The subcutaneous layer of the cartilaginous portion of the canal contains hair follicles, sebaceous glands, and ceruminous glands, and is up to 1 mm thick. The skin of the osseous canal does not have subcutaneous elements and is only 0.2 mm thick (Figure 472). The epithelium of the EAC has the capacity to migrate laterally, allowing the canal to remain unobstructed by debris. The rate of epithelial migration is 0.07 mm/d and is thought to occur at the basal cell layer.
The ceruminous glands are modified apocrine sweat glands surrounded by myoepithelial cells ; they are organized into apopilosebaceous units (Figure 473). Cerumen prevents canal maceration, has antibacterial properties, and has a normally acidic pH, all of which contribute to an inhospitable environment for pathogens. Innervation The pinna is innervated laterally, inferiorly, and posteriorly by the great auricular nerve (cervical plexus). Arnold's nerve (a branch of the vagus nerve) innervates the inferior bony canal, the posterosuperior cartilaginous canal, and corresponding segments of the tympanic membrane and the cymba concha. The posterosuperior bony EAC is innervated by branches of the facial nerve. The auriculotemporal branch of V3 supplies the anterior portion of the pinna. The glossopharyngeal nerve contribution to the external ear is not well delineated. Lymphatic Drainage The anterior and superior wall of the EAC and tragus are drained by the preauricular lymph nodes. The infra-auricular lymph nodes drain the helix and the inferior wall of the EAC, whereas the concha and antihelix are drained by the mastoid nodes. Vascular Supply The posterior auricular artery and the superficial temporal artery arise from the external carotid artery and supply the auricle and lateral EAC. The deep auricular branch of the maxillary artery supplies the more medial aspects of the canal and the external surface of the tympanic membrane. The posterior auricular and superficial temporal veins drain the external ear. Physiology The external ear aids in the efficient transmission of sound to the tympanic membrane by serving as a functional resonator and, in particular, boosts transmission in the speech frequencies. The hairs in the later canal, as well as the depth and tortuosity of the EAC, protect the tympanic membrane and structures of the middle ear. Embryology The mammalian ear is divided into external, middle, and inner ear components , which differ in their embryologic origin (Figure 474). The external ear consists of the pinna, the EAC, and the tympanic membrane, is embryologically derived from the first and second branchial arches, and includes both ectodermal and mesodermal components. The mesenchymal tissue of the arches is composed of paraxial mesoderm and neural crest cells. The pinna is formed by the gradual change in shape and fusion of components of the six auricular hillocks, which are derived from the first and second branchial arches (Figure 475). Formation of the external auditory meatus results from an ingrowth of a solid epithelial plate of ectodermal cells, the meatal plug, which eventually resorbs with only the lining of the canal remaining. The canal is lined by epithelial cells of ectodermal origin. The tympanic membrane begins to develop during the 28th week of gestation and arises from the most medial aspect of the meatal plug, which eventually becomes the external layer of the tympanic membrane.
| | Congenital Anomalies of the External Ear General Considerations Congenital anomalies of the external ear include a spectrum of malformations of the pinna as well as varying degrees of atresia and stenosis of the EAC. The causes of these disorders may be genetic or secondary to environmental exposures. These disorders include variants of microtia, lop ear, cup ear, Stahl's ear, cryptotia, and prominent ear. Patient evaluation requires a thorough head and neck examination to exclude additional congenital anomalies. The list of associated syndromes is extensive and includes Goldenhar (hemifacial microsomia), branchio-otorenal, Treacher Collins, and Robinow syndrome. Pathogenesis Multiple genes may have redundant roles in outer ear formation, which can account for phenotypically similar malformations. The sequence of such dysregulation is only beginning to be understood with the help of murine knock-out and knock-in models. The auricular hillocks that give rise to the pinna arise during the sixth week of embryogenesis, whereas the inner two thirds of the EAC are not formed until the 26th week. Untoward events throughout this period could give rise to structural anomalies of the external ear. Prevention Genetic counseling should be made available to parents who are known carriers of genetic anomalies associated with external ear deformities. However, many anomalies of the external ear occur without known patterns of genetic transmission. In these cases, genetic counseling opportunities are limited. Isotretinoin, vincristine, colchicine, cadmium, and thalidomide are among the known teratogens associated with anomalous hypoplasia of the external ear and should be avoided during pregnancy . Microtia Clinical Findings Patients typically present at birth with obvious auricular malformations. Several classification systems are used to further subcategorize this entity, one of which is detailed below. Grade I The ear exhibits mild deformity, typically with a slightly dysmorphic helix and antihelix. This group includes low-set ears, lop ears, cupped ears, and mildly constricted ears. All major structures of the external ear are present to some degree. The lop ear is characterized by inferiorly angled positioning of the auricular cartilage, whereas the cup ear protrudes with a deep conchal bowl. Grade II All pinna structures are present, but tissue deficiency and significant deformity exist. Grade III Also known as classic microtia or peanut ear, type III microtia has few or no recognizable landmarks of the auricle. The ear lobule is usually present and anteriorly positioned. This subgroup includes anotia, which is complete absence of the external ear. Treatment Classically, microtia has been treated by a multistage auricular reconstruction. Patients undergo observation until the age of 5 to allow for growth of rib cartilage, which is harvested for reconstruction, and the development of the contralateral ear. This approach offers the benefit of reconstruction with autogenous material, which ultimately requires little or no maintenance. However, it is difficult to achieve a perfect cosmetic result. Typically, reconstruction occurs in four stages: Stage I: Auricular Reconstruction The goals of this stage include symmetry in the position of the reconstructed cartilaginous ear framework with the normal ear. Postoperatively, the patient must be assessed for pneumothorax, which may arise with rib harvest. Stage II: Lobule Transposition This procedure should be performed 23 months after Stage I reconstruction and aligns the lobule with the reconstructed cartilage framework. Stage III: Postauricular Skin Grafting A postauricular sulcus is created to allow the ear to project away from the mastoid. This step should be performed 3 months after Stage II reconstruction. Skin for the creation of the sulcus may be harvested from the groin, lower abdomen, buttocks, contralateral postauricular sulcus, or back. Stage IV: Tragal Reconstruction and Soft Tissue Debulking This should be performed several months after Stage III reconstruction. Other Treatment Options Another option for reconstruction includes the placement of a prosthesis. This can be either glued on or anchored to bone. If the patient selects a bone-anchored prosthesis rather than auricular reconstruction, he or she must be aware that daily maintenance is required and that the anchor may compromise the vascularity of nonhair- bearing skin, complicating future reconstructive surgery if the patient becomes dissatisfied with the prosthesis. However, the cosmetic result of a bone-anchored prosthesis is usually excellent . Complications of all types of auricular reconstructions include infection, hematoma formation, skin-flap necrosis, scar contracture, and poor contouring . Protruding Ears Clinical Findings An increase in distance from the helical rim to the mastoid is thought to be due to a lack of the antihelical fold and prominence of the conchal bowl. This entity is most frequently bilateral. Treatment Otoplasty is the mainstay of treatment for protruding ears. Often used techniques include recreating the antihelical fold, postaurical skin excision , and conchal-mastoid suture. Atresia & Stenosis of the External Auditory Canal Clinical Findings Congenital anomalies of the EAC range from mild stenosis to complete atresia. These are often seen in association with malformations of the pinna and the structures of the middle ear. EAC cholesteatoma can develop in the face of severe of EAC stenosis. Audiologic evaluation via behavioral or electrophysiologic measures should be performed to confirm normal hearing in the contralateral ear in unilateral disease, and to assess for ipsilateral sensorineural hearing loss. The typical pattern of hearing loss in affected ears is a conductive hearing loss of 5070 dB. Axial and coronal computed tomography (CT) scans are essential in the evaluation of patients with canal atresia or stenosis. CT scanning assesses for ossicular, facial nerve, and otic capsule abnormalities as well as for the degree of temporal bone pneumatization. In addition, CT scanning can be used to identify a cholesteatoma medial to a canal stenosis. Treatment A discussion on reconstruction for aural atresia can be found in Chapter 48, Congenital Disorders of the Middle Ear. | | External Ear Trauma The external ear is subject to a wide variety of injuries. All trauma patients require appropriate stabilization and triage of associated injuries based on their severity. Adherence to basic surgical principles and wound care prevents complications and improves the likelihood of a successful outcome. Auricular Hematoma Essentials of Diagnosis - History of auricular trauma.
- Edematous, fluctuant, and ecchymotic pinna with loss of normal cartilaginous landmarks.
- Early diagnosis and treatment necessary to minimize cosmetic deformity.
General Considerations Auricular hematoma refers to the accumulation of blood in the subperichondrial space, usually secondary to blunt trauma. Pathogenesis Cartilage lacks its own blood supply; it relies on the vascularity of the surrounding perichondrium via diffusion. Shearing forces secondary to blunt trauma to the pinna lead to an accumulation of blood in the subperichondrial space. This creates a barrier for diffusion between the cartilage and the perichondrial vascularity, leading to necrosis of the cartilage and predisposing it to infection and further injury . Clinical Findings A patient with an auricular hematoma usually presents with an edematous, fluctuant, and ecchymotic pinna, with loss of the normal cartilaginous landmarks. Failure to evacuate the hematoma may lead to cartilage necrosis and permanent disfigurement known as "cauliflower ear." Treatment The evacuation of hematomas can be performed using a skin incision parallel with the natural auricular skin folds . The irrigation of evacuated hematomas with topical antibiotics reduces the likelihood of infection. Splinting after drainage prevents the reaccumulation of hematomas, and options include cotton bolsters, plaster molds, silicon putty, and water-resistant thermoplastic splints. Auricular Lacerations Sharp or severe blunt trauma may lead to laceration or avulsion of the auricle. The expeditious repair and prevention of infection are essential. Auricular lacerations should be cleansed and dbrided prior to repair. Simple lacerations can be closed primarily, whereas extensive injuries with tissue loss may require undermining, flap reconstruction, or tissue grafts. In certain circumstances, even completely avulsed segments may be re-attached. Repairs should be covered with pressure dressings to prevent edema and hematoma formation, and cartilage- penetrating antibiotics should be prescribed. Excellent cosmetic results can be achieved, even with extensive lacerations. Pham TV, Early SV, Park SS. Surgery of the auricle. Facial Plast Surg. 2003;19(1):53. (A thorough review of external ear anatomy and embryology, as well as the surgical management of auricular deformities and trauma.) [PMID: 12739182]
| Otitis Externa Essentials of Diagnosis - Otalgia, otorrhea, pruritus, hearing loss, history of water exposure.
- Tender pinna and canal; canal erythema, edema, and purulent debris.
- Culture for refractory cases.
General Considerations Otitis externa is an inflammatory and infectious process of the EAC. Pseudomonas aeruginosa and Staphylococcus aureus are the most commonly isolated organisms. Less commonly isolated organisms include Proteus species, Staphylococcus epidermidis , diphtheroids, and Escherichia coli . Fungal otitis externa is discussed in the next section. Pathogenesis In the preinflammatory stage, the ear is exposed to predisposing factors, including heat, humidity, maceration, the absence of cerumen, and an alkaline PH. This can cause edema of the stratum corneum and occlusion of the apopilosebaceous units. In the inflammatory stage, bacterial overgrowth ensues, with progressive edema and intensified pain. Incomplete resolution or persistent inflammation for more than 3 months refers to the chronic inflammatory stage. Clinical Findings Symptoms of otitis externa may vary, depending on the stage and extent of disease. The clinical diagnosis is suggested by the presence of otalgia, otorrhea, aural fullness, pruritus, tenderness to palpation, and varying degrees of occlusion of the EAC. The patient may also present with hearing loss that results from occlusion of the EAC by edema and debris. Signs of otitis externa include pain on distraction of the pinna, EAC erythema, edema, otorrhea, crusting, and, in more advanced disease, lymphadenopathy of the periauricular and anterior cervical lymph nodes. Skin changes of cellulitis may be present as well. In the chronic stage, the skin of the EAC may be thickened. A culture may be helpful for infections that are refractory to treatment. Treatment Treatment for otitis externa involves meticulous atraumatic debridement of the EAC with the aid of a microscope. Analgesia can be achieved with nonsteroidal anti-inflammatory drugs (NSAIDs), opioids, or topical steroid preparations. After cleansing is complete, otic drop preparations that are antiseptic, acidifying, or antibiotic (or any combination of these) should be used. If the degree of stenosis of the canal is severe, a wick may be carefully placed in an effort to deliver the drops to the medial portion of the canal. Available antiseptic preparations include acetic and boric acids, ichthammol, phenol, aluminum acetate, gentian violet , thymol, thimerosal (eg, Merthiolate), cresylate, and alcohol. Available antibiotic preparations include ofloxacin, ciprofloxacin, colistin, polymyxin B, neomycin, chloramphenicol, gentamicin, and tobramycin. Polymyxin B and neomycin preparations are often used in combination for the treatment of S aureus and P aeruginosa infections. Ofloxacin and ciprofloxacin are single-agent antibiotics with an excellent spectrum of coverage for pathogens encountered in otitis externa. Preparations with steroids help to reduce edema and otalgia. Systemic antibiotics are indicated for infections that spread beyond the EAC. For chronic otitis externa, a canalplasty may be indicated for thickened skin that has caused canal obstruction. Patients must be instructed to avoid EAC manipulation and water exposure if they have a history of recurrent otitis externa (Figure 476). Otomycosis Essentials of Diagnosis - Pruritus, otalgia, otorrhea, fullness, hearing loss, no response to topical antibiotics.
- Fungal elements on physical examination.
- Positive KOH prep or fungal culture.
General Considerations Otomycosis is an inflammatory process of the external ear canal due to infection with fungi and is responsible for more than 9% of the diagnoses of otitis externa. In 80% of cases, the etiologic agent is Aspergillus , whereas Candida is the next most frequently isolated fungus. Other more rare fungal pathogens include Phycomycetes , Rhizopus , Actinomyces , and Penicillium . Pathogenesis Otomycosis has similar predisposing factors to bacterial otitis externa. Patients with diabetes mellitus or an immunocompromised state are particularly susceptible to otomycosis. Clinical Findings Patients with otomycosis most frequently present with pruritus, aural fullness, and otorrhea, and may also complain of otalgia and hearing loss. The hearing loss associated with otomycosis usually results from the accumulation of mycotic debris. Otoscopy often reveals mycelia, establishing the diagnosis. The EAC may be erythematous and fungal debris may appear white, gray, or black. Patients have typically been tried on topical antibacterial agents with no significant response. The diagnosis can be confirmed by identifying fungal elements on a KOH preparation or by a positive fungal culture. Treatment The treatment of otomycosis includes cleansing and debriding the EAC, acidifying the canal, and administering antifungal agents. Nonspecific antifungal agents include thimerosal (eg, Merthiolate) and gentian violet. Commonly used specific antifungals include clotrimazole, Nystatin (otic drops or powder), and ketoconazole. Itraconazole is the only orally administered antifungal agent that is effective against Aspergillus . Skull Base Osteomyelitis Essentials of Diagnosis - Immunosuppressed patients with intense otalgia, otorrhea, hearing loss, fullness, and pruritus.
- Edema and erythema of the EAC, granulation tissue at the bonycartilaginous junction, cranial neuropathies in advanced stages.
- Elevated erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP). Culture of EAC. CT, MRI, and bone scan diagnostic; gallium scan to follow resolution.
General Considerations Skull base osteomyelitis, also known as malignant external otitis or necrotizing external otitis, is a bacterial infection of the EAC and skull base. This disease process is most frequently seen in elderly diabetics and immunocompromised patients. It most commonly begins as an external otitis that progresses to involve the temporal bone, and it may progress to fatal meningitis, sepsis, and death. Pathogenesis Skull base osteomyelitis commonly begins as an external otitis that progresses to cellulitis, chondritis, osteitis, and, ultimately, osteomyelitis. Unlike otitis media, which spreads through the pneumatized portion of the temporal bone, skull base osteomyelitis disseminates through the haversian canals and vascularized spaces of the skull base. As this progresses along the base of the skull, the facial nerve (stylomastoid foramen); hypoglossal nerve (hypoglossal canal); the abducens and trigeminal nerves (petrous apex); and the glossopharyngeal, vagus, and spinal accessory nerves (jugular foramen) may be involved. Cranial neuropathies portend a grave prognosis . The most frequently isolated causative organism is P aeruginosa , which may exhibit high levels of antibiotic resistance. Aspergillus may also be an etiologic organism and is thought to originate from the middle ear or mastoid. Elderly diabetics are thought to be particularly susceptible because of the microangiopathic changes that blunt an already attenuated immune response. In children, the clinical course of the disease progresses more rapidly , often manifesting with pseudomonal bacteremia. In contrast to that seen in adults, the tympanic membrane and middle ear are often involved. Clinical Findings Symptoms and Signs Patients may present with intense otalgia, otorrhea, aural fullness, pruritus, and hearing loss. As the disease advances to involve the temporal bone, granulation tissue is seen on the floor of the EAC at the osteocartilaginous junction. Bony sequestra can also be found in the EAC. Edema, periaural lymphadenopathy, and trismus may be present. Cranial neuropathies occur in more advanced presentations of disease, and the facial nerve is the most frequently affected cranial nerve. Further progression may lead to sigmoid sinus thrombosis, meningitis, sepsis, and death. Diagnostic Tests Inflammatory markers such as ESR and CRP may be elevated. Cultures and sensitivity should be obtained to aid in selecting appropriate antibiotics. CT and MRI are useful in the initial evaluation to determine the extent of disease. Bone scans are sensitive for assessing bony involvement but are not specific (Figures 477, 478, and 479). Gallium scans are used to track the resolution of the infection, since bone scans often remain positive long after the infection has resolved (Figure 4710).
Differential Diagnosis Carcinomas of the EAC, chronic granulomatous disease, Paget disease, fibrous dysplasia, and nasopharyngeal carcinomas must be considered in the differential diagnosis. Treatment Long- term parenteral antibiotics are the treatment of choice. Aminoglycosides (eg, tobramycin) and antipseudomonal  -lactam antibiotics, including piperacillin, ticarcillin, or ceftazidime, may be used. Some physicians recommend the use of outpatient fluoroquinolones such as ciprofloxacin or ofloxacin; however, this is appropriate only for patients with early presentations who can be followed up closely. Control of hyperglycemia and immunosuppression is necessary to maximize treatment. Surgical debridement may be necessary to remove necrotic tissue. The use of hyperbaric oxygen has been described in cases refractory to antibiotics, with variable results. In an effort to prevent skull base osteomyelitis, all diabetic and immunocompromised patients must be followed up closely and treated aggressively if they present with symptoms suggestive of external otitis. Rubin Grandis J, Branstetter BF IV, Yu VL. The changing face of malignant (necrotizing) external otitis: clinical, radiological, and anatomic correlations . Lancet Infect Dis. 2004;4(1):34. (An overview of the diagnosis and management of skull base osteomyelitis.) [PMID: 14720566]
| | | Dermatologic Diseases of the External Ear Essentials of Diagnosis - Atopic dermatitispruritic erythematous patches or weeping plaques.
- Psoriasisoval salmon-pink plaques with silvery scales on elbows, knees, scalp, and buttocks.
- Seborrheic dermatitispruritic greasy scales with erythematous bases on ears, scalp, forehead, eyebrows , glabella, or nasolabial folds.
- Contact dermatitispruritic, indurated, and erythematous lesions after exposure to allergen or irritant.
Atopic Dermatitis General Considerations Atopic dermatitis is a chronic skin disease of immune-mediated origin. It may remit spontaneously or endure as a chronic condition. Lesions presenting on the ear may be pruritic and erythematous. Patients often have a personal or family history of atopy and allergy. Atopic dermatitis often manifests in infancy on extensor surfaces and the face. Children may present with skin lesions on flexural areas and on the hands. Pathogenesis Though not completely understood, the clinical presentation of atopic dermatitis is thought to be secondary to immune dysfunction. Atopic skin lesions have been shown to have higher levels of Th2 T-lymphocytes, which produce inflammatory mediators such as interleukin 4, 5, and 10. Clinical Findings The diagnosis of atopic dermatitis is a clinical one. There is variability in skin lesions ranging from erythematous patches to weeping plaques. Lesions presenting on the ear are often pruritic and erythematous. Lesions typically persist for more than 1 month. Secondary infections with S aureus , herpes simplex virus, vaccinia, and molluscum contagiosum may occur. Atopic dermatitis is characterized by the absence of specific laboratory and histologic markers. Elevated IgE and eosinophilia may be present yet are not specific for the diagnosis. Differential Diagnosis The differential diagnosis includes seborrheic dermatitis and psoriatic dermatitis. Treatment Topical corticosteroids are the mainstay of treatment. Antihistamines and lubricants may be used for the treatment of accompanying pruritus. Moisturizers and mild soaps are preferred to minimize exposure to potential allergens found in many cosmetic products. Food elimination and desensitization are not recommended. Though often self-limited, the disease may recur spontaneously and can become chronic. Bacterial superinfection may require topical and systemic antibiotics. Psoriasis General Considerations Psoriasis is a chronic inflammatory disorder of the skin. Eighteen percent of patients with psoriasis have some involvement of the external ear, which may be secondary to extension from the scalp. Plaques may present on the concha and meatus of the EAC and are variably pruritic. The incidence of psoriasis in the United States ranges from 2% to 5%. Males and females are equally affected, with the onset of disease typically occurring in adolescence . Pathogenesis The cause of psoriasis is unknown, yet there is a strong genetic component. Attacks of psoriasis may be triggered by certain drugs such as NSAIDs, beta blockers, lithium carbonate, and antimalarial agents, as well as by infection, trauma, and stress. Clinical Findings Psoriasis is characterized by erythematous papules that coalesce to form round or oval salmon-pink plaques with silvery white scales found on the elbows, knees, scalp, and buttocks. These lesions bleed in pinpoint areas when scratched (Auspitz sign). Opacification or "oil spots" of the nails , as well as pitting and subungual hyperkeratosis, are also suggestive of this disease. Psoriatic lesions may present over areas of trauma, an entity known as Koebner phenomenon . Psoriatic arthritis occurs in 510% of all psoriatic patients. Treatment Patients should avoid excessive drying of the skin. For the ears and face, treatment includes low-dose topical nonfluorinated corticosteroids such as alclometasone, mometasone, desonide, clocortolone, hydrocortisone valerate, and butyrate creams and topical calcipotriene. Warm-water soaks, 15% coal tar treatment, and topical anthralin C may also be helpful. Oral psoralens and UVA phototherapy for patients with widespread disease may be necessary. Antihistamines are used to treat the associated pruritus. Methotrexate may be required for severe cases and for psoriatic arthritis. The response to treatment is variable, and the condition may become chronic. Seborrheic Dermatitis General Considerations Seborrheic dermatitis is a chronic inflammatory skin disease of unknown etiology with a predilection for areas of the skin rich with sebaceous glands. Seborrheic dermatitis affecting the ear is often distributed along the concha, scaphoid region, EAC, and postauricular crease . Pathogenesis The cause of seborrheic dermatitis remains unknown, but an association with Pityrosporum ovale and Malassezia furfur has led to the approval of ketoconazole shampoo for treatment. Clinical Findings Seborrheic dermatitis is characterized by greasy scales overlying erythematous and often pruritic plaques. The distribution is frequently not limited to the ears and often involves the scalp, forehead, eyebrows, glabella, and nasolabial folds. Scaling of the scalp or dandruff is common. Superimposed infection and edema may also occur. Differential Diagnosis Seborrheic dermatitis may be confused with atopic or psoriatic dermatitis, and scaling within the EAC may be confused with external otitis or otomycosis. Treatment Medicated shampoos with sulfur, tar, selenium sulfide, or zinc are helpful in the treatment of the associated dandruff. Intermediate- or high-dose glucocorticosteroids (eg, betamethasone or fluocinonide) are needed for more severe presentations and to alleviate pruritus. Fluorinated topical glucocorticoids may worsen lesions when used on the face or ear. Ketoconazole cream and shampoo are helpful in refractory cases. Seborrheic dermatitis can often become chronic with periods of exacerbation and remission. Superinfection should be treated with warm compresses, topical antibiotics, and selective use of oral antibiotics. Contact Dermatitis General Considerations Contact dermatitis can be an acute or chronic inflammatory disorder of the skin caused by contact with an allergen or irritant. This process may occur anywhere along the pinna or the EAC. Eruption may occur secondary to instrumentation, foreign objectsincluding jewelry , ear plugs, and hearing aidsand other objects used to scratch pruritic lesions. In addition, cosmetics and hair products are frequent culprits. Pathogenesis Allergic contact dermatitis is a Type IV hypersensitivity reaction, and cutaneous manifestations are often delayed by 13 days. This is in contrast to irritant-mediated contact dermatitis, which usually manifests earlier. Clinical Findings Allergic contact dermatitis is characterized by an indurated, erythematous, pruritic, and poorly demarcated process. This is in contrast to irritant dermatitis, which often presents with well-defined areas of exposure. Skin testing to identify contact allergens may be of use. Treatment The avoidance of exposure to irritants and allergens and high-dose topical glucocorticoids are the mainstays of therapy . First Branchial Cleft Anomalies Essentials of Diagnosis - Cyst or tract along anterior border of sternocleidomastoid muscle; corresponding tract at the bony-cartilaginous junction of the EAC.
- Recurrent neck or ear drainage and infection.
- CT scan may be helpful to identify tract.
- May be intertwined with the facial nerve.
Pathogenesis First branchial cleft anomalies occur as a result of anomalous fusion of the first and second branchial arches, with incomplete obliteration of the first branchial cleft. Clinical Findings Patients may present with a cyst or tract along the anterior border of the sternocleidomastoid muscle. One may also see a corresponding tract at the junction of the bony and cartilaginous ear canal. The patient may have a history of recurrent infection and drainage from the ear or neck. A Work type 1 anomaly is a duplication anomaly of the EAC. A Work type 2 anomaly may be intertwined with the facial nerve. Treatment The treatment for first branchial cleft anomalies is complete excision. Incomplete excision predisposes the patient to recurrence and re-infection. The tract may be intimately involved with the facial nerve, which is at risk during excision. Auricular Frostbite Essentials of Diagnosis - Cold exposure.
- Auricle initially numb, then subsequently painful.
- Auricle initially pale, cyanotic, and hypesthetic, then subsequently erythematous with bullae.
Pathogenesis Freezing temperatures lead to both direct cellular injury as well as vascular compromise. Prolonged exposure to cold temperatures can lead to vasoconstriction, cold-mediated dehydration, endothelial injury, thrombosis, and ischemia of auricular tissue. In the early stage, this process may be reversible, but over time, it leads to tissue necrosis. Clinical Findings Temperatures below 10 C may lead to hypesthesia, and the person is frequently unaware of impending frostbite. The ear is initially pale and then cyanotic. Ultimately, as the ear thaws, pain, erythema, and subcutaneous bullae secondary to extravasated extracellular fluid or blood may develop. Treatment The initial treatment for auricular frostbite consists of rapid rewarming of the ear to 4042 C. Nonhemorrhagic blisters may be dbrided, and patients should be given pain medicine and antibiotics. Aloe vera has antithromboxane properties and, together with ibuprofen, may aid in reestablishing circulation. More aggressive dbridement should be delayed for several weeks until demarcation is complete. Petrone P, Kuncir EJ, Asensio JA. Surgical management and strategies in the treatment of hypothermia and cold injury. Emerg Med Clin North Am. 2003;21(4):1165. (An overview of the current recommendations for the management of frostbite, including frostbite of the external ear.) [PMID: 14708823]
| Auricular Burns Essentials of Diagnosis - Superficial burnerythema and pain.
- Partial- thickness burnpainful blisters.
- Full-thickness and subdermal burnspainless, gray/black eschar.
General Considerations Thermal injury can be classified by the degree of the burn. Superficial burns involve the superficial layer of the epidermis. Partial-thickness burns extend into, but not through, the dermis. Full-thickness burns extend through the full thickness of the dermis. Subdermal burns extend into the subcutaneous tissue, including fat, muscle, tendon, cartilage, and bone. Clinical Findings Superficial auricular burns present with erythema secondary to dermal capillary dilation and vessel congestion. These burns are red and moderately painful. Patients with partial-thickness burns usually present with blisters that blanch on direct pressure and are very painful. Deep partial-thickness burns are associated with less pain, and there may be an eschar. Full-thickness and subdermal burns are painless because dermal nerve endings have been destroyed . The wound surface is of varying color , but may be gray or black and charred. Treatment Superficial burns do not scar and may be treated with moisturizing creams. The blisters of partial-thickness burns should be dbrided, and bacitracin ointment applied. When not deep, these burns heal without scarring as well. Full-thickness, subdermal, and deep partial-thickness burns of the auricle heal with scarring and contracture and may be complicated by suppurative chondritis. These burns should be treated with both topical (usually silver based) and systemic cartilage penetrating antibiotics. Early dbridement and closure with skin grafts should be considered. Secondary reconstruction is usually performed at approximately 1 year after injury. DeSanti L. Pathophysiology and current management of burn injury. Adv Skin Wound Care. 2005;18(6):323. (An overview of the current recommendations for the management of burns, including those of the external ear.) [PMID: 16096398]
| Foreign Bodies of the External Ear General Considerations Foreign bodies within the external ear may present in both children and adults. Common objects include erasers , pills, batteries, and insects . Clinical Findings Patients may present with pain, pruritus, conductive hearing loss, and bleeding. A persistent foreign body may lead to infection and the formation of granulation tissue. Batteries lodged within the EAC, when in contact with moisture, may cause liquefaction necrosis, low-voltage injury, or pressure necrosis of the EAC skin or tympanic membrane. Treatment The removal of foreign objects should be done in an atraumatic manner. Injury to the EAC is minimized with direct visualization using the operating microscope and proper instrumentation (eg, right angle pick, curet, forceps, and suction) as well as minimizing patient movement. In children, general anesthesia is often required. Irrigation may help dislodge cerumen or smaller objects. Cerumen impaction may require prior softening with an otic preparation. Two percent lidocaine may be used for the removal of insects both to achieve topical anesthesia and also to kill the insect. Complete occlusion of the EAC with cyanoacrylate adhesives (ie, "superglue") may require surgical removal with a postauricular approach. | | Neoplasms of the External Ear Essentials of Diagnosis - History of chronic sun exposure; usually found on sun-exposed areas of body.
- Basal cell carcinoma nodular, ulcerated, and/or bleeding lesion.
- Squamous cell carcinomaplaque, nodule, or ulceration.
- Melanomalesion with increasing size , ulceration, or bleeding.
- Any suspicious skin lesion should be biopsied.
- CT/MRI if concern regarding local extension or regional disease.
Basal Cell Carcinoma of the Auricle General Considerations Basal cell carcinomas are the most common malignant neoplasm of the auricle, representing 45% of auricular carcinomas. Pathogenesis Chronic long-term sun exposure is the predominant cause of basal cell carcinoma. Specifically, UVB radiation has been identified as a major carcinogen. The incidence of cancer increases with age. Other risk factors include fair skin, outdoor occupations, and a history of skin carcinoma. Classification Nodular Basal Cell Carcinoma The most common and least aggressive subtype, nodular basal cell carcinoma appears as a telangiectatic, pearly papule. Ulcerative Basal Cell Carcinoma This subtype presents with a central ulceration and pearly border. Pigmented Basal Cell Carcinoma This carcinoma is similar in gross appearance to the nodular form, but with brown pigmentation. Superficial Basal Cell Carcinoma This subtype occurs predominantly on the trunk, appearing as indurated, erythematous scaly patches. These lesions may be mistaken for other dermatologic conditions, including eczema and psoriasis. Morpheaform Basal Cell Carcinoma Occurring predominantly on the face, morpheaform basal cell carcinoma presents as yellowish cicatricial plaque lesions. Differentiated Basal Cell Carcinoma This subtype is characterized by slow-growing lesions with histologically differentiated glandular or ductal elements. Basaloid Basal Cell Carcinoma Composed of highly invasive keratinized lesions, this subtype represents 1% of basal cell carcinomas. Clinical Findings Patients may initially present with a skin lesion that is nodular, ulcerated, and/or bleeding. Basal cell carcinomas of the auricle typically occur on the posterior surface of the pinna and in the preauricular area. The diagnosis of any suspicious lesion should be confirmed with biopsy. CT scans and MRI may be used to evaluate advanced disease with tumor extension to the adjacent temporal bone and soft tissue structures of the head and neck. The overall rate of metastasis is 0.0030.1%. Staging Carcinomas of the EAC can be staged using the American Joint Committee on Cancer (AJCC) general staging system for nonmelanoma cancer of the skin, which is a TNM (tumor, node, metastases) staging system. This staging system is limited by the fact that it does not account for histologic subtypes or the anatomic variability of the skin of the external ear compared with other skin sites. Differential Diagnosis Given the variability of subtypes, the differential diagnosis includes benign nevi, amelanotic melanomas, cutaneous squamous cell carcinomas, eczema, and scleroderma. Treatment Nonsurgical Measures Topical 5-Fluorouracil Radiation Therapy Indicated for poor surgical candidates or unresectable lesions. Surgical Measures Curettage with Electrodissection Operator dependent and typically used to excise nodular lesions and desiccate the base. Cryosurgery Indicated for small basal cell carcinomas (< 1 cm) with well-defined borders. Local Excision Ninety-five percent of basal cell carcinomas < 2 cm in size can be successfully treated with local excision with a surgical margin of at least 4 mm. Auricular reconstruction may be required for large defects. Mohs Surgical Technique Refers to complete micrographic excision of the tumor using intraoperative histopathology to assess for positive margins. This technique is particularly useful for recurrent basal cell carcinomas, those larger than 2 cm, or those with an aggressive histology. Five-year cure rates using Mohs technique should approach 97.1%. Prevention Minimizing sun exposure between 10:00 AM and 3:00 PM, wearing protective clothing, and using UV-B-protective sunscreens are helpful measures for preventing basal cell carcinoma. Cutaneous Squamous Cell Carcinoma General Considerations Squamous cell carcinomas account for 20% of all cutaneous malignant neoplasms and commonly occur in elderly males. Pathogenesis Risk factors for squamous cell carcinoma include immunosuppression, advanced age, a nonhealing ulcer, and exposure to chemicals such as arsenic, soot, coal, tar, paraffin, and petroleum oil. The most important risk factor is exposure to UV radiation. Classification Adenoid Squamous Cell Carcinoma This is a classic nodular, ulcerative lesion. Bowenoid Squamous Cell Carcinoma This type of carcinoma has the histologic appearance of Bowen's disease, with invasive properties. Generic Squamous Cell Carcinoma Generic squamous cell carcinoma is the most common histologic group. Verrucous Squamous Cell Carcinoma The carcinoma is composed of wartlike lesions that are locally invasive. Spindle Cell Squamous Cell Carcinoma This type of squamous cell carcinoma consists of aggressive and deeply penetrating tumors named for their elongated fusiform cells. Clinical Findings The appearance of these tumors is variable and includes plaques, nodules, and ulcerations. They may be friable and prone to bleeding. Auricular lesions frequently occur on the helix or pre-auricular region, but may occur on any sun-exposed areas. CT scanning and MRI may be used to evaluate advanced disease with tumor metastasis to the adjacent temporal bone and soft tissue structures of the head and neck. The proper diagnosis should be made with biopsy. The overall risk of metastasis for cutaneous squamous cell carcinoma of the external ear is approximately 618%. Staging Carcinomas of the EAC can be staged using the AJCC general staging system for nonmelanoma cancer of the skin (ie, the TNM staging system). This staging system is limited by the fact that it does not account for histologic subtypes or the anatomic variability of the external ear skin compared with other skin sites. Differential Diagnosis The differential diagnosis includes basal cell carcinoma, actinic keratosis, seborrheic keratosis, keratoacanthomas, scars, psoriatic lesions, melanomas, and sarcomas. Treatment Nonsurgical Measures Radiation therapy may be indicated for unresectable lesions or those that may lead to significant cosmetic disfigurement with surgery. Surgical Measures Local Excision Ninety-five percent of squamous cell carcinomas < 2 cm can be successfully treated with local excision with a surgical margin of at least 6 mm. Auricular reconstruction may be required for large defects. Mohs Surgical Technique This technique is particularly useful for recurrent lesions, those > 2 cm, or those with an aggressive histology. Prevention As with basal cell carcinoma, minimizing sun exposure between 10:00 AM and 3:00 PM, wearing protective clothing, using UVB-protective sunscreens, and avoiding the sun are paramount for risk reduction. Prognosis In addition to the patient's age and overall immune status, the prognosis for squamous cell carcinoma is dependent on the histologic subtype, size, and location of the tumor. A better prognosis is associated with a well-differentiated histology. The 5-year cure rate for squamous cell carcinomas ranges from 75% to 92%. Melanoma of the External Ear General Considerations The incidence of melanoma in the United States is 11.1 cases per 100,000 individuals. Auricular melanoma accounts for 1% of all melanomas. Classification Lentigo Maligna Melanoma This subtype is characterized by hyperpigmented macules occurring on sun-exposed areas. The lesions expand laterally and may progress for years . This subtype carries the best prognosis. Superficial Spreading Melanoma This subtype accounts for approximately 75% of melanomas and often occurs on the lower extremities or the back. The lesions are irregular and hyperpigmented and may develop central nodularity. The natural history of these lesions begins with a superficial spreading lesion (radial growth phase) and subsequently ulceration, bleeding, and dermal invasion (vertical growth phase). Lesions that have already begun the vertical growth phase portend a worse prognosis. Nodular Melanoma Blue-black nodules of nodular melanoma invade deeply into the dermis. They occur predominantly on the trunk, but may present on the head and neck. This subtype carries the worst prognosis. Clinical Findings Most melanomas involving the ear present on the helix. Though initially painless, these lesions may change in size, ulcerate, and bleed. A thorough head and neck examination requires attention to enlarged lymph nodes that may occur with regional spread of disease. The diagnosis of melanoma is dependent on the histologic evaluation of a biopsy. At a minimum, metastatic evaluation should include a chest x-ray to rule out lung metastases and liver function tests to rule out liver metastases. CT scanning and MRI have added sensitivity in detecting metastatic disease. Radionuclide bone scans can be used to diagnose bony metastases. Staging At present, melanomas are staged using one of two systems: (1) the TNM staging system or (2) the staging system of the AJCC. Both systems incorporate the depth of invasion, measured in millimeters. Deeper lesions and lesions with ulceration are associated with higher stages and higher mortality rates. Differential Diagnosis The differential diagnosis is diverse and includes benign lesions as well as basal cell and squamous cell carcinomas. Treatment Nonsurgical Measures Adjunctive radiation therapy may have a role in palliation. Surgical Measures The extent of excision, including surgical margins, is dependent on the histologic type and stage of disease. Management of the regional lymphatics is controversial and may include elective regional lymph node dissection and parotidectomy. Recently, sentinel lymph node biopsy has become a well-accepted approach in the management of the N0 neck for lesions more than 1 mm deep. Prevention The avoidance of and protection from sun exposure are important in preventing disease, as is early detection. Early detection is also extremely important in improving prognosis. Glandular Tumors of the External Auditory Canal Essentials of Diagnosis - Otorrhea, fullness, otalgia, and conductive hearing loss.
- Sensorineural hearing loss indicates inner ear extension.
- CT and MRI to define tumor and surrounding anatomy.
- Biopsy essential.
Classification Glandular tumors of the EAC are rare and include four types: (1) adenoid cystic carcinomas; (2) ceruminous adenomas; (3) ceruminous adenocarcinomas; and (4) pleomorphic adenomas. Adenoid Cystic Carcinoma These are capsular tumors most often found in salivary gland tissue. They have a predilection for perineural, perivascular, and fatty infiltration. Patients with perineural invasion often present with otalgia. Histologically, these tumors may show cribriform, tubular, or solid patterns of cellular arrangement. Lymph node metastases are rare, but late distant metastasis is not an uncommon feature of these tumors. Ceruminous Adenoma Ceruminous adenoma consists of benign painless masses that may grow undetected for prolonged periods of time. Patients may present with a conductive hearing loss or otitis externa. They are histologically characterized by double-layered cuboidal or columnar cells, and the epithelium may show apical "snouts" of apocrine secretion. Ceruminous Adenocarcinoma These tumors share histologic features with ceruminous adenomas, but they have higher rates of mitoses and cellular atypia. Invasion into adjacent structures may be present, and lymph node metastases are rare. Pleomorphic Adenoma These tumors vary histologically but are characterized by epithelial and mesenchymal elements. These benign tumors do not display features of invasion. Clinical Findings Patients with glandular tumors of the EAC may present with otorrhea, aural fullness, otalgia, and conductive hearing loss. Sensorineural hearing loss signifies tumor extension into the inner ear. CT imaging is helpful in determining the amount of bony erosion and the size of the tumor. Generous tissue samples are important for histologic diagnosis. Treatment Benign glandular tumors are treated with wide local excision. Malignant tumors are treated with a variant of temporal bone resection, and consideration should also be given to adjuvant radiation. Devaney KO, Boschman CR, Willard SC, Ferlito A, Rinaldo A. Tumours of the external ear and temporal bone. Lancet Oncol. 2005;6(6):411. (Overview of the diagnosis and management of malignancies that affect the external and middle ear.) [PMID: 15925819]
| Osteomas & Exostoses of the External Auditory Canal Essentials of Diagnosis - Usually asymptomatic; may present with cerumen impaction, otitis externa, or conductive hearing loss.
- Osteomapedunculated bony EAC lesion.
- Exostosesmultiple EAC lesions.
General Considerations Osteomas are benign osseous neoplasms. Exostoses are firm, bony, broad-based lesions composed of lamellar bone (Figure 4711). Exostoses are formed by reactive bone formation and have been associated with cold water exposure. Both osteomas and exostoses arise from the bony portion of the EAC (Figure 4712).
Clinical Findings Osteomas are usually pedunculated and often have a vascular core (Figure 4713). Exostoses commonly present as multiple lesions. Although most osteomas and exostoses are asymptomatic, occlusion of the EAC with an enlarged lesion may lead to cerumen impaction, external otitis, and a conductive hearing loss on audiogram. Treatment Most exostoses and osteomas require no intervention. If surgery is necessary, a transcanal or postauricular approach can be used, depending on the size of the lesions. The preservation of skin flaps speeds healing. | | | |
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