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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)

23 Nasal Itching andSneezing inChildren
315
Mechanical trauma caused by nose scratching can release inammatory molecules that further increase itching, creating a vicious circle [21].
23.3 Allergic Rhinitis
Allergic rhinitis is IgE-mediated inammation of the nasal mucosa that develops
against specic allergens such as pollen, mold, feather, and house dust mites.
Symptoms occur after the release of inammatory mediators. Clinical ndings such
as runny nose, sneezing, nasal itching, and congestion are usually observed.
Symptoms such as itching, redness, and swelling in the eyes are often observed
together. Additional diseases such as rhinosinusitis, otitis, and asthma can sometimes be observed [22].
Observation of symptoms for more than 1h a day for 2weeks and two or more
additional symptoms suggests the diagnosis of allergic rhinitis in the child [23]. The
mentioned symptoms are not observed with the same intensity in every patient.
Some symptoms may seem more dominant than others.
Allergic rhinitis is the most common allergic disease in children [24]. Allergic
rhinitis is observed in approximately 40 percent of children [25]. It was observed
that the prevalence of allergic rhinitis in children in the United States increased from
13.4% in 1994 to 19.1% in 2003 [26]. In recent studies, the prevalence of allergic
rhinitis in children was 13% [27]. Although the number of boys with allergic rhinitis
was observed to be higher than girls at the ages of 6–7, it was observed that the
number of girls was higher than boys at the ages of 13–14 [28]. Allergic rhinitis is
the most common atopic disease under the age of 18 and is one of the leading
chronic conditions [29]. Most patients develop symptoms of AR before age 20, and
approximately half of these patients become symptomatic by age 6. If there is a history of allergy in the family on both the mother’s and father’s side, symptoms usually appear before adolescence. In the presence of a unilateral family history,
symptoms are observed at older ages [30]. AR is rare in children younger than
2 years of age because it usually requires several years of allergen exposure to
develop [31].
In children, sensitivity (presence of specic IgE) develops rst to allergens (dust
mites) constantly in the air. It has been observed that sensitivity to pollens and other
seasonal allergens develops before clinical complaints appear [32].
When symptoms of allergic rhinitis are evaluated in terms of time, they are classied as intermittent if they occur after specic exposures, seasonal if they occur at
certain times of the year, or perennial if the symptoms persist throughout the year
[33]. Allergic rhinitis affects the upper respiratory tract and can be seasonal or yearround. In seasonal allergic rhinitis, symptoms usually occur in spring, summer, or
fall and are often associated with pollen from trees, grass, and weeds. The number
and type of pollen varies according to geographical regions. Even within a given
area, weather patterns can cause annual changes in pollen count and the overall
prevalence and severity of allergic rhinitis. Exposure to indoor and outdoor air pollutants, pet dander, cockroaches, dust mites, molds, and others must be considered

316
N. Türe and F. Oğhan
in perennial allergic rhinitis. In some children, seasonal allergies may overlap and
cause persistent symptoms [34]. Allergic rhinitis: Patients’ daily activities, sleep,
and school routines are classied as mild, moderate, or severe (persistent or intermittent) according to the duration of symptoms [35].
It negatively affects the child’s quality of life and aggravates other allergic diseases, such as asthma [36]. At the same time, it disrupts the child’s quality of life by
negatively affecting their social activities, school performance, sleep status, and
psychosocial communication [37]. It has been reported that approximately two million school days are lost every year due to allergic rhinitis [38].
Young children suffer from acute infective rhinitis very frequently every year,
making it difcult to distinguish the condition from allergic rhinitis. If the condition
lasts longer than 2 weeks and there are other accompanying allergic symptoms,
allergic rhinitis, such as nasal itching, should be considered [39].
Allergic rhinitis can occur at any age, but patients with allergic rhinitis have been
reported to experience symptoms in childhood or young adulthood. Nasal itching is
very useful in distinguishing allergic rhinitis from other forms of rhinitis. Children
generally do not complain of nasal itching but show it through various nose-wiping
methods [40]. In patients, an “allergic salute” can typically be observed, which is
observed as a horizontal wrinkle on the nasal dorsum and occurs when the nose is
rubbed upwards with the palm [41].
Evaluation of AR requires a detailed history, including physical examination and
laboratory evaluation, in addition to questioning the patient’s environment and diet
and the presence of allergies in the family. History and laboratory ndings provide
clues to provoking factors. Symptoms such as sneezing, runny nose, nasal itching,
congestion, and laboratory ndings of high IgE and sIgE antibodies and positive
allergy skin test results indicate AR [42].
23.4 Non-allergic Rhinitis
The pathophysiology of networked conditions needs to be clearly dened. It is a
situation where the true incidence of the disease is unknown. Current treatment is
based on studies on adult individuals. There is no epidemiological data on the age at
which non-allergic rhinitis occurs in children. In addition, the gender and age distribution of non-allergic rhinitis in the pediatric age group are unknown. In summary,
only some aspects of pediatric non-allergic rhinitis in children have been explained,
and its pathophysiology has yet to be fully explained. The lack of accurate diagnosis
and appropriate treatment algorithms in managing the disease is noteworthy [43].
Non-allergic rhinitis is a disease that causes many clinical complaints with different etiologies and pathophysiologies.
Diagnosing non-allergic rhinitis in children is challenging due to disagreements
on the classication of different forms of non-allergic rhinitis and the need to elucidate its pathophysiology. This problem is clinically diagnosed as non-allergic rhinitis. The common denominator of the clinical conditions under this umbrella
diagnosis is the absence of systemic allergic sensitivity. Non-allergic rhinitis causes

23 Nasal Itching andSneezing inChildren
317
infrequent symptoms. Sneezing and nasal itching are less common in non-allergic
rhinitis than in allergic rhinitis but can be seen in the NARES subtype of non- allergic
rhinitis.
Non-allergic rhinitis at age four was reported to be 8.1%, and the prevalence at
age eight was reported to be 6.3% [32]. Another study reported that NAR was
observed in 24.9% of 6600 children with rhinitis symptoms. It has been reported
that NAR is more common than AR in children under the age of 6, that the diagnosis
of AR increases with age, and that NAR decreases to 10–15% in older children [44].
Under the non-allergic umbrella, conditions such as infectious rhinitis, nonallergic rhinitis with eosinophilia, vasomotor rhinitis, atrophic rhinitis, rhinitis due
to structural and mechanical factors, rhinitis medicamentosa, neoplasms, vasculitis,
and granulomatous disorders are included.
Children complain of runny nose, nasal congestion, and sneezing in infectious
rhinitis. The complaints usually disappear within the rst week, and the causative
agent is mostly rhinoviruses [25].
In non-allergic rhinitis, where high eosinophilia is observed, the symptomatology of the disease and response to treatment is similar to allergic rhinitis. Still,
unlike high IgE antibodies, high IgE antibodies are not observed [42].
Vasomotor rhinitis is characterized by the excessive response of the nasal mucosa
to physical stimuli [42]. In vasomotor rhinitis, intermittent nasal congestion and
runny nose are observed. A signicant increase in complaints is observed, especially after exposure to air pollution and cold weather [45].
Atrophic rhinitis is a rare clinical condition that begins with puberty and results
in slow and progressive atrophy of the nasal mucosa. It is typical for a crust to form
in the nose and a foul odor [46].
23.5 Infectious Rhinitis
The most common form of non-allergic rhinitis in children is infectious rhinitis,
which can be acute or chronic. Infectious rhinitis, commonly known as the common
cold, is an acute and self-limiting disease. The most common cause is rhinoviruses.
Children experience runny nose, nasal congestion, and sneezing, and the complaints
usually disappear within the rst week [47, 48]. Around 36% of patients have sneezing on the rst day of the disease, and sneezing continues on the fth day in more
than 35% [49].
Other symptoms, such as cough and sore throat, are more prominent in infective
rhinitis. Acute bacterial rhinosinusitis is a situation in which complaints sometimes
continue in viral rhinitis, and the sinuses are additionally included in the clinical
picture. Acute symptomatic bacterial sinusitis develops in approximately 0.5–2% of
viral upper respiratory tract infections in children [25].
Acute bacterial sinusitis presents similarly to an upper respiratory tract infection,
with a runny nose, congestion, cough, and sometimes fever and headache. Edema
and erythema are common in the nasal mucosa. Because sinusitis can develop as a
complication of an upper respiratory tract infection, a prior upper respiratory tract

318
infection is commonly reported. Unlike an upper respiratory tract infection, patients
with acute sinusitis experience signs and symptoms that worsen after 10days; purulent nasal discharge and halitosis are typical [50, 51].
In the presence of a chronic mucopurulent discharge, pathologies such as adenoid hypertrophy, anatomical abnormalities, primary immunodeciency, primary
ciliary dyskinesia, or cystic brosis should be considered [48].
Sometimes, allergic rhinitis and infectious rhinitis are observed together in children. In cases where these two conditions overlap, differential diagnosis becomes
difcult. It has been observed that an exaggerated response to viral upper respiratory tract infection is observed in atopic children [52]. Allergic rhinitis symptoms in
children are often confused with infectious rhinitis symptoms. If symptoms last
longer than 2weeks, a cause other than infection should be sought. When diagnosis
cannot be made by history and physical examination, a nasal swab can be taken,
which is helpful in differential diagnosis. Detection of more than 5% of eosinophils
in the nasal swab suggests allergy, and neutrophil predominance suggests infection [47].
N. Türe and F. Oğhan
23.6 NARES (Non-allergic Rhinitis
withEosinophilia Syndrome)
In Non-allergic Rhinitis with Eosinophilia Syndrome (NARES), which is evaluated
under the table of non-allergic rhinitis, the dominant symptoms are continuous
sneezing and excessive nasal discharge. Sometimes, it is accompanied by nasal congestion, itching, and a decreased sense of smell. The presence of increased eosinophils in the nasal swab, useful in differential diagnosis, is noteworthy. Failure to
monitor systemic sensitivity helps differentiate it from allergic rhinitis. The skin
prick test is negative. Specic IgE is not monitored. Its pathophysiology needs to be
clearly understood. The hypothesized view is that nasal neural dysfunction causes
symptoms [53].
23.6.1 Vasomotor Rhinitis
Vasomotor rhinitis is a diagnosis of exclusion. Common symptoms are primarily nasal congestion and runny nose but can also include nasal itching and
sneezing. The pathophysiology of vasomotor rhinitis is not well understood but
is believed to be due to autonomic dysregulation resulting in an imbalance in
sympathetic and parasympathetic activity. In vasomotor rhinitis, symptoms
begin suddenly and disappear quickly when the triggering factor is removed.
The allergy test is negative. Symptoms may change depending on weather
changes [54, 55].
Finally, it should not be forgotten that nonallergic, noninfectious rhinitis conditions occur due to exposure to irritants, hormonal dysfunction, and specic drugs.
This should be considered in the differential diagnosis.

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23.7 Evaluation
The ear, nose, and throat physical examination begins after the pediatric patient
complaining of nasal itching and sneezing states their rst complaint. Evaluation
should always start by taking a comprehensive medical history. During the interrogation, attention should be paid to what the patient does not say and specic situations such as mouth breathing, dry mouth, and speaking. Detecting an allergic or
infectious cause in children may be challenging, mainly when rhinitis is frequently
observed. Therefore, other distinctive physical examination ndings of allergic rhinitis should be questioned.
One of the characteristically noticeable ndings of allergic rhinitis in children is
the horizontal scar observed in the nose tip area. This is an important examination
nding that is observed as a result of repeating the movement called allergic salute,
which is performed by lifting the tip of the nose upwards with the palm of the hand,
for at least 2years to increase nasal breathing and reduce the feeling of itching. With
advancing age and adolescence, this movement can be observed as facial grimacing
[56, 57].
Notably, ndings in neighboring organs should be noticed. Venous pooling
occurs around the eyes secondary to inammation in the nasal mucosa. The pigmentation observed on the lower eyelid skin due to hemosiderin accumulated under
the skin during ponding is called allergic glitter. Venous pooling causes constant
muscle spasms in the lower eyelid. Spasm in the Müller muscle causes small scars
called Dennie-Morgan lines on the lower eyelid skin. Long and silky eyelashes
sometimes accompany allergic rhinitis complaints [56].
Anterior rhinoscopy provides valuable information about the septum and lateral
nasal wall. In allergic rhinitis, the nasal mucosa and turbinates may appear normal
but are usually edematous and pale. At the same time, the color of the discharge in
the nasal passage is helpful in distinguishing its uidity. In contrast, the color of the
nasal mucosa in patients with non-allergic rhinitis is usually standard, and acute
viral rhinosinusitis has a red appearance. In current practice, every otolaryngologist
successfully applies exible nasopharyngoscopy and endoscope, which allows the
anterior and posterior nasal structures to be distinguished more specically than
anterior rhinoscopy. Although nasal endoscope application is complex in young
children, its benet in clarifying nasal pathologies is excellent [58].
When the palate feels itchy, children may click while moving their tongue
towards the palate to relieve this itching feeling [59]. Depending on the timing of
allergen exposure, symptoms may be present year-round or seasonally [56].
Non-allergic rhinitis symptoms usually occur throughout the year. However, seasonal exacerbations can occur due to changes in humidity, temperature, and pressure. Differential diagnosis becomes difcult since these complaints overlap with
allergic rhinitis complaints in autumn and spring. The absence of eye and palate
symptoms is important in non-allergic rhinitis [60].
In non-allergic rhinitis, nasal secretions are generally normal except for edematous erythematous conchas. Nasal secretions can be observed as mucoid or transparent [61].

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N. Türe and F. Oğhan
Both nasal passages should be examined, and attention should be paid to the
color and consistency of the discharge detected in the nasal passage, the degree of
edema in the mucosa, and the presence of turbinate hypertrophy. Examination of the
oropharynx should also be included, and a postnasal drip should be noted. In addition, an ear examination should be performed, and the color and mobility of the
tympanic membrane and the presence of uid behind the membrane should be noted.
Perinatal infections such as Chlamydia can present as persistent rhinitis. In adolescence, inquiries about the onset of puberty may be helpful, as hormonal changes
may cause nasal congestion [62].
It is essential to determine whether the patient is also sexually active. In some
cases, syphilis may occur with chronic rhinitis [63]. All patients’ previous sinus
surgeries should be questioned.
Assessment of the chronicity of rhinitis is critical. Intermittent nasal congestion
is more closely associated with self-limiting rhinovirus infections. Chronic persistent nasal congestion may indicate more complicated conditions such as adenoid
hypertrophy or immobile cilia syndrome. Investigating all possible etiological factors is very important to make the correct diagnosis. Inquiry regarding exposure to
potential triggers commonly associated with nasal hyperreactivity, such as odors,
drafts, cold air, temperature changes, fatigue, stress, and spicy foods, will help the
clinician conrm the etiology of the patient’s chronic rhinitis. Reviewing past medication use and effectiveness may also help conrm the diagnosis [43].
Finally, nasal itching and sneezing symptoms are not sensitive or specic enough
to distinguish between bacterial sinusitis and allergic or viral rhinitis. This often
leaves patients in situations where the two conditions overlap.
23.8 Diagnosis
It is essential to question nose itching and other symptoms accompanying sneezing. Use
diagnostic tools according to etiology. Allergic rhinitis, infectious rhinitis, and non-allergic, non-infectious rhinitis should be considered in the differential diagnosis of pediatric
patients complaining of nasal itching and sneezing. Although almost all patients who
applied to health institutions with rhinitis complaints were diagnosed with allergic rhinitis, it is worth emphasizing that in studies conducted, allergy could not be identied as
the etiology in 40–64% of these patients. For this reason, after a preliminary diagnosis
of rhinitis is made in patients presenting with sneezing, diagnostic tests should be used
appropriately, and differential diagnosis should be made carefully.
Diagnosing allergic rhinitis in children is made by specic allergic complaints in
the history and diagnostic tests.
In the preliminary diagnosis, allergy tests are performed for this purpose in the
pediatric patient in whom allergy is suspected. Allergy tests to conrm the initial
diagnosis include a skin prick test and serum-specic IgE.Skin prick test is frequently preferred in children because it is easy to apply, gives results quickly, can
be used in ofce conditions, and has reasonable specicity and sensitivity. Serumspecic IgE is as sensitive as skin prick tests, which show the patient’s complaints
are due to allergies. Specic IgE is safely preferred, especially in patients who do

23 Nasal Itching andSneezing inChildren
321
not have a systemic reaction, have had a systemic reaction before, and have skin
diseases where objective data must be provided [25].
When an infection is suspected, complete blood count, white cell count, and
C-reactive protein (CRP) are helpful in differential diagnosis [1].
Nasal cytology is not a frequently used diagnostic method because it cannot be
standardized, its results are highly variable, and its results have different sensitivity
and specicity. Despite this, eosinophils in the nasal swab indicate inammation
and can help predict corticosteroid response [1].
Radiology for rhinitis is not routinely recommended. However, if rhinosinusitis
or nasal polyposis is suspected, especially if it does not respond to medical treatment, a Computed Tomography scan is helpful. However, remember that radiation
exposure in pediatric patients should be kept as low as possible [1].
Allergic rhinitis is often accompanied by eye symptoms (itchy and watery eyes),
and many patients have a positive family history of allergic rhinitis [64].
Sinusitis is primarily a clinical diagnosis; imaging is used to conrm it and evaluate its complications when necessary. A CT scan compatible with sinusitis shows
clouding, opacity, thickening of the mucosal interface, and air-uid levels in the
affected sinus [65].
Patients with non-allergic rhinitis often complain of nasal congestion and rhinorrhea, but they also complain less about sneezing and itching [66].
Blind cultures of the nasopharynx in children with rhinitis have little clinical
value because pathogenic bacteria are present in the normal ora in 92% of asymptomatic healthy children [25].
A careful history and physical examination are the most effective diagnostic
maneuvers in identifying allergic rhinitis in children. The distinction is sometimes
tricky as allergic and non-allergic rhinitis often cannot be distinguished based on
symptoms and require different management strategies and pharmacological treatments. Clinicians should perform specic diagnostic tests on pediatric patients
when indicated.
23.9 Treatment
The aim of treating Allergic Rhinitis, which is considered the main culprit in nasal
itching and sneezing and comes to mind rst in the differential diagnosis in children, is to control the patients’ symptoms, increase their quality of life and school
success, and prevent the development of complications.
The best treatment for nasal itching and sneezing due to allergic rhinitis is allergy
avoidance. Medical treatment is resorted to in pediatric patients who cannot achieve
sufcient success despite protection and rearrangement of the environment.
Immunotherapy is helpful in cases that fail medical treatment. Treatment includes
environmental control, allergen avoidance, pharmacotherapy, and allergen-specic
immunotherapy [33].
Informing families about avoiding allergen exposure is very important in managing pediatric patients. Although it does not seem possible to avoid allergens despite
all restrictions, it has been reported that this method reduces allergen load [25].

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Simple practices such as not being outdoors during pollen periods, using lters
in motor vehicles, using glasses and hats outdoors, and washing hands and face are
recommended [67].
To reduce contact exposure in managing allergic rhinitis caused by house dust
mites, the environment should be ventilated frequently, dust should be removed
often, items should be washed at temperatures higher than 55°C, and carpets with
less pile should be preferred. All the methods listed have been reported to relieve the
symptoms of allergic rhinitis caused by house dust mites. Oral antihistamines and
nasal steroids are both effective on sneezing and nasal itching.
23.10 Prognosis
In allergic rhinitis, where nasal itching and sneezing are frequently observed, the
positive impact on the child’s quality of life is excellent when compliance with the
treatment is ensured. It is expected to produce specic drugs based on genetic
sequences that target the cells, nerves, and cytokines involved in nasal itching and
sneezing and treat these two conditions as a systemic process.
23.11 Conclusion
Every child who complains of nasal itching and sneezing should undergo a detailed
history and physical examination, and other accompanying symptoms should be
questioned. Further assessment and treatment should be performed for differential
diagnosis of diseases in which nasal itching and sneezing occur together. Despite
the high prevalence of allergic rhinitis in the pediatric population, this disease is
often overlooked or undertreated.
Untreated allergic rhinitis impairs the child’s and his parents’ quality of life.
Accurate and timely diagnosis of allergic rhinitis in children depends on awareness of
the symptoms and signs of the disease and comorbidities, including asthma, sinusitis,
and otitis media. Rhinitis complaints can be reduced, especially with simple measures, and they contribute positively to quality of life and school performance.
Physicians should differentially diagnose nasal itching and sneezing in children
and perform specic diagnostic tests when necessary. Intranasal corticosteroids and
non-sedating antihistamines are successfully used in the treatment.
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