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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4534_Библиотеки_им_академика_М_И_Перельмана.pdf
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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)

34 Pediatric Allergic Rhinitis: Otolaryngology Perspective
441
decongestant sprays can be used before the procedure. Endoscopic examination is
crucial for the evaluation of the posterior nose and nasopharynx. Assessment of the
patency of both nasal passages, the condition of the mucosa, adenoid hypertrophy, and
ostium of the Eustachian Tube, and the detection of small polyps and foreign bodies
that cannot be seen with anterior rhinoscopy help detect malignancies. In the oropharynx and oral cavity examination, dental malocclusion or high-arched palate associated with chronic mouth breathing, cobblestoning of the oropharyngeal wall, and
pharyngeal postnasal discharge should be examined. Although viral upper respiratory
tract infections exhibit similar symptoms with allergic rhinitis, they can be differentiated by the short duration of symptoms and accompanying symptoms such as fever
and myalgia. Allergic conjunctivitis, watery eye discharge, and swelling in the conjunctiva are present in 50–70% of allergic rhinitis patients and are the most prominent
symptom that differentiates allergic rhinitis from other forms of rhinitis [20]
(Fig.34.1).
34.4.3 Diagnostic Tests
Allergy tests are generally conducted in patients who cannot be controlled despite
using antihistamines and intranasal corticosteroids for an adequate time and appropriate dose as empirical treatment, in patients with an unclear diagnosis of allergic
rhinitis, and in cases where it is essential to detect the specic antigen for immunotherapy. IgE-specic allergic tests are divided into two main categories: skin and
blood tests. Measurement of total Ig-E does not provide any benet for the
diagnosis of allergic rhinitis. Skin tests are considered more sensitive than blood
Fig. 34.1 Left nasal
passage view of a
6-year-old patient with
allergic rhinitis. Inferior
turbinate is observed in
hypertrophic and pale
appearance. *: serous
discharge due to allergic
rhinitis, **: purulent
discharge due to acute
sinusitis accompanying
allergic rhinitis

442
ab
M. C. Gökgöz et al.
tests, allowing us to observe the reaction against the antigen directly. It is performed
by measuring the swelling on the skin caused by the histamine released due to the
rapid interaction of the antigen with IgE antibodies through mast cells. It is cheaper
than blood tests but carries the risk of systemic allergic response (anaphylaxis). It
can be performed at any age and has been considered sensitive-specic over 80%.
Results are evaluated within 15–20min after the application. The medication usage
histories of the patients should be questioned before the allergy test (Fig.34.2).
Blood tests are implemented by measuring the IgE-specic antigen in the
patient’s serum. It is specically preferred in patients with skin-related problems, in
the presence of dermatographism and severe eczema, and when the interpretation of
skin tests becomes challenging. Its advantages include being unaffected by the history of medication use, no need to discontinue antihistamine therapy, and not having
the risk of anaphylaxis. In the absence of contraindications, the choice of skin or
blood testing can be left to the patient [21].
34.4.4 Nasal Cytology
The nasal mucosa comprises pseudostratied ciliated columnar epithelium containing mucinous cells responsible for mucus secretion. Nasal cytology is based on the
principle of identication of normal and pathological cells of the nasal mucosa by
Fig. 34.2 (a) Inhalant
panel skin prick test in
which 14 different
allergens are tested (grass
pollen, grain pollen, weed
pollen, cat, olive, etc.). (b)
It is applied to both
forearms. (c) Results are
evaluated within
15–20min after the
application. (d) 6mm level
of positivity against
allergen item 12 (olive)
c
d

34 Pediatric Allergic Rhinitis: Otolaryngology Perspective
examining the nasal cell types and morphology of the samples taken by various
means (nasal lavage, micro-suction aspiration, brushing, scraping, swap, or biopsy)
under the microscope [22]. It is an easy-to-apply, non-invasive, reproducible test
that can be implemented without age limitations. This procedure enables the detection of normal nasal mucosal cells and inammatory cells such as lymphocytes,
neutrophils, eosinophils, and mast cells. Depending on the dominant cell type, it can
help differentiate viral infections, allergic rhinitis, non-allergic rhinitis, and
NARES. In allergic rhinitis, intense inltration of eosinophils and mast cells is
detected, particularly in the symptomatic period. In conditions such as house dust
mite allergy that do not cause severe symptoms and last all year, cytology with minimal inammation in which neutrophils are more dominant is observed [23].
443
34.4.5 Imaging
Patient history, physical examination, and allergy tests lead to allergic rhinitis diagnosis. Although there is no radiological nding that will help in the diagnosis of
allergic rhinitis primarily, it can be performed in the presence of nasal polyps,
chronic rhinosinusitis, and suspected malignancy accompanying allergic ndings.
While CT should be preferred in evaluating bone structures, orbit should be selected
to assess soft tissues and tumoral structures, and MRI should be chosen to examine
the skull base and intracranial extension [24].
34.5 Differential Diagnosis inOtolaryngology Perspective
34.5.1 Adenoid Hypertrophy
It can be confused with the symptoms of allergic rhinitis since it causes difculty
breathing through the nose, sleeping with the mouth open due to nasal congestion,
predisposition to otitis media, and sleep disorders. Manifestations related to adenoid hypertrophy, like allergic rhinitis, often begin after the 2 years of age.
Mediators released due to the inammatory process in tonsil and adenoid tissue
are effective in clinical manifestations. Allergic rhinitis is associated with adenotonsillar hypertrophy and Obstructive Sleep Apnea (OSA). The incidence of allergic rhinitis has been reported to be nearly 40% in pediatric patients who have been
followed up via tonsillar hypertrophy and adenoid hypertrophy. In addition to the
adenoid size, allergy also occurs due to nasal congestion caused by inammation
of the nasal mucosa. In physical examination, nasal mucosa may be observed as
edematous due to nasal clearance deterioration, inammation in anterior rhinoscopy, and occlusion due to secretion. Endoscopic examination may reveal adenoid
hypertrophy, which narrows the nasopharynx and choana and closes the Eustachian
tube ostium. In treating adenoid hypertrophy, intranasal corticosteroid therapy
and follow-up with nasal irrigation may be recommended depending on the severity of the symptoms. OSA level, the level of obstruction caused by adenoid

444
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M. C. Gökgöz et al.
hypertrophy, serous otitis media, and hearing loss, are effective in the surgical
decision. Reducing OSA symptoms, particularly with intranasal corticosteroids,
supports the allergic background [25, 26] (Fig.34.3).
34.5.2 Nasal Septal Deviation
It may lead to obstruction, especially more prominently on one side in the pediatric
age group. It is accompanied by nasal congestion only, one of the signs of allergic
rhinitis. Regarding the timing of surgery, although some studies suggest that it
would not cause nasal and facial developmental disorders if performed after the age
of 6, there are also studies stating that surgery can be performed from the neonatal
period. There is no denite age limit for surgery yet [27]. Absolute indications
include septal hematoma, septal abscess, dermoid cyst, cleft lip with the nasal component, and severe deformity secondary to nasal fracture. In contrast, the relative
indication has been identied to be septum deviation causing signicant nasal airway obstruction [28].
34.5.3 Chronic Rhinosinusitis
Inammatory involvement of the sinus and nasal mucosa is dened as rhinosinusitis. Suppose nasal congestion, purulent nasal discharge, cough, facial pain
and pressure, nasal polyps, and mucosal edema symptoms persist for more than
3months despite standard treatment (antibiotics, oral or intranasal corticosteroids, nasal sprays, and nasal saline irrigation) in the pediatric age group, then
Fig. 34.3 Left nasal passage view of a 4-year-old patient with adenoid hypertrophy. (a) Adenoid
hypertrophy obstructing the nasal passage and serous discharge. (b) Minimal gap in choanae due
to adenoid hypertrophy. (S: Septum, Ad: Adenoid hypertrophy, *: Serous discharge, red arrow:
Choanal cavity)

34 Pediatric Allergic Rhinitis: Otolaryngology Perspective
it is considered as chronic rhinosinusitis [29]. Mucosal inammation, edema,
impaired mucociliary clearance, and obstruction of sinus drainage due to allergic rhinitis play a signicant role in the etiology of rhinosinusitis [30]. It has
also been suggested that patients with allergic rhinitis are predisposed to developing rhinosinusitis and that the deterioration in sinus functions is more
severe [31].
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34.5.4 Turbinate Hypertrophy
It leads to allergic rhinitis-like symptoms by showing manifestations of nasal
congestion and discharge, mouth breathing, and obstructive sleep apnea. In children, the effect of inferior turbinate hypertrophy is not clearly understood since
adenoid hypertrophy is the most common cause of nasal obstruction. Generally,
a conservative approach is followed in the pediatric age group. Patients with
continuing nasal obstruction after adenoidectomy should be considered a surgical indication [32]. Studies reveal that turbinate hypertrophy surgery provides
an additional benet in addition to adenoidectomy in patients who do not
respond adequately to medical treatment [33]. Surgical options include turbinectomy, cauterization or radiofrequency, and submucous micro debridement
[34, 35].
34.5.5 Nasal Foreign Body
Patients typically present with unilateral discharge and obstruction. Foul-smelling
unilateral discharge occurs depending on the foreign body’s duration in the nasal
passage. Nasal ow may be accompanied by nasal congestion, sneezing, and headache. Following anterior rhinoscopy evaluation, nasal endoscopy should be performed depending on the patient’s compliance. Radiological imaging may be
requested in cases where the foreign body cannot be seen, but its clinical utility is
limited as most foreign bodies are radiolucent. If a foreign body is detected, it is
used with a nasal speculum or endoscope-guided probe, curette, and alligator forceps removal [36].
34.5.6 Other Clinical Conditions
Although nasal polyps are rare in the pediatric age group, cystic brosis or ciliary
dyskinesia should be considered in the etiology. In the presence of unilateral polyps,
encephalocele should be considered. Nasal tumors lead to complaints of nasal discharge/nose bleeding and progression to adjacent structures, though rarely. Due to
pharyngonasal reux, symptoms such as chronic sinusitis and uid accumulation in
the ear due to Eustachian dysfunction, which can also be seen in allergic rhinitis,
can be observed (Table34.2).

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Table 34.2 Differential diagnosis of allergic rhinitis in children
Differential
diagnosis
Adenoid
hypertrophy
Nasal septal
deviation
Chronic
rhinosinusitis
Turbinate
hypertrophy
Nasal foreign
body
Cystic brosis/
ciliary dyskinesia
Encephalocele Unilateral nasal polyp Endoscopic examination,
Nasal tumors Nasal discharge, epistaxis, progression to
Symptoms
Difculty in breathing through the nose,
mouth breathing due to nasal congestion,
predisposition to otitis media, and sleep
disorders
Nasal obstruction, especially more
prominently on one side, and nasal
congestion
Nasal congestion, purulent nasal discharge,
cough, facial pain and pressure, mucosal
edema, polyp
Nasal congestion and discharge, mouth
breathing, and sleep disorders
Unilateral discharge and nasal obstruction,
foul-smelling discharge
Bilateral nasal polyps, decreased
mucociliary clearance
adjacent structures
M. C. Gökgöz et al.
Diagnostic tests
Lateral nasopharynx
X-ray graphy, endoscopic
examination
Anterior rhinoscopy,
endoscopic examination
Anterior rhinoscopy,
endoscopic examination,
paranasal CT, MRI
Anterior rhinoscopy,
endoscopic examination
Anterior rhinoscopy,
endoscopic examination,
radiological tests
Sweat chloride test,
genetic tests
paranasal, brain CT, MRI
Endoscopic examination,
paranasal CT, MRI
34.6 Prevention fromanOtolaryngology Perspective
34.6.1 Saline Irrigation (Douching)
Nasal irrigation has been determined to be benecial in relieving the symptoms of
allergic rhinitis in the pediatric age group [37, 38]. In addition to its mechanical
cleaning effect, it is considered helpful for mucociliary clearance and removing
allergens with inammatory mediators such as histamine, prostaglandin, and leukotrienes. Nasal irrigation can be used in drops, spray, and via a pump. It is subdivided into isotonic (0.9%), hypertonic (1.5–3%), and seawater-containing types.
For high-volume rinsing, pumps with a volume of 300mL are utilized in pediatric
forms. It has been suggested that adding nasal irrigation to the treatment and using
intranasal corticosteroids decrease patient symptoms compared to using intranasal
steroids (INS) alone and reducing the dose of INS [39]. A study on the compliance
and tolerance of nasal irrigation in the pediatric age group revealed that 86% could
tolerate the treatment, and 84% of the parents thought that nasal symptoms were
reduced by irrigation [40]. In the same study, 21% of parents in the under-5 age
group felt that their children could tolerate nasal irrigation, whereas the tolerance
rate of children was 86%. When combined with nasal steroids, the benet increases
compared to INS alone [41, 42]. In addition to the signs of allergic rhinitis, it also
relieves the symptoms and symptoms associated with asthma [43]. Nasal irrigation
solutions should be considered an alternative that is easy to use at home, inexpensive, and has few adverse effects (Fig.34.4). (a) The nasal irrigation bottle, used for

34 Pediatric Allergic Rhinitis: Otolaryngology Perspective
447
abc
Fig. 34.4 (a) The nasal irrigation bottle, used for 12years and older patients, provides high pres-
sure washing with approximately 200mL of water. (b) The nasal irrigation bottle, used for 4- to
12-years-old pediatric patients, provides high pressure washing with approximately 80–100mL of
water. (c) Shows how to use a nasal irrigation of a 6-year-old patient in standing position
12 years and older patients, provides high-pressure washing with approximately
200 mL of water. (b) The nasal irrigation bottle for 4- to 12-year-old pediatric
patients provides high-pressure washing with about 80–100mL of water. (c) Shows
how to use nasal irrigation in the standing position of a 6-year-old child.
34.7 Treatment
34.7.1 Oral Antihistamines
Histamine is the primary mediator responsible for the symptoms of allergic rhinitis.
H1 antihistamines are often used in allergic rhinitis in oral or nasal forms. They are
effective for nasal ow, sneezing, itching, and congestion. As a mechanism of
action, they inhibit the proinammatory effects of histamine by blocking the histamine H1 receptor [44]. Its development starts in 1–3h. First-generation antihistamines are not preferred as they cross the blood–brain barrier and lead to sedation,
drowsiness, decreased school performance, and increased appetite. Nowadays, second generation H1 antihistamines (desloratadine, loratadine, cetirizine, levocetirizine), which have less sedating properties, and antihistamines with minimal sedation
effects such as fexofenadine and bilastine have begun to be preferred [45]. Newgeneration antihistamines show high selectivity to H1 receptors and limitedly cross
the blood–brain barrier owing to their lipophilic effect. Thanks to their cost-effectiveness and ease of use once a day, which enhances compliance with treatment, oral
antihistamines are preferred, particularly in patients with mild allergic rhinitis.
34.7.2 Intranasal Steroids
Intranasal corticosteroids are the rst-choice treatment modality for all stages of allergic rhinitis, from mild to persistent and severe forms [46]. It is used effectively on
nasal ow, sneezing, congestion, and itching symptoms [47], in addition to reducing

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M. C. Gökgöz et al.
intranasal symptoms and relieving ocular symptoms [21]. It is in the rst place regarding treatment effectiveness, albeit the onset of the duration of action is late among
other allergic rhinitis treatment options. The time taken for the desired effect’s beginning is 6–48h. They are effective for nasal ow, sneezing, itching, and congestion. In
addition to its anti-inammatory effect, it reduces the release of mediators and cytokines and reduces eosinophilic, basophilic, and mononuclear cells in nasal secretions.
Moreover, INS reduces antigen-induced hyperresponsiveness [48]. Patients
should be trained for the use of intranasal sprays and drops. This training not only
prevents the feeling of pain in the nose and nose bleeding that may occur due to the
misuse of the jet but also ensures that the active substance reaches the desired ostiomeatal complex and over the turbinates [6]. It does not result in growth retardation
due to low systemic bioavailability. Fluticasone furoate, Mometasone furoate, and
Fluticasone propionate are preferred in the pediatric age group as they have the most
insufcient systemic bioavailability [6, 48–50]. It is also effective on ocular symptoms secondary to reducing the naso-ocular reex [51] (Fig.34.5).
34.7.3 Leukotriene Inhibitors
Montelukast is a selective antagonist of LTR type 1 and inhibits the proinammatory
effects of cysteinyl-leukotrienes. It has been reported that its impact is lower than antihistamines and INS [52]. Besides oral antihistamines and INS, its use helps reduce allergic rhinitis and asthma symptoms. Some studies have demonstrated that Montelukast is
benecial in combination therapy, particularly in the presence of asthma and allergic
rhinitis, rather than rst-line therapy [53]. It can cause mild upper respiratory tract infection, pharyngitis, headache, nausea, and vomiting as adverse effects. Still, it has been
reported to occur with a frequency similar to placebo and identical drug groups [54].
Fig. 34.5 (a) Shows how
to use a nasal spray in a
standing position using the
left hand for the right
nostril, and (b–d) Show
how nasal drops should be
used to reach the osteomeatal complex. (adopted
from Scadding etal. [6])
c
d

34 Pediatric Allergic Rhinitis: Otolaryngology Perspective
449
34.7.4 Oral Antihistamines-Leukotriene Receptor
Antagonists Combination
Studies demonstrate that this combination provides benets compared to oral antihistamines alone and leukotriene receptor antagonists alone [55]. It is benecial in treating persistent Allergic rhinitis (AR) in accompanying asthma and in treating grass
pollen allergic rhinitis in improving lung symptoms, reducing nasal congestion, and
increasing the quality of life [56]. Compared with INS, the effect of the combination on
nasal symptoms was lower than with INS alone [57]. This combination of treatments
should be used to assess which symptoms are predominant, specically in the pediatric
patient group [56].
34.7.5 Oral Steroids
Oral steroids should not be used except in very severe and acute conditions since
they are not superior in avoiding systemic side effects and efcacy compared to
intranasal steroids in the pediatric age group. It can only be used as a very shortterm, low-dose, short-rescue therapy in addition to INS in patients with severe
symptoms. On the other hand, depot steroid injections are not recommended since
the risk outweighs the benet [58].
34.7.6 Intranasal Antihistamines
As locally acting intranasal antihistamines, azelastine and olopatadine (there are 2
FDA-approved preparations) are used, and their effect starts in 30min–3h [59, 60].
For intranasal antihistamines, the age of use is 6years and over in the pediatric group,
while oral antihistamines can be used at 1year and above. Regarding the use of olopatadine and azelastine, one puff is recommended twice a day between the ages of 6–11,
while two breaths are recommended twice a day at 12 and over [61]. Some studies
have revealed that intranasal antihistamines have lower systemic effects than oral antihistamines and are more effective on nasal symptoms, particularly in nasal congestion
[62]. Nasal irritation, burning, accompanying pain, epistaxis, bitter taste in the mouth,
mild drowsiness, and headache are everyday adverse events of nasal antihistamines.
34.7.7 Immunotherapy (Sublingual-Subcutaneous)
Allergen-specic immunotherapy is the administration of controlled repetitive
doses of therapy aimed at increasing immune tolerance to the allergen in IgEmediated AR patient groups diagnosed via medical history and allergy tests. It is the
sole treatment modality with the potential to prevent AR.Merely 5% of patients can
reach immunotherapy. Two types of immunotherapies are used clinically, 75% of
patients receive subcutaneous therapy (SCIT), and 25% receive sublingual immunotherapy (SLIT) [63]. Immunotherapy was determined to be more effective in the

450
M. C. Gökgöz et al.
pediatric age group compared to adults [64]. Although there is no specic time for
the treatment period, it often takes 3–5years. In studies demonstrating efcacy after
treatment, efcacy has been shown to continue for 10years for SCIT and 8years for
SLIT following cessation of therapy [65, 66]. Studies show that SCIT and SLIT
reduce nasal symptoms more than medication use [67, 68].
Regarding the side effects, local redness and itching at the injection site can
reach 58% for SCIT and 97% for SLIT in some studies. In contrast, serious adverse
effects such as urticaria, wheezing, and anaphylaxis have been detected at 0.9% for
SCIT and 0.056% for SLIT.It has been reported that the incidence of death due to
SCIT is 1in 2.5 million injections, whereas no death occurred due to SLIT [69].
Immunotherapy should not be performed in the presence of uncontrolled asthma,
and to avoid adverse effects or unexpected effects, the rst dose of the therapy
should be administered under the control of a physician in the healthcare facility
instead of at home, and it would be appropriate to wait 30min after the shot, to
detect the adverse effects that may occur immediately.
34.7.8 New Treatment Options: Omalizumab andDupilumab
Omalizumab is an IgE-specic monoclonal antibody. It inhibits allergy steps by binding free-circulating allergen-specic IgEs [70]. Omalizumab can be used in children
older than 6, in patients with uncontrolled, moderate–severe, and severe asthma, with
increased IgE level and skin test positivity [71]. It is administered as a subcutaneous
injection for 2–4weeks. It is thought to reduce asthma exacerbations and the need for
inhaled steroid usage. Many studies have demonstrated its efcacy and safety [72, 73].
Dupilumab is a humanized Ig-G4-specic monoclonal antibody developed against
interleukin 4 receptor alpha. It blocks the communication of IL-4 and IL-13, suppressing the pro-allergic immune response induced by T helper two conversion [74]. It can
be used in patients with moderate-to-severe and severe asthma that cannot be controlled by treatment in the presence of eosinophilic phenotype and oral corticosteroiddependent asthma. It has been approved for use in adolescents aged 12 and over. As a
subcutaneous injection, 300mg injections are applied to two separate sites in patients
over 60kg, or 200mg is administered at two different locations in patients weighing
less than 60kg and is repeated as a dose every 2weeks. Comprehensive studies in the
pediatric population are needed for its long-term efcacy and safety prole [75].
34.8 Conclusion
Pediatric nasal obstruction is among the most common reasons for referral to pediatric
otolaryngologists. The presence of at least two of the complaints of nasal congestion,
rhinorrhea, sneezing, and itching accompanying the inammation of the nasal epithelium is sufcient for diagnosing rhinitis. Patient history, physical examination, and
allergy tests are primary in diagnosing allergic rhinitis. Intranasal corticosteroids and
oral antihistamines are the rst-choice treatment modality for all stages of allergic
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