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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

Otitis Media withEffusion
17
AyseYaseminGunduz, MahmutTayyarKalcioglu,
OzgurYigit, andHaythamKubba
17.1 Introduction
Otitis media with effusion (OME), also referred to as serous otitis media or secretory otitis media, as we dene it today, was named and explained by Mawson in the
1970s and is the occurrence of uid accumulation in the middle ear cavity without
showing any signs of acute infection [1].
Being one of the most common causes of hearing loss in children, OME stands
out as an important public health problem. Language development of these children
with hearing losses is impeded, leading to impaired communicative abilities and
negatively affected academic lives [2, 3]. For this reason, it is extremely important
to recognize OME in the early period and initiate the required treatment and followup procedure.
A. Y. Gunduz (*) · M. T. Kalcioglu
Faculty of Medicine, Department of Otorhinolaryngology, Istanbul Medeniyet University,
Istanbul, Turkey
Goztepe Prof. Dr. Süleyman Yalcin City Hospital, Istanbul, Turkey
O. Yigit
Department of Otorhinolaryngology, Istanbul Training and Research Hospital, Health
Sciences University, Istanbul, Turkey
H. Kubba
Department of Otorhinolaryngology, University of Glasgow, Glasgow, UK
e-mail: Haytham.Kubba@ggc.scot.nhs.uk
© 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_17
347

348
A. Y. Gunduz et al.
17.2 Definition
The lexical meaning of otitis media is middle ear inammation. Otitis media is a
range of diseases as different parts of inammatory processes dominate in various types of otitis media [4]. Acute otitis media (AOM) presents with otalgia and
fever and usually accompanies or follows upper respiratory tract infections [5].
When the high-pressure infected uid in the middle ear cavity ruptures the tympanic membrane, as in acute suppurative otitis media, and the perforation does
not heal over time, chronic suppurative otitis media occurs, which is characterized by persistent or recurrent otorrhea through the tympanic membrane perforation [6].
When uid collection is clinically silent as mentioned before, OME occurs.
In this type of otitis media, chronic transformation occurs while the tympanic
membrane still keeps its integrity; and when the process lasts longer than
3months, it is called chronic OME [7]. Persistent effusion that remains after
AOM even after treatment differs from chronic OME in that it lasts for a maximum of 2months [8].
17.3 Epidemiology andRisk Factors
In the early stages of life, the very rst origin of middle ear effusion is the uid of
the amniotic sac. More than two-thirds of term infants were shown to have amniotic
uid in their middle ear cavities [9]. The prevalence of OME in children under
2years of age is as high as 60%, and thereafter, middle ear uid begins to dissolve
with age [10]. After the age of 7, the prevalence of the disease signicantly decreases
and remains below 20% [11].
Children with craniofacial anomalies develop OME more often than their normal
peers. OME can be seen in up to 60% of children with Down syndrome and up to
75% of children with cleft lip and palate under 8years of age, [12, 13]. In young
girls with Turner syndrome, the prevalence of chronic OME is nearly as twice as
that of the general population of their peers [14]. In addition to this increased risk in
the preschool age of these girls, problems associated with chronic effusion can often
persist or even arise in the school-age period.
Although a direct pathophysiological connection has not been shown yet, it is
known that OME is seen more frequently in atopic children. The prevalence
increases if a child presents any allergic or asthmatic symptoms [11].
In addition to patient history, socioeconomic environment of the patient has a
considerable impact on the development of OME.The child has a higher risk of
developing OME if the parents have low education levels and lower status jobs.
Apart from that, children with parental secondhand smoke exposure also develop
OME more than their peers living in a smoke-free environment [11]. That being
said, OME appears as a signicant public health concern and should be considered
in this regard.

17 Otitis Media withEusion
349
17.4 Pathophysiology
The Eustachian tube develops with age and reaches almost adult conguration by
the age of 8 [15]. The main reason why OME is seen more frequently in children
than in adults is the failure of underdeveloped Eustachian tube to play its part in
normal middle ear function. Immature Eustachian tube is shorter, lies more horizontally, and dynamically cannot open and close adequately [16]. Consequently, the
middle ear begins to be affected by the pressure changes and microorganisms of the
nasopharynx. In other words, the immature dysfunctional Eustachian tube provides
the predisposition to the development of the disease. Inammatory and infectious
phenomena in the nasopharynx are thought to be the triggers of the pathological
process that begins in the middle ear. With local inammation arising in the middle
ear, vasodilation and cytokine production occur. These inammatory changes,
respectively, lead to a decrease in middle ear pressure by increased gas absorption
in the middle ear, and accumulation of exudate secretion due to goblet cell and
glandular metaplasia in the mucosal epithelium of the middle ear [17]. The uid that
starts to collect in the middle ear can be mucous, seromucous, or serous in nature.
Excess secretion obstructs the Eustachian tube, and the aeration of the middle ear
from the nasopharynx is thus also blocked. As a result, the negative pressure developing in the middle ear starts to damage the structure of tympanic membrane and
causes it to atrophy. Eventually, retraction pockets form primarily in the pars accida, which does not have the brous layer. Unless OME is treated and healthy
middle ear pressure is achieved, retraction involves the entire tympanic membrane
and complicates the development of atelectasis and adhesive otitis. As OME may
even lead to the development of cholesteatoma from retraction pockets in the future,
which occurs especially in children refractory to treatment, it should be recognized
and treated without delay and at a possible earlier age in order to minimize the duration of exposure to negative middle ear pressure [18, 19].
Eustachian tube dysfunction has been the traditional pathophysiological concept
in OME for a long time [20]. However, recent studies show that Eustachian tube
dysfunction is rather a predisposing factor than being the only and main etiological
factor [21]. Healthy middle ear is free of bacteria or viruses [22]; in contrast with
this, OME is not a sterile inammatory process. Conventional microscopy and
much more sensitive PCR studies have shown that bacteria possibly originating
from the nasopharynx are present in the middle ear cavity. Streptococcus pneu-
moniae, Haemophilus inuenza, and Moraxella catarrhalis, which are notably
abundant in the adenoids [23] and are the main pathogens in the etiology of AOM
and acute bacterial sinusitis, are also among the most commonly observed pathogens in OME [24, 25]. In pathogen reservoir hypothesis, adenoid tissue of the upper
respiratory tract serves as a bacterial source initiating infection in the middle ear
cavity in susceptible individuals [26]. These pathogens are thought to be involved in
the biolm layer formation in the middle ear [27, 28]. These bacteria, which need
less oxygen and nutrients and reach the appropriate pH by embedding into the biolm layer, are also protected from host phagocytes, antibodies, and systemic antibiotics by the extracellular matrix in the biolm [29, 30]. The infection becomes

350
A. Y. Gunduz et al.
chronic due to these bacteria that persist in the biolm layer. With novel genetic
sequencing techniques, the polymicrobiality of the disease process has been validated and become a well-known fact; moreover, it has been found that these bacteria
that dominate and persist in the middle ear effusion actually are not identical to the
bacteriome of adenoids [31]. Beyond the three common species of the upper respiratory tract mentioned above, Alloicoccus otitis, which is specic to the middle ear,
is found to be the most abundant bacterium in the middle ear uid of OME patients
[31–34]. These most recent ndings reveal the importance of middle ear’s own
microenvironment as well as the importance of adenoid microbiome in the formation of OME, thus the need for further studies to investigate the possible pathophysiological processes besides the pathogen reservoir theory [31, 32, 35].
It is thought that some other factors may also be effective in the development of
OME.Pepsin and Helicobacter pylori, a microaerophilic bacterium that nds the
appropriate pH in the middle ear biolm for its survival, found in the studies performed on middle ear effusion samples suggested that gastroesophageal reux may
have a role in the etiology of OME [36, 37]. However, studies have not yet shown
that a direct cause–effect relationship exists [38, 39]. It has been suggested several
times that there may be a relationship between allergic airway diseases and OME
[40–44], but again, a clear cause–effect relationship has not been demonstrated, and
anti-allergic treatment was shown to have no effect on the OME disease process
[45]. Allergy screening is recommended in OME patients only in the presence of
atopic symptoms suggestive of allergic rhinitis or asthma [46]. Besides all these, the
presence of middle ear effusion should be investigated in children with turbinate
hypertrophy, allergic rhinitis, or asthma in order not to miss and have a delay in the
diagnosis of OME [47].
17.5 Diagnosis
17.5.1 Clinical Evaluation
Most OME patients are diagnosed clinically. Hearing loss is the main symptom of
middle ear effusion. The anamnesis given by the parent is extremely important to
suspect a hearing loss and the presence of OME in children. The most commonly
stated complaints are not responding when called out and watching TV or videos on
tablet/phone with the volume turned up high. It is also very valuable and should not
be overlooked when the parents share their observations on their child such as a
drop in school success, deterioration in friendship relations and social behavior,
arising behavioral problems such as irritability and restlessness, and emerging sleep
problems [48, 49].
A clinical diagnosis is made with an ear examination performed after the anamnesis that arouses suspicion of OME.The presence of dullness, opacity, air-uid
level, air bubbles, or retraction pockets in the tympanic membrane in otoscopic
examination conrms the clinical diagnosis (Figs.17.1 and 17.2). Pneumatic otoscope is the main examination tool recommended to be used in the diagnosis of

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17 Otitis Media withEusion
Fig. 17.1 Image of a right (a) and the left (b) tympanic membrane of a 5-year-old child with
OME.The right tympanic membrane has the typical opaque appearance of OME, and an image of
a concomitant bullous myringitis can be seen. The left tympanic membrane has lost its translucency and looks dull due to the uid behind the membrane
351
Fig. 17.2 Preoperative image of the right (a) and the left (b) tympanic membrane of a 6-year-old
child with adhesive otitis. Air bubbles within the uid are visible through the tympanic membrane
OME, as it also provides the ability to evaluate the tympanic membrane movement
against pressure changes. Diagnosis of chronic OME is made when the same ndings persist at the end of 3months. Endoscopic or microscopic tympanic membrane
examinations could also be performed as alternative methods.
Nasal endoscopy and nasopharyngeal examination should especially be performed
in adults in the presence of unilateral OME.It should be kept in mind that a possible
nasopharyngeal mass or tumor may present only with OME in the early period. In
children, however, nasal endoscopy is not routinely required if the child does not have

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a nasal complaint. As will be discussed further in this chapter, in most of the cases,
adenoidectomy will be included in the treatment protocol whether there is a hypertrophy or not. When there is an accompanying complaint of nasal congestion or in the
presence of resistant OME, nasal endoscopic examination should be performed, and
the nasopharynx should be viewed for the diagnosis of a possible obstructive adenoid
vegetation as well as for the differential diagnosis of the other etiologies of nasal congestion such as turbinate hypertrophy or nasal septal deviation [50–52].
Recognizing craniofacial malformations is important as they predispose to resistant or recurrent OME [53]. In the absence of apparent phenotypic anomalies, a
careful oropharyngeal and oral cavity examination should be performed to determine whether there is an accompanying nding of a palatal defect, such as a bid
uvula, submucous cleft palate, or incomplete cleft palate. In the presence of these
palatal disorders in which resistant and recurrent OMEs can be seen, if there is a
presence of concomitant adenoid vegetation, extreme caution should be exercised
during adenoidectomy surgery due to the risk of velopharyngeal insufciency.
17.5.2 Audiological Workup andHearing Evaluation
Tympanometry testing is the gold standard investigation to conrm the diagnosis in
the presence of clinical OME.In the tympanometry test that assesses the mobility
of tympanic membrane, Type B tympanogram indicating a static tympanic compliance is the typical response and the curve with the highest specicity for OME [54,
55] (Fig.17.3).
Fig. 17.3 Preoperative
tympanogram of a
4-year-old child diagnosed
with bilateral chronic
OME.This is a Type B
tympanogram of both ears
with the at lines on the
graph indicating very
limited or no compliance
of the tympanic membrane
due to the uid
accumulated in the cavity
behind it and blocks its
movement

17 Otitis Media withEusion
353
As OME is most commonly seen in children during the language development
period, it is important to determine the degree of hearing loss after the diagnosis
before any treatment intervention. Tonal audiometry and speech audiometry with
measurement of air and bone conduction thresholds are the audiometric tests ideally recommended to be performed (Fig.17.4). Half of the children with OME
have hearing loss greater than 20dB, and one-fth of them have hearing loss
greater than 35dB between 500 and 4000Hz [56]. In cases which are left without
any treatment for a long time and there is a moderate or severe hearing loss of
more than 45–50dB, it should be considered that the inner ear also starts to get
affected and damaged. It should also be noted that the degree of hearing loss may
be higher in children with OME and craniofacial anomalies compared to their
normal peers with OME [13].
It is recommended to obtain auditory brainstem response or auditory steady-state
response recordings before any intervention, particularly in cases where audiometric tests cannot be performed due to patient incompatibility especially in very young
age or when very high free-eld thresholds are obtained [57].
Fig. 17.4 Preoperative
pure-tone audiogram of the
same 4-year-old child,
whose tympanogram was
shown in Fig.17.3,
diagnosed with bilateral
chronic OME.In both right
and left ears, air–bone gaps
can be noted clearly along
with the normal bone
conduction thresholds.
Pure-tone averages
between 500 and 4000Hz
show that the child had
mild conductive hearing
loss in his left ear, whereas
he had moderate
conductive hearing loss in
his right ear before the
intervention

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A. Y. Gunduz et al.
17.6 Treatment
17.6.1 Medical Treatment
Various maneuvers developed to mechanically resolve Eustachian tube dysfunction,
and negative middle ear pressure should be included as the rst-line treatment.
Toynbee and Valsalva maneuvers, which do not need any equipment, are selfadministered maneuvers instructed to the patient. In Toynbee maneuver, the patient
swallows after pinching his or her nose. In Valsalva maneuver, a deep breath is
taken, the nose is pinched again, and a strong expiration is performed while the
mouth is closed. Even 1week of successful Valsalva maneuver has been shown to
lead to signicant improvements in hearing [58]. Both maneuvers provide similar
improvements in middle ear pressures [59], are of very low cost, and have no side
effects. Therefore, they are recommended to be used either alone or as an adjunct to
medication treatment.
Intranasal corticosteroids are agents that suppress the local inammation in the
Eustachian tube and the middle ear. These molecules also help restore normal function in these anatomic regions by decreasing the viscosity of the middle ear effusion
uid, increasing the secretion of surfactant, and reducing the volume of lymphoid
tissue at the orice of Eustachian tube [60]. As topical steroids have short-term
benets in the resolution of effusion and OME symptoms, they may be preferred for
having early symptomatic relief [61]. Having no benets on OME in the long term,
topical steroids should only be included as an essential part of treatment in atopic
children [62]. Oral steroids do not have a place in the treatment of OME, as they
have not been shown to provide a signicant gain on hearing, besides having systemic side effects which is the most important handicap of using these medications [63].
Mucolytic agents indirectly alleviate inammation by decreasing mucus production and increasing excretion of secreted mucus. With these effects, they can provide relief in OME symptoms in the short term and can even omit the need for
ventilation tube (VT) insertion surgery in one out of every 5 children [64]. However,
since studies on mucolytics have not been able to clearly demonstrate their benets
in terms of cost-effectiveness, these agents are not recommended in the treatment of
OME in international guidelines [65].
Due to the fact that OME is a nonsterile inammatory process, oral antibiotherapy has occasionally been prescribed, especially more commonly by nonotorhinolaryngology specialists [66, 67]. However, none of these antibiotic drugs
given for varying durations have a benet on OME symptoms, hearing loss, or VT
application rates in the long term [68]. Middle ear effusion regressed in only 10% of
children who received antibiotics, whereas spontaneous resolution can be seen at
similar or even higher rates in patients who do not receive antibiotics [69]. The ineffectiveness of antibiotics is due to the sheltering effect of the biolm layer on the
pathogenic bacteria, as discussed before [29, 30, 70]. Therefore, the use of agents
from any antibiotic class is not recommended in the treatment of OME in international guidelines [65]. Macrolide group antibiotics can be preferred in the treatment

17 Otitis Media withEusion
355
of rhinosinusitis with accompanying OME due to their anti-inammatory effects in
addition to their antimicrobial effects [71].
It should be known that the use of antihistamines or decongestants in oral or
nasal form does not make a clinical contribution in OME treatment, and in addition,
side effects related to these drugs can be seen at a substantial rate [72]. However, in
the presence of concomitant atopy or upper respiratory tract infection, these agents
should be included in the prescription as the part of treatment protocols of these
conditions.
As argued above, there is no specic medical treatment for OME, and both
American and European guidelines recommend surgical treatment for chronic
OMEs that persist after a 3-month watchful waiting period [7, 73].
17.6.2 Surgical Treatment
In management of persistent OME, key treatment according to the global guidelines
is VT (or also referred to as tympanostomy tube) insertion [65]. VT insertion is an
effective treatment both in OMEs that have begun to develop tympanic membrane
damage and in OMEs that have caused hearing loss and thus affected the quality of
life. VT insertion is indicated in cases when atrophy or retraction of the tympanic
membrane starts to emerge when there is an objective hearing loss between 25 and
40dB on audiometry, or when the quality of life is affected for that individual in
milder hearing losses [74]. Signicant improvements are seen in hearing and quality
of life during the rst 9months after VT insertion [2, 7, 10, 75]. The long-term
benecial effect of VT insertion on language development has not been clearly
demonstrated yet [76]. However, rapid surgical treatment is recommended in order
not to allow the possible devastating effect of additional hearing loss in children
who are in the risk group for speech or learning disorders (children with autism
spectrum disorder, developmental dysphasia or speech delay, perception deafness,
craniofacial malformations, cleft palate) [77].
Ventilation tubes placed in the tympanic membrane allow the passage of air from
the external auditory canal to the middle ear cavity which cannot be ventilated via
the Eustachian tube, thus allowing the middle ear pressure to equalize with atmospheric pressure. There are several different types of VTs used in the surgical treatment of OME.Shepard-style grommet tubes that are generally used in Europe and
Asia stay in place for around 6months (Figs. 17.5, 17.6, 17.7, and 17.8), while
Armstrong-style grommet tubes that are more commonly used in America have beveled inner anges providing a relatively long lifetime of up to 1 and a half year [77].
Paparella-type grommet tubes are silicone tubes with a notched inner ange to aid
the insertion. Type I Paparella tube has a small inner ange as of Shepard style
grommet, which are both short-term tubes thus showing similar clinical features.
Type II Paparella tube, however, has a wider inner ange which makes it a longlasting tube [78, 79]. Apart from grommet tubes, there are also T-tubes for permanent middle ear aeration that stay in place for a much longer time and are not
expected to exhibit a spontaneous fall out into the external ear canal [80] (Fig.17.9).

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Fig. 17.5 Postoperative
follow-up view of a
13-year-old 1week after a
Shepard style grommet
tube insertion to a
tympanic membrane with a
large retraction pocket
A. Y. Gunduz et al.
Fig. 17.6 Postoperative images of a 5-year-old child at 1year follow-up of VT insertion surgery.
The Shepard-style grommet tube stays in place in the right ear (a), whereas the tube is expelled into
the external ear canal in the left ear (b). Note the healthy appearance of both tympanic membranes
Grommet tubes, which are expected to fall off between 6 and 18months, are preferred in the rst line in primary OME surgery. Since grommet tubes are short-term
VTs, except Type II Paparella tubes, their complication rates are also relatively low
[81]. Although complication rates are higher, T-tubes that are long-term tubes that
remain in place for more than 2 years are indicated in patients with chronic
Eustachian tube dysfunction and patients with resistant or recurrent OME who have
not beneted from a grommet tube.
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