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Ossicular coupling
Ossicular coupling
S. Mansour et al.
In case of failure of topical treatment to treat
CSOM, then systemic oral antibiotics should be
used. The best option is ciprooxacin, but it
should not be given to children below 12years.
Erythromycin or Bactrim are alternatives in these
cases. All systemic aminoglycosides should be
avoided.
Generally speaking, the topical ear drops
should be continued for 6 weeks, while systemic
antibiotics should not be used for more than 2
weeks. Systemic corticotherapy for a few days,
followed by tapering doses for another few days,
enhances the therapeutic control of the active
inammatory process.
5.13.2 Surgery forCSOM
All surgical procedures must be done in respect
of basic principles of ME mechanics in relation
to the mechanisms of acoustic sound gain [3, 11].
Middle ear mechanics: Sound is transmitted
from external auditory canal (EAC) to the cochlea
by three mechanisms:
2. Acoustic coupling: Difference of sound pres-
sure on the oval and round window because
they are not in the same anatomic localization.
Acoustic coupling role is minor in the normal
ear with intact TM and ossicles. The acoustic
coupling can explain why patients with normal TM and ossicular discontinuity will have
more signicant HL (60dB) than those with
ossicular discontinuity with perforated TM
(40–50 dB), as TM will restrict sound pressure difference transmission to oval and round
windows (Figs5.11, 5.12, and 5.13) [3].
Another consideration in middle ear
mechanics is Phase difference; a sound stimulus to the inner ear is detected as a net
Cochlea
1. Ossicular coupling: it is the transmission of
sound pressure from the TM to the oval window through the ossicular chains. Due to the
air–uid interface, the sound will be reected,
causing a 30-dB sound loss, but the coupling
effect will overcome this loss by three mechanisms [11]:
(a) The hydraulic lever effect: due to the Area
Ratio 21:1. It is the compression of sound
energy and increase of force on the oval
window due to the difference of surface
area between the TM and the oval window leading to an increase in gain of
26dB.
(b) Malleoincudal lever effect: results from
the difference in length between the
manubrium of malleus and the long process of incus (ratio of 1.3:1). Gain of
2dB.
(c) Catenary lever effect: results from stretch-
ing of the TM from the annulus to the
manubrium of malleus. Gain of 2dB.
RW
Acoustic coupling
Fig. 5.11 Middle ear mechanics in a normal ear
Cochlea
RW
Acoustic coupling
Fig. 5.12 Middle ear mechanics in ear with tympanic
membrane perforation and ossicular chain discontinuity.
Acoustic coupling with sound pressure difference on the
oval window and round window is the main mechanism
for transmitting sound energy into the cochlea
5 Chronic Suppurative Otitis Media (CSOM)
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Fig. 5.13 Middle ear
mechanics in ear with
intact tympanic
membrane and ossicular
chain discontinuity.
Sound energy will not
reach the cochlea neither
through ossicular
coupling nor through
acoustic coupling, which
will result in a maximal
conductive hearing loss
71
Ossicular coupling
Cochlea
RW
Acoustic coupling
difference in sound pressures between the
round and oval windows. This difference is
lost if tympano-ossicular mechanisms are
absent (as in tympanoplasty types IV and V);
in this situation, an unshielded round window
will have negative acoustic consequences.
3. Middle ear aeration is another essential fac-
tor in sound transmission. It contributes to a
normal stapes-cochlear impedance and plays
an important role in normal ossicular coupling. The minimum amount of air required to
maintain ossicular coupling within 10 dB of
normal hearing has been estimated to be
0.5ml [3].
Consideration in pediatric patients: It is
preferable to avoid tympanoplasty in pediatric
patients below 5 years, and delay it till he or she
is 6–9years old, as there are higher chances of
failure due to recurrent otitis media and poor ET
dysfunction. Adenoidectomy with or without
tonsillectomy could be considered in obstructive
cases. ET catheterization is considered. However,
conrmed and sustained clinical results remain
doubtful since the main issue is the mucosa
disease.
Surgical ear reconstruction success may be
disappointing to some patients: the hearing benet after surgery depends not only on the magnitude of the closure of the air-bone gap but also on
the level of cochlear function of the operated ear,
the hearing level of the contralateral ear, and the
symmetry of hearing levels between the two ears.
5.13.2.1 Surgical Techniques
inTympanoplasty (Middle
Ear Reconstruction)
The purpose is to reconstruct the TM, reconstruct
the ossicular chain (mechanics), and ensure an
adequate middle ear aeration.
Tympanic Membrane Repair
(Myringoplasty)
Surgical approaches: The choice of myringoplasty depends on the perforation size, the anatomy of EAC, and the surgeon’s preference. The
main three approaches are:
1. Transcanal: least invasive, used for small per-
foration or medium-sized perforation, but the
whole perforation, especially the anterior rim,
should be accessible and the EAC anatomy is
favorable.
2. Endaural: It is most useful if limited atticot-
omy is performed with tympanoplasty.
3. Postauricular: offers better visualization of the
anterior rim of the TM.
Canaloplasty can be used when there is bulging of anterior wall of the EAC, narrow EAC, or
anterior perforation.
Graft selection: See Table 5.1 for different
graft materials in tympanoplasty (Fig.5.14):
Graft Placement
1. Underlay: Graft put underneath or medial to
the perforation.
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72
Table 5.1 Different graft materials in tympanoplasty
Fascia Good results, easy to handle.
Perichondrium Same properties, easy to manipulate for beginners.
Cartilage Stronger but needs to be thinned. May be used for revision procedures.
Fat Small perforation, simple pathology (dry ear), inlay, outpatient procedure.
S. Mansour et al.
ab
Fig. 5.14 (a) Two years after right ear cartilage tympa-
noplasty for posterior perforation. (b) One year after right
ear cartilage tympanoplasty for subtotal perforation show-
2. Overlay technique: Graft put lateral to the
brous layer of the TM.However, it should be
medial to the manubrium to prevent lateralization of the graft. Complete and total removal
of the squamous epithelium from the lateral
surface of the TM must be insured to avoid
iatrogenic cholesteatoma.
The success of any technique depends on the
surgeon’s expertise rather than on the technique
itself.
The advantages and disadvantages of each
technique are summarized in Table5.2.
TM Repair Outcome
The success rate of myringoplasty is 90%.
Myringoplasty failure can be due to:
1. Reperforation: early reperforation is caused
by a faulty technique like inappropriate
approach selection, small graft, and inappro-
ing the good vascularization of the graft. The major
advantage of cartilage graft is that it retains its rigid quality and resists to reperforation or retraction [3]
Table 5.2 The advantages and disadvantages of each
technique (underlay/overlay)
Overlay Underlay
Advantages • Excellent
exposure
• High graft
uptake
• Applicable to all
cases
Disadvantages • Requires
precision
• Longer healing
time
• Blunting, Pearls
• Less
lateralization
• Simpler
technique
• Poor
visualization
• Difcult with
small EAC
priate placement of the graft, allowing it to
fall into the middle ear space. Late reperforation is often due to infection, graft atrophy,
and ET dysfunction.
2. Graft lateralization: happens more in the overlay technique. It can lead to insufcient sound
conduction.
5 Chronic Suppurative Otitis Media (CSOM)
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73
3. Atelectasis: ET dysfunction is the leading
cause. Other causes are thin graft, not reinforcing the graft by other materials like cartilage, or not ventilating the ear in the primary
surgery.
4. Postoperative myringitis: it is a granular reaction of the lateral surface of the TM graft. The
patient will complain of slight pain, ear fullness, or otorrhea. It can be an autoimmune
response, reaction to the packing materials, or
postoperative infection. Treatment options are
topical antibiotics, debridement, or silver
nitrate cautery. Tympanoplasty can be considered if these options failed.
Ossicular Chain Reconstruction
(Ossiculoplasty)
It can be achieved by an allograft (bone or cartilage) or by a synthetic prosthesis. Generally, the
prosthesis is divided into:
• Partial ossicular replacement prosthesis
(PORP), which is used in cases of absent incus
but stapes is present, and
• Total ossicular replacement prosthesis
(TORP), which is used in cases of absent incus
and stapes superstructure.
Biomechanics ofOssiculoplasty
There are number of factors to be considered in
reconstructing the middle ear ossicles:
1. Biological factors: which include:
(a) Biocompatibility of the prosthesis: a bio-
compatible prosthesis is an inert one that
remains stable in a biologic environment
without inducing foreign body reaction.
Titanium and hydroxyapatite are the most
widely used and the most successful
implants nowadays, as they have excellent
mechanical properties, low extrusion rates,
and good hearing results. Titanium prosthesis is more user-friendly. An interface
cartilage graft should be used between the
prosthesis and TM to minimize extrusion.
(b) Middle ear environment: Fibrotic middle
ear mucosa and denuded mucosa during
surgery are detrimental to hearing results
compared with that of normal middle ear
mucosa. The presence of a stapes superstructure is crucial for a favorable hearing
result. The presence of malleus is theoretically important for a favorable hearing
outcome as well: the malleus is thought to
provide better hearing results if incorporated in the reconstruction by preserving
the catenary lever.
(c) Healing process which varies with per-
sonal immunity conditions.
2. Mechanical factors: The primary goal of
ossicular reconstruction is to reach a maximum of coupling the stapes footplate to the
TM in order to re-establish the hydraulic
lever effect.
(a) Prosthesis Axis: the angle between the
stapes and a prosthesis should be less
than 45° for optimal sound transmission [12].
(b) Tension: A prosthesis that is too long
would stiffen the ME tympano-ossicular
system resulting in a reduction of motion
and an impaired closure of the air-bone
gap [13].
(c) Coupling: Coupling refers to how well
prosthesis adheres to the footplate or TM,
and the degree of coupling will determine
whether or not there is slippage at the end
of the prosthesis. Tilting and/or dislocation of the prosthesis are the major causes
of poor postoperative hearing results.
Apart from biological reasons, prosthesis
displacement is the most common cause
of the postoperative unsatisfactory hearing results.
Strategies andTechniques inOssiculoplasty
In cases where the malleus handle is much medialized, resection of the tensor tympani ligament
is accomplished to free and positioner the manubrium adequately for better reconstruction. The
malleus must be preserved for better stability [3].
Look at Fig. 5.15 for ossiculoplasty strategies
and Figs. 5.16, 5.17, 5.18, and 5.19 for further
demonstration.
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74
S. Mansour et al.
Fig. 5.15 Ossiculoplasty
strategies and techniques
Limited erosion
of incus
Ossicular
erosion
Significant
erosion of incus
PORP
Incus
interposition
Erosion of stapes
suprastructure
TORPBone cement
Fig. 5.16 Right ear intraoperative view showing recon-
struction of the incudostapedial joint with bone cement
Fig. 5.17 Ossiculoplasty in the left ear using incus
interposition
Fig. 5.18 Ossiculoplasty in the left ear using PORP
The Outcome ofOssiculoplasty
Postoperative hearing outcomes are considered successful if the postoperative air-bone gap is within
20dB.Ossiculoplasty may fail for one of three fundamental reasons: a problem with the prosthesis,
postoperative adhesions, and recurrent disease.
When only myringoplasty is needed,
80–90% of patients will have an air-bone gap of
20dB or less. When ossicular reconstruction is
necessary, long-term closure of the air-bone
gap to less than 20dB is achieved in 80% of
cases in cases where the stapes is intact, and
only in about 65% of cases where the stapes
superstructure is missing [14].
ab
5 Chronic Suppurative Otitis Media (CSOM)
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75
Critical to the success of the CSOM surgery is
the ability of the ME to maintain adequate aeration to ensure good ME mechanics.
Fig. 5.19 Right ear ossiculoplasty using TORP and carti-
lage shoe. After nishing middle ear reconstruction and
packing the ear canal, a 30° scope is placed in the mastoid
attic to look into the middle ear cavity; the TORP is in
proper position and is stable. Notice the pin (black arrow)
on the headplate of the TORP which is kept intentionally
so the TORP will incorporate in the TM cartilage
Complications ofMiddle Ear Reconstruction
1. Infection.
2. Postauricular incisional site hematomas.
3. Taste disturbance.
4. Ear numbness of the pinna and lobule.
5. CHL due to lateralization of the graft and failure of middle ear spaces aeration (40dB loss
secondary to ME dysventilation and granulation formations.).
6. SNHL, which is a serious complication, can
occur due to excessive manipulation of the
ossicular chain.
7. Vertigo (rule out stula).
Complications ofMastoidectomy or
Tympano-Mastoidectomy
When mastoidectomy is indicated, according to
imaging inputs and surgical strategy review, this
surgery may leave, in addition to the above-cited
complications, a cerebrospinal uid (CSF) leak if
the dura is violated during the dissection.
Moreover, meningoencephaloceles can occur
secondary to a large tegmen defect.
CT imaging provides information about the
status of the prosthesis and eventual displacement (Fig.5.20).
Fig. 5.20 (a) Axial CT image along the TORP, that is in
close contact with the tympanic membrane (empty arrow),
inserting medially on the posterior border of the footplate
(arrow): displacement. (b) Axial CT image showing a
PORP with thickening of the tympanic membrane in contact with the prosthesis (empty arrow), the medial part
inserting on the stapes head (arrow)
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76
S. Mansour et al.
5.14 Some Unusual Clinical
Presentations ofCSOM
Tuberculous Otitis Media: The typical feature
of the disease is profuse, painless otorrhea not
responding to topical and systemic antimicrobial
therapies in combined with aural toilet.
Examination shows multiple TM perforations
and pale exuberant granulations. Complications
like facial palsy and SNHL are signicantly
higher than CSOM without cholesteatoma.
Immunodeciency: The idiopathic hypogammaglobulinemia is characterized by a deciency
in the IgG fraction of serum globulin, which
often presents with otitis media at an early age.
Chronic ear disease is sometimes observed in
Job’s syndrome (lazy leucocyte syndrome).
Wegener’s Granulomatosis: Middle ear
infection, either as a primary or secondary
involvement of the disease, has been described.
Histiocytosis X (Langerhans Cell
Histiocytosis): Histiocytosis X involvement of
the middle ear is rare and manifests as recurrent
otitis with aural polyps.
Take-Home Messages
• In most cases, chronic suppurative otitis
media (CSOM) is the result of an initial
episode of acute otitis media, and this is
why it is of high importance to give
AOM the proper care and follow-up in
children of 2–3 years old to prevent
hearing loss; health workers should ask
for all procedures visualizing the eardrum be standardized and validated.
• Clinical evaluation must distinguish
between CSOM from other forms of
chronic otitis media.
• Imaging is a helpful tool in unresponsive cases to a medical treatment
enabling the extent of inammatory disease in the middle ear cleft so as to differentiate safe from unsafe ear.
• Despite the decrease of morbidity of
CSOM, it remains a real burden and residual hearing loss, especially in countries
with a lack of public health regimen.
References
1. Mawson S, Ludman H. Disease of the ear: a textbook of otology. 4th ed. London: Edward Arnold
Publication; 1979.
2. Matanda RN, Muyunga KC, Sabue MJ, Creten W,
Van de Heyning P. Chronic suppurative otitis media
and related complications at the University Clinic of
Kinshasa. B-ENT. 2005;1:57–62.
3. Mansour S, Magnan J, Nicolas K, Haider H.Middle
ear disease. Cham: Springer; 2018. p.311–81.
4. Elmorsy S, Shabana YK, Raouf AA, Naggar ME,
Bedir T, Taher S, Fath-Aallah M.The role of IL-8in
different types of otitis media and bacteriological correlation. J Int Adv Otol. 2010;6:269–73.
5. Si Y, Zhang ZG, Chen SJ, Zheng YQ, Chen YB, Liu
Y, Jiang H, Feng LQ, Huang X. Attenuated TLRs
in middle ear mucosa contributes to susceptibility
of chronic suppurative otitis media. Hum Immunol.
2014;75:771–6.
6. Stanford LE, Raisanen S.Opsonization of middle ear
bacteria during chronic suppurative and secretory otitis media. Acta Otolaryngol. 1992;112(1):96–101.
7. Stanford LE, Raisanen S. Secretory IgA- and IgGcoated bacteria in chronically discharging ears. J
Laryngol Otol. 1991;105(7):515–7.
8. Haidar H, Sheikh R, Larem A, Elsaadi A, Abdulkarim
H, etal. Ossicular chain erosion in chronic suppurative
otitis media. Otolaryngol (Sunnyvale). 2015;5:203.
9. Mehta RP, Rosowski JJ, Voss SE, O’Neil E,
Merchant SN. Determinants of hearing loss in perforations of the tympanic membrane. Otol Neurotol.
2006;27(2):136–43.
10. Cureoglu S, Schachern PA, Paparella MM, Lindgren
BR. Cochlear changes in chronic otitis media.
Laryngoscope. 2004;114:622–6.
11. Mansour S, Magnan J, Haidar H, Nicolas K,
Louryan S. Comprehensive and clinical anatomy of
the middle ear. Cham: Springer; 2013. https://doi.
org/10.1007/978-3-642-36967-4.
12. Vlaming MS, Feenstra L.Studies on the mechanics of
the reconstructed human middle ear. Clin Otolaryngol
Allied Sci. 1986;11(6):411–22.
13. Morris DP, Bance M, Van Wijhe RG.How do cartilage
and other material overlay over a prosthesis affect its
vibration transmission properties in ossiculoplasty?
Otolaryngol Head Neck Surg. 2004;131(4):423–8.
14. Altamimi Z, Haidar H, Larem A, etal. Innovation in
otology: stability of ossicular reconstruction. J Bioeng
Biomed Sci. 2016;6(5 Suppl).
Cholesteatoma
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SalahMansour, Ma’inAliAl Shawabkeh,
KarenNicolas, andHassanHaidar
6
6.1 Introduction
Cholesteatoma is an abnormal growth of thekeratinizing squamous epithelium in the middle ear. It
could be congenital or acquired. Cholesteatoma
is a destructive and expanding lesion that may
lead to fatal complications if left untreated.
6.2 Epidemiology
Its annual incidence is 9.2/100,000 in adults
and 0.3/100,000in children with male predominance [1].
It is higher in Caucasian and rare in African.
It peaks in the second and third decades [2]. The
mean age for congenital cholesteatoma is 6
years.
S. Mansour (*)
Centre Medical Westmount Square, Otology,
Westmount, QC, Canada
M. A. Al Shawabkeh
ENT Department, Hamad Medical Corporation,
Doha, Qatar
K. Nicolas
Radiology Department, Bsalim Hospital,
Beirut, Lebanon
H. Haidar
Hamad Medical Corporation, Doha, Qatar
6.3 Types ofCholesteatoma
6.3.1 Congenital Cholesteatoma
It is more common in males (3:1). Its location is
more common in the superior anterior part of the
middle ear facing the Eustachian tube opening
(2/3 of the cases). The second most common is
the superior posterior part near the incudostapedial joint (Fig.6.1).
Fig. 6.1 Small congenital cholesteatoma in the anterosu-
perior quadrant of a right ear. (Adapted from Mansour S.,
Magnan J., Nicolas K., and Haider H. (2018). Middle ear
disease)
© Springer Nature Switzerland AG 2021
A. Al-Qahtani et al. (eds.), Textbook of Clinical Otolaryngology,
https://doi.org/10.1007/978-3-030-54088-3_6
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78
Levenson criteriafor the diagnosis ofcongenital cholesteatoma are as follows:
(a) White mass behind anintact tympanic mem-
brane (TM).
(b) No prior history of otorrhea.
(c) No prior history of TM perforation.
(d) No prior history of otologic procedures.
Prior history of otitis media does not rule out
congenital cholesteatoma.
6.3.2 Acquired Cholesteatoma
Acquired cholesteatomahas two types:
S. Mansour et al.
• Primary acquired: It is the most frequent type
and arises from the progression of tympanic
membrane retraction pocket. It can be a retraction from the pars accida (more common in
adults), from pars tensa (more common in
children), or combined (Figs.6.2 and 6.3).
• Secondary acquired: It arises from the migra-
tion of epithelial membrane through a
marginal perforation of the TM, or due to
trapped skin through micro-perforation secondary to trauma or surgery.
Fig. 6.3 Left ear mesotympanic and retrotympanic cho-
lesteatoma. (Adapted from Mansour S., Magnan J.,
Nicolas K., and Haider H. (2018). Middle ear disease)
6.4 Histopathology
ofCholesteatoma
Light microscopy shows a cyst with three
components:
1. Amorphous center composed of squamous
keratin debris.
2. Matrix, a stimulated proliferative skin
(Keratinizing squamous epithelium).
3. Perimatrix which is granulation tissues and
inammatory cells. It is the site of the inammatory process.
6.5 Pathogenesis
ofCholesteatoma
6.5.1 Theories forCongenital
Cholesteatoma
Fig. 6.2 Left attical cholesteatoma. (Adapted from
Mansour S., Magnan J., Nicolas K., and Haider H. (2018).
Middle ear disease)
1. Epidermal rest theory: cell rests of non-
keratinizing squamous epithelium localized
near Eustachian tube ostium, having the
potential to become a cholesteatoma.
6 Cholesteatoma
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79
2. Inclusion theory: migration of cells originatimgfrom the external auditory canalskinto
the middle ear secondary to non-evident
injury to the TM [3].
6.5.2 Theories forAcquired
Cholesteatoma
1. Invagination theory: the precursors of cholesteatoma are retraction pockets secondary to
dysventilation syndrome of the middle ear
compartments. Two histological features
present in cholesteatoma but not found in
retraction pockets: epithelial hyperplasia
and skin migration.
2. Migration theory: squamous epithelium of the
TM or the ear canalskinmigrates through the
perforated eardrum into the middle ear.
3. Squamous metaplasia theory: this theory stipulated that under chronic inammation, middle ear mucosa changes into a squamous
epithelium. Butthis theory lackshistological
or experimental proof, so such ahypothesis is
not accepted anymore.
4. Basal cell hyperplasia (Papillary) theory: a
keratin-lled microcysts or buds arise from
the basal layer of accida epithelium that
invade the subepithelial tissue and fuse
togetherto form acholesteatoma [4].
Recent advances in the pathogenesis of cholesteatoma postulate that the cholesteatoma is a result
of the defective healing process, in which the normal maturation end-stage of the wound- healing
process will not be achieved (non-stop wound healing process). Moreover, the pathogenesis of this
condition does not rely only on the middle ear
pathological conditions but also on the immunological status of the bottom of the skin ear canal [5].
6.6 Molecular Biology
ofCholesteatoma
1. Histochemical studies found quantitative and
qualitative modications of Langerhans’
cells; these cells emit long dendritic expansions, which create a true network between
the neighboring cells: keratinocytes and lymphocytes. This close contact between these
cells is essential for the immune reaction production [6].
2. There are paracrine and autocrine interac-
tions between keratinocytes of the matrix and
broblasts of the perimatrix that regulate
homeostasis and tissue regeneration within a
cholesteatoma [4].
3. The fundamental difference between the healing process in a normal skin and in cholesteatoma is that in cholesteatoma, there is a loss of
the growth inhibition by “cell to cell contact”.
Two factors are involved in that:
(a) The cholesteatoma develops beyond its
normal anatomical site for a “skin”.
(b) The inammatory process produces a
self-maintained immunological cycle,
which enhances the epithelial growth.
4. The loss of balance between apoptotic and
antiapoptotic markers, the increased antiapoptotic activity in cholesteatoma favors its
continuing expansion [6, 7].
5. The presence of antibiotic-resistant bacterial
Biolms in cholesteatomas may also explain
their aggressiveness [8].
6.7 Cholesteatoma Origin
andGrowth Pathways [
Posterior epitympanic cholesteatoma: It is the
most common pattern of spread for cholesteatoma originating from Prussak’s space. The cholesteatoma spreads into the superior incudal
space lateral to the body of the incus, and from
there, it can potentially enter the mastoid through
theaditus ad antrum (Fig.6.4).
Mesotympanic cholesteatoma: the second
most common type is mesotympanic cholesteatoma whichspreads through the posterior pouch
of von Troeltsch, following the embryological
course of both saccus posticus and saccus superior. It grows medially along the lenticular process and stapes superstructure. Then it may grow
upward through the posterior tympanic isthmus
6]
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