Ceruminous Diseases of the Ear

Chapter 10 Ceruminous Diseases of the Ear



Norma White-Weithers, MS, DVM



Histopathology of the External Ear Canal


The epithelium of the external auditory meatus is composed of components similar to those of normal skin. The stratum corneum is the outermost layer; keratinocytes make up this layer of squamous anuclear cells. There are no rete ridges in the epithelium of the ear canal. The sebaceous glands are the outermost glands; they become progressively more numerous deeper into the meatus. Underlying the sebaceous glands are simple, coiled, tubular, apocrine glands called ceruminous glands, with ducts that open directly into hair follicles or onto the surface of the ear canal (Figure 10-1). During inflammatory reactions, sebaceous glands become hyperactive and hyperplastic; the ceruminous glands become dilated, thickened, and filled with secretions (Figure 10-2). Under normal physiologic conditions, ceruminous secretions (cerumen) combine with sebum produced by the sebaceous glands and epidermal debris to form earwax, the normal secretion of the ear.


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Figure 10-1 Multiple openings of the cerumen glands along the ear canal.


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Figure 10-2 Many diseases cause increased blood supply to the ears, increasing the metabolism within the ceruminous glands. Bacteria and yeasts secondarily grow on the roughened ear canal surface, using the glandular secretions as their nourishment.



Etiology of Ceruminous Otitis


When ceruminous glands and sebaceous glands of the ear canal become chronically irritated, the results are cystic dilation of ceruminous glands, hyperplasia, and increased activity of the overlying sebaceous glands. The excessive amount of cerumen produced by ceruminous glands forms a favorable medium for the growth of secondary bacteria and yeast. These organisms are normal flora of the ear and include Pseudomonas spp., Proteus spp., and Malassezia pachydermatis (see Chapter 9). With improper drainage and lack of air circulation (due to pendulous ears in some breeds), excessive growth of these organisms may occur within the ear canal.


In most cases of ceruminous otitis, the epidermal hyperplasia and inflammatory reaction occlude the external ear canal, making visual examination difficult. In both the dog and cat, hyperplasia of the ear canal can simulate neoplastic conditions that may lead to misdiagnoses and improper treatment. When hyperplasia does not respond to treatment and hardening of the ear canal ensues, surgical intervention is often the treatment of choice. Surgical opening of the ear canal allows proper drainage. The identification and treatment of underlying infections are important for surgical success.


Ceruminous otitis is inflammation of the glandular structures of the ear canal, with subsequent excessive epidermal proliferation and otitis externa that requires medical or surgical management. The causes of ceruminous otitis are many, and each condition is accompanied by other dermatologic or systemic manifestations.



Disorders of Keratinization



Primary Idiopathic Seborrhea


Ceruminous otitis can be due to an inherited or acquired keratinization defect. Inherited disorders include idiopathic primary seborrhea, commonly seen in West Highland White Terriers, American Cocker Spaniels, English Springer Spaniels, Basset Hounds, Irish Setters, Dachshunds, Chinese Shar-Peis, and German Shepherds. Primary idiopathic seborrhea, epidermal dysplasia of West Highland White Terriers, and lichenoid-psoriasiform dermatosis of English Springer Spaniels are examples of primary keratinization defects with ceruminous otitis externa. Secondary or acquired keratinization defects include vitamin A–responsive dermatosis, zinc-responsive dermatosis, and fatty acid deficiency.


The epidermis of the canine ear canal undergoes proliferation, differentiation, and desquamation with renewal of the viable epidermis in approximately 22 days. In American Cocker Spaniels that have idiopathic primary seborrhea, the proliferative, differentiative, and desquamative stages take an average of 8 days. This rapid turnover of epidermal cells increases the renewal stage that produces seborrhea (manifested as seborrheic dermatitis, ceruminous otitis, or both). This defect in differentiation includes hyperkeratosis or hypokeratosis and dyskeratosis.




Clinical Signs.


The clinical signs of primary and secondary ceruminous otitis are the same and can only be diagnosed on the basis of response to therapy. In-depth clinical and diagnostic evaluations are mandatory for animals that present with chronic ceruminous otitis. These animals usually present with other primary or secondary dermatologic manifestations.


Clinical signs can be mild or chronic, with secondary bacterial or Malassezia infections complicating the primary problem. Ears with ceruminous otitis are malodorous, and there is often secondary epidermal hyperplasia of the ear canal and pinna that may occlude the auditory meatus. Other presenting signs are usually generalized, focal to multifocal, seborrheic dermatitis with secondary bacterial and/or Malassezia infections.


In the author’s experience, animals with moist vertical canals due to pendulous ears and poor ventilation are presented more often with chronic ceruminous otitis that requires general anesthesia for proper ear examination. Examination under general anesthesia allows the clinician to visualize thoroughly, clean, and obtain biopsy specimens from the ear.


A biopsy is often necessary to differentiate chronic epidermal hyperplasia with chronic ceruminous otitis from ceruminous gland tumors. Secondary bacterial and Malassezia infections respond when the underlying cause is properly treated. If there is no response, evaluation should consist of bacterial and fungal culture and sensitivity testing.



Diagnosis.


Histologic evaluation of noninfected seborrheic areas usually supports a diagnosis of primary seborrhea. After identification of secondary invaders and appropriate medical management, diagnosis is most frequently confirmed by response to treatment.



Treatment.


Because ceruminous otitis is only the manifestation of a more serious problem, finding the underlying cause should be the clinician’s primary goal. Treatment of primary seborrhea should attempt to control the disease rather than produce a complete cure. Treatment of the ears should focus on (1) control of secondary infections and of production of scales and crust, and (2) reduction of inflammation. Frequent ear cleaning with appropriate topical medication can control the odor associated with this condition. Steroids, cytotoxic drugs, and retinoic acid have variable effects. Results with the use of synthetic retinoid (etretinate) in Cocker Spaniels and other breeds to treat idiopathic seborrhea are disappointing. In the Cocker Spaniel, for example, there is a reduction of scales, crust, and alopecia, but the ceruminous otitis is not responsive to this therapy. It is less effective in other breeds affected with this condition.



Endocrine Dermatosis


The most common endocrine diseases associated with ceruminous otitis are hypothyroidism and hyperadrenocorticism.



Hypothyroidism.


Breed predilections for hypothyroidism include Golden Retrievers, Alaskan Malamutes, Chow Chows, Boxers, English Bulldogs, Chinese Shar-Peis, Great Danes, Afghan Hounds, Doberman Pinschers, Newfoundlands, Dachshunds, and Cocker Spaniels. Hypothyroidism in cats is extremely rare.



Etiology.


The causes of hypothyroidism are classified as primary, secondary, tertiary, and congenital. Examples of causes of primary hypothyroidism include lymphocytic thyroiditis, thyroid atrophy, thyroid gland hyperplasia, neoplasia, and thyroid cell destruction due to radioactive iodine treatment or antithyroid drug therapy. Secondary hypothyroidism in the dog is the result of pituitary destruction and malformation or suppression of thyrotropic cell function. There are no known causes of canine tertiary hypothyroidism. Defects in iodine organification and thyroid gland dysgenesis are the two most common causes of congenital hypothyroidism in the dog.



Clinical Signs.


Thyroid hormone is an important regulator in the body’s metabolic function. A deficiency causes a decrease in the normal cellular metabolic functions of the body. The clinical signs of hypothyroidism in the dog are extremely variable, being those of metabolic, dermatologic, reproductive, neuromuscular, ocular, gastrointestinal, cardiovascular, hematologic, and behavioral disorders.


Serum and cutaneous fatty acid concentrations are affected by thyroid hormones. Thyroid hormones stimulate the synthesis, mobilization, and degradation of lipids, with the most dramatic effect being a decrease in degradation. This may present as an increase in serum low-density lipoprotein (LDL).


Thyroid hormone increases the sebum production necessary for the normal lipogenesis and synthesis of sterol by keratinocytes and increases cutaneous linoleic acid, with a decrease in gamma linolenic and arachidonic acid concentrations. The decrease in arachidonic acid concentration alters epidermal proliferation. This alteration is responsible for the seborrhea, seborrheic dermatitis, and ceruminous otitis so often present in hypothyroid dogs. This may be the only presenting sign in a hypothyroid dog. The dryness or greasiness associated with the alteration of cutaneous fatty acid levels can manifest as a dry or a greasy form of seborrhea.


Secondary bacterial and Malassezia infections are complicating factors in ceruminous otitis and can be a dermatologic nightmare if not treated properly. Other dermatologic abnormalities in dogs with hypothyroidism are myxedema, thin skin, hyperkeratosis, seborrheic ear pinnae, pyoderma, symmetrical or patchy endocrine alopecia, and various degrees of hyperpigmentation. Otic pruritus is often present with secondary bacterial or Malassezia infection.



Diagnosis and Treatment.


The resolution of the ceruminous otitis largely depends on the proper diagnosis and control of hypothyroidism. History and physical examination findings are important in the diagnosis of hypothyroidism. A complete blood count, serum biochemistry profile, urinalysis, and thyroid stimulation test are some of the few laboratory tests used to diagnose hypothyroidism.


Because the availability of thyroid-stimulation hormone is limited due to factors of price and supply, in most cases the interpretations of total tetraiodothyronine (T4), free T4, and thyroid-stimulating hormone (TSH) in combination with clinical manifestations are the only diagnostic tools at the clinician’s disposal. For this reason, it is important to note that misdiagnosis of this disease can be easily made if the appropriate tests are not performed. Drugs such as glucocorticoids, anticonvulsants, trimetoprim/sulfamethoxazole, phenylbutazone, quinidine, salicylates, and radiocontrast agents can adversely affect thyroid levels in the body. It is recommended that these medications be withdrawn, if possible for up to 2 weeks, before a thyroid test is performed. These drugs can reduce the conversion of T4 to triiodothyronine (T3), inhibit thyroxine synthesis in the gland, inhibit TSH secretion from the pituitary gland, and interfere with the binding of serum thyroxine to binding proteins. Thyroid testing should not be performed immediately after anesthesia. Due to its adverse effect on serum thyroid levels, a waiting period of up to 1 or 2 weeks is recommended before performing a thyroid profile on these animals. A free T4 using the equilibrium dialysis (ED) method is recommended in veterinary medicine. This test measures the quantity of T4 in the dialysate and does not use the thyronine-binding globulin as a high-affinity binding protein, as in the radioimmunoassay (RIA) test. The level of this binding protein is low in the dog, compared with humans. The free T4 by the ED method as compared with the RIA method is a more specific and sensitive test in the dog.


Epidermal hyperplasia and pain often occur in the treatment of ceruminous otitis. Topical steroid preparations are useful in controlling pain and inflammation and reducing epidermal hyperplasia. Because steroids affect baseline thyroid levels, thyroid profiles should be performed before or 1 or 2 weeks after discontinuing any topical otic medications with steroids.



Hyperadrenocorticism.


Bilateral adrenocortical hyperplasia due to pituitary adenoma is the most common cause of hyperadrenocorticism in the dog. The excessive production of cortisol by the adrenal gland results in systemic as well as dermatologic abnormalities. The prolonged exogenous use of oral, intramuscular, or intravenous (and possibly otic and ophthalmic) corticosteroids may also cause iatrogenic hyperadrenocorticism. Other causes are adrenal adenomas and carcinomas.


The cutaneous manifestations of excessive serum cortisol are as follows:


• Alopecia

• Failure or slowness of hair growth after clipping

• Thin skin

• Pyoderma

• Seborrhea

• Comedone formation

• Bruising

• Striae formation

Seborrhea dermatitis may manifest as ceruminous otitis with secondary bacterial or Malassezia infections.


Glucocorticoids inhibit epidermal proliferation and sebum production through antimitotic, protein-catabolic, and antienzymatic effects. The decrease in hair growth is manifested clinically through bilateral symmetrical or “moth-eaten” alopecia. The antimetabolic and antiproliferative effects on fibroblasts are evident as poor wound healing. There is also an increase in susceptibility to infections. Because animals with hyperadrenocorticism show signs of secondary hypothyroidism, clinical signs of seborrhea and skin infection may be exaggerated due to the dermatologic effects of low thyroid levels.


The combination of seborrhea and bacterial or Malassezia infections can be manifest as ceruminous otitis, which is not as common in the cat as in the dog.



Diagnosis and Treatment.


Diagnosis of hyperadrenocorticism is based on history, complete blood count, serum biochemistry, urinalysis, adrenocorticotropic hormone (ACTH) stimulation test, low- or high-dose dexamethasone suppression tests, and ultrasonographic and radiographic findings. Because steroids affect thyroid levels, a thyroid stimulation test, if available, or a thyroid profile (T4, free T4 [ED], and TSH) is part of the diagnostic plan. However, a thyroid profile should be performed after hyperadrenocorticism has been diagnosed and controlled to minimize the adverse effects of steroids outlined previously. Treatment of otitis externa secondary to hyperadrenocorticism depends on proper diagnosis and treatment of the hyperadrenocorticism. Any secondary bacterial or Malassezia infection should also be treated.


Several factors are important in the treatment of hyperadrenocorticism. Most animals with this disease are presented with other problems such as a secondary bacterial, parasitic (Demodex), or fungal skin infection, as well as otitis. When these are encountered, individual treatment modalities are recommended for each specific problem. Therefore, in treating an animal with hyperadrenocorticism, secondary problems can complicate the picture, making therapy prolonged and complicated at times.

Related posts:

  1. Simple Diagnosis and Treatment of Pruritic Otitis
  2. Ototoxicity
  3. Inflammatory Polyps
  4. Diagnostic Imaging of the Ear

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Ceruminous Diseases of the Ear

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