C h a p t e r 3 8
Disorders of Special Sensory Function: Vision, Hearing, and Vestibular Function
979
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.
