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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)

284
Y. S. S. Yıldırım et al.
Furthermore, it is worth noting that rhabdomyosarcoma and neuroblastoma can also
present as tumors within the auditory canal in children [13].
Less commonly, otorrhea may arise from the following conditions:
Contact Dermatitis
Topical medications or cosmetics may cause local irritation and inammation with
ear drainage. A typical history reveals the offending agent being used, often for
a pre-existing condition such as otitis externa or cerumen impaction. Pruritus,
pain, and inammation on examination accompany the otorrhea. Treatment con-
sists of topical corticosteroids and avoidance of the allergen.
Bullous Myringitis
Often associated with respiratory symptoms or acute otitis media, bullous myringi-
tis describes serous liquid-lled blisters, or “bullae,” on the tympanic membrane.
When the bullae rupture, thin bloody otorrhea may occur, and pain is often
relieved. The external ear canal is not typically involved.
Granulation Tissue
Granulation tissue can develop in several conditions and can be associated with
otorrhea. As mentioned, this tissue can accumulate around a foreign body (such
as a tympanostomy tube). It can also be seen in granulomatous disease (such as
Langerhans cell histiocytosis) or chronic inammatory conditions (such as
chronic otitis media). The rich vascular supply can also lead to leakage of lym-
phatic uid [14].
21.5.7 Polyps
Polyps within the ear canal’s external region can develop as a reaction to inammation or infections, such as chronic otitis media, cholesteatoma, or the presence of a
foreign body (e.g., a dislodged tympanostomy tube). In rare instances, they might
originate from a tumor, such as Langerhans Cell Histiocytosis, teratoma, or a neoplasm. These polyps often result in the discharge of bloody or serous uid from the
ear, particularly when manipulated, displaying characteristics akin to granulomas.
Treatment for ear polyps can lead to rapid resolution through the application of topical antibiotics and/or anti-inammatory therapy [15].
21.5.8 Otomycosis
Otomycosis is a fungal infection of the external auditory canal and a common reason for external otitis treatment failure, usually caused by Aspergillus species.
Patients with fungal external otitis commonly report itching, discomfort, discharge,
discomfort, and feeling that something is in the ear canal. Otorrhea is generally
thick and purulent. Deep-seated itching is the most troublesome symptom; pain is
less intense than bacterial otitis externa. Fungal organisms have a very characteristic
appearance in the ear canal, especially under magnied vision [16]. Topical

21 Otorrhea inChildren
285
antifungals are given, and thorough suction cleaning of the meatus is performed.
And meautus should kept dry. In persistent infections, oral antifungals like
Itraconazole may be prescribed.
21.5.9 First Branchial Cleft Cysts
The rst branchial pouch originates within the pharynx and extends outwards and
upwards to connect with the rst branchial cleft, ultimately giving rise to the eustachian tube. Rarely, congenitally anomalous rst branchial cleft cysts may drain into
the external ear canal. A mass in the periauricular region may suggest this diagnosis
in the face of chronic drainage with a normal tympanic membrane.
21.5.10 Cholesteatoma
A cholesteatoma is an anomalous development of squamous epithelial tissue. These
growths can manifest within the middle ear and mastoid region (referred to as middle ear cholesteatoma) or, less frequently, within the ear canal itself (termed external
ear canal cholesteatoma). Over time, a cholesteatoma may progressively expand,
encompassing, and damaging the ossicles, which can result in conductive hearing
impairment. Hearing loss may also occur if the cholesteatoma blocks the orice of
the eustachian tube, leading to the accumulation of uid in the middle ear. Typically,
surgical intervention is necessary for the treatment of most cholesteatomas [17, 18].
21.5.11 Spontaneous Cerebral Spinal Fluid Otorrhea
Apart from basilar skull fractures resulting from head injuries, spontaneous cerebrospinal uid (CSF) otorrhea can also originate from defects in the tegmen tympani, located in the oor of the temporal bone. The possibility of these defects
should be considered in situations where otorrhea persists after ruling out more
typical causes, or in cases involving a child who has experienced multiple episodes
of meningitis. A noninvasive approach to diagnosis involves utilizing high- resolution
computed tomography (CT) with thin slices through the temporal bone [19].
References
1. Schulze SL, Kerschner J, Beste D.Pediatric external auditory canal foreign bodies: a review of
698 cases. Otolaryngol Head Neck Surg. 2002;127:73–8.
2. Macfadyen CA, Acuin JM, Gamble C. Systemic antibiotics versus topical treatments for
chronically discharging ears with underlying eardrum perforations. Cochrane Database Syst
Rev. 2006;(1):CD005608.
3. Boyce TG.Otitis externa and necrotizing otitis externa. In: Long SS, Pickering LK, Prober CG,
editors. Principles and practice of pediatric infectious diseases. 4th ed. Edinburgh: Elsevier
Saunders; 2012. p.220–2.

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4. Heikkinen T, Ruuskanen O.Signs and symptoms predicting acute otitis media. Arch Pediatr
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Y. S. S. Yıldırım et al.

Nasal Congestion inChildren
22
MuratGümüşsoy andİbrahimÇukurova
22.1 Introduction
Nasal congestion is common in newborns, infants, and older children and is a signicant problem. It is one of the most common reasons for consultation in ear, nose,
and throat (ENT) practice, where it is requested to be evaluated by pediatricians
under outpatient clinic conditions. Although the subjective perception of difculty
or difculty breathing through the nose and expressing this situation as disturbing is
dened as nasal congestion, the problem is slightly different for children. It should
not be forgotten that nasal congestion, considered a simple nding, can cause serious, life-threatening consequences such as malnutrition, respiratory distress, and
sleep apnea, especially in the neonatal period [1].
The rst 3months are when the newborn’s air needs are met only through nasal
breathing. Partial or complete nose obstruction as an entrance to the upper respiratory tract causes the child to experience respiratory failure. While both nasal
obstructions inevitably result in emergency airway obstruction, partial or single
nasal obstruction clinically results in more difculty in feeding. Both situations may
require a critical and urgent approach. For older age groups, a blocked nose is more
likely to result in poor quality of life rather than an emergency approach and constitutes a substantial patient group in ENT practice [2].
The history taken from the families regarding nasal congestion is signicant for
diagnosis. In the past, children’s day and night ndings should be questioned in
detail, especially the child’s feeding, sucking, sleep, and wakefulness status provide
clues for the approach to nasal congestion. Additionally, runny nose, bleeding, and
snoring are other ndings that should be questioned [3].
M. Gümüşsoy · İ. Çukurova (*)
Health Sciences University Izmir Tepecik SUAM ENT Clinic, Izmir, Turkey
Department of Otolaryngology-Head and Neck Surgery, Izmir Tepecik Training and Research
Hospital, University of Health Sciences, Izmir, Turkey
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2024
H. Yüksel et al. (eds.), Pediatric Airway Diseases, Comprehensive ENT,
https://doi.org/10.1007/978-3-031-74853-0_22
287

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M. Gümüşsoy and İ. Çukurova
ENT examination should be performed as thoroughly and completely as possible
in pediatric patients. Anatomical structures, especially those involving the upper
airway, should be evaluated in detail with rigid or exible endoscopy. Although
radiological imaging methods are not routine after endoscopic evaluation with the
preliminary diagnosis of nasal obstruction in children, they can be used when necessary in suitable patients. Imaging in children may be limited for different reasons,
especially compliance problems. In addition, it is almost impossible to apply nasal
airow tests, acoustic rhinometry, rhinomanometry, and similar methods in children, which we can use for nasal congestion in adult patients [1–3].
Nasal congestion in children can generally occur due to congenital or acquired
anatomical disorders, mucosal pathologies, and many different and various diseases
that block air passage due to the mass effect. In addition, the obstruction may be
unilateral, bilateral, permanent, or temporary (during the day). The most crucial difference is that the causes of nasal congestion in children may differ etiologically
depending on the child’s age. While physiological and congenital causes cause
nasal congestion in the newborn period, infectious causes come to the fore as the
child grows. For all these reasons, it can be challenging to focus on the problem in
children who complain of nasal congestion. Therefore, detailed history, ENT examination, and endoscopic examination contain important clues for diagnosis.
Radiological imaging, even a biopsy, may sometimes be required for diagnostic
purposes [4, 5].
22.2 Nasal Breathing intheNeonatal Period
Especially in children, the rst 12weeks following birth are critical in terms of the
need for mandatory nasal breathing. Any obstacle in nasal breathing can cause
severe and life-threatening problems in the child. Anatomical structures in the neonatal period differ between infants and children. Inside the mouth, the tongue is
more extensive, complicated, and attached to the soft palate than the oropharynx
opening. The epiglottis is located above the level of the soft palate. Placing the epiglottis and larynx in a higher position than usual allows the newborn to feed and
breathe air simultaneously. Therefore, nasal congestion negatively affects breathing
and nutrition [4–6].
The nasal cavity contributes approximately half of the total resistance of commonly inhaled air. Therefore, the degree of obstruction and the ndings are at the
forefront. As a sign of respiratory distress, the nasal ap participates in breathing,
trying to balance breathing by reducing inspiratory airow resistance. However, due
to the degree of obstruction and increased air resistance, rapid desaturation and
respiratory difculty will occur for newborns with nasal obstructions following
birth. The situation is urgent and fatal if left untreated. Airway patency should be
ensured quickly, and the newborn should be intubated. If intubation cannot be performed, tracheotomy should be performed in emergencies. Unilateral nasal obstruction occurs in later periods in direct proportion to the degree to which it affects
breathing and nutrition [5, 6].

22 Nasal Congestion inChildren
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Several physiological changes from the neonatal period and childhood can
trigger nasal congestion. The physiological mechanism controlled by the autonomic nervous system on both sides of the nasal cavity, which we call the nasal
cycle, ensures the nasal airow resistance remains balanced. The nasal cycle is
increased on one side of the nose by the erectile properties of the turbinates and
decreased on the other, resulting in physiological nasal congestion that may last
between 30min and 6h. In addition, positionally, nasal congestion may occur due
to congestion in the underlying nasal cavity when the child is laid on its side. In
the rst year of life, nasal congestion is expected due to physiological reasons,
especially nasal congestion, and affects sleep quality. Nevertheless, with the rapid
growth pattern of the newborn and the nasal volume approximately doubling in
the rst 6months of life, a signicant improvement in the symptoms of nasal
congestion is observed [6, 7].
Evaluation of a newborn with nasal congestion begins with a history taken from
the mother, father, and relatives. In addition to nasal congestion, it is learned whether
symptoms such as runny nose, wheezing, or feeding problems are accompanied. It
is essential when the ndings are noticed and whether they are intermittent or continuous. The diseases the mother had during pregnancy, the medications she used,
familial genetic disorders, and conditions detected before birth should be questioned in detail. Learning the details of the labor process and its aftermath (early
birth, prematurity, prolonged labor time, difcult birth, birth trauma, postnatal
resuscitation, or intubation history) may be helpful in diagnosis [8].
After the newborn has an adequate airway after birth, a detailed physical
examination should be performed to investigate the presence of deformity, asymmetry, and skin lesions in the newborn’s body. Afterward, nasal patency should
be evaluated. The most commonly used practical and easy method to assess nasal
patency is to evaluate the patency by advancing from the tip of the nose towards
the nasopharynx with a plastic catheter or cannula. However, today, the most
valid method for nasal obstruction is direct examination and examination of the
nasal cavity up to the nasopharynx using exible or rigid endoscopy. After endoscopic examination, pathology is detected, and radiological evaluation (Computed
Tomography (CT) and Magnetic Resonance Imaging (MRI)) is performed. CT is
more valuable for evaluating bone structures such as choanal atresia and piriform
aperture stenosis, and MRI is more practical for soft tissues and intracranial
extension and connections. In the presence of an obstructive lesion, biopsy
should also be considered. However, a biopsy should only be performed with
radiological evaluation [9].
22.3 Etiology ofNasal Congestion inChildren
The complaint of nasal congestion, which we frequently encounter in children from
birth to adulthood, is the most important of the clinical problems that sleep disturbance, snoring, OSAS ndings, and regression in growth, development, and learning abilities can accompany.

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Nasal and paranasal symptoms may accompany nasal congestion. These are the
basics of common diseases, such as allergic rhinitis, rhinosinusitis, septal deviation,
adenoid hypertrophy, or nasal trauma.
It may be a symptom. In addition, lung-related pathologies such as asthma may
also accompany it.
Different classications have been used in the literature for the etiology of nasal
congestion in children. Nasal congestion is a comprehensive issue that can be seen
due to congenital or acquired anatomical disorders, mucosal level, or structural disorders that can block the nasal passage due to mass effects, trauma, and iatrogenic
reasons. The obstruction may be bilateral or unilateral, or it may be permanent or
temporary.
This section will discuss the etiological causes of nasal congestion, their prevalence according to age, and their diagnosis and treatment [7–10].
Nasal congestion in children can be evaluated in two groups according to age.
1. Causes of nasal congestion in newborns and babies.
(a) Physiological (Nasal cycle and positional congestion).
(b) Neonatal rhinitis.
(c) Congenital.
(d) Trauma.
(e) Neoplasia (benign, malignant).
2. Causes of nasal congestion in children.
(a) Inammatory/infectious.
(b) Adenoid hypertrophy.
(c) Foreign body (unilateral obstruction).
(d) Septal deviation.
(e) Neoplasia (benign, malignant).
(f) Systemic diseases.
Generally, the etiological causes of nasal congestion in children are classied in
Table22.1.

22 Nasal Congestion inChildren
291
Table 22.1 Causes of nasal
congestion in children
1. Physiological
2. Congenital
(a) Choanal atresia
(b) Pyriform aperture stenosis
(c) Nasal dermoid
(d) Nasal glioma
(e) Encephalocele
(f) Nasolacrimal duct cysts
3. Infectious
(a) Neonatal rhinitis
(b) Infectious rhinitis (rhinosinusitis)
(c) Adenoid hypertrophy
4. Inammatory
(a) Allergic rhinitis
(b) Nonallergic rhinitis
(c) Nasal polyp-Antrochoanal polyp
(d) Inferior turbinate hypertrophy
5. Neoplasia
(a) Benign
• Juvenile nasopharyngeal angiobroma
• Nasopharyngeal teratoma
(b) Malignant
• Adenocarcinoma
• Esthesioneuroblastoma
• Lymphoma
• Metastatic disease
• Nasopharynx carcinoma
• Rhabdomyosarcoma
• Squamous cell carcinoma
6. Systemic
(a) Cystic brosis
(b) Primary ciliary dyskinesia
7. Trauma/iatrogenic
(a) Septal hematoma
(b) Septum deviation
(c) Foreign body in the nose
22.4 Congenital Causes
22.4.1 Choanal Atresia
Many congenital facial deformities in childhood can cause nasal congestion. The
most common is choanal atresia, in which the opening between the nasal cavity and
the nasopharynx is impaired due to one or bilateral atresia obstruction in the posterior part of the nasal cavity (Fig.22.1). In 30% of the cases, it is bilateral, and in
70% of the cases, bone and membranous components are seen together. Its

292
ab
Fig. 22.1 The newborn was evaluated for respiratory distress. (a) Paranasal axial CT, white arrow,
bone atretic plaque in the choanal region, (b) Silicone tube stent placed in both noses after surgery
M. Gümüşsoy and İ. Çukurova
incidence is 1/5000–7000 births. Regarding gender, the female/male ratio is 2/1, it
is unilateral, and the right side is predominant. It may be accompanied by additional
congenital anomalies in approximately 40–60% of cases. Choanal atresia and
CHARGE syndrome [C: “coloboma,” H: “heart defects (congenital heart disease),”
A: “atresia (choanal),” R: “retardation (mental),” G: “genital hypoplasia,” E: “ear
abnormalities/deafness”] is more common than other anomalies [11] (Fig.22.1).
For the newborn, bilateral choanal atresia is a vital condition accompanied by
immediate respiratory failure and cyanosis. In unilateral atresia, the diagnosis may
be made late. Children may be asymptomatic or apply to the clinic with complaints
of runny nose, sleep disorders, and feeding problems. Atresia is often noticed when
the nasogastric tube cannot be passed through the nose. Diagnosis can be made by
ENT examination and exible endoscopic nasal examination. Radiological analysis
should be performed to evaluate the atresia’s location, position, and anatomical
structures. Paranasal CT in the axial-coronal plane should be the rst choice. Before
radiological imaging, aspiration of both nasal cavities should be performed in a
child with suspected choanal atresia to evaluate CT more efciently [12].
22.4.1.1 Points toConsider inAxial-Coronal Paranasal CT
1. Unilateral or bilateral atresia, bone and membranous association, and thickness
of atresia.
2. In axial imaging, the portion of the airway opening to the nasopharynx is less
than 3 mm; that is, it shows narrowing, evident in the posterior part of the
nasal cavity.
3. Monitoring the air-liquid level above the obstruction level.

22 Nasal Congestion inChildren
293
4. Thickening in the vomer.
5. Hypertrophic inferior turbinates are ndings that can be determined radio-
logically.
The treatment of choanal atresia is surgery, and today, transnasal endoscopic
surgery is the most frequently preferred approach. Surgery aims to eliminate the
atresic plaque. Different studies have reported that transnasal endoscopic surgery
success rates are between 70 and 90%. After nasal passage patency, silicone tube
stents are placed and kept for at least 3weeks (Fig.22.1). Re-occlusion of the atresia area opened in choanal atresia surgery is still the biggest obstacle to success.
Risk factors include gastroesophageal reux, bilateral bone atresia, and age at surgery less than 10years old. Since bilateral nasal passage obstruction is an airway
emergency in children, it should be treated surgically as soon as possible. In necessary patients, the patient should be provided with an oral airway until surgical treatment. In unilateral patients, it can wait until 18–24months at the earliest or often
until school age. Children with feeding difculties can benet from McGovern
paciers until surgical intervention [13, 14].
22.4.2 Pyriform Apertura Stenosis
Also known as stenosis of the front part of the nose, it is a rare congenital anomaly
that occurs as the pyriform aperture of the maxillary bone, which forms the entrance
to the nose, grows more than usual towards the medial or becomes ossied, resulting in a narrowing of the aperture. In children, symptoms similar to children with
bilateral choanal atresia are observed, with feeding difculties and cyanosis attacks.
It may be accompanied by anomalies such as prominent central incisors, hypoplastic maxillary sinuses, or holoprosencephaly. Diagnosis is made by showing on CT
that the maxillary aperture in the front of the nose is narrower than usual. Airway
management is the most critical aspect of treatment [15].
Medical interventions include McGovern paciers, oral airway, or endotracheal
intubation. Publications state that surgical intervention will be necessary when the
distance between piriform openings is less than 5.7mm. The transnasal sublabial
approach is the preferred surgical method. With the sublabial approach, the bone is
opened laterally and downwards, gaining a wide airway. Particular attention should
be paid to tooth buds. It is recommended that nasal stents be retained for 4–6weeks
following surgery [16].
22.4.3 Nasal Midline Congenital Masses
22.4.3.1 Nasal Dermoid Cyst
It is the most common congenital midline nasal lesion. Nasal dermoid cysts refer to
cystic congenital anomalies lined with squamous epithelium, which is located on
the midline nasal dorsum and has a channel that can pass through the skin, through
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