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12 Auricula Anomalies andAuricula Atresia
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ossicular chain abnormalities include a hypoplastic stapes superstructure, a merged
malleus–incus complex, a shortened malleus, and the absence of a manubrium.
Bony atretic plates can fuse with malleus necks [1].
The establishment of the otic placode, a local thickening of the ectoderm, initiates inner ear development as early as the third week of fetal life. The otic pit is
formed when the otic placode invaginates. The otic pit’s epithelium merges to create
the otic vesicle, making the inner ear’s membrane labyrinth. Divided into the vestibule, cochlea, and endolymphatic regions, the membrane labyrinth is formed by a
sequence of infoldings of the otic vesicle. Patients with CAA typically have a functional and stimulative cochlea since the inner ear nishes developing by the 20th
week of fetal life, before the ear canal forms [1].
Microtia and CAA often live together. However, CAA can manifest in a seemingly healthy auricle on a rare occasion. Located near the rostral end of the branchial apparatus, the axonal hillocks are a sequence of ectodermal elevations that
serve as the embryologic ancestors of the auricle. In and around the early ear canal,
the axonal hills blend. Each of the six hills forms a unique feature of the auricle. In
this formation, hillocks 1–6 are responsible for different anatomical characteristics:
the tragus, crus helicis, helix, antihelix, antitragus, and ear lobule. By the 20th week
of gestation, the auricle looks adult, regardless of size. After these mounds stop
growing, a condition known as microtia (“small ear”) develops. The middle ear
typically appears underdeveloped in cases of severe microtia [3].
12.3 Congenital Abnormalities oftheEar
Some ear abnormality affects about 5% of the population. Plastic surgeons often see
protruding ears and external ear microtia or a variant when treating congenital ear
defects. While many medical professionals see patients with the former, only a few
surgeons specialize in the latter. Due to their prevalence, prominent ears will be the
primary focus of this article. Many new otoplasty techniques have recently appeared
in surgical journals, attesting to the eld’s rapid evolution. Just as certain hospitals
focus on craniofacial osteotomy surgery, only a few centers employ highly regarded
surgeons to treat congenital ear microtia and atresia [4].
12.3.1 Pathophysiology
In descending order of importance, the following [4] characteristics are observed in
patients with prominent or projecting ears:
Antihelical fold is not present.
The scaphoconchal angle is acute.
The helical rim is now closer to the scalp.
Subtle conchal basin.
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To x the anomaly, consider all of these issues when planning and carrying out
the operation [4]. There is minimal difference between the ear structures of adults
and children. Ears develop and grow to their full size by the third year and then stop
growing after 10years. A person’s ears may get taller as they enter adulthood, but
after age 10, they don’t vary much concerning the scalp. This means that children as
young as ve or six years old can have setback otoplasty without risk [4].
A Prominent or Bulging Ear
• Antihelical fold is not present
• Augmented Scaloconchal angle
• Subtle conchal bowl
• Prolonged space between the helical rim and the scalp
• Leveling off of upper cervical
• A typical helical length [4]
Deformity of the Ear Canal (Lop-Ear, Constricted Ear)
• Hydroplaning the antihelix
• Concha enlargement
• The helix’s overhang
• Contraction of the triangular fossa and scapha
• Difference between crura and antihelix
• Reduced helix length
• No change in size; however, the ear seems tiny [4]
Cryptotia
• Because there is no retro auricular sulcus, the ear’s top part seems buried
• The antihelical crus is rmly curving
• The auricle is not foreshortened [4]
Stahl Ear
• The existence of the third crus
• Curved antihelix
• Saboid fossa deformity [4]
12.3.2 Management
Ears that stick out too much have traditionally been surgically removed. The good
news is that nonsurgical options are now for treating newborns in the hours following birth [5]. Surgical tape secures the back helix rim to the back of the ear. You can
use an ear wrap or a tubular elastic net bandage for support. For these methods to
12 Auricula Anomalies andAuricula Atresia
263
work, therapy must be ongoing and careful for at least a few weeks, if not months,
beginning in the rst few weeks of life [4].
The following four surgical procedures are used to x ears that stick out:
• Removal of skin
• Mattress sutures positioned radially
• Sutures that are conchomastoid
• Excision of conchal cartilage
Incisionless and sutureless methods have been discussed in detail by the authors.
One of these methods is the incisionless otoplasty technique, which involves splitting the ear cartilage without sutures [6, 7].
Cartilage Remodeling with Laser Assistance
While several methods exist for hiding or reshaping enlarged ears, more than one
approach has yet to achieve universal acceptance. While not every surgeon will use
every one of the following [4] methods, the vast majority will:
Removal of Skin
Most procedures involving a posterior auricular approach now incorporate excision,
likely the rst therapy for projecting ears. In the posterior auricular incision, a crescent-shaped area of three to ve millimeters of skin is often removed. A little further
up on the outside of the external auricle, nearly pole to pole, is where the incision
should be performed [4] rather than in the posterior sulcus.
Making a Score on the Skin
This method’s popularity has grown, thanks to Stenstrom and Davis. To create the
absent antihelical fold, the cartilage might be bent away from the incised or abraded
side utilizing anterior perichondral scoring. It is possible to score the front cartilage
using various methods and instruments. Most surgeons will use more than just this
method to get the job done. According to research out of Turkey, Erol, you must
consistently score the cartilage from the front and put horizontally buried mattress
sutures from the back [8].
The Luckett Method
This method of severing cartilage has lost popularity due to the severe antihelical
fold it produces, yet it is mentioned here for historical reasons. A crescent of medial
skin and cartilage is excised as a part of the Luckett operation to reconstruct the
antihelical fold. Plastic surgeons have adopted this method, and a more rened antihelical fold is now possible [4].
Radial Mattress Sutures
Surgeries typically include the use of sutures, which are commonly inserted posteriorly. They make the scaphoid–conchal angle fold look more precise and organic.
The operator has a lot of discretion to get the right amount of angulation and setback
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Z. Öztürk et al.
because all ve sutures are inserted before tying and tightening. The anterior perichondrium should be included in the sutures that continue through the entire thickness of the cartilage [4].
Conchomastoid Sutures
Furnas popularized this mattress suture to achieve a successful outcome for setback
otoplasty [9, 10]. These sutures would go from the conchal cartilage to the mastoid
fascia, from the scaphoid fossa to the temporal fascia, from the scapha to the concha, and from the earlobe to the sternocleidomastoid muscle insertion [4].
Excision of Conchal Cartilage
According to Chicago-based Bauer and colleagues, many ENT doctors overlook
conchal hypertrophy as a signicant contributor to the noticeable ear deformity
[11]. This author frequently includes the removal of conchal cartilage in their surgical procedures and patient care.
Incisionless and Sutureless Techniques
The authors have described the incisionless otoplasty technique and methods for
slicing the ear cartilage without sutures [7].
Using a Laser
Leclère etal. discovered a decent success rate for projecting ear cartilage reshaping
with laser assistance in their literature study. Results from three different wavelengths—1064nm (Nd:YAG), 10,600nm (CO2), and 1540nm (Er:Glass)—were
addressed in the seven clinical investigations that made up the article [12].
Alternative Methods
The recurrence rate was higher in patients treated with combined Congchet/Furnas
surgery, which involved scoring the anterior cartilage and the use of conchomastoid
mattress sutures, compared to patients treated with the Mustardé surgical approach,
which involves using mattress sutures to create a new antihelical fold [18]. Wound
infections and hematomas, however, occurred at similar rates in the two groups [13].
In describing an otoplasty procedure for prominent ears, Hendrickx etal. utilized
a posterior approach to remove wedges of partial-thickness cartilage in a “Wi-Fi
symbol” pattern using micro chondrectomies. Mustardé sutures were also used. Out
of 200 bilateral otoplasties, no serious problems were reported; however, three
patients (or 1.5%) did experience a full recurrence of the deformity [14].
Auricular Atresia That Is Present at Birth
The external ear canal does not expand or fully develop; this is the primary morphological abnormality in congenital amaurosis (CAA). The degree to which atresia is
present can vary. Where development is halted in the embryological pathway determines the ear’s anatomy. It is impossible to discern the ear canal in the most severe
congenital amaurosis (i.e., when ear development is abruptly stopped). The space
that the ear canal usually occupies is lled or blocked by bone, and there is no
12 Auricula Anomalies andAuricula Atresia
265
meatus or external aperture. The ear canal is still there in less severe instances but is
pretty small and stenotic. The presence of a primitive tympanic membrane and its
connection to the ossicular chain are both uncertain [1].
In highly unusual instances of ear canal stenosis (narrowing), the usually lining
skin of the ear canal can become stuck and unable to self-clean. Infection and skeletal remodeling of the surrounding bone might result from this trapped skin. The
surgical removal and cleaning of trapped skin, known as cholesteatoma, is necessary to create a secure ear that will not trap skin again. When a stenotic canal’s
pinpoint opening experiences drainage or dampness, cholesteatoma should be considered a possible diagnosis. Thorough computed tomography (CT) scans of the
temporal bone provide a more conclusive diagnosis. To verify the existence of skin
in the stenotic canal, a diffusion-weighted imaging (DWI) sequence can be used in
magnetic resonance imaging (MRI). Among the imaging ndings is bony remodeling in the surrounding bone and opacication (soft tissue lling) of the canal [1].
While the ear canal and middle ear develop later in fetal development, the inner
ear forms somewhat sooner. Furthermore, unlike the middle and outer ears, the
inner ear originates from a distinct anatomy. Most people with CAA have normal
functioning of the cochlea. All it comes down to is that the sound isn’t reaching the
inner ear. A conductive hearing loss is what this is known as. A bone-conducting
hearing aid, an osseointegrated bone-conducting device, or atresia repair or surgery
can all help increase sound transmission to the healthy inner ear by opening the ear
canal and restoring the natural mechanism that transmits sound there [1].
12.3.3 Etiology
Accidents involving motor vehicles, gunshot wounds, or otologic surgeries are the
most common causes of acquired aural atresia, a rare condition in and of itself.
There have been very few reports of canal stenosis and atresia occurring alongside
neoplastic alterations or idiopathic inammatory processes [15, 16].
Several factors may come together to induce congenital aural atresia. Several
known disorders can cause ear abnormalities, although most instances are unidentied. Ultimately, it is the product of abnormalities in embryological development
that start as early as the sixth week of gestation [17]. These abnormalities impact the
formation of the external auditory canal, which is responsible for creating the rst
pharyngeal cleft. Although this disturbance often happens randomly, it is associated
with several syndromes, such as Goldenhar, Treacher Collins, and Crouzon. A vascular insult to the stapedial artery, which forms the rst and second pharyngeal
arches during development, is the most commonly held but unproven idea regarding
the origin of Goldenhar syndrome. The aficted ear is most often located on the
right side of the face, and symptoms can extend beyond the skull to the mandible,
vertebrae, or even beyond the face itself [18].
Multiple genetic abnormalities could be at play if it shows signs of an autosomaldominant or recessive inheritance pattern. Mutations in the TCOF1 gene are the
most common cause of Treacher–Collins syndrome, characterized by auditory
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atresia. The rst and second pharyngeal arches are involved in early craniofacial
development, inuenced by the TCOF1 gene. A mutation on chromosome 10 affecting FGFR2 or FGFR3 causes Crouzon syndrome. It follows an autosomal-dominant
inheritance pattern and typically results in craniosynostosis and, on rare occasions,
aural atresia [19]. Other syndromes that can cause this include Mobius, Klippel–
Feil, Fanconi, DiGeorge, and Pierre Robin syndromes. The only known genetic
cause of congenital aural atresia is the distal 18q22.3 deletion. In this case, the
patient will have normal auricles but bilateral complete atresia and other craniofacial abnormalities [20].
We have also discovered several external risk factors. Some examples of this
include diabetes, vascular insults frequently caused by maternal cocaine addiction,
isotretinoin and thalidomide use by mothers, and other similar conditions [16, 21].
12.3.4 Epidemiology
One in 10,000–20,000 babies are born with congenital aural atresia. Most cases are
unilateral, and there seems to be an unexplained preference for the right ear in some
studies. It affects 2.5 times more males than females. Microtia, to varying degrees,
is often present, which may be related to the amount of middle ear deformity. When
one ear is unaffected, children with unilateral aural atresia usually have normal
speech development and hearing in the unaffected ear. Due to functional monoaural hearing, they are more likely to experience delayed language development;
thus, it is crucial to identify this condition early on. The child’s preferred seating
arrangement in class allows the unaffected ear to face the teacher, and speaking into
the unaffected ear contributes to the child’s normal language development.
12.3.5 Assessing
Conducting thorough hearing tests on all infants diagnosed with an ear abnormality
during the rst few months of life is crucial. Because conductive and sensorineural
hearing loss can manifest in either ear in individuals with unilateral or bilateral aural
atresia, the initial step in evaluating these patients is typically to conduct an auditory
brainstem response (ABR) or balance-of-function (BAER) test. Even though conductive hearing loss is the most common type, additional testing may be necessary
for 15% of individuals with sensorineural hearing loss [21].
Further testing can be postponed until six months of age if the hearing test in the
unaffected ear is standard, which indicates that speech and language development
will occur properly. However, to keep the unaffected ear’s hearing normal, it is necessary to treat middle ear effusion quickly and conduct comprehensive routine
examinations [22].
In the event of an abnormal hearing test, ABR testing is necessary to guarantee
that language development can proceed generally because at least one ear must
function normally. Patients suspected of having syndromic symptoms may benet
12 Auricula Anomalies andAuricula Atresia
267
from genetic testing. Initial workups should wait until the child is ve years old or
until the Jahrsdoerfer grading scale recommends surgery before recommending a
computed tomography (CT) scan of the temporal bone. An open oval window, facial
nerve, mastoid pneumatization, incus–stapes link, external ear, middle ear space,
malleus–incus complex, and the existence of a stapes bone each receive one point
on the Jahrsdoerfer grading scale. Ten points are in play here [23].
12.3.6 Treatment
When it comes to acquired auditory atresia, surgical correction is considered the
gold standard treatment. On the other hand, early stage management is contentious.
While some otologists advocate for anti-inammatory and antibacterial treatment,
others maintain that medial canal brosis worsens with postponed surgical intervention. In any case, meticulous clinical monitoring is required [24].
Considerations such as the laterality of the defect, the patient’s hearing ability,
their aesthetic goals, and the practicality of hearing restoration dictate the course of
treatment for congenital types. When audiological testing for bilateral auditory atresia fails, the patient must wear bone-conduction hearing aids as soon as possible.
Decisions to implant hearing aids are contentious because new research suggests
that unilateral aural atresia may impact academic achievement. While this becomes
more convoluted when considering cost, the answer becomes clear in areas where
these aids are readily available: they improve the patient’s hearing and should be
acquired without delay. The situation regarding hearing aids is highly situational; in
places where they must be privately purchased, the child’s benets must outweigh
the family’s costs [25]. In such cases, teachers and speech therapists may need to
closely monitor these patients to ensure they usually develop in terms of speech and
language. To maintain normal hearing, getting a hearing test every 6–12months is
advised as part of a regular medical evaluation. A middle ear infection or effusion
requires immediate and severe medical attention [16].
Coordination of the time of canal atresia repair and pinna restoration is essential
in microtia-atresia situations. No hard and fast rules apply, and improving one’s
hearing takes precedence over supercial concerns. Since the contralateral ear has
yet to reach>85% of its adult size, rib cartilage is usually only utilized for grafting
or microtia repair once the child is 5 or 6years old. As a result, many surgeons will
recommend canal atresia repair before pinna reconstruction or creation. In contrast,
others will suggest a bone-conduction hearing aid until the child is old enough to
have a multi-staged atresia and pinna repair procedure. This is why it is common
practice to wait until this age to apply alloplastic repair materials like Medpor to
achieve the best possible auricular symmetry. To lessen emotional and mental strain,
this should coincide with the start of the school year and the beginning of puberty.
Patients who wear hearing aids that conduct bone conduction before surgical surgery have better outcomes. There are several reasons why children around the ages
of 5 or 6 are the best candidates for surgical surgery to repair bilateral aural atresia.
Preventing middle ear problems requires, among other things, enough time for the
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Z. Öztürk et al.
eustachian tube to mature and the temporal bone to pneumatize. The development
of an external canal cholesteatoma, a recognized complication that can cause irreversible damage to the middle ear, is an exception to this age. Improving patient
knowledge and compliance with postoperative treatment is another rationale
[26–28].
Many things must be considered while dealing with unilateral situations, such as
the child’s degree of maturity, hearing capacity in the opposite ear, and academic,
linguistic, and speech development. When the patient’s contralateral ear usually
functions, some wait until adolescence before deciding between atresiaplasty and
bone-anchored hearing aids (BAHA). Various forms of atresiaplasty are performed
surgically. A mentoplasty is commonly used to x lateral atresia, while a canaloplasty is used to x more medial atresia. The Jahrsdoerfer grading system, which
gives points for different anatomical traits, is used to decide whether or not to have
surgical repair atresiaplasty [29].
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Otoplasty
13
RemziDogan, TamerErdem, andOrhanOzturan
13.1 Introduction
Prominent ear, also known as protruding ear, is an auricular deformity that exhibits
an autosomal-dominant inheritance pattern and occurs in 5% of the Caucasian population [1–3]. It occurs equally in males and females. The primary pathologies causing prominent ears are absence of the antihelical fold and/or conchal hypertrophy
[4]. Over 200 techniques have been described for the surgical correction of prominent ears [5]. This indicates that there is no single “best” technique and that new
techniques and modications will continue to be developed [6].
Techniques for correction of prominent ears fall into four main groups: cartilagecutting techniques (CCTs), cartilage-sparing techniques (CSTs), combined techniques, and incisionless techniques.
Although prominent ears do not affect hearing function, they can cause psychological distress, emotional trauma, and behavioral problems, especially in children
[7]. The generally accepted timing for surgery is that children with prominent ears
should be operated on between the ages of 3 and 6 before they enter school [8]. The
goal is to correct the deformity before socialization and prevent the child from being
ridiculed by peers. In addition, due to the greater exibility of the cartilage at a
younger age, surgery for prominent ears is easier to perform in childhood and there
is less need for CCTs at these ages [9].
Rigid and thick cartilage is preferred for CCTs. CCTs break the elastic resistance
in the cartilage structure to create the antihelical fold. Incisions, excisions, scoring,
and abrasion are performed on the anterior and/or posterior portions of the
R. Dogan (*) · O. Ozturan
Faculty of Medicine, Department of Otorhinolaryngology, Bezmialem Vakif University,
Istanbul, Turkey
T. Erdem
Privat Clinic, Istanbul, Turkey
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2024
M. T. Kalcioglu et al. (eds.), Otology Updates, Comprehensive ENT,
https://doi.org/10.1007/978-3-031-76173-7_13
271