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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)

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187

Upper Airway Evaluatıon: Dıagnostıc
Clues fromUpper Respıratory Tract
SedefNarinTongal, AdaezeAyuk, andHasanYüksel
14.1 Upper Airways
Flexible bronchoscopy is frequently used for anatomical and functional evaluation
of the upper and lower airways in childhood. The upper airway starts from the nasal
cavity and continues to the extrathoracic part of the pharynx, larynx, and trachea.
1. Flexible airway endoscopy provides insight into the causes and appearance of
congenital and acquired anomalies of the nasal cavity, pharynx, and larynx.
(a) The nasopharyngeal region: Choanal stenosis and atresia, nasal masses, cra-
niofacial abnormalities, adenotonsillar hypertrophy, and base of tongue
lesions can be investigated using bronchoscopy.
(b) The laryngeal region: Laryngomalacia, subglottic stenosis, subglottic
edema, vocal cord paralysis, hemangioma, cyst, papillomatosis, web, cleft
and vocal cord dysfunction, and upper respiratory tract disease associated
with gastroesophageal reux can be evaluated.
In children, the airway diameter is narrower and the subglottic region is the
narrowest. In addition, the larynx is softer and the epiglottis is omega-shaped in
children. Flexible airway endoscopy provides insight into pathologies of the
upper airways that lead to airway obstruction, although rare in newborns and
early infancy and more common in older children. Obstruction can lead to the
collapse of the extrathoracic airways. Early diagnosis and treatment is imperative as there is associated morbidity and mortality.
14
S. N. Tongal · H. Yüksel (*)
Department of Pediatric Pulmonology, Manisa Celal Bayar School of Medicine,
Manisa, Turkey
A. Ayuk
Department of Pediatrics, College of Medicine, University of Nigeria– Enugu Campus/
University of Nigeria Teaching Hospital, Enugu, Nigeria
© 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_14
189

190
S. N. Tongal et al.
Bronchoscopic appearance of the upper airway: For ease of visualization of the
upper airway, a face mask is used with sedation and exible bronchoscopy is performed through the nose and advanced along the middle or lower meatus. If the
patient is intubated under anesthesia or a laryngeal mask is applied during the bronchoscopy procedure, examination of the upper airway may not be possible. Using
the facemask method, with the patient lying on his/her back, the base of the nose is
observed above and the roof of the nose below. İn a normal anatomy, the turbinate
should appear smooth and clean. No pathologies like polyps or purulent secretions
should be seen obstructing the course of the bronchoscope. The upper turbinate is
rarely seen in this procedure. In the presence of a deviated septum, the bronchoscope can be passed more easily from one side than the other. The opening of the
Eustachian tube can be seen on the lateral wall of the nasopharynx in older children.
Adenoidal tissue in the posterior part of the nasopharynx can also be seen, especially in preschool children while tonsillar tissue is best evaluated in oral procedures. The epiglottis and laryngeal opening should also be seen clearly.
Bronchoscopic appearance of the larynx: The larynx is best examined under light
anesthesia with spontaneous breathing. Anatomically, there are marked differences
between the larynx of children and adults. In young children, it is located anteriorly
and superiorly, whereas it becomes more centralized and inferiorly positioned with
increasing age. The larynx is also smaller and the lower end of the cricoid cartilage
is at the middle level of C5in the newborn and in the shape of a cone, while in adults
it is at the lower level of C6.
During bronchoscopy, the vocal cords should move equally and converge centrally. The arytenoids are usually more mobile in infancy and their prolapse toward
the laryngeal inlet may be normal in the early infancy period. If there is evidence of
obstruction, surgical intervention should be considered. In the child, the cuneiform
and corniculate cartilages may not be distinguished as separate structures. A cleft if
present, may be visualized in the posterior laryngeal wall. Because it may be difcult to see this area with a exible bronchoscope, it is technically more successful
in visualizing anterior structures [1–3].
14.2 Indıcatıons forUpper Aırway Imagıng
14.2.1 Pathologıes ofUpper Airway wıth Noisy Breathing
Diagnostic airway endoscopy is used in children with symptoms such as nasal congestion, sleeping with an open mouth, snoring, stridor, and hoarseness, who hitherto
had not responded to medical treatment or have had an atypical course. Although it
may sometimes be difcult to decide very young infants, evaluation of the airway
should be performed without delay in children with persistent or recurrent stridor,
especially if there are accompanying ndings such as hoarseness, apnea, feeding
difculties, or growth retardation.
When children present with stridor, endoscopic examination can be performed, looking out for laryngomalacia and further excluding other possible

14 Upper Airway Evaluatıon: Dıagnostıc Clues fromUpper Respıratory Tract
191
differentials. For most procedures, the exible endoscope is passed through the
nose and this gives the opportunity for the upper airways to be examined in detail
as the pharynx and larynx can be well observed with the head and neck in the
neutral position.
Depending on the indication, in some cases where examination under anesthesia
is planned for the upper airway, evaluation of the lower airway may also be required
. Upper airway lesions may frequently coexist with lower airway lesions.
VCD can present with inspiratory sounds (stridor) and in children with suspected
vocal cord dysfunction (VCD), the diagnosis is made by visualization of paradoxical narrowing of the anterior portion of the vocal cords during inspiration.
Upper airway endoscopy is also useful for the evaluation of patients with postextubation stridor. While reintubation may be required immediately in some patients.
The development of scar tissues on extubation following prolonged intubation takes
a longer time to develop; thus, initial endoscopic ndings may be normal and
reevaluation should be kept in view [4–10].
14.2.2 Nasopharyngeal-Related Pathologıes (Congenital
andAcquired)
Many of these disease entities may present as dysmorphic syndromes with attendant
craniofacial abnormalities and associated mandibular or maxillary hypoplasia. İn
such patients, it may be difcult to provide airway stability due to concomitant
micrognathia, glossoptosis, adenotonsillar hypertrophy, cleft palate, midface hypoplasia, or a narrowed nasopharynx associated with tongue hypertrophy [11].
(a) Choanal Atresia: This is the most common congenital anomaly of the nose.
Coanal atresia is frequently associated with other anomalies, the association
with CHARGE syndrome being the most common and serious [11, 12].
Unilateral atresia is more common and may not be detected until later in childhood. However, when bilateral, it can cause severe airway obstruction. The
diagnosis can be conrmed using exible endoscopy. Computed tomography
CT scan of the head is usually necessary to determine the exact location of the
obstruction and whether the defect is bony or membranous.
(b) Congenital Masses of the Nasal Region: These are rare, cystic structures or
sometimes more solid masses such as hemangiomas, neurobromas, and gliomas. Solid masses may be associated with midline defects such as cleft palate.
If a polyp is visualized in a newborn, differentials to be considered include
encephalocele or glioma until the denitive diagnosis is made [11, 13].
(c) Adenotonsillar Hypertrophy: This is a common cause of obstructive sleep
apnea in children and may worsen airway obstruction in patients with pharyngeal collapse.
(d) Cysts or mass lesions arising from the dorsal surface of the tongue are rare
and can cause signicant airway obstruction, often with feeding difculties [11].

192
S. N. Tongal et al.
14.2.3 Laryngeal Pathologıes
(a) Laryngomalacia: This is the most common congenital laryngeal anomaly. It is
uncertain if laryngomalacia develops due to an anatomical problem or delayed
neuromuscular development. It is usually dened by the onset of inspiratory
stridor in the rst 4–6weeks of life. Stridor increases during crying, agitation,
feeding, and respiratory tract infections. Stridor tends to improve as the child
grows. Surgical treatment is rarely required. It is frequently associated with
other airway problems and gastroesophageal reux [14, 15] (Fig.14.1).
(b) Subglotic Stenosis: Membranous bilateral symmetrical stenosis may develop
with the thickening of the soft tissues in the subglottic area, resembling the
appearance of acute subglottic edema. Cartilaginous subglottic stenosis is due
to malformation of the cricoid cartilage and causes variable stenosis that is not
symmetrical in appearance. Children with subglottic stenosis may present with
different clinical ndings depending on the grade ranging from severe respiratory distress in the neonatal period to the development of inspiratory or biphasic
stridor within the rst few months of life. Thus the signs and symptoms depend
on the severity of the stenosis; Myer etal. proposed a grading of the proportion
of stenosis, (I to IV); with grade 1 having up to 50% obstruction of the lumen,
grade 2 having 51–70% obstruction, grade 3 having more than 71% obstruction
of the lumen, and grade 4 having no detectable lumen. Cases in which stenosis
develops due to airway trauma caused by prolonged intubation and tracheostomy are more common than congenital ones [14, 16, 17] (Fig.14.2).
(c) Subglottic Edema: This can be caused by infection, allergy, or trauma.
Endoscopically, the subglottic area is symmetrically narrowed, often with
supraglottic edema. It is the most common complication of rigid
bronchoscopy.
(d) Vocal Cord Paralysis and Dysfunction: If due to traumatic causes are usually
unilateral and especially affect the left side and can be visualized as the absence
Fig. 14.1 Laryngomalacia

14 Upper Airway Evaluatıon: Dıagnostıc Clues fromUpper Respıratory Tract
Fig. 14.2 Subglottic
stenosis
193
of movement on the affected side. Unilateral vocal cord paralysis is difcult to
diagnose. Bilateral paralysis may be due to a severe central nervous system
malformation such as Arnold-Chiari malformation. In the more common abductor paralysis (closed appearance of the glottis), bilateral paralysis may present
with stridor, hoarseness, and respiratory distress, whereas unilateral paralysis
may be asymptomatic. Aphonia and aspiration may develop in the rarer adductor paralysis (open glottis). For optimal diagnostic evaluation, the movement of
the vocal cords and arytenoids should not be evaluated under general anesthesia, but rather imaging while the patient is awake or under mild sedation/
reawakening from anesthesia as it wears off [18]. Vocal cord dysfunction is
characterized by paradoxical closure of the vocal cord during inspiration or during both inspiration and expiration. The resulting symptoms and signs include
sudden onset of dyspnea, wheezing, inspiratory or biphasic stridor, and cough;
with these ndings, they can often be misdiagnosed as asthma. The diagnosis is
usually difcult; it can be conrmed by laryngoscopy performed without sedation, and it is seen that the anterior part of the vocal cords is closed, leaving a
narrow gap [19, 20].
(e) Hemangiomas are among the most common laryngeal masses seen in infancy.
Infants may present with mild to moderate stridor or with sudden (biphasic)
stridor and recurrent or atypical croup. They are more commonly found in the
subglottic area and more rarely in the supraglottic area as an asymmetric mass.
Subglottic hemangiomas are usually unilateral. Endoscopic diagnosis may be
difcult because they may have a normal epithelial appearance. Cutaneous
hemangiomas may also be seen simultaneously in some infants. These hemangiomas usually grow rapidly until about 6–10months and then usually start to
shrink at around 1.5years of age [21] (Fig.14.3).

194
Fig. 14.3 Hemangioma
S. N. Tongal et al.
(f) Supraglottic Laryngeal Cysts: These are usually located in the aryepiglottic
fold or epiglottis and are often congenital. They develop as a result of iatrogenic
trauma such as intubation. Diagnosis is easy if the cysts are covered with thin
mucosa, while others appear as a submucosal mass. Infants usually present with
stridor, hoarseness, or aphonia and sometimes feeding difculties [14].
(g) Laryngeal Papillomatosis: Although rare, it is the most common benign neo-
plasm of the larynx after infancy. It is caused by human papillomavirus types 6
and 11. It may regress spontaneously or may show a tendency to recur and spread
all over the airways and lungs. The vocal cord is the most common site of lesions
and they are typically multiple, irregular, and fragile masses. They usually present
with hoarseness and stridor, less frequently with cough or respiratory distress [22].
(h) Laryngeal Web (Vocal Folds): They are usually seen at the level of the glottis,
but may also be present in the supraglottic and subglottic regions. Webs can be
classied as complete or incomplete. The presentation may vary from hoarseness and aphonia to (biphasic) stridor and respiratory distress [14] (Fig.14.4).
(i) Congenital Posterior Laryngeal Cleft: This is a rare condition that develops
between the larynx and hypopharynx; and in severe cases, it may extend inferior
to the trachea. It may be associated with other anomalies of the trachea or esophagus and other congenital anomalies. It can be classied as type 1 supraglottic
interarytenoid cleft not extending below the level of the vocal cord, type 2 cleft
extending below the level of the vocal cord (partial involvement of the cricoid
cartilage), type 3 cleft along the cricoid cartilage with or without extension into
the cervical trachea, type 4 cleft extending into the thoracic trachea (may extend
to the carina). Aspiration, cyanosis, and cough may occur with feeding. First
suspicion is required for diagnosis. Rigid rather than exible bronchoscopy is
more ideal for detecting cleft. Bid epiglottis and anterior cleft of the larynx are
very rare; while bid epiglottis is usually associated with other anomalies, anterior cleft may be found as an isolated defect [14, 23, 24] (Fig.14.5).

14 Upper Airway Evaluatıon: Dıagnostıc Clues fromUpper Respıratory Tract
Fig. 14.4 Anterior
laryngeal web
Fig. 14.5 Type 1
laryngeal cleft
195
(j) Gastroesophageal Reux Disease: Though not an anatomical structural defect
has been associated with many respiratory symptoms in infants and children,
including hoarseness, chronic cough, stridor, and wheezing, and with chronic
sinusitis, otitis media, chronic laryngitis, recurrent croup, and laryngomalacia.
Endoscopic ndings that may reveal granular changes in the epiglottis, erythema, and edema in the mucosa covering the arytenoid cartilage and posterior
wall of the glottis (posterior laryngitis), vocal cord nodules, ulcers and granulation tissue, and rarely subglottic stenosis [25, 26].
In conclusion, endoscopy can be used to examine only the upper airway, but
since upper and lower airway lesions can frequently be seen together, it should be
preferred to visualize both upper and lower airways in the same procedure unless
there is an exceptional situation for the child.

196
S. N. Tongal et al.
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