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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

Retraction Pockets andAdhesive Otitis
Media
BeldanPolat, KadirSerkanOrhan, andBadrEldinMostafa
20.1 Introduction
Adhesive otitis media (AdOM) is the condition in which a portion of the tympanic
membrane (TM) inseparably adheres to anatomical structures in the middle ear cavity (MEC). This is usually preceded by tympanic membrane retraction pockets (RP)
and atelectasis. As the RP progresses, the middle ear volume decreases and eventually the middle ear cavity is obliterated by atelectasis of the tympanic membrane. At
this stage, the membrane adheres to the middle ear structures but can be elevated
because the mucosal covering is preserved. Retraction pockets do not always progress to atelectasis. Inammation of the middle ear mucosa is the basic underlying
process of all these events. The clinical picture that occurs in a signicant part of the
patients is conductive hearing loss.
20
20.2 Physiology
In order to understand the development of the RP of the TM, it is necessary to examine the ventilation and gas exchange of the middle ear cavities. The middle ear cavity, Eustachian tube (ET), and mastoid air cells form an interconnected system to
regulate middle ear pressure.
B. Polat · K. S. Orhan (*)
Faculty of Medicine, Department of Otorhinolaryngology, Istanbul University,
Istanbul, Turkey
e-mail: beldanp@istanbul.edu.tr
B. E. Mostafa
Department of Otorhinolaryngology, Ain-Shams University, Cairo, Egypt
© 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_20
409

410
B. Polat et al.
20.2.1 Role oftheMucosa
The air in the middle ear, the mucosa and submucosal blood vessels of the middle
ear, and mastoid air cells can be compared to an alveolus. Just as oxygen and nitrogen with high partial pressure in the lung alveoli tend to diffuse into the blood in the
vascular structures and carbon dioxide from the blood to the air into the alveoli, a
similar situation exists in the MEC.As long as the mucosa is healthy and the MEC
is balanced with the atmosphere, the rate of passage of oxygen and nitrogen into the
blood and the rate of passage of carbon dioxide into the middle ear cleft is equal
[1–3]. Gas concentrations in the MEC are very similar to gas concentrations found
in venous blood [4]. The diffusion rate is affected by possible changes in blood ow
and mucosa. However, the rate of absorption of gases increases in conditions such
as mucosal inammation where blood ow increases [5]. Even body positionrelated changes in blood ow to the middle ear mucosa affect gas diffusion
rates [6, 7].
20.2.2 The Role oftheEustachian Tube
The ET, which is closed at rest, opens by the contraction of the tensor palatini
muscles. This allows the air pressure in the nasopharynx to equalize with the air
pressure in the MEC.When ET is dysfunctional, middle ear ventilation is impaired.
Nitrogen is gradually absorbed by the mucous membrane of the middle ear. This
creates a negative pressure in the middle ear cavity.
20.2.3 Role ofMastoid Air Cells
According to Boyle’s law, pressure (P) and volume (V) in a closed environment are inversely related. A low mastoid air volume means large changes in
pressure which can have undesirable effects on the eardrum in the long run.
Prolonged negative pressure in the middle ear is known to cause medialization
of the tympanic membrane. However, in addition to the high mastoid air volume, the width of the mucosal surface that will allow gas diffusion is also
important [8, 9].
20.2.4 Tympanic Isthmus
The MEC is anatomically composed of three parts: the ET, the tympanic cavity, and
the mastoid air cells. The part of the tympanic cavity above the lateral process of the
malleus is called the epitympanum (attic), the part between the lateral process of the
malleus and the inferior border of the bony external auditory canal is called the
mesotympanum, and the part that is inferior to the bony external auditory canal is
called the hypotympanum.

20 Retraction Pockets andAdhesive Otitis Media
Fig. 20.1 Connection between mesotympanum and epitympanum via tympanic istmuses in right
ear. AML Anterior Malleolar Ligament, LML Lateral Malleolar Ligament, PIL Posterior Incudal
Ligament, PE Pyramidal Eminence, FN Facial Nerve, CP Cochleariform Process, TTM Tensor
Tympani Muscle, TTF Tensor Tympani Fold, AMLF Anterior Malleolar Fold, LMF Lateral
Malleolar Fold, M Malleus, I Incus
411
Clinically, it can be divided into attico-antral and tubotympanic parts which are
separated by the tympanic diaphragm. This diaphragm is composed of bony and
membranous structures, including the incus body, medial and lateral incudal folds,
malleus head, lateral and anterior malleal mucosal folds, and tensor tympani folds.
It is perforated by two openings: the posterior and anterior tympanic isthmuses
which allow gas passage between the atticoantral part and the tubotympanic parts.
Medial to the incus and posterior to the tensor tympani is the anterior tympanic
isthmus. Located between the medial incudal fold and the posterior tympanic wall
is the smaller posterior tympanic isthmus. If the tensor tympani fold is incomplete,
a greater transition is achieved between the mesotympanum and anterior epitympanum (Fig.20.1). If these passages are blocked for any reason, the mastoid air cells
are disconnected from the mesotympanum, negative pressure occurs in the mastoid
area, which may result in effusion. The probability of isthmus blockade and tensor
fold closure in patients with attic disease was found to be 96% [10]. Furthermore, in
patients with attic retraction pockets, retraction could not be prevented by any
method (cartilage tympanoplasty, attic lateral wall reconstruction) without removing the cog and tensor fold and providing anterior epitympanic aeration [11].
20.3 Retraction Pockets oftheTympanic Membrane
The retraction pocket of the tympanic membrane (TM) serves as a distinctive feature observed during otoscopic examination. All or parts of the tympanic membrane
are drawn inwards towards the middle ear. The pars accida and posterosuperior
part of the pars tensa are the most frequently affected areas of TM [12]. Retraction

412
B. Polat et al.
pockets can resolve spontaneously and persist in a stable state over an extended
period. The loss of anatomical and structural integrity of the drum can lead to progression and the development of further complications and cholesteatoma.
20.4 Pathophysiology
The development of retraction pockets involves several factors. Areas of the tympanic
membrane can be weakened by the inuence of elastase and collagenase secreted by
inammatory cells during otitis media, the gradual loss of lamina propria in specic
regions of the TM, and the impact of middle ear dysventilation syndrome. Trauma to
the tympanic membrane by perforation, infection, or ventilation tube insertion can
increase the risk of retractions. Dysfunction of the ET can lead to negative pressure
affecting the entire middle ear. This overall condition is referred to as global middle
ear dysventilation. On the other hand, when the tympanic isthmus is obstructed, localized conditions arise, which are termed selective middle ear dysventilation [13]. When
the tensor tympani fold is closed and the anterior tympanic isthmus is closed, the
epitympanic space is disconnected from the mesotympanum. With the gas decit,
negative pressure is formed in the attic, resulting in selective epitympanic dysventilation occurs. In pars accida, independent of the function of the ET medial collapse
and formation of a retraction pocket are observed (Fig.20.2).
Dysventilation of the retrotympanum occurs with occlusion of the posterior
tympanic isthmus. With the variations in the depth of this region, if the effusion
stays in this space for a long time, persistent inammatory reactions accelerate the
formation of a retraction pocket in the posterosuperior part of pars tensa [14]. In
certain cases, the promontory may be situated at a similar level to the long arm of
the incus, extending nearly to the level of the malleus handle or even the head of
the stapes. A high promontory and a deep retrotympanum favor the prolonged
Fig. 20.2 Bony erosion in
lateral attic wall in
retraction pocket of pars
accida in left ear

20 Retraction Pockets andAdhesive Otitis Media
Fig. 20.3 Retraction
pocket in right ear in
posterior part of pars tensa.
Dotted ellipse shows
retraction pocket
Fig. 20.4 Elevation of
retraction pocket with
nitrogen before surgery in
right ear
413
retention of effusion. Furthermore, when the pars tensa is more retracted, it can
readily make contact with both the incus and the promontory simultaneously,
potentially leading to adhesion formation either with the incus or at the incudostapedial joint (Fig.20.3) [13]. If adhesion has not yet occurred, this pocket can be
ventilated with the Valsalva maneuver (Fig.20.4). Inammation caused by chronic
otitis media causes more serious problems around the bony chain. In this environment where drainage is more difcult, occlusion of the isthmus can easily occur,
and even if the ET functions return to normal, the dysventilation process may
become permanent [15].

414
B. Polat et al.
20.5 Clinical Picture
Retraction pockets are commoner in children. They affect the pars accida more
frequently than the pars tensa [16, 17]. The most prominent symptom in RP is
conductive hearing loss, regardless of stage. Hearing loss can uctuate over time.
A crackling sound from the ear and a feeling of congestion in the ear can also be
seen. Intermittent ear discharge after exposure to water is also among the
symptoms.
On examination, the location of the retraction pockets, their depth, their
relationship with other structures in the middle ear, and the condition of the
visible bony chain should be noted. Erosion of the long arm of the incus is the
most common bony chain abnormality. Bony annulus erosion is also rarely
seen. Testing the mobility of the drum by Valsalva’s maneuver or pneumatic
otoscopy is important to check areas of adhesions as well. Examination with
otoendoscopy is mandatory to check the fundus of the pocket and its selfcleaning ability.
There are many classications for tympanic membrane retractions either pars
tensa [18–20], pars accida [12, 19, 21] or generalized retractions [12, 22–24]. All
of the following refers to the behavior of the pocket, whether or not it is a selfcleaning retraction pocket, bone erosion of the scutum, annulus, and/or ossicular
chain, or xation of the TM retraction pocket to the ME ear structures. This staging
assumes that each stage is distinct and that there is a natural progression between
stages which will also determine the management strategy. However, this is not true
and, although they have a benet in follow-up teaching and research, they are not
practical due to the high intra-observer variability and lack of correlation to specic
management policies (Table20.1).
Radiologically, on CT examinations the most important image to note is the sclerotic or poorly ventilated mastoid. In the retraction pockets, varying degrees of condensation are observed in the anterior epitympanic recess, attic, and antrum. In
these spaces, condensation is observed in 80% of pars accida retractions and
around 50% of pars tensa retractions [13].
Table 20.1 Sade and Tos classications of pars tensa and pars accida
Sade
Stage
I TM is slightly retracted over its
annular fold
II TM is touching incudostapedeal
joint
III TM is touching the promontory,
but it is not adhering.
IV The pars tensa is in contact with
the promontory
V Atelectatic otitis media Attic cholesteatoma
Tos
There is a slight retraction toward the neck of the
malleus, but the air space is still visible
Retraction up to the neck of the malleus, no air
space is visible behind the TM
Retraction extends beyond the bony annulus. The
full extent of the retraction pocket can be seen
Outer attic wall erosion

20 Retraction Pockets andAdhesive Otitis Media
415
20.6 Management
Decision-making in the management of RP is a complex issue. Individualized decisional trees are constructed depending on the surgeon’s priorities for each patient.
To date, there are no high-level studies to support any particular approach. There are
no objective criteria to be considered when deciding between surgical intervention
or close follow-up options. However, evaluation of the Eustachian tube function
may be central in inuencing further management and follow-up. Persistent ETD
mandates proper management and elimination of predisposing sinonasal and/or
nasopharyngeal problems. Improvement of ET function may be achieved by control
of nasal and nasopharyngeal problems, repeated Valsalva maneuvers, autoination,
or balloon tuboplasty. If there is no ear discharge, no hearing loss, or if there is aeration in the anterior epitympanum, attic, and antrum on CT, follow-up may be recommended. However, surgery is considered if there is bone erosion, condensation in
the spaces mentioned above, conductive hearing loss exceeding 30 dB, ear discharge, debris accumulation in the pocket (Fig.20.5), granulation or cholesteatoma
(Fig.20.6) on CT.The location of the RP may also inuence the management strategy. Postero-superior retractions are more dangerous and are liable to progression
and possible complications, whereas antero-inferior pockets can be followed up for
longer periods of time.
Fig. 20.5 Squamous
debris in retraction pocket
of pars tensa in right ear.
*Squamous debris in
retraction pocket

416
Fig. 20.6 Cholesteatoma
formation in retraction
pocket of pars accida in
right ear. *Cholesteatoma
in attic retraction pocket
B. Polat et al.
20.6.1 Surgical Management
Depending on the stage of the RP, its location and the presence or absence of bony
erosion, various surgical procedures have been described for retraction pockets.
20.6.1.1 Myringotomy withTubes
This involves placing a ventilation tube to address early-stage RPs associated with
middle ear effusion. This may include temporary or permanent ventilation tubes or
even subannular tubes for permanent aeration.
20.6.1.2 Tympanoplasty
With ongoing retraction and fragilization of the TM, grafting with excision of the
RP may also be done, especially if it is limited to one-quarter of the eardrum. The
choice between medial and lateral grafting depends on the surgeon’s preference and
experience. Future medialization of the graft should be anticipated and prevented.
Cartilage grafts are used to separate, elevate, and support the RP.Cartilage is preferred because of its resistance to resorption and inammation, but complications
and recurrence can occur. It may cause some conductive loss and make follow-up
difcult. During tympanoplasty the status of the ossicular chain must be evaluated
and reconstruction planned to avoid post-operative conductive hearing loss.
20.6.1.3 Mastoid Surgery
Resection of RP and mastoid obliteration: This surgery reduces mucosal gas
exchange in the middle ear to address advanced RPs and prevent cholesteatoma
recurrence.

20 Retraction Pockets andAdhesive Otitis Media
Mastoidectomy-atticotomy with anterior epitympanotomy: A functional
approach that aims to address the underlying causes of RP by restoring ventilation
pathways. Anterior epitympanic recess surgery involves removing the folds in the
middle ear cleft, especially in the epitympanum and retrotympanum spaces, opening the ventilation pathways, and ensuring proper gas exchange.
417
20.7 Adhesive Otitis Media
AdOM occurs as an undesirable consequence of prolonged serous otitis media and
ET dysfunction [25, 26]. It is often bilateral and is sometimes associated with cholesteatoma [27]. Most otitis media patients with chronic effusion either heal spontaneously or are treated with tympanostomy tubes. A proportion of neglected patients
(3–5%), develop advanced atelectasis and AdOM [28]. It is critical to prevent this
situation before it occurs, otherwise the result is irreversible.
20.7.1 Pathogenesis
AdOM is a sequelae of chronic otitis media with long-lasting effusion and is mostly
accompanied by ETD [29]. Middle ear inammation, negative middle ear pressure,
and loss of TM strength play a role in the development of AdOM.With the disappearance of the lamina propria of the tympanic membrane, the atrophic membrane
collapses into the entire mesotympanic cavity. With the disappearance of middle ear
aeration, the tympanic-ossicular system loses its function. The TM adheres to the
medial wall of the middle ear with a granulation-rich reaction in the mucoperiosteum, an increase in broblast activity, and eventually an increase in connective
tissue due to prolonged inammation in the mesotympanic mucosa. With hyperplasia in the epidermal layer of the tympanic membrane, its self-cleaning feature is lost.
20.7.2 Clinical Findings
The most common symptom is fullness in the ears, caused by negative pressure in
the middle ear. Hearing loss occurs gradually over months and years and then
remains stable. It does not show improvement in between as in some retraction
pockets. In some patients, there is no hearing loss and the pure tone audiogram may
be normal. The presence of otorrhea may be a warning of the presence of
cholesteatoma.
During the physical examination, a complete collapse of the tympanic membrane
is observed. Despite various maneuvers, it proves impossible to elevate the tympanic membrane, resulting in the full exposure of all anatomical details of the
medial wall (Fig.20.7). Erosion of the ossicular chain can be evident. The most
commonly affected ossicle in AdOM is the incus. Due to the vascular structure of
the long arm, erosion was detected in 55% of the patients. Erosion in the stapes was

418
Fig. 20.7 Elevation of
atelectatic tympanic
membrane with Valsalva
maneuver in the left ear
B. Polat et al.
detected at rates of up to 22%. Malleus is the least affected ossicle in AdOM and
erosion is rarely seen (12.7%) [30]. The manubrium mallei may be displaced medially and adhere to the promontory.
Hearing loss is mostly of the conduction type and the air–bone gap can reach up
to 45–50dB.Tympanometric examination is at type.
Cholesteatoma formation is not uncommon in patients with AdOM.The incidence of cholesteatoma in the literature varies from 8% to 25% [30, 31]. Recurrent
infections and otorrhea may be a precursor to cholesteatoma in AdOM.The development of cholesteatoma occurs frequently in the attic region and
retrotympanum.
20.7.3 Imaging
Imaging is not required unless there is cholesteatoma development. Erosions in the
bony chain, in which the entire TM adheres to the medial wall of the middle ear, can
be detected (Fig.20.8). Another notable thing about CT is that the mastoid is almost
always sclerosed.
20.7.4 Treatment
It is one of the most difcult ear pathologies to treat. Therefore, RP and atelectasis
should be treated appropriately before AdOM develops. Atelectasis is best treated
with ventilation tubes. The best treatment strategy for AdOM is not agreed upon.
Medical treatment is not effective. Surgical options are controversial.
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