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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4507_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface
- •Contents
- •1.3.4 The Eustachian Tube
- •1.3.5 Muscles
- •1.3.6 Innervation
- •1.3.7 Vascular Supply
- •1.4 The Inner Ear (Labyrinthine Cavity)
- •1.4.1 The Vestibule
- •1.4.2 Semicircular Canals
- •1.4.4 The Cochlea
- •1.4.5 Innervation
- •1.1 Introduction
- •1.2 The External Ear
- •1.2.1 The Auricle
- •1.2.3 The Eternal Auditory Canal/External Acoustic Meatus
- •1.3 The Middle Ear (Tympanic Cavity)
- •1.3.1 The Tympanic Membrane
- •1.3.3 Ossicles
- •1.4.6 Cochlea Nerve Anatomy
- •1.4.7 Vestibular Nerves
- •1.4.8 The Vestibulocochlear Nerve
- •1.5 The Central Hearing System
- •1.5.3 Auditory Input
- •1.5.4 The Auditory Nerve’s Descending Routes
- •References
- •2: Outer–Middle–Inner Ear Embryology
- •2.1 Introduction
- •2.2 Embryology
- •2.3.1 First Week
- •2.3.3 Third Week
- •2.3.4 Fourth Week
- •2.3.5 Sixth Week
- •References
- •3.1 Introduction
- •3.3 The Outer Ear
- •3.3.1 Anatomy
- •3.3.3 Localization
- •3.4 The Middle Ear
- •3.4.3 Middle Ear Muscles
- •3.4.4 The Eustachian Tube
- •3.4.5 Impedance Matching
- •3.5 The Inner Ear
- •3.5.1.1 Lateral Wall
- •3.5.1.2 Reissner’s Membrane
- •3.5.1.3 The Basilar Membrane
- •3.5.2.1 Hair Cells
- •Inner Hair Cells
- •Outer Hair Cells
- •3.5.3 The Tectorial Membrane
- •3.5.4 The Osseous Spiral Lamina
- •3.5.5 Cochlear Mechanics
- •3.5.5.1 Passive Mechanics
- •3.5.5.2 Active Mechanics
- •3.6.1 Auditory Nerve Fibers
- •3.6.2 The Subcortical Auditory Nuclei
- •3.6.2.1 The Cochlear Nucleus
- •3.6.2.2 The Superior Olivary Complex
- •3.6.2.3 The Lateral Lemniscus
- •3.6.2.4 Inferior Colliculus
- •3.6.2.5 The Medial Geniculate Body
- •3.6.3 The Auditory Cortex
- •3.7 Conclusion
- •References
- •4.1 Introduction
- •4.2 Eustachian Tube Anatomy
- •4.4 Eustachian Tube Dysfunction
- •References
- •5: Temporal Bone Radiology
- •5.1.1 Introduction
- •5.1.2 Computed Tomography (CT)
- •5.1.3 Temporal Bone CT Angiography
- •5.1.4 Magnetic Resonance Imaging (MRI)
- •5.1.5 Diffusion-Weighted Imaging (DWI)
- •5.1.6 Conclusion
- •5.2.1 Introduction
- •5.2.2.1 The External Auditory Canal (EAC)
- •5.2.3 Temporal Bone Fractures
- •5.2.4 Conclusion
- •5.3.1 Introduction
- •5.3.2 Necrotizing Otitis Externa
- •5.3.3 Middle Ear
- •5.3.3.2 Chronic Otitis Media
- •5.3.3.3 Cholesteatomas
- •5.3.3.4 Cholesterol Granulomas
- •5.3.4 Inner Ear
- •5.3.4.1 Labyrinthitis
- •5.3.4.2 Petrous Apicitis
- •5.3.5 Conclusion
- •5.4.1 Introduction
- •5.4.2.1 Cerebellopontine Angle Tumors
- •Vestibular Schwannomas
- •Arachnoid Cysts
- •Meningiomas
- •5.5.2 External Auditory Canal Aplasia
- •5.5.4 Inner Ear Malformations
- •5.5.4.1 Complete Labyrinthine Aplasia/Michel Anomaly
- •5.5.4.2 Rudimentary Otocysts
- •5.5.4.3 Common Cavity Malformation
- •5.5.4.4 Incomplete Partition (IP) Type I
- •5.5.4.5 Incomplete Partition Type II/Mondini Malformation
- •5.5.4.6 Incomplete Partition Type III
- •5.5.4.7 Cochlear Anomalies
- •5.5.4.8 Semicircular Canal Anomalies
- •5.5.6 Conclusion
- •5.6.1 Introduction
- •5.6.2 Otospongiosis/Otosclerosis
- •Epidermoids
- •5.4.2.2 The Middle Ear
- •5.4.2.4 Petrous Bone
- •5.4.2.5 Metastatic Tumors
- •5.4.3 Conclusion
- •5.5.1 Introduction
- •5.6.3 Third Window Lesions
- •5.6.4 Conclusion
- •References
- •6.1 Introduction
- •6.3.1 What Is Sound?
- •6.3.2 Sound Intensity
- •6.4 Psychoacoustics
- •6.4.1 Signal Detection Theory
- •References
- •7.1 Introduction
- •7.1.1 What Is Sound?
- •7.2 Fundamental Acoustic Concepts
- •7.2.3 Period
- •7.2.4 Frequency
- •7.2.5 Wavelength
- •7.3 Psychoacoustics
- •7.3.1 Loudness
- •7.3.2 Auditory Masking
- •7.3.2.1 Simultaneous Masking
- •7.3.2.2 Temporal Masking
- •7.4.2 Spatial Hearing
- •References
- •8.1 Introduction
- •8.2 Case History
- •8.3 The Audiology Test Room
- •8.4.1 Pure-Tone Audiometry
- •8.4.1.1 Masking
- •8.4.2 Speech Audiometry
- •8.4.3 Pediatric Assessment
- •8.5.1 Acoustic Immittance Audiometry
- •8.5.1.1 Tympanometry
- •Tympanogram Interpretation
- •8.5.1.2 Multifrequency Tympanometry
- •8.5.1.3 Wideband Tympanometry
- •8.5.1.4 Acoustic Reflex Test
- •8.5.1.5 The Reflex Decay Test
- •8.5.1.6 Eustachian Tube Evaluation
- •8.5.2 Otoacoustic Emissions
- •8.5.2.2 Performing Otoacoustic Emission Tests
- •8.5.3 Auditory Evoked Potentials
- •8.5.3.2 Auditory Evoked Brainstem Response
- •Stimulus Types
- •Stimulus Polarity
- •Stimulus Presentation Rate
- •Stimulus Intensity
- •Analysis Time (Recording Epoch)
- •Filters
- •Artifact Rejection Level
- •Electrodes
- •8.5.3.3 Auditory Steady-State Responses
- •8.5.3.4 Electrocochleography
- •Electrocochleography Analysis
- •8.5.3.5 Cortical Auditory Evoked Potentials
- •8.5.3.6 Event-Related Auditory Potentials
- •P300
- •Mismatch Negativity
- •Acoustic Change Complex
- •8.6 Conclusion
- •References
- •9.1 Introduction
- •9.2.3 Conductive Hearing Loss
- •9.2.4 Sensorineural Hearing Loss
- •9.2.4.1 Internal Acoustic Canal Tumors
- •9.2.4.2 Auditory Neuropathy Spectrum Disorder
- •9.2.4.3 Third Window Syndrome
- •9.2.4.4 Dead Region
- •9.2.5 Mixed Hearing Loss
- •9.3 Hearing Loss Configuration
- •9.3.3 Unilateral or Bilateral Hearing Loss
- •9.3.4 Symmetric or Asymmetric Hearing Loss
- •9.3.5 Fluctuating or Stable Hearing Loss
- •9.4 Diagnostic Tests
- •9.4.1 Pure Tone Threshold Testing
- •9.4.2 Speech Recognition Tests
- •9.4.3 Tympanometric Tests
- •9.4.4 Stapedial Reflex
- •9.4.5 Otoacoustic Emission Test
- •9.4.6 Auditory Brainstem Responses
- •9.6 Reporting Audiological Findings
- •9.7 Conclusion
- •References
- •10.1 Introduction
- •10.2.1 Anamnesis
- •10.2.2 Hearing Loss
- •10.2.3 Ear Pain (Otalgia)
- •10.2.4 Ear Discharge (Otorrhea)
- •10.2.5 Itchy Ear
- •10.2.8 Physical Examination
- •10.2.8.1 Inspection
- •10.2.8.2 Palpation
- •10.2.8.3 Otoscopy
- •10.2.12 Hearing Examination
- •10.2.13 Hearing Assessment
- •10.2.13.1 Whisper Test
- •10.2.13.2 Tuning Fork Tests
- •Rinne Test
- •Weber Test
- •Schwabach Test
- •Gelle Test
- •10.3 Conclusion
- •References
- •11.1 Introduction
- •11.2.1 Microphone
- •11.2.2 Amplifier
- •11.2.3 Receiver
- •11.2.4 Batteries
- •11.2.5 Earmolds/Domes
- •11.4 Hearing Aid Types
- •11.5.1 Directional Microphone Technologies
- •11.5.2 Digital Noise Reduction
- •11.5.3 Frequency Lowering
- •11.5.4 Feedback Canceller
- •11.5.5 Bluetooth
- •11.6 Other Hearing Aid Technologies
- •11.7 Pediatric Hearing Aid Application
- •11.7.3.7 Hearing Aid Fitting
- •Prescription Formula Preference
- •Objective Verification Tools
- •Subjective Verification Tools
- •Fine-Tuning
- •11.8 Adult Hearing Aid Application
- •11.8.1.1 Medical Evaluation
- •11.8.1.2 Audiological Evaluation
- •11.8.1.3 Physical Evaluation
- •11.8.1.4 Psychological Evaluation
- •11.8.2 Hearing Aid Application Process
- •11.8.2.1 Anamnesis
- •11.8.2.6 Hearing Aid Fitting
- •Fine-Tuning
- •11.9 Conclusion
- •11.10 Case Studies
- •11.10.1 Case 1
- •11.10.2 Case 2
- •11.10.3 Case 3
- •11.10.4 Case 4
- •References
- •12.1 Introduction
- •12.3.1 Pathophysiology
- •12.3.2 Management
- •12.3.3 Etiology
- •12.3.4 Epidemiology
- •12.3.5 Assessing
- •12.3.6 Treatment
- •References
- •13: Otoplasty
- •13.1 Introduction
- •13.2 General Information
- •13.2.1 Auricular Anthropometry
- •13.3 History
- •13.8.1 Conservative Treatment
- •13.8.2 Surgical Treatment
- •13.11 Patient Follow-Up
- •13.12 Case Examples
- •13.13 Complications
- •13.13.1 Early Complications
- •13.13.2 Late Complications
- •13.13.3.1 Telephone Ear Deformity
- •13.13.3.2 Reverse Telephone Ear Deformity
- •13.13.3.5 Antihelical Malposition
- •13.13.3.6 Tragal Prominence
- •13.13.3.7 Auricular Lines
- •13.14 Revision Otoplasty
- •References
- •14: External Ear Tract Diseases
- •14.1 Introduction
- •14.2.1 Atopic Dermatitis
- •14.2.2 Allergic Contact Dermatitis
- •14.2.3 Photoallergic Dermatitis
- •14.2.4 Psoriasis
- •14.2.5 Relapsing Polychondritis
- •14.2.6 Gout
- •14.3 Traumatic Disorders
- •14.3.1 Irritant Contact Dermatitis
- •14.3.2 Phototoxic Dermatitis
- •14.3.3 Phototrauma
- •14.4 Infectious Diseases
- •14.4.1 Otitis Externa
- •14.4.1.1 Background
- •14.4.1.2 Anatomy
- •14.4.1.3 Classification
- •14.4.1.5 Diagnosis
- •14.4.1.6 Management
- •References
- •15: Auricula Tumors
- •15.1 Introduction
- •15.2 Benign Tumors
- •15.2.1 Chondrodermatitis Nodularis Chronica Helicis
- •15.2.2 Cystic Chondromalacia
- •15.2.3 Ceruminous Gland Adenoma
- •15.3 Malign Tumors
- •15.3.1 Basal Cell Carcinoma (BCC)
- •15.3.2 Squamous Cell Carcinoma
- •15.3.3 Ceruminous Gland Adenocarcinoma
- •15.4 Conclusion
- •References
- •16: Acute Suppurative Otitis Media
- •16.1 Introduction
- •16.2 Pathophysiology
- •16.3 Etiology
- •16.3.1 Host Factors
- •16.3.1.1 Immune System
- •16.3.1.2 Hereditary Susceptibility
- •16.3.1.3 Mucins
- •16.3.1.4 Anatomic Abnormalities
- •16.3.1.5 Physiologic Dysfunction
- •16.3.2 Infectious Factors
- •16.3.2.1 Bacterial Pathogens
- •16.3.2.2 Viral Pathogens
- •16.3.3 Environmental Factors
- •16.3.3.1 Infant Feeding Methods
- •16.4 Classification
- •16.6 Diagnosis
- •16.7 Treatment
- •16.7.1 Antibiotic Therapy Versus Observation
- •16.7.2 Initial Antibiotic Therapy
- •16.7.3 Supplemental Programs
- •References
- •17.1 Introduction
- •17.2 Definition
- •17.4 Pathophysiology
- •17.5 Diagnosis
- •17.5.1 Clinical Evaluation
- •17.6 Treatment
- •17.6.1 Medical Treatment
- •17.6.2 Surgical Treatment
- •17.7 Conclusion
- •References
- •18: Chronic Suppurative Otitis Media
- •18.1 Introduction
- •18.2 Epidemiology
- •18.3 Pathophysiology
- •18.4 Microbiology
- •18.5 Histopathology
- •18.6 Clinical Manifestations
- •18.6.1 Tubotympanic Type
- •18.6.2 Atticoantral Type
- •18.7 Diagnosis
- •18.7.1 Anamnesis
- •18.7.2 Otoscopic Examination
- •18.7.3 Audiological Evaluation
- •18.7.4 Imaging
- •18.8 Treatment
- •18.8.1 Medical Treatment
- •18.8.2 Surgical Treatment
- •18.9 Complications
- •18.10 Future Directions
- •18.11 Conclusion
- •References
- •19: Cholesteatoma
- •19.1 Introduction
- •19.2 Definition
- •19.3 Epidemiology
- •19.4 Histopathology
- •19.7 Cholesteatoma Types
- •19.7.1 Congenital Cholesteatoma
- •19.7.2 Acquired Cholesteatoma
- •19.7.2.2 Epithelial Migration Theory
- •19.7.2.3 Basal Cell Hyperplasia Theory
- •Tos Staging
- •Sade Staging
- •19.7.3 Unclassified Cholesteatomas
- •19.7.4 Petrous Bone Cholesteatomas
- •19.8 Practical Classification
- •19.8.1 Attic Cholesteatomas
- •19.8.2 Sinus Cholesteatomas
- •19.8.3 Pars Tensa Cholesteatomas
- •19.9 Clinical Presentations
- •19.9.1 Cholesteatoma Microbiology
- •19.10 Diagnosis
- •19.10.2 Computed Tomography
- •19.10.3 Magnetic Resonance Imaging
- •19.10.4 Audiometric Evaluation
- •19.11.1 Closed Techniques
- •19.11.2 Open Techniques
- •19.12 Conclusion
- •References
- •20.1 Introduction
- •20.2 Physiology
- •20.2.4 Tympanic Isthmus
- •20.4 Pathophysiology
- •20.5 Clinical Picture
- •20.6 Management
- •20.6.1 Surgical Management
- •20.6.1.2 Tympanoplasty
- •20.6.1.3 Mastoid Surgery
- •20.7 Adhesive Otitis Media
- •20.7.1 Pathogenesis
- •20.7.2 Clinical Findings
- •20.7.3 Imaging
- •20.7.4 Treatment
- •20.8 Conclusion
- •References
- •21.1 Introduction
- •21.2 Intratemporal Complications
- •21.2.1 Acute Mastoiditis
- •21.2.2 Facial Nerve Paralysis
- •21.2.3 Labyrinthitis
- •21.2.4 Labyrinthine Fistula
- •21.2.5 Petrositis
- •21.3 Intracranial Complications
- •21.3.1 Meningitis
- •21.3.2 Lateral Sinus Thrombosis
- •21.3.3 Brain Abscess
- •21.3.4 Otitic Hydrocephalus
- •21.3.5 Epidural Abscess
- •21.3.6 Subdural Empyema
- •21.4 Conclusion
- •References
- •22: Basic Otological Surgical Techniques
- •22.1 Introduction
- •22.3 Atticotomy
- •22.4 Mastoidectomy
- •22.4.1 Simple (Cortical) Mastoidectomy
- •22.4.2 Canal Wall-Up Mastoidectomy
- •22.4.3 Canal Wall-Down Mastoidectomy
- •22.4.4 Retrograde Mastoidectomy
- •22.4.5 Modified Radical Mastoidectomy
- •22.4.6 Radical Mastoidectomy
- •22.4.7 Mastoid Obliteration
- •22.5 Petrosectomy
- •22.6 Conclusion
- •References
- •23: Tympanoplasty
- •23.1 Introduction
- •23.2.1 Chronic Otitis Media
- •23.2.2 Traumatic Perforations
- •23.5 Tympanoplasty Types
- •23.7 Graft Materials
- •23.8 Graft Techniques
- •23.8.1 The Perichondrium/Cartilage Island Graft
- •23.8.2 The Palisade Graft
- •23.8.3 The Temporalis Fascia Graft
- •23.9 Surgical Approaches
- •23.9.1 Microscopic Approach
- •23.9.2 Endoscopic Approach
- •23.10.1 Transmeatal Incisions
- •23.10.1.1 The Rosen Incision
- •23.10.1.3 Anterior Tympanomeatal Flap
- •23.10.2 Endaural Incision
- •23.10.3 Postauricular Incision
- •23.11 Pediatric Tympanoplasty
- •23.12 Prognostic Factors
- •23.14 Conclusion
- •References
- •24: Ossiculoplasty
- •24.1 Introduction
- •24.4 Indications/Contraindications
- •24.5 Reconstruction Materials
- •24.7 Surgical Preparation
- •24.8 Surgical Technique
- •24.9 Ossiculoplasty Results
- •24.10 Complications
- •24.11 Postoperative Care
- •24.12 Follow-Up
- •24.13 Conclusion
- •References
- •25: Tympanomastoidectomy
- •25.1 Introduction
- •25.2 Surgical Anatomy
- •25.4 Indications
- •25.5 Technique
- •25.5.1 Patient’s Preparation
- •25.5.3 Simple Mastoidectomy
- •25.5.4 Posterior Tympanostomy or Facial Recess Approach
- •25.5.5 Epitympanectomy
- •25.5.6 Endolymphatic Sac Procedures
- •25.5.8 Atticotomy-Atticoantrotomy

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13.12 Case Examples
Three long-term results are shown in the Fig.13.4. All cases underwent an operation
including the Mustarde sutures, medial conchal excision, and conchomastoid
sutures.
Fig. 13.4 Long term
results of otoplasty

13 O t opla s t y
293
13.13 Complications
There are relatively few published reports of otoplasty complications and long-term
outcomes in the literature. Complications can be divided into early and late complications. The early postoperative period covers the rst 14days, while the late period
covers the period after 14days [120]. Early complications include hematoma, infection, chondritis, pain, bleeding, itching, and necrosis. Late complications include
poor scarring, patient dissatisfaction, suture problems, and decreased sensation.
Otoplasty complications are well described in the literature [57, 121–123].
Overall complication rates are low, and when they do occur, they tend to be minor.
Major destructive complications such as chondritis, necrosis, and large hematomas
are now rare. The most common complication is patient dissatisfaction, which is to
be expected in a facial aesthetic procedure. Depending on the technique used, recurrence can be a common complication and can be reduced with careful surgical technique [56].
13.13.1 Early Complications
(a) Hematoma
In the early postoperative period, the most feared complications are hematoma
and infection [59]. Inadequate hemostasis during surgery or other surgical technique errors can lead to hematoma formation. Less commonly, other causes such as
rebound vasodilation due to local anesthesia, hypertension, postoperative trauma,
and coagulation problems can also lead to hematoma [2, 124].
Disproportionate unilateral pain shortly after surgery is a harbinger of hematoma
[1, 5, 59]. If a hematoma has formed, the clotted blood should be drained, and the
area is closed. If bleeding vessels are visible, they should be cauterized. This is an
undesirable situation. The ear is closed with a loose passive drain. Broad-spectrum
antibiotic therapy is then initiated. If left untreated, wound infection, perichondritis,
or postoperative deformity may develop [56]. If left untreated, a hematoma may
compress the auricular cartilage, disrupting local blood ow and leading to necrosis
of the undernourished cartilage [59].
According to Colpaert and Missotten [125] and Robiony etal. [126], the rates of
early complications are low. Hematoma is seen at a maximum rate of 2.2% in the
studies conducted. This rate is consistent with rates in previous studies (1.4–1.7%)
[127, 128]. Lee and Bluestone [129] and Di Mascio [130] also have similar incidences of hematoma. In the event of a hematoma, it should be evacuated as soon as
possible to avoid circulatory compromise of adjacent tissues and skin.
(b) Infection
Infection is rare in the auricle due to its abundant blood supply (supercial temporal artery, postauricular artery) [5, 131]. Inadequate sterile technique during

294
R. Dogan et al.
surgery may result in hematoma or dehiscence, which may contribute to the development of wound infection [1, 2]. Wound infection manifests as deep, throbbing
pain, pus formation, or erythema 12 hours postoperatively [5, 59, 61]. If left
untreated, the patient’s symptoms can progress to perichondritis or chondritis,
resulting in cartilage necrosis and deformity [5, 59].
Four trials used antibiotic prophylaxis to prevent infection [114, 130–133], and
no infections were reported in any of them. However, the use of prophylactic antibiotics has not been shown to make a signicant difference [114, 130, 132, 133].
The reported incidence of infection in the literature ranges from 0% to 3.5% [67,
117, 127, 128]. A study by Tan etal. found a high infection rate of 15.5% in cases
using the Mustarde method [134]. The authors attributed this to the presence of
white silk sutures. Post-otoplasty infection is a signicant complication and requires
antibiotic therapy and removal of the source of infection if it occurs.
(c) Bleeding
Surgical complications that can occur with any surgery can also occur with otoplasty. Bleeding during surgery is due to inadequate hemostasis. It is an early postoperative complication. Bleeding can be a sign of hematoma as it may require
bandage changes. In addition, hemorrhage and hematoma formation have similar
etiologies. In case of bleeding, further investigation and hemostasis should be
ensured [61, 135]. Bleeding is mentioned in many publications, but rates vary from
0% to 6% in six publications [29, 114, 115, 117, 132, 133].
(d) Skin Necrosis and Wound Dehiscence
The high blood supply to the auricle protects the auricular skin from infection.
Skin necrosis is usually not due to inadequate circulation but to obstruction of the
venous circulation of the subdermal plexus caused by tight bandaging [125, 131].
Necrosis can also occur secondary to excessive hematoma or infection. In addition,
necrosis can occur with excessive cauterization [61]. Postoperative skin necrosis
was present in the studies of Colpart and Missotten [126] and Robiony etal. [126].
In both cases, it was thought to be associated with high rates of early complications.
Older publications provide little information on skin necrosis. It is only reported at
a rate of 5.4% in the study by Nielsen etal. [128]. There are three studies in the
literature on wound dehiscence. In the rst two studies, the incidence rates were
0.2% [117] and 0.6% [114], while in the third study, the rate was 10% [115].
13.13.2 Late Complications
In general, late complications are more common and there is a wide variation in the
incidence of these complications, ranging from an average of 0% to 47.3%. The
highest rate is reported by Colpaert and Missotten [118]. Late sequelae: They usually appear around the sixth month postoperatively and can be single or multiple

13 O t opla s t y
295
[136]. Most often the cause of residual deformity is related to poor surgical planning
and technical problems [73].
(a) Patient Dissatisfaction
This complication is the most common after otoplasty, as with all facial aesthetic
procedures. Postoperative patient dissatisfaction is related to patient selection and
preoperative patient expectations. The situation should be thoroughly discussed
with the patient before surgery, and it should be emphasized that the condition will
be improved, but the result may not be perfect. A difference of up to 3 millimeters
between the ears in the distance between the auricle and the scalp after otoplasty is
acceptable. Patients want reassurance about the outcome of their otoplasty. However,
the surgeon should not give a 100% guarantee for this operation. It is also necessary
to inform the patient that revision may be required [57]. Unsatisfactory aesthetic
results include various sequelae; overcorrection, undercorrection, retroposition,
telephone ear, reverse telephone ear, and cartilage irregularities are some of
them [57].
The incidence of unsatisfactory aesthetic results varies from 0% to 11.1%. The
highest incidence rates are found in the studies by Nordell [121] and Sylaidis and
Gault [124]. The high rate in the Nordzell study may be due to working with a limited number of patients, such as 16 patients. Residual deformities in otoplasty are
noted by the surgeon, not the patient or the patient’s family. If patient follow-up is
done by chart review, the results may be missed because deformities in these patients
can only be noticed by trained individuals. In addition, patients may not return for
follow-up because they are satised. Therefore, patients who typically go unnoticed
and do not return for follow-up are not included in complication rates. Older studies
have mixed data on dissatisfaction rates. The incidence of these rates varies from
5.9% to 16.7% [124, 127, 134].
(b) Loss of Correction
Recurrence of the original correction of the ear can be due to various reasons,
such as postoperative trauma, insufcient cartilage weakening, especially when
dealing with stiff or thick cartilage, inadequate, or weak sutures. This loss of postoperative correction and retroposition is mainly due to the reliance on skin excision
alone for correction in the techniques used [25]. Loss of correction is one of the
most common postoperative complications, with rates ranging from 6.5% to
12% [123].
Cartilage-sparing techniques (CST) require intraoperative overcorrection due to
the elastic nature of cartilage, which can relax up to 40% in the postoperative period
[12]. The main objection to suture techniques is that they can cause recurrence by
cutting or tearing the cartilage. To avoid this complication, a suture can be placed on
the cartilage and perichondrium. However, care must be taken when passing the
suture through the thin anterolateral ear skin and subcutaneous tissue. Therefore,
hydrodissection can be used to open the space between the skin and perichondrium,

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allowing the suture to pass between the skin and perichondrium [99]. Adamson
et al. found that overcorrection is better tolerated than undercorrection because
undercorrection is perceived by the patient as a surgical failure [57]. In cases of
persistent superior pole protrusion, a suture can be placed between the fossa triangularis and the temporal fascia. Similarly, for inferior pole protrusion, the suture is
placed between the cauda helix and the mastoid [88]. Loss of correction due to the
suture cutting through the cartilage and the use of suture-only techniques in thick
and strong cartilage often fail to control cartilage memory [137]. The Mustarde
technique is currently the most preferred and used technique, especially in soft and
at auricular cartilage [11].
Loss of correction is most common with CSrT.If it is due to a technical error, it
will occur in the rst few months after surgery. Technical errors include excessive
tension due to incorrect suture placement, too few sutures, pulling through one or
more sutures, or inadequate correction during surgery. Technical failure is not
always related to suture placement but can also be related to failure to achieve sufcient conchal setback or dealing with thick and non-bending cartilages. External
trauma is a notable factor in many cases associated with late loss of correction. The
complication of loss of correction is gradually decreasing due to proper suture
placement [54].
(c) Suture Complications
Suture extrusion is caused by sutures that are not placed in the correct location
during closure, sutures that place excessive tension on the cartilage, or infection [5,
59] (Fig.13.5).
Absorbable sutures are a common source of local skin infection and short-term
abscess formation. Permanent sutures, especially various braided sutures, are more
likely to cause slow-developing infections or foreign body granulomas. Removal of
the suture is curative in these cases. This procedure can be postponed for a few
months as it may cause loss of correction. Monolament sutures cause less reaction.
There is a tendency to use these sutures because they can affect the negative cosmetic result [138].
Suture-related complications are mostly due to technical errors. Mustarde’s
sutures are more extruded than conchomastoid sutures. This is because they are
more supercial in the subcutaneous plane, especially at the superior pole. If the
suture is placed too distally when creating the antihelical fold, it can cause aesthetic
and functional deformities in the form of a tethered appearance. This can be a problem for patients who wear glasses.
Excessive excision of postauricular skin increases suture extrusion. Tight skin
closure means weak suture placement. As a result, improper suture placement may
be responsible for anterior displacement of the conchal cartilage, leading to obstruction of the external auditory canal [61]. In all six studies in the literature, suture
extrusion was attributed to non-absorbable sutures, which were 3–0 and 5–0 diameter Gore-Tex, prolene, nylon, or polyester sutures [94, 109, 129, 133, 137, 139,
140]. There are high complication rates with suture techniques (12.5% suture

13 O t opla s t y
Fig. 13.5 A case of suture
extrusion
297
extrusion rate). Polyester (non-absorbable braided silk-like suture) was used in 10%
of these cases and Gore-Tex (single lament suture) in 2.5% [84]. The rate of suture
extrusion varies from 0% to 3.1% [94, 132, 137, 139, 140]. Very high incidences are
reported in studies by Bogetti [132] (11.9%), Yugueros and Friedland [133] (19.0%),
and Cho [140] (22.2%). Although Cho etal. used a small group of nine individuals,
which could explain the high incidence in their study, this is not the case in the other
two studies.
(d) Hypersensitivity
Hypersensitivity is the sensitivity in the postauricular skin that is generally
caused by axonal regeneration and is expected to decrease over time [68]. It is one
of the most common late complications.
(e) Hypoesthesia
Persistent paresthesia or sensory loss is rare after otoplasty. Although damage to
the greater auricular nerve may initially cause these symptoms, they usually resolve
spontaneously over months. Another symptom is cold insensitivity, and there is a
high risk of frostbite after otoplasty. This is due to possible impairment of blood
ow to the ear. Patients are informed of these conditions and encouraged to consider
these possibilities. They are advised to take appropriate measures regarding these
conditions [57].

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(f) Asymmetry
Asymmetry is another important complication to include in our evaluation. A
difference of 3mm or less in the auriculocephalic distance between the auricles
provides a symmetrical appearance [5]. Asymmetry is usually a preexisting condition and is not solely related to protrusion of the prominent ear [65, 84]. The incidence of asymmetry is 2.5–18.3% [109, 114, 117, 140].
Postoperative residual asymmetry is acceptable if there is preexisting asymmetry, and the current asymmetry is mild [2]. If it is at an unacceptable level and has
occurred postoperatively, it should be revised.
(g) Unacceptable Scar Tissue
Abnormal scarring includes hypertrophic scars or keloid formation. Both can be
largely prevented by avoiding excessive suture tension [5, 59]. Keloids are more
common in African American patients [59, 124].
Rates of hypertrophic scar and keloid formation range from 1.2% to 2.5% [133,
141]. The studies reporting the highest rates generally approach from the posterior.
The effect of the thickness of the postauricular skin and subcutaneous tissue on this
outcome is uncertain [139].
13.13.3 Specific Complications Related toTechnique
13.13.3.1 Telephone Ear Deformity
Insufcient correction of the superior helix and lobule or excessive correction of the
middle 1/3 of the ear can result in relative protrusion of the superior and inferior
portions of the ear, known as telephone ear deformity [5, 59, 68]. Insufcient or no
correction of the superior crus or cymba conchae can lead to this condition. A balanced correction should be performed to avoid this result [57].
13.13.3.2 Reverse Telephone Ear Deformity
Reverse telephone deformity is characterized by a relatively prominent concha or an
inadequately corrected overdeveloped concha, along with excessive correction of
the superior and inferior portions [57, 59].
13.13.3.3 Overcorrection andHidden Helix Deformity
Excessive conchal cartilage or skin excision can sometimes result in excessive attening of the concha. This gives the ear an unnatural appearance of being overly
compressed. This condition is more commonly seen as follows: the concha is attened downward, and the antihelix is overcorrected to compensate. In this case, the
antihelix is seen most laterally in the frontal view, so it is considered a hidden helix
deformity [57].

13 O t opla s t y
299
13.13.3.4 Antihelical Folding andCrinkling
If Mustardé sutures are placed too tightly, a very narrow segment of cartilage is
formed. This results in folding and crinkling of the antihelix. To create a smooth
structure, sutures should be placed wider than 6mm [57].
13.13.3.5 Antihelical Malposition
This is a deformity associated with the unnatural anterior position of the helix when
a new antihelix is created. The scaphoid fossa in these ears is quite wide [57].
13.13.3.6 Tragal Prominence
This occurs when there is insufcient excision of the postauricular skin during conchal setback. As a result, permanent postauricular soft tissue exerts anterior and
outward pressure on the concha, causing the tragus to become prominent [57].
13.13.3.7 Auricular Lines
Cartilage manipulation techniques signicantly destabilize the cartilage. Changes
in tensile forces during healing often result in step deformities, leading to line formation in patients exposed to these techniques. Therefore, cutting techniques should
be used sparingly and replaced with scoring techniques to avoid contour irregularities [57].
13.14 Revision Otoplasty
Cases requiring secondary surgery include recurrent protrusion, overcorrection, cartilage irregularities, telephone ear deformity, and other primary aesthetic complications (postauricular sulcus obliteration, contour irregularities in the antihelical fold,
external auditory canal obliteration, postperichondritis deformity) [73, 142–144].
Approaches to these deformities are described by Walter and Nolst Trenite [142].
To correct postauricular sulcus obliteration, zigzag incisions are made in the posterior skin, triangular approximation points are made, and the remaining gaps are
lled with full-thickness skin grafts.
Minor irregularities in the antihelical fold can be treated with curettage, while
larger defects can be corrected with temporal fascia, cartilage grafts, or prosthetic
materials [73]. Inappropriate conchal setback results in external auditory canal stenosis, which is treated with conchal resection through a posterior approach [73].
Patients should avoid toys or objects that may cause inadvertent trauma. In cases
requiring revision surgery, half of the loss of correction was found to be related to a
history of external trauma [132].
Revision cases are particularly challenging. Patients often have psychological
problems that have been hidden for years. As a result, patients may sometimes be
overly demanding of the surgeon. For patients who have undergone otoplasty with
family consent, the time lapse is one to two years. During this time, the occurrence
of serious complications is a signicant event in their lives. The principles outlined

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here are intended to optimize the likelihood of a satisfactory outcome and improve
the psychological state of these patients [4].
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