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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)

11 Radiologic Evaluation ofUpper Respiratory System
135
11.3 Pharynx
Pharynx is divided into three parts: nasopharynx, oropharynx, and hypopharynx.
11.4 Nasopharynx
Nasopharynx is continuous with the nasal cavity and forms the uppermost part of
the pharynx. Its borders are the skull base above and the soft palate below.
11.4.1 Adenoid Hypertrophy
The posterior and superior walls of the nasopharynx are rich in lymphoid tissue.
Hypertrophy of nasopharyngeal lymphoid tissue in children, particularly between
the ages of 3–6, is called as adenoid hypertrophy or nasopharyngeal lymphoid
hypertrophy and probably due to recurrent infections and allergic conditions [10,
11]. Adenoid hypertrophy may cause chronic adenoiditis; chronic sinusitis, snoring,
sleep apnea due to obstruction of nasopharynx; otitis media, serous otitis media
related with the obstruction of the eustachian tube, and either medical or surgical
treatment might be required [12]. The presence of adenoid hypertrophy and the
degree of airway obstruction can be evaluated by exible beroptic nasal endoscopy
or lateral neck radiograph. Different results have been reported in the literature by
comparing these two methods [13, 14]. Airway patency can be evaluated by measuring the adenoid/nasopharynx ratio (thickness of the adenoid in the craniocaudal
direction/distance between basiocciput and hard palate) on lateral radiograph
(Fig.11.6). However, with lateral neck radiography the radiation exposure is the
main concern. If the radiography is not obtained with optimum positioning and timing (with the neck in slight extension and at the end of inspiration) may lead to
misinterpretation of the exact obstruction of the nasopharynx. Although it is presumed that hypertrophied adenoid regresses after the age of 6–7, can be encountered incidentally in imaging at later ages. Adenoid hypertrophy has typical CT and
MRI appearance that helps differentiate from nasopharynx cancer: It grows symmetrically with a smooth surface and the Rosenmüller fossa is not obliterated.
Following IV contrast administration, hypo- and hyperintense lines from front to
back, especially on MR images, are in favor of adenoid hypertrophy (Fig.11.7).
11.4.2 Nasopharyngeal Carcinoma
Nasopharyngeal carcinoma is encountered less frequently in children compared to
adults and constitutes less than 1% of childhood cancers [15]. It usually occurs during the adolescence. Since the clinical ndings are nonspecic and mostly related
with the obstruction of the nasopharynx and eustachian tube, locally advanced
tumors are most likely to be encountered at the time of diagnosis. It is seen as a mass

136
Fig. 11.6 Lateral neck
radiograph of 6-year-old
boy with adenoid
hypertrophy. Measurement
of adenoid/nasopharynx
ratio is shown. a adenoid;
n nasopharynx
G. Koc et al.
a
Fig. 11.7 Adenoid hypertrophy of a 14-year-old girl. (a) T2-weighted MR image shows homog-
enous adenoid hypertrophy with smooth surface (white arrows). (b) On T1-weighted contrastenhanced MR image, note the hypo- and hyperintense vertical lines suggesting adenoid hypertrophy
rather than carcinoma (white arrows)
b
in the posterior wall of the nasopharynx, which often grows asymmetrically and
obliterates the Rosenmüller fossa. In contrast-enhanced examinations, the typical
linear pattern observed in adenoid hypertrophy disappears, the lesion enhances heterogeneously. The involvement of the parapharyngeal, prevertebral, and masticatory
spaces; skull base indicates locally advanced disease. MRI with IV contrast is the

ab
11 Radiologic Evaluation ofUpper Respiratory System
Fig. 11.8 MR images of 13-year-old boy with nasopharynx carcinoma. (a) T2-weighted axial
image. Note the irregular surface of nasopharyngeal mass (white arrows). (b) T1-weighted postcontrast image is revealing asymmetric nasopharyngeal mass more prominent on the left (asterisk).
Lateral retropharyngeal lymph node is also seen (white arrow)
137
choice of imaging to reveal the extent of the disease and has mostly been replaced
CT.MRI is also superior to CT in demonstrating the lateral retropharyngeal lymph
nodes, which are the primary nodal spread site of the disease [16] (Fig.11.8).
11.5 Oropharynx
Oropharynx is the middle part of the pharynx that is continuous with the oral cavity.
The borders; superiorly and anteriorly soft palate, inferiorly upper border of the
epiglottis, posteriorly the posterior wall of the pharynx. It contains the root of the
tongue and palatine tonsils.
11.5.1 Thyroglossal Duct Cyst
The development of the thyroid gland begins with the proliferation of endodermal
cells at the base of the tongue in the third week of gestation. It then descends from
the root of the tongue through the thyroglossal canal, anterior to hyoid bone and
larynx, to its normal location in the neck. Thyroglossal duct cyst develops due to
incomplete obliteration of the thyroglossal duct and is the most common congenital
cystic neck lesion of children. Approximately 65% of the cases has infrahyoid localization and tongue root localization is extremely rare (1–2%) [17]. It typically has
midline or paramedian location.

138
G. Koc et al.
a
Fig. 11.9 Thyroglossal duct cysts with various locations. (a) T1-weighted postcontrast image
shows a thick-walled cystic lesion with median location at the level hyoid bone (white arrows). It
has central enhancing septae. (b) Another thyroglossal duct cyst of root tongue on sagittal
T1-weighted MR image (white arrow)
b
Patients with thyroglossal duct cyst present with painless soft tissue swelling of the
neck. When infected redness of the skin and pain may also be added to the clinical
scenario. Diagnosis is mostly based on clinical ndings. Ultrasonography (US) helps
establish cystic nature of the lesion. In the oropharynx, imaging with MRI or CT is
required for the delineation of the lesion. CT reveals a homogeneous, hypodense, thinwalled cystic lesion with no signicant contrast enhancement if it is not infected.
While high signal intensity on T2-weighted MR images is expected, its signal on
T1-weighted images varies depending on proteinaceous or hemorrhagic content. The
thick wall and internal septae would suggest infection or hemorrhage (Fig.11.9).
11.5.2 Hypertrophied Palatine Tonsils andPeritonsiller Abscess
Palatine tonsils are lymphoid tissue clusters located on both lateral walls of the
oropharynx, showing continuity with the soft palate at the top and front, the root of
the tongue at the bottom and front, and the posterior wall of the pharynx in the back.
Tonsillitis is mostly viral and 30% bacterial caused by group A beta hemolytic
streptococcus. The diagnosis is solely based on clinical ndings. In conjunction
with inammation of the nasopharyngeal adenoid tissue, it may cause airway
obstruction. If any complication is suspected imaging methods are considered.
Peritonsillar abscess is the most common infection of the neck region and occurs
when tonsillitis turns into cellulitis and then into abscess [18]. Radiological imaging
has an important role in the diagnosis and management of the treatment. CT neck
with IV contrast administration is the choice of imaging modality (Fig.11.10).

11 Radiologic Evaluation ofUpper Respiratory System
Fig. 11.10 Contrastenhanced CT image of
12-year-old girl with
peritonsillar abscess.
Right-sided hypodense,
rounded peritonsillar
abscess is seen (white
arrows)
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11.6 Hypopharynx
Hypopharynx forms the most distal part of the pharynx and is continuous with the
oropharynx above, the cervical esophagus below. It starts at the level of hyoid bone
above and ends just below the cricoid cartilage consisting of three parts: Pyriform
sinuses, posterior pharyngeal wall, and postcricoid region [19].
11.6.1 Retropharyngeal Abscess
The retropharyngeal region is a potential space located posterior to the pharynx. It
extends from the skull base to the mediastinum below, is surrounded by the prevertebral muscles posteriorly and the carotid sheath on the sides. It contains lymph
nodes and fatty tissue [20]. The retropharyngeal abscess is frequently encountered
in early childhood, up to 4–5years of age, as this is the age group that upper respiratory tract infections are more common. The abscess is thought to occur as a result of
lymph adenitis of this region. Rarely, trauma caused by the foreign body aspiration
may be the reason for the abscess. Early diagnosis and treatment are profoundly
important since delay may lead to respiratory tract obstruction, mediastinal extension and cause sclerosing mediastinitis.
Lateral nasopharyngeal radiography should be obtained during the inspiration with
the neck in slight extension. Normally the thickness of the soft tissue anterior to the
second cervical vertebra does not exceed the thickness of ½ vertebral body. When this

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a
Fig. 11.11 Retropharyngeal abscess vs. uid. (a) Sagittal reformatted contrast-enhanced CT
image of 8-year-old boy revealing retropharyngeal abscess (white arrows) with enhancing capsule
(black arrow). (b) Retropharyngeal uid of 5-year-old boy (white arrows)
b
is the case, it might be the sign of infection of the retropharyngeal region. The radiograph should also be examined carefully for the presence of a foreign body. Intravenous
contrast-enhanced CT of the neck is the gold standard imaging method in the diagnosis, localization, and extension of retropharyngeal abscess. A hypodense, peripherally
enhancing uid collection is dened as retropharyngeal abscess (Fig. 11.11).
Treatment includes abscess drainage and antibiotics. Since the treatment is usually
conservative, other infections of retropharyngeal region as retropharyngeal edema,
cellulitis, and phlegmon that reveal nonloculated uid collection without any capsular
enhancement should be differentiated from retropharyngeal abscess.
11.6.2 Lymphatic Malformation
As the most common vascular malformation of the neck, the majority of lymphatic
malformations are located in the cervical region [21]. The diagnosis might be established antenatally; however, patients may also present with various symptoms
related with intralesional bleeding and infection in the postnatal period. They
develop due to drainage obstruction of the lymphatic channels to venous system. If
the size of the lesion large enough might cause airway compression.
The rst-line imaging method is US.The lesion consists of single or multiple
cysts with various sizes and contains septa. The echogenicity of the cyst content
alters depending on whether it is complicated by bleeding or infection. MRI with IV
contrast is the modality of choice due to its higher soft tissue resolution to show
extent of the lymphangioma. The signal intensity of the cysts varies depending on
whether the content is hemorrhagic or proteinaceous. Lack of solid component and
contrast enhancement solely in the septa and cyst walls distinguishes lymphangioma from teratoma (Fig.11.12).

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11 Radiologic Evaluation ofUpper Respiratory System
Fig. 11.12 Lymphatic malformation of the neck. (a) Two-year-old girl presented with soft tissue
swelling of the neck. T2-weighted axial MR image shows left-sided multiloculated cystic lesion of
the neck (white arrows). It has hypointense component suggesting hemorrhage (white asterisk) and
retropharyngeal extension (black arrow). (b) Contrast-enhanced CT neck of newborn with antenatal diagnosis of lymphatic malformation and respiratory distress. Left-sided cystic mass of the
neck (white arrows), with enhancing septae (black arrow) and airway compression (white asterisk)
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11.6.3 Hemangioma andVenous Malformations
Hemangiomas and vascular malformations of the head and neck region constitute of
60% of vascular lesions of childhood and may affect airway when they seat deep
and reach big sizes [22]. Infantile hemangiomas present after few weeks following
birth while vascular malformations are usually encountered at birth.
Hemangioma is a benign vascular tumor and characterized as solid mass lesion.
When it is located at airway usually diagnosed with bronchoscopy during the rst
1.5–2years of life at rapidly growing phase due to obstructive respiratory symptoms.
When bronchoscopic ndings are vague or for the delineation of the extension of the
lesion radiological imaging is conducted. On CT vivid enhancement of the lesion following contrast administration is suggestive of the diagnosis of hemangioma. MRI
would be more advantageous due to its higher soft tissue resolution and lack of radiation exposure. Signicant increased signal on T2-weighted images and vivid and early
enhancement on postcontrast images are the features indicative of hemangioma.
Venous anomalies usually present at birth and grow proportionally as the child
grows up. They are blue, soft, compressible lesions and may enlarge during valsalva
maneuver. Supercial lesions may be diagnosed with US and Doppler US with
radiological ndings of vascular channels with slow ow. When the lesions have
deeper extensions MRI may help show the extent of the lesion.

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If the lesions are causing airway compromise, treatment options for hemangioma
are propranolol, steroids, laser ablation, surgical excision of the lesion. Venous malformations are decreased in size with Sirolimus and embolization and following
surgical resection might be conducted.
11.6.4 Lymphoma
In children, lymphoma is the most common malignant tumor of the head and neck
region. It often arises with lymph node involvement. While extranodal involvement is
observed at a rate of approximately 30% in non-Hodgkin lymphoma, it is extremely
rare in Hodgkin’s disease [23]. Involvement of the sinonasal region and Waldeyer’s
ring may be associated with airway-related symptoms and be observed as polypoid
masses with smooth surfaces in the submucosal region. Advanced imaging of masses
can be performed with contrast-enhanced CT or MRI (Fig.11.13). CT is superior in
revealing bone destruction, while MRI is superior in showing soft tissue extension and
intracranial spread. The masses have soft tissue density on CT.On MRI, the lesions are
hypointense on T1-weighted image and hypo- or hyperintense on T2-weighted image.
It may show diffusion restriction and contrast enhancement with varying degrees.
Fig. 11.13 Eight-year-old
girl with right-sided tonsil
mass. Axial CT image is
revealing mass of right
tonsil obliterating
prevertebral (black arrows)
and right parapharyngeal
spaces (white arrow). The
patient was diagnosed as
Burkitt lymphoma

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11 Radiologic Evaluation ofUpper Respiratory System
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11.6.5 Rhabdomyosarcoma
Rhabdomyosarcoma (RMS) is the most common malignant tumor of head and neck
following lymphoma in children [24]. The average age at diagnosis is under
5–6 years old, and 72–81% of cases are diagnosed before the age of 10 [25].
Rhabdomyosarcomas located in the sinonasal cavity and parapharyngeal space are
dened as parameningeal RMS and have the worst prognosis due to their close relation to cranium and advanced local disease at the time of diagnosis. Findings of
skull base invasion, intracranial extension, and cranial nerve invasion are encountered in approximately 1/3 of the cases [25]. Patients may often present with persistent, nonspecic or sometimes airway-related symptoms (such as nasal congestion).
In the presence of a rapidly growing head and neck mass in the childhood age group,
RMS should be at the forefront of the differential diagnosis list.
Although radiological ndings are nonspecic, imaging plays a key role to dene
the local extension, staging, and evaluation of treatment response. US can be utilized to identify supercial lesions and to reveal their solid nature. However, the
lesions usually have deep location. MRI is the rst-line imaging method due to its
capability of showing the location and local spread of the lesions due to its high
spatial and contrast resolution. The lesion is hypo-isointense relative to the muscle
on T1-weighted images and hyperintense on T2-weighted images, might be heterogeneous due to bleeding or necrosis. Signicant enhancement with IV contrast
material and diffusion restriction are other features of RMS (Fig.11.14). CT should
be reserved for the investigation of lung metastases to minimize radiation exposure.
Fig. 11.14 Ten-year-old boy with rhabdomyosarcoma. (a) Axial T2-weighted MR image show-
ing T2 hyperintense and slightly heterogeneous mass lling both nasal cavity more prominently on
the right (arrows) and chonoae (asterisk). (b) On postgad axial T1-weighted image the mass is
enhancing vividly with some heterogeneity

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11.7 Larynx
The larynx locates between the hypopharynx and the trachea. It basically has a cartilage structure and is divided into three parts by the vocal cords: supraglottic, glottic, and infraglottic.
11.7.1 Subglottic Stenosis
The subglottic region is dened as the region between the inferior of the vocal cords
and the inferior border of cricoid cartilage. Stenosis may be congenital or acquired.
Necrosis due to pressure created by the cuff during the prolonged intubation is the
most common cause of subglottic stenosis. Congenital and idiopathic forms are
encountered less frequently, and congenital subglottic stenosis may be accompanied
by pathologies such as tracheoesophageal stula and vascular ring anomalies.
Bronchoscopy is the basic imaging method in the diagnosis. However, 3 plane
CT and MRI images can be implemented in the diagnosis and surgical planning.
Virtual endoscopy and VRT images of CT may further help understand the degree
and length of the stenosis (Fig.11.15). Contrast-enhanced CT images also rule out
the possibility of vascular compression.
11.7.2 Laryngotracheal Papillomatozis
The causative agent of laryngotracheal papillomatosis is human papilloma virus.
Children develop the disease by ingesting the virus from a contaminated birth canal
during birth. It is the most common laryngeal neoplasia of the childhood [26]. The
a bc
Fig. 11.15 Five-year-old girl with the history of previous intubation is presenting with inspiratory
stridor. (a) Sagittal CT image reveals long segment subglottic stenosis of the trachea. (b, c)
Volume-rendered 3D CT images on coronal and sagittal plain help better visualization of the stenosis. Arrows on coronal image show the narrowest segment (asterisk pyriform sinuses)
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