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TITLE: External Auditory Canal Lesions
SOURCE: Department of Otolaryngology, UTMB: Grand Rounds Presentation 
DATE: April 9, 1997 
RESIDENT PHYSICIAN: Kyle Kennedy, M.D. 
FACULTY PHYSICIAN: Jeffrey Vrabec, M.D. 
SERIES EDITOR: Francis B. Quinn, Jr., M.D.


"This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion." 


Introduction 
Lesions of the external auditory canal (EAC) are disease entities frequently encountered by the otolaryngologist. These disorders range in complexity from the simple impaction of cerumen to neoplasia of the temporal bone. The EAC is not simply a conduit for sound from the environment to the tympanic membrane. A thorough understanding of the basic aspects of EAC development, anatomy, and physiology are requisite for the rational management of diseases affecting this structure. A discussion of these topics will be followed by an overview of the most frequently encountered EAC lesions with which the practicing otolaryngologist should become familiar. 

Development 
The EAC derives from the 1st branchial cleft or groove which lies between the 1st (mandibular) and 2nd (hyoid) branchial arches. The 1st branchial cleft is derived from ectoderm and initially consists of dorsal and ventral portions. During embryogenesis, the dorsal portion persists to form the EAC while the ventral portion disappears. Persistence of the ventral portion may later result in the development of a 1st branchial cleft anomaly such as a cyst, sinus, or fistula. The ectoderm of the medial 1st branchial cleft begins to invaginate around the 4th week of embryonic development and lies adjacent to the endoderm of the corresponding 1st pharyngeal pouch. This pouch subsequently becomes the tympanic cavity. By the 5th week of embryonic development, mesoderm has grown between the ectodermal and endodermal layers, and ultimately, the tympanic membrane forms at this site. Invagination of the 1st branchial cleft toward the tympanic cavity during the 8th week results in formation of the primary external meatus, and this structure corresponds to the future lateral third of the EAC. Thickening and extension of the 1st cleft ectoderm medially during the 9th week forms a solid cord of cells known as the meatal plate. The meatal plate remains solid until the 21st week when the medial cells in the plate begin to degenerate. Recanalization of the developing EAC thus occurs in a medial to lateral direction and is complete by the 7th month. 

Although the tympanic membrane, ossicles, and otic capsule have reached adult size at birth, the EAC undergoes further developmental changes from birth through approximately 9 years of age. At birth, the tympanic membrane is oriented almost horizontally, and, together with squama of the temporal bone, form the roof of the EAC. The EAC is almost straight. The tympanic ring is incompletely fused, and the floor of the bony canal is only partially ossified, a portion of which is composed of the lamina fibrosa. The tympanic ring is completely fused by the age of 2, and the bony canal is completely ossified by age 3 or 4. Incomplete ossification in the anteroinferior canal may result in a persistent defect known as the foramen of Huschke. By about age 9, the tympanic membrane is oriented at approximately 45 degrees from the horizontal, and the EAC has developed the characteristic S shape, as seen in the adult. 

Anatomy 
In the adult form, the EAC is an S-shaped structure approximately 2.5 cm in length. Due the oblique orientation of the tympanic membrane, the posterosuperior canal wall is approximately 6 mm shorter than the anteroinferior canal wall. The narrowest portion of the canal is the isthmus located at the bony-cartilaginous junction. The lateral portion of the EAC is oriented in a posterosuperior direction, and the medial portion of the canal is oriented in an anteroinferior direction. For this reason, pulling the auricle outward, upward, and backward permits adequate visualization of the tympanic membrane in most instances. 

The lateral one-third of the canal is composed of an incomplete tube of elastic cartilage in its anterior, inferior, and a portion of its posterior walls. The superior and the remainder of the posterior wall are composed of a bridge of dense fibrous connective tissue which is adherent to the squamous portion of the temporal bone and is continuous with the periosteum of the bony canal medially. Two or three vertically-oriented fissures of Santorini in the anteroinferior aspect of the cartilaginous canal render it more flexible but also permit the possible extension of infection from the EAC to the parotid gland. The medial two-thirds of the EAC is composed of a complete bony canal in the temporal bone extending laterally from the tympanic membrane. The tympanic portion of the temporal bone contributes the anterior and inferior aspects of the bony canal while the squamous and mastoid portions of the temporal bone contribute the superior and posterior aspects, respectively. 

When examining the EAC, it is important to bear in mind the anatomical relationship of the EAC to surrounding structures. Medially, the anterior wall lies adjacent to the temporomandibular joint, and laterally, it lies adjacent to the parotid gland. The inferior wall also lies adjacent to the parotid. As previously mentioned, defects in the EAC wall such as the fissures of Santorini or the foramen of Huschke may allow pathologic processes originating in the EAC to reach adjacent structures. The tympanic margin of the temporal bone is a wedge-shaped portion of bone at the medial end of the superior canal wall which separates the EAC from the epitympanum. Laterally, the superior canal wall is separated from the middle cranial fossa by a thicker bony plate. A thinner bony plate separates the posterior canal wall from the mastoid air cells. 

Keratinizing stratified squamous epithelium lines the EAC. The skin of the bony canal is thin (approximately 0.2 mm in thickness) and continuous with the epithelium of the lateral aspect of the tympanic membrane. Epidermal rete ridges and skin adnexal structures are absent in the skin of the medial canal as is a subcutaneous layer, and the skin is adherent to the underlying periosteum of the bony canal. The skin of the cartilaginous canal is approximately 0.5 to 1 mm thick and contains a well-developed dermis and subcutaneous layer. Hair follicles are present as are numerous sebaceous and ceruminous glands (modified apocrine glands). No eccrine sweat glands are located in the EAC. Large, coarse terminal hairs and small, fine vellus hairs can be seen and are mostly present in lateral third of the cartilaginous canal. The glandular secretions combine to produce cerumen, which is principally composed of lipids. 

The blood supply of the medial EAC is provided by the deep auricular artery, a branch of the internal maxillary artery. The deep auricular artery enters the canal at the bony cartilaginous junction and sends a group of vessels medially along the superior canal wall toward the tympanum, and this comprises the vascular strip. The lateral canal is supplied by the posterior auricular and superficial temporal arteries. Venous drainage is via posterior auricular and superficial temporal veins, which subsequently combine to form the external jugular vein. Lymphatics typically follow the veins and drain to parotid and postauricular lymph nodes as well as superficial cervical nodes along the external jugular vein. 

Innervation of the EAC is complex and overlapping. Cranial nerves V, VII, IX, and X provide contributions. The auricle itself also receives a portion of its sensory innervation from the cervical plexus via the great auricular nerve. The auriculotemporal branch of the mandibular division of CN V supplies the superior and anterior aspects of the canal, as well as the anterior portion of the tympanic membrane. The posterior and inferior aspects of the canal are supplied by CN VII, IX, and X via the auricular branch of the vagus (Arnold's nerve). Arnold’s nerve branches from the vagus in the jugular foramen and then enters its own canaliculus within the temporal bone. It receives contributions from CN VII and IX as it traverses the temporal bone and then exits the bone via the tympanomastoid suture or stylomastoid foramen. This complex innervation mediates clinical phenomena such as referred otalgia from other structures within the head and neck and the initiation of coughing during manipulation of the ear canal. 

Physiology 
As mentioned previously, the EAC does not merely serve as a simple conduit for sound. Its physiology is more complex than would be expected from its usual appearance, and the EAC has important auditory and nonauditory functions. The structure of the canal and the physical barriers it presents act to prevent excess moisture and various foreign bodies from entering the medial EAC. This helps to maintain the stability of medial EAC environment adjacent to the tympanic membrane under a wide variety of climatic and other circumstances. 

In terms of its acoustic properties, the EAC has a unique structure which results in the canal becoming a resonator for frequencies between 3000 and 4000 Hertz. This augments the transmission of sound from the environment to the middle and subsequently the inner ear. 

Cerumen is primarily a lipid-containing material produced by the ceruminous or modified apocrine glands of the lateral portion of the EAC. Under normal circumstances, the cerumen which is produced in the EAC is usually transported laterally along the canal wall in conjunction with the normal epithelial migration and is subsequently extruded. Mechanical disruption of this process, as with a Q-tip or placement of a hearing aid, may result in formation of a cerumen impaction. This condition is arguably one of the most common disorders of the EAC and is treated with cerumenolytics or physical removal of the inspissated cerumen. The hydrophobic properties of cerumen render it an important physical barrier to moisture entering the EAC, and components of cerumen such as lysozyme are thought to provide antibacterial characteristics to cerumen. 

Epithelial migration of the lining of the EAC is a well-known phenomenon and is essential for the self-cleansing mechanism of this structure. In most cases, the epicenter of this migratory process appears to reside in the vicinity of the umbo of the tympanic membrane. The epithelial migration takes place at a rate of approximately 0.07mm/day and serves to cleanse the canal of debris, foreign bodies, and bacteria. 

The warm, dark, moist environment of the EAC is ideal for bacterial growth. The composition of the normal flora of the canal tends to remain relatively stable and acts as a deterrent to colonization of the canal by pathologic organisms. Studies of culture results from normal ears show a predominance of Staphylococcus epidermidis, Corynebacterium species, and micrococci. A variety of less prominent bacterial species such as Staphylococcus aureus and assorted Gram negative bacilli may be found, along with the occasional presence of a saprophytic fungus. Of note, Pseudomonas aeruginosa is not typically cultured from normal ears, and its presence suggests evidence of infection. 

EAC Atresia and Stenosis 
Congenital aural atresia or stenosis is reported to occur in approximately 1 in 10,000 to 1 in 20,000 live births. As noted previously, the external and middle ear structures are derived from the 1st and 2nd branchial arches and 1st branchial cleft and pharyngeal pouch. The EAC/tympanic cavity anomalies typically occur together and microtia may be present. The membranous labyrinth is derived from the ectodermal otocyst, and cochlear and vestibular function are usually normal. The vestibular portion of the stapes footplate derives from the otic capsule, and stapes mobility is usually present despite deformity of the superstructure. The lateral ossicles are typically deformed in conjunction with the EAC atresia or stenosis. These auricular malformations may occur in isolation or in conjunction with other recognizable craniofacial syndromes, and when combined with one of these syndromes, a predictable mode of inheritance is often present. Approximately one-third of the cases demonstrate bilateral involvement. 

For simplicity, these congenital aural malformations may be classified into two broad categories, major and minor malformations. This classification scheme is based on auricular and EAC/tympanic cavity development. Major malformations are those involving absence of the EAC and tympanic membrane, and EAC stenosis is sometimes included in this category. The tympanic cavity is often reduced in size with ossicular deformity. Microtia and abnormalities of the facial nerve are common. Minor malformations primarily involve middle ear abnormalities. The tympanic cavity may be normal in size, but there is absence, deformity, or fixation of the ossicles. The EAC and tympanic membrane are normal or only slightly reduced in size, and the auricle itself is normal or only slightly deformed. Again, facial nerve abnormalities are common. 

Surgical correction of these abnormalities may be possible, albeit quite challenging, depending upon evaluation of the individual patient. Inadvertent facial nerve or labyrinthine injury during the procedure are major concerns. The presence of EAC stenosis may predispose to the formation of canal cholesteatoma. 

First Branchial Cleft Anomalies 
1st branchial cleft anomalies are rare and represent approximately 1% of all branchial cleft anomalies. As mentioned previously, these anomalies are thought to arise as a result of failure of the normal obliteration of the ventral portion of the 1st branchial cleft. As with other branchial cleft anomalies, a cyst, sinus, or fistula may develop. Type I and Type II anomalies are usually described. The Type I anomaly originates from ectoderm of the 1st branchial cleft only and represents a duplication anomaly of the membranous EAC. The usual location is posterior, medial, and inferior to the conchal cartilage, and there may be an opening into the EAC itself. The Type II anomaly consists of elements of both ectodermal origin from the 1st branchial cleft and mesodermal origin from the 1st and 2nd branchial arches. These lesions are usually located in the anterlateral neck anterior to the sternocleidomastoid muscle and often have a tract coursing over the mandible and through the parotid toward the bony-cartilaginous junction of the EAC. The relationship of this tract with regard to the location of the facial nerve is variable. 

These lesions may go undiagnosed for long periods of time and often come to clinical attention as a result of an infection, which sometimes requires incision and drainage. Treatment consists of careful, complete surgical excision with particular attention toward preservation of the facial nerve. 

Local Trauma 
Local trauma to the epithelial lining may occur as a result of a variety of insults. There is no end to the types of objects that patients will place into their ear canals in an attempt to alleviate a sense of pruritus or remove a piece of real or imagined cerumen. The ubiquitous Q-tip is not the least of these offenders. Iatrogenically, overzealous or inappropriate attempts at cerumen removal or other canal manipulation by the physician may achieve the same result. Damage to the canal epithelium may lead to abrasion, hematoma, or laceration. Indeed, perforation of the tympanic membrane occurs all too frequently. Any disruption of the integrity of the epithelial protective mechanisms predisposes to the possibility of infection and otitis externa. Avoidance of unnecessary canal manipulation of all types is the best treatment. 

Foreign Bodies 
Any object small enough to fit into the meatal opening of the EAC is a potential canal foreign body. This is a frequent problem in the pediatric patient. Inanimate objects, as well as insects, may be encountered. If the object is small enough to pass the isthmus into the medial EAC, removal may require additional finesse. Otoscopic or microscopic visualization and the appropriate instruments are mandatory for removal of the foreign body. In the uncooperative and many pediatric patients, sedation or general anesthesia may become necessary for safe removal. After removal of the foreign body, careful inspection of the EAC and tympanic membrane should be performed to assess for any additional injury which needs to be addressed. 

Temporal Bone Injury 
Temporal bone injury with resultant trauma to the EAC may occur as a result of blunt or penetrating forces. Blunt head trauma may result in temporal bone fracture, classically described as longitudinal or transverse based on the orientation of the fracture line in relation to the long axis of the petrous pyramid. Approximately 80% of temporal bone fractures are longitudinal and result from a blow to the lateral aspect of the skull. These fractures usually extend through the EAC and tympanic membrane into the middle ear then lateral to the otic capsule and parallel to the course of the eustachian tube. The fracture line is usually in the posterosuperior aspect of EAC and may be visible at this site. Conductive hearing loss predominates, and approximately 20% of the cases involve facial nerve injury. Transverse temporal bone fractures are usually the result of trauma to the frontal or occipital aspects of the skull. EAC injury rarely occurs with this type of fracture. Sensorineural hearing loss and vestibular symptoms are more common, and facial nerve injury is seen in approximately 50% of the cases. In patients suspected of having temporal bone fracture, careful examination of the EAC may give important clues as to the character and extent of the injury, and cranial nerve assessment is imperative. Management is individualized based on the nature of the injuries discovered. 

Penetrating temporal bone injuries such as those from stab or gunshot wounds may be devastating to the auditory and vestibular apparatus, and the incidence of associated neurovascular injury is substantial, especially with gunshot wounds. Approximately 50% of gunshot wounds to the temporal bone involve the EAC. Depending on the nature of the injury, aggressive management may be necessary in order to prevent adverse sequelae such as infection or canal stenosis. This may include debridement, topical therapy with antibiotic and or steroid preparations, and packing. 

Dermatologic Diseases 
As the EAC is a skin-lined cul-de-sac, an extensive variety of dermatologic disorders may affect this area. Since the majority of dermatologic therapy is topical and the epithelium of the EAC is somewhat less readily accessible, some of these lesions may be more difficult to manage than their counterparts in other epidermal locations. 

Acne 
Acne is the result of obstruction of hair follicles with the subsequent accumulation of sebum and cellular debris. An open or closed comedone is the consequence. Should the process become progressive, extension outside the hair follicle may occur with local inflammation and possible infection. Severe cases may become cystic or nodular. The etiology is multifactorial and not fully understood. The condition is common in adolescence and typically improves with the passage of time. Topical therapy with preparations such as benzoyl peroxide, retinoids, and/or antimicrobials is adequate in most cases and control of infection and inflammation is important to limit residual cutaneous effects. 

Furuncles and Carbuncles 
A furuncle is typically a localized infectious process which develops within a hair follicle in the skin near the junction of the concha and canal skin. The infection is usually by a Gram positive organism such as Staphylococcus aureus. Several adjacent lesions may coalesce to form a carbuncle. The lesions may be quite painful and may result in EAC obstruction if large. Local care and topical or oral antibiotic therapy is usually sufficient for therapy, but larger lesions with sufficient purulent collections may require incision and drainage if spontaneous drainage does not occur. 

Atopic Dermatitis 
Atopic dermatitis is a chronic, generalized dermatitis which displays intensely pruritic lesions in a patient with a strong personal and family history of atopy. It may occur in conjunction with allergic rhinitis or asthma, and the activity of the disease may wax and wane. Exacerbations or flares may be caused by various allergens or environmental stresses depending upon the patient. The mechanism by which atopic dermatitis is not entirely clear but is thought to be related to alterations in the activity of T helper lymphocytes. The gross appearance of the lesions themselves is often nonspecific, especially in the early stages. Erythematous patches with small papules may be evident in involved areas of the skin with secondary changes such as excoriations due to the intense pruritus. Spongiosis or intercellular edema is often visible histologically in the epidermis of early lesions. When chronic, lesions frequently display lichenification and other evidence of cutaneous chronic inflammatory changes. The lesions are also prone to bacterial superinfection with organisms such as Staphylococcus aureus. Subsequent impetiginization with formation of characteristic honey-colored crusts may then follow. Dermatographism can often be demonstrated in these patients in which mechanical stimulation of the skin produces a wheal and flare reaction. Onset typically occurs early in life with lesions present on the face and extensor surfaces. Later on, lesions often arise on the flexural surfaces such as the antecubital or popliteal fossae. Topical steroid preparations are the mainstay of therapy, and antihistamines are an important adjunct to alleviate the pruritus. Systemic steroids may become necessary to control severe cases, and topical or oral antibiotics may be necessary where infection is present. 

Contact Dermatitis 
Contact dermatitis is a localized cutaneous reaction which occurs in response to contact with an inciting agent. Irritant or allergic contact dermatitis are the two forms of this disease which may be distinguished. Innumerable substances may act as irritants which may result in a localized cutaneous inflammatory response if the degree of exposure is adequate. These substances range from frankly noxious stimuli such as acids or alkalis to less obvious items such as grooming products. Allergic contact dermatitis requires exposure to an actual initial exposure to an antigenic hapten followed by a period in which an anamnestic response may be developed. Subsequent exposure to the inciting agent then produces a magnified response. Lesions are typical erythematous, edematous, pruritic lesions which may display vesiculation or exudate. The lesions cannot be distinguished histologically from those of atopic dermatitis. The external ear is a frequent site of involvement. Of note to otolaryngologists is the fact materials used in the manufacture of hearing aids and ear plugs are common offending substances, as is neomycin, a frequent component of many otic preparations. A sensitivity to neomycin should be suspected in any patient being treated with one of these preparations for an otitis which is not improving as anticipated. These patients may also be sensitive to related antibiotics such as gentamicin. Identification and avoidance of the offending substance is the treatment of choice. 

Seborrheic Dermatitis 
Seborrheic dermatitis is a chronic inflammatory condition typically affecting particularly oily areas of the skin. The scalp, face, ears, or trunk may be involved. Mild cases may range from simple dandruff to involvement of the periorbital areas about the eyebrows, nasal alae, and periauricular area, as well as the EAC. Lesions may be mildly erythematous and slightly raised with a greasy scale. They may be pink or orange in color and demonstrate thickening of the plaques and lichenification if chronic. Malassezia furfur, a lipophilic yeast, is thought to play at least some role in the development of this condition. Treatment consists of topical steroids and keratolytics, as well as medicated shampoos for scalp involvement. 

Psoriasis 
Psoriasis is a chronic, inflammatory condition affecting approximately 2 to 5% of the U.S. population, and the external ear is involved in about one-fifth of the cases. The etiology is unclear and appears to be multifactorial. The lesions are typically raised, scaly, and proliferative in nature. Circumscribed erythematous papules may coalesce to form larger patches with thick scale which is silver-white in color. Histologically, epithelial hyperplasia is evident with hyperkeratosis and parakeratosis. Microabscesses are often present and there is uniform elongation of rete ridges into an edematous papillary dermis. A superficial perivascular lymphocytic infiltrate can be seen in the dermis also. Removal of the plaque often results in pinpoint bleeding known as Auspitz’s sign. Koebner’s phenomenon describes the formation of lesions induced in areas of involved skin by minor trauma. Topical therapy suffices in most patients and consists of topical steroids and tar preparations. Some patients require ultraviolet phototherapy or photochemotherapy and systemic therapy with agents such as azulfidine, cyclosporine, and methotrexate are reserved only for the most severe cases. 

Herpes Zoster 
Herpes zoster is known to affect the EAC and usually does so in a unilateral dermatomal distribution. The involvement typically begins with pain or burning sensation and may be followed by a vesicular eruption in several days. Adjacent vesicles may coalesce and rupture to form crusts. The Ramsay Hunt syndrome or herpes zoster oticus describes herpetic vesicular eruption in the EAC with concomitant facial nerve involvement resulting in paresis or paralysis. Treatment is with local care and antibiotics for any secondary infection. Antivirals such as acyclovir are of benefit, particularly if the diagnosis is established and therapy is instituted early in the course of the illness. It has been noted that patients receiving antiviral therapy experience a significantly more rapid clinical improvement in the pain associated with this disorder. 

Infectious Eczematoid Dermatitis 
Eczematoid dermatitis may occur when infectious material from the middle ear or EAC itself causes inflammation of the epithelium of the EAC and periauricular skin. The otorrhea can lead to additional infection and crust formation and requires thorough local care and topical antimicrobials. 

Psychocutaneous Disorders 
Primary (essential) pruritus occurs when a patient has a sense of itching in the absence of any local or systemic illness which may cause this symptom. It is important to eliminate the possibility of these underlying causes (e.g. diabetes mellitus, hepatic or renal disease, leukemia, lymphoma) to encourage the patient not to induce local trauma to the canal by scratching. Topical steroid therapy may be necessary. 

Patients with psychiatric disorders which manifest as compulsive behavior may produce neurotic excoriations by repeated scratching. The skin of the EAC may become thickened and lichenified by chronic inflammation. Topical steroids and local care may be of help, and it may become necessary to treat an infection should it arise. 

Other patients display delusions of parasitosis, in which they are convinced that they have something crawling in their ears or on their skin. They may complain of intense pruritus, and it is necessary to rule out infestations or systemic illnesses which may cause this symptom. Factitial dermatitis may result from a patient intentionally producing local ear trauma in order to achieve some secondary gain and should be suspected when no recognizable clinical pattern to the lesions is apparent. 

Bacterial Otitis Externa 
Otitis externa is a term which represents a spectrum of inflammatory changes in the EAC typically of an infectious etiology. The EAC, with its normal protective and self-cleansing mechanisms intact, is usually quite resistant to infectious processes. When a local insult of any nature results in disruption of the integrity of the epithelium, infectious organisms may gain access to the underlying tissues and cause an inflammatory response of varying degrees. 

The usual offending organisms involved in otitis externa are Pseudomonas aeruginosa, Proteus mirabilis, Staphylococcus species, Strepotococcus species, and various other Gram negative bacilli. Mixed infections are not uncommon, and cultures from the canal are usually not necessary in the typical case of otitis externa. 

Patients may present with complaints of aural pain, itching, fullness, or decreased hearing. Depending upon the time of initial presentation, the physical examination may reveal different stages of involvement, including pre-inflammatory, acute, and chronic stages. In the pre-inflammatory stage, mild edema and erythema of the canal are evident. The acute inflammatory stage may further be categorized as mild, moderate, or severe. These represent a progressive increase in the degree of edema, erythema, and exudate which are evident in the canal. It may no longer be possible to visualize the tympanic membrane. The more severe the involvement, the more likely that infectious inflammatory changes may extend outside the confines of the EAC to the adjacent tissues, thus leading to perichondritis, chondritis, or cellulitis. Recalcitrant cases of otitis externa may evolve into a chronic inflammatory stage which results in thickening of the EAC epithelium with scaling and other changes. This situation, if it persists, could lead to acquired stenosis of the canal. 

Effective medical management of otitis externa requires frequent meticulous cleansing of the canal, appropriate topical or systemic antibiotic coverage, alleviation of inflammation and pain, and steps for prevention of future episodes. Aural toilet with thorough removal of debris and exudate on a regular basis is mandatory. Antibiotic coverage for Pseudomonas aeruginosa and Staphylococcus species is necessary and Cortisporin otic suspension and gentamicin are frequent choices of topical therapy. Oral antibiotic therapy with penicillinase-resistant penicillins and the cephalosporins often provide adequate coverage, and the oral fluoroquinolones have been a valuable addition to the armamentarium. Intravenous antibiotics may be required in more extensive infections. Topical steroid preparations and aluminum sulfate-calcium acetate solutions are beneficial in alleviating inflammation, edema, and crusting in the EAC. Placement of a wick is often necessary in those instances in which canal edema is extensive to provide stenting of the canal walls and topical medications to penetrate the canal adequately. Surgery therapy is rarely required but may be needed to correct sequelae of chronic inflammation and prevent recurrence. 

Otomycosis 
Otomycosis results from fungal infections of the EAC and is often secondary to chronic infections of bacterial origin. Fungal otitis externa comprises approximately 10% of the cases of otitis externa in the U.S., and this percentage is even larger in warmer, more humid areas. Aspergillus and Candida are the most common species. Patients particularly complain of EAC pruritus, and physical examination may reveal fungal debris in the canal which may be white, black, or gray in appearance. Thorough cleansing of the canal is important in treatment, and administration of topical antifungal preparations may be necessary to alleviate the infection. Acidifying agents and drying powders alter the microenvironment of the EAC and make it inhospitable for fungal growth. Treatment of any other underlying bacterial infection is important as well. 

Bullous Otitis Externa 
Bullous otitis externa involves the formation of vesicular or bullous lesions of the bony canal. The of ten hemorrhagic lesions may rupture with resultant secondary infection. Pseudomonas may be an etiologic agent and appropriate topical therapy is indicated with avoidance of unneccessary manipulation of the canal. 

Granular Otitis Externa 
Granular otitis externa demonstrates the formation of usually small lesions of granulation tissue in the EAC. It may occur in the setting of an untreated or partially treated otitis externa of some cause and is treated by careful removal of visible granulations and administration of appropriate topical antimicrobials. In the diabetic, debilitated, or immunocompromised patient, it is imperative that this condition be distinguished from necrotizing otitis externa. 

Necrotizing (Malignant) Otitis Externa 
Necrotizing otitis externa is a serious infection usually encountered in elderly diabetic, immunocompromised, or otherwise debilitated patients. Pseudomonas aeruginosa is the pathogen most often involved. These patients present with persistent otalgia, persistent otorrhea, granulation tissue in the EAC, and sometimes cranial nerve involvement, particularly of cranial nerve VII. The granulation tissue in the canal is characteristically present in the floor of the canal at the bony-cartilaginous junction. Computed tomography is study of choice to image the extent of these lesions and gallium and technetium scanning may provide information in localizing the focus of infection. The gallium scan will revert to normal with quiescence of disease, whereas the changes evident on technetium scanning may lag behind for many months. This disease may progress to frank osteomyelitis of the skull base if left unchecked. Management must be aggressive and meticulous with frequent, thorough debridement of canal granulations and topical as well as systemic antibiotic therapy. Oral or intravenous antibiotic therapy is based on severity of infection, and anti-pseudomonal coverage is mandatory. However, other pathogens may be involved, and therapy is modified based on culture and sensitivity results. Medical management may suffice if intervention is early in the course of disease, but more aggressive surgical therapy may be indicated in recalcitrant cases or those which are progressive. 

Aural Polyps 
Aural polyps are the result of hyperplastic inflammatory proliferation of middle ear mucosa as a consequence of chronic otitis media. The polyps may extend into the EAC via tympanic membrane perforations and even completely obstruct the canal lumen in severe cases. These are friable masses which, on histology, demonstrate pseudostratified columnar epithelium often with squamous metaplasia. The stroma is edematous, and acute and chronic inflammatory cell infiltrates are evident. Management is by removal and treatment of the underlying chronic ear disease. 

Exostosis 
An exostosis is a benign bony growth originating from periosteum, usually in the bony medial EAC. They are often multiple and demonstrate a characteristic concentric lamellar bony organization without intervening vascular tissue. They are often asymptomatic and are seen in surfers and others with chronic exposure to cold water. These sessile lesions may become obstructive and lead to conductive hearing loss, infection, or otalgia. 

Osteoma 
Osteomas are the most common bony neoplasm of the temporal bone and are benign, usually pedunculated lesions often seen arising from the anterior EAC wall at the bony cartilaginous junction. They consist of fibrovascular tissues covered by a layer of disorganized bony tissue and present the same symptoms as exostoses. Treatment is the same for both and consists of complete excision with preservation of as much of the normal EAC architecture as possible. 

Fibrous Dysplasia 
Fibrous dysplasia is a disorder of unclear pathogenesis in which proliferating fibroosseus tissue replaces normal medullary bone. It is classified as monostotic, polyostotic, and McCune-Albright syndrome. McCune-Albright syndrome is characterized by polyostotic involvement with skin pigmentation and endocrinopathies. These white to red, rubbery, cystic masses are composed of a vascular stroma surrounding irregularly woven bone. The monostotic form is the most common, occurring in approximately 70% of the cases. Of these cases, 20 to 25% involve bones in the head and neck. Approximately one-fifth of head and neck cases involve the temporal bone. Cholesteatoma formation is the most common complication, and the disease usually becomes quiescent after puberty. Therefore, conservative management is most often indicated in the pediatric patient. 

Eosinophilic Granuloma (Histiocytosis X) 
Histiocytosis X represents an idiopathic group disorders involving histiocytic proliferation and eosinophilic infiltration in the skull and other tissues throughout the body. Onset is often in childhood, and on electron microscopy, the histiocytes demonstrate characteristic cytoplasmic organelles known as Birbeck bodies. Eosinophilic granuloma is the mildest, localized form of the disease. Hand-Schuller-Christian syndrome is more chronic and involves multiple organs. Letterer-Siwe syndrome entails aggressive, multisystem involvement and has the worst prognosis. Only about 10% of patients demonstrate the classic triad of osteolytic skull lesions, exophthalmos, and diabete insipidus. Approximately 80% of the cases of eosinophilic granuloma have head and neck involvement. Temporal bone lesions are bilateral in about 30% of cases and lead to pain and swelling with otorrhea, canal granulations and edema, and bony erosions. Localized lesions may resolve spontaneously but surgical excision with or without adjunctive radiotherapy or chemotherapy may is often required, depending on localized or systemic involvement. 

Cholesteatoma and Keratosis Obturans 
Canal cholesteatoma is an often cystic collection of squamous epithelium usually seen in an older age group. Unilateral involvement with pain, purulent otorrhea, bony erosion, and periostitis are often present. Topical antibiotic therapy is administered for supervening infection. Frequent, meticulous debridement in the office setting is necessary to control the lesions, and the majority of patients do not require surgical intervention. Indications for surgery would include failure of medical management with evidence of impending complication from extension of the lesion into the middle ear or mastoid, including conductive hearing loss or facial nerve paresis or paralysis. Keratosis obturans, an accumulation of squamous debris in the EAC, is often bilateral in a younger age group and causes pain, canal hyperemia, and granulation with occasional hearing loss. Thorough debridement on a regular basis is required to successfully manage keratosis obturans. Chronic inflammation plays at least some role in the propagation of these lesions, and it evident that the application of topical steroid is beneficial in slowing this process. 

Ceruminous Gland Tumors Ceruminous gland tumors of the EAC are relatively uncommon neoplasms. They usually present as polypoid masses with or without an antecedent history of otorrhea or infection. The ceruminous adenoma demonstrates normal glandular structures on histology with hyperproliferation of the myoepithelial component. These lesions may become obstructive and lead to complications. They are difficult to distinguish from their malignant counterparts on clinical grounds, and biopsy is required. 

Malignant Neoplasms 
When a mass lesion of the EAC is discovered, perhaps 80 to 90% of the time it is benign. Unfortunately, when a malignant lesion does present, it has often progressed to an advanced stage. Symptoms may mimic those of chronic infection. Otalgia, otorrhea, an EAC mass, and hearing loss are the most common presenting features. Increased pain and evidence of bony erosion are indicators which are suspicious for malignancy. Malignant neoplasms of the ear arise from the EAC in approximately 20 to 30% of the cases. Furthermore, malignancies of the temporal bone usually originate from the EAC. The lesions may arise from the epithelium or its adnexa. Squamous cell carcinoma is by far the most common histologic type encountered, comprising approximately 80% of the cases. Glandular neoplasms such as ceruminal adenocarcinoma occur as well. As already mentioned, these difficult tumors are often insidious and quite advanced at the time of diagnosis. The prognosis is usually poor, and the lesions are very challenging to manage. Metastases are uncommon, and death is usually the result of extension to vital contiguous structures. Treatment is based on feasibility of resection with extent of resection dependent upon extent of tumor involvement. The limits of resection may include lateral, subtotal, or total temporal bone resection. Adjuvant radiation therapy may also required, depending on the extent of the lesion. 

Conclusions 
The external auditory canal is a more complex anatomic and physiologic structure than is often initially appreciated. A thorough understanding of its development, structure, and function is necessary to rationally manage the wide variety disorders that the otolaryngologist encounters in this area of the head and neck.

BIBLIOGRAPHY 

  1. Anderson JE. The Head. In: Grant's Atlas of Anatomy 8th edition. Baltimore: Williams & Wilkins, 1983: 7. 
  2. Benjamin B, Bingham B, Hawke M, Stammberger H. The Ear. In: A Color Atlas of Otorhinolaryngology. Philadelphia: JB Lippincott, 1995: 1. 
  3. Linstrom CJ, Lucente FE. Infections of the External Ear. In: Bailey BJ, et al, eds. Head and Neck Surgery-Otolaryngology. Philadelphia: JB Lippincott, 1993: 117. 
  4. Lucente FE, Lawson W, Novick NL. The External Ear. Philadelphia: WB Saunders, 1995: 1, 4-14. 
  5. Sadler TW. Langman's Medical Embryology 6th edition. Baltimore: Williams & Wilkins, 1990: 17. 
  6. Selesnick SH, ed. Diseases of the External Auditory Canal. Otolaryngol Clin North Am, 1996: 725-886. 
  7. Wenig BM. Non-neoplastic Diseases of the Ear and Neoplasms of the Ear. In: Atlas of Head and Neck Pathology. Philadelphia: WB Saunders, 1993: 24, 25. 

Posted 4/9/1999
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