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208
A. Larem et al.
Table 19.1 Tumor-Node-Metastasis (TNM) staging
adapted from AJCC Cancer Staging Manual 8th Edition
Tx Primary tumor cannot be identied
Tis Carcinoma in situ
T1 Tumor smaller than 2cm in greatest dimension
T2 Tumor 2cm or larger, but smaller than 4cm in
greatest dimension
T3 Tumor 4cm or larger in maximum dimension or
minor bone erosion or perineural invasion or deep
invasion*
T4a Tumor with gross cortical bone/marrow invasion
T4b Tumor with skull base invasion and/or skull base
foramen involvement
Clinical N (cN)
Nx Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in a single ipsilateral lymph node,
3cm or smaller in greatest dimension and
ENE(−)
N2a Metastasis in a single ipsilateral node larger than
3cm but not larger than 6cm in greatest
dimension and ENE(−)
N2b Metastasis in multiple ipsilateral nodes, none
larger than 6cm in greatest dimension and
ENE(−)
N2c Metastasis in bilateral or contralateral lymph
nodes, none larger than 6cm in greatest
dimension and ENE(−)
N3a Metastasis in a lymph node larger than 6cm in
greatest dimension and ENE(−)
N3b Metastasis in any node(s) and ENE(+)
Pathological N (pN)
Nx Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in a single ipsilateral lymph node,
3cm or smaller in greatest dimension and
ENE(−)
N2a Metastasis in single ipsilateral or contralateral
node 3cm or smaller in greatest dimension and
ENE(+)
N2b Metastasis in multiple ipsilateral nodes, none
larger than 6cm in greatest dimension and
ENE(−)
N2c Metastasis in bilateral or contralateral lymph
nodes, none larger than 6cm in greatest
dimension and ENE(−)
N3a Metastasis in a lymph node larger than 6cm in
greatest dimension and ENE(−)
N3b Metastasis in a single ipsilateral node larger than
3cm in greatest dimension and ENE(+);or
multiple ipsilateral. Contralateral, or bilateral
nodes, any with ENE(+)
M
M0 No distant metastasis
M1 Distant metastasis
19.2.7 Rhabdomyosarcoma
• It is considered a disease of pediatrics [13].
• Auricular rhabdomyosarcoma is extremely
rare. Temporal bone involvement represents
less than 7% of all rhabdomyosarcoma cases
[13, 14].
• Appearance: like a polypoid lesion [14]
19.2.8 Merkel Cell Carcinoma
• Considered neuroendocrine cells [15].
• It is a rare tumor [15].
• Risk factors: elderly, fair skin, sun exposure,
and immunocompromised [15].
• Appearance: it is a subcutaneous lesion that
has reddish-blue or pink color [15].
• Histology: small round cells, stain positive for
neurons specic enolase, cytokeratin (CK),
and chromogranin, which can help of other
cutaneous malignancies [15].
• It has a high rate of metastasis [16].
• Had 30–50% local recurrence rate, and
50–80% lymph node spread [2].
• Male and young age patients have a worse
prognosis [2].
• It has 55% 3-year survival rate [2].
• Treatment: complete surgical excision with a
wide surgical margin (2cm margin for those
more than 2 size) and elective neck dissection.
Postoperative radiotherapy is indicated for
aggressive malignancy [15].
• It is considered radiosensitive and chemosensitive [15].
19.3 Malignancy ofEAC
19.3.1 Spread
The bony ear canal limits tumor growth. However,
it can still spread through the following:
1. Fissures of the Santorini: an embryologic
remnant that leaves small anterior
19 External Ear Malignancies
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209
ab c
Fig. 19.3 Steps of the resection of auricular SCC with reconstruction: (a) Resection of the SCC with wide margin. (b)
Utilizing the surrounding tissue as a ap for closure. (c) The shape of the auricle at the end of the procedure
Fig. 19.4 Complete left auricular excision for a patient with SCC of left auricle
dehiscence in the cartilaginous part of the
19.3.2 Basal Cell Carcinoma
ear canal, which connects to parotid inferiorly [17].
2. Bony and cartilaginous junction part of the ear
canal.
3. Huschke’s foramen (Foramen tympanicum): a
defect found in the tympanic ring in the inferior anterior margin and opens into the temporomandibular joint (TMJ). It is found in 5%
[17].
• It is the second most common primary malignant tumor of the EAC.SCC is considered the
most common [18].
• BCC in this location tends to have an aggressive course and has high recurrence rates with
high mortality rates [19].
• Treatment: Even with aggressive treatment, it
is common to have a local recurrence.
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A. Larem et al.
Table 19.2 Comparison between BCC and SCC
BCC SCC
Aggressiveness Low incidence
of metastasis
Appearance A pearly skin
lesion with
rolled borders
and
telangiectasias
Treatment Surgical
excision with
2–4mm
margins.
Radiotherapy
can also be
used. Moh’s
micrographic
mapping can be
utilized
It has a capacity for
metastasis and local
destruction
Indurated
erythematous patch,
and its border cannot
be distinguished. It
has an area of
ulceration that can
bleed easily
Excision with 1cm
margins
circumferentially,
which might require
auriculectomy.
Radiotherapy might
be indicated
postoperatively.
Close follow-up of
the patient is
required to monitor
the resected area and
to detect any new
lesion in sunexposed areas
Treatment of choice is complete excision with
negative margins, and that necessitates subtotal or total temporal bone resection depending
on the extension of the disease [19].
19.3.3 Squamous Cell Carcinoma
• It is an aggressive disease [20].
• It constitutes 80% of the malignant tumor of
EAC. However, it occurs less common than
those in the auricle [2].
• Signs and symptoms:
– Ear pain: which can resemble otitis externa
or media; so, the persistence of pain despite
treatment should raise the suspicion of
such a condition [21, 22].
– Bloody otorrhea [20].
– Hearing loss [20]
– Other symptoms or signs are cervical
lymphadenopathy and cranial nerve
involvement. Facial paralysis and vertigo
occur in cases at an advanced stage [2,22].
• Imaging:
• Assess the following: the EAC, middle ear,
mastoid, facial nerve, sigmoid sinus, jugular
bulb, carotid canal, tegmen, middle and posterior cranial fossa, TM joint, and parotid and
infratemporal fossa [5].
– CT scan: to look for erosion and extension
of the disease [5].
– MRI with contrast to look for soft tissue
involvement and intracranial extension [5].
– Angiography can be obtained if other
imaging modalities showed the possibilities of internal carotid artery (ICA)
involvement. The balloon occlusion test
can be utilized to check the patency of
ICA in the contralateral side[5].
• Investigation: Biopsy of the lesion: obtain a
deep biopsy [5].
• Staging: There are several staging systems
available
• Treatment:
– T1 and tumor localized to cartilaginous
part: sleeve resection [23].
– T1 with bone involvement or T2: Lateral
bone resection (± radiotherapy) [23]
– T3: lateral temporal bone resection plus
subtotal petrosectomy followed by radiotherapy, or subtotal temporal bone resection plus postoperative radiotherapy
[5,24].
– T4 with limited dural involvement “less
than 1 cm” and no intraparenchymal extension: subtotal or lateral temporal bone
resection with postoperative radiotherapy
[5, 24].
• See Table 19.3 for the type of temporal bone
resection.
• Neck management:
• If the node is positive, then a modied radical
neck dissection is performed.
• If the node is negative, then selective neck dissection for level II, III, Va, and parotidectomy
(either supercial if facial nerve function is
not affected or total if facial nerve function is
affected) [5, 24]
• The patient is considered inoperable in case
of:
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211
Table 19.3 Types of temporal bone resection [25]
Sleeve
resection
Lateral bone
resection
Subtotal
temporal bone
resection
Total bone
resection
Removal of the cartilaginous part of
the ear canal along with the skin over
the bony part
Removal of the cartilaginous and bony
EAC with the TM, malleus, and incus
Same as lateral bone resection with the
contents of the middle ear, mastoid,
otic capsule, and middle ear medial
wall
Same as subtotal bone resection with
petrous apex and neurovascular bundle
– ICA encasement.
– Extension to petrous apex
– Dural involvement of more than 1cm intra-
parenchymal extension [24].
19.3.4 Rhabdomyosarcoma
• A rare malignant tumor [2].
• EAC rhabdomyosarcoma is usually an extension from the middle ear [2].
• Appearance: polyps causing destruction of the
bone and neurological decit like facial nerve
palsy [2].
19.3.5 Melanoma
• It usually arises as a primary tumor [26].
• EAC melanoma is considered a high-risk
lesion as the tumor will be hidden in the ear
canal, so it will grow to a signicant thickness
[26].
• Treatment: Complete surgical excision with
negative margin (total or subtotal temporal
bone resection), neck dissection, and postoperative radiotherapy [26].
19.3.6 Langerhans Cell Histiocytosis
• Symptoms: mass in the ear canal, ear pain, ear
discharge, bloody ear discharge, and hearing
loss [2].
This usually involves the medial bony part of
•
the EAC [2].
• CT will show EAC soft tissue along with bony
erosion [2].
19.3.7 Malignant Ceruminous
Tumors
19.3.7.1 Ceruminous Adenoid Cystic
Carcinoma
• Constitutes around 2.4% of all primary malignant tumor of EAC [27].
• They arise from the ceruminous gland [27].
• Symptoms: ear pain and mass in the ear canal
[27].
• They have an indolent course and tend to have
a perineural invasion, which is considered a
hallmark feature of this tumor [28].
• Treatment: complete surgical excision with
negative margin along with parotidectomy (to
remove the tumor cells that spread through the
ssures) and neck dissection with postoperative radiotherapy [2].
19.3.7.2 Ceruminous
Adenocarcinoma
• Less frequent than adenoid cystic carcinoma
with EAC [2].
• They are classied as low and high grade.
• Symptoms are similar to ceruminous adenoid
cystic [2].
• Treatment: complete surgical excision with
negative margin with postoperative radiotherapy [2].
19.3.7.3 Ceruminous
Mucoepidermoid Carcinoma
• Rare tumor, appears less frequent than the previous two [2].
• Symptoms: ear pain and mass in the lateral
part of the ear canal, ear discharge, bloody ear
discharge, hearing loss, and facial nerve paralysis [2].
• Treatment: complete surgical excision [2].
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A. Larem et al.
Take Home Massages
Auricular Malignancies
• Actinic keratosis is a premalignant condition that can be treated by curettage,
cryotherapy, or some local applicants.
• Keratoacanthoma is considered a lowgrade skin tumor.
• BCC is the least aggressive skin cancer
and the most common skin cancer in the
head and neck. Histologically, it has different subtypes like supercial, nodular,
pigmented, inltrative, morpheaform
(sclerosis), and basal squamous (last
two have an aggressive clinical course).
It is treated by surgical excision with
2–4mm margins.
• SCC is the most common malignancy of
the auricle. It is treated by excision with
1cm margins circumferentially.
• Melanoma can arise de novo or from
pre-existing lentigo maligna lesion. It
has four subtypes: supercial spreading
(most common), nodular, lentigo
maligna, and acral lentiginous. TNM,
Breslow, and Clerk are some staging
systems in use. It is treated by surgical
excision with surgical margin depending on the thickness of the tumor.
• Merkel cell carcinoma is considered a
neuroendocrine cell tumor that can
affect the auricle. It has a high rate of
metastasis. Thirty to 50% local recurrence rate and 50% to 80% lymph node
spread rate. It is treated by complete surgical excision with a wide surgical margin (up to 3 cm) and elective neck
dissection. Postoperative radiotherapy is
indicated for aggressive types.
EAC Malignancy
• BCC of the EAC tends to have an
aggressive course and has high recurrence rates.
• SCC constitutes 80% of the malignant
tumor of EAC.There are different stag-
ing systems like Manolidis Staging
System, Stell–McCormick Staging
System, and Arriaga (University of
Pittsburgh) Revised by Moody. It is
treated by temporal bone resection like
(sleeve, lateral, subtotal, and total).
However, in cases like ICA encasement,
an extension to petrous apex, dural
involvement more than 1cm, and intraparenchymal extension, the tumor will
be considered inoperable.
• Rhabdomyosarcoma, melanoma, and
langerhans cell histiocytosis are other
tumors that can affect EAC.
• Malignant ceruminous tumors can
affect the ear canal. Ceruminous adenoid cystic carcinoma, ceruminous adenocarcinoma, and ceruminous
mucoepidermoid carcinoma are examples of those tumors.
Acknowledgment Authors of the chapter would like to
appreciate the help of Dr. Adham Aljariri, an ENT resident in Hamad medical corporation, for his help and effort
in editing the chapter.
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https://doi.org/10.5152/
AL GRAWANY
Cochlear Implant and Other
Implantable Hearing Devices
HassaninAbdulkarim, AbdulsalamAl-Qahtani,
andAliAl-Saadi
Key Points
In this chapter, we will learn:
• What is a cochlear implant device?
• Pathophysiology and causes of sensorineural hearing loss
• Indications and cocntraindications for
cochlear implant surgery
• Investigations needed for diagnosis
• Surgery of cochlear implant and its
complications
• Short description about other implantable hearing devices (middle ear and
bone anchored)
20.1 Introduction
• Cochlear implants are surgically implanted
prosthetic devices that use electrical stimulation to the cochlear nerve to provide hearing.
It collects sound through the external device
microphone and then changes to electrical
impulse to the internal device’s electrodes
(Fig.20.1a, b).
H. Abdulkarim · A. Al-Qahtani (*) · A. Al-Saadi
Hamad Medical Corporation, Doha, Qatar
e-mail: habdulkarim@hamad.qa; aaa2009@qatar-med.
cornell.edu; aalsaadi1@hamad.qa
20
• Simulating the physiology of the ear, the
sound collected from the external device
microphone is processed and changed to electrical current passing to the inner device’s corresponding electrodes tonotopically.
• Cochlear implantation has become a routine
procedure worldwide for the management of
severe-to-profound sensorineural hearing loss.
It is a phenomenal example of success that
was made possible through collaboration
among engineers, surgeons, scientists, and the
medical community.
• As of 2012, more than 300,000 implants have
been performed worldwide, and this number
is in constant rise every year.
• Patient candidacy is through an evaluation of a
big team made of ENT surgeons, audiologists,
psychologists, speech and language therapists,
and social workers.
20.2 History oftheProcedure
• In 1957, Djourno and Eyries observed that
activation of the auditory nerve with an electried device gives auditory stimulation in a
patient.
• 1963, Doyle and Doyle’s early experiments in
scala tympani implantation [1].
• In 1972, the rst House/3M single-channel
implant was done [2].
© 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_20
215
216
Receiver Antenna
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H. Abdulkarim et al.
a
Coil
Coil magnet
Coil cable
Microphones
Processing
Uint
Ear hook
b
Receiver magnet
Receiver
Electrode array
Fig. 20.1 Cochlear implant device components. (a)
Components of external device. (b) Component of internal device
• In 1984, multichannel devices were
introduced.
• In 2008, image-guided minimally invasive
cochlear implantation was developed and is
still under research.
• Adult patients
– Progressive hearing loss that began in
childhood
– Viral-induced sudden hearing loss
– Ototoxicity
– Otosclerosis (cochlear)
– Ménière disease
– Trauma
– Autoimmune conditions
– Presbycusis
– Bacterial infections
20.4 Pathophysiology
• Severe-to-profound deafness patients had a
direct or indirect injury to the organ of Corti,
causing hair cell degeneration or dysfunction.
• Success of cochlear implantation depends on
stimulation of surviving spiral ganglion neurons.
• The number of surviving neuron populations
needed for successful implantation remains
unknown till now. However, studies do report
better postimplantation performance with
higher residual spiral ganglion cells [3].
• Also, delayed loss of residual hearing in
implantation done is connected with intracochlear brosis; thus, interventions aimed at
reduction of cochlear trauma and inammation, that is, perioperative steroids and hearing
preservation approaches, are routinely used
successfully [3].
20.5 Diagnosis andSelection
20.3 Etiology
In adults, most of the patients reaching for
cochlear implantation are already following with
Common etiologies that result in congenital and
delayed-onset hearing loss needing cochlear
implant:
• Pediatric
– Idiopathic
– Genetic hearing loss (dominant or
recessive)
– Acquired usual infectious: bacterial and
postviral meningitis
an ENT surgeon or audiologist regarding his
sensorineural hearing loss with hearing aid use,
so the nal decision to proceed for cochlear
implant is an eventual expected step of the
management.
For children, most of the developed countries
have a neonatal screening program right after
birth to early pick deafness in neonates.
From these programs, diagnosis of SNHL
(sensorineural hearing loss) is made,
AL GRAWANY
20 Cochlear Implant and Other Implantable Hearing Devices
217
investigations and radiological imaging are
requested, and hearing aid tting is also done.
Failure of benets from hearing augmentation
is later on referred for cochlear implant
programs.
Candidates will be further referred to psychologists and social workers to assess readiness and
address expectations of the patient or the parents
for the procedure.
20.6 Indications
Any patient with moderate-to-profound sensorineural hearing loss or a patient who still struggles
to hear and understand despite appropriately t
hearing aids is a candidate for cochlear implant.
Although cochlear implants are mainly used
for those with bilateral hearing loss, they may also
be used in patients with severe unilateral sensorineural hearing loss, with or without tinnitus.
Candidates do not need to be totally deaf.
Indeed, most patients have some hearing, and the
sentence recognition scores can be up to 60% in
best-aided conditions.
The clinical scenarios indicating cochlear
implant are as follows:
• Congenital hearing loss and prelingual
deafness
• Acquired hearing loss and postlingual
deafness
• Severe hearing loss that can be aided and that
deteriorates to profound loss in childhood,
adolescence, or adulthood (perilingual) and
coexists with various degrees of language
development.
Generally, the candidacy for implantation is
considered separately for adults and children as
outlined in the 1995 National Institutes of Health
(NIH) consensus statement on cochlear implantation [4, 5].
Prelingually deafened adults, although potentially suitable for cochlear implantation, must be
counseled in regard to realistic expectations, as
language and open-set speech discrimination outcomes are less predictable.
Children are considered suitable for cochlear
implantation at age of 1 year, and because of
meningitis-related deafness with progressive
cochlear ossication, occasional earlier implantation is necessary [6].
Differences between cochlear implants in
children and adults include:
• The best candidates for cochlear implants are
postlingual (had speech and language skills
before losing their hearing), and most adult
candidates for a cochlear implant fall into this
category.
• Adults typically perceive more of a mechan-
ical sound after implantation; the sound
typically becomes more natural after
4–8weeks.
• Adults with bilateral hearing loss benet
from bilateral implants, which improve
speech perception, allow better hearing in
conditions with signicant background
noise, enhance sound localization, and
allow the patient to hear sound coming from
either side without having to turn one’s head
[7–10].
20.7 Contraindication
• Contraindications to cochlear implantation
may include deafness due to lesions of the
eighth cranial nerve or brain stem (those
patients may benet from brain stem implant
although controversial).
• In addition, chronic infections of the middle
ear and mastoid cavity or tympanic membrane
perforation can be contraindications
(relative).
• Cochlear aplasia as demonstrated on CT scans
remains an absolute contraindication.
• Certain medical conditions such as specic
hematologic, pulmonary, and cardiac condi-
tions also may be contraindications.
• The lack of realistic expectations regarding
the benets of cochlear implantation and/or a
lack of strong desire to develop enhanced oral
communication skills poses a strong contrain-
dication for implant surgery.
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20.8 Evaluation
20.8.1 History
Obtain a detailed otological history including
family history of hearing loss, patient’s developmental history, and immunizations.
20.8.2 Physical Examination
Conduct a comprehensive physical including
general ENT with focus on otologic exam. Pay
specic attention for any infectious, chronic ear
component that will inuence the decision and
sequences of procedures to make the ear safe
before implantation.
20.9 Investigations
20.9.1 Laboratory Studies
1. CBC (complete blood count) count
2. Electrolytes
3. Clotting time studies
4. Immunologic workup for patient has rapidly
progressive hearing loss or other signs or
symptoms of autoimmune hearing loss like a
Western blot analysis for antibodies to the
heat shock protein. Thyroid and renal function
for Pendred and Alport syndrome
5. Genetic testing such as the test for connexin
26 mutations
20.10 Imaging Studies
1. High-resolution CT scanning of the temporal
(imaging of choice)
This study helps determine the absence of
malformations that contraindicate implantation (e.g., cochlear aplasia, absence of the
auditory nerve). Additional relative contraindications, such as chronic otitis media, are
revealed with high-resolution CT (Figs.20.2,
20.3, 20.4, and 20.5).
CT scanning also reveals abnormalities
that alter the standard insertion procedure of
H. Abdulkarim et al.
Fig. 20.2 Axial cut of temporal bone CT scan showing
basal turn of the cochlea (white asterisk) and a bony ridge
obscuring the round window niche (red asterisk)
the electrode array. These abnormalities
include Mondini dysplasia, common cavity,
and cochlear ossication. Suspect cochlear
ossication in patients with a history of meningitis (Figs.20.2, 20.3, 20.4, and 20.5).
2. High-resolution T2-weighted fast spin echo MRI
is complementing and even replacing CT scanning because of its increased ability to reveal
cochlear ossication with identication of nerves
inside internal auditory canal (Fig.20.6a, b).
3. Plain lm radiography of the cochlea in the
anteroposterior plane (transorbital) is useful to
conrm correct placement of the electrode
array is used to provide evidence and conrmation of correct initial placement in the event
that delayed implant malfunction arises and
electrode migration is suspected (Fig.20.7).
4. Intraoperative uoroscopy to conrm electrode placement and also guides the right trajectory of placement in cases of malformed
cochlear anatomy.
20.11 Treatment
20.11.1 Medical Therapy
Steroid therapy preoperatively and can be
extended till activation of the implant postoperatively for prevention of delayed loss of
residual hearing and intracochlear brosis
postop.
AL GRAWANY
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