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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)

208
a
b
c
d
–1
Volume (L)
zs
−
V. Koucký and N. Cobanoglu
10
8
6
4
)
2
0
–2
Flow (L·s
–4
–6
–8
–10
Volume (L)
e
4
2
10 4
8
6
4
2
6
0
–2
–4
–6
–8
–10
f
3
2
1
0
4
2
–1
–2
–3
–4
Volume (L)
g
12
2
h
Fig. 16.3 Typical shapes of the ow-volume loops. (a) Normal ow volume loop; (b) peripheral
airway obstruction; (c) one-sided main bronchus obstruction; (d) large (central) airway instability
(tracheomalacia); (e) xed upper airway obstruction (mild); (f) xed upper airway obstruction
(severe); (g) variable extrathoracic upper airway obstruction; (h) variable intrathoracic upper airway obstruction
percentage of the norm (% n), and 80% was traditionally considered as a level of
normality (values >80% n were ‘healthy’, and those <80% were ‘diseased’). This
approach has several limitations and is no longer recommended [9]. The main reason for that is the fact that the reference data distribution of the respective outcomes
is not uniform and the standard deviations differ for the respective outcomes. Thus,
80% may be still within the norm for one outcome but not for the other. Moreover,
the classication of the impairment severity is not uniform for all the parameters
(see example in Table16.2, which is based on Zapletal’s reference values) [8].
Currently, use of z-score is preferred. Z-score may be calculated as follows:
−=
standard deviation
measured value reference value
core

16 Spirometry andUpper Respiratory Tract
209
Table 16.1 Forced spirometry outcome parameters
Abbreviation
Parameter
(unit)
Denition
Forced vital capacity FVC (L) Maximal forcefully exhaled volume from
maximal volume level (TLC) to minimal
volume level (RV)
Forced volume exhaled in
the rst t-seconds
FEVt (L) Maximal forcefully exhaled volume during
the rst t-seconds (usually 0.5, 1 and 6s)
Peak expiratory ow PEF (L/s) Maximal ow during exhalation
Maximal expiratory ow at
25%, 50% and 75% levels
a
of FVC
MEF25, MEF50,
MEF75 (L/s)
Maximal expiratory ow when 25, 50, or
75% of FVC remains to be exhaled
Area under the curve Aex (L*L/s) Area under the expiratory part of the FV
loop
Maximum inspiratory ow MIF (L/s) Maximal ow during inspiration
Maximum inspiratory ow
at 50% level of FVC
a
Alternatively (typically in US), FEFxx may be used. XX denotes how much of the FVC has
MIF50 (L/s) Maximal inspiratory ow when 50% of
FVC has been inhaled
already been exhaled. Thus, MEF75=FEF25, MEF50=FEF50, and MEF25=FEF75. We use MEFxx in
the text, which is preferred in Europe. TLC = total lu ng capacity
Table 16.2 Zapletal’s classication of airway obstruction based on MEF25, MEF50 and PEF for
preschool children
Peripheral airway Central airway
Degree Description
MEF
% n
25
MEF
50
PEF
1 Mild 70–60 75–66 80–72
2 Moderate 59–50 65–58 71–64
3 Severe < 49 < 57 < 63
and when comparing to norm, it reects also the variability of the reference
population (standard deviation). Thus, there is just one level of normality for all
the outcomes, which is usually set to 1.65SD (Fig.16.4). Moreover, the classication of the impairment severity is uniform for all outcomes (Table16.3).
Additionally, for the rst-line evaluation of the results, lower and upper limits
of norm (LLN and ULN) may be used. Limits of the norm are borderline values
of the parameter, which are just in the norm. Everything, that is under (LLN) or
above (ULN), is already pathologic. Limits of the norm may be used to simplify
the interpretation of lung function results.

210
–4
Probability that a healthy individual has abnormal results
V. Koucký and N. Cobanoglu
95% of population
–3 –2 –1
–1,645 SD
LLN
0.01
0.11510203050
1:10 000 1:1000 1:1001:201:10
01234
z-score
70 80 90 95 99
Percentile
1,645 SD
ULN
Fig. 16.4 Z-score, percentiles and impairment probability for normally-distributed. SD standard
deviation; LLN lower limit of norm; ULN upper limit of norm
Table 16.3 Classication of
impairment severity based on
z-score for whatever
parameter proposed by ERS
2022 [9]
Degree
Description
1 Mild
2 Moderate
3 Severe
SD standard deviation
a
For whatever outcome parameter
a
z-score
−1.65 to −2.5 SD
−2.5 to −4 SD
< −4 SD
16.3 Forced Spirometry andUpper Airway Pathology
Spirometry is not primarily intended to evaluate upper airway pathology. Other lung
function methods such as rhinomanometry, body plethysmography (airway resistance measurement), etc., may be more helpful. The value of spirometry in assessing upper airway obstruction is based on the fact, that it is widely available and may
raise suspicion about upper airway obstruction during the rst-line lung function
testing. The most common clinical scenarios, when upper airway obstruction may
be present include laryngomalacia and tracheomalacia (airway instability—variable
obstruction), xed obstruction in laryngeal stenosis, (bilateral) vocal cord palsy,
laryngeal oedema, tracheal stenosis—extraluminal (compression by great vessels,
goitre), intraluminal (mucus stagnation, granulation tissue, foreign body, tumours)
or intramural (complete cartilaginous rings). It is important to note, that both the

16 Spirometry andUpper Respiratory Tract
211
specicity and sensitivity of spirometry for upper airway pathology are not very
high. Other methods such as computed tomography or exible endoscopy are necessary to conrm the suspicion.
The value of forced spirometry and FV loop for diagnosing upper airway obstruction has been evaluated previously and different criteria have been proposed. Upper
airway obstruction may be suspected based on the shape of the FV loop (so-called
visual criteria). Variable extrathoracic upper airway obstruction (e.g. laryngomalacia) is characterised by ow limitation during the inspiration, while the expiratory
part of the FV loop is without alteration (Fig.16.3g). In the case of variable intrathoracic upper airway obstruction, ow limitation is present during expiration,
while the inspiratory part of the FV loop is without alteration (Fig.16.3h). In xed
upper airway stenosis (e.g. laryngeal stenosis, subglottic stenosis, etc.), both inspiratory and expiratory ows at higher levels of FVC (more than 50%) are limited.
Thus, PEF, MEF75 and MIF50 are reduced, while those at lower volume levels
(MEF50 and MEF25) may be normal. The typical FV loop shapes are shown in
Fig.16.3e, f. In upper airway obstruction, the lung volumes (FVC and others) are
usually not affected. Typical shapes of FV curves in upper airway obstruction mentioned above have been described by different authors [10–13] and are usually
called sawtooth (or knee) shape (Fig.16.3d), FV loop with plateau, oscillations, etc.
Quantitative criteria to detect upper airway obstruction have been developed [10,
14–18]. The most frequently used criteria include:
1. Ratio of FEV1 (in ml) to peak expiratory ow (PEF, in l/min)>10ml/(l/min)1
(based on the criteria of Empey [14]).
2. Difference between PEF z-score and FEV1 z-score≤−2 (based on the criteria of
Zapletal [18]).
3. Ratio of MEF
(MIF
); an abnormal MEF
50%
to the ow at the mid-point of the forced inspiratory manoeuvre
50%
50%
/MIF
is dened as <0.30 or >1 (based on the
50%
criteria of [15]).
4. Ratio of FEV1 to forced expiratory volume in the rst 0.5s (FEV
) >1.5 (based
0.5
on the criteria of Rotman etal. [17]).
5. MIF
<100L/min (based on the criteria of Rotman etal. [17]).
50%
Although they are primarily intended for use in adults, some of them may be
used even in children. Their sensitivity and specicity have been studied previously.
Modrykamien et al. [19] examined spirometry in 475 adults, who had acceptedstandard tests for upper airway obstruction available (bronchoscopy, laryngoscopy,
neck CT and chest CT). The prevalence of upper airway obstruction was low (7.5%)
in a population of patients referred for spirometry to a tertiary centre. The authors
concluded that the diagnostic performance of the individual quantitative criteria for
detecting upper airway obstruction from the ow-volume loop was poor. The
sensitivity ranged from 5.5 to 47.2% and the specicity from 60.5 to 96.8%. There
1
In children, the cut off value >8mL/L/min was proposed by some authors to increase the sensitiv-
ity [22].

212
V. Koucký and N. Cobanoglu
was a signicant risk of undetecting upper airway obstruction when relying on spirometry alone. When aggregated, the diagnostic performance could be slightly
improved: the sensitivity of the aggregated criteria (≥ 1 quantitative criterion) was
69.4% and specicity 30.2%; area under the receiver-operator characteristic curve
for the aggregate criteria exceeded 0.6, while for the individual criteria, it ranged
from 0.4 to 0.5.
Spirometry indices in children with tracheomalacia were studied by Boonjindasup
etal. [20]. The ‘knee’ shape of the FV loop was common in children with tracheomalacia and PEF was signicantly reduced in children with tracheomalacia.
However, the Empey index was normal (8.21± 1.59, mean ±standard deviation)
and could not be used to characterise tracheomalacia. In children with subglottic
stenosis, the role of spirometry has been investigated by Abdullah etal. [21]. The
Empey index ranged from 7.34 to 21.40mL/L/min and signicantly improved after
dilation. It did not correlate with the severity of the stenosis. The authors concluded
that spirometry might be a useful marker in following up patients with subglottic
stenosis and a good indicator to determine intervention outcomes. Olbers etal. [22]
studied spirometry results in children after surgical repair of oesophageal atresia
with tracheoesophageal stula. They found elevated Empey index (FEV1/
PEF>8mL/(L/min)) in 58% of cases. Recurrent pneumonias were more frequent
in children with elevated Empey index (73% vs. 27%). About 87% of children with
increased Empey index had respiratory symptoms of any kind.
Especially in children, special attention must be paid to the quality and reproducibility of the FV loop as improper technique may result in falsely pathological
results. For instance, muscle weakness, collapsibility of the soft tissues in the upper
airway, mouthpiece obstruction via tongue or improper position of mouthpiece may
all result in ndings mimicking upper airway pathology. For these reasons, repeated
manoeuvres are helpful in distinguishing artefacts from true pathology. Development
of the ndings during follow-up may also be helpful.
In conclusion, different visual and quantitative criteria to detect upper airway
obstruction from forced spirometry have been proposed. Their diagnostic value was
studied in different clinical situations and seems to be limited. Despite this fact, they
should not be neglected when spirometry is available as it may raise suspicion of
upper airway pathology. Conrmation using other standard diagnostic tests (endoscopy, computed tomography) is required.
References
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16 Spirometry andUpper Respiratory Tract
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8. Zapletal A, Chalupová J.Forced expiratory parameters in healthy preschool children (3-6
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213

Allergen Testing: Purpose, Procedure, Interpretation
CansuÖzdemiral andÜmitMuratŞahiner
Abbreviations
AECs Allergen Exposure Chambers
BAT Basophil activation test
CAMP Childhood Asthma Management Program
CRD Component resolved diagnosis
CCD Cross-reactive carbohydrate determinants
EAACI European Academy of Allergology and Clinical Immunology
EMA European Medicines Agency
ECP Eosinophilic cationic protein
FDA Food and Drug Administration
FEV1 Forced expiratory ow in 1s
GA2LEN Global Allergy and Asthma European Network
ICDRG International Contact Dermatitis Research Group
NAC Nasal allergen challenge
nsLTP Non-specic lipid transfer proteins
PNIF Peak nasal inspiratory ow
RAST Phadebas radioallergosorbent test
PAF Platelet activating factor
PFAS Pollen Food Allergy Syndrome
sAT Serum acute tryptase
sBT Serum baseline tryptase
SPT Skin prick test
sIgE Specic IgE
17
C. Özdemiral · Ü. M. Şahiner (*)
Department of Pediatric Allergy and Asthma, Hacettepe University Faculty of Medicine,
Ankara, Türkiye
e-mail: cansuozdemiral@hacettepe.edu.tr; umit.sahiner@hacettepe.edu.tr
© 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_17
215

216
TNSS Total Nasal Symptom Score
VAS Visual analog scale
C. Özdemiral and Ü. M. Şahiner
17.1 Introduction
Allergic diseases exert a signicant global burden, impact individuals across all age
groups. Allergies to food, aeroallergens, drugs, and venom complicate patients’ lives
and, at sometimes pose life-threatening risks. Type 1 immediate hypersensitivity and
Type 4 delayed hypersensitivity constitute major underlying mechanisms in allergic
diseases. Clinical history takes a light for the allergist to make a diagnosis and frequently diagnosis is completed with the basic tests. Skin prick/puncture tests, intradermal tests, and patch tests are skin tests that have been utilized to diagnose allergic
diseases. The SPT is the most frequently used method that is safe and reliable. SPT
typically induces a wheal and are reaction, indicative of Type 1 hypersensitivity.
Positive SPT results are dened by wheal diameters ≥3mm, taking into account the
results of both positive and negative controls. In intradermal skin testing, allergen
extracts are administered into the dermis at a concentration that is 100–1000 times less
than that used in SPT.Patch tests are typically used for patients experiencing delayedtype hypersensitivity reactions. Nevertheless, conducting skin tests and accurately
interpreting the results need adequate training and also involve the possibility of unexpected systemic responses. Total serum IgE measurement has limited utility in allergic
diseases. Serum-specic IgE (sIgE) measurement, as a complementary or alternative
diagnostic tool, is widespread. Component-resolved diagnosis might be benecial in
cases where polysensitization complicates the diagnosis, or when negative skin prick
test (SPT) ndings are obtained despite a potential history of allergy. The allergen
provocation test could be used as a gold standard method in particular patients.
17.2 Tests
17.2.1 Skin Tests
Skin tests involve introducing an allergen through a break in the skin, which are
could be utilized for detecting allergies to inhalants, food, insect venom, or drugs.
When sensitivity to the relevant allergen exists, specic IgE molecules bound to
mast cell surface receptors become cross-linked, triggering mast cells to degranulate and release histamine along with other mediators. Skin tests result in the formation of a wheal and are response, which is indicative of Type 1 hypersensitivity [1].
In 1865, Charles H.Blackley, a physician suffering from allergic rhinitis, conducted
the rst skin test on himself. Using a lancet, he scratched a quarter-inch area of his
skin and applied grass pollen grains placed on wet gauze to the scarred area, covering it with an occlusive bandage. This experimental procedure resulted in signicant
itching and a large cutaneous response [2]. Due to the increased pain, reduced

17 Allergen Testing: Purpose, Procedure, Interpretation
217
repeatability, and possibility of maintaining several linear depigmented patches following scratch testing, as well as the higher risk of causing a systemic allergic
response, it is no longer recommended to use scratch tests. Instead, skin prick/puncture tests, intradermal tests, and patch tests have been widely utilized in diagnosing
allergic diseases [3].
Skin prick test (SPT): In 1959, H.Ebruster reported the identication of Type 1
hypersensitivity reactions through the use of the SPT [4]. Pepys modied the SPT
at 1970, and it is still frequently utilized for allergy diagnosis today [5]. Both the
EAACI (European Academy of Allergology and Clinical Immunology) and the US
Council of Allergy Asthma and Immunology recommended the initial use of skin
prick/puncture tests for individuals whose clinical histories suggest Type 1 hypersensitivity reactions to inhalant allergens [1, 6]. SPTs are minimally invasive, quick,
inexpensive, reproducible, and reliable, exhibiting a strong correlation with symptoms [7]. The implementation of standardized procedures became imperative owing
to variances in performing SPT, selecting allergens, and interpreting the results. The
Global Allergy and Asthma European Network (GA2LEN) conducted a study
across 17 centers in 14 countries, leading to the development of a standardized SPT
protocol [8]. Standardized protocol, includes using Histamine dihydrochloride
0.1% as positive control, NaCl 0.9% as negative control, and an allergen panel
Table 17.1 Standard skin prick test panel [7]
Positive control Histamindihydrochloride 0.1%
Negative control NaCl 0.9%
Alder Alnus incana
Birch Betula alba
Cypress Cupressus sempervirens
Grass mix Smooth meadow grass/Poa pratensis, cock’s foot grass/Dactilis
glomerata, perennial rye grass/Lolium prenne, timothy grass/Pheleum
pratense, meadow fescue/Festuca pratensis, meadow oat grass/
Helictotrichon pretense
Hazel Corylus avellana
Mugwort Artemisia vulgaris
Olive Olea europaea
Parietaria Parietaria
Plane Platanus vulgaris
Ragweed Ambrosia artemisiifolia
Dermatophagoides
farinae
Dermatophagoides
pteronyssinus
Blatella Blatella germanica
Alternaria Alternaria alternata (tenuis)
Aspergillus Aspergillus fumigatus
Cladosporium Cladosporium herbarum
Cat
Dog

218
lancet
tip lancet
C. Özdemiral and Ü. M. Şahiner
involving common allergens, as detailed in Table17.1 [7]. A minimal amount of an
allergen extract containing particular components, both genuine and cross-reacting,
is required for the test [9]. The allergen panel selection can be determined according
to patients’ age, clinic, and geographic area, typically encompassing 8–12 allergens,
which is usually adequate [10, 11]. The allergen extracts must possess high potency
and stability, while also considering their shelf life. The pricking device should be
sterile and only be used once for each allergen. They are available in a variety of
sizes (single or multiple puncture devices), shapes (lancet, needle, bifurcated lancet,
with or without guard), materials (plastic or metal), and preparations (precoated
with the allergen extract, or not) [9]. The examples of pricking devices are depicted
in Fig.17.1. No SPT device has been established as the gold standard in the literature [9]. SPT is conducted on the anterior arm or back and is limited to healthy skin
[12]. To prevent cross-contamination, a minimum of 2cm spacing between prick
tests is recommended. The most commonly used SPT method involves applying a
drop of the allergen extract to a marked area of the skin and then inserting the device
through the drop at a 45–60° angle, ensuring it does not penetrate beyond the epidermis. If the device is inserted at a 90° angle, it is referred to as a skin puncture test,
skin test methods are illustrated in Fig.17.2 [12]. A different SPT technique was
used, in which submerge the device into the allergen, then drop to the test area, and
apply vertical pressure. Comparable results were found with less effort and expense
[13]. It’s important to note that performing the SPT should not cause bleeding [12].
The best outcomes can be anticipated by selecting a single prick/puncture tool and
effectively training skin technicians in its use. Skin test prociency protocols should
be used to establish consistency in skin test performance among technicians in order
to achieve quality assurance. Post-histamine control applications have been advised
to adhere to proposed standards, such as a coefcient variation of less than 20% (as
per EAACI) and less than 30% (as per Childhood Asthma Management Program—
CAMP) [14, 15]. The peak reactivity of prick/puncture tests occurs between 15 and
20min, then the diameters of the erythema and wheal should be measured in millimeters (mm) and compared with positive and negative controls. An example of the
SPT is exhibited in Fig.17.3. The wheal diameter is determinative while interpreting the test result. In clinical studies, wheal diameters ≥3mm are considered positive in SPTs whereas less than 3mm may be accepted positive in epidemiologic
studies [16]. Although the severity of clinical symptoms is not always predicted by
wheal size, larger wheal sizes may indicate a favorable positive response to nasal
provocation. The correlation between wheal size and clinical symptoms may be
Fig. 17.1 The examples
of skin prick test devices
ALK SPT lancets
Stallerpoint
ALK Duo
ALK multitest
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