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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

368
landscapes. The total number of new episodes of CSOM per year is estimated to be
31 million, of which 22% occur in children under 5years of age [4].
The prevalence of CSOM varies signicantly by region, with rates ranging from
as low as 0.3% to as high as 14% in the surveyed populations [3]. Factors contributing to this variability include suboptimal hygiene practices, poor nutrition, limited
healthcare access, and certain societal behaviors, which may account for its
increased incidence in populations with lower socioeconomic status. Additionally,
lifestyle and health-related factors such as smoking, recurrent or chronic upper
respiratory infections, genetic predispositions, and compromised immune systems
have been identied as factors that heighten the risk of developing CSOM.
M. İ. Şahin et al.
18.3 Pathophysiology
CSOM is typically a sequela of a single or repeated episodes of AOM.The factors disrupting the recovery from an AOM episode or causing recurrent AOM episodes lead to
persistent infection and inammation of the middle ear mucosa and eardrum. The
enzymes and toxins produced by the bacteria, along with the body’s immune response
to the infection result with tissue damage and breakdown of the protective epithelial
layer. The ongoing battle between the immune system and bacteria leads to the formation of highly vascular granulation tissue in the middle ear which cause further discharge.
Among the factors causing chronic inammation of the middle ear mucosa and
eardrum, the dysfunction of Eustachian tube (ET) is the most prominent one. When
ET doesn’t function well, the middle ear is not ventilated, and the secretions are not
drained properly. Such a condition potentially causes the collapse of the normal balance of commensal bacteria of the middle ear and possibly predispose the pathogen
bacteria to create biolm on the surface of the middle ear leading to persistent discharge. Tissue damage caused by the chronic inammatory status involves eardrum
and ossicles, which eventually results with hearing loss.
The dysfunction of ET is particularly evident in early childhood due to it’s immature physiological state. Furthermore, developing immune system is another factor
causing recurrent and persistent infections in the middle ear of the children.
Additionally, a range of familial and environmental risk factors including allergic rhinitis, exposure to tobacco smoke within the home, inadequate breastfeeding, residing
in a large family or an overcrowded nursery, and frequent upper respiratory tract
infections contribute to the risk. The pathogenesis of CSOM, therefore, is a multifaceted process inuenced by the complex interplay of these various factors [5, 6].
18.4 Microbiology
The patients having CSOM suffer from infectious episodes with ear discharge
which leads to repeating doctor visits and antibiotic use either topical or systemic.
Although ampiric antibiotic use is the rst choice of physicians, swab culture is
used for the patients who do not respond ampiric antibiotic therapy. The most

18 Chronic Suppurative Otitis Media
369
commonly isolated microorganisms are Staphylococcus aureus and Pseudomonas
aeruginosa in CSOM.Methicillin-resistant S. aureus (MRSA) and anaerobic organisms such as Peptostreptococcus, Fusobacterium spp., Porphyromonas spp.,
Prevotella, Proteus species, Klebsiella pneumoniae, and diphtheroids are also iso-
lated in some cases [1, 2, 7–13].
Nevertheless, the knowledge on the microbiology of CSOM and healthy middle
ear has been based on conventional culture techniques for a long time. Healthy
middle ear has been assumed as a “sterile space” according to those techniques [14].
Standing on this assumption, infectious episodes in CSOM patients are thought to
occur due to the entrance of bacteria ascending from the nasopharynx via the ET or
invading from the ear canal through a perforation of the tympanic membrane [15].
However, persistent infections were explained by some theories such as antibiotic
resistance or toxin production of bacteria, as well as biolm formation [2, 9, 16].
Recently, molecular-based studies indicated that middle ear is not sterile [17–19].
The Proteobacteria is the dominant phylum, and Novosphingobium, Staphylococcus,
Streptococcus, Escherichia-Shigella, and Burkholderia are the dominant bacterial
families in the normal mucosa of the middle ear in both children and adults, where
the bacterial loads are low though [2, 12]. Surprisingly, Staphylococcus, Pseudomonas,
Streptococcus, and Moraxella, which have been acknowledged as the pathogens in
CSOM, were also detected among healthy middle ears [2]. Furthermore, the microbiomes of the middle ears of non-suppurative chronic otitis media are very similar to
the healthy middle ears [12]. However, the microbiome of CSOM consists of a broad
range of bacteria and the dominant phyla found to be Firmicutes, Actinobacteria, and
Proteobacteria, including Staphylococcus, Corynebacterium, Anaerococcus, and
Raoultella genera. The most prominent ndings of those studies indicate that
Proteobacteria phylum bacteria have lower incidences and Firmicutes phylum bacteria have higher incidences in CSOM than healthy middle ear [2, 12]. In a study of
patients with tympanosclerosis or cholesteatoma using sequence analysis of the gene
responsible for transcription of 16 ribosomal RNA (rRNA) and next-generation
sequencing, the presence of bacterial genomes was reported as Alloiococcus otitis,
Staphylococcus aureus, Achromobacter xylosoxidans, Escherichia coli,
Staphylococcus sciuri, Staphylococcus caprae, Parvimonas spp., Bacillus sp.,
Clostridiales, Staphylococcaceae, Peptoniphilaceae, and Turicella otitidis [20].
From the aforementioned ndings, it becomes clear that the persistent infection
within the middle ear and mastoid arises from a disruption of the normal balance of
commensal bacteria of the middle ear and mastoid, as opposed to bacterial invasion
into sterile regions.
18.5 Histopathology
AOM is typically limited to the mucosal lining unless it leads to a complication.
Inammatory blood cells inltrate the mucosa, which cause edema and hemorrhage. According to the ndings of animal studies, goblet cell density in the middle
ear mucosa increases in 2weeks [21]. The progression to CSOM is characterized by

370
M. İ. Şahin et al.
the formation of mucosal ulcerations and granulation tissue. Mucosal thickening
causes polyp formation, additonally brous adhesions arise in the following weeks
when the infection persists [21]. Over time, persistent otorrhea and mucosal alterations drive a refractory mucoperiosteal disease and osteitis. Osteoresorption leads to
erosion of the temporal bone and ossicles in the advanced stages of the condition
and followed by massive osteoneogenesis [3, 21, 22].
Granulation tissue, ossicular erosions and/or ankylosis, tympanosclerosis, tympanic membrane perforation, cholesterol granuloma, and cholesteatoma are the pathologic ndings most frequently encountered within the temporal bones of CSOM
patients. Ossicular erosion rate in CSOM cases has been reported as 31.8% [23].
18.6 Clinical Manifestations
The main symptoms of the patients having CSOM suffer from ear discharge and
hearing loss. Upper respiratory infections or immersion of the middle ear in water
during activities such as swimming or bathing may precipitate episodes of ear discharge. These episodes’ frequency and severity can vary widely among individuals.
Some patients may require medical treatment roughly once per month, while others
may only need it a few times per year. The duration, frequency, and features of the
discharge correlate with histopathologic changes in the ME and mastoid. It may be
continuous or intermittent, may persist for several months to many years, and
mucoid or mucopurulent in feature. Medical treatment helps alleviating the infection and inammation, consequently, stops the ear discharge in most of the cases.
However, the inammation may not respond to the medical treatment in some cases.
Major risk factors for persistent inammation have found to be rural residence,
bilateral CSOM, and being infected by multidrug-resistant bacteria [24]. Resistant
inammation leads to continuous discharge and associated with the increased risk
of complications.
Patients with CSOM typically experience mild to moderate conductive hearing
loss. The severity of the conductive hearing loss depends on the size and localization of eardrum, as well as the pathologies affecting the continuity and mobility of
the ossicles. The ossicles remain intact in many cases. However, erosion of the
ossicles, particularly the long arm of incus and the stapes superstructure, which are
more susceptible to damage, worsen the hearing loss. Erosions may occur due the
damaging effect of cholesteatoma or and the chronic inammatory process that
leads to osteitis. Besides the erosions, the pathologies, such as tympanosclerosis,
granulation tissue, brosis, and adhesions restrict the mobility of the ossicles and
diminish their ability to transmit sound efciently into the inner ear [25, 26].
Additionally, a signicant proportion of patients may suffer from severe or profound hearing loss due to sensorineural involvement.
The consequences of hearing loss include impaired language development in
affected children, hindered academic success in school-aged children and teenagers,
and diminished communication skills across all ages. Collectively, these issues signicantly lower the quality of life for those impacted. Furthermore, CSOM is associated with the risk of serious complications, potentially leading to persistent health
issues and, in severe cases, fatality.

18 Chronic Suppurative Otitis Media
The clinical course of the patients is highly depended on the types of the
CSOM.According to the commonly accepted classication, there are two types: 1.
tubotympanic and 2 atticoantral.
371
18.6.1 Tubotympanic Type
This type of CSOM is relatively safer, and its clinical course is benign. It is characterized by centrally localized perforation, which is limited to the pars tensa of the
tympanic membrane. The pathology typically involves the anteroinferior region and
do not exceed to the mastoid region.
The ear discharge may be profuse, purulent or mucous, and odorless. The degree
of the hearing loss varies. It is uncommon to see serious complications in this type
of CSOM.
18.6.2 Atticoantral Type
This is the unsafe and potentially dangerous type of CSOM, characterized by attic
or marginal perforations, involving the pars tensa of tympanic membrane and the
posterosuperior region including the mastoid bone.
The ear discharge may be malodorous. The degree of the hearing loss varies.
Existence of cholesteatoma, which erodes bones, is very typical in this type of
CSOM. Therefore, the patients having atticoantral CSOM are prone for serious
complications.
18.7 Diagnosis
18.7.1 Anamnesis
Obtaining a thorough patient history is the rst and most crucial step in the diagnostic
process. At least one of the abovementioned symptoms, namely ear discharge and hearing loss, should be existing for minimum 3months. Most of the cases have a medical
history of doctor visits due to recurrent ear infections either in childhood or later. Also,
history of having upper airway allergies, recurrent infections, and surgeries, such as
adenoidectomy, tonsillectomy, and nasal surgeries are common. The cases having congential maxillofacial anomalies are also candidates for the diagnosis of CSOM.
18.7.2 Otoscopic Examination
Examination of the ear should at least be performed with a conventional otoscope.
Better than that, an otoendoscope or a microscope will exhibit more detailed information about the eardrum and middle ear as well as the pathologies within those.
Serumen and secretions in the ear canal should be cleaned well to make sure that the
eardrum is visualized entirely. If there is discharge from the middle ear through a

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M. İ. Şahin et al.
tympanic membrane perforation, together with the anamnesis, it is the most important sign of CSOM.Suctioning of the discharge as much as possible will facilitate
demonstrating the pathologies within the middle ear. However, interventions should
be performed carefully that bleeding caused by those interventions will make the
examination very difcult.
The size and localization of the tympanic membrane perforations should be
noted. The retractions of the tympanic membrane, particularly those localized in
pars accida and contain keratin debris, should alert the physician for the potential
existence of a cholesteatoma (Fig.18.1a). The sclerosis of the tympanic membrane
and middle ear mucosa is also important sign of chronic inammation for long term
(Fig.18.1b).
cThe existence of moisture, edema, polyps, and granulation tissue in the middle
ear are the other signs of CSOM in otoscopic examination (Fig.18.1c).
a
b
c
Fig. 18.1 Various appearances of the tympanic membrane in CSOM. (a) Perforation of the tym-
panic membrane localized in pars accida containing keratin debris (cholesteatoma). (b) Central
perforation and sclerosis of the tympanic membrane. (c) Central perforation of the tympanic membrane, also moisture, edema, and granulation tissue in the middle ear

18 Chronic Suppurative Otitis Media
373
18.7.3 Audiological Evaluation
Tuning fork tests, namely Weber and Rinne, are practical and informative tests in
the initial evaluation of the patients. Weber indicates lateralization of the sound to
the ear with conductive hearing loss when the opposite ear is normal. If there is
bilateral CSOM, patient will hear the sound of the tuning fork from the worse hearing ear. The expected result of the Rinne test is negative in the ears with conductive
hearing loss.
Pure tone audiometry is also needed for the evaluation of the hearing function in
elder kids and adults. The type and the degree of the hearing loss will support the
diagnosis and lead the selection of the treatment options. Mild to moderate conductive hearing loss is common in CSOM patients. However, severe to profound mix
type hearing loss may be detected in patients having chronic inammation for long
term. Furthermore, total sensorineural hearing loss indicates a complication or a
sequele of CSOM.
Auditory brainstem response (ABR) test may be prefered in young children for
the hearing evaluation, if cooperation to the behavioral audiometry cannot be
obtained. When performing ABR test, bone conduction stimuli besides the air conduction stimuli should be used in CSOM patients to make sure that the type of the
hearing loss is conductive or mix in CSOM patients.
18.7.4 Imaging
Historically, Schüller’s plain radiography had been used to image the mastoid
part of the temporal bone. Nowadays, first choice of imaging CSOM patients is
high-resolution computerized tomography (CT) of the temporal bone
(Fig.18.2).
Pneumotization of the mastoid bone is usually diminished in the ears with
CSOM.The duration of the inammation is correlated with the diminishing. The
patients having CSOM starting from early childhood have sclerotic mastoid bone
with very low or no pneumotization. CT is superior for the evaluation of the bony
structures; therefore, besides the mastoid cellules, ear canal, ossicles, labyrinth,
and fallopian canal are demonstrated well with CT.The erosions caused by cholesteatoma as well as sclerosis and osteolysis are well observed with CT.However,
CT is not good at distinguishing pathologic soft tissue, such has edematous
mucosa, granulation tissue, brosis, and cholesteatoma within the middle ear and
mastoid bone [27]. Magnetic resonance imaging (MRI) is the best option of
imaging for the differentiation of the soft tissue, if needed. Non-echoplanar diffusion weighted magnetic resonance imaging (non-EPI DWI MRI) has a high
sensitivity (91%) and specicity (92%) in detecting cholesteatoma [28]. This
technique is capable of detecting cholesteatomas as small as 2mm, which makes
it very suitable for the follow up of the operated patients under risk of cholesteatoma recurrence [29].

374
Fig. 18.2 Computerized
tomography (CT) images
of the temporal bone. (a)
Pneumotization of the
mastoid bone is diminished
in the right side, left
mastoid is wellpneumatized. (b)
Pneumotization of the
mastoid bone is diminished
in both sides, bone erosion
appears in the left side
(cholesteatoma)
a
M. İ. Şahin et al.
b
18.8 Treatment
CSOM carries potential risks of serious complications, some of which may be mortal. If there is an infection and discharge in the middle ear, rst step of the management is to control the infection and dry the middle ear. Controling the infection by
a medical treatment is needed not only for increasing the life quality of the patient
but also avoiding from complications.
18.8.1 Medical Treatment
The initial treatment for acute episodes of CSOM should be the topical use of antibiotics. The mostly preferred antibiotics are uoroquinolones, such as ciprooxacin
and ooxacin [3, 30]. One or two weeks of use is adequate in most of the cases.
However, the efcacy of the long-term treatment is unknown regarding the protection of the ear from recurrent infections [31]. In addition to the antibiotic ear drops,
topical steroids are commonly used to alleviate the inammation within the middle
ear. However, evidence of low certainty suggests that certain topical antibiotics
alone may be more effective than combinations of topical antibiotics with steroids
at resolving discharge [30]. Also, some magistral antiseptic ear drops, such as Boric
acid, Burow’s, and Castellani’s solutions, are used as alternatives for the topical
treatment of ear discharge in CSOM patients [32–34]. However, antibiotic ear drops
seem to be more effective than topical antiseptics in resolving the discharge [35].
An important point to emphasize is the potential ototoxicity risk of topical ear
drops when the eardrum is perforated. Aminoglycosides, known for their ototoxicity, are contraindicated for topical use in these patients. Conversely, quinolones are
deemed safe and are the only antimicrobials approved by the United States Food

18 Chronic Suppurative Otitis Media
375
and Drug Administration (FDA) for topical use on a non-intact tympanic membrane
[36, 37]. Although data on the ototoxic potential of common antiseptics like boric
acid and acetic acid are limited and inconclusive, it is prudent to avoid those in the
treatment of CSOM when possible. Despite several reports on the ototoxic potential
of antiseptic ear drops, the applicability of animal studies to human ototoxicity must
be carefully considered due to signicant anatomical and physiological differences [37].
Current evidence does not strongly support the use of systemic antibiotics for the
treatment of discharge in CSOM, as their effectiveness and side effects remain
poorly understood, with little indication that they improve outcomes when used
alongside topical treatments [38]. However, systemic use of antibiotics is suggested
in complicated CSOM.
18.8.2 Surgical Treatment
This topic will be discussed in another chapter of this book.
18.9 Complications
CSOM may cause complications when the infection spreads out of the air-lled
cavities of the temporal bone, namely the middle ear and mastoid cells. Existence of
a cholesteatoma increases the risk of the occurance of the complications [39].
Studies indicate that the occurrence rates of complications vary between 0.69% to
0.78% in developing countries [40, 41]. However, these rates are estimated to be
much lower in high-income countries.
The complications of CSOM are classified as intratemporal and exratemporal. Intratemporal complications include mastoiditis, facial paralysis, labyrinthitis, labyrinthine fistula, and petrositis. The presence of bone erosions makes
these patients particularly susceptible to complications such as facial palsy and
labyrinthine fistula. In one study, the rate of facial canal dehiscence detected in
CSOM cases that underwent canal wall down mastoidectomy was reported to
be 11.29% [42]. Those complications lead to significant morbidities and
sequelas.
Most of the extratemporal complications are intracranial, such as meningitis,
epidural, subdural, and brain abscess, lateral sinus thrombosis, and otitic hydrosephalus. Those complications are lifethreatening, and most of the deaths are caused by
particularly brain abscess. Despite the proper management including antibiotic
usage and surgical techniques, the mortality rate associated with intracranial complications is reported to be 8% [43]. Therefore, the patients with intracranial complications should be managed by a multidisciplinary team including otolaryngologists
and neurosurgeons. Very rarely, extracranial extratemporal complications, such as
Benzold’s abscess and Zygomatic abscess may occur due to CSOM.

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M. İ. Şahin et al.
18.10 Future Directions
Developments in diagnostic and therapeutic tools, as well as surgical techniques in
medicine, have signicant potential to improve the management of chronic suppurative otitis media (CSOM). Firstly, one of the challenges in diagnosing CSOM is
differentiating between ears with and without cholesteatoma. Recent advancements
in imaging technologies, particularly CT and MRI, have already facilitated the diagnosis of primary and recurrent cholesteatoma. However, these techniques still
require further improvement. Eroglu at al [44]. reported that articial intelligence
(AI) modeling can accurately differentiate between CSOM with and without cholesteatoma using CT images, demonstrating similar reliability to MRI in diagnosing
cholesteatoma. It is likely that AI will play a signicant role in the diagnosis of
CSOM in the near future [45].
Currently, surgery is the only effective treatment for CSOM.Microscopic tympanoplasty and mastoidectomy have been performed successfully for decades, and
surgical techniques and tools continue to improve. The development of the transcanal endoscopic approach has reduced surgical morbidity and lowered the recurrence
rate of cholesteatoma. Clinicians and scientists are also working to develop nonsurgical treatment alternatives for CSOM.Previously, the application of sodium
2-mercaptoethanesulfonate (MESNA) alongside surgical dissection has been shown
to reduce cholesteatoma recurrence in humans [46, 47] Subsequent studies have
suggested that MESNA application in cholesteatoma surgery is an effective and safe
supportive tool during surgical treatment [48]. Experimental studies have reported
that the use of MESNA is safe for important structures such as the facial nerve [49]
and may prevent cholesteatoma formation [50]. Furthermore, recent research has
shown that controlling histone modication through intratympanic injections of the
menin-MLL inhibitor (MI503) has promise as a potential therapeutic target for the
conservative treatment of cholesteatoma in animals [51]. It appears that non- surgical
treatment of cholesteatoma may become possible with the discovery of novel therapeutic targets to combat the growth and recurrence of cholesteatoma in the future.
18.11 Conclusion
Chronic suppurative otitis media (CSOM) remains a signicant health issue affecting millions globally. This persistent middle ear infection often arises from acute
otitis media, particularly in settings with poor hygiene and limited healthcare access.
The condition is marked by chronic ear discharge and varying degrees of hearing
loss, often due to ET dysfunction and a disrupted middle ear microbiome. Effective
management of CSOM requires thorough patient history, detailed otoscopic examinations, audiological assessments, and advanced imaging techniques like high-resolution CT and MRI.Treatment strategies primarily include topical antibiotics and,
when necessary, systemic antibiotics and surgical intervention. Recent advances in
diagnostic tools, such as AI and novel therapeutic approaches, offer promising
improvements in managing CSOM.Emphasizing preventive measures, addressing

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377
risk factors, and enhancing public health initiatives are crucial for reducing the incidence and complications of CSOM ultimately improving the quality of life for those
affected.
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