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Chapter 631 External Otitis (Otitis Externa)
Joseph Haddad, Jr.
In an infant, the outer two thirds of the ear canal is cartilaginous and the inner one third is bony. In an older child and adult only the outer one third is cartilaginous. The epithelium is thinner in the bony portion than in the cartilaginous portion, there is no subcutaneous tissue, and epithelium is tightly applied to the underlying periosteum; hair follicles, sebaceous glands, and apocrine glands are scarce or absent. The skin in the cartilaginous area has well-developed dermis and subcutaneous tissue and contains hair follicles, sebaceous glands, and apocrine glands. The highly viscid secretions of the sebaceous glands and the watery, pigmented secretions of the apocrine glands in the outer portion of the canal combine with exfoliated surface cells of the skin to form cerumen, a protective, waxy, water-repellent coating.
The normal flora of the external canal consists mainly of aerobic bacteria and includes coagulase-negative staphylococci, Corynebacterium (diphtheroids), Micrococcus, and, occasionally, Staphylococcus aureus, viridans streptococci, and Pseudomonas aeruginosa. Excessive wetness (swimming, bathing, increased environmental humidity), dryness (dry canal skin and lack of cerumen), the presence of other skin pathology (previous infection, eczema, or other forms of dermatitis), and trauma (digital or foreign body, cotton tip applicators [Q-tips]) make the skin of the canal vulnerable to infection by the normal flora or exogenous bacteria.
External otitis (swimmer’s ear, although it can occur without swimming) is caused most commonly by P. aeruginosa, but S. aureus, Enterobacter aerogenes, Proteus mirabilis, Klebsiella pneumoniae, streptococci, coagulase-negative staphylococci, diphtheroids, and fungi such as Candida and Aspergillus also may be isolated. External otitis results from chronic irritation and maceration from excessive moisture in the canal. The loss of protective cerumen may play a role, as may trauma, but cerumen impaction with trapping of water also can cause infection. Inflammation of the ear canal due to herpesvirus, varicella-zoster, other skin exanthems, and eczema also may predispose to external otitis.
The predominant symptom is acute ear pain, often severe, accentuated by manipulation of the pinna or by pressure on the tragus and by jaw motion. The severity of the pain and tenderness may be disproportionate to the degree of inflammation, because the skin of the external ear canal is tightly adherent to the underlying perichondrium and periosteum. Itching often is a precursor of pain and usually is characteristic of chronic inflammation of the canal or resolving acute otitis externa. Conductive hearing loss may result from edema of the skin and tympanic membrane (TM), serous or purulent secretions, or the canal skin thickening associated with chronic external otitis.
Edema of the ear canal, erythema, and thick, clumpy otorrhea are prominent signs of the acute disease. The cerumen usually is white and soft in consistency, as opposed to its usual yellow color and firmer consistency. The canal often is so tender and swollen that the entire ear canal and TM cannot be adequately visualized, and complete otoscopic examination may be delayed until the acute swelling subsides. If the TM can be visualized, it may appear either normal or opaque. TM mobility may be normal or, if thickened, reduced in response to positive and negative pressure.
Other physical findings may include palpable and tender lymph nodes in the periauricular region, and erythema and swelling of the pinna and periauricular skin. Rarely, facial paralysis, other cranial nerve abnormalities, vertigo, and/or sensorineural hearing loss are present. If these occur, necrotizing (malignant) otitis externa is probable. This invasive infection of the temporal bone and skull base requires immediate culture, intravenous antibiotics, and imaging studies to evaluate the extent of the disease. Surgical intervention to obtain cultures or debride devitalized tissue may be necessary. P. aeruginosa is the most common causative organism of necrotizing otitis externa. Fortunately, this disease is rare in children and is seen only in association with immunocompromise or severe malnourishment. In adults it is associated with diabetes mellitus.
Diffuse external otitis may be confused with furunculosis, otitis media (OM), and mastoiditis. Furuncles occur in the lateral hair-bearing part of the ear canal; furunculosis usually causes a localized swelling of the canal limited to 1 quadrant, whereas external otitis is associated with concentric swelling and involves the entire ear canal. In OM, the TM may be perforated, severely retracted, or bulging and immobile; hearing usually is impaired. If the middle ear is draining through a perforated TM or tympanostomy tube, secondary external otitis may occur; if the TM is not visible owing to drainage or ear canal swelling, it may be difficult to distinguish acute OM with drainage from an acute external otitis. Pain on manipulation of the auricle and significant lymphadenitis are not common features of OM, and these findings assist in the differential diagnosis. In some patients with external otitis, the periauricular edema is so extensive that the auricle is pushed forward, creating a condition that may be confused with acute mastoiditis and a subperiosteal abscess; in mastoiditis,
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