Ear

Surgical procedures of the ear fit into two basic categories. They are adjunctive to medical therapy of ear disease, or they attempt to provide complete resolution of local neoplastic or inflammatory disease. Occasionally, traumatic injuries to the ear are resolved surgically. Ear disease is most commonly inflammatory and complicated by secondary infection with bacteria and/or yeast. The ear canal, as an extension of the skin is affected by generalized skin disorders such as atopy, food allergy, and generalized seborrhea. The warmer, more humid microclimate is a predisposing factor to secondary infection. Neoplastic processes, whether benign or malignant, obstruct ear canal drainage, alter defense mechanisms, and often result in secondary local infection. Congenital stenosis, stenosis from wound healing processes, and vascular disorders also may affect the ear canal and pinna. Whereas the middle ear is most commonly affected because it is the near neighbor of the external ear canal, disease that begins within the middle ear can secondarily affect the external ear canal and nasopharyngeal passages. The proximity of the temporomandibular joint and facial and sympathetic nerve branches may result in clinical signs being referred to more distant structures. The ear may also be affected by vascular disorders that in some instances require surgery. My mission in this chapter is to focus on pathophysiologic processes that affect the ear and how surgery may be used to support treatment efforts or to resolve the disease process.

External Ear Canal

The pinna of the external ear is a breed characteristic, but more importantly, it has specific functions. As a funnel, its cartilaginous plate and shape receive vibrations and transmit or direct them down the ear canal to the tympanic membrane. The ear canal provides protection for the tympanic membrane from direct injury, and provides or maintains an open conduit for conduction of sound to the eardrum [1]. The shape of the pinna is altered by 19 auricular muscles attached to each ear that control movement independently [2]. The convex surface of the pinna is the medial and caudal surface of the ear, whereas the concave surface is the rostral and lateral surface and directs sound down the ear canal. The blood supply to the pinna is provided by the medial, intermediate, and lateral branches of the caudal auricular arteries, which arise at the base of the ear in subcutaneous tissue at the base of the convex side of the ear [2].

Auricular Cartilage

The auricular cartilage includes the helix, anthelix, tragus, and antitragus. The helix is the free edge of the auricular cartilage, which has medial and lateral parts that meet at the apex. The anthelix is located on the medial wall of the ear canal, forms a low horizontal ridge, and has a prominent tubercle that is seen near the entrance. The tragus is the lateral wall of the entrance to the ear canal. The intertragic notch separates the thicker dense tragus from the more caudal and thinner antitragus. The aforementioned structures and the medial and lateral crura of the helix encircle the ear canal (Fig. 59-1). The auricular cartilage of the ear canal attaches to the skull at the dorsolateral-facing external acoustic meatus. The vertical ear canal extends to the transversely oriented horizontal canal, which terminates at the end (most medial aspect) of the ear canal, formed by the tympanic membrane. The tympanic membrane is also the lateral wall of the middle ear (Fig. 59-2). The annular cartilage is located medial to, and in part telescopes into, the rolled portion of the auricular cartilage and then has ligamentous attachment to the temporal bone.

Figure 59.1. Diagram of pinna and auricular cartilages. (Redrawn from Miller’s Anatomy of the Dog, 2nd ed. Evans HE, Christensen GD, (Eds). Philadelphia: WB Saunders, 1979).

Figure 59.2. Diagram of the middle ear and inner ear. (Redrawn from Miller’s Anatomy of the Dog, 2nd ed. Evans HE, Christensen GD, (Eds). Philadelphia: WB Saunders, 1979).

External Acoustic Meatus

The external acoustic meatus is lined by a continuation of stratified squamous epithelium from the ear canal and the adnexa, which include the more superficial sebaceous glands, tubular apocrine (ceruminous) glands located in the deeper connective tissue layer, and hair follicles. Both apocrine and sebaceous glands are responsible for the production of the cerumen. Although there is breed variation, hair follicles are located on the pinna and within the ear canal. The density of follicles, sebaceous glands, and tubular glands decreases in the depth of the canal and is least within the osseous meatus. Dogs with heavy hair coats have more compound hair follicles and have a consistent follicle density throughout the horizontal canal. Short-coated breeds tend to have fewer follicles and simple follicles near the eardrum [1,3]. Cats have little hair in the ear canal, and have more adnexa in the proximal third of the horizontal canal. Hair tends to point outward and, therefore, facilitates cerumen and debris moving out of the ear canal and resists movement toward the eardrum.

The skin of the entire ear canal is supported by a dense layer of connective tissue and gradually becomes thinner as it extends into the external acoustic meatus (Fig. 59-3). Coiled apocrine glands are noted in the deeper dermal layers of the peripheral ear canal. Normal canine ear canals contain actively secreting sebaceous follicles, which produce a holocrine substance that is secreted through ducts near the surface of the skin and occasionally directly to the skin surface [2]. Cerumen is a combination of desquamated corneocytes, apocrine secretions and sebaceous secretions, which contain protein, lipids, amino acids, and mineral ions. Cerumen tends to be sticky, and this adhesive character is considered a local protective mechanism, helping to prevent debris from moving toward the tympanum. Small coiled tubular apocrine glands are not common in healthy ears and are located below the sebaceous glands. In long-standing otitis externa, secretions from both sebaceous and apocrine glands become copious and accumulate within the external auditory meatus. The increased activity of the cerumen glands results in excessive cerumen accumulation, which is a good growth medium for bacteria, especially for pathologic microorganisms [2,3].

Figure 59.3. Histopathologic photomicrograph of a transverse section of a normal canine ear canal (H & E). Photomicrograph courtesy of Dr. Pam Ginn, University of Florida. (Reprinted with permission from Bellah JR. When should you recommend total ear canal ablation and lateral bulla osteotomy? Vet Med June:544-550, 1997).

Peripheral Nerves

Peripheral nerves that supply the ear canal are the vagus nerve, which provides sensory innervation to the external auditory meatus, and the facial nerve, which is responsible for motor innervation but also provides two branches that enter the caudal and caudolateral aspect of the vertical canal. These branches provide sensory innervation to a portion of the pinna [4]. These small sensory branches of the facial nerve are transected during ear canal ablation [4].

Epithelial Migration

The ear is hypothesized to have a self-cleaning function that is thought to be a mechanism that keeps the external auditory meatus clean [5]. Investigative work has suggested that epithelial migration occurs from the tympanic membrane outward toward the opening of the ear canal. The tympanic membrane has a generation center (a region where epithelial cell mitosis is increased) that is thought to replace cells that migrate actively off the tympanum and outwardly or distally along the ear canal wall. Cells in the stratum basale and stratum spinosum are implicated as being important in this process because of their asymmetrical shape and their long-axis orientation in the direction of epithelial movement. These cells also have a high concentration of contractile proteins when compared with other cells [2]. In this way, the debris is passively transported toward the canal opening. The hypothesized lateral epithelial migration may explain, in part, the rapid wound healing potential within the ear canal and the general lack of debris within the canal.

Tympanic Membrane

The eardrum or tympanum is a thin, transparent barrier between the external ear canal and the middle ear. It is made up of the pars flaccida, the small triangular region that is located between the lateral process of the malleus and the margins of the tympanic incisure, and the pars tensa, the larger region of the membrane. The umbo membranae tympani is a depressed point opposite to the distal end of the manubrium. Otoscopically, the stria malleolaris is seen running dorsocaudally from the umbo membranae tympani toward the pars flaccida. The pars tensa is attached firmly to the surrounding bone by a fibrocartilaginous ring, known as the annulus fibrocartilaginous, and the latter is attached by fibrous tissue to the external acoustic meatus [1].

The Middle Ear

The middle ear is located just medial to the ear drum in the tympanic cavity, which is an oval-shaped cavity in the petrous temporal bone. The middle ear includes the auditory (Eustachian) tube, the larger bulbous or pear-shaped cavity known also as the osseous bulla, and the epitympanic recess, which houses the three auditory ossicles. In the cat, the tympanic cavity is bisected into a dorsolateral compartment and a ventromedial compartment by a boney septum. Structures of importance in the middle ear are the auditory ossicles (malleus, incus, and stapes), the vestibular (oval) window, the cochlear (round) window, and the auditory tube (Eustachian tube). The vestibular window is occupied by the base of the stapes (Fig. 59-4). The auditory tube ostia is located rostrodorsally near the cochlear window. The chorda tympani nerve, a branch of the facial nerve, passes through the dorsal aspect of the tympanic bulla, crossing the manubrium of the malleus, and eventually joins the lingual nerve. The vital structures within the tympanic bulla are located dorsomedial in the cranial-most region. The tympanic bulla is bordered externally by the digastricus muscle laterally and by the styloglossus and hyoglossus muscles medially. The hypoglossal nerve is located medial to the bulla. The tympanohyoid cartilage of the hyoid apparatus attaches to the mastoid process of the skull, which is caudal to the external acoustic meatus and caudolateral to the tympanic bulla. The air-filled tympanic cavity is lined by columnar ciliated epithelium, which forms an essentially translucent membrane lining which continues into the Eustachian tube. Simple squamous epithelium lines the ventral aspect of the tympanic cavity and also invests the auditory ossicles, the inner surface of the tympanic membrane, and the membranes over the vestibular (oval) and cochlear (round) foramina.

Figure 59.4. Sculptured medial view of the right middle ear and cochlea. (Redrawn from Miller’s Anatomy of the Dog, 2nd ed. Evans HE, Christensen GD, (Eds). Philadelphia: WB Saunders, 1979).

The Inner Ear

The osseous labyrinth within the petrous temporal bone contains the cochlea, vestibule, and the semicircular canals. Within the osseous labyrinth are membranes that form a closed system that contains endolymph and is termed the membranous labyrinth. The membranous labyrinth is made up of three parts - the vestibule (saccule and utricle), the cochlea, and three semicircular canals - and is the sensory end organ for the vestibulocochlear nerve and the vestibular mechanism. Changes in the position of the head are detected by this proprioceptive apparatus, which then directs tenseness of postural muscles. It is this mechanism of the ear that when damaged results in vestibular signs, including a head tilt toward the affected side and horizontal nystagmus. The fast phase of horizontal nystagmus is away from the affected side when the injury or disease is peripheral. Small animals that are severely affected often cannot walk and will roll toward the affected side. The median longitudinal fasciculus and accompanying cranial nerves III, IV, and VI allow communication from the vestibular nuclei to the ocular muscles and, therefore, are the neurologic pathway that results in nystagmus.

Developmental Anomalies

Congenital problems within the ear canal are rare in dogs and cats. Anotia, the absence of an ear canal, usually occurs in conjunction with anophthalmia and other deformities, and affected animals often die or are euthanized prior to weaning. In puppies the external ear canal membrane occludes the ear canal until 14 to 17 days of age, when the canal opens. Complete failure of this membrane to disintegrate usually results in deafness, whereas a partially retained ear canal membrane will predispose to otitis externa secondary to poor aeration and drainage. Suspected atresia of the distal acoustic meatus has been reported in a Bouvier des Flandres, and associated otalgia was resolved by total ear canal ablation and lateral bulla osteotomy [6].

Dentigerous cysts and temporal odontomas may occur from ectopic tooth development. The incompletely developed tooth is usually found near the mastoid process of the petrous temporal bone and causes a sinus tract to form and drain near the base of the ear canal. Surgical removal of the sinus tract and the cyst resolves the condition.

Congenital deafness occurs as a result of a defect of the inner ear or because of a lesion of the auditory center and is either perceptive or central, respectively. These defects are associated with a lack of cilia in the organ of Corti, improper development of the cochlear nerve, or agenesis of the cochlea.

Acquired Disease of the Ear Canal

Otitis Externa

Inflammation of the ear canal may be caused by predisposing, primary, and perpetuating factors, and the degree of involvement may include one or more regions of the ear. Factors that alter the microenvironment of the ear canal predispose the canal to pathogenic and opportunistic microorganisms. Examples of such factors include pendulous ears, congenital stenosis of the ear canal, and mechanical obstruction of the canal by ear canal tumors or foreign bodies. It is known that ear anatomy plays a role in the development of otitis externa, and otic humidity seems to play a more important role than temperature [3,7]. Dogs with pendulous ears have significantly more otitis externa than dogs with erect ears, and some breeds (Labrador retrievers, American cocker spaniels, and English Springer spaniels) have greater numbers of apocrine (ceruminous) glands and, therefore, increased wax production [3]. The aforementioned breeds also had a higher density of hair follicles throughout the horizontal canal when compared with greyhounds and mongrel dogs [3]. Poodle and Lhasa apso breeds have a higher density of compound hair follicles, which promotes accumulation of ear wax and debris and interferes with migration of material out of the canal. Beagles and setters are breeds that are the exception to the above and are less frequently affected by otitis than are other pendulous-eared breeds. Alternatively, German shepherd dogs, as an erect-eared breed, are over-represented. The Chinese Sharpei breed tends to have a narrow, long vertical ear canal, which is essentially a stenosis in comparison with other breeds. Ear canal stenosis can be coincidental in other breeds; Chow-chows and their crosses also tend to have narrow canals. Acquired canal stenosis occurs from periaural masses such as neoplasia. Microflora that normally occur in the ear may be more apt to cause otitis externa when the microenvironment of the ear canal better supports organism growth. The stratum corneum can be broken down by increased moisture content in the ears, as maceration of the epidermis occurs, allowing microorganisms to colonize the ear canal resulting in otitis. Excessive moisture in the ear from swimming, excessive bathing, and environmental humidity and temperature (characteristic of the southeast region of the United States) can cause maceration of the surface of the ear canal and can influence the incidence of otitis externa. An investigation of first-time otitis externa cases over five geographic regions in North America found that monthly variations in ambient temperature, rainfall, and relative humidity correlated positively with the incidence of initial ear infection. The investigation found a 2-month delay between a climatic change and an increased incidence of otitis externa [3].

Mechanical trauma to the ear canal from excessive cleaning or from the excessive use of cleaning agents or drying agents may damage the ear canal. Systemic diseases may predispose to otitis externa as they may impair cell-mediated immunity. Ulcerative otitis externa has been reported to respond to immunosuppressive therapy in dogs [8]. Examples of diseases that may result in such immune impairment include feline leukemia virus, feline immunodeficiency virus, canine distemper, and canine parvovirus. Endocrine disease such as hyperadrenocorticism, hypoadrenocorticism, hypothyroidism, and diabetes mellitus may also be associated with otitis externa [3].

Parasites such as Otodectes cyanotis and Demodex canis are commonly responsible for otitis externa in young animals [9], especially in cats in which approximately 50% of cases are secondary to mite infestation. Ear mites cause mechanical irritation but the dog or cat can also become sensitive to antigens in mite saliva. When hypersensitization is present, it takes very few mites to cause severe inflammation. Demodex mite infestation generally causes a severe ceruminous otitis in dogs and in cats, and the presence of otitis may be the only sign of infestation. Other mites and Otobius megnini, the spinous ear tick may also be found in the canal, but these are less common than those previously mentioned. Grass awns, foxtails, and other foreign material including impacted wax may initiate otitis. The most common cause for bilateral otitis externa in the dog is hypersensitivity. Allergic conditions that commonly produce secondary otitis externa include atopy, food allergy, and contact allergy. Atopy, for example, affects as many as 50% of dogs at a given time, and is commonly associated with secondary infection. When atopy and other hypersensitivities that affect the ear are uncomplicated, the pinna and the vertical ear canal are reddened and pruritic, and the horizontal canal can be normal [2]. Otitis externa is present in 88% of dogs with food allergy [10]. Contact allergies are most commonly due to topical therapy; the indication of this is a worsening of the otitis and lack of improvement with the initiation of therapy [3,5].

Seborrhea is a disorder of keratinization that can result in ceruminous otitis. Other endocrine disorders that may be associated with otitis externa include hypothyroidism, male feminizing syndrome (Sertoli or interstitial cell tumors), and ovarian imbalance [3].

Tumors within the ear canal cause mechanical interference with normal movement of the cerumen from the ear canal and with drainage of exudates once otitis externa has occurred. Ceruminous gland adenoma and adenocarcinoma, sebaceous adenocarcinoma, mast cell tumor, squamous cell carcinoma, and benign conditions such as polyps can obstruct the ear canal.

Perpetuating factors that prevent resolution of otitis externa or that worsen preexisting otitis are usually microorganisms. The normal ear canal has microflora in low numbers that include both commensal and pathogenic bacteria. Staphylococcus intermedius is a common bacterium involved in otitis externa, and other species frequently encountered include Pseudomonas spp., Proteus spp., Escherichia coli, Enterococcus spp., and Corynebacterium spp. Pseudomonas is cultured from 12 to 35% of ears with otitis externa [11]. Multiple organisms can occur in otitis externa. In 20% of cultures another organism may be missed, and this is one criteria that should be considered in treatment failure [12]. These organisms benefit by alteration of the microenvironment within the ear canal and impaired drainage from the canal, which results in their proliferation and potentiation of the inflammatory response. Malassezia spp. is the most common fungal organism found in the ear canal, and it can be present in both normal and inflamed ears, but is highly opportunistic in macerated and inflamed ears, and is common as a secondary complication in atopic skin disease or food allergy. Other fungi, such as Candida, Aspergillus, and Microsporum may cause otitis externa [3].

Otitis externa results in progressive injury to the ear canal if medical therapy is not able to control the cause and the inflammatory response. Initially, when otitis is acute, canal erythema and swelling occur as many inflammatory cells infiltrate the dermis and epidermis. Apocrine glands hypertrophy and dilate, with an accompanying increase in the production of cerumen. The cerumen that is produced differs in composition as well. Normally, epidermal migration occurs toward the opening of the ear canal, but if the inflammatory response is progressive the epidermis begins to fold (Fig. 59-5) and epidermal migration is inhibited. Eventually, the increased glandular activity, epidermal thickness, and decreased epidermal migration lead to excessive wax production with a buildup of keratinaceous debris, and proliferation and overgrowth of bacteria occurs. Persisting inflammation results in dermal fibrosis within the horizontal canal and calcification of annular and auricular cartilages, usually from deeper regions to the exterior, and ossification can occur late. The end-stage result is permanent stenosis of the ear canal lumen [3,5]. Complete obstruction of the ear canal lumen can result, and the inflammatory process can "break-out" of the ear canal and result in development of periaural fistulae (Fig. 59-6 and Fig. 59-7)

Figure 59.5. Histopathologic photomicrograph of a transverse section of an ear canal in a dog with otitis externa (H & E). Note hyperplasia of apocrine tubular glands, thickening of the epidermis, and a buildup of keratinaceous debris. (Photomicrograph courtesy of Dr. Pam Ginn, University of Florida).

Figure 59.6. Labrador retriever with end-stage otitis externa and break-out abscessation with the draining fistulae. The ear canal was ablated (see Figure 59-7). (Reprinted with permission from Bellah JR. When should you recommend total ear canal ablation and lateral bulla osteotomy? Vet Med June:544-550, 1997).

Figure 59.7. Histopathologic photomicrograph of a transverse section of an ear canal in a dog with severe end-stage otitis externa (the dog in Figure 59-6). Note the obstruction of the ear canal owing to cartilage mineralization and the severe hyperplasia and microabscessation within the canal lumen (H & E). Photomicrograph courtesy of Dr. Pam Ginn, University of Florida. (Reprinted with permission from: Bellah JR. When should you recommend total ear canal ablation and lateral bulla osteotomy? Vet Med June:544-550, 1997).

Clinical signs of ear canal disease do not necessarily differentiate the varying causes of otitis. Pruritus, pain, erythema, swelling, and drainage are common. Depending on the severity and amount of drainage from the ear and whether the middle ear is involved, a head tilt may be noted to the affected side. Excessive head shaking may lead to aural hematoma. A discharge or foul order is often present. Periauricular excoriations and alopecia may be noted. In uncomplicated allergic otitis externa, erythema of the pinna and the vertical canal may occur and the horizontal canal may be relatively unaffected. Proliferative disease may be limited to the vertical canal. Ulcerations and erosions of the ear canal may occur with contact dermatitis or gram-negative bacterial infections. As the otitis externa becomes more chronic, the compliance of the cartilage support of the ear canal is lost as it becomes mineralized. Acute otitis externa is painful to dogs and cats; but as the condition becomes more chronic, less dramatic pain responses are elicited during examination. However, calcified ear canals are associated with intense pain. Hearing loss is often detected by the owners as otitis becomes end-stage.

Tympanic Injury

Tympanic injury is most commonly secondary to otitis externa in small animals [13]. Proteolytic enzymes that accumulate from bacterial release and from the degradation of inflammatory cells have destructive effects on the epithelial surface of the tympanic membrane. Once a perforation occurs, the bacteria, enzymes, and debris have access to the respiratory epithelium of the middle ear [13]. Traumatic perforations occur from direct trauma (i.e., cotton-tipped applicator or excessive fluid pressures against a weakened membrane) during ear canal cleansing. Masses, such as nasopharyngeal polyps in cats, may cause pressure necrosis as they push against the tympanic membrane, and secondary infection and its by-products cause additional injury.

The tympanum is capable of healing, and will attempt to do so if remnants of the eardrum remain. Two factors are required to accomplish tympanic membrane healing: a satisfactory blood supply and an intact germinal epithelium. The blood supply to the germinal epithelium arises from vessels within the pars flaccida; therefore, this region of the eardrum must be intact for healing to occur. The germinal epithelium that produces the epidermal layer of the tympanum is located near the manubrium of the malleus. From that location, the tympanic epithelium grows radially toward the annulus of the tympanic membrane, and healing can be complete in a period of 3 weeks to 4 months [13].

Tympanic membrane wound healing has been investigated. Keratinocytes proliferate on the external surface of the eardrum simultaneously with proliferation of fibrous connective tissue cells in the middle layer. The inner layer of epithelium differentiates into ciliated and secretory cells at the border of the perforation. Early healing and closure of the tympanic wound is by the migration of the superficial epithelial layers of the eardrum, and permanent apposition and closure of the defect is by the slower-migrating basal epithelium [13]. In naturally occurring eardrum perforations, pathologic changes tend to be progressive, such that inflammation, fibrosis, tympanosclerosis, and hyperkeratosis are found to impair wound healing progress. Keratinized epithelial proliferation may localize to the medial side of the tympanum and protrude into the middle ear cavity. Otitis media, because of the production of mucous and purulent exudates, including proteolytic enzymes, impairs eardrum healing. If lysis of the malleus occurs and the germinal epithelium is destroyed, or if fibrous scar devitalizes the pars flaccida, perforation will be permanent [13]. A ring of hyperkeratotic epithelium in the region of the perforated tympanum is an indication of chronic permanent perforation. Persistent drainage with relapsing otitis media occurs in this condition.

Surgery of the External Ear Canal

Surgical treatment of the external ear canal is done to treat relapsing or persisting otitis externa, stenosis of the vertical or horizontal ear canal, neoplasia, vascular disease of the pinna, and traumatic injuries to the ear canal. Specific techniques for specific conditions of the ear are not the objective of this chapter, but commentary on specific areas of the ear and the surgery appropriate for those areas follows.

Pinna

The pinna of dogs and cats is important functionally to pets but also cosmetically to pet owners. Traumatic lacerations and injuries to the pinna are common and result from skirmishes between cats, between dogs, between cats and dogs, and from gunshot and other missiles. Many partial-thickness lacerations do not require suturing, but apposition using fine sutures (3-0 to 5-0) often improves the cosmetic result. Full-thickness lacerations benefit by including the cartilage of the ear canal in the suture loop (i.e., vertical mattress), so careful apposition of the cartilage edges is done, followed by suturing the skin on the opposite side. Lacerations on the haired (convex) side of the ear canal may be more easily apposed and sutured because subcutaneous tissue separates the dermis and cartilage on that side of the pinna [2,14].

When it is necessary to remove a mass, from the pinna, the haired surface of the convex surface of the ear canal has sufficient skin that may be undermined and closed after tumor excision. Depending on the location of the mass, it is possible to remove masses up to 2 cm in size 14 with the expectation of achieving primary closure without creating a flap from the head or neck. Moveable skin is more readily available near the base of the pinna. On the concave surface, the skin and cartilage are in close contact, so undermining is difficult. Small non-malignant masses may be excised with narrow margins, and the small minor wound may heal by second intention. Small malignant masses may be excised by removing skin, mass, and underlying perichondrium and cartilage, whereas larger masses with known malignant character are best aggressively removed by excision of the entire pinna. This results in cosmetic asymmetry but is preferable to leaving microscopic tumor at the excision site.

Large defects of the lateral non-haired skin of the pinna are difficult to correct because of the inability to undermine skin extensively and because the auricular cartilage is inelastic. Various reconstructive techniques are available including the creation of local skin flaps from the skin of the cheek or neck. Flaps of varying shapes may be designed to repair the ear cosmetically using staged techniques. The different hair color or direction and the thickness of the skin are disadvantages to consider. Defects of the central portion of the pinna may also be resolved with similar techniques.

Amputation of a portion of the pinna is simplest when neoplastic involvement or traumatic devitalization of a portion of the pinna is located at the periphery of the ear. Full-thickness incisions, using a scalpel blade, can be done by obtaining a margin of normal pinna to be removed with the tumor. A scalpel is the instrument of choice as it is the least traumatic instrument for incision versus traumatically crushing the auricular tissues with scissors. Occasionally, curvilinear incisions at the edge of the pinna may be made with very sharp scissors as it is sometimes easier to make a more cosmetic (rounded) incision. The concave and convex skin margins are sutured over the cartilage, using fine suture. Excisions of masses along the anterior or posterior margins of the ear canal may done by removing a triangular portion of the edge of the canal (a wedge), and apposing the full-thickness margins in two layers. Sometimes this will narrow the pinna of pendulous ears or make the pinna slightly more convex in erect ears, but once the hair grows back, a good cosmetic result is often attained.

Lateral Ear Resection (LER)

Lateral ear resection, the Zepp procedure, has been done to aid management of otitis externa in dogs since 1949 [15]. Over the years, veterinary surgeons have altered their approach to otitis externa, from recommending lateral ear resection frequently in dogs that have relapsing otitis externa, to rarely recommending this surgery. The advent of better ear care in general and the knowledge that the results of lateral ear resection surgery are not the panacea for resolution of otitis that might have been anticipated. The potential for adjunctive surgical therapy to be efficacious was a sincere goal, as approximately 4% of veterinary hospital admissions involve some form of otitis externa [16]. Lateral ear resection does result in a significant change in the microclimate of the ear, and in one study relative humidity was reduced by 10% in operated external ear canals [17]. In a study of 281 dogs with otitis externa, Tufvesson found LER to resolve approximately 50% of otitis externa in dogs, with another 15% of the dogs showing improvement, and the remaining 35% showing minimal or lack of improvement [18]. In this study, age or breed did not affect the outcome; however spaniels, poodles, and Airedale terriers were predisposed [18]. A similar outcome was reported by Gregory and Vasseur in a small number of dogs (N=26), where 41% had good outcomes, 12% improved, and 47% had a poor outcome [19]. They concluded that a technically correct LER does not ensure a successful outcome, but also noted that clinical signs improved in some instances where the surgery was a technical failure [19]. A post-surgical investigation by Lane and Little, of 135 dogs with persistent aural drainage after ear surgery found concurrent otitis media, irreversible disease of the medial vertical ear canal, and unsatisfactory drainage from the horizontal canal to be the most common factors recognized with surgical failure [20]. Surgical outcome in another study showed LER to achieve acceptable results in 45% of the dogs treated and 55% to be unacceptable. Acceptable outcomes were rated excellent (the ears no longer required regular cleaning and the dog had no more than 2 bouts of otitis externa since the surgery) or good (the ears had occasional flare-ups of otitis externa, no more that 2 per year that readily responded to topical medical management. Unacceptable outcomes were rated fair (the ears required regular cleaning in order to prevent a relapse of the otitis and the dog experienced an average of 3 or more bouts of otitis annually) or poor (the ears progressed to an end-stage with an occluded canal as determined by follow-up physical examination). The Cocker spaniel breed had poorer results than other breeds, showing a failure rate of 86.5%. Non-Cocker spaniel breeds had an LER acceptable result percentage of 63%. The Shar pei breed was found to have narrower vertical ear canals [21]. Other studies have shown varied acceptable results from LER surgery [19]. Johnston found disappointing results when LER was performed in 41 dogs, after otitis media was present and severe changes developed in the ear canal with ruptured tympanums. Aggressive middle ear flushing and appropriate antimicrobial use based on culture and susceptibility testing in addition to LER found in these dogs clinical improvement, but head shaking and drainage from the horizontal canal persisted [22]. A lesser affected group in this study, 70 dogs with a history of 1 to 2 years of otitis externa and minimal canal changes were treated by LER. In this group, 50 had severe eardrum perforations and the other 20 had diseased and likely ruptured eardrums; LER resulted in slight to moderate discharge with reduced discomfort and head shaking [22]. The third group of 33 dogs in this study were dogs that had been affected by lifelong otitis externa at 12 to 18 months of age (based on breed, a minimum of 3 episodes of otitis externa after treatment and evidence of atopy or other allergic skin disease). Dogs in this group did not have tympanic rupture. In this latter group of 33 dogs, all dogs had resolution of ear discharge and discomfort at 6 months after surgery, and no dogs had eardrum perforation [22]. The conclusion was made that LER (Zepp) was definitively indicated once a predisposition to otitis externa was diagnosed and before irreversible changes are present within the ear canal, tympanum, and the middle ear [22]. If surgical intervention is considered a last resort after proliferative disease and canal obstruction is in progress, the procedure is doomed to fail.

Indications for recommending surgical resection of the lateral wall of the vertical ear canal or creating a lateral ear canal flap that is positioned ventrally (Zepp) may be when masses involve the lateral aspect of the vertical ear canal or when opening the vertical canal to change the microclimate of the ear canalis judged beneficial to the individual dog with otitis externa [23]. The latter indication presents a more difficult decision as lateral ear resection is an adjunctive measure and not considered a curative procedure for otitis externa. The procedure does change the microclimate of the ear canal and can have a positive impact on aiding treatment of otitis externa. In addition to altering the microclimate of the ear canal, LER improves drainage of fluid and exudates from the horizontal canal by eliminating the vertical canal "reservoir" that must be overcome by head shaking. The region aerates better and is more easily cleaned, and in some dogs at the least this is palliative. A horizontal ear canal with minimal chronic proliferative changes is necessary for this surgery to be considered [24].

Lateral ear resection does not require special equipment and it is not a difficult procedure to complete. The most common error made is an inaccurate incision of the vertical canal. This can happen if the lateral canal flap is made too thin on the lateral aspect, making the base of the flap too narrow, or on the medial side, resulting in a narrow strip of vertical ear canal remaining and a lateral canal flap that is difficult to bend to a ventral location. The goal is to incise the flap so the ventral aspect of the horizontal canal is wide open and the lateral flap makes a smooth cranioventral bend. The flap created is trimmed to a length of approximately 2 cm and sutured such that it remains ventral. The method of suturing is up to the individual surgeon's preference. The most difficult area to suture is the deep corner of the lateral ear canal flap where it bends away from the vertical ear canal. A figure-of-eight mucocutaneous suture pattern (similar to that used for mucocutaneous apposition) may be used to make the sutures more accessible at suture removal [23,25].

Vertical Ear Resection (VER)

A slightly more aggressive ear canal excision is the vertical canal resection. It is less commonly used for otitis externa [26]. Complete resection of the vertical ear canal is more commonly done when trauma has lacerated and injured the vertical canal badly or when neoplasia involves the vertical segment of the ear canal. Atopic dogs and dogs with food allergy, in which inflammation and swelling are more focally located within the vertical canal, benefit by having the proliferative changes in the vertical ear canal removed [27]. The horizontal canal is commonly spared severe inflammatory effects in these two allergic conditions; the most pruritic region seems to be the vertical canal and extending upward toward the pinna [3]. When vertical ear canal excision is considered for aural tumor excision, the most important factor is determining the presence of sufficient horizontal canal for wound closure after resection. Imaging the ear canal and skull by computed tomography (CT) prior to surgery aids preoperative decisions. In the absence of CT, local inspection to explore the canal during surgery by means of a lateral ear resection approach may be necessary. If the horizontal canal is insufficient, a total ear canal ablation is done to achieve the best surgical margin possible beyond the tumor. The surgical approach for vertical canal resection requires conservation of periaural skin for wound closure and, therefore, differs from lateral ear canal resection. A T-shaped incision is commonly used, and the incision correlating to the top of the "T" can meander along the margin of the tragus cartilage if the skin is normal. to preserve all available skin for closure under the pinna. Conserving skin facilitates apposition of wound edges between the horizontal ear canal stoma and the pinna.

The vertical canal is isolated around its entire circumference by dissection next to the cartilage of the ear canal and pushing or making a minor incision in the parotid salivary gland to aid exposure. Remaining directly adjacent to the ear canal is especially important on the concave surface of the canal so the auricular vessels that supply the pinna of the ear are not damaged. The level of the incision at the dorsal aspect of the ear canal is dependent on the position of the tumor being excised or the level of proliferative disease if done for atopy. Once the resection is completed and hemostasis obtained, the horizontal canal remaining may be divided into dorsal and ventral baffle plates if enough canal is present. If not, the skin is sutured directly to the circular remnant of the horizontal canal. The figure-of-eight mucocutaneous suture pattern is useful when little horizontal canal remains. The apposition of skin around the horizontal canal is done first, followed by apposing the skin to the pinna from the anterior and posterior edges.

Total Ear Canal Ablation and Lateral Bulla Osteotomy (TECA-LBO)

End-stage otitis externa results in obstruction of the ear canal to the extent that normal lateral epidermal migration of debris and keratinized epithelium does not occur, and in most canals the eardrum is ruptured, and otitis media is present as well. Removing the entire ear canal is a common procedure in dogs, and less common in cats [28-30]. In cats, the most common indication for TECA-LBO in one investigation was neoplasia [29], with 86% of the neoplasms being ceruminous gland adenocarcinoma [29]. Total ear canal ablation is indicated to resolve the discomfort and chronic infection and drainage from end-stage otitis externa and calcified canals, from neoplastic disease located deep within the ear canal with or without secondary infection, and to resolve para-aural abscessation that results from traumatic avulsion and secondary stricture of the ear canal [31,32]. Traumatic avulsion of the annular cartilage from the external auditory meatus in a cat has also been reported and was treated by ablation of the ear canal [33]. Traumatic ear canal separations may be managed by isolating the distal end of the horizontal ear canal (annular cartilage) and suturing the open end to the skin to allow cleaning and maintenance of patency [34].

Many references and texts contain reviews of the surgical technique for ablation of the ear, and each surgeon has specific methods to facilitate exposure and completion [28-30,35,36]. Many surgeons use a "T-shaped" incision similar to that used for vertical canal resection; however, the author's preference is to make an incision from the cranial aspect of the opening of the ear canal in a caudoventral direction but following the edge of the ear canal to the caudal aspect of the ear canal opening, and then extending ventrally parallel to the vertical ear canal to a level below the horizontal canal. The purpose of this incision is to conserve as much skin as possible to aid closure after resection of the ear canal, essentially in the manner of a single pedicle advancement toward the concave surface of the pinna. Once the incision is made, dissection is carried to the level of the cartilage and soft tissues are removed by sharp and blunt dissection around the entire circumference of the vertical ear canal. The level of the incision made to release the dorsal aspect of the vertical canal depends on where the proliferative disease extends. All proliferative disease should be removed, but the higher the level of the vertical canal resected the more important it is to carefully remain intimate with the cartilage of the ear canal so auricular vessels supplying the pinna are protected. Dissection down to the horizontal ear canal and continuing down to the external acoustic meatus is carefully continued. Note that branches of the facial nerve, the caudal internal auricular nerve and the lateral internal auricular nerve penetrate the caudal and lateral aspects of the horizontal canal, respectively [4]. Each is associated with an artery that is ligated. The facial nerve is located just caudal and ventral to a boey protuberance about 5 o'clock or 7 o'clock, depending on whether the left or right ear canal is being ablated. The facial nerve need not be identified at surgery as its trunk is located just caudal to the external acoustic meatus and just ventral to the mastoid process, a protuberance that can be palpated during surgery. These landmarks allow the location of the facial nerve to be kept in mind so careful retraction of neighboring soft tissues may be done and care is taken not to compress this region as the nerves movement is restricted by the close proximity to the stylomastoid foramen where the nerve exits the skull. Rarely, facial nerve is incorporated in an inflammatory response that extends from the ear canal, but more often is simply pushed away by the expansion of the canal tissues.

The dorsal-most aspect of the circumference of the horizontal canal is the location that allows the most convenient entry into the tympanic cavity. The ear canal can usually be pushed away from the meatus using a Freer elevator. The remainder of the circumference is then released by gradually extending the separation around the entire circumference. The caudo-ventral aspects of the canal attachment are the most difficult and this is also where bony proliferation is the most extensive. The retroarticular foramen should be avoided so hemorrhage from the retroglenoid vein does not occur. Tissues or debris are collected for culture and histopathologic examination once the canal is released. Bacteria cultured from TECA-LBO sites commonly include Streptococcus canis and E. coli [37]. One investigation showed bacteria to remain after debridement and lavage of the tympanic cavity, and in this study, only 26% of isolates showed susceptibility to cefazolin [38].

Access to the tympanic bulla is accomplished by lateral bulla osteotomy and is done to allow thorough removal of debris and tissue extending into the middle ear. An air drill is the most efficacious method for removing the thick cortical bone of the external acoustic meatus. Ronguers can be used effectively. Care must be taken to avoid wrapping up soft tissues around the canal if a drill is used and also to carefully inspect the tissues just ventral to the external meatus so no secretory epithelium remains. Branches of the carotid artery are located deep to the tympanic bulla and severe hemorrhage may result if these vessels are torn during dissection. Thorough lavage is done and closure of the surgical wound is performed.

Drains are not necessary to maintain drainage after TECA-LBO [35]. Primary closure is most commonly done after TECA-LBO but passive drains may be used at the discretion of the surgeon. Drains may be used in some instances where "breakout" abscessation has occurred and fistulae are apparent prior to ablation, as the extent of wound infection can be well beyond the region of the ear canal. Soft tissues are apposed, being careful to avoid deep suture bites that may penetrate vessels. Subcutaneous tissues are apposed and cartilage may be included in the suture pattern if necessary for wound strength. The apposition of the wound margin of the pinna (remainder of the auricular cartilage) to the skin flap is done from a cranial to caudal direction, as "dog-ear" correction is simple to do at the caudoventral aspect of the incision.

Facial paralysis is the most common complication and likely results from ischemia caused by compression or traction of the facial nerve near the mastoid process. Incidences vary from 5% to 58% [30]. Ischemia, if sustained long enough, will cause fiber degeneration within the nerve and result in loss of function. As long as the facial nerve is intact, function should return, as the fibers regenerate at a rate of approximately 1 mm per day. Although the incidence of facial nerve paralysis is high, careful technique in the region of the mastoid process and ventral to the external acoustic meatus will protect nerve function. In cats, facial nerve paralysis occurred in 56% of cats that underwent TECA-LBO, and 42% had Horner's syndrome [29]. Nerve fragility was suggested to be greater in cats in comparison with dogs [29].

Persistent otitis media and development of periaural sinus have been reported to be as high as 30% in dogs undergoing total ear canal ablation [30,39]; however, most veterinary surgeons would estimate that less than 10% are affected [40,41]. The source of the fistulae may be tissue or material within or outside the tympanic cavity [40]. Plain radiographs and sinography may be used to demonstrate the source of drainage [42]. It is uncommon for persisting otitis media with sinus tract development to be successfully treated with drainage and antimicrobial therapy; only 1 of 17 and 1 of 8 dogs in 2 reports were successfully treated in that way [41,43]. In the author's opinion, lateral bulla osteotomy is the procedure of choice to attempt resolution of draining sinuses and persisting otitis media. Although a ventral bulla osteotomy may be used and will accomplish good exposure of the tympanic cavity, it is difficult with this procedure to access the region of the acoustic meatus, especially laterally where remnants of secretory epithelium may be found. Retraction of the external carotid artery and at least partial transaction of the digastricus muscle is required to obtain exposure to the lateral aspect of the external acoustic meatus if a ventral approach is used [40]. Facial nerve location is difficult with the lateral approach after TECA-LBO as the canal landmark is not present. The mastoid process is still palpable, however, and careful dissection along the deeper portions of the sinus will help protect the facial nerve. A lateral approach allows the sinus tract to be followed (inserting a red rubber catheter into the tract is an effective method for following the tract during surgery) to the remnant of the external acoustic meatus and for the tympanic cavity to be reopened to a wide enough dimension and be debrided of debris and any adnexal structure that may be causative.

Vestibular signs, including nystagmus, head tilt, and postural abnormalities may occur when trauma to the promontory and the oval and round windows occurs during curettage of the tympanic cavity [30]. This is a rare complication but is probably the most disconcerting to an owner because the dog shows such anxiety as it tries to walk. Usually, vestibular signs abate over a period of weeks, but residual signs such as a persisting head tilt may remain [40].

Necrosis of the pinna from careless dissection, hemorrhage, and airway obstruction have been reported to occur after ear canal ablation. The latter complication has been noted when severe hemorrhage occurs, and when bilateral ear canal ablations are done during one anesthetic episode. Airway structures are in close proximity to the tympanic bullae such that severe hemorrhage or edema may result in airflow resistance when dogs are extubated. Cervical bandages that are too tight may also restrict good airflow.

Multiple regimens exist to provide analgesia for aural surgery. Opioids and combinations of systemic administration and local nerve blocks are used commonly [44]. Bupivacaine splash blocks and bupivacaine administration by analgesia catheter placement have also been used [45]. A comparison of systemic opioids with systemic opioids and preoperative nerve blocks found no advantage to the latter protocol [44]. The great auricular and auriculotemporal nerves may be blocked [36]. Extended release morphine tablets and transdermal patches may be used as well [36]. Tranquilization may be necessary, not for analgesia, but to provide restraint from head shaking and pawing at the incision in some animals. Physical restraint with E-collars to prevent the dog or cat from traumatizing the surgical site is also used.

Perioperative antimicrobial use is recommended for ear canal surgery, especially for TECA-LBO, and therapeutic use beyond the post-operative period should be based on the results of culture and susceptibility testing [38].

Auditory Function after Ear Canal Ablation

Pet owners are commonly worried about the effect of ear canal ablation on their pet's hearing. Dogs with bilateral end-stage otitis externa have been evaluated before and after surgery by auditory evoked response [46]. Prior to surgery, all dogs could hear a loud voice or noise, 3 dogs could hear a voice at a normal volume level, and 13 of 14 ears of the 7 dogs had a positive brainstem auditory-evoked response (air-conducted or bone conducted). After surgery, 2 dogs responded to a normal voice and all 7 dogs responded to a loud voice or noise. There were 3 of 13 ears that did not respond to an air-conducted stimulus that did prior to surgery, but all 13 ears in the dogs responded to a bone-conducted stimulus [46]. Experimentally, normal dogs that underwent ventral bulla osteotomy had reduced auditory evoked potentials after wound healing [47]. Proliferation of scar and bone in a subperiosteal location in some dogs impaired function of the auditory ossicles and tympanum. Although most dogs in the study reformed a tympanic cavity without hearing impairment, the internal surfaces were found to easily produce new bone, which if extensive, can affect hearing function in dogs [47].

Conductive hearing loss was evaluated in dogs experimentally using brain stem auditory evoked response threshold and latency-intensity. Dogs had their ears canals obstructed by an ear plug rated at 26 decibels, had mechanical irritation to induce transient stenosis of the external ear canal, a needle puncture of the tympanum, and extensive destruction of the tympanum with electrocautery [48]. The investigators found that only the mechanical plug and the destruction of a major portion of the eardrum produced pronounced hearing loss [48]. The size and location of the perforation and especially the loss of integrity of the auditory ossicles were factors that affected the severity of auditory-evoked response [48].

Otoacoustic emission (termed tinnitus in humans), an audible ringing from the ear canal, has been reported in a dog. Otoacoustic emission is the term used in animals because it cannot be determined if the animal consciously perceives the sound [49]. The dog was reported to have a normal brain-stem auditory evoked-response test, indicating the initial phases of sound processing in the affected ear were normal [49].

Otitis Media

Otitis media is defined as inflammation of the middle ear, and is usually caused by bacterial infection that has extended directly from the external ear canal [50,51]. In most situations the tympanum has ruptured, but the tympanum may appear intact at examination, as small defects may have healed [52]. Positive cultures of the middle ear cavity may often be obtained by myringotomy in the presence of an intact eardrum. In one investigation of 46 ears in dogs with otitis media, 71% of the ears had intact eardrums [52]. Bacteria are the most common cause of otitis media but yeast may be the causative agent as well [52]. Hematogenous route and the Eustachian tube are also sources of infection for otitis media [53]. Bacterial infection of the middle ear is usually secondary, from extension of otitis externa or cholesteatoma. Primary otitis media may occur owing to neoplasia, inflammatory polyps, and rarely, primary infections. Middle ear disease has been associated with congenital palatine defects in both dogs and a cat, without evidence of external ear disease [54].

The initial clinical sign of primary otitis media is pain, causing the dog to hold the affected ear down [2]. Clinical signs of disease involving the middle ear can be similar to those in other types of ear disease, but the routine head shaking, pawing at the ear, and drainage from the ear canal are more common in otitis media. Drainage may occur if the eardrum should perforate. Otoscopic or videoscopic examination of the eardrum, which often requires anesthesia, may reveal it to be discolored or possibly bulging into the external ear canal, and to have congested blood vessels [2]. A bulging discolored tympanum (dull, and grey to yellow) in the presence of a normal external ear canal suggests an origin of disease to be hematogenous or via the Eustachian tube. A myringotomy is done to obtain specimens for cytologic examination and for culture and susceptibility testing.

Disease of the middle ear can be expansile and result in an enlargement of the volume of the tympanic cavity ventrally, or the disease process can break through the boundaries of the tympanum. This can result in a mass that is sometimes palpable ventral to the bulla. Because of the proximity of the osseous bulla to the nasopharynx, if the expansile mass becomes large enough that it extends down toward the soft palate and compresses against these structures, oral examination may reveal the region of the dorsal tonsillar pillar and soft palate to bulge into the oropharynx. Noisy respiration may be noted if the nasopharynx is compromised. In addition, the osseous bulla is in close proximity to the temporomandibular joint so disease processes that cause inflammation and pain in this region may cause irritation when the mandible moves, resulting in dysphagia.

Diagnostic evaluation includes basic otoscopic examination, radiographs of the tympanic bulla, and cytologic evaluation of drainage from the ear. Computerized tomography is an ideal imaging technique for the middle ear, and use of contrast can provide valuable diagnostic information [22,55]. One report showed that CT was more accurate than skull radiographs for diagnosing middle ear disease when the degree of disease was moderate to high; however, when the severity of involvement of the middle ear was low, skull radiographs and CT were more variable in their ability to detect abnormalities [56]. Findings of proliferation of bone, lysis of bone, and in particular, extension of invasive processes toward or into the calvarium allow judgments to be made to avoid surgery as well as to help plan exploratory surgery. Once the diagnostic imaging is done, specimens from the middle ear can be obtained if the ear canal is not obstructed. Soft catheters may be placed by myringotomy if the tympanum is intact, or through a perforated tympanum, to obtain specimens for cytologic examination and for culture and susceptibility testing.

In dogs, aural cholesteatoma can be a sequel to ear canal occlusion and chronic otitis externa [3]. A cholesteatoma is an epidermal cyst that is found within the middle ear cavity and originates from a pocket of tympanic membrane that bulges into the tympanic cavity. This prolapse of epidermis adheres to the inflamed mucosa of the middle ear cavity and fills with keratin lamellae (Fig. 59-8) which is produced by the tympanic membrane epidermis [3,57]. This process can result in expansion of the osseous tympani bulla with remodeling of the bone that normally borders the dimensions of the normal tympanic cavity (Fig. 59-9). Cholesteatomas are most commonly secondary to otitis externa in dogs, but can be congenital or acquired [57]. Cholesteatomas that expand within the middle ear can cause oropharyngeal compression and partial obstruction of the nasopharyngeal tube [57,58]. Cholesteatomas that are secondary to chronic otitis externa can be managed successfully by total ear canal ablation and lateral bulla osteotomy. The large epidermal-lined cystic structure can be gently removed from the middle ear cavity. A ventral bulla osteotomy can be done and the epidermal cyst removed; however, if the cholesteatoma is secondary to chronic otitis externa, the tympanum and residual epidermis may remain.

Figure 59.8. Histopathologic photomicrograph of a section of the tympanic bulla in a dog with cholesteatoma. Note the epithelium and keratin flakes. (Photomicrograph courtesy of Dr. Pam Ginn, University of Florida).

Figure 59.9. Lateral radiograph of the affected tympanic bulla (Figure 59-8) in a dog with cholesteatoma. Note the lacy expanded margin of the tympanic bulla (open arrows).

Surgical Approaches to the Middle Ear

The three methods of access to the middle ear include myringotomy, ventral bulla osteotomy, and lateral bulla osteotomy. The most conservative approach is myringotomy, which is most commonly done to obtain specimens for culture and susceptibility testing and cytology when otitis media is suspected. Lateral bulla osteotomy is the more common surgical approach but is done in conjunction with total ear canal ablation for the purpose of debriding tissue and debris from the tympanic bulla. Ventral bulla osteotomy is done to explore the tympanic bulla, to remove tissue, tumors, and debris for histopathology and for culture and susceptibility testing. It is also done for removal of cholesteatomas and to promote ventral drainage. The ventral approach to the tympanic bulla is usually done when diagnostic evaluation reveals focal disease within the bulla, or if otitis media is not responsive to myringotomy and medical therapy, and if all efforts done to salvage hearing function are desired by the owner.

Surgical judgment is required when deciding which approach to perform for middle ear disease. Lateral bulla osteotomy is most appropriate for treatment of otitis media secondary to end-stage otitis externa. A ventral approach can be done but provides poor access to the lateral aspects of the external acoustic meatus. Ventral bulla osteotomy provides the most complete exposure to the tympanic cavity and is used when primary otitis media and other middle ear diseases are present. In dogs, breed differences cause ventral bulla osteotomy to vary in difficulty. For example, dissection is deep in stocky breeds such as the English bulldog and Boxer, whereas in dolicocephalic breeds the dissection seems easier. In cats, the osseous bullae are palpable prior to incision; however the tympanic bulla is partitioned into dorsolateral and ventromedial compartments. The surgical anatomy is basically the same, but the degree of difficulty of getting to the bulla may vary greatly. Vital structures encountered during the approach include the hypoglossal nerve, the external carotid artery, the lingual artery, and the sublingual salivary gland. Remember, the vital structures within the tympanic bulla are located dorsally and cranially; thus, the initial osteotomy approach must be made ventrally and caudally. The bulla is located between the angle of the mandible and the jugular process of the skull, but a convenient landmark that aids in finding the bulla is the hyoid apparatus. The tympanohyoid cartilage (attached at the stylohyoid bone) attaches caudal to the external auditory meatus, which is caudolateral to the tympanic bulla. It is also important to remember that, in addition to the vital structures in the periphery of the approach to the ventral aspect of the tympanic bulla, the oropharynx is just a few millimeters away and cavalier medial dissection can result in exposure of the oral cavity.

Inflammatory Polyps in Cats and Dogs

Inflammatory polyps are common in young cats and have been rarely reported in dogs [59-61]. These polyps are non-neoplastic and the exact etiology is not known, as neither a congenital origin or a secondary result of middle ear infection has been confirmed [62]. Polyps in cats do not appear to be associated with feline leukemia virus or feline immunodeficiency virus infections [62]. Attempts to find viral evidence by polymerase chain reaction (PCR) have been unsuccessful [63]. Chronic irritation to the mucosal surface of the middle ear may lead to the production of the inflammatory polyp, which is typically composed of well vascularized fibrous tissue stroma covered with respiratory epithelium. The ulcerated epithelium has an underlying stroma that contains both acute and inflammatory cells. Although the polyps can occur in cats of any age, the average age at diagnosis is 1.5 years [62]. Inflammatory polyps in cats are thought to originate most commonly in the middle ear near the junction of the auditory tube and the tympanic bulla, and from this location migrate into the horizontal ear canal by protrusion through the tympanum or into the nasopharynx via the auditory tube. Because the respiratory epithelium is continuous within the tympanic cavity, the Eustachian tube, and the nasopharynx, it is difficult to know the exact location of origin [62]. In the pharynx, polyps may attain a large enough size to cause stertorus respiration. Rarely, dysphagia may result. Surgical removal is accomplished by avulsing the polyp from the horizontal ear canal, or by ventral bulla osteotomy, or by an oral approach that may or may not require incision of the soft palate. Ventral bulla osteotomy to allow removal of the septum of the middle ear and curretage of the polyp base decreases recurrence of the polyps [64,65]. The polyp usually originates from the dorsolateral compartment. Curettage of both areas must be complete or recurrence of the polyp is likely. Horner's syndrome is usually transient after bulla curettage in cats (as many as 48% can have this complication) [62].

Traction or avulsion of the inflammatory polyp can be done from either canal or nasopharyngeal locations. A lateral ear resection can improve exposure [62]. Regrowth of the polyp may occur if the polyp stalk remains. In 22 cats that had inflammatory polyps treated by traction alone, 41% had recurrence [66]. Prednisolone was also used in cats reported in this investigation and was believed to aid suppression of recurrence, as 8 cats that received the corticosteroid did not have recurrence and 9 of 14 cats that did not receive the drug had recurrence of the polyps [66]. It has also been reported that nasopharygeal polyps are 4 times more likely to be successfully treated by traction alone than those that occur in the ear canal [62,66]. Perendoscopic trans-tympanic excision (PTTE) has been described and utilizes endoscopic view and endoscopic forceps to pinch away the polyp. In one report, 8 of 10 cats had complete resolution for 24 months, 2 cats required repeating PTTE, and 2 cats had temporary Horner's syndrome [67].

Laser ablation of inflammatory polyps can be done using videoscopic exposure and a CO2 laser [62]. Small polyps may be vaporized and gradually removed until the polyp stalk can no longer be seen. Larger polyps are removed by initially vaporizing a portion of the polyp stalk, avulsing the polyp, and then going back to finish vaporization of the polyp stalk [62]. Corticosteroid and azithromycin therapy are also recommended [62]. Antimicrobial therapy should be based ultimately on antimicrobial culture and susceptibility testing.

The tympanum is commonly destroyed when inflammatory polyps extend out into the horizontal canal. Although remnants of the tympanum and proliferation of scar tissue may result in reformation of the tympanum and partitioning of the middle ear from the external ear, persistence of this communication may result in relapse of otitis externa and media with persisting drainage from otitis media. In some cats, TECA-LBO may be necessary to resolve chronic otitis externa and media that may result.

In dogs, nasopharyngeal polyps and aural polyps rarely develop [62]. Polyps can enter the nasopharyngeal tube and affect the airway. In one dog, a polyp was removed by a staphylotomy approach, which allowed the polyp to be grasped and removed [59]. Polypoid masses are often large ceruminous-gland adenomas, rather than inflammatory polyps [62].

Complications of bulla osteotomy include injury to vital structures such as the hypoglossal or glossopharyngeal nerves, creation or exacerbation of otitis interna (vestibular signs), Horner's syndrome when sympathetic fibers are damaged, facial nerve paralysis, and hemorrhage. Head tilts present prior to surgery, especially if chronic, may persist despite resolution of disease.

Aural Hematomas

Aural hematomas are most commonly diagnosed in dogs but are occasionally seen in cats. They occur within the cartilaginous plate (intrachondral) of the auricle (pinna) of the ear. The hematoma, which consists of blood, serum, or both, has classically been thought to result from self-inflicted trauma to the ear. Pruritus, owing to allergy or ectoparasites or secondary to otitis externa, results in head shaking or scratching. The trauma is believed to cause a shearing force that causes separation of the cartilage of the pinna. The hematoma is painful and irritating to the dog or cat and causes more head shaking and pawing at the ear with subsequent extension of the region of involvement. In cats, aural hematomas are most commonly diagnosed when ear mite infestation and otitis externa are concurrent [2]. Aural hematomas show trauma to be a precipitating rather than an underlying factor. They are uncommonly associated with chronic skin diseases, and commonly occur when there is no other evidence of ear disease in the affected dog [68].

The aforementioned pathogenesis of aural hematomas in dogs was challenged in the late 1980s. Most veterinary surgeons have made the diagnosis of aural hematoma in the presence of a pristine ear canal; therefore, understanding the association of otitis externa and trauma is sometimes in question. An immune-mediated pathogenesis had been hypothesized on the basis of one study where 30% of affected dogs were LE cell positive, 100% of affected dogs were Coomb's test positive, and 52% of affected dogs had positive antinuclear antibody titers [69]. It was suggested that the inflammatory disease in the ears might serve as a triggering mechanism for an autoimmune reaction that could be responsible for cartilage degeneration, cartilage clefts, and subsequent development of the aural hematoma. Local treatment of aural hematoma remains unchanged, but judgment as to whether systemic therapy is appropriate is warranted. Dexamethasone has been recommended, based on these papers, to control the immune-mediated component thought to be responsible. This treatment remains controversial, and what works for some veterinarians may not work for others. Reported causes (or associations) include fungi, bacteria, parasites, atopy, aural foreign bodies, and aural neoplasia. An autoimmune pathogenesis posited in the literature in the past, has not been substantiated by more recent investigation [68]. The latter investigation did find cartilage degeneration associated with fibrovascular granulation tissue that may have been the end result of a macrophage-mediated process [62,68].

It is important to treat aural hematomas, because if left untreated, the result is usually a thickened fibrous scar that causes the ear to fold. The auricular cartilage perichondrium is highly chondrogenic, and chondroblast invasion into an organizing aural hematoma results in a firm hard cartilaginous mass of scar, and distortion of the pinna occurs. The end result of a conservatively treated aural hematoma is an abnormal shape that is most noticeable in breeds with erect ears. Various methods of treatment exist but all must be combined with careful otoscopic examination to discern whether self-inflicted trauma or head shaking is evident, as medical management of a concurrent problem is important for complete treatment.

Conservative techniques to drain aural hematomas are effective, and because a large incision is not made, minimal scarring of the pinna occurs. Active drainage technique or pressure can be an aid to evaluation of fluid from the aural cavity [70]. Each type of drain is placed into the cavity encompassing the hematoma after a small stab incision is made. The teat cannula is placed in the dependent portion of the hematoma. The drain must be cleansed daily to assure patency, and it may be necessary to leave it in place 14 to-21 days. If the drain becomes clogged by exudate, or if it is removed prematurely, recurrence of the hematoma is likely. Bandaging protects the ear from further trauma related to head shaking and also prevents soiling of areas in the home when drainage occurs.

More invasive techniques usually involve making incisions parallel to the pinna, evacuating the fluid, and suturing to appose the tissue layers with the hope of resolving and preventing recurrence of the aural hematoma. Various incision and suture patterns can be used to accomplish this; the choice depends on the individual surgeon. Too much tension on sutures may cause secondary contracture and deformation of the ear so care should be taken when placing sutures. Some surgeons feel a large curvilinear incision does not allow contraction to deform the pinna of the ear. A narrow gap is desired to aid maintenance of drainage from the concave surface of the ear. Non adherent contact dressings are used. Bandaging techniques also vary but are used to protect the ear from head shaking and to absorb drainage. Sutures are often left in place for 14 or more days.

More chronic aural hematomas may be firm and organized, as after 7 to 10 days fibroblastic infiltration of the hematoma occurs, and eventually cartilage forms. It is helpful to remove this material surgically and obliterate the space using sutures. In this state, drainage by the aforementioned techniques is not feasible. Organized hematomas must be removed by incision on the concave surface of the ear. The hematoma is removed and bleeding vessels are cauterized or ligated. The incisional margins are excised such that the edges do not meet and drainage is promoted. The dead space in the cavity is obliterated with through-and-through mattress sutures placed parallel to and on each side of the incision, with the knots on the external surface of the ear. An alternative technique is to place the mattress sutures from inside the ear through the cartilage without penetrating the opposing skin surface. A better cosmetic result is obtained as the development of stitch abscesses on the haired side of the pinna is prevented. Non capillary suture material should be used (i.e., monofilament nylon or polypropylene), and mattress sutures should be placed parallel to the long axis of the pinna to preserve blood vessels that are oriented in that direction. The carbon dioxide laser can also be used to treat aural hematomas [71]. Regardless of technique, a protective bandage and head wrap are applied and changed every 2 to 3 days, and sutures are removed in 10 to 14 days.

Antibiotic therapy is not indicated unless infection is suspected or confirmed by culture and sensitivity testing, but corticosteroids are used by those who feel an immune-mediated component contributes to the development of aural hematomas. Corticosteroids are also important to lessen head shaking and for patient comfort. Use of corticosteroids may also be therapeutic if the inflammatory response is in part responsible for cartilage separation and development of the aural hematoma.

Marginal Auricular Dermatosis and Ear Margin Fissures

Short-haired dogs with pendulous ears occasionally develop thickened areas at the apical edges of the pinna. These areas eventually become scab-like, which when removed reveal a raw bleeding surface. As these wounds heal, exposed cartilage disappears but the edge of the flap remains eroded and thickened [2]. Pinnal necrosis, often idiopathic, can affect toy breeds and requires surgical excision of the edge or apex of the pinna. (Fig. 59-10A and Fig. 59-10B) Biopsy of lesions of the pinna, especially on the concave surface, may be done using a 3 mm skin punch. Hemorrhage can be controlled by digital pressure, needle-tip cautery, or a cauterizing agent. It is important to obtain dermal tissue in the specimen. A small hypodermic needle can be used to tease the fibrous tissue off the cartilage base.

Figure 59.10A. Photograph of the ear of a Chihuahua with idiopathic pinnal necrosis. Surgical biopsy of this lesion is indicated and (B) cosmetic distal pinna excision, depicted by the dashed line, may be curative. (Photograph courtesy of Dr. Robert Kennis, Auburn University).

Figure 59.10B. Photograph of the ear of a Chihuahua with idiopathic pinnal necrosis. Surgical biopsy of this lesion is indicated and (B) cosmetic distal pinna excision, depicted by the dashed line, may be curative. (Photograph courtesy of Dr. Robert Kennis, Auburn University).

Ear margin fissures occur as a result of scratching or flapping the ears. This lesion appears as small wounds at the margin of the distal aspect of the pinna, and with continued trauma may become several centimeters long [2]. Treatment of the primary reason for the discomfort and head shaking (flapping) is important to break the cycle that results in recurrent injury. Treatment of long fissures requires debridement and suturing. Multiple small fissures are usually treated by excision of the most superficial edge of the pinna. A scalpel or sharp scissors (depending on the thickness of the edge of the pinna) can be used to excise the affected edge just proximal to the fissure. Sutures are not always required, but the ear must be bandaged across the head to prevent trauma to the wound margin from head shaking. Alternatively, the medial and lateral edges of the skin can be apposed gently over the cartilage edge with fine interrupted sutures of non-absorbable material, taking care to avoid penetrating the cartilage where possible. While the ear margin is healing primarily or by secondary wound healing, the primary cause for the irritation and trauma must be treated, so that once the ears are left unbandaged, ear flapping is minimized.

Auricular chondritis, resulting in bilateral thickening of the pinnae was reported in a cat. Slight curling of the pinna, intense erythema, and pain were evident. The cat responded to treatment with prednisolone [72].

Otolithiasis

Rarely, mineralized opacities may occur in the tympanic bullae. Mineralized necrotic material from previous otitis media may be the source of otolithiasis. Otolithiasis has been reported in three dogs and was detected by skull radiographs and CT [73]. Otoliths may be identified in active cases of otitis media, or in some dogs, maybe an incidental finding.

Aural Neoplasia

In dogs and cats, tumors of the ear canal are relatively rare, comprising between 2% and 6% of dog ear surgery admissions and 1% to 2% of cat ear surgery admissions, respectively [74]. Malignant aural tumors in dogs and cats include ceruminous gland adenocarcinoma, squamous cell carcinoma, and carcinoma of undetermined origin [74]. It has been stated that malignant tumors in dogs are less aggressive than those in cats [75]. It is expected that dogs generally live longer than 2 years after surgical excision of an aural tumor, whereas cats' median survival is about 1 year [75]. The median survival rates for dogs and cats with malignant tumors in a 1996 study were longer than 58 months and 11.7 months, respectively [74]. A more recent study in cats showed a median survival time of 50.3 months for those with ceruminous gland adenocarcinoma [29]. Negative prognostic factors were extensive tumor involvement, neurologic signs at the time of diagnosis, diagnosis of squamous cell carcinoma or of carcinoma of undetermined origin, and lymphatic or blood vessel invasion [74]. Squamous cell carcinoma is known to arise from the middle ear in cats, and may cause Horner's syndrome, vestibular dysfunction, and facial paralysis [29,76]. In the more recent study in cats, a mitotic index of greater or equal than 3 found cats living significantly less than cats with a mitotic index of less than or equal to 2 [29]. Approximately 25% of malignant aural tumors will have tympanic bulla involvement; therefore, imaging studies such as CT are helpful to plan surgical removal [75]. Metastasis to the thorax or to regional lymph nodes is present in about 10% of dogs and cats at the time of diagnosis [75]. For both dogs and cats, aggressive surgical resection of malignant tumors (i.e., total ear canal ablation with lateral bulla osteotomy), results in the longest survival times. Benign ear canal tumors can be managed with more conservative surgical resection, depending on the location of the tumor and the condition of the ear canal. Radiation may be used adjunctively where resection is incomplete, but little is known about the efficacy of chemotherapy [75].