Managing Chronic Otitis Externa
Brittany Lancellotti, DVM, DACVD
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Chronic otitis externa (OE) can be a frustrating relapsing disease leading to pet discomfort, permanent disfigurement, increased caregiver burden, damage to the human-animal bond, and financial strain. A systematic approach using the Primary, Secondary, Perpetuating, and Predisposing (PSPP) classification systemic allows the practitioner to consider each of these important aspects for more successful management.1-4
Primary Diseases
The Source of the Disease
Food, flea, and environmental allergies can all trigger otitis externa. Hormonal diseases (hypothyroidism, Cushing’s syndrome) often cause recurrent infections. The presence of masses or foreign objects (grass lawns) can be a trigger. Ectoparasitic (Sarcoptes spp., Demodex spp.), fungal (Dermatophyte), and epithelialization (primary seborrhea, sebaceous adenitis, zinc responsive dermatosis) disease can also occur.
Secondary Infections
Bacteria and/or Yeast
Cytology is a key tool for evaluating the presence and response to topical treatment of secondary Staphylococcal, Malassezia, and Pseudomonas infections. Culture and systemic treatment are typically only warranted with otitis media or severely proliferative deep horizontal canals.
Perpetuating Factors
Chronic Changes
Excess cerumen and damaged epithelial migration, biofilm production, glandular hyperplasia, mineralization, edema and stenosis of the canal, development of cysts, scar tissue and chronic inflammatory changes are all perpetuating factors that interfere with resolution and control of clinical signs.
Predisposing Risks
Anatomic Risk Factors
Certain breed-influenced conformation factors will increase risk of frequency and severity of infection when primary disease is present, including narrowed horizontal canals (e.g. brachycephalics), excessive hair (e.g. poodles and mixes), pendulous pinnae (e.g. bassett hounds), and primary secretory otitis media (e.g. cavalier King Charles spaniels).
Hypersensitivity dermatitis is the most common cause of chronic OE and can include environmental, food, and insect triggers.5 Up to 40% of patients with canine adverse food reactions (CAFR) may develop signs before 1 year of age.6 A well performed 8-12 week strict hydrolyzed or novel protein diet trial is recommended to evaluate control of clinical signs with elimination of food triggers.7 Other common clinical signs of CAFR include gastrointestinal upset (vomiting and diarrhea), conjunctivitis, anaphylaxis, and increased frequency of stools.8 Addressing pruritus and inflammation with glucocorticoids when initiating an elimination diet trial may allow for abbreviated trials if pruritus and inflammation do not relapse within two weeks of finishing the course of glucocorticoids.9 After 8-12 weeks of an elimination diet trial, challenge feeding by reintroducing the pet’s original diet may result in a relapse of clinical signs within five days and fourteen days for 50% and 90% of dogs with CAFR respectively.10 Relapsing OE despite control of food allergens may indicate ongoing environmental triggers and warrant referral to a dermatologist and discussion of allergy immunotherapy for long term control.11,12
Endocrinopathies, such as hypothyroidism and Cushing’s syndrome (hyperadrenocorticism, HAC), may result in recurrent secondary infections from a poorly functioning immune system.13 A detailed history may reveal other systemic signs, such as lethargy, weakness, weight gain, appetite change or thinning hair coat. Thyroid testing should include Total T4, free T4 by equilibrium dialysis, and thyroid stimulating hormone (TSH) in order to differentiate between euthyroid sick syndrome and true hypothyroidism. Complete blood count and serum chemistry (CBC/Chem) can increase clinical suspicion of HAC if common abnormalities such as thrombocytosis or elevated alkaline phosphatase are present, but normal CBC/Chem should not rule out HAC as a primary trigger for OE.
Secondary infections should be investigated with cytology to determine the presence and type of microorganisms. Cytology guides selection of appropriate topical antimicrobials and/or ear cleaners, as well as evaluates response to treatment. Culture of infections is typically not recommended for OE and is more appropriate for otitis media.5 Resistance profiles can vary significantly between samples depending on the region of the ear canal sampled. In addition, topical antimicrobial therapy allows for significantly higher concentrations of antimicrobials than systemic antibiotics. Because susceptibility testing often evaluates for expected response to concentrations of systemic antibiotics, topicals may often overcome reported resistance due to the significant increase in antimicrobial concentration when applied directly to the external ear canal, rather than passing through systemic absorption.
Perpetuating factors may result in ongoing secondary infection despite appropriate antimicrobials. Inflammation leads to significant changes such as glandular hyperplasia, edema of the canal, damage to normal epithelial migration, and stenosis.14 Antiinflammatory medications such as glucocorticoids and modified cyclosporine are helpful in reducing acute and chronic inflammation respectively.5 Prednisolone at 1mg/kg can help treat acute inflammation and then be tapered to minimize adverse effects. Owners should be informed of possible adverse effects with glucocorticoids, both short and long term. Modified cyclosporine (Atopica; Elanco) is a calcineurin inhibitor indicated for the control of atopic dermatitis in dogs weighing at least four pounds. A significant reduction in inflammation is achieved about 4 weeks after starting 5mg/kg daily and steroid-sparing benefits of this medication can be used in the long term management of chronic, proliferative OE.11,12 Modified cyclosporine may be an effective alternative to total ear canal ablation surgery in the management of end-stage ear disease.15
Biofilm is most often produced by Pseudomonas bacteria, however, other microorganisms such as Staphylococcus and Malassezia have been shown to produce biofilm.16 This extracellular matrix of exopolysaccharides makes microorganisms 10 to 1000 times more resistant to topical antibiotics as the result of impaired drug penetration, reduced growth of microorganisms having entered a quiescent state, and the expression of multi drug resistance pumps.17 Although certain topical agents have demonstrated anti-biofilm efficacy, including Triz-EDTA, N-acetyl cysteine, chlorhexidine, polyhexanide, and hypochlorous acid, biofilm is most effectively treated by physical removal during deep ear cleaning with video otoscopy.5
Predisposing factors can increase the risk of frequency or severity of OE in animals with a primary disease and make management more challenging. These risk factors include (but are not limited to) copious ear hair, narrowed or congenitally stenotic canals, pendulous pinnae and excess moisture (swimming, bathing, excessive cleaning). Ear hair may prevent penetration of topical therapy and therefore resolution of secondary infection. When considering hair plucking, sedation, analgesia, and antiinflammatory treatment is recommended. Maintenance hair plucking should not be necessary if the primary disease and perpetuating factors are managed.
Ear flushing is a helpful tool in removing excess cerumen, adjusting pH, and providing additional antimicrobial action.18,19 Practitioners should familiarize themselves with available ear flushes and select an appropriate cleaner(s) based on each individual pet’s needs. Cooperative care techniques and use of technical staff to educate clients can help improve the client’s confidence and capability in performing this helpful treatment for long term management.
Communicating to clients that OE is often caused by chronic, lifelong primary diseases can help manage expectations, minimize frustrations, and improve compliance with workup of the underlying cause and implementation of the long term plan.
This content is provided by Blue Buffalo. Clinician's Brief does not inherently endorse any product or organization advertised across its properties. The appearance of an advertisement on Clinician's Brief properties is neither a guarantee nor an endorsement of the product or advertising claims. Clinician's Brief is not responsible for the content promoted in this article or the referenced sources. Questions about the accuracy of the information presented or sources cited may be directed to the listed sponsor.