Treatment

Corticosteroids have a definite place in the treatment of otitis externa. Systemic corticosteroids reduce both the intense pruritus associated with acute otitis externa and the inflammation in the epithelium of the ear canal.

Antibiotics that kill Staphylococcus, Pseudomonas, and other gram-negative bacte­ria are used in many otic preparations. They may be formulated with other topical pharmaceuticals such as antifungals, corticosteroids, insecticides, and topical anes­thetics. Antibiotics such as gentamicin, neomycin, and polymyxin B are potentially ototoxic, so if the patient has no eardrum, these antibiotics should be avoided. In addi­tion, neomycin has been implicated as a sensitizer in contact dermatitis in the ear. If the ear becomes worse with neomycin treatment, the antibiotic should be stopped immediately. Although an aminoglycoside antibiotic, ophthalmic tobramycin solution can be safely instilled into the external ear canal to treat resistant bacterial infections.

Fluoroquinolones are used in otic formulations, but their use should be reserved for Pseudomonas infections that do not respond to other antibiotics.

Ticarcillin has been used in severe cases of Pseudomonas otitis externa, both as a topical infusion into the tympanic bulla and as an intravenous antibiotic. This antibiotic is very expensive, and the intravenous route of administration requires the patient to be in the hospital for treatment. A treatment regimen is described using 1 to 2 mg/kg prednisolone orally once daily and a cleansing and drying ear cleaner, followed by topical administration of injectable ticarcillin solution four times daily. The patient with a ruptured eardrum receives 15 to 25 mg/kg ticarcillin three times daily intravenously until the membrane heals. Topical ticarcillin and the ear cleaner are continued twice daily for 14 days after clinical resolution.

Silver sulfadiazine cream has been used to treat resistant Pseudomonas infections. A small amount of the cream is dispersed in a volume of normal saline to make a 1% solution and is used as an ear drop twice daily. This compound has the potential to cause inflammation in the ear canal and may be ototoxic.

Another useful compound for resistant ear infections is ethylenediamine tetraacetic acid-tris (tris-EDTA) in alkaline solution. The solution can be mixed up in the veterinary hospital and dispensed fresh (Box 8-1). This mixture is also avail­able commercially for the treatment of otitis externa (TrizEDTA, DermaPet, Inc., T8 Solution, DVM). Tris-EDTA is particularly useful for otitis externa caused by gram­negative bacteria. It affects the cell membranes of bacteria by chelating minerals such as calcium and magnesium, essentially “stripping off’ the outer membrane layer, rendering the membranes more porous so that the antibiotic can diffuse into the bacteria and kill them. Even if culture and sensitivity results indi­cate that a gram-negative bacterium is resistant to a certain antibiotic in vitro, pretreatment with tris-EDTA may render the organism sensitive to the antibiotic in vivo. Tris-EDTA is used as a pretreatment in the external ear 5 minutes before the

BOX 8-1 Tris-EDTA Ear Solution for Gram-Negative Ear Infections

HOW TO MAKE

1. Mix:

EDTA (disodium salt) 1.2 g

Tris (tromethamine) (Trizma, Sigma Chemical) 6.05 g Distilled water 1 L

Glacial acetic acid 1 ml

2. Adjust pH to 8.0 with additional glacial acetic acid.

3. Autoclave and store sterile.

4. Dispense in 4-ounce bottles. Keep refrigerated.

HOW TO USE (TWICE DAILY)

1. Fill ear canal with tris-EDTA solution.

2. Wait 5 minutes, then wipe out any excess with a cotton ball.

3. Immediately instill antibiotic solution into the ear canal.

instillation of topical antibiotics, most of which require an alkaline medium for maximum efficacy.

Alterations in cerumen lipid composition caused by underlying skin diseases such as atopy or hypthyroidism may play a role in the pathogenesis of Malassezia otitis externa. Low levels of free fatty acids in surface lipids coupled with increased levels of surface triglycerides favor Malassezia infections. Malassezia growth is inhibited in an acid medium, so manufacturers of otic products directed against Malassezia usually formulate them with organic acids that provide an intra-otic pH in the range of 4.5 to 5.0. Lactic, acetic, salicylic, malic, citric, boric, and benzoic acids are all used to acidify the ear canal. For otitis externa complicated by Malassezia, the author prefers the use of a combination of acetic acid and boric acid solution (Malacetic Otic, DermaPet). The cleansing and desquamating effects of the acetic acid solution essentially remove fatty acid substrates necessary for the metabolism and reproduction of Malassezia. This organism produces a chemotactic factor for neutrophils that is a hydrophilic protein. The presence of this factor may help explain why only a few Malassezia organisms can cause such profound erythema and pruritus. The cleansing effect of the acetic acid-boric acid solution removes this chemoat­tractant and may account for the reduction in inflammation. Boric acid, which is hygroscopic (drying out the humid ear canal), removes moisture necessary for this hydrophilic chemoattractant. Boric acid also dehydrates the surface of the epithelial cells lining the ear canal so the Malassezia yeasts cannot reattach to them. Wiping the ear cleaner on the lower part of the concave pinna also aids in decreasing the numbers of yeasts in the ear canal.

It has been demonstrated that more than 50% of atopic dogs with pruritic skin disease may have increased cutaneous Malassezia populations. Humans with atopic dermatitis also demonstrate Malassezia infections. With Malassezia otitis externa, treatment failures are frequent even though there appears to be temporary resolution of symptoms. Presumably, these “relapses” are often related to the initial diminution of inflammation due to the corticosteroid used in the ear medications or administered parenterally in atopic patients. The reduction in inflammation reduces clinical symp­toms, but when the topical medication is discontinued and the infectious organism is still present, symptoms of erythema and pruritus reappear.