External ear disease in dogs and cats- Part 1
External ear diseases are particularly pertinent to dermatology, as the outer ear is formed by an invagination of skin within which various cutaneous disorders can occur. It is important to emphasize that the word otitis refers to an inflammatory sign, not a specific diagnosis; in other words, when treating otitis, the veterinarian is usually treating a sign rather than the primary or underlying disease that causes it. Ear disorders have a prevalence of about 15-20% in dogs and 6-7% in cats (1). There is no gender predilection but the condition is most common in dogs aged 5-8 years and cats aged 1-2 years (2).
Etiopathogenesis of otitis externa
When considering otitis externa, it is helpful to regard the outer ear as an L-shaped dermoepidermal structure with follicles and ceruminous and sebaceous apocrine glands (1,3). Alterations to this anatomical structure produce a microenvironmental imbalance that can give rise to inflammation and consequent infection. The following are all important factors:
• The external ear conformation, which can impair ventilation.
• The vertical canal, which can impair natural drainage.
• The natural narrowing and bend of the canal, which favors stenosis.
• The presence of hairs, which can obliterate the canal lumen.
• The abundance of secretory glands, which can produce excess exudate.
• The relatively sealed compartment of the middle ear.
It is also important to emphasize three other points:
• The external ear glands secrete cerumen; this is important for homeostasis of the auditory canal, as it has bacteriostatic and fungistatic properties (2).
•The concept of epithelial migration (1), a self-cleaning mechanism whereby the epithelial cells lining the external auditory canal grow in a synchronized manner towards the exterior, eliminating detritus via a sweeping action. Any alteration of the epithelium, due to edema, hyperkeratosis or chronic inflammation, stops this migration, and detritus and waste accumulates. If the condition is allowed to continue, inflammation can lead to ossification of the external auditory canal and the associated cartilage elements (1,3).
• The integrity of the eardrum (tympanic membrane) is very important when considering otitis externa and media.
In order for otitis to develop, a number of factors and causes must be present (1-5). These can be considered under the headings of predisposing factors, primary causes, secondary factors and perpetuating factors. A combination of these affects the development of otitis and should be identified by the clinician via the history and clinical examination; the correct approach to otitis is not simply to treat the condition but to address these underlying factors. Predisposing factors and primary causes are set out in Table 1. These primary causes are thought to be direct inducers of otitis externa; many of them are suspected but are not definitively confirmed. Identification and control of the primary cause is essential in order to avoid otitis relapse. An animal may have a primary cause of otitis but no disease develops as secondary factors (e.g. bacteria, yeasts or drugs) are absent. Note that any hypersensitivity reaction can induce otitis (1), causing inflammation of the skin and adnexa in the external auditory canal; in fact any self-inflicted trauma, pruritus or itching can lead to otitis. In general the first symptoms are usually erythema of the pinna and vertical canal, with excess cerumen production; this alters the cutaneous ecosystem which is then taken advantage of by bacteria and/or yeasts. In many cases, no exudates is observed until the secondary agents appear.
Note that 80% of all dogs and 20% of all cats with adverse reactions to food are susceptible to otitis externa (1,5). The latest theories reinforce the notion that there may be a close relationship between atopy and adverse reactions to food; indeed a hypoallergenic or elimination diet may prove essential to control otitis externa induced by hypersensitivity phenomena (7).
Secondary and perpetuating factors – pathological changes produced by the combination of primary causes and secondary factors which make otitis chronic or prone to relapse – are shown in Table 2. Failure to identify these factors can lead to ineffective treatment, and a subsequent loss of client confidence.
Persistent treatment is required to avoid relapse of ear problems – in some cases treatment may need to continue for many months. In advanced otitis externa the dermis surrounding the cartilage components undergoes calcification, requiring prolonged systemic antibiotic therapy. The tympanic membrane is also affected in these cases, with color change and a loss of transparency so that the insertion of the malleus is not visible. Note that accumulation of keratin or impacted exudates can be mistaken for an altered tympanic membrane.
It is good practice to first examine the healthy or less painful ear in order to avoid resistance on the part of the animal (4). However animal reluctance should not be used as an excuse to avoid a full examination and anesthesia should be employed if necessary. Should there be a ruptured eardrum the ear should first be cleaned using safe cleaning fluids such as warm saline. Drying of the canal is essential – fluid accumulation inhibits vision and will impede adequate exploration – and can be performed with a rubber medical pear, surgical aspirators or abundant gauze. A thorough examination is then possible and the integrity of the eardrum should be verified. This can be a true diagnostic challenge as damage may not be obvious – a ruptured membrane may develop adhesions which can form folds or pockets that mimic an intact membrane (1). If necessary one of the following may be required to confirm rupture:
• Filling the canal with saline to check for bubbles, swallowing or coughing.
• Palpating and measuring the length of the canal compared with the contralateral canal, using a flexible probe (e.g. cat urinary catheter).
There are a number of signs to be taken into account in diagnosing otitis and differentiating the affected part(s) of the ear (Table 3). The appearance, smell, texture and color of the auricular exudate may provide clues as to the underlying etiopathogenesis (Table 4).
Come back next week for Part 2 covering cytology and treatment!
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2. Scott D, Miller W, Griffin C. Muller and Kirk’s Small Animal Dermatology. 6th ed. Philadelphia: Saunders, 2001;1203-1235.
3. McKeever P. Otitis externa. In: Manual de Dermatología en pequeños animales. Colección BSAVA – Ediciones S - 1999;147-158.
4. Hill PB. Small Animal Dermatology. Elsevier Science 2002;143-147.
5. Griffin C. Otitis externa and media. Dermatology I. ESAVS 2002;115-143.
6. Colcuc M, Degasperi B, Alton K. Ear polyps of the cat: two case reports and a model for pathogenesis-chronic otitis media with effusion. Euro J Comp Anim Practice 2011;21.
7. Favrot C, Steffan J, Seewald W, et al. A prospective study on the clinical features of chronic canine atopic dermatitis and its diagnosis. Vet Dermatol 2010;21:23-31.
8. Colombini S, Merchant S, Hosgood G. Microbial flora and antimicrobial susceptibility patterns from dogs with otitis media. Vet Dermatol 2000; 11:235-239.
9. Gotthelf LN. Extracción de cerumen y cerumenolíticos, in: Proceedings. 16th Annu AAVD-ACVD Meet, Norfolk, Virginia 2001.
10. DeBoer D. Chronic and severe otitis externa: primary treatment, longer management II, in Proceedings. Workshop on Dermatological Therapy, Cuneo, Italy 2008;81-92.
11. Kelley LS, Flynn-Lurie AK, House RA, et al. Safety and tolerability of 0.1% tacrolimus solution applied to the external ear canals of atopic beagle dogs without otitis. Vet Dermatol 2010;21:554-565.
12. Videmont E, Pin D. Proliferative and necrotising otitis in a kitten: first demonstration of T-cell-mediated apoptosis. J Small Anim Pract 2010; 51:599-603.