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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

22 Basic Otological Surgical Techniques
Periodic cleaning of the EAC and mastoid cavity is required in the postoperative
follow-up as the anatomy and physiological cleaning of the cavity cannot be preserved with the CWD approach. Hearing aid amplication and the effects of external physical factors are the main obstacles in the mastoid cavity.
451
22.4.4 Retrograde Mastoidectomy
Retrograde mastoidectomy (inside-outside) is a type of combined CWD mastoidectomy approach. This approach, described by Dornhoffer [12], is used in cases of
cholesteatoma limited to the attic, epitympanum, and upper mesotympanum. The
EAC is partially lowered with a burr, starting from the attic and following the disease posteriorly and superiorly. This technique allows limited removal of the attic
cholesteatoma and reconstruction of the ossicular chain. The defect in the EAC wall
is closed with palisade-shaped cartilage. Similar cholesteatoma recurrence rates of
5–10% have been observed when comparing cases operated with the retrograde
mastoidectomy approach and CWD mastoidectomy [13].
22.4.5 Modified Radical Mastoidectomy
The modied RM (MRM) approach involves removal of the posterior and superior
walls of the EAC, like CWD mastoidectomy, terminologically, CWD mastoidectomy and MRM are often used to refer to the same surgical technique. The Bondy
approach [14], which is less commonly used today, involves the removal of disease
from the attic and mastoid cavity in limited cholesteatomas that do not extend to the
middle ear. Fascial grafts are placed lateral to the head of the malleus and the body
of the incus and mastoid cavity without involving the middle ear.
22.4.6 Radical Mastoidectomy
The RM approach is also a CWD procedure. In contrast, RM does not preserve
middle ear function, removes malleus and incus, and closes the Eustachian tube. No
fascial or cartilaginous grafts are placed, allowing the epithelial lining of the entire
middle ear and mastoid cavity to remain intact.
22.4.7 Mastoid Obliteration
This approach aims to reduce the size of the mastoid cavity in cases such as CWD,
MRM, and retrograde mastoidectomy where the canal wall is lowered. This makes
it easier to obliterate the mastoid cavity and amplify the device in patients who use
postoperative cavity care and hearing aids. LSSC is exposed to external factors in an
open cavity. Obliteration may be indicated in recurrent skin infections or when

452
H. Bayraktar et al.
thermal changes, wind, or water exposure cause dizziness or vertigo. Autologous
materials used for obliteration include bone pate, bone chips, minced cartilage,
muscle ap, and fat, and allograft materials include hydroxyapatite bioactive glass
and tricalcium phosphate. Palva [15, 16] rst described ap obliteration by placing
postauricular pedicled musculoperiosteal tissue into the mastoid cavity.
22.5 Petrosectomy
The most common pathologies affecting the petrous apex include cholesterol granuloma, cholesteatoma, aneurysm, asymmetric aeration and presence of bone marrow,
arachnoid cyst, petrous apicitis (Gradenigo syndrome), mucocele, and petrous apex
effusion. Surgical intervention may be required in symptomatic cases that do not
respond to conservative management. Several surgical approaches can be used for
petrous apex lesions depending on the surgeon’s experience, the location of the
lesion in the petrous bone, and the preservation of hearing. Approaches to the
petrous apex include transcanal infracochlear, transmastoid infralabyrinthine, middle fossa craniotomy, translabyrinthine, suboccipital, transsphenoidal endoscopic,
and infratemporal fossa (ITF) types A and B.
22.6 Conclusion
The primary purpose of all otological techniques dened in COM surgery is to
remove the disease that may cause complications from the middle ear and associated mastoid region or to manage the complication that occurs before surgery. The
secondary purpose is hearing reconstruction through ossiculoplastic interventions
by creating a ventilated and functional middle ear cavity. For these purposes, the
microscope has long been used in all otological surgical interventions. In addition,
recently the transcanal endoscopic approach, both in combination with microscopic
surgery and alone, has become popular in the eld of otology. Although endoscopic
ear surgery requires a more difcult learning process and experience than microscopic surgery. Since it is less invasive and provides an easier healing period, it will
be the preferred method in the eld of otology in the future.
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22 Basic Otological Surgical Techniques
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org/10.3109/00016487809123502. PMID: 377902.
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Tympanoplasty
23
IsaKaya, TayfunKirazli, andJohnL.Dornhoffer
23.1 Introduction
Tympanoplasty is a surgical procedure that aims to reconstruct the tympanoossicular system. The primary goal of this procedure is to remove diseased tissue
from the tympanic membrane (TM) and middle ear cavity, reconstruct the tympanoossicular structures, and create a functional, closed cavity that is aerated. The secondary goal is to improve the patient’s hearing as much as possible.
Tympanoplasty can be broadly divided into four categories: myringoplasty,
ossiculoplasty, canaloplasty, and meatoplasty. Myringoplasty is the surgical
reconstruction of the TM.The goal of myringoplasty is to restore the ability of the
TM to vibrate, which is necessary for hearing. Ossiculoplasty is the surgical
reconstruction of the ossicular chain. The ossicular chain comprises the malleus,
incus, and stapes, which transmit sound waves from the TM to the inner ear.
Ossiculoplasty is performed when the ossicular chain is damaged and prevents
sound waves from reaching the inner ear. Canaloplasty is the surgical restoration
of the normal width and contour of the ear canal. Canaloplasty is performed to
improve the patient’s ability to clean the ear canal and to facilitate a second-stage
ossiculoplasty, if necessary. Meatoplasty is the surgical widening of the cartilaginous ear canal relative to the diameter of the medial bony canal. Meatoplasty is
performed to improve the patient’s hearing by increasing the surface area of the
TM exposed to sound waves.
I. Kaya (*) · T. Kirazli
Faculty of Medicine, Department of Otorhinolaryngology, Ege University, Izmir, Turkey
J. L. Dornhoffer
Arkansas Children’s Hospital, Department of Otolaryngology/Head and Neck Surgery,
University of Arkansas for Medical Sciences, Little Rock, AR, USA
e-mail: dornhofferjohnl@uams.edu
© 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_23
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23.2 Etiology ofTM Perforations
23.2.1 Chronic Otitis Media
Chronic otitis media (COM) is a disease characterized by persistent or recurrent
episodes of acute otitis media lasting more than 12weeks, typically culminating in
a nonhealing perforation of the TM [1]. Affecting more patients worldwide than any
other infectious disease [2], the development of COM is inuenced by multiple risk
factors, including upper respiratory tract infections, malnutrition, poor hygiene,
familial predisposition to ear infections, low birth weight, craniofacial anomalies,
and ethnic background, particularly in populations of Native American, Native
Alaskan, and Aboriginal Australian descent [3].
The cardinal symptoms of COM are otorrhea, discharge leakage through the perforated TM into the external ear canal, and hearing loss [4]. The latter typically manifests as a mild conductive decit in the range of 10–20 decibels (dB). However,
larger perforations can result in more signicant hearing impairment. Ossicular chain
erosion, a potential complication, can further exacerbate audiologic decits, resulting in a loss of 50–70 dB. In such cases, careful evaluation for cholesteatoma is
crucial, as its presence signicantly complicates both management and prognosis [4].
Tympanic membrane perforations (TMP) can be classied according to their
location, size, and presence of drainage. The vast majority occur in the pars tensa,
while the pars accida is less commonly involved [5]. Based on their location relative to the annulus, perforations can be classied as marginal or central [6]. In addition, the presence or absence of active otorrhea (persistent discharge) denes them
as wet or dry [6]. This classication system is crucial for guiding appropriate treatment strategies, as different types of perforations may require different surgical
approaches or medical interventions [5, 6].
Tympanoplasty remains a cornerstone procedure in the management of chronic
otitis media with the dual goals of eradicating infection and restoring TM integrity
[7]. The two goals of this surgical procedure are to achieve an intact TM and
improved hearing function [8]. Reconstruction of the perforated TM by graft placement is the core of tympanoplasty, as complete TM healing is the basis for establishing a healthy middle ear environment free of chronic inammation and infection [9].
23.2.2 Traumatic Perforations
The TM can be injured by both direct or indirect forces. Direct trauma can result
from a blow to the ear, a foreign body penetrating the TM, or direct exposure of the
TM to heat or ame. Indirect trauma can result from a skull fracture, either with or
without a temporal bone fracture. Longitudinal skull fractures can injure the TM
and other middle ear structures. Sounds of 195dB or greater can cause acoustic
trauma that can damage the TM.Sudden changes in pressure can cause barotrauma,
which can also damage the TM.Disruption of the ossicular chain and window stulas may occur, especially after traumatic perforation of the TM.

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23.3 History ofTympanoplasty
The history of tympanoplasty reveals a dynamic evolution of graft materials.
Pioneering efforts by Banzer in 1640 used pig bladder, followed by Blake’s paper
patch in 1877 and Berthold’s rst skin graft in 1878 [10–12]. Microscopic tympanoplasty with skin grafts became the dominant technique in the 1950s [13]. Soon
after, canal skin pedicle grafts were introduced to repair extensive perforations [13].
Vein grafts gained traction in the late 1950s, and House and Sheehy provided further
innovations with canal skin overlay grafts in the early 1960s [13, 14]. Storrs’ landmark report in 1961 described the fascia graft technique, adding another valuable
option to the growing repertoire [15].
Tympanoplasty techniques have evolved over time and include approaches such
as overlay, underlay, and over-underlay procedures [14, 16]. While microscopic
tympanoplasty has dominated since the 1950s, endoscopic techniques have gained
popularity since the 1990s [17, 18]. This diversity extends to graft materials, with
temporalis muscle fascia remaining the most common choice due to its approximately 90% success rate in primary tympanoplasties [19, 20]. However, there is
concern for larger perforations where success rates have been reported to decrease
[21]. A possible explanation lies in the unpredictable shrinkage of the fascia, which
is attributed to its disorganized arrangement of elastic bers and interspersed brous
connective tissue, with the latter exhibiting greater shrinkage than elastic bers
[22]. This highlights the need for further investigation of alternative materials and
techniques to optimize tympanoplasty outcomes, particularly for challenging cases.
In 1963, cartilage emerged as a promising alternative to temporalis fascia for TM
reconstruction, especially in difcult cases [23, 24]. Unlike fascia, which is free of
unpredictable brous components, cartilage has an inherent stiffness that resists
resorption and retraction even in chronic Eustachian tube (ET) dysfunction [25].
This superior structural stability increases its attractiveness, not only in advanced
middle ear pathologies but also in subtotal or total perforations. However, the rigidity of the cartilage has sparked debate regarding its impact on audiological outcomes [26]. Therefore, meticulous preoperative assessment of the degree and type
of hearing loss, including the potential detection of occult pathology, is crucial to
optimize material selection and surgical planning.
23.4 Anatomy andPhysiology
The middle ear cleft, also termed the tympanic cavity, resides within the petrous
portion of the temporal bone. It houses key anatomical structures, including the
inner layer of the TM, the ET orice, and the three ossicles (malleus, incus, stapes)
that form the ossicular chain. Posteriorly, the middle ear cleft communicates with
the mastoid air cell system via the tympanic antrum and the aditus ad antrum. This
connection facilitates aeration and pressure equalization. Anteriorly, the ET connects the middle ear cavity to the nasopharynx, allowing for pressure equalization
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The TM forms most of the lateral wall of the middle ear. This tri-layered structure
has unique properties that are critical for sound transmission. The outermost layer, a
seamless extension of the external auditory canal epithelium, consists of stratied
squamous epithelium. The middle layer, the brous stratum (lamina propria), represents the core and primary determinant of TM stability. Robust collagen bers traversing this layer limit stretchability, enabling the TM to exhibit high compliance at
minimal acoustic pressure displacements while resisting excessive stretching at higher
pressures. This compliance allows for efcient sound transmission. Finally, the innermost layer, which is continuous with the cuboidal middle ear mucosa, completes the
composite structure. The collagen bers of the brous stratum play a critical role in
regulating compliance, ensuring that the TM responds effectively to changes in acoustic pressure. Approximately 10mm in diameter and 0.1mm thick, the TM typically
appears pearly gray and slightly translucent, allowing visualization of the underlying
ossicular chain. This transparency facilitates clinical assessment and diagnosis [27].
The TM exhibits a distinct topographic division. The pars accida, located anteriorly and posteriorly to the malleolar ligaments, occupies the superior region. This area
lacks the central brous layer of the pars tensa, making it thinner and more compliant.
As a result, the pars accida has greater exibility and responsiveness to acoustic pressure than the more rigid, brous pars tensa, which makes up the majority of the TM and
covers the area below the neck of the malleus. In clinical practice, the TM is further
subdivided into four quadrants for precise localization. These quadrants are delineated
by horizontal and vertical lines intersecting at the umbo and passing through the handle
of the malleus. A comprehensive understanding of these intricate spatial relationships
within the middle ear is crucial for the otologic surgeon, as both functional and anatomical considerations signicantly inuence surgical approaches [5].
The TM and the ossicular chain serve as the exquisitely designed sound transmission apparatus of the middle ear. Airborne sound waves, manifested as air pressure uctuations, impinge on the TM, initiating a cascade of mechanical energy
transfer [28, 29]. This energy transmission unfolds via the ossicular chain, a series
of intricately linked ossicles—the malleus, incus, and stapes—that amplify the
incoming signal. The amplied mechanical vibrations are delivered to the oval window of the inner ear, ultimately creating a uid wave within the cochlea [29]. This
uid wave interacts with specialized hair cells organized tonotopically on the basilar membrane, triggering the conversion of mechanical energy into electrical nerve
impulses [30]. These neural signals, encoded with auditory information, are then
transmitted via the cochlear nerve to the brainstem, completing the remarkable journey of sound from the outside world to the central nervous system.
Hearing losses that occur in the case of TMP are shown in Table23.1.
Table 23.1 Hearing loss
resulting from total
membrane perforation and
ossicular chain dislocation
Lack of leverage 7.3dB
Lack of hydraulic effect 26.5dB
Elimination of phase
protection effect
Total loss 50dB
16.2dB

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23.5 Tympanoplasty Types
According to the classication made by Wullstein in 1956, there are ve types of
tympanoplasty [31]. The methods are named according to the condition of the
ossicles.
Wullstein Classication (Adapted from Reference [31])
• Type I: There is no problem in the middle ear and ossicles. Only the TM is
repaired. It is synonymous with myringoplasty.
• Type II: There is a defect in the malleus. The graft is placed on the incus.
• Type III: There is erosion of the malleus and incus. The graft is placed on the
suprastructure of the stapes.
• Type IV: The ossicles are eroded except for the base of the stapes. The graft is
placed on the stapes foodplate, which is mobile.
• Type V: The stapes base is xed. The fenestration is made and the graft is placed.
The Bellucci classication is based on the discharge in the middle ear [32].
Bellucci Classication (Adapted from Reference [32])
• Group I.The ear has been stable for a long time. The prognosis is good.
• Group II.The middle ear is stable, but discharge develops during upper respira-
tory tract infections. The middle ear is sometimes dry and sometimes wet. The
prognosis is fair.
• Group III.There is a constant discharge from the ear. There is no period when the
middle ear is dry. It may be mastoiditis. The prognosis is poor.
• Group IV.There is a persistent discharge from the ear accompanied by nasopha-
ryngeal problems such as cleft palate or choanal atresia. The prognosis is
very poor.
23.6 Perforation Size andLocation
Based on the percentage of the TM surface that is perforated, TMPs are classied as
small, medium, subtotal, and total (⩽25%, ⩽50%, ⩽75%, and ⩾76%, respectively).
The severity of conductive hearing loss, a hallmark consequence of TMPs, has been
shown to increase with the size and duration of the perforation [33]. In addition,
subtotal and total perforations have limited self-healing potential and provide fewer
suitable sites for graft adherence during surgical repair [34]. Reconstruction of total
TMPs presents the most signicant challenge in tympanoplasty due to the complete
absence of the annular remnant that serves as the primary vascular bed for the graft.
Therefore, the choice of surgical approach depends on the condition of the protympanum. In cases with intact protympanic mucosa, the underlay technique utilizing
the mucosa as a vascular bed can be employed. Conversely, in situations where the
protympanum is obliterated or signicantly compromised, the overlay technique
may be required. Interestingly, spindle-shaped perforations have been shown to

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disproportionately disrupt sound conduction compared to circular perforations,
especially at high frequencies [33]. These observations underscore the signicance
of perforation size, shape, and chronicity in determining both the degree of hearing
impairment and the success of reparative interventions.
TMP classication based on location includes posterior, anterior, marginal,
median, and attic perforations. Notably, marginal and attic perforations carry a
higher risk of retraction and cholesteatoma development compared to median perforations, raising safety concerns [35]. This increased risk in marginal and attic
locations stems from their vulnerability to retraction, a process in which the TM is
pulled inward, creating a potential pocket for debris accumulation and subsequent
cholesteatoma formation. In contrast, median perforations, which are centrally
located, exhibit a lower propensity for retraction and cholesteatoma development.
However, their location, particularly around the umbo/manubrium region, can signicantly impact sound transmission through the middle ear, resulting in signicant
conduction disturbances [36, 37]. Additionally, anterior and marginal perforations
present surgical challenges due to limited graft attachment sites and anatomical
constraints. The transcanal approach commonly used for tympanoplasty is often
hampered by the narrower ear canal, angular TMP, and medial canal curvature associated with these perforations, compromising surgical access.
The anatomical limitations of certain perforation sites, particularly anterior and
marginal sites, pose signicant challenges to surgical reconstruction using the transcanal approach. As a result, surgeons may opt for more invasive alternatives such as
postaural and endaural approaches to ensure optimal graft placement [5, 38]. The
choice of approach ultimately depends on the specic anatomic features of the perforation and the surrounding ear structures. By carefully considering these factors,
surgeons can ensure effective and safe material placement to maximize the success
of the TM repair.
Perforations extending into the anterior quadrants require meticulous graft placement to avoid complications. To prevent anterior blunting, the graft should be positioned deep to the anterior portion of the annulus, effectively tucked under the bony
ring. However, lateralization must also be avoided. Therefore, the graft should be
placed medial to the manubrium mallei to ensure proper positioning. In addition, it
is critical that the graft adequately covers the posterior wall to ensure intimate contact with the remaining TM and middle ear mucosa.
23.7 Graft Materials
Tympanoplasty is essentially a tissue transfer procedure aimed at reconstructing the
TM.Surgeons have a repertoire of graft materials at their disposal, each with different characteristics that inuence their suitability for different scenarios. Temporalis
fascia remains the mainstay of choice due to several advantages. Located in close
proximity to the surgical site, temporalis fascia offers ease of harvest with minimal
donor site morbidity. Its inherent properties, characterized by a dense collagenous
structure and low vascularity, contribute to excellent stability and minimal

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shrinkage after grafting. This makes it ideal for primary tympanoplasty, promoting
successful long-term TM closure and improved hearing outcomes [23, 39]. However,
some surgeons prefer to use the loose areolar fascia of the temporalis muscle, especially in revision cases or when true fascia needs to be preserved for future procedures. This alternative offers comparable ease of harvest but with increased
vascularity, requiring careful selection in specic cases where graft vascularity may
be a concern [40]. The popularity of cartilage grafts has increased dramatically over
the past few decades. The ease of harvesting from the tragus or concha of the auricle, coupled with promising results in numerous studies, has fueled this trend [40,
42]. Cartilage grafts have several potential advantages. Their limited size minimizes
donor site morbidity, while their inherent rigidity and resistance to resorption provide superior structural support compared to fascial grafts. This robustness makes
them an attractive option for complex perforations with a history of failed repair
[40, 41]. In addition, the passive diffusion of nutrients offered by cartilage may
contribute to higher graft acceptance rates [43]. However, concerns regarding the
effect of cartilage on sound transmission due to reduced sound conductivity compared to other materials have sparked ongoing debate.
Full-thickness cartilage grafts may actually cause some hearing loss compared to
other materials due to their stiffness [44]. Fortunately, research suggests that this
can be mitigated by utilizing partial-thickness grafts, which have been shown to
improve hearing outcomes [45]. Interestingly, despite initial concerns regarding
potential conductive hearing loss associated with cartilage thickness, several studies
have reported surprisingly positive results [46]. Evidence from both experimental
and clinical studies indicates comparable hearing outcomes with cartilage and fascia grafts [40, 42, 47]. In particular, the middle ear appears to tolerate cartilage well,
with long-term graft survival consistently observed. These ndings challenge previously held concerns about the impact of cartilage on hearing and suggest that its use
as a graft material is not inherently detrimental to auditory function compared to
alternatives such as fascia.
The growing body of literature documenting favorable outcomes with cartilage
grafts in tympanoplasty underscores their efcacy and durability as a middle ear
reconstruction material [48, 49]. To achieve this reconstruction, surgeons implement two different techniques: the perichondrium/cartilage island ap and the palisade technique. Each technique offers distinct advantages that require careful
consideration during surgical planning. The selection of the optimal technique
depends on a nuanced understanding of the specic middle ear pathology, the condition of the ossicular chain, and the experience of the surgeon.
Ultimately, the optimal choice of graft material depends on careful consideration
of several factors: the surgeon’s expertise and preference, the unique characteristics
of the perforation (size, location, chronicity), and whether the procedure is a primary or revision surgery. The variety of options available, including temporalis fascia, cartilage, perichondrium, and various composites, allows surgeons to tailor
their approach to the specic needs of each case, maximizing the success of the
tympanoplasty and ultimately improving patient outcomes [41]. A listing of potential graft materials is provided in Table23.2.
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