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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4534_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Contents
- •1.1.9 Laryngeal Atresia
- •1.1.10 Laryngeal Webs
- •1.1.11 Congenital Subglottic Stenosis
- •1.1.12 Laryngeal Cleft
- •1.1.13 Tracheoesophageal Fistula
- •1.1.14 Tracheal Bronchus
- •1.2.2 Mesenchyme Development
- •1.2.4 Lung Development
- •1.2.4.1 Embryonic Stage
- •1.2.4.2 Pseudoglandular Stage
- •1.1.1 Oral Cavity
- •1.1.2 Nasal Cavity
- •1.1.3 Palate
- •1.1.4 Primitive Pharynx
- •1.1.5 Upper Airway Anomalies
- •1.1.6 Cleft Lip/Palate
- •1.1.7 Choanal Atresia
- •1.1.8 Laryngomalacia
- •1.2.4.3 Canalicular Stage
- •1.2.4.4 Saccular Stage
- •1.2.4.5 Alveolar Stage
- •1.2.5 Congenital Respiratory System Defects
- •1.2.5.1 Tracheal Agenesis
- •1.2.5.2 Congenital Tracheal Stenosis
- •1.2.5.3 Lung Agenesis
- •1.2.5.4 Lung Hypoplasia
- •References
- •2.1 Introduction
- •2.2 Nasal Cavity
- •2.2.1 Vestibule
- •2.2.2 Respiratory Mucosa
- •2.2.3 Olfactory Mucosa
- •Supporting Cells
- •Basal Cell
- •Olfactory Receptor Cell (Bipolar Neuron)
- •Brush Cell (Microvillar Cell)
- •2.2.3.2 The Lamina Propria
- •2.2.3.3 Olfactory Glands (Bowman’s Glands)
- •2.3 Paranasal Sinuses
- •2.4 Pharynx
- •2.5 Larynx
- •2.6 Trachea
- •2.6.1.1 Ciliated Columnar Cells
- •2.6.1.2 Goblet Cells
- •2.6.1.3 Brush Cells
- •2.6.1.4 Basal Cells
- •2.6.1.5 Enteroendocrine System Cells (Kulchitsky Cells or DNES Cells)
- •2.6.2 Lamina Propria
- •2.7 Lungs
- •2.7.1 Pleura
- •2.7.2 Bronchi
- •2.7.3 Bronchioles
- •2.7.3.1 Terminal Bronchioles
- •2.7.3.2 Respiratory Bronchioles
- •2.7.4 Ductus Alveolaris
- •2.7.5 Alveoli
- •2.7.5.2 Type II Alveolar Cell (Septal Cell, Large Alveolar Cell)
- •References
- •3.1.1.3 Nerves
- •Ophthalmic Division
- •Maxillary Division
- •Parasympathetic Nerve Supply
- •3.1.1.4 Bony Anatomy
- •3.1.1.5 Cartilaginous Pyramid
- •3.1.1.6 Structure
- •External Nasal Anatomy
- •Internal Nasal Anatomy
- •3.1.2 Nasal Physiology
- •3.1.2.1 Nasal Airflow
- •3.1.2.2 Abnormal Nasal Physiology
- •3.2.1 Larynx Anatomy
- •Cricoid Cartilage
- •Thyroid Cartilage
- •Epiglottis
- •Arytenoid Cartilages
- •Corniculate Cartilages
- •Cuneiform Cartilages
- •Extrinsic Ligaments
- •Intrinsic Ligaments
- •Laryngeal Cavity
- •Piriform Recesses
- •Cricothyroid Muscles
- •Posterior Cricoarytenoid Muscles
- •Lateral Cricoarytenoid Muscles
- •Transverse Arytenoid Muscle
- •Thyroarytenoid Muscles
- •Superior Laryngeal Nerve
- •Arteries
- •Veins
- •Lymphatics
- •Swallowing
- •Respiration
- •Phonation
- •3.2.2.1 Reflex Glottic Closure
- •References
- •4.1 Introduction
- •4.2.1 Choanal Atresia
- •4.2.2 Pyriform Aperture Stenosis
- •4.2.3 Cleft Lip Nasal Deformity
- •4.2.4 Nasolacrimal Duct Cysts
- •4.2.5 Encephaloceles
- •4.3 Craniofacial Anomalies
- •4.3.1 Pierre Robin Syndrome
- •4.3.2 Treacher-Collins Syndrome
- •4.3.3 Crouzon Syndrome
- •4.3.4 Down Syndrome
- •4.3.5 Apert Syndrome
- •4.4.1 Thyroglossal Duct Cyst
- •4.4.2 Laryngomalacia
- •4.4.3 Vocal Fold Paralysis
- •4.4.5 Subglottic Stenosis
- •4.4.6 Subglottic Hemangioma
- •4.4.7 Laryngeal Cysts
- •4.4.8 Laryngeal Cleft
- •4.5 Conclusion
- •References
- •5.1 Innate Immunity
- •5.2 Adaptive Immunity
- •References
- •6.1 Introduction
- •6.2 Innate Immunity
- •6.3 Adaptive Immunity
- •References
- •7.1 Introduction
- •References
- •8: Respiratory Microbiome
- •8.1 Introduction
- •8.2.1 Childhood Asthma
- •8.2.2 Asthma Exacerbation
- •8.3 Bacteriome
- •8.4 Virome
- •8.5 Mycobiome
- •References
- •9.1 Introduction
- •References
- •10.1 Introduction
- •10.3.3 The Appointment Process, Explained
- •10.3.5 Parental Involvement
- •10.4 Coordinating Care When Your Child Is Ill
- •10.4.3 Exhibit Cohesion
- •10.6 Conclusion
- •References
- •11.1 Introduction
- •11.2 Nasal Cavity
- •11.2.1 Choanal Atresia
- •11.2.2 Rhinosinusitis
- •11.2.4 Juvenile Nasopharyngeal Angiofibroma
- •11.3 Pharynx
- •11.4 Nasopharynx
- •11.4.1 Adenoid Hypertrophy
- •11.4.2 Nasopharyngeal Carcinoma
- •11.5 Oropharynx
- •11.5.1 Thyroglossal Duct Cyst
- •11.6 Hypopharynx
- •11.6.1 Retropharyngeal Abscess
- •11.6.2 Lymphatic Malformation
- •11.6.4 Lymphoma
- •11.6.5 Rhabdomyosarcoma
- •11.7 Larynx
- •11.7.1 Subglottic Stenosis
- •11.7.2 Laryngotracheal Papillomatozis
- •11.7.3 Croup
- •11.7.4 Epiglottitis
- •11.7.5 Foreign Body Aspiration
- •References
- •12.2.1 Plain Radiography
- •12.2.1.1 The Thymus
- •Tracheal Buckling
- •Hilum
- •Diaphragm
- •Mediastinal Borders
- •Lung Opacities
- •Cystic Lung Diseases
- •Pulmonary İnterstitial Emphysema (PIE)
- •Unilateral Hyperlucent Lung
- •12.2.2 Fluoroscopy
- •12.2.3 Ultrasound
- •12.2.4 Computed Tomography
- •12.2.5 Magnetic Resonance Imaging (MRI)
- •12.2.6 Angiography
- •12.2.7 Positron Emission Tomography (PET)
- •12.3 Conclusion
- •References
- •13.1 Introduction
- •13.2 Nasal Diagnostic Procedures
- •13.2.1 Indications
- •13.2.2 Contraindications
- •13.2.3 Anatomical Features
- •13.2.4 Technical Considerations
- •13.2.5 Technique
- •13.2.5.1 First Pass
- •13.2.5.2 Second Pass
- •13.2.5.3 Third Pass
- •13.3 Flexible Laryngoscopy
- •13.4 Direct Laryngoscopy
- •13.5 Video Laryngoscopy
- •13.5.1 Indications
- •13.5.2 Contraindications
- •13.5.3 Outcomes
- •13.5.4 Equipment
- •13.5.5 Approach Considerations
- •References
- •14.1 Upper Airways
- •14.2.3 Laryngeal Pathologıes
- •References
- •15.1 Introduction
- •15.2 Airway Measurements
- •References
- •16.1 Introduction
- •16.2 Background
- •References
- •17: Allergen Testing: Purpose, Procedure, Interpretation
- •17.1 Introduction
- •17.2 Tests
- •17.2.1 Skin Tests
- •17.2.3 Component Resolved Diagnosis (CRD)
- •17.2.4 Tryptase
- •17.2.5 Basophil Activation Test (BAT)
- •17.2.6 Provocation Tests
- •17.2.7 Nasal sIgE
- •17.2.8 Nasal Smear Eosinophilia
- •17.2.9 Eosinophilic Cationic Protein (ECP)
- •References
- •18: Smell Testing: Purpose, Procedure, Interpretation
- •18.1 Introduction
- •18.2 Possible Olfactory Disorder Diagnosis
- •18.2.1 Conductive Defects
- •18.2.3 Inherited Disorders
- •18.2.3.1 Hormonal Disturbances
- •18.4 Odor Threshold Tests
- •18.8.1 Butanol Threshold Test
- •18.8.1.1 The Penn State University Odor Identification Exam
- •18.8.2 Cross-Cultural Smell Identification Test
- •18.8.3 Sniffin’ Sticks
- •References
- •19: Taste Testing: Purpose, Procedure, Interpretation
- •19.1 Introduction
- •19.2 Definitions
- •19.2.1 Taste Dysfunction Abnormalities
- •19.4.1 Taste Dysfunction
- •19.4.2 COVID-19
- •19.5 Taste Disorder Diagnosis
- •19.6.2 Magnitude Matching
- •19.6.3 Spatial Test
- •References
- •20.1 Introduction
- •20.2 Primary Otalgia Causes
- •20.2.1 Auricle
- •20.2.1.1 Infections
- •20.2.1.2 Trauma
- •20.2.1.3 Allergic Angioedema
- •20.2.1.4 Thermal Damage
- •20.2.2 External Auditory Canal
- •20.2.2.1 Otitis Externa
- •20.2.2.2 Malignant Otitis Externa
- •20.2.2.3 Eczematous Dermatitis
- •20.2.2.4 Furunculosis
- •20.2.2.5 Foreign Body
- •20.2.2.6 Cerumen Impaction
- •20.2.2.7 Tumors
- •20.2.3 Middle Ear
- •20.2.3.1 Acute Otitis Media
- •20.2.3.3 Eustachian Tube Dysfunction
- •20.2.3.4 Cholesteatoma
- •20.2.3.5 Trauma
- •20.3 Secondary Otalgia Causes
- •20.3.1 Oropharyngeal Infections
- •20.3.2 Dental Causes
- •20.3.3 Auricular Lymphadenitis
- •20.3.4 Neck Abscess
- •20.3.5 Parotitis
- •20.3.6 Temporomandibular Joint Dysfunction
- •20.3.7 Sinusitis
- •20.4 Differential Diagnosis
- •References
- •21.1 Introduction
- •21.2 Bacterial Otitis Externa
- •21.3 Acute Otitis Media
- •21.4 Chronic Suppurative Otitis Media
- •21.5 Foreign Body
- •21.5.1 Cerumen
- •21.5.2 Tympanostomy Tube Drainage
- •21.5.3 Traumatic Cerebrospinal Fluid Otorrhea
- •21.5.5 Necrotizing Otitis Externa (Malignant External Otitis)
- •21.5.6 Neoplasms
- •21.5.7 Polyps
- •21.5.8 Otomycosis
- •21.5.9 First Branchial Cleft Cysts
- •21.5.10 Cholesteatoma
- •21.5.11 Spontaneous Cerebral Spinal Fluid Otorrhea
- •References
- •22.1 Introduction
- •22.4 Congenital Causes
- •22.4.1 Choanal Atresia
- •22.4.2 Pyriform Apertura Stenosis
- •22.4.3 Nasal Midline Congenital Masses
- •22.4.3.1 Nasal Dermoid Cyst
- •22.4.3.2 Nasal Glioma
- •22.4.3.3 Encephalocele (Encephalo-Meningocele)
- •Differential Diagnosis
- •22.4.3.4 Nasolacrimal Duct Cyst (Dacryocystocele)
- •22.5 Infectious Causes
- •22.5.1.1 Rhinitis Etiology
- •22.5.2 Neonatal Rhinitis
- •22.5.3 Bacterial or Viral Rhinitis
- •22.5.4 Iatrogenic Rhinitis
- •22.5.5 Infectious Rhinitis (Rhinosinusitis)
- •22.6 Adenoid Hypertrophy
- •22.7 Inflammatory Causes
- •22.7.1 Allergic Rhinitis
- •22.7.2 Nonallergic Rhinitis
- •22.7.3 Eosinophilic Nonallergic Rhinitis (NARES)
- •22.7.4 Nasal Polyp
- •22.7.5 Antrochoanal Polyp
- •22.7.6 Inferior Turbinate Hypertrophy
- •22.8 Neoplasia
- •22.8.1 Benign Tumors (Juvenile Nasopharyngeal Angiofibroma)
- •22.8.2 Malignant Tumors
- •22.9 Systemic Causes
- •22.9.1 Cystic Fibrosis
- •22.9.2 Primary Ciliary Dyskinesia
- •22.10 Trauma/Iatrogenic Causes
- •22.10.1 Nasal Trauma-Septal Hematoma
- •22.10.2 Septum Deviation
- •22.10.3 Nasal Foreign Bodies
- •References
- •23.1 Introduction
- •23.2 Pathophysiology
- •23.3 Allergic Rhinitis
- •23.4 Non-allergic Rhinitis
- •23.5 Infectious Rhinitis
- •23.6.1 Vasomotor Rhinitis
- •23.7 Evaluation
- •23.8 Diagnosis
- •23.9 Treatment
- •23.10 Prognosis
- •23.11 Conclusion
- •References
- •24.1 Introduction
- •24.2 Pathogenesis
- •24.3 Diagnosis
- •24.3.1 History
- •24.3.2 Examination
- •24.4 Differential Diagnoses
- •24.5 CSF Rhinorrhea
- •24.5.1 CSF Physiology
- •24.5.1.1 Pathogenesis
- •24.6 Diagnosis
- •24.6.1 Chemical Diagnosis
- •24.6.2 Imaging Diagnosis
- •24.7 Treatment
- •24.7.1 Surgical Technique
- •References
- •25.1 Introduction
- •25.1.1 Waldeyer Ring
- •25.3 Anatomy
- •25.3.1 Lymphatic Drainage
- •25.3.1.1 Nerve Supply
- •25.6 Tonsillary Hypertrophy
- •25.7 Physical Examination
- •25.8.1 Obstructive Sleep Apnea
- •References
- •26.1 Introduction
- •26.5 Halitosis Physiopathology
- •26.6.1 Oral Halitosis (Intraoral Halitosis, Oral Malodor)
- •26.6.1.1 Periodontal Infections
- •26.6.1.2 Tongue Oriented Halitosis
- •26.6.1.3 Peritonsillar Abscess
- •26.7 Paranasal Sinus Diseases
- •26.8 Adenoid Vegetation
- •26.9 Chronic Pharyngitis
- •26.10 Chronic Tonsillitis
- •26.11 Tonsillolith
- •26.12 Non-Oral Halitosis
- •26.13 Gastroesophageal Reflux
- •26.14 Diagnosis
- •26.14.1 Organoleptic Measurement
- •26.14.2 Sulfur Monitoring
- •26.14.2.1 Indirect Methods
- •26.14.2.3 Ammonia Monitoring
- •26.14.2.4 Polymerase Chain Reaction (PCR)
- •26.15 Physical Examination
- •References
- •27.1 Introduction
- •27.2 Epidemiology
- •27.4 Diagnosis
- •27.5.1 Clinical Assessment
- •27.6 Treatment
- •27.6.1 Voice Therapy
- •27.7 Phonosurgery
- •References
- •28.1 Introduction
- •28.2 Epidemiologic Characteristics
- •28.3 Swallowing Physiologic Phases
- •28.3.1.1 Prematurity
- •28.3.1.2 Neuromuscular
- •28.3.1.5 Cardiopulmonary Disease
- •28.4 Symptoms
- •28.5 Clinical Feeding Assessment
- •28.7 Flexible Endoscopic Swallowing Evaluation
- •28.8 Imaging
- •28.9 Endoscopic Assessments
- •28.9.1 High-Resolution Manometry
- •28.10 Medical Management
- •28.11 Surgical Management
- •28.11.1 Ankyloglossia
- •28.11.2 Laryngomalacia
- •28.11.3 Laryngeal Cleft
- •28.12 Conclusions
- •References
- •29.1 Introduction
- •29.2 Reactive Lymph Node Enlargements
- •29.3 Vaccines
- •29.4 Acute Suppurative Lymphadenitis
- •29.6 Granulomatous Lymphadenitis
- •29.6.1 Mycobacterial Infection
- •29.6.2 BCG Vaccine
- •29.6.3 Cat-Scratch Disease
- •29.6.4 Sarcoidosis
- •29.6.5 Kikuchi-Fujimoto Disease
- •29.7 Malignancies
- •29.8 Diagnosis
- •References
- •30.1 Introduction
- •30.2 Upper Airway Cough Syndrome
- •30.3 Chronic Rhinosinusitis
- •30.5 Otogenic Cough
- •30.6 Laryngeal Clefts
- •30.7 Conclusion
- •References
- •31.1 Introduction
- •31.5.1 Vocal Cord Disfunction (VCD)
- •31.5.2 Obstructive Sleep Apnea Syndrome (OSAS)
- •31.5.3 Allergic or Non-Allergic Rhinitis
- •31.6 Conclusion
- •References
- •32.1 Introduction
- •32.2.1 Non-massive Hemoptysis
- •32.2.2 Massive Hemoptysis
- •32.4 Diagnostic Evaluation
- •32.4.1 History
- •32.4.1.1 Infection Warning Signs
- •32.4.1.2 Choking
- •32.4.1.3 Exposures
- •32.4.1.4 Underlying Medical Problems
- •32.4.2 Physical Examination
- •32.4.3 Laboratory Evaluation
- •32.4.4 Imaging
- •32.5.1 Respiratory Illness
- •32.5.3 Trauma
- •32.5.4 Hemoptysis Mimics
- •References
- •33.1 Introduction
- •33.6 Conclusion
- •References
- •34: Pediatric Allergic Rhinitis: Otolaryngology Perspective
- •34.1 Introduction
- •34.2 Epidemiology
- •34.2.1 Prevalence
- •34.2.2 Risk factors
- •34.3.1 Classical Pathway
- •34.3.2 Nasal Pathway
- •34.4.2 Physical Examination
- •34.4.3 Diagnostic Tests
- •34.4.4 Nasal Cytology
- •34.4.5 Imaging
- •34.5.1 Adenoid Hypertrophy
- •34.5.2 Nasal Septal Deviation
- •34.5.3 Chronic Rhinosinusitis
- •34.5.4 Turbinate Hypertrophy
- •34.5.5 Nasal Foreign Body
- •34.5.6 Other Clinical Conditions
- •34.6.1 Saline Irrigation (Douching)
- •34.7 Treatment
- •34.7.1 Oral Antihistamines
- •34.7.2 Intranasal Steroids
- •34.7.3 Leukotriene Inhibitors
- •34.7.5 Oral Steroids
- •34.7.6 Intranasal Antihistamines
- •34.7.7 Immunotherapy (Sublingual-Subcutaneous)
- •34.8 Conclusion
- •References
- •35: Allergic Rhinitis: Pediatric Pulmonologist Perspective
- •35.1 Introduction
- •35.2.1 Epidemiological Relationship
- •35.2.4 Immunopathology
- •35.2.7 Non-pharmaceutical Treatment Method
- •35.2.8 Pharmaceutical Medication Policy
- •35.2.9 Immunotherapy Against Allergens
- •35.6 Conclusion
- •References
- •References
- •37.1 Introduction
- •37.2 Adenoid Hypertrophy
- •37.7 Preoperative Evaluation
- •37.8 Contraindications
- •37.9 Complications
- •37.9.1 Bleeding
- •37.9.2 Hypernasality
- •37.9.3 Surgical Traumas
- •37.9.4 Torticollis
- •37.9.5 Otitis Media
- •37.9.6 Psychological Trauma
- •37.9.7 Nasopharyngeal Stenosis
- •37.9.8 Recurrence
- •37.10 Postoperative Care
- •37.11 Surgery
- •37.12.1 Adenoiditis
- •References
- •38.1 Introduction
- •38.2 Anatomy
- •38.2.1 Palatine Tonsils (Faucial Tonsils)
- •38.2.2 Lingual Tonsil
- •38.2.3 Adenoids (Pharyngeal Tonsil)
- •38.2.4 Tubal Tonsils
- •38.5.1 Viral Tonsillitis
- •38.5.2 Bacterial Tonsillitis
- •38.5.3 Candida
- •38.6.1 Suppurative Complications
- •38.6.1.1 Peritonsillar Abscess (Quincy Tonsil)
- •Lemierre’s Syndrome
- •38.6.2 Nonsuppurative Complications
- •38.6.2.1 Acute Rheumatic Fever
- •38.6.2.2 Poststreptococcal Glomerulonephritis
- •38.6.2.3 Scarlet Fever
- •38.6.2.6 Palmoplantar Pustulosis (PPP)
- •38.6.2.7 IgA Nephropathy
- •38.7 Clinical Manifestation
- •38.7.1 Infection
- •38.7.2 Obstruction
- •38.7.3 Neoplasia
- •38.8 Diagnosis
- •38.8.2 Physical Examination
- •38.8.3 Laboratory
- •38.8.4 Imagining
- •38.8.5 Polysomnography
- •38.9 Treatments
- •38.9.1 Medical Treatment
- •38.9.2 Surgery
- •38.9.2.2 Tonsillectomy
- •38.9.3.1 Intraoperative Complications
- •38.9.3.4 Postoperative Long-Term Complications (>weeks)

366
İ. Çukurova and İ. Denizoğlu
27.6 Treatment
Treatment of pediatric dysphonia should be managed in a dynamic approach [25].
Although pediatric dysphonia may be expected to disappear after puberty [37], they
may lead to severe communicative, psychosocial, and organic problems if neglected.
So, verifying and explaining the situation to the child and family is necessary.
Laryngopharyngeal reux, sinonasal infections and allergies, ADHD, and other
pathologies must also be considered.
Although nodules are known to respond to voice therapy well, Rosen 2012 treatment strategies may change according to duration and severity of symptoms. Needs
of the individual child, especially if the communication problem affects social, academic, and personal well-being, dene treatment process. Phonomicrosurgery may
be the choice of treatment in recalcitrant nodules [38]. Pediatric vocal fold nodules
generally resolve spontaneously at puberty [39]. On the other hand, if patients with
puberphonia are not treated, they may continue with similar voice problems to
adulthood.
27.6.1 Voice Therapy
Voice therapy in childhood is not the same with adults because it is not easy to communicate with children in a therapeutic sense. The motivational interview is the
most crucial step in the treatment of pediatric dysphonia in the beginning. This
increases awareness and adherence to therapy. Counseling should explain how to
breathe quietly and give a comfortable, calm, easy-to-extract sound. The practice
and exercises must be regarded as a play instead of homework. Anna Freud’s words
“play is the business for the child” shed light on the clinicians to add curiosity and
play into therapy exercises. Anything can be transferred into a play; the clinician
must be exible and provide a playground within the therapy process.
Children prefer to be active and determined through the therapy process. It is not
easy to make them passively obey the rules and do the homework exercises. So, it is
better to make them feel independent, actively participate, and use their creativity;
otherwise, a constructive relationship a friendship cannot be constituted. Every success must be celebrated together. The clinician must not be in a dictating, punishing
state, which decreases motivation and therapy adherence.
Awareness of the child and family about vocal hygiene should be increased.
Collaboration with the school and teacher is essential. Excessive crying, yelling in
the play (football), cough, and throat clearing habits (attention should be paid to
differential diagnoses such as laryngopharyngeal reux, allergy, sinusitis, etc.) can
be explained with examples. While exemplifying a child with a complex glottic
attack and vocal abuse, it can be said to clap with his hands, for example, to explain
that the same situation will also happen to the vocal folds by showing the redness
and discomfort of their hands when the intensity of the applause increases gradually. Somatization of therapy exercises as much as possible will also help by using
devices (e.g., tube phonation) associated with the play and the toy [40].

27 Dysphonia inChildren
367
Empathy and being a playmate are critical skills for clinicians who are interested
in pediatric dysphonia. Indirect conversations with puppets (nger puppets are a
practical solution) can be made to make puppets give vocal hygiene suggestions. By
using prosody, the child can feel the sense of music in the sound. For this, the
stressed phonemes in a sentence can be represented by lines by doing the exercise
of “drawing the sound” [41]. Various interactive cartoon programs, pictures, and
toys prepared for pediatric voice therapies can be used.
The family must be included in therapy. Eliminating the environments where the
child will shout and preventing the family from talking too loudly in the home environment affects the child. It is a fact that telling the child not to shout is a suggestion
that cannot be realized. Shouting is a normal behavior, especially during the play
with his/her peers. The child must either learn to shout correctly or nd something
that can be put in place to identify him/herself. For example, he can blow a whistle
hanging on his neck when angry and shouting. However, it is necessary to arrange
proper place and time; otherwise blowing a whistle in an unlikely place (e.g., in a
school canteen) will not be acceptable.
Duration and number of sessions of voice therapy are another issues in pediatric
dysphonia treatment. Pediatric voice therapy addressing benign vocal fold lesions
and laryngeal edema was reported to require an average of 7.54 sessions [30].
Duration and time between sessions are adjusted according to child’s compliance.
In puberphonia, patients can shift quickly to chest register from falsetto. The
voice may improve in a few sessions, but the change at the vocal personality must
be considered well. The therapy does not end when chest register is obtained; but
when the patient can use the chest register properly in speech and singing activities [22].
27.7 Phonosurgery
The developing physioanatomy of the vocal fold structure makes surgical interventions more challenging to decide in the pediatric group. The dimensions of the surgical site are extremely smaller than adult larynx. The developing layers of the vocal
fold mucosa are also critical. Because of the high risk of scar formation and trauma
to the anterior and posterior macula avas, microsurgical principles including technique and instruments must be considered carefully. Treatment of cysts and mature
polyps usually requires surgery, but the surgical decision can be made according to
impairments of the dysphonia on social and personal communication skills. The
decision for surgery may be postponed for a while, provided that the patient is
closely monitored.
Results should be interpreted cautiously due to the heterogeneity of the studies,
techniques, and surgeries used. However, a systematic review and meta-analysis did
nd that pediatric patients with vocal fold nodules may see a reduction in dysphonia
following surgery [17].
It should be noted that surgery, no matter how well it is performed, will not
change the phonation patterns in motor memory. Before, and more importantly after

368
İ. Çukurova and İ. Denizoğlu
surgery, it is essential to add voice therapy to the treatment. Patients and their relatives should be informed that surgery is only a part of the treatment and should be
made aware of the importance of voice therapy. It is clear that the best treatment
results will be obtained when surgery and therapy are combined to promote safe and
economic voice use and prevent future injury [42].
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İ. Çukurova and İ. Denizoğlu

Dysphagia inChildren
28
DoganBarut , GraziaFenu , andFundaCetin
28.1 Introduction
Dysphagia, a condition characterized by difculty in swallowing, comprises a range
of challenges that impede safe, efcient, and sufcient food transport to the stomach [1, 2].
While the name “dysphagia” adequately characterizes the problem in adults,
it fails to encompass the full complexity of the condition when it occurs in the
pediatric population. The act of swallowing, considered one of the fundamental
physiological processes in humans, initiates during the early stages of gestation
and undergoes further development and variations following birth [3]. Given that
swallowing is a dynamic and ongoing process, pediatric dysphagia (PD) exhibits
diverse, intricate symptoms and indications similar to those observed in
adults [1–3].
D. Barut
Division of Gastroenterology, Hepatology and Nutrition Disease, Department of Pediatrics,
Medical School of Ege University, Izmir, Turkey
G. Fenu
Pulmonology Unit, Meyer Children Hospital, IRCCS, Florence, Italy
e-mail: grazia.fenu@meyer.it
F. Cetin (*)
Division of Gastroenterology, Hepatology and Nutrition Disease, Department of Pediatrics,
Medical School of Ege University, Izmir, Turkey
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2024
H. Yüksel et al. (eds.), Pediatric Airway Diseases, Comprehensive ENT,
https://doi.org/10.1007/978-3-031-74853-0_28
371

372
D. Barut et al.
28.2 Epidemiologic Characteristics
The reported prevalence of PD varies signicantly, with estimates ranging from
0.9% to 80% [4]. This variation might be attributed to differences in the denition
of dysphagia, the specic population under study, and the methodologies employed
in the research [4, 5]. Feeding and swallowing dysfunction are diagnosed more
frequently in children with preterm, neuromuscular abnormalities, cardiac diseases,
anatomic malformations of the upper aerodigestive tract, and gastrointestinal tract
issues [6, 7]. Children’s swallowing difculties must be managed with an early
diagnosis and multidisciplinary team intervention [3].
28.3 Swallowing Physiologic Phases
The preparation phase, the oral phase, the pharyngeal phase, and the esophageal
phase are the four traditional phases of a typical swallow. During the preliminary
stage, the ingestion of food occurs in the oral cavity, where it is moistened with
saliva, chewed, and shaped into a bolus using the oral tongue and hard palate. At
around 6months of age, this period begins to develop. Sucking from a nipple constitutes the preliminary stage before 6 months. The oral phase involves the oral
tongue propelling the food bolus into the oropharynx and inducing the swallow
reex. The elevation of the soft palate prevents food’s regurgitation into the
nasopharynx.
The food bolus travels through the oropharynx and hypopharynx toward the
esophagus using synchronized muscle contractions during the pharyngeal phase. The
tongue and pharyngeal muscles propel the bolus into the pharynx. As the velum
approaches the pharyngeal muscles, the larynx rises, and the vocal folds adduct [3,
8]. During the pharyngeal phase, breathing stops; when eating, breathing becomes
faster and more erratic than during tidal breathing [9]. In the esophageal phase, the
cricopharyngeus relaxes to allow the food bolus to enter the esophagus, and then the
bolus is passed into the stomach by synchronized smooth muscle peristalsis [3–10].
Beginning in pregnancy, as early as gestational week 10 or 11, the suck and swallow
develop. Most children typically begin to develop oral feeding prociency and tolerance between weeks 34 and 38 of pregnancy. Involuntary reexes in babies control
all four phases. The preliminary and oral stages are controlled voluntarily in children
and adults, but the pharyngeal and esophageal phases are still involuntary [6].
Dysphagia can be further classied into other categories based on the affected
swallowing phase. Signs indicative of oral dysphagia include uncoordinated biting
and chewing, underdeveloped or absent sucking, and inadequate manipulation of
the food bolus. Laryngeal penetration, aspiration, food ingress into the airway
below the vocal folds, asphyxiation, airway obstruction due to food, pharyngeal
reux, and nasopharyngeal reux are all indicative manifestations of pharyngeal
dysphagia. Esophageal dysphagia is caused by either a blockage in the esophagus
that prevents food from passing through or poorly coordinated esophageal muscle
contractions [2].

28 Dysphagia inChildren
373
28.3.1 The Etiology ofDysphagia
The etiology of dysphagia can be a single medical problem, but it is typically complex and brought on by a combination of diseases and comorbidities. Table28.1 lists
some typical causes of swallowing difculties. To choose the best solution, it is
essential to establish the etiology of dysphagia.
28.3.1.1 Prematurity
Infants’ dysphagia is frequently brought on by prematurity. The prevalence of feeding issues was shown to be 10.5% in premature children born at fewer than 37weeks
gestation and to increase to 24.5% in infants born with a very low birth weight of
less than 1500 g, according to a signicant population-based cohort study [11].
Delays in developing head control, tongue movement, palate function, gag reex,
and laryngeal feeling can cause poor swallowing. Dysphagia is more distinct and
complex because of the common comorbidity of pulmonary and central nervous
system disorders in premature newborns. The formation of a normal swallow can be
further complicated and delayed by anomalies of the aerodigestive system, such as
laryngomalacia, or iatrogenic damage brought on by respiratory assistance, such as
prolonged intubation or tracheostomy [12].
28.3.1.2 Neuromuscular
The intricate coordination of sensory and motor activities required for a secure
swallow is disrupted by neuromuscular diseases—dysphagia results from delayed
reexes, hypotonia, and generalized incoordination. The degree of the central nervous system injury and whether it is static or progressive affect the presentation and
clinical course of the dysphagia [7]. Several medical diseases can have a signicant
impact on swallowing. These include cerebral palsy, congenital viral infections,
Arnold-Chiari malformation, microcephaly, hydrocephalus, intraventricular hemorrhage, periventricular leukomalacia, traumatic brain injury, muscle dystrophies, seizure disorders, and malignancies. Cerebral palsy is the neurologic disorder most
commonly associated with dysphagia in pediatric populations [3, 13].
28.3.1.3 Abnormalities oftheAerodigestive Tract’s Anatomy
Anatomical anomalies of the upper aerodigestive tract might disrupt the intricate
coordination needed for a good swallow. Common causes are listed in Table28.1 by
anatomical subsite and frequently change based on the patient’s age [6, 7].
28.3.1.4 Disorders oftheGastrointestinal Tract
In healthy infants, gastroesophageal reux, the ow of stomach contents back into
the esophagus with or without regurgitation or vomiting, is a normal physiological
process. The condition is referred to as gastroesophageal reux disease (GERD)
when accompanied by symptoms or consequences and is regarded as pathologic. A
newborn with GERD typically exhibits signs of irritability, inability to thrive,
unwillingness to eat, posturing, cough, stridor, and hoarseness. The youngster may
experience epigastric pain, dysphagia, odynophagia, tooth erosion, and chest pain

374
D. Barut et al.
Table 28.1 Disorders that
predispose children to
swallowing difculties and
dysphagia
Prematurity
• Low gestational age at birth
• Low birth weight
Respiratory and cardiac disorders
• Respiratory distress syndrome
• Bronchopulmonary dysplasia (chronic pulmonary
disease)
• Laryngo−/tracheo−/bronchomalacia
• Cyanotic and acyanotic heart defects
Gastrointestinal disorders
• Tracheoesophageal stula and esophageal atresia
• Congenital diaphragmatic hernia
• Gastroesophageal reux disease (GERD) and achalasia
• Eosinophilic esophagitis
• Food allergies and intolerances
Neurological disorders
• Microcephaly
• Hydrocephalus
• Intraventricular hemorrhage
• Periventricular leukomalacia
• Birth asphyxia and cerebral palsy
Congenital abnormalities
• Tongue tie
• Cleft lip/palate
• Moebius syndrome
• Down syndrome
Iatrogenic complications
• Tube feeding
• Tracheostomy
• Certain medications (especially those that affect
arousal, muscle tone)
Ingestional (caustic) injuries
• Cleaning agents, battery
as they get older. In older kids, frequent vomiting and regurgitation are not thought
to be physiological. By lessening the upper aerodigestive tract’s mucosal feeling,
GERD can cause oropharyngeal dysphagia [13].
Eosinophilic esophagitis is an additional inammatory disorder of the gastrointestinal tract that can impact the swallowing process in pediatric patients.
Eosinophilic esophagitis (EoE) is a pathological condition characterized by immune
system involvement associated with food allergies, genetic susceptibility, and several environmental variables. Children often appear with failure to thrive, vomiting
during meals, dysphagia to both liquids and solids, retrosternal discomfort, and
food impaction. During an esophagogastroduodenoscopy and biopsy, eosinophilic
esophagitis is identied. Endoscopy frequently reveals esophageal edema and
inammation along with a lack of vascularity. Linear furrows, concentric rings (also

28 Dysphagia inChildren
375
known as trachealization), and white ecks on the mucosa can all be found inside
the esophagus. The diagnosis made after a biopsy sample and more than 15 intraepithelial eosinophils per high-power eld indicate eosinophilic esophagitis [14].
A rare cause of dysphagia in young children is cricopharyngeal achalasia. The
symptoms of cricopharyngeal achalasia include coughing, choking, gagging, and
nasal regurgitation. It leads to pharyngeal phase dysphagia. Due to a higher risk of
laryngeal penetration, patients with cricopharyngeal achalasia may nd it more difcult to swallow liquids. A tonically constricted upper esophageal sphincter that
occasionally relaxes is a pathophysiologic feature of cricopharyngeal achalasia. A
modied barium swallow study that identies a typical bar in the cricopharyngeus
region is frequently used to determine the disease. Esophageal manometry demonstrates that the cricopharyngeal muscles cannot relax [15].
28.3.1.5 Cardiopulmonary Disease
Premature and term infants with complex medical conditions, such as congenital
heart disease and bronchopulmonary dysplasia, are at risk for swallowing dysfunction. Based on available reports, it has been shown that newborns who undergo heart
repair surgery have a higher likelihood of experiencing dysphagia, with prevalence
rates ranging from 22% to 50%. Dysphagia associated with cardiac defects and
cardiac surgery can arise from various factors, including abnormal thoracic anatomy, iatrogenic injury such as damage to the recurrent laryngeal nerve, the need for
prolonged intubation, ventilation or respiratory support, as well as the inuence of
anesthetics and narcotics [16].
28.4 Symptoms
Depending on the underlying etiology of the dysphagia, different children present
with varying symptoms of swallowing difculty. A caregiver should seek evaluation
for feeding problems if a child exhibits symptoms like prolonged feeding times,
little interest in feeding, or food refusal; postural changes like back arches and neck
extensions; failure to thrive; nasal regurgitation; coughing; choking; wet respirations during and after feeding; and increased work of breathing. It is possible to
have laryngeal penetration and aspiration without the typical eating symptoms [17].
The occurrence of laryngeal penetration and aspiration may manifest even in the
absence of typical feeding signs. The term “silent aspiration” refers to the occurrence of aspiration without the presence of coughing or deliberate efforts to remove
the food bolus from the airway. The stimulation of the laryngeal cough reex is
absent. Silent aspiration is believed to be associated with reduced laryngopharyngeal sensation, neurological weakness or lack of coordination in the pharyngeal
musculature, or a weak cough. It is recommended that children who experience
recurrent respiratory tract infections in the absence of any apparent indicators of
swallowing difculty should be subjected to an evaluation for dysphagia [18]. A
comprehensive history and physical examination by a doctor are the rst steps in
evaluating a child for swallowing difculties. Children with feeding difculties are
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