PATHOLOGICAL CHANGE IN CHRONIC OTITIS

Chronic damage occurs in both horizontal and vertical ear canals in dogs with ongoing episodes of otitis externa. This damage can be caused through a variety of primary triggers, the most common of which is allergy including both atopic dermatitis and adverse food reaction. Other primary triggers which will lead to longstanding damage to the ear canal include parasitism with either otodectic or demodectic mange mites, keratinisation disorders either secondary problems in the form of endocrinopathies such as hypothyroidism or primary keratinisation disorders such as sebaceous adenitis. Perpetuating factors such as secondary bacterial and yeast infections can be superimposed on primary triggers contributing to an increase in inflammation and a further deterioration in clinical signs and the damage to the ear canals.

In the early stages of acute inflammation the damage that occurs to the ear canal is reversible. Unfortunately though the more chronic the disease process becomes the less likely it is that the clinician can reverse the changes that have occurred. Where the canal is chronically irreversibly damaged then surgery will be necessary and will become the only available option.

In order to undertake successful surgery in ears that have significant hyperplastic change present it is essential the clinician is able to recognize the degree of damage within the ear to assess whether medical therapy is appropriate.

Acute changes

Three principle changes occur in the early stages of disease. Initially an increased vascular permeability is seen leading to dermal oedema. Alteration in epidermal barrier function occurs and with it an accompanying change in the composition of the cerumen. Microscopically these changes are seen as oedema, erythema and hyperplasia of the canal. The change in barrier function leads to increased penetration of micro-organisms which exacerbates inflammatory change. As a result of inflammation cerumen production is increased which leads to further occlusion of the canal with ceruminous debris. The overall effect of narrowing of the canal and increased cerumen production leads to changes in the micro-environment within the ear canal and micro-organism overgrowth. The ceruminous glands themselves can become dilated or hyperplastic at this stage which macroscopically is seen as a cobblestone appearance on the lining of the ear canal. This slightly raised clinical appearance at this stage is still reversible.

Chronic changes

As the inflammation becomes more advanced the superficial epithelium changes to a hyperplastic stratified squamous epithelium. This leads to abnormal epithelial migration and a further accumulation of debris within the lumen of the canal. If bacterial numbers have increased due to changes of micro-environment in the canal then neutrophil chemotaxis leads to the formation of a purulent exudate in the canal lumen. This further leads to damage of the epithelium which can cause erosion and ulceration.

Irreversible changes

As inflammatory changes progress hyperplastic change occurs in both the sebaceous glands, ceruminous glands and the fibroblasts within the dermis of the ear canal. As glandular hyperplasia occurs the lumen of the ear canal decreases further leading to stenosis of the canal. At this stage both sebaceous and ceruminous gland hyperplasia is advanced and the canal is becoming irreversibly damaged. Fibrosis at this stage can rarely be reversed with medical therapy usually needing surgical intervention in the form of a total ear canal ablation. Fibrosis at this stage usually progresses further to osseous metaplasia unless medical intervention can prevent further chronic change occurring. It is a common misconception that calcification of the ear canal at this point is due to transformation of the cartilage in the canal. It is in actual fact the fibroblasts that transform to produce bone-like tissue rather than the cartilage which undergoes transformation. The calcification therefore is found in the soft tissue outside the cartilaginous boundaries. Calcification at this stage can be picked up on palpation of the ear canals and also by a variety of different diagnostic techniques including computed tomography or radiography. This change is now irreversible and end stage.

The progression from oedema to epidermal hyperplasia associated with glandular hyperplasia following on to fibrosis and osseous metaplasia represents the spectrum of histopathological change associated with otitis externa. It is important to identify the chronicity of the changes present in the ear canal when assessing suitability for medical therapy. Once fibrosis has occurred within the canal and glandular hyperplasia is advanced, medical therapy is usually of little benefit. It may still be possible to enlarge the lumen of the canal, resolve infection and keep the animal comfortable but the ear canal, at this stage, will never be returned to its original anatomical conformation. Calcified ear canals, in the author's opinion are never amenable to medical therapy and should be removed surgically.

ASSESSMENT OF EAR CANAL HYPERPLASIA AND STENOSIS

It is essential that examination of the ear canal is undertaken to decide on the chronicity and reversibility of the changes that are present. The animal should be adequately restrained with heavy sedation or a general anaesthetic to allow a thorough visual inspection of the canal. This is best achieved via video otoscopy where magnification and good illumination allow accurate visualisation of the internal anatomy of the canal itself. Where hyperplastic or polypoid change is present in the ear canals biopsy of the lining may be useful to establish the chronicity of the change that is present. Radiography or more advanced imaging techniques may be useful to assess the canals and also the middle ear as well as more simple direct examination techniques such as palpation of the canals themselves.

THERAPY

Flushing of the ear canal is an important first therapeutic step as it is in any ear disease. However, when the canal is narrowed, particularly where there is glandular hyperplasia present, this can be difficult to accomplish. In these situations therefore steroid therapy can be employed to reduce the swelling in the ear canals and help widen the lumen. The author will generally prescribe systemic steroid therapy to achieve this.

Typically a dog will be admitted to the clinic, heavily sedated or anaesthetised for examination of the ear canal. Appropriate imaging techniques are often undertaken at this stage to assess the degree of chronic changes to the canal. The author, however, finds video otoscopic examination the most useful. Cytology of the canals will be undertaken to assess the presence of an inflammatory infiltrate and pathogenic organisms which should be treated before steroid therapy is employed. Culture and sensitivity will also be performed where cytology is suggestive of a Gram-negative or mixed population of bacteria. Biopsies can be undertaken where hyperplastic change is present or to confirm the presence of benign inflammatory change rather than a more sinister neoplastic component. This is usually accompanied via the grasping forceps down the video otoscope head.

Days 1 - 14

In the initial stages of therapy, after ear cleaning has been performed a broad spectrum anti-bacterial/anti-yeast flush will be used to keep the ear clean and also provide an environment within the ear canal that is hostile to bacterial and yeast colonisation.

Initial systemic therapy is started after ear flushing in the form of prednisolone. This is given, providing there are no contra-indications, at a dose of 1.0mg/kg once daily by mouth for the first two weeks. It is important when using systemic steroids at full anti-inflammatory dose rates that the clinician is aware of the dog's general health status. Such medication should be avoided in debilitated animals or where concurrent disease makes steroid therapy an inadvisable risk. It is also imperative to warn owners of the potential side-effects associated with steroid therapy including polydipsia, polyuria and polyphagia. However, despite the side-effects that are inevitably seen with steroid therapy, owners will generally report after two weeks that the dog has become far more comfortable and much more active and lively.

Day 15 - 28

Within two weeks the steroid therapy will start to decrease the inflammatory change in the canal and open up the lumen. At this stage the author will generally switch from daily prednisolone therapy to an alternate-day regimen at the same 1mg/kg dose rate. In addition to this the flushing solution will be maintained but a more potent steroid medication will be added in. This will generally be a product containing one of the more potent steroids such as dexamethasone or betamethasone. As previously described, it is important at this stage to use an appropriate volume of solution to ensure that the eardrops actually permeate through the full length of the ear canal. A minimum of 0.5ml of solution should be added to each ear and up to 1.0ml in a big dog. Video otoscopy of the ear canal is generally performed at Day 0 and after two and four weeks to assess the progress of the canal. Where the eardrum is intact the author will also use an off-licence mixture of steroid, antibiotic and Dimethyl sulphoxide (DMSO). This can be mixed into either 12ml of an appropriate ear cleaner, the author uses a 1% acetic acid /1% boric acid /1% hydrocortisone-based ear cleaner or 12ml of EDTA-tris solution. In addition to the DMSO, fluorinated quinolones, which are generally well tolerated in the ear canal are added to the mixture combination with aqueous solution and dexamethasone. The solution can be instilled directly into the ear canal or can be used in combination with ear wicks.

Ear wicks

Ear wicks are small porous sponges made in polyvinyl alcohol (PVA). These highly absorbent structures can be placed in ear canals and soaked in a variety of different solutions. They expand within the canal and conform to the lumen of the canal. They are an excellent way to deliver and maintain drugs in the dogs' ear. When the ear wicks are soaked in a combination of steroid, antibiotic, cleaner and DMSO it allows an intimate contact of the drug with the ear canal, the DMSO allowing better penetration of the active ingredients within the ear canal further widening the ear canal lumen. Where the eardrum is ruptured the presence of the wick can be used to prevent medication leaking into the middle ear.

Day 29 - 43

The overall length of course of anti-inflammatory therapy that is needed in cases of ear canal hyperplasia depends on the chronicity of the hyperplastic change that is present. Four to six weeks of therapy is usually required as a bare minimum. Oral anti-inflammatory doses of prednisolone are given initially on a daily basis for two weeks and then on an alternate-day basis for approximately four weeks in combination with potent topical steroid treatment. Once the canal has been widened so that an adequate lumen has been created the author tapers medication down to the lowest possible maintenance dose rate. Where possible systemic steroids are withdrawn but topical therapy is maintained. In view of the fact that the micro-environment inside the ear will still be abnormal, if improved, she will generally use an acid-based ear cleaner once or twice a week in combination with some topical steroid therapy. Where possible hydrocortisone should be used in preference to the more potent steroid such as dexamethasone or betamethasone.

Where hyperplasia has been associated with allergic disease efforts should also be made to address the underlying primary trigger.

Further reading