Infections of the External Ear

Key Points

The external ear and ear canal are affected by various bacterial, fungal, and viral infections as well as noninfectious inflammatory conditions.
Meticulous debridement of the ear canal is a crucial first step in managing all infections.
Most cases of external otitis should be managed with topical medications.
Infections that have spread beyond the confines of the ear canal skin require culture-directed systemic antibiotics. Until the culture results become available, patients should be started on a quinolone antibiotic.
Malignant or necrotizing otitis externa is a life-threatening infection that requires a high index of suspicion and proper selection of radiographic and possibly nuclear studies for prompt diagnosis.
There should be a low threshold to biopsy an ear canal process that is not responding appropriately to therapy or is associated with cranial nerve deficits.
Infection of the auricular cartilage can lead to significant cosmetic deformity and requires aggressive treatment with systemic antipseudomonal antibiotics and, in many cases, surgical debridement.
Viral infections of the ear canal include zoster oticus and bullous myringitis; both may be associated with sensorineural hearing loss.
Keratosis obturans and external auditory canal cholesteatoma (keratoma) are two poorly understood disorders marked by the accumulation of squamous debris and bony remodeling of the ear canal; although both are treated by debridement, they occasionally require aggressive surgical management.

Introduction

Otitis externa (OE) represents a state of infection or inflammation of the external auditory canal (EAC). The severity can range from a mild inflammation to osteomyelitis of the skull base; this can represent an acute episode or a process lasting years. OE is responsible for hundreds of millions of dollars of health care expenditures yearly and has a significant impact on the quality of life of those affected.

The pathophysiology of OE has been described in terms of three clinical stages: preinflammatory, acute inflammatory, and chronic. The preinflammatory stage consists of edema of the skin of the EAC and subsequent obstruction of the glands induced by local trauma or moisture, predisposing to further trauma. The acute inflammatory stage can be classified as mild, moderate, or severe. Mild acute inflammation is characterized by an erythematous and edematous EAC with clear, odorless secretions. The inflammation becomes moderate with increasing edema and pain, as well as mucopurulent secretions. In severe inflammatory OE, the EAC becomes obstructed with debris and secretions, is intensely painful, and is often associated with periauricular edema and adenopathy. If the inflammatory process spreads to surrounding tissues, it becomes necrotizing OE. Chronic inflammation is defined as a single episode lasting greater than 4 weeks or four or more episodes within one ear. The differential diagnosis should extend to primary malignancy and prompt tissue biopsy in cases that do not respond to therapy in a timely fashion or those associated with facial nerve deficits and/or deep-seated pain (see Chapter 178 ).

Anatomy of the External Ear

The external ear includes the auricle and the EAC. The auricle consists of keratinizing squamous epithelium covering a framework of elastic cartilage with perichondrium tightly bound to its lateral surface and more loosely bound to its medial surface. Sebaceous glands and hair follicles are found in the subcutaneous layer, with adipose tissue restricted to the cartilage-free lobule.

The EAC extends from the lateral surface of the tympanic membrane (TM) to the external auditory meatus; it measures approximately 2.5 cm in adults. A bony wall surrounds the medial two-thirds of the canal, with the lateral one-third possessing a cartilaginous skeleton. The cartilaginous portion contains hair follicles along with sebaceous and apocrine glands beneath a squamous epithelial surface layer. Cerumen is found in this portion of the canal; it is a hydrophobic, slightly acidic (pH 6.0 to 6.5) substance formed by glandular secretions and sloughed epithelium. Transverse slits in the cartilaginous canal (the fissures of Santorini) allow for the spread of infection or neoplasms from the external canal to the surrounding soft tissues.

The tympanic portion of the temporal bone forms the majority of the osseous EAC. The bone is covered by a thin layer of squamous epithelium that is tightly adherent to the bone and continuous with the lateral surface of the tympanic membrane. There is no subcutaneous layer and no glands or hair follicles. The junction of the bony and cartilaginous canal is known as the isthmus and represents the narrowest portion of the canal. The foramen of Huschke is a defect in the anterior bony canal from incomplete ossification that allows for the spread of disease to the deep lobe of the parotid gland.

The ear canal possesses a unique self-cleansing mechanism. The sloughed keratinous layer of the tympanic membrane migrates in a centrifugal fashion toward the annulus and subsequently to the cartilaginous canal, where it is combined with glandular secretions and extruded as cerumen.

Normal flora isolated from the EAC and cerumen is overwhelmingly gram positive. The most common bacteria include Staphylococcus auricularis and Staphylococcus epidermidis . Coryneform bacteria (diphtheroids), streptococci, and enterococci represent the next most common groups in descending order. Pseudomonas aeruginosa and fungal species are rare in the EAC of normal subjects.

Otitis Externa

Acute Otitis Externa

Acute otitis externa (AOE), also known as “swimmer's ear” or “tropical ear,” involves the rapid onset (<48 hours) of signs and symptoms of ear canal inflammation. It is generally unilateral and associated with exposure of the ear canal to water or local trauma. This diagnosis accounts for approximately 2.4 million health care visits per year in the United States and is more common in the summer months. The age group with the highest incidence of AOE includes 5- to 10-year-olds. However, over half of such cases are seen in adults over 20 years of age, and there appears to be a decline in incidence among those over 50 years of age.

Factors that may predispose to AOE include a congenitally narrow canal or a canal narrowed by exostoses; skin conditions including eczema, seborrhea, or psoriasis; trauma from ear plugs or hearing aids; or attempts at wax removal.

Medical comorbidities can have a dramatic impact on the course of OE. Conditions such as immunocompromised states, including diabetes and HIV, can predispose to malignant OE and should be evaluated carefully. Any history of radiotherapy and the status of the tympanic membrane should also be considered.

Chronic Otitis Externa

Chronic otitis externa (COE) represents a state of prolonged inflammation of the EAC, although the causes of this inflammation are incompletely understood and likely varied. Several proposed mechanisms include the following:

Exposure: Allergic OE may result from an allergic reaction to topical agents, most commonly neomycin. A contact dermatitis can result from contact with various agents, including hair sprays, shampoos, ear buds, and hearing aid molds. Allergic reactions of the EAC associated with fungal infections elsewhere in the body have also been described.
Systemic: Amyloidosis, sarcoidosis, Wegener granulomatosis, Sjogren disease, psoriasis, lichen planus, or systemic dermatitides such as seborrhea can involve the ear canal. The chronic inflammatory reaction typically results in hyperkeratosis and lichenification of the ear canal skin.
Chronic infection: Granular OE is thought to result from chronic infection of the ear canal by bacteria, fungi, or both. The ear canal skin and tympanic membrane manifest granulation and excoriation.
Local factors: including moisture or elevated pH.

COE is bilateral in over half of patients and affects 3% to 5% of the population. It often has a prolonged and variable course and is associated with poor quality-of-life measures. Although the majority of cases are indolent, some patients will develop fibrosis of the TM and medial canal skin. This will result in a blind-ending ear canal in a process known as postinflammatory medial canal fibrosis.

Signs and Symptoms

Acute Otitis Externa

The presenting symptom for bacterial AOE is often moderate to severe otalgia worsened with manipulation of the pinna. Symptoms are often present from several days to a week. Early AOE may include pruritus and erythema with a scant clear discharge. As the infection progresses, the pain and edema become worse and the discharge becomes seropurulent. The edema of the canal skin combined with otorrhea and debris in the canal may lead to a feeling of fullness and a conductive hearing loss.

Signs of AOE include erythema and circumferential edema of the EAC, otorrhea, and lymphadenopathy of the preauricular or cervical lymph nodes. There is tenderness with manipulation of the pinna in AOE, which must be differentiated from tenderness of the mastoid tip in acute mastoiditis. A Weber test should localize to the side of the infection if the canal is obstructed, and Rinne testing may show bone conduction greater than air conduction. A complete neurologic examination should be conducted to ensure that there is no evidence of extension to the facial nerve, vestibular organs, or other cranial nerves.

Viral acute OE is rare. Offending organisms include varicella, measles, and herpesvirus. Herpes zoster can affect the ear canal without (herpes zoster oticus [HZO]) or with facial paralysis (Ramsay Hunt syndrome) and may also be associated with sensorineural hearing loss or vertigo.

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