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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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11 Radiologic Evaluation ofUpper Respiratory System
c
145
Fig. 11.16 Five-year-old girl with laryngotracheal papillomatosis. (a) On 3D CT volume-ren-
dered image, multiple lling defects of left main and lower lobe bronchi created by papillomatosis
(arrows). Cystic lung nodules of both lungs are also seen (asterisks). (b) Axial CT image of right
lung reveals cysts (arrows) and nodules (asterisks) of the lung. (c) On axial CT image, circumferential tracheal stenosis, by papillomatosis (black arrow)
papillomas may spontaneously regress, but in 1% the disease spreads to the lungs
and cause respiratory symptoms [27]. The symptoms usually present prior to age of
5 [27]. Multiple surgical procedures and tracheostomy may be needed to ensure the
airway patency. In decreasing recurrency frequency of the papillomas, some nonsurgical treatments including interferon alfa, cidofovir, indol-3-carbinol, celecoxib,
heat shock of protein have been investigated and seem to be promising [28].
CT is the basic imaging method to reveal polypoid lesions of the airway. A large
number of polyps of various sizes originating from the larynx, trachea, and bronchi
are encountered. When the disease spreads to the lungs, nodules and cavitations are
seen, with lower lobes distribution. Over time, cavities tend to coalesce (Fig.11.16).
11.7.3 Croup
Croup or laryngotracheobronchitis is dened as infection of upper airway caused by
viral agents in early childhood. The causative agent is often rhinosincytial virus or
parainuenza, and children aged 6months to 3years are mostly affected [29]. Cases

146
G. Koc et al.
a b
Fig. 11.17 Two views of neck radiograph of a 2-year-old boy presented with inspiratory stridor.
(a) AP view of the neck is showing signicant narrowing of subgottic trachea (arrows) compatible
with Steeple sign. (b) On lateral view dilatation of the hypopharynx (asterisk) and narrowed subglottic trachea (arrows) are again noted
present with inspiratory stridor and dog-barking cough. The diagnosis is made clinically. When lateral and AP radiographs of the neck are obtained for the differential
diagnosis of foreign body aspiration, retropharyngeal abscess, and epiglottitis,
which may cause similar symptoms, narrowing of the subglottic airway called as
Steeple sign is observed. Subglottic stenosis and dilatation of the hypopharynx
(occurs to overcome airway resistance) are typical ndings of the disease observed
on radiographs (Fig.11.17).
11.7.4 Epiglottitis
Epiglottitis is a rapid inammatory process of epiglottis usually caused by bacterial
agents. Haemophilus inuenzae type B, prior to introduction of the vaccination, was
the foremost etiologic agent of the epiglottitis. Due to widespread immunization of
Hemophilus inuenza type B, the incidence of the disease amongst children has
been decreased [30]. Patients rapidly present with the symptoms of fever, difculty
in swallowing and breathing, anxiety. The diagnosis is usually established clinically
and with direct visualization of the epiglottitis via laryngoscopy. Lateral neck radiography acquired in erect position in order to secure airway may help make the

ab
11 Radiologic Evaluation ofUpper Respiratory System
147
diagnosis with the ndings of thickened epiglottitis (thumb sign) and aryepiglottic
folds, increased prevertebral soft tissue thickness, and dilated hypopharyngeal
air column.
CT and MRI of the neck are not preferable due to airway compromise in supine
position. The treatment of epiglotitits is including intravenous antibiotherapy, steroid, supportive therapy as intravenous uid and oxygen.
11.7.5 Foreign Body Aspiration
Aspiration of foreign body into the airways is of particular concern in infants and
preschool young children and fourth leading cause of death [31]. Organic material,
particularly food with rounded shape including peanuts, fruit, and candies are most
often aspirated. When the aspirated material is involving upper airway the main symptoms are usually sudden onset coughing and respiratory distress. If the patient is clinically stable the radiological evaluation may start with lateral neck and two views chest
radiography. Radiopaque foreign bodies can be vizualized with the radiographs. In
case the aspirated material is not demonstrated with physical examination or radiographs prior to endoscopic procedures and for delineation of postraumatic complications CT of neck and/or chest might be acquired with low dose protocols (Fig.11.18).
The removal of foreign body from upper airway is conducted via laryngoscopy.
Fig. 11.18 Fourteen-year-old girl, with posttraumatic retropharyngeal collection, its mediastinal
extension, and subcutaneous emphysema caused by aspirated foreign body. (a) Axial CT image of
the neck reveals air-lled retropharyngeal collection (asterisk) and soft tissue emphysema of bilateral cervical chain (white arrows). (b) Sagittal contrast-enhanced CT image of the neck and chest
show retropharyngeal collection extending down to the mediastinum lled with air and water-soluble contrast medium (black arrows)

148
G. Koc et al.
References
1. Adewele L. Anatomy and assessment of pediatric airway. Pediatr Anaesth.
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Radiologic Evaluation ofLower
Respiratory System
SevinçTaşar andRecepSavaş
12.1 The Differences intheLower Respiratory Tract
inChildren andAdults Are asFollows [1]
– In infants, contrary to adults, infections such as bronchiolitis can lead to signi-
cant respiratory distress.
– The larynx, trachea, and bronchi have thinner walls compared to lumen diameter.
Consequently, the lumen can collapse easily during inspiration.
– Children have shorter tracheas compared to adults, making it easier for tubes to
enter the bronchi during endotracheal intubation.
– Newborns have a barrel-shaped thorax, which gradually transforms into a cylin-
drical shape as they age.
– In newborns and early childhood, the diaphragm muscle is more effective in
ventilation due to the weakness of intercostal muscles and the prevalence of car-
tilage over bone in the thorax. This leads to a focus on abdominal breathing.
– Intra-abdominal organs and mediastinal structures affect breathing.
– Proximal and distal airways grow proportionally up to the rst 5 months.
However, after 1 year, growth is more prominent in the distal airways.
Consequently, up to the age of 5, resistance in the distal airways is higher than
in adults.
– Bronchospasm is rare in children, especially in the rst 6months, due to insuf-
cient bronchial musculature.
– In children, bronchial walls can easily adhere to eachother due to insufcient
cartilage support. This leads to positive pleural pressure during expiration in
12
S. Taşar
Pediatric Radiology, University of Health Sciences Ümraniye Training and Research
Hospital, İstanbul, Türkiye
R. Savaş (*)
Department of Radiology, Faculty of Medicine, 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_12
151

152
ab
ab
S. Taşar and R. Savaş
obstructive pulmonary diseases, potentially causing the collapse of the respira-
tory tract.
– The number of alveoli rapidly increases until the age of eight to ten. After this
age, while the formation of new alveoli signicantly decreases, structural
development in the existing alveoli becomes more prominent. As collateral
airways (Lambert and Kohn pores) do not develop before the age of 8years,
telectasis and pleural-based round pneumonia are more likely to be observed
(Fig.12.1).
– In children, lung compliance is lower than in adults, making the lungs more sus-
ceptible to collapse. Surfactant reduces surface tension and enhances lung com-
pliance. Respiratory distress syndrome, which is secondary to surfactant
deciency, may develop in premature infants (Fig.12.2).
Fig. 12.1 On the PA chest X-ray (a), a nodular opacity is evident in the upper zone of the right
lung. Simultaneously, in the CT examination (b) of the patient, a consolidated area, consistent with
pleural-based round pneumonia, is observed in the upper lobe posterior in the axial section
Fig. 12.2 On the rst day of birth, a 29-week-old newborn presented with diffuse, hazy, granular
pulmonary airspace opacication on CXR (a). After 5days of surfactant treatment, chest X-ray
ndings returned to normal (b)

12 Radiologic Evaluation ofLower Respiratory System
153
12.2 Imaging Methods Used inRespiratory System Diseases
• Plain Radiography
• Fluoroscopy
• Ultrasonography (US)—Color Doppler US
• Computed tomography (CT)
– High-resolution computed tomography (HRCT)
– Spiral tomography
– CT angiography
• Magnetic resonance imaging (MRI) and MR angiography
• Angiography
• PET
12.2.1 Plain Radiography
Chest radiography offers several advantages, including easy acquisition, availability, and cost-effectiveness. Despite signicant advancements in radiological imaging methods today, chest radiography remains the most commonly and initially
preferred imaging method for diagnosing, monitoring, and assessing treatment
response in pediatric respiratory system diseases (Fig.12.3). It allows for the evaluation of the lungs, heart, airways, major vascular structures, and bone structures
such as vertebrae, ribs, and the clavicle.
Chest radiography is obtained during full inspiration in cooperative older pediatric patients and during quiet inspiration in uncooperative infants and young children. For infants and young children (under 5years), a standard chest X-ray is taken
in the anterior-posterior position, while in older patients, it is taken in the posterioranterior position. In neonates, X-rays can be obtained within incubators using modern mobile X-ray equipment. Certain areas, such as the anterior-upper mediastinum,
retrocardiac, and sub-diaphragmatic lung regions, may not be well evaluated due to
being in superposition and may require lateral radiographs for assessment.
Lateral X-rays are taken close to the pathology side to enhance the visibility of
lesions. If the side is not specied, a left lateral chest X-ray is taken to minimize
cardiac magnication. In lateral X-rays, density decreases from top to bottom, making it useful for detecting small inltrates in hidden areas, such as the retrocardiac
region, which can be challenging to detect on anterior-posterior X-rays. While lateral radiographs were previously used to detect pleural uid, ultrasonography is
now the preferred imaging method for this purpose due to its portability. It is essential to minimize unnecessary radiation exposure to nonthoracic structures like the
lower neck, proximal upper extremity, and upper abdomen by using proper collimation and shielding [2].
When interpreting X-rays, it is crucial to ensure that both hemithoraxes of the
patient are equally pressed against the detector, as unequal compression can lead to
misleading radiolucent appearances. The symmetry of the X-ray can be assessed
practically by examining the ribs. On the side of rotation, the ribs appear shorter

154
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S. Taşar and R. Savaş
c
Fig. 12.3 In the case of a newborn with a gestational age of 28weeks, on the rst day of life, a
chest X-ray (CXR) reveals diffuse hazy granular pulmonary airspace opacication (a). The patient
received mechanical ventilation and surfactant treatment within the rst 5days of life, and a focal
radiolucent area consistent with pulmonary interstitial emphysema is observed in the left lung. It
is challenging to distinguish this condition from congenital pulmonary airway malformation
(CPAM) based on this image alone (b). By the 17th day of treatment, the lungs appear normal (c)
anteriorly and longer posteriorly. Obtaining inspiratory radiography in young children can be challenging. In a good inspiratory radiograph, the diaphragmatic border
should align with the fth and sixth anterior ribs or the tenth and 11th posterior ribs
on the posterior-anterior view. In infants, unlike in adults, the thorax expands in all
directions, diaphragmatic movement is minimal, and distinguishing between inspiration and expiration is difcult.
12.2.1.1 The Thymus
The thymus gland is visible on chest radiographs from birth to 3years of age, with
its largest volume occurring, particularly during the rst 2years [3]. Its contours
appear convex until the rst 4years of age, after which they become concave. In a
normal thymus gland, there should be no compression of adjacent anatomical structures. At the junction of the thymus gland with the heart, you may observe the “cardiothymic notch,” and its more prominent form is referred to as the “sail sign”
(Fig.12.4a). Additionally, the “wave sign” can be seen due to the pressure exerted
by the ribs (Fig.12.4b).

12 Radiologic Evaluation ofLower Respiratory System
155
a
Fig. 12.4 The extension of the thymus toward the minor ssure is referred to as the “sail sign” (a).
Its indentation into the intercostal spaces is known as the “wave sign” (b)
b
Prominent thymus tissue can create the appearance of a mediastinal mass. This
can be differentiated using ultrasonography, where the normal thymus exhibits
echogenicity similar to that of the liver (Fig.12.5).
Thymus tissue is very soft. Even in marked hyperplasia, it does not compress the
surrounding tissues. It can change shape with breathing and position. It contracts
and elongates on inspiration and shortens and expands on expiration. It does not
change the location of the tracheobronchial tree.
Thymus size can be reduced by stress (fever, infection, congenital heart and lung
disease, malnutrition, and chemotherapy). When the stress factor disappears,
rebound hypertrophy can be observed. Those with abnormal ndings on a direct
X-ray are rst evaluated by ultrasound (US) and then by MRI if necessary. On MRI,
the normal thymus has a homogeneous signal and an intermediate signal on
T2-weighted images, similar to the spleen and lymph nodes.
Tracheal Buckling
Anterior and rightward displacement of the trachea due to ligamentous laxity is
physiologic and is called tracheal buckling in young infants (Fig. 12.6). This
becomes more evident in expiration. Normal deviation to the left is observed only
when the aortic arch is located to the right of the trachea.
Hilum
The hilar regions are not prominent in the neonatal period. Hilar density gradually
increases with age. Unlike adults, hilar growth in children is usually secondary to an
acute infection, not a tumor. In infancy, it can also be seen secondary to congenital
anomalies such as bronchogenic cysts. It may be difcult to distinguish the vein from
nodal enlargement. In nodal enlargement, the outer contour of the hilum becomes convex.
Diaphragm
Normally, the left hemidiaphragm is lower than the right due to the impact of the
heart. There should be no more than a 2cm height difference between the two
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