Porth's Essentials of Pathophysiology, 4e

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Disorders of Special Sensory Function: Vision, Hearing, and Vestibular Function

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with uncomplicated AOM. This approach involves joint decision making between the clinician and parents, a system for close follow-up, and beginning antibiotics if symptoms worsen or there is no improvement within 48 to 72 hours. 52 Most cases of OME resolve spontaneously within a 3-week to 3-month period. The management options for this duration include observation only, antimicrobial therapy, or combination antimicrobial and corticosteroid therapy. 52,54 A hearing evaluation is recommended when OME persists for 3 months or longer or at any time that language delay, learning problems, or a significant hearing loss is suspected. Children with recurrent OM should be evaluated to rule out any anatomic variations (e.g., enlarged adenoids), allergies, and immunologic abnormalities. Referral to an otolaryngologist is indicated if the effusion persists for 4 months or longer. Surgical treatment (e.g., tympanostomy tubes, adenoidectomy) may be indicated for OME if the effusion has persisted for 4 months or longer and is accompanied by persistent hearing loss and other manifestations; if recurrent or persistent effusion occurs in children at risk regardless of hearing status; or if there is structural damage to the tympanic membrane or middle ear. 54 Tympanostomy tube insertion is the preferred initial procedure and does not typically include the removal of adenoids unless the child has additional indications, such as postnasal obstruction from enlarged adenoids. Adenoidectomy plus myringotomy (without tube insertion) has been shown to have comparable efficacy in children 4 years of age or older but is more invasive, with additional surgical and anesthetic risks. 54 Complications of Otitis Media. The complications of OM include hearing loss and extratemporal complications, including those affecting the middle ear, mastoid, adjacent structures of the temporal bone, and intracranial structures. Hearing loss, which is a common complication of OM, usually is conductive and temporary based on the duration of the effusion. Hearing loss that is associated with fluid collection usually resolves when the effusion clears. Permanent hearing loss may occur as the result of damage to the tympanic membrane or other middle ear structures. Cases of sensorineural hearing loss are rare. The mastoid antrum and air cells constitute a portion of the temporal bone and may become inflamed as an extension of acute or chronic OM. 51 The disorder causes necrosis of the mastoid process and destruction of the bony intercellular matrix, which are visible by radiologic examination. Mastoid tenderness and drainage of exudate through a perforated tympanic membrane can occur. Chronic mastoiditis can develop as the result of chronic middle ear infection. The usefulness of antimicrobial agents for this condition is limited. Mastoid or middle ear surgery, along with other medical treatment, may be indicated. Cholesteatomas are cystlike lesions of the middle ear, usually associated with chronic otitis media (see Fig. 38-19B). Measuring 1 to 4 cm in diameter, they are lined with keratinizing squamous epithelium or mucus-secreting epithelium and filled with amorphous

debris (derived largely from desquamated epithelium). 51 Although precise mechanisms involved in their devel- opment are unclear, it is proposed that chronic inflam- mation and perforation of the eardrum with ingrowth of squamous epithelium or metaplasia of the secretory epithelium of the middle ear are contributing factors. These lesions can erode the ossicles, the labyrinth, the adjacent mastoid bone, and the surrounding soft tis- sues. Although often thought of as a complication of otitis media, a cholesteatoma may also occur as a con- genital condition. Symptoms commonly include pain- less drainage from the ear and hearing loss. Treatment involves microsurgical techniques to remove the choles- teatomatous material. Intracranial complications are uncommon since the advent of antimicrobial therapy. Although rare, these complications can develop when the infection spreads through vascular channels, by direct extension, or through preformed pathways such as the round window. 48 These complications are seen more often with chronic suppurative OM and mastoiditis. They include otogenic meningitis, brain abscess, lateral sinus thrombophlebitis or thrombosis, labyrinthitis, and facial nerve paralysis. Any child who develops persistent headache, tinnitus, stiff neck, or visual or other neurologic symptoms should be investigated for possible intracranial complications. Otosclerosis Otosclerosis refers to the formation of new spongy bone around the stapes and oval window, which results in progressive deafness 55,56 (see Fig. 38-19C). In most cases, the condition is familial and follows an autosomal dominant pattern with variable penetrance. Otosclerosis may begin at any time in life but usually does not appear until after puberty, most frequently between the ages of 20 and 30 years. The disease process accelerates during pregnancy. Otosclerosis begins with resorption of bone in one or more foci. During active bone resorption, the bone structure appears spongy and softer than normal (i.e., otospongiosis). The resorbed bone is replaced by an overgrowth of new, hard, sclerotic bone. The process is slowly progressive, involving more areas of the tempo- ral bone, especially in front of and posterior to the sta- pes footplate. As it invades the footplate, the pathologic bone increasingly immobilizes the stapes, reducing the transmission of sound. Pressure of otosclerotic bone on middle ear structures or the vestibulocochlear nerve (CN VIII) may contribute to the development of sensorineu- ral hearing loss, tinnitus, and vertigo (to be discussed). The symptoms of otosclerosis involve an insidious conductive hearing loss. Initially, the affected person is unable to hear a whisper or someone speaking at a distance. In the earliest stages, the bone conduction by which the person’s own voice is heard remains relatively unaffected. At this point, the person’s own voice sounds unusually loud, and the sound of chewing becomes intensified. Because of bone conduction, most of these persons can hear fairly well on the telephone, which provides an amplified signal.