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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)

294
M. Gümüşsoy and İ. Çukurova
the septum, through the cribriform plate, and extend to the skull base and even to the
dura. They can be somewhere between the glabella and columella. Cystic expansion
of the duct is dened as a dermoid cyst [17].
Nasal dermoid cysts may contain skin appendages (mesodermal). About 60% of
the cysts are seen outside the nose, 30% are inside the nose, and the remaining 10%
are of mixed type. Radiological examination is vital for diagnosis. CT is used for
bone structures and relationships, and MRI with Gadolinium is used to evaluate
intracranial extension and soft tissue. The treatment is surgical, and total excision is
essential. Inadequate surgery may result in recurrence [18].
22.4.3.2 Nasal Glioma
Nasal gliomas are craniofacial masses developed from remnants of congenital
benign neuro-glial tissues. Although they are perceived as tumors, they are accumulations of glial tissue in the extradural region. These are abnormal connections
between the embryonic ectodermal and neuroectodermal parts due to the incomplete closure of the anterior fontanelle between the nasal and frontal bones. About
30% of nasal gliomas are intranasal, and 15–20% have an intracranial connection
with a brous band. On examination, it is smooth, not compressed by pressure;
the overlying skin may be discolored or telangiectatic, and the mass is not attached
to the mobile skin. Gliomas that have grown inside the nose can cause septal
deviation. Sometimes, they can look like antrochoanal polyps. They may protrude
from the anterior or posterior nasal cavity as pink-red polypoid masses. In MRI
evaluation, detailed information about the intracranial distance can be obtained,
and it also provides differentiation from other midline anomalies (encephalocele,
dermoid cyst, etc.). Gliomas appear isointense on T1 and heterogeneous on T2
and do not capture contrast material. Treatment involves total excision of the mass
[19, 20].
22.4.3.3 Encephalocele (Encephalo-Meningocele)
They are considered congenital neural tube defects. They always appear as extracranial herniation of meninges and brain tissue in the cranial defect area. They can
be meninges (encephalocele), brain, and meninges (encephalo-meningocele). In
nasal encephalocele formation, there is a bone defect between the frontal and
ethmoid bones. The mass can be seen to grow with crying or with pressure on the
jugular vein (Furstenberg test). Fronto-ethmoid encephaloceles are observed as
compressible masses that give intranasal translucency. Clinically, they may present with nasal congestion, cerebrospinal uid rhinorrhea, or recurrent attacks of
meningitis [21].
CT and MRI examinations are required for diagnosis. While CT is used to show
the location of the bone defect at the skull base, MRI provides information about the
sac content and intracranial extension (Fig.22.2). In cases where encephalocele is
suspected, biopsy is not recommended due to intracranial relationship. When diagnosed in the rst months of life, surgery should be planned to avoid the risk of
meningitis and cosmetic deformity due to the growth of the mass. Treatment
includes total removal of the group and repair of the dura [22, 23] (Fig.22.2).

22 Nasal Congestion inChildren
295
ab
Fig. 22.2 A 6-year-old girl complains of long-term nasal congestion and snoring. (a)
Encephalocele extending to the inferior of the left frontal lobe with a brous band in the coronal
MRI T1 section of the patient. (b) T2 section Coronal MRI imaging of the case
Differential Diagnosis
(a) Nasal glioma and dermoid cysts do not shrink upon examination, whereas
encephalocele is consistently soft and shrinks when pressed.
(b) Unlike nasal glioma and dermoid cysts, encephalocele may show
transillumination.
(c) The formation associated with cerebrospinal uid is encephalocele (herniation
of the meninges).
(d) Nasal glioma has no connection with the intracranial region.
(e) Encephalocele is pulsative (positive Furstenberg).
(f) There is no pulsation in nasal glioma and dermoid cysts (negative Furstenberg).
(g) Radiological imaging is sufcient for diagnosis.
(h) Preoperative biopsy should not be performed.
(i) While cranial bone defects are seen radiologically in encephalocele and der-
moid cysts, CT, and MRI, they are not seen in nasal glioma.
22.4.3.4 Nasolacrimal Duct Cyst (Dacryocystocele)
A nasolacrimal duct cyst develops due to incomplete canalization of the nasolacrimal duct during fetal development and can cause signicant nasal obstruction in the
newborn. Clinically, it is usually seen unilaterally, and the most common nding is
epiphora. It is typical to see a bluish cystic lesion located in the medial canthus or
an intranasal cystic mass [24].
Congestion in both noses occurs in 14% of cases and can close the nasal cavity
and cause severe respiratory distress. CT is the method of choice for diagnosis. On
CT, it can be seen as a cystic mass in the medial canthus region, expansion of the
nasolacrimal duct, and a cystic mass lling the nasal passage at the level of the inferior turbinate. Its treatment is surgery [25].

296
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22.5 Infectious Causes
22.5.1 Rhinitis intheNeonatal Period
Since effective breathing for the newborn is only possible with an open nose, nasal
congestion is vital, and severe hypoxia can have serious consequences. In the differential diagnosis, the most common cause of nasal congestion, apart from physiological and congenital causes, is rhinitis [4–6].
22.5.1.1 Rhinitis Etiology
1. Neonatal rhinitis.
2. Bacterial or viral rhinitis.
3. Iatrogenic rhinitis.
22.5.2 Neonatal Rhinitis
It is the most common cause of nasal congestion in the neonatal period. Regardless
of the causative pathology, it is observed as runny nose and congestion in children
under 3. Although its etiology is unknown, many causes have been blamed: viral,
inammatory, vascular, drug-related, traumatic, hormones and drugs transmitted
from the mother, etc. Nasal examination reveals bilateral nasal mucosa edema and
mucoid nasal discharge. A regression in symptoms is observed after nasal lavage
with physiological saline. Rhinitis symptoms resolve spontaneously over time
[5, 26].
22.5.3 Bacterial or Viral Rhinitis
The causative agent is often bacteria such as maternal streptococci, staphylococci,
chlamydia, gonorrhea, and syphilis, and less frequently, viral agents, especially
respiratory syncytial virus. The clinical picture is nasal congestion after nasopharyngitis and rhinitis [27, 28].
22.5.4 Iatrogenic Rhinitis
Iatrogenic rhinitis is due to secondary infection, trauma, nasal catheterization, or
uncleaned residues such as meconium remaining in the nose. Another factor associated with rhinitis ndings in the neonatal period is gastroesophageal reux. Nasal
congestion causes an increase in negative intralaryngeal pressure during inspiration,
thus facilitating reux. Therefore, in the presence of a persistent nasal obstruction
in the neonatal period, the possibility of gastroesophageal reux should be investigated and treated [27–29].

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22.5.5 Infectious Rhinitis (Rhinosinusitis)
Infectious rhinitis is often seen in childhood as inammation of the nose and sinuses
due to viral, bacterial, and less fungal reasons. Acute upper respiratory tract infections (rhinovirus) are infections of viral origin that are transmitted via droplets.
Rhinitis clinically manifests with complaints of local itching and sneezing, congestion, and discharge (serous) in the nose, along with systemic symptoms such as
chills, weakness, and fever. Flu (inuenza) has a more severe course than rhinovirus. It causes more serious damage to the upper respiratory tract, often leading to
secondary infection. The incidence of sinusitis increases in children after rhinovirus
or inuenza is the causative agent of rhinitis. Sinusitis is seen in 5–10% of children
due to upper respiratory tract infections, especially between 6 and 8. It is more
appropriate to call this condition, which clinically concerns both the nose and
sinuses, rhinosinusitis rather than sinusitis [30, 31].
When we examine it physiopathologically, viral infections disrupt nasal mucociliary activity, cause mucosal edema, and narrow the sinus ostium, thus preparing
the ground for the development of sinusitis. Due to the anatomical neighborhood of
the sinuses with the nasal cavity, colonized Streptococcus pneumoniae, Haemophilus
inuenzae, and Moraxella catarrhalis can pass into the sinuses. The mechanism can
be summarized as ostium occlusion, negative sinus pressure, and infection. Impaired
sinus circulation, mucus, and bacterial colonization in the sinus can easily result in
acute bacterial rhinosinusitis. The most common viral agent that disrupts this
defense mechanism is rhinoviruses. Rhinoviruses have a very high infection capacity [32].
Rhinosinusitis is more straightforward to develop in children in two ways. The
rst reason is that the sinuses are small in volume, and their physiological defense
mechanisms are not as fully developed as in adults due to their incomplete
development.
Second, they experience frequent viral infections during childhood. The most
critical risk factor for frequent infections is that the child goes to nursery or school.
In the clinic of acute bacterial rhinosinusitis in children, nasal congestion, runny
nose, posterior nasopharyngeal drainage, fever, cough, pain, especially on the side
of the face where sinusitis occurs, edema, and halitosis (bad breath) are observed.
ENT examination, especially nasal anterior rhinoscopy and endoscopic examination, is vital for diagnosis. Nasal endoscopic examination is essential for evaluating
many different structures, such as anatomical structures (septum deviation, turbinate hypertrophy), adenoid hypertrophy, and foreign bodies. Additionally, nasal
endoscopy provides essential clues to show allergic rhinitis, nasal polyps, mucosal
edema, scarring, discharge, and crusting within the nose [33].
In children under age 6, clinical ndings compatible with rhinosinusitis, history,
and ENT examination are sufcient for diagnosis, and radiological evaluation is
unnecessary. Radiological evaluation is useless, especially in children younger than
1year old. It cannot be evaluated because it is not radiologically developed except
for the ethmoidal and maxillary sinuses. Ethmoid and maxillary sinuses are present

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at birth. The remaining sinuses begin to ventilate after age four and reach adult size
by age twelve.
In summary, maxillary and ethmoid sinusitis may occur in the neonatal and
infant period. The most frequently requested plain radiograph is the Waters radiography. However, its contribution is limited; no radiological evaluation alone
can diagnose rhinosinusitis. Clinical ndings are always more valuable. The
diagnosis of uncomplicated rhinosinusitis can be made based on history and
clinical ndings. In radiological evaluation, CT and MRI are useful in evaluating cases with chronic or recurrent sinusitis that are clinically considered complications [31–34].
Rhinosinusitis treatment in children is applied as antimicrobial treatment and
supportive treatment for the causative agent. In treating rhinosinusitis, antimicrobial
therapy shortens the duration of clinical recovery, especially for the causative agent,
and prevents possible complications. In case of antibiotic resistance during treatment, it may be necessary to reconsider the following criteria in the history. Suppose
the child goes to kindergarten or nursery, has received antibiotic treatment in the last
3months, is less than 2years old, has recently been hospitalized, and has received
antibiotic treatment. In that case, there is a high probability of being infected with a
Streptococcus pneumoniae strain that has reduced sensitivity to penicillin, especially amoxicillin. If these risks do not exist, amoxicillin is started orally at 45mg/
kg/day. However, if these risks exist, the amoxicillin dose is increased to 80–90mg/
kg/day [35].
As a supportive treatment, the main goal is to reduce edema in the nasal mucosa,
open the Ostia, facilitate sinus drainage, and reduce fever. Decongestants, nasal
steroids, nasal lavage, and mucolytic drugs are used for these purposes. However,
no signicant advantage of these drugs over placebo has been demonstrated. It
should not be forgotten that long-term use of decongestant medications can cause
rhinitis medicomentosa. The effectiveness of topical steroids in the treatment has
been investigated, and it is stated that they may be benecial only for rhinosinusitis
caused by allergy. Nasal lavage is helpful in moistening and mechanical cleaning of
the mucosa. However, it is challenging to apply to children under two. Pressure
nasal lavage should be used cautiously, especially in children under six. Care should
be taken in case of acute otitis media because the nasal ora passes to the middle ear
via the eustachian tube [33–37].
22.6 Adenoid Hypertrophy
Adenoid hypertrophy is essential for nasal congestion and rhinosinusitis in children,
especially between the ages of 2 and 6. Adenoid is anatomically located in the posterior nasopharynx and is an important member of the Waldeyer Ring. It is essential
in developing and maturing non-immune B-lymphocytes, especially in the neonatal
period, against environmental antigens during infection processes from the oral cavity and pharynx. Adenoid tissue grows in volume until age 6–7 and shrinks and
atrophy during early puberty [38].

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The presence of nasal congestion, purulent nasal discharge, postnasal discharge,
fever, and cough suggests adenoid hypertrophy and infection. Rhinosinusitis and
otitis media may often accompany the condition. Nasal congestion impairs orofacial
facial development in the child, causing the typical appearance referred to as an
adenoid face. This condition is a result of prolonged nasal congestion. A characteristic adenoid facial appearance with an open mouth appearance, short upper lip,
widened nasal dorsum, dome palate, and retrognathic mandible formation can be
mentioned in a child who breathes through the mouth instead of the nose [39, 40].
Adenoid hypertrophy in children causes eustachian tubal dysfunction and ear
pathologies (serous and recurrent otitis media). In advanced cases, proportional to
the degree of nasal obstruction, sleep-disordered breathing and regression in attention and learning skills may be added to the clinical picture [41].
The diagnosis is easily made by history and endoscopic examination (Fig.22.1).
Direct radiography has no place in diagnosis; it causes the child to receive unnecessary radiation. Instead, adenoid hypertrophy can be quickly evaluated with nasal
and nasopharyngeal endoscopy. Treatment is surgical removal of adenoid tissue
[39–41].
22.7 Inflammatory Causes
22.7.1 Allergic Rhinitis
It is one of the most common causes of nasal congestion in children, as a type 1
hypersensitivity reaction mediated by immunoglobulin E due to exposure of the
nasal mucosa to the allergen, seen in 6–18% of children [42].
In its physiopathology, it is a picture of inammatory origin, clinically characterized by watery eyes, itching, nasal discharge (serous), sneezing, and nasal congestion, as a result of the nasal mucosa, which has been previously sensitized, that is,
encountered with the antigen, facing the same antigen. If the child is not treated
early, maxillofacial anomalies may develop due to open-mouth breathing and nasal
congestion. While questioning the history, the time when the symptoms appeared,
whether they continue seasonally or throughout the year, accompanying cough,
sleeping with the mouth open, snoring, sleep quality, growth and development, and
nutritional status should be learned. In addition to the ndings, whether there are
frequent complaints of acute or serous otitis media or rhinosinusitis should be investigated. Pets and conditions that may cause allergies should be noted [43].
The most common symptom of allergic rhinitis in children is the allergic salute
gesture. In this movement, the nose tip is involuntarily pressed upward with the
palm to relieve nasal itching and ease nasal breathing. In addition, allergic shiners,
which are characterized by the appearance of dark circles on the lower eyelid skin
that turn into permanent pigmentation over time, and small half-moon-shaped lines
(Dennie-Morgan lines) that appear on the lower eyelid are typical for allergic rhinitis. Endoscopic nasal examination is critical in the diagnosis of the disease. In
endoscopy, mucosa and turbinates are pale, serous discharge is present, and inferior

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turbinate hypertrophy may also accompany. Additionally, adenoid hypertrophy,
antrochoanal polyp, nasal polyp, acute otitis media, serous otitis media, and rhinosinusitis ndings may also occur [44].
Clinical and anamnesis information is usually sufcient for the diagnosis of
allergic rhinitis. Diagnosing and conrming allergy in children, considered in the
history and examination, is possible with allergic skin tests. The sensitivity reaction
to a specic antigen applied to the skin is measured. In this way, it is determined
whether immunotherapy can be used or not [45].
The main goal in treating allergic rhinitis is to protect and stay away from allergens. If this is not possible, medical treatment, immunotherapy, and surgical treatment can be applied. Surgical treatment aims to include anatomical pathologies
such as turbinate hypertrophy, where medical therapy fails, and septum deviation,
where it is ineffective [42–45].
M. Gümüşsoy and İ. Çukurova
22.7.2 Nonallergic Rhinitis
This group includes all rhinitis in the absence of non-IgE-related immunological
mechanisms. It is less common in children and occurs in 70% of adult patients after
age twenty [45].
22.7.3 Eosinophilic Nonallergic Rhinitis (NARES)
Nasal congestion and runny nose are the most common symptoms. Although
the disease occurs throughout the year, it is more common in autumn and winter, when the temperature difference between home and outdoor environments
is highest. Sneezing, watery serous runny nose, itching, and symptoms such as
nasal congestion are observed. It is a condition in which eosinophils are more
than 20% in the smear. Additionally, this disease is characterized by the negativity of the prick skin test and the absence of serum IgE antibodies. It may
occur alone or in association with nasal polyps, non-IgE-dependent asthma, or
aspirin sensitivity. Corticosteroids are the most critical drug group in treatment [46].
22.7.4 Nasal Polyp
It is a chronic inammatory disease whose etiology is not fully explained and is less
common in children than antrochoanal polyps. It is often observed on both sides of
the nose. Complaints of nasal congestion, runny nose, rhinosinusitis, or allergic
rhinitis may accompany patients. Nasal polyps are more common in allergies,
asthma, aspirin/nonsteroidal anti-inammatory sensitivity, and cystic brosis (CF)
patients. Therefore, nasal polyps in children are a clinical warning sign to investigate cystic brosis [47].

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Nasal polyps are seen as pale, transparent, and smooth-surfaced mass lesions
during endoscopic nasal examination. Approximately one-third have a unilateral
antrochoanal polyp, another third have polyps secondary to the infective process
associated with mucus retention that occurs in cystic brosis (CF), and the remainder are associated with a range of inammatory conditions, although most remain
idiopathic. Nasal examination and CT are sufcient for diagnosis and treatment
planning. A prick skin test can be performed if there is a history of allergy. Although
its treatment is planned medically and surgically, it is sometimes tricky.
Corticosteroids are the most critical agents in medical treatment. Endoscopic sinus
surgery is preferred in surgical treatment. Management of pediatric polyposis is
often disappointing because the recurrence rate is high, except in those with antrochoanal polyps. Therefore, some authors recommend treatment with topical steroids as a routine approach in treating nasal polyps and resort to surgery only in case
of failure [48, 49] (Fig.22.3).
22.7.5 Antrochoanal Polyp
They are inammatory polyps that originate from the mucosa of the maxillary sinus
and extend from the maxillary ostium to the nasal cavity and often to the nasopharynx. It has two components: cystic and solid. Antrochoanal polyps are rare in children but occur at a higher rate than in the adult population. While antrochoanal
polyps constitute 4–6% of all nasal polyps, they constitute 33% of the pediatric
population. Although it is thought to develop as a complication of chronic inammatory sinus disease in its physiopathology, studies in the pediatric population have
reported that it creates an allergic basis in approximately half of the patients. Unlike
adults, allergic polyps are more common than inammatory polyps among children.
Fig. 22.3 Visualization of hypertrophic adenoid tissue from the nasal cavity with exible
endoscopy

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Fig. 22.4 Antrochoanal polyp originating from the left maxillary sinus extends to the middle
meatus and then to the nasopharynx on paranasal axial CT
M. Gümüşsoy and İ. Çukurova
Although they often originate from the maxillary sinus, they may also arise from the
septum, sphenoid sinus, ethmoid sinus, hard and soft palate, and turbinates.
Although they are primarily unilateral, bilateral patients have been reported. They
are frequently observed in children and young adults. The main symptoms are unilateral nasal congestion, runny nose, and postnasal drip. Computed tomography is
the radiological evaluation of choice for evaluating antrochoanal polyps. Classically,
they are considered as an opaque hypodense mass originating from the maxillary
sinus and extending from the middle meatus to the nasal cavity (Fig.22.4). The
treatment is surgery, and endoscopic sinus surgery is preferred. To reduce recurrence rates, it is necessary to remove altogether the mucosa from which the polyp
originates in the maxillary sinus [50, 51] (Fig.22.4).
22.7.6 Inferior Turbinate Hypertrophy
Turbinates are functional anatomical structures important in humidifying and warming the inhaled air. The autonomic nervous system changes the size of the erectile
turbinates with sympathetic and parasympathetic stimulation according to physiological needs. Inferior turbinate hypertrophy often occurs due to infection or inammation caused by allergic rhinitis, vasomotor rhinitis, or infectious rhinitis. In
physiopathology, acute or chronic mucosal-submucosal hypertrophy occurs due to
congestion. This situation causes nasal congestion and negatively affects the child’s
quality of life. Inferior turbinate hypertrophy causes runny nose, nasal congestion,
mouth breathing, obstructive sleep apnea, and craniofacial development disorder in
children [52, 53].
The endoscopic nasal examination is sufcient to evaluate the hypertrophic inferior turbinates and the appearance of the mucosa (pale or hyperemic). As an imaging method, paranasal CT is preferred when medical treatment is inadequate, and
surgery is considered [54].

22 Nasal Congestion inChildren
In inferior turbinate hypertrophy, nasal steroids, antihistamines, and decongestants are used in medical treatment. Long-term drug use in children is challenging
and reduces the effectiveness of treatment due to compliance problems. There is
no denitive consensus for inferior turbinate surgery in children. Surgery aims to
preserve the bone and erectile submucosa of the turbinate while preserving the
inferior turbinate mucosa and to maximize nasal airow by reducing nasal tissue [55].
Various surgical options have been recently described for treating medically
resistant inferior turbinate hypertrophy in children, including laser ablation, submucosal microdebrider, and radiofrequency methods. Pediatric otolaryngologists have
turned to mucosal protective procedures such as submucosal microdebrider turbinectomy and RF instead of turbinectomy, the preferred surgical method [52–55].
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22.8 Neoplasia
22.8.1 Benign Tumors (Juvenile Nasopharyngeal Angiofibroma)
It manifests only in males and typically during adolescence, with recurrent nosebleeds and unilateral nasal obstruction. Although this is considered a benign tumor,
it can be locally invasive. In nasal endoscopy, it is observed as a vascular mass in the
posterior lateral part of the middle turbinate at the level of the sphenopalatine foramen. On endoscopy, it is seen as a light pinkish mass with a supercial vascular
structure. Endoscopic nasal examination and radiological evaluation are essential in
diagnosis. In cases of clinical suspicion of angiobroma, biopsy is contraindicated
due to the risk of bleeding. It is recommended that CT and MRI be evaluated
together in imaging. CT is signicant in assessing bone structures. A lobulated,
unencapsulated soft tissue mass is typically centered over the sphenopalatine foramen. The posterior wall of the maxillary sinus may bend anteriorly (Holman-Miller
sign). MRI is critical in evaluating the orbital and intracranial spread of the lesion.
Treatment consists of primary embolization followed by surgical resection within
48h, usually via an endonasal approach. Recent advances in radiological imaging,
embolization, and endonasal surgical techniques and instruments have greatly
improved the prognosis [56, 57].
22.8.2 Malignant Tumors
Although malignant nasal masses are rare, they are most commonly seen with nasal
congestion and other symptoms such as a change in smell, nosebleeds, nasal/facial
pain, nasal asymmetry, swelling, or numbness. Rhabdomyosarcoma, esthesioneuroblastoma, lymphoma, and squamous cell carcinoma can rarely be seen among other
malignant nasal masses with minor salivary glands (adenocarcinoma or adenoid
cystic adenomas), which can lead to the development of salivary gland tumors in the
nasal cavity mucosa [58].
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