EAR PINNA

The pinna, which is the first portion of the ear that is visible from a distance, is important to hearing because its anatomy is designed to capture sound waves. It also is involved with nonverbal communication between cats, and between cats and other animals, including human beings. Ear position, in association with facial expression and body position, can relay a number of feelings such as fear, anger, happiness, and curiosity.

Cats have pinnae that are more consistent in size and shape than in dogs. Most cats (except Scottish Folds) have erect pinnae unless a disease is present.

The pinna is triangular in appearance with the tip of the triangle distal (Figure 30-1). There is a concave surface that faces rostrolaterally and a convex surface that faces caudomedially. This shape is valuable in collecting sound and directing it toward the ear canal and eventually the tympanic membrane.

Figure 30-1 Cat pinna. Note the triangular appearance. Unlike dogs, the pinna of cats is almost uniform across breeds. The arrow points to the cutaneous marginal pouch.

Both the concave and convex surfaces are covered by skin that is lightly haired compared with the cat’s body. The concave surface is less haired than the convex surface. Sandwiched between these surfaces is the auricular cartilage. This cartilage is responsible for the shape of the pinna. When this cartilage is damaged, either through trauma or inflammation (e.g., auricular chondritis), the shape of the pinna will change (e.g., droop).

Because the epidermis, regardless of its location, is avascular, there are numerous small vessels located in the dermis to supply nutrients to the skin. When vessels rupture, the blood that escapes fills the space between the firm cartilage and the encasing epidermis, creating an aural hematoma. The exact cause of this occurrence is unclear. Historically it has been reported to be associated with otitis externa usually caused by ear mites; however, the author has seen more aural hematomas that are unassociated with concurrent ear infection. This may reflect the author’s specialty practice.

The skin of the pinna is the same as other areas of the body, consisting of epidermis and dermis. The associated adnexal structures, hair follicles, and sebaceous and apocrine glands are present also.

Traveling more proximally, the auricular cartilage rolls to form a tube. This tube is a modified L-shaped structure; however, instead of the two parts of the L being unequal lengths, they are both approximately the same length—approximately 1 centimeter. Cats, in contrast to dogs, have a fairly constant length to their external ear canal.

The first step in an otic examination is to examine the pinna. This examination should be performed in a systematic manner in order not to miss an abnormality. Any alopecia, erythema, ulceration, crusting, scaling, or swelling present on the pinna should be noted, because these may be major clues of underlying disease. During the examination, note whether the lesions are primary or secondary. Because certain primary lesions are associated with a limited number of diseases, identifying primary lesions is helpful in establishing a logical list of differential diagnoses. Primary lesions are changes in the skin caused directly by the disease process. Secondary lesions may evolve from primary lesions, or may be caused by scratching, trauma, infection, or the healing process. The distinction between a primary and secondary lesion is not always clear. Some lesions may be considered both a primary and secondary lesion depending on the disease process (e.g., alopecia).

PRIMARY LESIONS THAT MAY BE SEEN ON THE PINNA

Macule

A macule is a circumscribed flat area of the skin, less than one centimeter in diameter, which has a different color from the surrounding skin. Macules may be hyperpigmented, depigmented, or erythematous. When the skin is red it is called erythroderma. Erythroderma may be caused by erythema or purpura. Erythema occurs as the result of increased blood flow through the skin, or from dilatation and congestion of the cutaneous blood vessels. If pinnal erythema is present, an inflammatory process caused by infection (e.g., bacterial), neoplasia (e.g., squamous cell carcinoma), autoimmune disorder (e.g., vasculitis), hypersensitivities (e.g., atopy or cutaneous adverse food reaction), or a burn (radiation) should be considered as differential diagnoses. In addition, pinnal erythema may also be caused by exercise, fear, or excitement.

Erythroderma also may occur as a result of purpura. Purpura is hemorrhage in the skin. All forms of purpura involve microvascular disruption leading to extravasation of erythrocytes into the surrounding dermis. Description of purpura is modified depending on the size of the lesion. Petechiae are areas of hemorrhage one centimeter or less in diameter, whereas ecchymoses are purpuric lesions larger than one centimeter. The causes of purpura may be divided into two categories, intravascular and vascular. Intravascular causes are the result of platelet defects or coagulopathies; the most common vascular cause, excluding direct trauma, is vasculitis. Diascopy can be performed to differentiate erythema from purpura. To perform this procedure, a glass slide is pressed firmly on the area in question. The area under the slide then is evaluated to see if it has blanched. By applying pressure to the lesion, red blood cells that are present in the vessels are moved away from the lesional site. If erythroderma resolves while pressure is applied, the erythema is the result of inflammation. Purpuric lesions do not blanch with pressure. This is because the redness associated with purpura is caused by hemorrhage into the tissue rather than dilated or congested blood vessels that occur with erythema. Pressing on the tissue will not dramatically displace the red blood cells from the tissue.

Papule

A papule is a raised, circumscribed, firm elevation of skin less than one centimeter in diameter. This occurs because of cellular infiltration or edema in the epidermis or superficial dermis. When present on the pinna, etiological causes such as bacterial infections, fungal infection (e.g., dermatophyte), demodicosis, Notoedres infestation, fly bites (mosquito), and cutaneous drug reaction (systemic or topical) should be considered.

Plaque

A plaque is a coalescence of papules creating a raised portion of the skin larger than one centimeter in diameter. The same etiologies that induce papule formation cause plaques. Rarely ear tumors may present as plaques.

Pustule

A pustule is a circumscribed, elevated lesion that contains polymorphonuclear cells (neutrophils, eosinophils). It may be caused by infections (bacterial or fungal infection [e.g., dermatophyte]) or may be sterile such as in pemphigus foliaceus. Pemphigus foliaceus (PF) is the most common cause of pustules on the pinna of cats and cytological examination of these pustules often reveals acanthocytes compatible with PF (Figure 30-2). In fact, if pustules are seen on the pinna of a cat, the author considers PF to be the working diagnosis until histopathological examination proves otherwise. (See Chapter 29 in the fifth volume of this series for a complete discussion of pemphigus foliaceus.)

Figure 30-2 Impression smear of a pustule from a cat’s ear. Note the rafts of deeply basophilic rounded epithelial cells. These are acantholytic cells, found commonly in pustules from animals with pemphigus foliaceus.

Alopecia

Alopecia is loss of hair (hypotrichosis is partial alopecia or thinning of hair). Alopecia occurs as a primary lesion in demodicosis, bacterial folliculitis, and dermatophytosis in cats. It also may occur in immune-mediated/autoimmune disease such as alopecia areata or pemphigus foliaceus. Congenital pinnal alopecia may occur in breeds such as the Sphynx or Abyssinian. Preauricular alopecia is normal in cats and is most obvious in darkly haired cats. These types of hair loss are noninflammatory. Alopecia also may be a secondary lesion. An example would be pruritus associated with a hypersensitivity reaction. If alopecia is present, the first step is to determine if it is posttraumatic alopecia. If it is posttraumatic, then atopy, flea allergy dermatitis, cutaneous adverse food reaction, dermatophytosis, and otitis externa would be possible etiological causes. Inflammatory alopecia is the most common cause of alopecia.

SECONDARY LESIONS THAT MAY BE SEEN ON THE PINNA

Scale

Scale is an accumulation of fragmented (desquamated) corneocytes from the stratum corneum. Scales per se are not abnormal; in fact, human beings shed approximately one billion cells each day.¹ Normally, scale fragments are so small that they are not visible to the naked eye. Abnormal scaling is an accumulation of these fragments so that they are visible without magnification. Any process that affects the degradation of the intercellular lipids or corneodesmosomes, or increases the proliferation of the basal keratinocytes, will create scale. Inflammation is a common cause of scale. Inflammatory cytokines that are produced when the epidermis is damaged include tumor necrosis factor-alpha (TNFα) and interleukin-6 (IL-6). Damaged epidermis also stimulates the production of lipid mediators. These inflammatory lipid mediators are produced by the metabolism of phospholipids in keratinocyte cell membranes into free arachidonic acid that is further metabolized into inflammatory eicosanoids, such as prostaglandins, thromboxanes, and leukotrienes. These cytokines and inflammatory eicosanoids stimulate epidermal proliferation in an effort to remove the noxious insult. However, this epidermal hyperproliferation also leads to defective differentiation of the keratinocytes. Inflammation that occurs with allergic skin disease (atopy, cutaneous adverse food reaction), cheyletiellosis, Otodectes infestation, or dermatophytosis is a common cause of pinnal scaling. Pemphigus foliaceus, vasculitis, cutaneous T cell lymphoma, and cutaneous drug reaction (allergic or irritant) also may be accompanied by scaling.

Less common causes of pinnal scaling include nutritional and environmental causes (e.g., solar dermatitis). Deficiencies in a variety of vitamins, minerals, proteins, or essential fatty acids may cause scaling. Clinically these are very uncommon. In contrast to a true nutritional deficiency, scaling also may be associated with vitamin A–responsive or fatty acid–responsive dermatoses. In an arid environment there may be inadequate water content in the skin. With inadequate water content the enzymes necessary for separation of corneocytes (normal desquamation) will not occur, leading to scale.

Crusts

Crusts are the result of dry plasma or exudate on the skin. Cats frequently will have a lesion that is a combination of a papule and a crust known as a papulocrust. When crusts or papulocrusts are identified, dermatophytosis, autoimmune disease (PF, vasculitis, drug reaction), environmental allergen–induced atopic dermatitis, cutaneous adverse food reaction, flea allergy dermatitis, a bacterial skin infection (caused by an underlying hypersensitivity), Notoedres cati infestation, Trombicula (usually Neotrombicula automnalis) infestation, or a louse infestation (Felicola subrostrata) should be considered as possible causes (Figure 30-3).

Figure 30-3 Severe crusting on the margin and concave surface of the pinna of a 7-month-old female cat with pemphigus foliaceus.

On the caudal lateral surface of the proximal pinna is a small pouch, the cutaneous marginal pouch (see Figure 30-1). The purpose of this pouch is unknown; however, it is an easily accessible area for collecting skin biopsies of the pinna when needed (e.g., confirming PF, cutaneous small vessel vasculitis).

After examining the pinna visually, the external ear canals should be palpated for pain or firmness. Causes of firmness of the external ear canal include calcification of the cartilage of the external ear canal and thickening from fibrosis or edema.

EAR CANALS

The next step is an otoscopic examination, which involves examining the ear canals and tympanic membrane (Figure 30-4). To evaluate the ear canals and the tympanic membrane, the tip of the otoscope cone should be placed in the opening of the external vertical ear canal. In order to perform a proper otoscopic examination, it is important to understand the path that the vertical ear canal travels. Because the vertical canal travels ventrally and slightly rostrally, the otoscope cone initially should be directed vertically rather than horizontally, while gently pulling up on the pinna. There is a curve in the canal at the point where the vertical ear canal changes into the horizontal ear canal. This area is identified by a ridge of cartilage on the dorsal surface of the canal. This landmark is important to identify, because to gain entrance to the horizontal ear canal and visualize the tympanic membrane, the otoscope cone must be passed gently under this ridge. This is best accomplished by gently pulling on the pinna dorsally and laterally as the otoscope cone is advancing proximally in the ear canal.

Figure 30-4 Schematic views of the feline middle and inner ear.

(From Hudson LC, Hamilton WP: Atlas of feline anatomy for veterinarians, Philadelphia, 1983, Saunders.)

The lining of the vertical and horizontal ear canal in cats contains very few to no visible hairs. The lining is a glistening pink and the dermal vessels should be visible on otoscopic examination. The inability to visualize the dermal vessels is one of the first signs of inflammation in the ear canal.

The most medial border of the horizontal ear canal ends at the tympanic membrane. As the auricular cartilage approaches the tympanic membrane, the annular cartilage replaces it. The annular cartilage ends just lateral to the tympanic membrane, and the osseous external auditory meatus begins. This bony part of the external ear canal, which is an extension of the temporal bone, forms the most proximal part of the horizontal ear canal and terminates lateral to the tympanic membrane (see Figure 30-4). The temporal bones originate from the ventrolateral wall of the skull. Within the temporal bones are the sensory organs for hearing and balance (middle and inner ear). They also surround the proximal end of the external ear canal. This enclosure protects these important structures.

In contrast to our stereotypical skin, there are very few hairs in the ear canal of cats (unlike dogs, who may have copious amounts depending on breed). The external ear canal is lined by skin that, like skin on other parts of the body, contains hair follicles, and sebaceous and apocrine sweat glands. The sebaceous glands tend to secrete an oily substance, whereas the ceruminous glands (modified apocrine glands) secrete a milky white fluid that changes to a brown color when exposed to air. The combined product of these sweat glands is called cerumen. In human beings cerumen contains saturated and unsaturated long-chain fatty acids, cholesterol, cholesterol esters, wax esters, squalene, and triglycerides.²

Sweat glands (sebaceous and apocrine glands) secrete their contents into ducts by two different mechanisms. The first is known as holocrine secretion. In this process the secretion consists of the disintegrated cells of the gland. This is how sebaceous glands secrete their product. In contrast is apocrine secretion, in which just the apical portion of secretory cells is shed and incorporated into the secretion. This is the method by which ceruminous glands secrete their product.

Cerumen, along with trapped debris, normally is carried away from the tympanic membrane by the migration of the epithelial cells that line the ear canals. This movement of the epithelial cells is known as epithelial migration. Epithelial cells originate on the tympanic membrane and move from the tympanic membrane laterally to the opening of the vertical ear canal. This allows a “cleaning” mechanism to the ear canal. Defective epithelial migration may occur as the result of damage to the tympanic membrane from previous episodes of otitis externa, or from current inflammation (with or without a secondary bacterial or yeast infection) of the ear canal caused by allergies or previous Otodectes infestation. This defect leads to an accumulation of cerumen. The accumulation may appear as debris in the horizontal canal, or it may form into a large ball known as a ceruminolith. In the author’s experience it is very common to see ceruminoliths in cats presented for neutering. When questioning the owners it is often reported that these cats have a history of previous Otodectes infestation. Once the ceruminolith is removed in these patients it does not recur. If it does recur, however, an additional underlying disease should be sought (e.g., environmental allergen-induced atopic dermatitis, cutaneous adverse food reaction).

There are different consistencies to the cerumen in human beings and dogs, varying from a very dry flaky appearance to the more typical moist form.² The type of cerumen that is present in human beings is a reflection of the macroenvironment, especially the humidity, and also genetics. The author has not appreciated any pattern to the form that is present in dogs. Cats do not appear to have both forms, just the moist form.

Even though we focus frequently on cleaning ears to remove cerumen, it is important to understand that cerumen performs some very important functions. As mentioned previously, the purpose of cerumen is to protect the ear canals and the tympanic membrane by trapping and then mechanically removing resident bacteria and yeast and toxins produced by these organisms.³ Cerumen also removes foreign material that may have entered the ear canal. The lipids and free fatty acids that are present in cerumen contribute to the barrier function of the epidermis of the ear canals. They perform this function by keeping the epidermis of the ear canals and the tympanic membrane moist. Also, by maintaining proper moisture, normal desquamation of the epidermis may occur.

Fatty acids present in cerumen are derived from the breakdown of sebaceous gland triglycerides. This hydrolysis occurs as the triglycerides are excreted onto the surface of the ear canal. The lipids that are present in cerumen have potent antibacterial activity. Recently two sebaceous gland–derived fatty acids (sapienic acid, C16:1D6, and lauric acid, C12:0) have been identified that are especially potent antimicrobial molecules.⁴ The issue of whether cerumen has antimicrobial properties is undecided in human medicine.⁵ What confuses the issue at this time is that in the presence of infection, cerumen, with its antimicrobial molecules, is produced in excess yet the infection continues.⁶ This may be explained by studies suggesting that the lipid-rich cerumen is an ideal medium for proliferation of bacteria and fungi.^7,8 This apparent disconnect between the presence of excessive cerumen in cases of bacterial otitis externa and the antimicrobial properties of cerumen may be explained by differences in the components of the cerumen. When inflammation occurs in the ear canal, with or without a concurrent bacterial or yeast infection, the ceruminous glands will become hyperplastic and secretion from the glands will accumulate in the ear canals. In addition, the amount of sebaceous secretion decreases. Perhaps this difference in cerumen content has an impact on its antibacterial properties. Other investigators report that immunoglobulins, not cerumen, are responsible for protecting the external ear canal.⁶ More research in this area will have to be performed before an answer is found.

As mentioned previously, the ability to visualize the dermal vessels of an inflamed ear canal is lost when performing an otoscopic examination. This may be caused by thickening of the epidermis and/or dermal edema. In addition, the epidermis of an inflamed ear canal will have a red appearance. Excessive waxy secretions and hyperplastic ceruminous glands may be present. These glands will create a “cobblestone” appearance to the lining of the ear canals. If inflammation continues, these glands will progress to form inflammatory polyps. These inflammatory polyps are not the same as the nasopharyngeal polyps that will be discussed later.

Treatment with a 10- to 21-day course of oral prednisolone and topical corticosteroids with or without antimicrobial agents, if appropriate, may reverse these hyperplastic and inflammatory changes, returning the ear canals to normal. In other situations they will only undergo partial regression, making the ear canal prone to infection owing to the inability of the natural ear-cleaning process to properly remove the cerumen and associated debris. In those cases an ear cleaning program should be established with appropriate owner education.