TIPS AND TECHNIQUES FOR IMPROVING OTOLOGIC SURGERY
From Clinical Frontiers in Otolaryngology, presented by the Research Study Club of Los Angeles
Richard J. Wiet, MD, Professor of Clinical Otolaryngology and Neurosurgery, Department of Otolaryngology–Head and
Neck Surgery, Northwestern University Feinberg School of Medicine, and Ear Institute of Chicago, Chicago, IL
Educational Objectives
| The goal of this program is to improve otologic surgery and the management of hearing loss after surgery. After
hearing and assimilating this program, the clinician will be better able to:
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 | 1. Classify the main types of chronic ear disease.
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| 2. Discuss how conductive hearing loss may persist or return after apparently successful ossiculoplasty.
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| 3. Compare stereotactic radiosurgery and gamma knife surgery in the management of acoustic neuromas.
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| 4. Describe the causes of immediate and delayed hearing loss after stapes surgery.
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| 5. Cite recent advances in medical therapy for otosclerosis.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning
committee 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, Dr. Wiet disclosed that he designs instruments
for Medtronic and Xomed. The planning committee reported nothing to disclose.
Acknowledgements
This program was recorded at the 76th Midwinter Conference, Clinical Frontiers in Otolaryngology, held January 11-
12, 2008, in San Marino, CA, and sponsored by the Research Study Club of Los Angeles. The Audio-Digest Foundation
thanks Dr. Wiet and the Research Study Club for their cooperation in the production of this program.
| RECENT ADVANCES IN CHRONIC EAR AND OSSICULAR CHAIN SURGERY
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| Classification of chronic ear disease
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| Tubotympanic disease: affects mucoperiosteum; central membrane perforation and draining
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| Atticoantral disease: usually associated with cholesteatoma; worsens over time
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| Patient evaluation: history, otologic examination, including use of microscope and tuning fork; x-rays ordered in cases
of revision, or when symptoms suggest problem such as perilymphatic fistula, bone disease, or complication of untreated infection;
magnetic resonance imaging (MRI) ordered only when tumor or extratemporal disease suspected
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| Causes of recurrent hearing loss: poor aeration, persistent disease, tympanic membrane problem, ossicular chain
coupling
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| Poor aeration: causes include Eustachian tube dysfunction; persistent mucosal disease; sclerotic mastoid pneumatization;
persistent aeration problems associated with disease recurrence; estimated incidence of residual disease 8% to 40%;
true recurrence relatively rare, but can result from persistent aeration problems when protection of eardrum inadequate;
consider preoperative staging for stapedial fixation, or when perforation coupled with ossicular deficit (air-bone gap
higher)
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| Persistent disease or development of biofilm: biofilm does not respond to antibiotics; does respond to mechanical ventilation
or subsequent surgery; lessening residual cholesteatoma—advances include wall replacement and intraoperative
dyes; use of methylene blue followed by saline rinse during surgery may isolate cholesteatoma; aids in visualizing border
or margin under unusual circumstances; wall replacement option in primary acquired cases, but only if mastoid
well pneumatized (contraindicated if mastoid sclerotic)
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| Tympanic membrane: size of perforation or effective membrane surface important for driving stapedial footplate; depending
on location of perforation, round window may require protection; cavity infection also influences degree of hearing
loss; large perforation causes greater hearing loss; paper patch will not improve hearing when ossicular problem
present; assess ossicular status preoperatively (if ossicle not intact, hearing will not improve); no difference in hearing
between canal-wall-up and canal-wall-down procedure when ossicular structures comparable
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| Ossicular chain coupling: small changes in position lead to big changes in hearing
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| Kartush revision of Austin ossicular fixation classification: absent incus considered Class A deficit; can correct
with implants
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| Passive implants: autografts—patient’s own tissue; lowest incidence of extrusion; homografts—rarely used due to fears
about prions (Jakob-Creutzfeldt disease); allografts—speaker treats distal erosion of incus tip with hydroxyapatite cement
(low extrusion; not recommended for large defects); total or partial ossicular replacement prosthesis (TORP or
PORP)—TORP materials include hydroxyapatite and titanium; however, long-term results discouraging; only 59% of
PORPs and 30% of TORPs associated with <20 decibel (dB) gap at 5 yr, due to recurrent or persistent disease; better
stabilization of TORPs—perforation of footplate not recommended because of high incidence of sensorineural hearing
loss (SNHL); may stabilize distal end with “shoe” in oval window; proximal end may be stabilized with glues and
hooks on tympanic membrane side; results poor if malleus hookup angle >45o (measure distance); when using metal
prosthesis on proximal (tympanic membrane) side, use cartilage for protection to prevent extrusion (less common with
hydroxyapatite or autograft)
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| Emerging technologies: intraoperative hearing assessment—can use audiometers and tuning forks during stapes surgery
with local anesthesia; new active implants—improvement on Soundbridge
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| Type IV tympanoplasty: requires no implant; line shallow oval window with split-thickness skin; maintain aeration by
placing cartilage over round window, so sound energy goes directly to vibratory surface of stapes
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| ACOUSTIC NEUROMA: CONTROVERSIES IN MANAGEMENT
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| Microsurgery: 3 goals; completely resect tumor; eliminate disease; minimize morbidity
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| Radiotherapy: arrests tumor growth
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| Important difference: results of surgery apparent quickly (≤1 yr); results of radiotherapy often not known for 5 to 20 yr
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| Pregnancy concurrent with acoustic neuroma: neuroma growth rate accelerates during pregnancy; tumors contain
estrogen receptors and bind estradiol; pregnant women have higher incidence of sudden hearing loss; rapid tumor
growth rate probably due more to progesterone than estrogen; evaluate individually; waiting usually appropriate, unless
growth rate and hearing loss excessive
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| Only-hearing ear: often associated with small or medium-sized tumors; consider possibilities of brainstem compression
and progression of hearing loss; treatment options include cochlear implantation and auditory brainstem implant; watchful
waiting often advised to preserve hearing as long as possible; however, if evidence of central brainstem compression
appears, treatment necessary; patients often advised to attend lip-reading classes, consider hearing rehabilitation (eg, contralateral
cochlear implantation); follow up with repeated magnetic resonance imaging (MRI)
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| Hearing preservation surgery: in one large review (2007; 1132 articles), middle fossa surgery associated with
slightly better auditory outcomes than retrosigmoid surgery; however, review did not include several important more
recent studies; in those papers, hearing preserved postoperatively in 60% to 70% of patients
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| Neuroma associated with neurofibromatosis type 2 (NF2): case—NF2 in man 33 yr of age; symptoms of brainstem compression;
on right side, had neurosurgery for decompression, followed by debulking 1 yr later; gamma knife surgery on
left side; right ear (deaf) underwent translabyrinthine removal and auditory brainstem implant; observation of only
hearing ear; cochlear implants often not helpful after auditory brainstem implant due to involvement of cochlear nerve
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| Radiotherapy: stereotactic—provides tumor control (growth cessation, possible shrinkage); patient must be followed for
5 to 20 yr; overall rate of complications low; rate of hearing preservation ≈50% (rising with fractionation; delivery of
multiple fractionated doses now possible); gamma radiation—delivery platform 201 cobalt radiation sources placed
inside helmet; patient lies on gantry, with head in helmet and head frame in helmet; radiation delivered directly to tumor
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| Outcomes: early treatments (1987-1992) involved average dose margin of 16 gray (Gy) and associated with high rate of
complications (facial weakness or numbness; hearing loss); later articles reported good outcomes, including tumor
shrinkage; tumor control rate 98.6% in one series, with low rates of facial nerve weakness and trigeminal neuropathy,
and good rates of hearing preservation; outcomes similar in other studies; gamma knife—rates of local control 87% to
100%, depending on center; hearing preservation 33% to 78%; rates of facial and trigeminal neuropathy low;
fractionation—more variation in control rates (patients undergo ≥6 treatments, with total dose of 30-50 Gy, but radiation
delivered in short bursts, which accounts for variable results; local control rate ≥90%; hearing preservation rate
53% to 93%, with low rates of facial and trigeminal neuropathy; allows higher dose delivery to tumor
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| Complications of stereotactic radiotherapy: hydrocephalus, malignant transformation (secondary neoplasms); increase in
risk for radiation-induced changes ≤12-fold
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| Ideal indications for radiotherapy: older or medically infirm patients; attempts at hearing preservation; patient choice
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| Failure of radiotherapy: decrease of dose from 12 to 10 Gy associated with 6-fold increase in incidence of tumor regrowth;
in series of ≥500 cases, regrowth rate varies from 0.3% to 3.0%; with radiotherapy, rate ranges from 2% to 6%,
even in best of hands; failure rate will probably increase over time as doses decrease
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| Lack of central necrosis: radiation therapy considered failure if central necrosis does not occur and tumor growth resumes;
80% of tumors may lose central enhancement and continue to swell in first 6 mo after irradiation; 30% of those
tumors remain large; wait ≥2 yr before concluding treatment failure; microsurgical resection technically challenging
after radiation failure
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| HEARING LOSS AFTER STAPES SURGERY
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| American Academy of Otolaryngology–Head and Neck Surgery (AAOHNS) guidelines for stapes
surgery: minimum air-bone gap of 25 dB, preferably verified with tuning forks; success defined as 10-dB closure of
postoperative air to postoperative bone; success of primary surgery 85% to 90%; success of revisions ranges from 16%
to 80%
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| Types of postsurgical hearing loss: persistent conductive loss immediately after surgery; immediate neurosensory
loss; delayed sensorineural loss; delayed conductive loss
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| Persistent conductive loss: usually due to unrecognized pathology or surgical problem; unrecognized pathologies—epitympanic
fixation, round window otosclerosis, dehiscence of superior semicircular canal, Paget’s disease (cochlear
deterioration with fibrous change at stapes footplate)
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| Epitympanic fixation: usually seen in people ≥50 yr; diagnosis sometimes possible by gently palpating malleus handle
if patient permits; best managed by removing malleus head and incus and performing ossiculoplasty
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| Round window obliteration: unusual (occurs in <1% of stapes surgery); key is otosclerosis beginning during teen years;
becomes very advanced; round window reflex missing (must check for it)
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| Superior canal dehiscence syndrome: patient often has history of Tullio phenomenon (loud sound induces vertigo);
Hennebert’s sign with Valsalva maneuver (nystagmus in response to sound or pressure); conductive hearing
loss; check stapedial reflex to avoid missing diagnosis; diagnose with vestibular evoked myogenic potential
(VEMP; response elicited at lower threshold), special computed tomography (CT) with oblique planes reformatted
for observing superior semicircular canal (shows dehiscence extending from dura to edge of canal)
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| Surgical problems: case abandoned due to overhanging facial nerve; incus subluxation; prosthesis too short
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| Immediate neurosensory loss: incidence 0.5% to 4.0% in case series; usually due to surgical trauma, suctioning, viral or
foreign body reactions, and suppurative labyrinthitis (potentially serious; at least 3 reports mention mortality associated
with stapes surgery); often associated with perilymphatic “gushers”
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| Gushers: usually seen in young men (X-linked deafness); stapedial reflex present due to underpressure of cerebrospinal
fluid (CSF) against stapes footplate (ominous sign; surgery contraindicated); widening of internal auditory canal or
malformation of area next to cochlear capsule more common
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| Hearing loss from surgical trauma: examples—overaggressive suctioning or drilling in patients with advanced otosclerosis;
laser-associated trauma—argon penetrates perilymph and may hit macula and saccule; however, rare in actual
practice; overaggressive use of CO2 laser may overheat perilymph, leading to SNHL; avoid fishing footplate
particles out of vestibule; common cause of SNHL
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| Wide vestibular aqueduct syndrome: may cause conductive hearing loss; acts as “third window”
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| Delayed SNHL: causes include granuloma; perilymphatic fistula; advanced otosclerosis; cochlear otosclerosis
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| Granuloma: characterized by initial hearing gain, followed by hearing loss, within 6 wk of surgery; patients may complain
of dizziness as well as progressive hearing loss; blue-red color may develop on tympanic membrane
(Schwartze’s sign); early recognition and intervention (revision surgery) can save hearing
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| Perilymphatic fistulas: rare today; associated with wire, polyethylene, or Gelfoam struts; characterized by fluctuating
SNHL and Hennebert’s sign; negative pressure shows quick phase of eye away from affected ear; dizziness lasts ≥4
wk; diagnose by history and pneumatic otoscopy; rule out prosthesis or granuloma; light pressure on incus may reveal
fistula; repair with blood patch or fibrin glue
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| Advanced otosclerosis: in very advanced cases, bone score not measurable and audiogram seems blank; consider
stapes revision plus hearing aid for those patients; otic capsule trilaminar structure, consisting of perichondrium,
endosteum, and periosteum; osteoclasts produced in otic capsule; rationale for medical therapy—bone from cartilage;
conductive hearing loss results from abnormal bone growth over oval window; SNHL thought to result
from enzymatic or inflammatory response from spongiotic focus; may be slowed by medical therapy
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| Types of medical therapy: bisphosphonates (can arrest SNHL associated with Paget’s disease if used early enough);
sodium fluoride, zoledronic acid (decreases cytokine expression in osteoblasts; recently published information)
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| Cochlear otosclerosis: likely signs and symptoms include SNHL disproportionate to age; CT evidence of disease; family
history of otosclerosis; Schwartze’s sign (florid flamingo color during active phase); progressive hyalinization of
stria vascularis probably contributes to SNHL; active phase sometimes called otospongiosis, compared to inactive
phase, or otosclerosis (hardening of tissue)
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| Delayed conductive hearing loss: causes include incus necrosis, loose prosthesis attachments, prosthesis detachment or
dislodgement, and obliterative otosclerosis
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| Incus problems: hydroxyapatite glue can fix small problems; for larger defects, speaker uses Lippy modification of Robinson
prosthesis to bridge defect, or considers malleus-to-oval window–and-incus bypass procedure; loose attachments
at incus—fluctuations in conductive component may be key; dislodged prosthetics—lining membrane can migrate
(revision indicated); prosthesis itself may migrate (typically seen with thin wire prosthetic)
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| Obliterative otosclerosis: characterized by early preoperative onset of hearing impairment; if air–bone gap not closed
properly, hearing loss may recur within weeks to months of surgery, due to rapid reformation of otosclerotic foci that
dislodge prosthesis; key is accurate assessment of rapidly progressing hearing loss during childhood; use of long
prosthesis that goes ≈0.25 mm below oval window recommended so otosclerosis cannot push prosthesis out of position
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Suggested Reading
Banerjee R et al: Comparison of the surgical and follow-up costs associated with microsurgical resection and stereotactic
radiosurgery for vestibular schwannoma. J Neurosurg 108:1220, 2008; Battista RA et al: Revision stapedectomy.
Otolaryngol Clin North Am 39:677, 2006; Bush ML et al: Long-term hearing results in gamma knife radiosurgery for
acoustic neuromas. Laryngoscope 118:1019, 2008; Ju DT et al: Hypofractionated Cyberknife stereotactic radiosurgery
for acoustic neuromas with and without association to neurofibromatosis type 2. Acta Neurochir Suppl 101:169, 2008;
Kaylie DM et al: Revision chronic ear surgery. Otolaryngol Head Neck Surg 134:443, 2006; Neff BA et al: Cochlear
implantation in the neurofibromatosis type 2 patient: long-term follow-up. Laryngoscope 117:1069, 2007; Venail F et al:
New perspectives for middle ear implants: first results in otosclerosis with mixed hearing loss. Laryngoscope 117:552,
2007; Wang YP, Young YH: Experience in the treatment of sudden deafness during pregnancy. Acta Otolaryngol
126:271, 2006; Wiet RJ et al: Acoustic neuroma (vestibular schwannoma) revision. Otolaryngol Clin North Am 39:751,
2006; Yetiser S et al: Management of tympanosclerosis with ossicular fixation: review and presentation of long-term results
of 30 new cases. J Otolaryngol 36:303, 2007; Yung M: Long-term results of ossiculoplasty: reasons for surgical failure.
Otol Neurotol 27:20, 2006.
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