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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)

124
partner about sharing that responsibility. This may already be covered if you have a
right of rst refusal clause in your parenting agreement [11].
C. C. Cingi
10.4.2 Inform Your Co-parent oftheSpecifics
When handing off parental duties to your co-parent, ensure everyone understands
their responsibilities. Put all drugs and their dosages and administration times down
on paper. Before entrusting someone else with your child, ensure they know how
things have been going so far [11].
When you’ve nished communicating the necessary information, your co-parent
can take over. Have faith in their ability to nurse your child back to health and commit to doing what is in the child’s best interest. Although it may be challenging to
relinquish control, you must do so in this situation [11].
10.4.3 Exhibit Cohesion
Maintain a cheerful environment for your ill youngster. Treat your co-parent with
respect before your child, and consider increasing your co-parent’s visitation rights.
They could make more frequent phone or text checks. If your kid is genuinely sick,
consider inviting them to spend time with them [11].
A child can benet from seeing their parents work together as co-parents at any
time, but the effect is magnied when one is ill. Feel free to set aside your differences and focus on getting your sick child well again if that youngster is yours. Put
aside your differences and work together as a team for the sake of your child [11].
It’s not easy to deal with a sick kid, but you must do it effectively when it happens. Before your child is sick, discuss how you’ll improve them quickly and implement your plans [11].
10.5 Talking toOne’s Siblings andPals
Children with life-limiting illnesses may have a different concept of death and dying
than children of the same age. This comprehension results from their participation
in discussions about their sickness and its management, as well as their exposure to
the deaths of other children [8].
Siblings and close friends of a child with a terminal disease need to have discussions about death and dying that are appropriate for their age. Parents and caregivers
often have their losses to contend with. The palliative care team members may need
to help them to have these conversations [1, 12].
Siblings can gain from:
• being included in family conversations
• being given information about their sibling’s condition

10 Communication withSick Child’s Parents
125
• being given time to discuss concerns with medical professionals
• making connections with support groups or other children dealing with similar
circumstances
• receiving individualized attention and care
• being encouraged to express negative emotions like sadness and anger
• having these feelings and emotions normalized [13, 14]
They are reassured about their own health and permitted to visit their sick sibling.
10.6 Conclusion
When talking to kids, keeping their developmental level in mind is essential [15,
16]. Age-appropriate strategies for communicating with kids are outlined in the
below [17–22].
Stability can be fostered for children of all ages by upholding consistent routines
and expectations. Having “regular” family time that isn’t constantly focused on the
child’s condition is also benecial. To keep things as normal as possible for their
sick kid, parents often need guidance in recognizing how these reminders impact
their child’s life [20–22].
References
1. PCC4U.Topic 3 | Activity 5: Communication with children and their families. https://pcc4u.
org.au/learning/topics/topic3/t3_section2/t3_activity5/. Accessed 4 Oct 2023.
2. Wiener L, Zadeh S, Battles H, Baird K, Ballard E, Osherow J, Pao M.Allowing adolescents
and young adults to plan their end-of-life care. Pediatrics. 2012;130(5):897–905.
3. CareSearch. Communicating with health professionals. 2011. www.caresearch.com.au/care-
search/tabid/1107/Default.aspx. Accessed 6 Dec 2012.
4. Zwaanswijk M, Tates K, van Dulmen S, Hoogerbrugge PM, Kamps WA, Beishuizen A, Bensing
JM.Communicating with child patients in pediatric oncology consultations: a vignette study
on child patients’, parents’, and survivors’ communication preferences. Psychooncology.
2011;20(3):269–77.
5. Rollins JA.Tell me about it: drawing as a communication tool for children with cancer. J
Pediatr Oncol Nurs. 2005;22(4):203–21.
6. Turner J, Clavarino A, Yates P, Hargraves M, Connors V, Hausmann S. Development of a
resource for parents with advanced cancer: what do parents want? Palliat Support Care.
2007;5(2):135–45.
7. Sandler I. Parental grief and palliative care require attention. Pediatr Adolesc Med.
2004;158(6):590–1.
8. Bluebond-Langner M, Belasco J, DeMesquita Wanda M. “I want to live, until I don’t want to
live anymore”: involving children with life-threatening and life-shortening illnesses in decision making about care and treatment. Nurs Clin North Am. 2010;45(3):329.
9. Klick JC, Hauer J. Pediatric palliative care. Curr Probl Pediatr Adolesc Health Care.
2010;40(6):120–51.
10. Clark M.Common sense pediatric patient and parent communication tips. https://etactics.com/
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C. C. Cingi

Part II
Diagnostic Testing

Radiologic Evaluation ofUpper
Respiratory System
GoncaKoc, AloisiaPalomaHernandezMorales,
andHuseyinHudaverAlper
11.1 Introduction
The upper airway is dened as the airway passage located between the nostrils and
the trachea. It consists of the nasal passage, pharynx (naso- and oropharynx), and
larynx. Diseases of upper airway and its obstructive pathologies are more common
in children due to certain anatomical and physiological characteristics specic to
the respiratory system: The children have enlarged adenoid tissue and narrower
nasopharynx compared to adults. Conus elasticus lining the region between the
vocal cords and the cricoid is vulnerable to edema related to its loose connective
tissue. Children also have weaker respiratory muscles to compensate the respiratory
distress [1]. Laryngeal rest during current expiration, a variable resistance mechanism, allows maintaining a stable and adequate residual functional capacity through
a compliant rib cage and lung. The variety of the symptoms and the fact that they are
not specic to the disease, clinicians (pediatricians, otolaryngologists) may need to
implement radiological imaging to establish a diagnosis. The basic radiological
imaging method in the upper airway diseases is radiography of associated anatomic
region, subsequently computed tomography (CT) can also be obtained. Although
magnetic resonance imaging (MRI) is not acquired in the emergency setting due to
11
G. Koc (*)
Department of Radiology, King Hamad University Hospital, Royal Medical Services,
Muharraq, Bahrain
e-mail: gonca.koc@khuh.org.bh
A. P. H. Morales
Department of Radiology, Instituto Nacional de Enfermedades Respiratorias, Ismael Cosío
Villegas, México City, Mexico
H. H. Alper
Division of Pediatric Radiology, Department of Radiology and Medical Imaging, Ege
University School of Medicine, 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_11
129

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G. Koc et al.
its prolonged examination time, has signicant contribution to the diagnosis of
tumoral lesions of the airway and sleep apnea. In this section, pediatric upper airway diseases will be discussed according to the anatomical regions. First, the diseases specic to the anatomical regions, subsequently the common diseases that
may affect all regions will be discussed with a specic emphasize on their radiological ndings.
11.2 Nasal Cavity
The nasal cavity forms the initial part of the airway as anteriorly connected to the
external environment with the nasal vestibule. Posteriorly, it has continuity with
the nasopharynx via choanae. The borders of the nasal cavity are; cranially cribriform plate of the ethmoid bone, caudally the hard and soft palate, laterally the
turbinates, and medial walls of the maxillary sinuses. Due to the direct connection between the nasal cavity and paranasal sinuses, their diseases are closely
related. During the childhood, the most common disease is the inammatoryinfectious diseases. The physical examination is the basic diagnostic method of
the diseases of paranasal cavity. The radiological imaging, particularly CT and
MRI, should be reserved for the chronic, complicated inammatory, and neoplastic diseases.
11.2.1 Choanal Atresia
The denition of choanal atresia is the lack of development of the posterior part of
the nasal cavity (choana) and therefore the interruption of the connection between
the nasal cavity and the nasopharynx. The incidence is 1 per 5000–7000 live births
[2]. It can be encountered as uni- or bilateral forms. The bilateral forms occur less
frequently. Since the neonates present with respiratory distress immediately following the birth due to compulsory nasal breathing during the neonatal period, surgery
is an emergency [3]. Children with unilateral choanal atresia show the symptoms of
unilateral nasal discharge and congestion at later stages. CT scan obtained following the failure to advance the nasogastric tube is the rst choice imaging method for
conrmation of choanal atresia and surgical planning. There are two forms of choanal atresia: In the bony atresia, the lateral walls of the nasal cavity bend medially
and the enlarged vomer come together to cover the choana. In membranous atresia,
bony structures are generally normal. The posterior nasal cavity and nasopharynx
connection is interfered with a thin membrane. In the CT examination of the nasopharynx accumulation of a small amount of water-soluble contrast material dripped
through the nostrils at the level of atretic choana might be helpful in making the
diagnosis of choanal atresia (Fig.11.1).

11 Radiologic Evaluation ofUpper Respiratory System
131
a
Fig. 11.1 CT images of membranous and bony atresia of the choana. (a) One-month-old boy with
left-sided membranous type choanal atresia. Thin membrane separating choana and nasopharynx
is seen (white arrow). The water-soluble contrast medium is accumulated within the atretic pouch
of the choana (black asterisk). (b) Three-month-old boy with left-sided bony type choanal atresia.
Vomer is thickened (black asterisk) and bent laterally to obstruct the choana (white arrow)
b
11.2.2 Rhinosinusitis
Rhinitis is dened as the inammation of the nasal mucosa. However, since it is
almost always accompanied with the inammation of the paranasal sinuses, the use
of the term rhinosinusitis would be more accurate. Rhinosinusitis can be classied
as acute (less than 1month) or chronic (more than 3months); and as viral or bacterial. In children, most cases occur as viral rhinosinusitis. The American Academy of
Pediatrics denes acute bacterial sinusitis as a persistent illness with nasal discharge
of any quality and/or daytime cough lasting for >10days without improvement, a
worsening clinical course, a severe onset of symptoms with concurrent fever (temperature≥39°C), and purulent nasal discharge for at least 3 consecutive days [4].
Since the radiological imaging does not change the treatment approach, it is not
recommended for the diagnosis of uncomplicated acute rhinosinusitis [5].
Radiography is not benecial for the diagnosis and follow-up of acute/chronic rhinosinusitis of pediatric patients due to difculty in positioning and evaluating particularly the ethmoid sinuses. Furthermore, paranasal sinus opacication on CT and
MRI can be encountered even in healthy children without a clinical sign of rhinosinusitis. Therefore, radiological imaging has a limited role in the diagnosis (6). As
recommended by the American College of Radiology, the imaging modality of
choice should be paranasal sinus CT without intravenous (IV) contrast administration for surgical planning if functional sinus surgery is planned for chronic or recurrent rhinosinusitis, and as paranasal and brain CT/MRI with IV contrast if
rhinosinusitis/invasive fungal sinusitis with intracranial or orbital complication is
suspected [6].
Complications of the rhinosinusitis occur in the form of spread of the infection to the orbit, intracranial region, or bone. Orbital complications are the
most common and develop with the dispersal of ethmoid or frontal sinus

132
ab
Fig. 11.2 Subperiosteal
abscess. CT orbits with
intravenous contrast
administration of a
12-year-old boy reveals
right-sided subperiosteal
abscess (white arrows) and
bilateral ethmoid sinusitis
(black asterisk)
G. Koc et al.
Fig. 11.3 Orbital and intracranial abscess as the complication of rhinosinusitis. (a) Postcontrast
T1-weighted coronal MR image of 10-year-old girl with left-sided ethmoid sinusitis (white arrow),
intraorbital abscess (black arrow), and orbital cellulitis (black asterisk). (b) T2-weighted coronal
MR image of a 15-year-old boy previously diagnosed with leukemia and fungal sinusitis.
Pansinusitis, defect of nasal septum (white arrows) associated with fungal infection, intracranial
abscess (black arrow), and intraorbital extension of the infection (white asterisks) are seen
infections. Orbital complications are as follow, preseptal cellulitis, orbital cellulitis, orbital abscess, subperiosteal abscess, and cavernous sinus thrombosis
(Figs.11.2 and 11.3). In orbital complications, a favorable response to medical
treatment compared to particularly intracranial complications is expected [7].

11 Radiologic Evaluation ofUpper Respiratory System
133
Pottt’s Puffy tumor is the subperiosteal abscess of the frontal bone caused by
the extension of rhinosinutis. Intracranial spread is the most serious complication and appears as inflammation of any structure within the brain or intracranial abscess.
11.2.3 Sinonasal Polyposis andAntrochoanal Polyp
Nasal polyp is a benign and inammatory growth of the nasal mucosa and its extension into the nasal cavity and/or paranasal sinuses. It is often associated with chronic
and allergic rhinosinusitis and less common during the childhood. Nasal polyposis
might be a sign of cystic brosis, immune deciency, or ciliary dyskinesia in children [8].
A single polyp is albeit rarely encountered in anywhere in the nasal cavity. When
it originates from the maxillary sinus antrum and extends posteriorly to the choana
is called as antrochoanal polyp. The major symptom caused by anthrochoanal polyp
is chronic nasal obstruction.
The radiological ndings associated with nasal polyps are expansion of the
sinus ostia and remodeling of the bony walls of the nasal cavity and sinuses without causing any destruction. On MRI, they are hyperintense on T2 and hypointense on T1-weighted images, and might peripherally enhance following IV
gadolinium injection. If sinonasal surgery is planned, a paranasal sinus CT or
MRI examination, preferably without IV contrast, can be obtained for preoperative planning (Fig.11.4).
a
Fig. 11.4 MR images of antrochoanal polyp. (a) T2-weighted MR image reveals left-sided antro-
choanal polyp lling left maxillary sinus (asterisk) and extending to the nasal cavity via accessory
maxillary sinus ostium (white arrow). It is hyperintense on T2-weighted image. (b) T1-weighted
MR image, note enlarged maxillary sinus accessory ostium (asterisk) and extension of antrachoanal polyp into the nasal cavity (white arrow)
b

134
G. Koc et al.
11.2.4 Juvenile Nasopharyngeal Angiofibroma
Albeit rare, nasopharyngeal angiobroma is the most common benign tumor of the
nasal cavity [9]. It is a locally aggressive and highly vascular tumor frequently
encountered in adolescent boys. Patients usually present with nasal congestion and
bleeding. The common thought of its origin is sphenopalatine foramen. Extension
of the tumor in all directions, primarily by lling the pterygopalatine fossa, and
intracranial extension may also be encountered. Due to its increased blood supply,
biopsy may cause excessive bleeding. Therefore, radiological diagnosis is extremely
important. The most important radiological ndings of the tumor on CT and MRI
are typical location of pterygopalatine fossa and intense contrast enhancement following IV contrast medium administration (Fig.11.5). CT is useful in revealing
bony erosion. On MRI, dot like signal void areas are indicative of increased vascularity of the tumor.
Fig. 11.5 Contrastenhanced CT image of
14-year-old boy reveals
vividly enhancing
right-sided nasopharyngeal
angiobroma (asterisk). It
is lling pterigopalatine
fossa and extending to the
posterior of right nasal
cavity, parapharyngeal, and
masticator spaces (black
arrows)
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