Diagnosing and Treating Chronic and Recurrent Otitis Externa

Otitis remains one of the most common diseases among dogs.¹ To help categorize clinical cases and formulate therapy, a recent review proposed definitions for recurrent and chronic otitis (see GLOSSARY).² Successful management and treatment of chronic and recurrent otitis externa (CROE) can be challenging because they require an understanding of the pathogenesis, diagnostics, and multimodal therapy.^2-5 Preventing chronic and irreversible changes to the ears requires early recognition and medical intervention.^2,3,5 Furthermore, patience and adherence from clients and patients are vital for positive outcomes.^3,6 Appropriate intervention leads to better patient outcomes, client satisfaction, improved antimicrobial stewardship,^2,6 and ultimately saves ears from end-stage CROE requiring surgical removal through total ear canal ablation and bulla osteotomy (TECABO).^3,7-9

Pathogenesis of CROE

Understanding the primary, secondary, predisposing, and perpetuating (PSPP) factors of otitis externa (OE) can help clinicians create effective treatment plans (TABLE 1).^2,3,5,10,11 Identifying the causes through a detailed history and physical examination prioritizes differentials and diagnostic workup.^2-5,10 CROE may have more than one primary cause and multiple other contributing factors.^3,5,10

Primary Causes

Primary causes of OE are conditions that can induce clinical disease in a healthy ear with no secondary, predisposing, or perpetuating factors (i.e., dermatologic diseases that also affect the ear epithelium).^2-4,10 Atopic dermatitis is the primary cause in 43% to 75% of dogs with OE and in 31% to 50% of dogs with CROE.^12-14 Cases of unilateral otitis should prompt prioritization of other causes such as foreign bodies (e.g., plant awns), otitis media (OM), polyps, and neoplasia (particularly in cats as allergic otitis is less common).¹⁵ For successful management of CROE, obtaining an accurate diagnosis for the underlying cause and its appropriate management is crucial.^2-4,10

Secondary Contributors

Secondary contributors to otitis lead to clinical disease in abnormal ears,^3-5 which compound the effects of primary causes, exacerbating clinical signs.^2,3 Bacterial or yeast infections of the ear can incite inflammation³; however, they result from a combination of primary causes, predisposing factors, and perpetuating factors.³ Ear infections become chronic or recurrent despite treatment of the infection itself because of uncontrolled underlying disease.³

Predisposing Factors

Predisposing factors are present before the onset of otitis, alter the ear canal anatomy and physiology, and increase the likelihood of OE development.^3,11 Alone, each factor is unlikely to cause disease.^2,11 However, the presence of any predisposing factor(s) warrants active surveillance for the development of primary causes, which may then lead to otitis.^10,11 A classic example is the pendulous pinnae of basset hounds, especially because not every dog breed with pendulous pinnae is at increased risk for OE.^11,16 Some individuals and breeds may have multiple predisposing factors.^3,11,17

An often overlooked predisposing factor is iatrogenic trauma from hair plucking or vigorous cleaning that induces inflammation or injury to delicate epithelial cells.¹¹ The authors believe that hair plucking may be required for select patients (e.g., those with entrapped biofilm or matting) and should be done responsibly with use of appropriate analgesia and anti-inflammatory medications.⁸

Perpetuating Factors

Perpetuating factors include changes to the normal anatomy and physiology resulting from chronic inflammation and OM; ultimately, they are the result of uncontrolled otitis.^2,18 These changes are initially very mild but become prominent with time. The significance of perpetuating factors is that they sustain otitis regardless of resolution or control of the primary cause.^2,3,5

The first change detectable during otoscopic examination is a cobblestone appearance of the lining of the canal walls, resulting from epidermal nodular and glandular hyperplasia (FIGURE 1).^2,3,5 Treatment at this stage can most effectively reverse the changes and prevent end-stage otitis; however, if untreated, the changes progress to epidermal and dermal hyperplasia, stenosis, fibrosis, and finally mineralization (FIGURE 2).^2,3 Although medical management may be able to reverse hyperplasia and fibrosis, it cannot reverse mineralization of the canal; therefore, ears with mineralized canals are often called end-stage ears,^2,3 at which stage a TECABO may be recommended to improve patient comfort by removing a source of pain.^2,3,7,9

Figure 1. Video otoscopy image of classic cobblestone appearance and moderate erythema in a horizontal canal of a dog.

FIGURE 2. Video otoscopy image of marked ceruminous and nodular hyperplasia with stenosis, fibrosis, and purulent material in a dog. The deep structure may represent an abnormal opaque tympanic membrane or a mass.

The above changes can all result in OM and tympanic membrane alterations, if not rupture.^2,3,18,19 The natural, self-cleaning mechanism of the ear becomes disrupted, and cerumen along with other debris will no longer migrate out of the canal.^2,3,5,8

Diagnosis of otitis media/interna (OMI) can be more apparent when patients exhibit Horner syndrome, facial paralysis, or peripheral vestibular signs.^3,19 However, in a study evaluating 121 dogs with CROE and no overt evidence of OMI in either their history or clinical presentation, magnetic resonance imaging (MRI) detected subclinical OM in 20.8% of dogs.¹⁸ OM should be considered for patients with recurrent otitis, an abnormal tympanic membrane, and a history of treatment failures.^3,19,20

Clinical Presentation of CROE

History

Patients with CROE can exhibit a variety of clinical signs (e.g., head shaking, malodorous ears, hearing loss).³ Hearing loss caused by OE can be conductive or sensorineural.^3,5,21,22 In a study of dogs referred for chronic OE, hearing deficits were bilateral for 53% and unilateral for 25%.²¹ The more severe cases of hearing loss were statistically significantly associated with OM; therefore, patients with hearing loss should be referred for advanced imaging so they can receive appropriate diagnosis and treatment.²¹

OE always results from an underlying disease that must be addressed to minimize recurrence. A detailed history regarding recurrent skin infections, pruritus or pruritic behaviors, and seasonal changes may reveal concerns for atopic dermatitis. Alternatively, changes in appetite, thirst, urination, and energy levels may indicate an endocrinopathy.

Physical Examination

The entire patient should always be examined because general examination can provide valuable insight into the underlying cause, perpetuating factors, or adverse drug effects. Oral examinations are relevant for detecting potential diseases affecting the middle ear or temporomandibular joint.^3,19

The clinical signs of OE depend on the primary cause, secondary infections, and chronicity.³ Ear canal palpation is a valuable part of examination, tolerated to some degree by most patients. A healthy ear canal is made up of soft and pliable cartilage.^2,3,23,24 Chronic inflammation makes the ears firm, thickened, and nonpliable, often corresponding to the degree of hyperplasia and calcification.^2,3 Palpation also helps with assessment of facial asymmetry and identifying unilateral versus bilateral disease.

External visual examination of the ear canal can reveal hyperplasia and stenosis of the vertical canal (FIGURE 3),^3,8 which may be reversible depending on whether the cartilage in the canal has mineralized.³ A subset of patients will have purulent exudate with erosions to ulcerations, which may indicate Pseudomonas species infection.^2,25 These conditions typically are particularly painful, although pain is likely underrecognized in most patients with chronic otitis.^3,25 Characterizing the exudate can provide insight as to expected cytologic findings; however, ear cytology should never be replaced by smell or macroscopic visual inspection.

FIGURE 3. Canine hyperplastic otitis. Courtesy: Dr. Sandra Koch

When otoscopic examination is possible, a cobblestone appearance of the canal epithelium indicates ceruminous gland hyperplasia. Concurrent stenosis or masses can be seen.^2,3,5 For dogs of certain breeds, especially brachycephalic breeds, the normal horizontal canal is often slightly stenotic, which is a predisposing factor for OE and should not be confused with pathologic stenosis.^3,8,25 Hair may be present within the canals of breeds such as poodles, bichon frises, and terriers, making deep structures difficult to visualize.^3,8

A healthy tympanic membrane is translucent, but when chronically inflamed it becomes opaque and thickened and/or ruptures.^2,3,5,19 Depending on their size, partial ruptures can be difficult to diagnose. In stenotic ears, visualization of the tympanic membrane may not be possible.^18,26 Note that an intact tympanic membrane does not rule out OM.^3,18,27,28

OMI may be identified during examination of facial symmetry and neurologic examination. Head tilt can sometimes be a nonspecific finding because it can result from pain, causing abnormal head carriage, or from temporary or permanent sequelae to vestibular syndrome.³ Middle ear disease can damage the postganglionic sympathetic neurons, leading to Horner syndrome: miosis, third eyelid elevation, enophthalmos, and ptosis.^3,22 In dogs, it is more common to also see facial nerve paralysis from middle or inner ear disease.^3,22 These dogs can have neurogenic keratoconjunctivitis sicca, making tear production evaluation relevant.^3,22 Patients with neurologic deficits benefit greatly from early referral for diagnosis and intervention.

Diagnostics for CROE

Ear Cytology

Ear cytology is a foundational part of chronic otitis management because it enables quick identification and quantification of infectious organisms and inflammatory cells. Ear cytology should be performed at every visit to help measure treatment effectiveness and particularly at the end of a treatment course to prove infection resolution. Cytology may reveal cocci (usually Staphylococcus species), rods (e.g., Pseudomonas, Proteus), or yeasts (e.g., Malassezia species).^2,5,29,30 Rarely, filamentous fungi (e.g., Aspergillus) are also identified.^3,30 Inflammatory and red blood cells are not seen in healthy ears and enter the lumen of the canal only through ulceration, exudate, masses, or middle ear effusion.²⁹ The presence of rods and inflammatory cells is associated with a higher risk for OM.^18,28

Biofilm can be produced by a variety of organisms, including Malassezia and Staphylococcus, but predominantly Pseudomonas.^2,31 Most bacteria noted on cytology are in their planktonic form; however, a biofilm is an aggregate of bacteria suspended in a liquid matrix.^2,31 Presence of biofilm can be suggested by clinical and cytologic evaluation of sticky mucus and a net-like cluster of bacteria and neutrophils (FIGURE 4).^2,31 However, a definitive diagnosis requires specialized testing, such as periodic acid–Schiff staining.³² Identification of biofilm is valuable because biofilm makes the bacteria less susceptible to antibacterial agents and increases adherence to the epithelium, both of which can make infections more difficult to resolve.^2,31

FIGURE 4. Oil immersion showing biofilm containing rod bacteria and inflammatory cells from a dog with chronic otitis externa secondary to a mass. Diff-Quik stain, 1000× magnification. Courtesy: Dr. Kim Devos Davies.

Bacterial Aerobic Culture and Susceptibility

The usefulness of ear aerobic bacterial culture and susceptibility for OE treatment is controversial. When interpreted along with cytology, culture results can provide insight to predominant pathogens.^2,3,29 The controversy arises from the lack of clinical breakpoints for topical formulations, and the in vivo therapeutic concentrations for topical therapy are significantly higher than plasma drug concentrations.^2,3,5,33 Culture results do not seem to be predictive of in vivo response.³⁴ The literature reports that cultures are potentially useful for cases of atypical bacterial infections or failure to respond despite adequate treatment and adherence.^2,5 It is the authors’ opinion that with adequate treatment of the underlying disease and anti-inflammatory therapy, proper application technique, and selection of medications and cleanser, along with compliant clients and patients, true treatment failure resulting from resistance is uncommon. However, from a public health perspective, identifying multidrug-resistant bacteria is useful because resistance genes can be shared between bacteria. In addition, bacterial culture and susceptibility of material collected from within the tympanic bulla during a myringotomy is recommended because OM is frequently treated with a systemic antibiotic, whereas OE is treated topically.¹⁹ Although the relevance of ear cultures will remain controversial, a smaller sample study showed cultures better correlated with cytology than with 16S rRNA gene profiling.³⁵

Advanced Imaging

Advanced imaging is crucial for detecting masses, congenital abnormalities, mineralization of the external ear canals, and OMI. The decision between computed tomography (CT) and MRI depends on case presentation, differentials, and availability.^18,28 CT is better for evaluating osseous tissue, including evaluating the thickness of the bullae and mineralization of the external canal (FIGURE 5).²⁸ For patients with neurologic deficits, depending on the constellation of clinical signs, MRI may be preferred because it enables better evaluation of soft tissue (FIGURE 6). When a mass is suspected, contrast should be used if available and not contraindicated.

FIGURE 5. Computed tomography scan showing end-stage otitis externa with hyperplasia and mineralization of the ear canals (circles) and left-sided otitis media (arrow) in a dog.

FIGURE 6. Magnetic resonance image of T1-weighted fluid-attenuated inversion recovery after contrast administration, showing otitis media (circle) and interna (arrow) with meningeal enhancement secondary to otitis media in a dog.

Treatment of CROE

At-Home Ear Cleaning

When done correctly, ear cleaning is a crucial component of managing OE because it removes exudate, debris, and foreign material, which affect the effectiveness of medications and serve as nidi for infection.⁸ Clients must be shown how to correctly clean the ears, including introducing the product into the ear, gently massaging the ears if it is comfortable for the patient, and then allowing the patient to shake its head.⁸ Clients can gently clean debris from the visible parts of the ears but should never insert objects (e.g., a cotton-tip swab) into the canal as it can cause an impaction and trauma.⁸

The market for ear cleaners is continually changing; therefore, being familiar with desired active ingredients is recommended (TABLE 2).^8,36 Many of the active ingredients can potentially irritate the middle ear or be ototoxic; therefore, when the status of the tympanic membrane is unknown, a good option for minimizing risk for ototoxicity is use of tromethamine (tris) and EDTA-tromethamine (tris-EDTA).³⁷

Patients with CROE may be very sensitive to topical medications.⁸ If a contact reaction is suspected, discontinue topical therapy and allow the ears to recover; saline should be considered as a safe alternative if cleaning is necessary.⁸ Some ear cleaners may also contain topical glucocorticoid(s). If one of these cleaners is to be used, choose a product with low-potency glucocorticoid(s) and use it infrequently to avoid the adverse effects of steroids.^8,20

In-Clinic Ear Cleaning

At-home cleaning may be sufficient for patients with acute OE; however, in-clinic cleaning or deep ear flushing may need to be performed in clinic for patients with more chronic OE. When material is tightly adhered deep in the canal, as is common for patients with CROE, deep ear flushing by a veterinarian is usually recommended. Recent studies on collaborative care showed deep ear flushing leads to faster patient improvement and resolution of otitis.^6,38,39 The distinction between in-clinic ear cleaning and deep ear flushing is that in-clinic ear cleaning using commercial cleaners can be helpful when the client is unable to perform ear cleaning at home⁴⁰; however, deep ear flushing involves visualization of the canal and tympanic membrane to remove as much material as possible while often using specialized equipment to mitigate damage.^8,20

Patients undergoing deep ear flushing need to be anesthetized with a protected airway in case of tympanic membrane rupture or compromise because the fluid will drain through the auditory canal and into the oropharynx.^8,20 Ideally, irrigation is performed through a video otoscope.^3,8,20 If a video otoscope is not accessible, a hand-held otoscope with a red rubber catheter and a syringe may enable adequate flushing, although visualization throughout the procedure may be more difficult.^3,8,20 Saline is typically considered the best option for flushing because it is safe for the middle ear and provides excellent visibility.^3,8,20 Soaking with a ceruminolytic product could be considered before flushing.⁸

Complications may result from deep ear flushing and anecdotally seem to be more common among cats; therefore, the risks should be discussed with clients before flushing.⁸ Commonly reported complications include ruptured tympanic membrane, peripheral vestibular syndrome, facial nerve paralysis, Horner syndrome, and hearing loss.^3,8,20

Antimicrobial Therapy

Topical

Historically, topical antimicrobial therapy has been empirically based on cytology and tympanic membrane status.^2,3,41,42 If tympanic membrane integrity is compromised, ototoxic medications (TABLE 3) should not be used.^3,41-44 It has recently been suggested to also base therapy on antibiotic tiers, similar to those outlined in the International Society for Companion Animal Infectious Diseases guidelines for antimicrobial use for pyodermas.^2,45,46

A study evaluating chronic, unresponsive Malassezia infections found that within 4 weeks of initiating a course of glucocorticoids, performing a deep ear flush, and following up with otic antifungal ointment resolved the infections.³⁹ Common antifungals include the azoles (clotrimazole, miconazole, and posaconazole), allylamines (terbinafine), and polyene (nystatin).^2,41 Empiric treatment failure is often a sign that a PSPP factor is unidentified or inadequately addressed or that cleaning and medication application have been improperly performed.^3,5,8

Systemic

Use of systemic antimicrobials for OE has been controversial and is now discouraged with the emergence of antimicrobial resistance and emphasis on antimicrobial stewardship as the likelihood of obtaining therapeutic drug concentrations within the ear lumen is low.^2,41,47 Use of systemic antimicrobials should be reserved for patients with OM with or without otitis interna and ideally based on culture and susceptibility of material from within the tympanic bulla.^{2,20,41,46,47}

Glucocorticoids

Glucocorticoids provide the best chance for reversing chronic changes from inflammation and should be considered for OE patients with stenosis, erythema, ulcerations, or pain.^48,49 Early use of systemic glucocorticoids is associated with better outcomes and fewer relapses of CROE.⁶ Prescribing considerations include case selection, treatment phase (induction or maintenance), formulation, potency, and route of administration. Patients that are sensitive to glucocorticoids may experience fewer adverse effects from different formulations of triamcinolone, methylprednisolone, or dexamethasone.⁴⁹ For some patients, glucocorticoids are contraindicated and alternative therapy should be investigated, which may make treatment challenging.

Treatment Phases of CROE

Induction

The goals for the induction phase are to improve patient comfort, identify and address PSPP factors, treat infection, and determine whether permanent physiologic changes are present.⁴⁸ The success of the treatment plan strongly depends on patient and client adherence.^2,3 Patients often have otalgia and form negative associations with the ears.^2,3,50 Reassessing pain and behavior at every visit enables the practitioner to intervene with pain medication and anxiolytics to improve patient comfort and therefore adherence to the treatment plan.

Typically, an induction dose of glucocorticoids starts at the high end of the anti-inflammatory dosing range and continues for 1 to 3 weeks.^{2,20,41,48,49} Depending on the degree of pain, it can take a few days of systemic glucocorticoids before the patient will tolerate topical ear medications, after which it is recommended to start a topical glucocorticoid for a local effect.⁴⁹ Similar to systemic glucocorticoids, the potencies of topical formulations vary (TABLE 4). Fluocinolone, which is in Synotic (fluocinolone acetonide 0.01% and dimethyl sulfoxide 60%; Zoetis, zoetis.com), is among the most potent glucocorticoids. Synotic also has the benefits of dimethyl sulfoxide, and together these ingredients can effectively address hyperplasia.^20,41,48,49 Betamethasone, dexamethasone, hydrocortisone aceponate, and mometasone furoate are all potent glucocorticoids and are appropriate for use during the induction phase. Hydrocortisone aceponate and mometasone furoate are considered “soft steroids” and are less likely to cause local and systemic adverse effects.⁵¹ However, even these steroids can be systemically absorbed.^48,49,52,53 The steroid vehicle also contributes to potency.^3,41,49 Ointments are more potent because they form an occlusive barrier.⁴⁹ For adequate effect, recommended frequency for administration of most otic glucocorticoids is twice daily.⁴⁹

During the induction stage, ear cleaning and topical antimicrobials are started. The topical antimicrobial selection should be based on cytology results. Many commercially available otic medications contain a combination of a topical steroid, an antibacterial agent, and an antifungal agent. However, more targeted treatment is based on cytology (e.g., using a sole topical azole for Malassezia infections). Furthermore, an in vitro study showed that miconazole has some antistaphylococcal activity.⁵⁴ Because mechanical removal of material from the ear canal via cleaning is a valuable component of treatment, it is the authors’ opinion that long-lasting topical gels be used only for patients for which at-home treatment is not possible and that lanolin-based products be avoided entirely. When used, long-lasting topical gels should be applied after thorough in-clinic cleaning and verification of an intact tympanic membrane. If otalgia precludes medicating at home, long-lasting topical gels can be considered to improve patient comfort while clients can practice veterinarian-guided behavior modification to help reset negative associations with ear interactions to enable future at-home ear treatment.

To monitor treatment response, patients with CROE should ideally be evaluated every 2 to 4 weeks until resolution of infection and abnormal otoscopic findings.⁴¹ The induction phase ends when only irreversible chronic changes remain and infection is resolved.

Maintenance

The goal for the maintenance phase is to prevent recurrence of OE. The focus should be to reduce inflammation in the ear as a noninflamed ear canal is less likely to support bacterial or yeast overgrowth.^5,55 After the infection is treated and stenosis is improved, systemic glucocorticoids should be tapered down to the lowest effective dose and frequency.^48,49 PSPP factors should be reassessed to ensure that infection and stenosis remain controlled. Depending on the primary etiology, this can be a time to transition to other allergy medications. For patients with severe cases, modified cyclosporine is frequently a good option for long-term control and may prevent the need for surgery.⁵⁶

For patients with CROE, at-home maintenance ear cleaning should be performed 1 to 2 times weekly.⁸ Regular intermittent administration of the least-potent steroid possible can help decrease systemic medications needed for long-term control and prevent flares.^48,55 In addition, topical otic solutions containing aqueous solution of aluminium triacetate (Burow’s solution) or enzymatic solutions can be used a few times per week to help prevent infection return.^48,49

Effects of CROE

Treating CROE is associated with a significant emotional and financial burden for clients.^2,6,38 Patients and clients experience reduced quality of life as a result of CROE, and it can also fracture the human–animal bond.^6,38 In the authors’ experience, initial encounters at the referral level for patients with CROE can be very emotionally charged, particularly when concern for end-stage otitis is raised. Recent studies showed that outcomes are worse for patients that have had CROE for more than 6 months from diagnosis to referral.^6,38 Another benefit of early referral is availability of the special equipment for video otoscopy and deep ear flushing, which has been associated with improved patient outcomes.^6,38,39

When clinical signs concerning CROE are found during examination, appropriate expectations should be explained to the client (i.e., if these changes are not reversed, they can lead to end-stage otitis). Medical management of end-stage otitis is unlikely to be successful over the long term without flares, and affected ears are a source of pain. A TECABO is considered a salvage procedure to remove the painful and infected canals.^2,3,7,9,57 Although surgery is not free of potential complications, if surgery goes well, clients usually report that their dog is more playful and has a significantly improved demeanor, underscoring how much unaddressed pain accompanies CROE.⁷

Summary

CROE is a complex, multifaceted condition with a significant emotional and physical burden to patients and clients. Understanding all the factors leading to its development is crucial for treatment success. For patients with CROE, glucocorticoids provide the best chance of reversing detrimental changes and improving patient comfort. Topical treatment of secondary infections should be based on cytology, with or without culture. Systemic antimicrobials are indicated for treatment of OMI. Chronic cases may require advanced diagnostics and procedures that are not always available in a primary care setting. When treatment for the initial stages of CROE is successful, long-term management is necessary to prevent further recurrence. Ultimately, avoiding cycles of inflammation that can lead to end-stage otitis depends on early recognition of PSPP factors and aggressive intervention.