CARE AND REPAIR IN OTOLOGY
| REFLECTIONS ON GUIDELINES FOR MANAGING ACUTE OTITIS MEDIA —S. Michael Marcy, MD, Clinical Professor
of Pediatrics, Keck School of Medicine of the University of Southern California, Los Angeles, and the David Geffen
School of Medicine at the University of California, Los Angeles
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| Recommendation on modifying clinical definition of acute otitis media (AOM): to diagnose AOM—
confirm history of acute onset; identify signs and symptoms of middle ear effusion and inflammation; other factors—
pain usually in context of upper respiratory tract infection (URI); fever absent in ≤50% of cases; pneumatic otoscopy
key to diagnosis
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 | Differentiating otitis media with effusion (OME) from AOM: confusing clinical definitions—middle ear effusion
based on clinical signs alone (ie, bulging tympanic membrane [TM], air-fluid level, or reduced mobility of TM); middle
ear inflammation based on scarlet redness of TM or otalgia that interferes with sleep or normal daily activity; problems
with definition—bulging drum need not be painful or have erythema; drum may be another color, eg, white, not
red; to avoid confusion, guidelines might recommend—assessing TM status independently, without considering
presence of otalgia; looking for otorrhea and opacified bulging discolored TM (ie, consider green, yellow, or creamy
white discoloration along with redness as key finding); eliminating otalgia as requirement for diagnosis of AOM
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| Recommendation that observation without antibacterial therapy is option for selected children,
based on diagnostic certainty, age, illness severity, and assurance of follow-up
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| Managing child: <6 mo of age—treat regardless of whether diagnosis certain or uncertain; failure to treat may lead to unanticipated
adverse consequences in preverbal child; 6 mo to 2 yr—treat when diagnosis certain; if diagnosis uncertain,
treat if illness severe, ie, moderate to severe otalgia or fever ≥39°C; observation sufficient if disease nonsevere, ie, mild
or intermittent ear pain and fever <39°C; ≥2 yr—treat severe illness; treat nonsevere illness if diagnosis certain
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| Amoxicillin: antimicrobial of choice; selection based on cost, taste, and availability; administering 80 to 90 mg/kg per
day in 2 divided doses kills nonsusceptible Streptococcus pneumoniae; points—community susceptibility patterns
should determine whether child receives high- or low-dose therapy; standard doses sufficient for children who received
≥3 doses of pneumococcal vaccine
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| Changing microbial flora in AOM: heptavalent pneumococcal vaccine reduced incidence of AOM caused by S
pneumoniae; Haemophilus influenzae now causes 55% to 60% of AOM (50% β-lactamase–positive); Moraxella catarrhalis
causes 3% to 10% of AOM (all organisms β-lactamase–positive); incidence of viral infection varies with intensity
of investigation
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| Cephalosporins for managing increased incidence of AOM caused by H influenzae: cefdinir effective and
better tasting
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| Nontype-1 or uncertain reaction: late onset (>72 hr); first-generation cephalosporins safe in penicillin-allergic patients;
patients who experienced non–life-threatening (ie, not anaphylactic IgE-mediated) reaction to penicillin or cephalosporin
can still receive repeated courses of those antibiotics, ie, clinician does not have to abandon β-lactams;
point—no fatal anaphylaxis reported in children receiving oral cephalosporins; single IM dose of ceftriaxone recommended
in children—who are vomiting or unable to tolerate treatment; when compliance uncertain or parent or
care-giver unreliable
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| Options for patients who fail antimicrobial therapy at 48 to 72 hr: high-dose amoxicillin and potassium clavulanate
for β-lactamase–positive organisms (eg, H influenzae and M catarrhalis); cephalosporin, eg, ceftriaxone, for
patient with nontype-1 allergy to amoxicillin
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| Recommendations on reducing risk for AOM: promoting breast-feeding; reducing group day-care activities;
avoiding supine bottle feeding, pacifier use, and passive exposure to tobacco smoke; vaccination; detection of allergies
and immunodeficiency; no data show—AOM can be caused by tobacco smoke or propping bottle of child with intact
TM; definite risk from pacifier use; additional observations—data on efficacy of influenza vaccination in preventing
AOM remains limited; complementary and alternative medicine remain controversial
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| COMPLICATIONS OF ACUTE OTITIS MEDIA —John S. Oghalai, MD, Assistant Professor, Bobby R. Alford Department
of Otolaryngology–Head and Neck Surgery, Baylor College of Medicine, Houston, TX
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| Mastoiditis: characterized by—swollen external auditory canal; postauricular edema or erythema; protruding ear; disease
types—noncoalescent mastoiditis differentiated from routine AOM by presence of swollen or protruding ear; coalescent
mastoiditis characterized by destruction of bony trabeculae or cortex of temporal bone; myringotomy—approach
depends on patient’s age and where procedure performed; when performing procedure in clinic, do not place pressure
equalization (PE) tube; procedure indicated in newborn infant with middle ear effusion and increased risk for meningitis
(use small spinal needle attached to suction to penetrate TM and to aspirate material for culture); when procedure performed
in operating room, place PE tube to drain middle ear space and mastoid (without tube, hole closes and myringotomy
must be repeated); myringotomy—decreases risk for intra- and extracranial complications; provides culture
specimen for antibiotic therapy; successfully treats most children with mastoiditis; mastoidectomy more definitive
means of clearing infection when—hospitalized patient with AOM does not respond to IV antibiotics; PE tubes cannot
provide adequate drainage (good connection does not exist between mastoid air cell system, antrum, and middle ear
space); complications other than mastoiditis present
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| Acute coalescent mastoiditis with subperiosteal abscess: Bezold’s abscess (infection within mastoid air cell
system that goes downward and medially through mastoid tip around digastric muscle, producing neck abscess); Luc’s
abscess goes up squamous portion of temporal bone and underneath periosteum of temporalis muscle; management—
myringotomy with PE tube; drain purulent material from areas that cannot be drained adequately by tube; place Penrose
drain to promote continued drainage of infection (drain contraindicated for simple mastoiditis without subperiosteal abscess);
speaker usually performs simple mastoidectomy; caveat—patient with one intracranial complication may have others
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| Facial paralysis associated with AOM: uncommon, even though ≥55% of patients have clear dehiscence of fallopian
canal; ≈75% of cases involve incomplete paralysis; treatment—myringotomy with PE tube whenever possible
(drain infection; culture aspirate); obtain infectious disease consultation and administer intravenous (IV) antibiotics; steroids
typically avoided when managing infection; consider mastoidectomy; facial nerve decompression usually not done
(advocated by some clinicians for managing total paralysis); once infection resolves, facial nerve function usually recovers
over months
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| Labyrinthitis: stages—serous labyrinthitis (bacterial toxins enter inner ear and produce inflammation, vertigo, and
mild to moderate sensorineural hearing loss [presumably reversible if sterile]); purulent labyrinthitis (develops as bacteria
enter inner ear and trigger release of inflammatory mediators; produces irreversible hearing loss); fibrous stage
(fibroblastic proliferation with granulation develops in inner ear); osseous stage, ie, labyrinthitis ossificans
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| Treatment: if patient becomes deaf, consider immediate implantation; in patients believed to have labyrinthitis associated
with AOM—image for intracranial extension or other complications; obtain lumbar puncture, because bacteria
can spread to cerebrospinal fluid and produce meningitis; place PE tube; administer IV antibiotics; consider mastoidectomy
to help eliminate infection
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| Diseases mimicking mastoiditis: include rhabdomyosarcoma and Langerhans cell histiocytosis
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| Petrous apicitis, ie, Gradenigo’s syndrome: patient has history of frontal headaches, eye pain, diplopia, dizziness,
nausea, and left abducens nerve palsy; AOM on otoscopy; magnetic resonance imaging (MRI) shows—inflammation
of petrous apex and mastoid air cell system; constricted precavernous carotid artery on affected side; on computed tomography
(CT)—bone erosion in petrous apex; less erosion in mastoids; treatment—myringotomy with PE tube; culture-directed
IV antibiotic therapy; reserve surgery for nonresponders or patients with impending or established
intracranial complications; tailor surgical approach to focus of pathology
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| Intracranial complications: meningitis—meningeal signs mandate lumbar puncture; follow with serial audiometry;
encephalomalacia—complication of meningitis; can cause severe brain damage; epidural abscess—remove bone
from area of abscess; go down to dura and eliminate abscess
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| Any patient with AOM unresponsive to oral antibiotics must be taken seriously: radiographic
imaging—CT with contrast of temporal bones (visualizes bony trabeculae of mastoid; detects intracranial complications);
MRI (indicated in absence of CT with contrast); treatment—hospitalize all patients for IV antibiotic therapy;
consult with infectious disease specialist; perform myringotomy with PE tube for culture and drainage; if situation does
not improve quickly, proceed to more extensive surgery; any patient with meningeal signs requires lumbar puncture
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| BACTERIOLOGY OF CHRONIC OTITIS MEDIA: NEW CHALLENGES —James Saunders, MD, Associate Professor
of Otolaryngology, Department of Otorhinolaryngology, University of Oklahoma Health Science Center, Oklahoma City
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| Biofilms in chronic otitis media (COM): clinical data show—biofilms on mucosal surfaces of patients with rhinosinusitis;
high percentage of biofilms in cholesteatoma matrix; characteristics—bound to surfaces; glycocalyx provides
superstructure; antimicrobial resistance; slow growing; bacteria enter dormant state within biofilm; quorum sensing (genetic
change that occurs when bacteria switch from planktonic to biofilm state); diagnostic imaging—scanning electron microscopy
(EM); transmission EM; confocal laser scanning microscopy (CLSM); data show biofilms—present in COM;
contribute to difficulty encountered with antibiotic therapy; exist on tympanostomy tubes (TT), within cholesteatoma matrix,
and on mucosal surfaces; current research looking for—genetic markers to identify quorum sensing; effective treatment
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| Antibiotic-resistant bacteria: external otitis—Staphylococcus present in ≈50% of cases; methicillin-resistant Staphylococcus
aureus (MRSA) present in ≈10% of draining ears; corynebacteria becoming prominent in bacterial population
(as pathogen, not contaminant) and show significant resistance patterns; myringitis—mostly primary myringitis;
broad range of organisms, but MRSA plays significant role; otitis media (OM) with perforation—staphylococci;
Pseudomonas, including quinolone-resistant strains; bottom line—assessment of all conditions studied show ≈30% incidence
of resistant strains in bacterial isolates from different diagnoses
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| Otomycosis: fungal spores—classic finding; often found in drainage of ear not expected to contain fungus; as percentage
of culture isolates, otomycosis—fairly low for external otitis, myringitis, and TT; fungus found growing in ≈50%
of cultures obtained from draining ears of patients with OM with perforation; observation—in significant number of
cases with other initial diagnoses, discovery of otitis externa tended to alter treatment
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| Management: cultures of draining ear—recommended at initial visit; more difficult for refractory cases (previous antibiotic
therapy complicates effort to obtain clean culture); impact on management uncertain; ear drops—not recommended for
treating ear with copious amounts of purulent drainage; systemic antibiotics recommended for treating more refractory disease;
high-dose trimethoprim–sulfamethoxazole (Bactrim)—often effective against MRSA (data show 15% of cultures resistant
to Bactrim); should resistance problems occur, convert to vancomycin
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| TYMPANIC MEMBRANE PERFORATIONS IN CHILDREN —Kay W. Chang, MD, Assistant Professor of Otolaryngology,
Pediatric Otolaryngology, Stanford University School of Medicine, Palo Alto, CA
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| TM perforations: risk factors—placement for recurrent AOM rather than for effusion; placement of 2 TT; multiple insertions
of TT; duration of intubation >18 mo; ≥3 episodes of otorrhea during intubation; etiologic factors—infection
(AOM); COM with severe eustachian tube dysfunction; chronic mastoid disease; cholesteatoma; trauma; iatrogenic injuries;
main causes of perforation—TT and AOM in children; trauma and COM in adults; analysis of pars tensa perforations
in children—72% of perforations related to prior TT placement; 60% of perforations found in anteroinferior
quadrant of TM (typical location for tube placement); size of perforation determines amount of hearing loss; tube removal
mandated by granulation in 50% of cases (perforation rate 11% after removal); point (intubation lasting >3 yr increases
rate of persistent perforation)
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| Office management of TM perforations: determine whether perforation—acute or chronic (perforations lasting
>3 mo considered chronic); central or marginal; assess—size of perforation (percentage of TM surface); quadrant(s)
containing perforation; whether perforation dry or draining, and has sharp or rough edges; look for—dimeric membranes
resulting from healed perforations (identified with pneumatic otoscopy); perforation involving pars flaccida (superior
to short process of TM; maintain high suspicion for cholesteatoma); marginal perforations (ingrowth of keratinizing
epithelium into middle ear can cause cholesteatoma); traumatic perforations (often have irregular rough edges; folded-in
flaps can adhere to mucosal undersurface of middle ear; epithelium may be implanted into middle ear space)
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| Typical TM rupture from AOM: treat otorrhea with antibiotics and nonototoxic ear drops; evaluation urgent if patient
has—traumatic perforation; symptoms of vertigo or facial weakness; suspected intracranial infection; persistent otorrhea
despite medical therapy or persistent perforation after 3 mo; severe hearing loss; diagnostic tools—binocular
microscopy (improves depth perception and illumination; helps visualize foreign bodies); suction when blood or secretions
obscure detail; irrigation can cause significant hearing loss in patients with large TM perforations; tuning fork examination
(Weber test; Rinne test); audiography before surgery; CT unnecessary unless perforation caused by temporal bone fracture, or
ossicular anomaly or cholesteatoma suspected; conductive hearing loss—usually 15 to 30 dB; if >30 dB, suspect ossicular
problem
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| Factors determining need to repair chronic perforation: include—draining ear (should usually be dry before
repair; repair immediately if drainage caused by nasopharyngeal reflux); size of perforation; degree of hearing loss; duration
of perforation; patient’s age (controversial); status of contralateral ear; point—indications for surgery often related
to complications caused by TM perforation
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| Treatment: dry ear precautions for large perforations; follow-up audiography; for 3 yr after repair, children have high incidence
of reperforations, TM retraction, infections, effusion, and conductive hearing loss; graft options—temporalis
fascia for standard tympanoplasty; cartilage for more involved tympanoplasty; paper patch or fat for myringoplasty; data
show—after repair, ≈90% of patients have air–bone gap closed to 20 dB; adenoidectomy and status of contralateral ear
can affect outcome
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| Algorithm for managing TM perforation after tube extrusion: if granulation present and tube does not fall
out, try medical treatment and remove tube; if tube falls out and perforation persists, clear ear of otorrhea before performing
fat-graft or Gelfilm/paper patch myringoplasty; results—approach achieved 91% success rate initially; 8 patients required
second intervention (all patients responded successfully to additional therapy)
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Suggested Reading
Albera R et al: Tympanic reperforation in myringoplasty: evaluation of prognostic factors. Ann Otol Rhinol Laryngol
115:875, 2006; Bluestone CD: Clinical course, complications, and sequelae of acute otitis media. Pediatr Infect Dis J
19:S37, 2000; Butbul-Avivel Y et al: Acute mastoiditis in children: Pseudomonas aeruginosa as a leading pathogen.
Int J Pediatr Otorhinolaryngol 67:277, 2003; Cober MP, Johnson CE: Otitis media: review of the 2004 treatment
guidelines. Ann Pharmacother 39:1879, 2005; Ford-Jones EL et al: Microbiologic findings and risk factors for antimicrobial
resistance at myringotomy for tympanostomy tube placement — a prospective study of 601 children in Toronto.
Int J Pediatr Otorhinolaryngol 66:227, 2002; Haddad J et al: Nonsusceptible Streptococcus pneumoniae in children
with chronic otitis media with effusion and recurrent otitis media undergoing ventilating tube placement. Pediatr Infect
Dis J 19:432, 2000; Hydén D et al: Inner ear and facial nerve complications of acute otitis media with focus on bacteriology
and virology. Acta Otolaryngol 126:460, 2006; Marcy SM: New guidelines on acute otitis media: an overview of
their key principles for practice. Cleve Clin J Med 71 Suppl4:S3, 2004; Uyar Y et al: Tympanoplasty in pediatric patients.
Int J Pediatr Otorhinolaryngol 70:1805, 2006; Viastarakos PK et al: Biofilms in ear, nose, throat infections:
how important are they? Laryngoscope 117:668, 2007; Zapalac JS et al: Suppurative complications of acute otitis media
in the era of antibiotic resistance. Arch Otolaryngol Head Neck Surg 128:660, 2002.
Educational Objectives
| The goal of this program is to improve the management of otitis media and tympanic membrane perforations in children.
After hearing and assimilating this program, the clinician will be better able to:
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| 1. Evaluate current guidelines for managing acute otitis media (AOM).
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| 2. Diagnose and treat complications associated with AOM.
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| 3. Review current data on the role of biofilms in chronic otitis media (COM).
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| 4. Discuss current trends in bacterial resistance associated with COM.
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| 5. Manage tympanic membrane perforations in children.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members to disclose relevant
financial relationships within the past 12 months that might create any personal conflicts of interest. Any identified conflicts
were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial
interest. For this program, the faculty reported nothing to disclose.
Acknowledgements
Drs. Chang and Marcy gave their scientific lectures at Pediatric Otolaryngology Update 2006, presented October 27-
28, 2006, in Palo Alto, CA, by Lucile Packard Children’s Hospital at Stanford and Stanford University School of
Medicine; Dr. Oghalai gave his scientific lecture at Stanford Otology and Neurotology Update 2006, presented November
2-4, 2006, in San Francisco, CA, by Stanford University School of Medicine; and Dr. Saunders gave his scientific
presentation at the Ultimate Colorado Mid-Winter Meeting: An Otolaryngology Update and the Colorado
Otology—Audiology Conference presented January 28 to February 1, 2007 in Vail, CO, by the University of Colorado
School of Medicine. The Audio-Digest Foundation thanks the speakers and the sponsors for their cooperation in
the production of this program.
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