Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4534_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •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)

304
M. Gümüşsoy and İ. Çukurova
22.9 Systemic Causes
22.9.1 Cystic Fibrosis
It is the most common autosomal recessive genetic disease in Caucasians. Water
and salt transport in the cell membrane is disrupted, and there is a change in the
composition of the uid secreted from the respiratory tract, pancreas, gastrointestinal tract, sweat glands, and other exocrine tissues. Because cystic brosis is a disease that affects more than one system, it manifests itself with very different clinical
signs and symptoms. Recurrent lung infections during childhood and adolescence,
purulent sputum production, nasal congestion, nasal polyposis, chronic and persistent rhinosinusitis, asthma, clubbing of ngers, hemoptysis, biliary cirrhosis, meconium ileus, diabetes mellitus, delayed puberty, and infertility are among the ndings
suggestive of cystic brosis. In addition to these clinical ndings, measuring 100mg
of sweat chloride concentration above 60mEq/L in three separate periods conrms
the diagnosis. Its treatment can be achieved with a multidisciplinary approach.
Medical treatment (corticosteroids) and surgical treatment may be required in
patients with polyps in the nasal cavity. The monitoring and treatment team should
include a pulmonologist, gastroenterologist, metabolism and nutrition specialist,
dietitian, physiotherapist, and microbiologist. Depending on the complications that
arise, assistance from other branches is provided, thus prolonging the patients’ quality and duration of life [59–61].
22.9.2 Primary Ciliary Dyskinesia
It is characterized by chronic sinopulmonary infections starting from the neonatal
period due to disorders in the structure and functions of cilia. It is characterized by
ciliary immotility and ciliary dyskinesia. It is an autosomal recessive disease. There
is a congenital disability in the structure and function of motile cilia. An increased
incidence of infertility and situs in versus characterizes impairment in mucociliary
ltration. Increased mucus and bacterial load in the airways is typical. While the
diagnosis of cystic brosis can often be made at the age of one, in primary ciliary
dyskinesia, if there is cardiac pathology, it may be delayed until the age of four or
six if there is no [62].
For a denitive diagnosis, the nasal biopsy sample should be evaluated by
video microscopy for cilia function and by electron microscopy for ultrastructural cilia defect. The diagnosis must be conrmed by genetic evaluation. It is
essential to have a history of recurrent respiratory tract infections, sinusitis and
otitis attacks, cardiac pathology with bronchiectasis, or a history of a relative
diagnosed with primary ciliary dyskinesia. In cases where nasal polyps are seen
together with chronic rhinosinusitis in children, the most common differential
diagnosis is cystic brosis and rarely direct rhinosinusitis. Ciliary dyskinesia
should be considered [63].

ab
22 Nasal Congestion inChildren
305
22.10 Trauma/Iatrogenic Causes
22.10.1 Nasal Trauma-Septal Hematoma
Septal deformity in children is often seen after trauma and can occur anytime. The
nose and mandible are the facial bones most frequently traumatized. During newborns and childhood, fractures are not seen as often as in older children since most
of the nasal skeleton has not developed and is cartilaginous. Therefore, nasal fractures are very rare in children under ve. Instead of fractures in the nasal bones,
septal hematoma, abscess, or septum deviation are more common. Septal hematoma
can be dened as bleeding between the mucoperichondrium, which vascularly supplies the septum cartilage, and the septal cartilage, and the separation of the mucoperichondrium from the septum. This condition blocks blood ow to the nasal
septum and causes avascular cartilage necrosis. The collected blood and necrotic
tissue become an excellent focus for infection of the nasal mucosa, and an abscess
forms. Septal hematoma clinic manifests itself with nasal obstruction, and if not
intervened, septal necrosis occurs, resulting in septal perforation and irreversible
nasal deformities (Fig.22.5). Therefore, septal hematoma is a critical ENT emergency requiring early childhood diagnosis and treatment [64].
Examination of children after nasal trauma is more complex than for adults.
Nasal palpation, deformity, and crepitation are problematic in pediatric patients.
Endoscopic nasal examination is the gold standard. As an imaging modality, CT is
the gold standard for imaging craniofacial and nasal fractures. Plain radiographs do
not help diagnose nasal fractures in children. Signs and symptoms of septal hematoma after nasal trauma may develop within 24–72h after the injury.
Fig. 22.5 (a) Septal hematoma anterior rhinoscopy nasal examination image, black star septal
hematoma. (b) White arrow, septal hematoma image on paranasal coronal CT

306
M. Gümüşsoy and İ. Çukurova
For this reason, if nasal congestion occurs after nasal trauma, it should be shared
with the children’s families that it may be caused by septal hematoma. Septal hematoma and abscess treatment is performed under general anesthesia with incision,
drainage, and tampons placed in the nose. Antibiotics and nasal care should be recommended to patients. The nasal tampon is usually left on for 2–3days. It may be
difcult for children to tolerate tampons [65].
22.10.2 Septum Deviation
While some authors mention that birth trauma is an essential factor in forming septum deviation in children, it has been reported that it can occur without birth trauma.
As a result, septal deviation can cause nasal congestion in children and adults,
whether congenital or acquired. The diagnosis of septum deviation can be easily
made by endoscopic nasal examination. Its treatment is surgery, and its clinical
indications must be based on solid foundations. These relate to the severity of the
child’s nasal congestion, such as sleeping with an open mouth, sleep-disordered
breathing, and craniofacial anomalies. Septoplasty is possible at any age but rarely
performed before age seven. The reason is that septoplasty may negatively affect the
development of the nose and face. This view stems from the fact that, anatomically,
the story of the septal cartilage continues until the age of ve to six, and the vomer
and perpendicular lamina continue until adolescence. On the other hand, waiting
instead of surgically correcting a septum deviation that causes nasal congestion in a
pediatric patient may be more harmful, considering the complications that may
occur. Radiologically, paranasal CT is necessary for planning surgery [66, 67].
Surgically, to avoid disrupting the development of the nose and face, rearranging
the septum with minimal resection of the cartilage part blocking the passage is a
correct approach. In children, active growth foci should not be touched, and the
bony septum should not be removed to avoid changes in facial development [68].
22.10.3 Nasal Foreign Bodies
Nasal foreign bodies are frequently encountered in children under the age of ve.
The most important reason is that children in this age group put objects in their
hands into their noses while crawling or playing on the ground. We can divide foreign objects into two parts: living and non-living. Inanimate objects such as grains,
beads, or buttons are more commonly seen in children. They often fall on the kitchen
oor during cooking or are found by children at home [69].
When organic foreign bodies (chickpeas, beans, peas, etc.) come into contact
with the nasal mucosa, they swell and become difcult to remove as they remain in
the nose. Organic foreign bodies tend to swell and are generally more symptomatic
than inorganic ones. For this reason, one should not wait for the removal of such
foreign bodies and should be removed as soon as possible. Button batteries are
attractive to children because of their small size and bright appearance; they are

22 Nasal Congestion inChildren
307
often inserted into the nose, ear, or mouth. Early diagnosis and urgent removal are
essential. Any delay may lead to necrosis of the nasal mucosa and septal perforation [70].
The most critical complaints of patients with foreign bodies in the nose are nasal
congestion and foul-smelling nasal discharge. It may also cause symptoms such as
nosebleeds, facial pain, nasal regurgitation, facial swelling, nasal crusting, and
cough. Objects can be located in any nasal cavity region, inferior to the inferior
turbinate or anterior to the middle turbinate. Sometimes, the foreign body is not visible on nasal examination. When in doubt, the ideal method is rigid or exible nasal
endoscopy (Fig.22.6). Edema, inammation, or bleeding around the foreign body
may prevent the foreign body from being seen. Foreign body and unilateral choanal
atresia, nasal tumor, nasal polyp, septal abscess, and septal hematoma should be
considered in the differential diagnosis in pediatric patients presenting with unilateral nasal obstruction or foul-smelling, purulent nasal discharge. In diagnosing
nasal and paranasal sinus foreign bodies, the most important diagnostic methods
besides examination are plain radiographs, CT, and MRI [71].
In immobile patients with full cooperation, foreign bodies can usually be
removed using appropriate tools without leaking into the nasopharynx, esophagus,
or trachea. Organic foreign objects that do not have corners are round (balls, beads,
etc.) or may break apart when held. They should be removed by going behind the
thing and pulling it forward with a curved tool such as an Itard probe or an angled
hook. No attempt should be made to grasp or remove round foreign objects from the
front with a bayonet or forceps. Meanwhile, the foreign body may return to the
a b
a
b
Fig. 22.6 (a) The foreign body is in front of the middle turbinate during an endoscopic examina-
tion of the left side of the nose. (b) The foreign body (plastic toy part) was removed from the nose

308
M. Gümüşsoy and İ. Çukurova
nasopharynx, trachea, or esophagus. Suppose the foreign body is angular and prominent. In that case, it can be removed by grasping it with special tools such as bayonet Hartman forceps, and if it is angular and small, alligator forceps. In cases where
the nasal foreign body cannot be seen or retained, a balloon catheter can be applied
[69–71].
References
1. Esmaili A, Acharya A.Clinical assessment, diagnosis and management of nasal obstruction.
Aust Fam Physician. 2017;46:499–503.
2. Van Cauwenberge P, etal. Anatomy and physiology of the nose and the paranasal sinuses.
Immunol Allergy Clin N Am. 2004;24(1):1–17.
3. Jones N. The nose and paranasal sinuses physiology and anatomy. Adv Drug Deliv Rev.
2001;51(1):5–19.
4. Valero A, Navarro AM, Del Cuvillo A, etal. Position paper on nasal obstruction: evaluation
and treatment. J Investig Allergol Clin Immunol. 2018;28:67–90.
5. Leboulanger N. Nasal obstruction in children. Eur Ann Otorhinolaryngol Head Neck Dis.
2016;133(3):183–6.
6. Trabalon M, Schaal B.It takes a mouth to eat and a nose to breathe: abnormal oral respiration
affects neonates’ oral competence and systemic adaptation. Int J Pediatr. 2012;2012:207605.
7. Smith MM, Ishman SL.Pediatric nasal obstruction. Otolaryngol Clin N Am. 2018;51(5):971–85.
https://doi.org/10.1016/j.otc.2018.05.005.
8. Lale A, Mason J, Jones N.Mucociliary transport and its assessment: a review. Clin Otolaryngol.
1998;23(5):388–96.
9. Neskey D, Eloy JA, Casiano RR.Nasal, septal, and turbinate anatomy and embryology.
Otolaryngol Clin N Am. 2009;42(2):193–205.
10. Patel VA, Carr MM.Congenital nasal obstruction in infants: a retrospective study and literature
review. Int J Pediatr Otorhinolaryngol. 2017;99:78–84.
11. Teissier N, Kaguelidou F, Couloigner V, Francois M, Van Den Abbeele T.Predic-tive factors
for success after transnasal endoscopic treatment of choanal atresia. Arch Otolaryngol Head
Neck Surg. 2008;134(1):57–61.
12. Blake KD, Prasad C.CHARGE syndrome. Orphanet J Rare Dis. 2006;1:34.
13. Strychowsky JE, Kawai K, Moritz E, etal. To stent or not to stent? A meta-analysis of endonasal congenital bilateral choanal atresia repair. Laryngoscope. 2016;126(1):218–27.
14. Willging JP.Transpalatal repair of choanal atresia. In: Potsic WP, Cotton RT, Handler SD,
etal., editors. Surgical pediatric otolaryngology; 2016. p.193–215.
15. Tate JR, Sykes J. Congenital nasal pyriform aperture stenosis. Otolaryngol Clin N Am.
2009;42:521–5.
16. Wormald R, Hinton-Bayre A, Bumbak P, et al. Congenital nasal pyriform aperture stenosis
5.7 mm or less is associated with surgical intervention: a pooled case series. Int J Pediatr
Otorhinolaryngol. 2015;79(11):1802–5.
17. Zapata S, Kearns DB. Nasal dermoids. Curr Opin Otolaryngol Head Neck Surg.
2006;14:406–11.
18. Paradis J, Koltai PJ. Pediatric teratoma and dermoid cysts. Otolaryngol Clin North Am.
2015;48(1):121–36.
19. Bonne NX, Zago S, Hosana G, Vinchon M, Van den Abbeele T, Fayoux P.Endonasal endoscopic approach for removal of intranasal nasal glial heterotopias. Rhinology. 2012;50:211–7.
20. Özgür A, Dursun E, Şehitoğlu İ, Özergin Z, Çelebi Ö, Terzi S.Two cases of nasal glioma
treated by endoscopic transnasal surgery. Kafkas J Med Sci. 2016;6:145–8.
21. Cukurova I, Gumussoy M, Yardim BG, Imamoglu T, Yigitbasi OG.Transnasal endoscopic
approach for the treatment of the nasal encephalocele causing respıiratory distress. Nobel
Med. 2011;7(2):117–2.

22 Nasal Congestion inChildren
22. Gumussoy M, Ugur O, Cukurova I, Uluyol S.Recurrent meningitis and frontal encephalocele
as delayed complications of craniofacial trauma. J Craniofac Surg. 2014;25(2):529–30.
23. Cukurova I, Gumussoy G, Yaz A, Bayol B, Yigitbasi OG.A benign teratoma presenting as an
obstruction of the nasal cavity: a case report. J Med Case Rep. 2012;6(1):1–4.
24. Lecavalier M, Nguyen LH.Bilateral dacryocystoceles as a rare cause of neonatalrespiratory
distress: report of 2 cases. Ear Nose Throat J. 2014;93(1):26–8.
25. Barham HP, Wudel JM, Enzenauer RW, etal. Congenital nasolacrimal duct cyst/dacryocystocele: an argument for a genetic basis. Allergy Rhinol (Providence). 2012;3(1):e46–9.
26. Mallol J, Crane J, von Mutius E, etal. The international study of asthma and allergies in childhood (ISAAC) phase three: a global synthesis. Allergol Immunopathol. 2013;41:73–85.
27. Workowski KA, Berman S, Centers for Disease C, Prevention. Sexually transmitted diseases
treatment guidelines, 2010. MMWR Recomm Rep. 2010;59:1–110.
28. Gumuşsoy M, Gumuşsoy S, Çukurova I.The most frequently encountered rhinologic problems during pregnancy: appropriate approaches in diagnosis and therapy. J Tepecik Educ Res
Hosp. 2017;27:13–9. https://doi.org/10.5222/terh.2017.013.
29. Cingi C, Özdoğanoğlu T, Songu M.Nasal obstruction as a drug side effect. Ther Adv Respir
Dis. 2011;5:175–82.
30. Wallace DV, Dykewicz MS, Bernstein DI, Blessing-Moore J, Cox L, Khan DA, etal. The
diagnosis and management of rhinitis: an updated practice parameter. J Allergy Clin Immunol.
2008;122(2):S1–84. https://doi.org/10.1016/j.jaci.2008.06.003.
31. Catlı T, Atilla H, Miller EK.Acute viral rhinitis. All around the nose. Heidelberg: Springer;
2019. p.199–202. https://doi.org/10.1007/978- 3- 030- 21217- 9_23.
32. Monto AS. Epidemiology of viral respiratory infections. Am J Med. 2002;112(Suppl
6A):4s–12s.
33. Settipane RA, Charnock DR, Baraniuk JN, Shusterman D, et al. Epidemiology of rhinitis:
allergic and nonallergic. Nonallergic rhinitis. NewYork, NY: Informa; 2007. p.23–34.
34. Jeffe JS, Bhushan B, Schroeder JW Jr. Nasal saline irrigation in children: a study of compliance and tolerance. Intern J Pediatr Otorhinolaryngol. 2012;76:409–13.
35. Shaikh N, Wald ER, Pi M.Decongestants, antihistamines and nasal irrigation for acute sinusitis in children. Cochrane Database Syst Rev. 2012;(9):CD007909.
36. Shapiro DJ, Gonzales R, Cabana MD, Hersh AL.National trends in visit rates and antibiotic
prescribing for children with acute sinusitis. Pediatrics. 2011;127(1):28–34.
37. Revai K, Dobbs LA, Nair S, Patel JA, Grady JJ, Chonmaitree T.Incidence of acute otitis
media and sinusitis complicating upper respiratory tract infection: the effect of age. Pediatrics.
2007;119(6):e1408.
38. Feres MF, Hermann JS, Cappellette M, Pignatari SS. Lateral X-ray view of theskull for
the diagnosis of adenoid hypertrophy: a systematic review. Int J Pediatr Otorhinolaryngol.
2011;75(1):1–11.
39. Brietzke SE, Brigger MT.Adenoidectomy outcomes in pediatric rhinosinusitis: a meta-analysis. Int J Pediatr Otorhinolaryngol. 2008;72(10):1541–5.
40. Ramadan HH, Cost JL. Outcome of adenoidectomy versus adenoidectomy with maxillary
sinus wash for chronic rhinosinusitis in children. Laryngoscope. 2008;118(5):871–3.
41. Almac A, Elicora SS, Yumuk Z, Dundar V, Willke A.The relationship between chronic otitis media with effusion and surface and deep ora of hypertrophic adenoids. Int J Pediatr
Otorhinolaryngol. 2009;73(10):1438–40. https://doi.org/10.1016/j.ijporl.2009.07.014.
42. Orlandi RR, Kingdom TT, Hwang PH, Smith TL, Alt JA, Baroody FM, etal. International
consensus statement on allergy and rhinology: rhinosinusitis. Int Forum Allergy Rhinol.
2016;6:S22–S209.
43. Tharpe CA, Kemp SF. Pediatric allergic rhinitis. Immunol Allergy Clin N Am.
2015;35(1):185–98.
44. Gentile D, Bartholow A, Valovirta E, etal. Current and future directions in pediatric allergic
rhinitis. J Allergy Clin Immunol. 2013;1:214–26.
45. Smart BA.The impact of allergic and nonallergic rhinitis on pediatric sinusitis. Curr Allergy
Asthma Rep. 2006;6:221–7.
309

310
46. Ellis AK, Keith PK.Nonallergic rhinitis with eosinophilia syndrome. Curr Allergy Asthma
Rep. 2006;6(3):215–20. https://doi.org/10.1007/s11882- 006- 0037- 0.
47. Fokkens WJ, Lund VJ, Mullol J, etal. EPOS 2012: European position paper on rhinosinusitis
and nasal polyps 2012. A summary for otorhinolaryngologists. Rhinology. 2012;50:1–12.
48. Weber SAT, Ferrari GF.Incidence and evolution of nasal polyps in children and adolescents
with cystic brosis. Braz J Otorhinolaryngol. 2008;74(1):16–20. https://doi.org/10.1016/
S1808- 8694(15)30745- X.
49. Fokkens W, Lund V, Bochert V, Clement P, Hellings P, Holmstrom M, etal. EAACI position
paper on rhinosinusitis and nasal polyps executive summary. Allergy. 2005;60:593–601.
50. Bakshi SS, Vaithy KA.Antrochoanal polyp. J Allergy Clin Immunol Pract. 2017;5:806–7.
51. Yaman H, Yilmaz S, Karali E, Guclu E, Ozturk O.Evaluation and management of antrochoanal polyps. Clin Exp Otorhinolaryngol. 2010;3:3.110-114.
52. Jiang ZY, Pereira KD, Friedman NR, Mitchell RB.Inferior turbinate surgery in children: a
survey of practice patterns. Laryngoscope. 2012;122(7):1620–3. https://doi.org/10.1002/
lary.23292.
53. Arganbright JM, Jensen EL, Mattingly J, etal. Utility of inferior turbinoplasty for the treatment of nasal obstruction in children: a 10-year review. JAMA Otolaryngol Head Neck Surg.
2015;141(10):901–4.
54. Kaya E, Özüdoğru E, Nogueira JF.Surgical management of the turbinates. All around the
nose; 2020. p.469–87. https://doi.org/10.1007/978- 3- 030- 21217- 9.
55. Komshian SR, Cohen MB, Brook C, Levi JR.Inferior turbinate hypertrophy: a review of
the evolution of management in children. Am J Rhinol Allergy. 2018;33:212–9. https://doi.
org/10.1177/1945892418815351.
56. Cloutier T, Pons Y, Blancal JP, Sauvaget E, Kania R, Bresson D, etal. Juvenilenasopharyngeal
angiobroma: does the external approach still make sense? Otolaryngol Head Neck Surg.
2012;147(5):958–63.
57. Gerth DJ, Tashiro J, Thaller SR.Pediatric sinonasal tumors in the United States:incidence and
outcomes. J Surg Res. 2014;190(1):214–20.
58. Yi JS, Cho GS, Shim MJ, Min J-Y, Chung Y-S, Lee B-J. Malignant tumors of the sinonasal tract in the pediatric population. Acta Otolaryngol. 2012;132:21–6. https://doi.org/10.310
9/00016489.2012.660730.
59. Sarafoleanu C, Manea C. Nasal manifestations of systemic diseases—a literature review.
Romanian J Rhinol. 2014;4:81–92.
60. De Vincentiis GC, Sitzia E, Botteroa S, Giuzioa L, Simonetti A, Rossi P. Otolaryngologic
manifestations of pediatric immunodeciency. Int J Pediatr Otorhinolaryngol. 2009;73:S42–8.
61. Lahiri T, Hempstead SE, Brady C, Cannon CL, Clark K, Condren ME, Guill MF, Guillerman
RP, Leone CG, Maguiness K, Monchil L, Powers SW, Rosenfeld M, Schwarzenberg SJ,
Tompkins CL, Zemanick ET, Davis SD.Clinical practice guidelines from the cystic brosis
foundation for preschoolers with cystic brosis. Pediatrics. 2016;137(4):e20151784. https://
doi.org/10.1542/peds.2015- 1784.
62. Lucas JS, Burgess A, Mitchison HM, Moya E, Williamson M, Hogg C.Diagnosis and management of primary ciliary dyskinesia. Arch Dis Child. 2014;99(9):850–6. https://doi.org/10.1136/
archdischild- 2013- 304831.
63. Guo Z, Chen W, Wang L, Qian L.Clinical and genetic Spectrum of children with primary
ciliary dyskinesia in China. J Pediatr. 2020;225:157–165.e5. https://doi.org/10.1016/j.
jpeds.2020.05.052.
64. Wright RJ, Murakami CS, Ambro BT.Pediatric nasal injuries and management. Facial Plast
Surg. 2011;27(5):483–90. https://doi.org/10.1055/s- 0031- 1288931.
65. Cakabay T, Ustun BS.Pediatric nasal traumas: contribution of epidemiological features to
detect the distinction between nasal fractures and nasal soft tissue injuries. J Craniofac Surg.
2018;29(5):1334–7. https://doi.org/10.1097/SCS.0000000000004550.
66. Reitzen SD, Chung W, Shah AR.Nasal septal deviation in the pediatric and adult populations.
Ear Nose Throat J. 2011;90(3):112–5.
M. Gümüşsoy and İ. Çukurova

22 Nasal Congestion inChildren
67. Lawrence R.Pediatric septoplasy: a review of the literature. Int J Pediatr Otorhinolaryngol.
2012;76(8):1078–81.
68. Cristophel JJ, Gross CW.Pediatric septoplasty. Otolaryngol Clin N Am. 2009;42:287–94.
69. Abou-Elfadl M, Horra A, Abada RL, Mahtar M, Roubal M, Kadiri F.Nasal foreign bodies:
results of a study of 260 cases. Eur Ann Otorhinolaryngol Head Neck Dis. 2015;132:343–6.
70. Regonne PE, Ndiaye M, Sy A, Diandy Y, Diop AD, Diallo BK.Nasal foreign bodies in children in a pediatric hospital in Senegal: a three-year assessment. Eur Ann Otorhinolaryngol
Head Neck Dis. 2017;134:361–4.
71. Cetinkaya EA, Arslan İB, Cukurova İ. Nasal foreign bodies in children: types, locations,
complications and removal. Int J Pediatr Otorhinolaryngol. 2015;79(11):1881–5. https://doi.
org/10.1016/j.ijporl.2015.08.036.
311

Nasal Itching andSneezing inChildren
23
NurullahTüre andFatihOğhan
23.1 Introduction
Nasal itching and sneezing occur after neural activation stimulation by environmental irritants and biological agents released during the local inammation process. In
particular, sneezing protects the body by playing an essential role in protecting and
clearing the airway from irritating substances. A runny nose, nasal itching, and
nasal congestion often accompany sneezing. This condition is generally observed
due to rhinitis seen in allergies and viral upper respiratory tract infections.
Rhinitis is inammation of the nasal mucosa. In rhinitis, nasal itching, sneezing,
runny nose, and nasal congestion are observed. Along with rhinitis symptoms,
accompanying complaints in the eyes, ears, and throat may be observed. Rhinitis is
generally classied as allergic and non-allergic rhinitis [1, 2].
Regarding complaints, there is no signicant difference between allergic and
non-allergic rhinitis. For this reason, most pediatric patients presenting with rhinitis
complaints are diagnosed with allergic rhinitis. Treatment management is carried
out according to this diagnosis. Sometimes, differential diagnosis can be difcult in
pediatric patients due to overlapping conditions. It is difcult to determine its incidence epidemiologically due to the need for more data on the prevalence of nasal
itching and sneezing in allergic and non-allergic rhinitis in pediatric patients.
This chapter explains the pathophysiology and etiology of nasal itching and
sneezing in children, the differential diagnosis of co-occurring diseases, and appropriate treatment options.
N. Türe · F. Oğhan (*)
Kütahya Health Sciences University, Evliya Çelebi Training and Research Hospital,
Izmir, Turkey
e-mail: fatih.oghan@ksbu.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_23
313

314
N. Türe and F. Oğhan
23.2 Pathophysiology
Itching is a nociceptive primitive defense mechanism that stimulates avoidance of
inhaling harmful substances involving innate and adaptive immune mechanisms
[3]. On the other hand, sneezing is caused by neural activation triggered by external
environmental stimuli (irritants) or biological products formed in a local inammatory process. Sneezing is a central reex whose afferent arm begins in the nasal
mucosa and whose efferent arm includes the nerves innervating the diaphragm,
accessory respiratory muscles, and larynx. Sensory nerves in the nasal mucosa originate from the ophthalmic and maxillary branches of the trigeminal nerve [4].
Terminal sensory nerve endings are mostly unmyelinated nociceptor C bers.
Sometimes Aδ bers (Aβ bers) are also included [5, 6]. Nociceptor nerves respond
to noxious external and internal stimuli through a series of receptors, such as transient receptor potential vanilloid type 1 (TRPV1) and transient receptor potential
ankyrin type 1 (TRPA1) [7].
Nasal nerve endings contain receptors for chemicals such as the Histamine 1
(H1) receptor or the cysteinyl leukotriene 1 receptor (CysLTR1) [8, 9].
While H1 receptors in nasal sensory nerve endings explain the sneezing that
occurs during exposure to allergens, transient receptor channels explain the
sneezing and itching that occur when exposed to non-antigenic irritating substances [10].
Many pruritogens and receptors mediate itching, which occurs due to allergic
rhinitis. After stimulation of nerve bers in the nasal mucosa and activation of mast
cells, histamine is released, which causes nasal itching [11]. Histamine increased in
the nasal lavage uid of allergic patients, but no increase was observed in nonallergic patients [12]. Neuropeptides such as substance P, CGRP, and vasoactive
intestinal polypeptide (VIP) have been reported to be increased in the nasal lavage
wash of patients with allergic rhinitis, which are thought to play a role in nasal itching. Furthermore, nerve growth factor (NGF) is expressed in the nasal epithelium
and peripheral nerves in the nasal mucosa, and the expression of this neuropeptide
is signicantly increased after nasal allergen challenge in patients with allergic rhinitis compared to controls [13, 14]. House dust mites are affected by proteaseactivated receptor 2 (PAR2).
It has been shown to induce the release of inammatory cytokines and ultimately
cause nasal itching [15]. Additionally, it has been reported that nasal itching
increases when a TRPV1 activator such as capsaicin is administered to patients with
allergic rhinitis during seasonal allergen exposure [16]. Nerve expression of TRPV1
is also increased in patients with non-allergic rhinitis [17]. This phenomenon suggests inammatory cytokines such as histamine and bradykinin cause nasal itching
through TRPV1 receptors [18].
Physicians should know its close relationship with other allergic diseases, such
as allergic conjunctivitis and asthma. Interestingly, pruritus has been reported as a
preliminary symptom in patients with asthma [19]. Additionally, in a study investigating non-respiratory symptoms of acute asthma, nasal itching was observed
before the asthma attack [20].
Соседние файлы в папке Библиотека им академика М.И. Перельмана
