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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)

29 Cervical Lymphadenopathy inChildren
the possibility of abscess formation. Ultrasonography is useful for detecting abscess
formation. If the lymphadenitis is highly suspicious for abscess formation and is
present in an anatomical area requiring more detailed information, a computed
tomographic (CT) scan or magnetic resonance image (MRI) will give more detailed
information.
An abscess smaller than 1cm may not require surgical drainage. Clinicians may
consider a trial of 24–48h of intravenous antibiotics before incision and drainage
for abscesses less than 1.5–2cm if the child is clinically stable. If the location of the
abscess is anatomically tricky, or if the abscess is small but persistent, image-guided
needle aspiration with or without drain placement may be appropriate. Cultures
should be taken to help direct the antibiotic regimen.
387
29.5 Infectious Mononucleosis DuetoEBV
Infectious mononucleosis due to EBV infection is frequent in the pediatric age
group. Main symptoms are fever (98.3%), tonsillitis (100%), tonsillar white exudate
(83.6%), cervical lymphadenopathy (98.3%), hepatomegaly (37.7%), splenomegaly
(42.6%), eyelid edema (41.0%), and nasal obstruction (49.2%) [8]. Among the laboratory ndings, leukocytosis with lymphocytosis and monocytosis are common as
well as elevations in the levels of alanine aminotransferase, aspartate aminotransferase, and lactic dehydrogenase in the blood.
29.6 Granulomatous Lymphadenitis
The granulomatous lymphadenitis is a group of disorders that are rarely seen in
children. Among them, the caseating granulomatous lymphadenitis is the result of
mycobacterial infections [1]. The noncaseating granulomatous lesions are seen in
cat-scratch disease, toxoplasmosis, toxocariasis, brucellosis, Kikuchi-Fujimoto disease, Kimura disease, and sarcoidosis.
29.6.1 Mycobacterial Infection
Mycobacterial infections, mainly due to Mycobacterium tuberculosis and
Mycobacterium avium are the major causes of cervical granulomatous lymphadenopathy in children [9, 10]. These lymph nodes grow chronically with a purplish
overlying skin color, and rm to palpation. Abscess and stula formations are
expected in clinical courses.
29.6.2 BCG Vaccine
BCG vaccine can cause lymphadenitis in 4–5 cases of 100,000 vaccine administrations [11]. The location is usually the axillary area, but supraclavicular and cervical
lymph nodes can also be affected.

388
M. Kantar and E. Ataseven
29.6.3 Cat-Scratch Disease
Cat-scratch disease (CSD) is characterized by regional lymphadenitis with fever
caused by Bartonella henselae, a gram-negative bacillus. Cat-scratch disease follows the inoculation of Bartonella henselae through broken skin or mucous membranes and is usually transmitted by the scratch or bite of a cat [12]. A skin papule
typically develops at the site of inoculation, followed by regional adenopathy 5days
to 2months later. The cervical, axillary, or supraclavicular lymphadenopathy locations are the most frequently affected. The involved lymph nodes are initially
mobile, elastic, and tender, with a typical size from 1 to 5cm. In about 10–15% of
the cases, the adenopathy evolves in a suppurative phase, lasting for months [13]. In
most cases, the diagnosis is clinical and supported by a history of exposure to a cat.
Serological tests can be used to conrm the diagnosis.
Cat-scratch disease is usually self-limited. In most cases, nodal enlargement
resolves spontaneously after 1–3months. In some patients, the lymph nodes may be
painful and have a protracted course with the formation of abscesses and stulas.
Several studies have highlighted the need for antibiotic therapy or multiple drainages in these cases [14]. The rst line of antibiotic treatment is azithromycin; however, clarithromycin, ciprooxacin, or trimethoprim/sulfamethoxazole may be
considered.
29.6.4 Sarcoidosis
Among all the causes of lymphadenopathy, sarcoidosis is reported in 0.37% as an
underlying disease [1]. In pediatric sarcoidosis, there are two clinical forms reported.
Children younger than 5years of age have a triad of rash, uveitis, and arthritis. But
older children have a multisystem disease that involves LAP, pulmonary involvement with fever, fatigue, and weight loss. In a pediatric series of sarcoidosis with 48
cases, peripheral lymphadenopathy is reported at 40% and hilar LAP at 71% [15].
In another large series of pediatric sarcoidosis, the percentage of peripheral LAP is
30%, hilar adenopathy 40%, and hepatosplenomegaly 30% [16]. According to the
radiological ndings of sarcoidosis described by Hofmann etal., chest radiographs
were found normal (stage 0) in 39%; 34% had isolated bilateral hilar lymphadenopathy (stage I), 10% had bilateral hilar adenopathy with pulmonary inltrates
(stage II), and 15% had parenchymal inltrates without hilar adenopathy (stage
III) [15].
29.6.5 Kikuchi-Fujimoto Disease
Children with Kikuchi-Fujimoto disease may have enlarged cervical lymph nodes,
fever, symptoms of upper respiratory tract infection, and less frequently chills, night
sweats, arthralgia, rash, and weight loss. Lymph nodes are usually painful and tender; splenomegaly or hepatomegaly have sometimes been described [17].

29 Cervical Lymphadenopathy inChildren
389
29.7 Malignancies
Neck region may be the primary site of lymphomas, either Hodgkin’s (HL) or nonHodgkin’s lymphoma (NHL), and granulocytic sarcoma, or secondary metastasis
from nasopharyngeal and oropharyngeal tumors such as carcinoma, NHLs, neuroblastoma, rhabdomyosarcoma or thyroid tumors. Clinically, 70% of the HL begins
in the cervical lymph nodes in children. Mediastinal involvement accompanies cervical lymph node enlargement in many cases. In NHLs, head and neck tissues may
be the primary sites such as cervical lymph nodes, tonsils, nasopharyngeal area,
nasal cavity, sinuses, and scalp. In acute lymphoblastic leukemia, generalized LAP
is more frequent than it is in acute myeloid leukemia. Granulocytic sarcoma (chloroma) cases may primarily begin in the cervical lymph nodes without accompanying acute myeloid leukemia. Cervical lymph nodes may also be involved in
histiocytosis, thyroid carcinoma, nasopharyngeal carcinoma, rhabdomyosarcoma,
neuroblastoma, malignant rhabdoid tumors, osteogenic sarcoma, and Ewing family
tumors of the region. In malignancies, lymph nodes are enlarged, xed, rmed, and
conglomerated without pain in palpation.
29.8 Diagnosis
All children with cervical lymphadenopathy should be evaluated clinically rst.
History, patient symptoms, and ndings of physical examination are necessary to
make the diagnosis in many cases. Laboratory (peripheral blood smear, cell count,
biochemistry, serological tests) and radiological tests (especially ultrasonography)
are helpful for diagnosis and differential diagnosis. In case of pathological lymphadenopathy with systemic B symptoms (fever >1week, night sweats, weight loss
>10% of body weight), palpable supraclavicular nodes, generalized lymphadenopathy, xed, painless, matted, nontender lymph nodes, abnormal chest X-ray with
mediastinal mass or adenopathy, and dyspnea, lymph node biopsy is taken to make
a denitive diagnosis [16]. However, sometimes a biopsy is unnecessary. Malignancy
is not found frequent among the excised lymph nodes. In a surgical analysis, biopsy
yielded 48% of reactive lymph nodes, 25% tuberculosis, 11.6% neoplasm, 11.5%
granulomatous lesions, 2.5% miscellaneous infections, and 1.5% normal [18].
References
1. Deosthali A, Donches K, Del Vecchio M, etal. Etiologies of pediatric cervical lymphadenopathy: a systematic review of 2687 subjects. Glob Pediatr Health. 2019;6:1–7.
2. Bshesh K, Khan W, Vattoth AL, etal. Lymphadenopathy post-COVID-19 vaccination with
increased FDG uptake may be falsely attributed to oncological disorders: a systematic review.
J Med Virol. 2022;94(5):1833–45.
3. Belsky JA, Carroll WR, Xu G. Side effects with a focus on lymphadenopathy following
COVID-19 vaccination in pediatric and AYA oncology patients. J Pediatr Hematol Oncol.
2023;45(2):88–90. https://doi.org/10.1097/MPH.0000000000002621.

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4. Howard-Jones AR, Al Abdali K, Britton PN.Acute bacterial lymphadenitis in children: a retrospective, cross-sectional study. Eur J Pediatr. 2023;82(5):2325–33. https://doi.org/10.1007/
s00431- 023- 04861- 0.
5. Kwon M, Seo JH, Cho KJ, etal. Suggested protocol for managing acute suppurative cervical lymphadenitis in children to reduce unnecessary surgical interventions. Ann Otol Rhinol
Laryngal. 2016;125(12):953–8. https://doi.org/10.1177/0003489416665194.
6. Gosche JR, Vick L. Acute, subacute, and chronic cervical lymphadenitis in children. Semin
Pediatr Surg. 2006;15(2):99–106. https://doi.org/10.1053/j.sempedsurg.2006.02.007.
7. Weinstock MS, Pattel NA, Smith NP. Pediatric cervical lymphadenopathy. Pediatr Rev.
2018;39(9):433–43. https://doi.org/10.1542/pir.2017- 0249.
8. Wu Y, Ma S, Zhang L, et al. Clinical manifestations and laboratory results of 61 children with infectious mononucleosis. J Int Med Res. 2020;48(10):1–8. https://doi.
org/10.1177/0300060520924550.
9. Haverkamp MH, Arend SM, Lindeboom JA, et al. Nontuberculous mycobacterial infection in children: a 2-year prospective surveillance study in The Netherlands. Clin Infect Dis.
2004;39(4):450–6. https://doi.org/10.1086/422319.
10. Durmuş SY, Tanır G, Kaman A. Tuberculous lymphadenitis in children. J Pediatr Inf.
2021;15(3):e139–45. https://doi.org/10.5578/ced.20219716.
11. Szczuka I.Adverse events following immunization with BCG vaccine in Poland 1994–2000.
Przegl Epidemiol. 2002;56:205–16.
12. Pecora F, Abate L, Scavone S, etal. Management of infectious lymphadenitis in children.
Children. 2021;8(10):860. https://doi.org/10.3390/children8100860.
13. Ridder-Schröter R, Marx A, Beer M, etal. Abscess-forming lymphadenopathy and osteomyelitis in children with Bartonella henselae infection. J Med Microbial. 2008;57(4):519–24.
14. Stevens DL, Bisno AL, Chambers HL, etal. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005;41:1373–406.
15. Hoffmann AL, Milman N, Byg KE. Childhood sarcoidosis in Denmark 1979-1994: incidence, clinical features and laboratory results at presentation in 48 children. Acta Pediatr.
2004;93(1):30–6.
16. Gedalia A, Khan TA, Avinash KS, etal. Childhood sarcoidosis: Louisiana experience. Clin
Rheumatol. 2016;35:1879–84.
17. Lelii M, Senatore L, Amodeo I, et al. Kikuchi—Fujimoto disease in children: two case
reports and a review of the literature. Ital J Pediatr. 2018;44:83. https://doi.org/10.1186/
s13052- 018- 0522- 9.
18. Moore SW, Schneider JW, Schaaf HS. Diagnostic aspects of cervical lymphadenopathy
in children in the developing world: a study of 1,877 surgical specimens. Pediatr Surg Int.
2003;19:240–4.
M. Kantar and E. Ataseven

Chronic Cough inChildren: Upper
Respiratory Tract Related Etiologies
TugbaRamasli Gursoy andLauraGochicoa-Rangel
30.1 Introduction
Cough is a forced expiratory mechanism against the glottis and protective reex
with both voluntary and involuntary control elements, necessary for the clearance of
inhaled particles and mucus from airways [1]. Cough is the most common complaint in respiratory system diseases and is an irritating complaint when it is intense
and prolonged [2, 3]. The presence of a persistent cough in pediatric patients has the
potential to negatively impact their overall well-being, resulting in diminished quality of life, increased frequency of medical consultations, and perhaps inappropriate
utilization of medications. In addition, cough can be a sign of a serious underlying
disease [4]. A cough that persists for more than 4weeks in children aged 14years
and younger is dened as a chronic cough [3]. In both adults and children aged
14years and above, the duration of a cough over 8weeks is classied as a chronic
cough [4]. The causes of chronic cough in children are given in Table30.1. The
most common causes of upper respiratory tract related etiologies of chronic cough
in children are discussed in this section.
30
T. Ramasli Gursoy (*)
Department of Pediatric Pulmonology, Van Training and Research Hospital, Health Sciences
University, Van, Turkey
L. Gochicoa-Rangel
Department of Respiratory Physiology, National Institute of Respiratory Diseases “Ismael
Cosío Villegas”, Mexico City, Mexico
© 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_30
391

392
Table 30.1 Causes of chronic cough in children
Pulmonary causes
Asthma Congenital lung disease
Aspiration due to swallowing dysfunction,
GERD, or TEF
Cystic brosis Vascular anomalies
Immunodeciency (primary or secondary) Environmental pollutants (tobacco smoke,
Primary ciliary dyskinesia Extrapulmonary causes
Post infection Cardiac diseases
Protracted bacterial bronchitis Upper respiratory tract diseases
Bronchiectasis Ear disease
Retained inhaled foreign body Psychogenic cough
Interstitial lung disease Drugs (ACE inhibitors)
GERD gastroesophageal reux disease, TEF tracheoesophageal stula, ACE angiotensin-converting enzyme
T. Ramasli Gursoy and L. Gochicoa-Rangel
Tracheobronchomalacia
vaping, air pollution)
30.2 Upper Airway Cough Syndrome
The pathogenesis of Upper Airway Cough Syndrome (UACS) is hypothesized to
result from postnasal drip, wherein nasal secretions run into the nasopharynx. This
condition can be associated with allergic, chronic nonallergic, or vasomotor rhinitis
or rhinosinusitis. The initiation of the cough reex is largely triggered by the activation of cough receptors situated in the mucous membranes of the larynx. This
response is particularly prominent when there is a buildup of secretions in the upper
respiratory tract [5]. The exact mechanism by which UACS contributes to chronic
cough remains uncertain [6]. However, numerous studies have consistently demonstrated that UACS, particularly when accompanied by postnasal drip, is a common
underlying factor in cases of subacute and chronic cough. The reported prevalence
of UACS-associated cough varies considerably, ranging from 9% to 82% across
different studies [6, 7]. The signicant variation in prevalence can be primarily
attributed to the slow integration of the term into clinical practice and disparities in
treatment approaches across different countries. There is a prevailing agreement
among experts that UACS is commonly acknowledged as either the major or secondary most prevalent cause of chronic cough in non-smokers, on a global level.
UACS is frequently associated with comorbidities that can lead to the manifestation
of a chronic cough [5–7]. According to Irwin etal., cough is associated with three
or more etiologies (such as gastroesophageal reux disease (GERD), drugs, asthma)
in up to 42% of patients [6]. The term “postnasal drip syndrome” was commonly
employed until 2006, at which point the American College of Chest Physicians
(ACCP) recommended substituting it with the acronym UACS [8]. While it was
previously believed that purulent nasal secretions were solely responsible for causing persistent cough, numerous studies have demonstrated that there are various
underlying causes, such as inammation and irritation of upper airway tissues, that
can lead to coughing, including cases involving postnasal drip. The divergence of

30 Chronic Cough inChildren: Upper Respiratory Tract Related Etiologies
393
opinions within the academic community led the ACCP to revise the nomenclature,
resulting in the adoption of the term UACS. There remains ongoing discourse
regarding the appropriate terminology to delineate the experience of postnasal drip
in relation to coughing [5, 8]. The reason why the European Respiratory Society
(ERS) does not dene UACS is that postnasal drip cannot fully explain the cough
and some patients with postnasal drip do not cough. UACS and postnasal drip syndrome are classied as “rhinitis/rhinosinusitis” or upper respiratory tract diseases
causing cough according to ERS [3, 5].
Initially, it is imperative to obtain a comprehensive anamnesis regarding the initiation, duration, and nature (intermittent or persistent) of the disease in children
being evaluated for UACS.Additionally, it is important to inquire about symptoms
such as rhinorrhea, nasal congestion, any history of allergies, sensitivity to seasonal
or daily variations, as well as the severity of associated cough and headache.
Characteristic features of the examination for UACS include nasal discharge and
congestion, postnasal drip that can lead to symptoms of throat discharge, wheezing,
and snoring, as well as a cobblestone appearance resulting from lymphoid hypertrophy in the oropharynx [5, 8].
The prioritization of therapy for UACS should be focused on addressing the
underlying medical conditions that are commonly linked with it, such as GERD,
uncontrolled asthma, or bronchiectasis. Nevertheless, when a specic reason cannot
be determined, it is advisable to commence empirical treatment [9]. The treatments
of UACS and most common underlying medical conditions are given in Table30.2.
When symptoms of rhinitis or chronic rhinosinusitis (CRS) persist despite initial
empirical therapy, secondary UACS may necessitate further therapeutic approaches.
Decongestants, which are believed to restrict the secretion of inammatory cytokines, are advised for use. Patients diagnosed with allergic rhinitis (AR) are advised
to utilize next-generation antihistamines; however, those with non-allergic rhinitis
(NAR) or CRS should be administered rst-generation antihistamines for treatment.
There is a suggestion that the anticholinergic action exhibited by rst generation
antihistamines has a notable impact on patients with NAR and CRS in comparison
to individuals with AR.In cases when antihistamines and decongestants are ineffective in managing UACS related to non-allergic rhinitis, it is advisable to explore
other therapy modalities. The treatment for vasomotor rhinitis accompanied with
cough typically involves the administration of antihistamines and decongestants, as
Table 30.2 The treatments of upper airway cough syndrome and most common underlying medical conditions
Allergic rhinitis Next-generation antihistamines, decongestant, nasal steroid
Non-allergic rhinitis First generation antihistamines, decongestant, ipratropium bromide
nasal spray (alternative treatment)
Chronic rhinosinusitis Nasal saline, nasal corticosteroids, antibiotics, endoscopic sinus
surgery in selected cases
Post viral cough First generation antihistamines, decongestants, montelukast
Gastroesophageal reux
disease
Dietary recommendations, proton pump inhibitors, antacids,
histamine receptor antagonists, surgery in selected cases

394
T. Ramasli Gursoy and L. Gochicoa-Rangel
these medications include anticholinergic properties, particularly in the case of rstgeneration antihistamines. The utilization of ipratropium bromide nasal spray may
be considered in situations when contraindications are present or when alternative
treatment options are deemed necessary. First generation antihistamines and decongestants may also provide relief for post viral cough resulting from a viral upper
respiratory tract illness. Additionally, studies have demonstrated the potential benets of Montelukast in the treatment of post viral cough. The management of symptoms associated with chronic rhinosinusitis often involves the use of nasal saline,
topical nasal corticosteroids, and antibiotics. In certain instances where conventional medical interventions are ineffective, the necessity for endoscopic sinus surgery may arise [10]. Insufcient data exist to establish a denitive dosage or duration
for the administration of non-sedating or sedative H1-histamine receptor antagonist
treatment. Two distinct studies have examined the improvement in cough score at
different time intervals, indicating that there is currently no universally accepted
standard period for medical therapy. In a study involving a cohort of 20 patients
presenting with AR, characterized by cough and rhinoconjunctivitis, the patients
underwent a 4-week treatment regimen involving the administration of loratadine,
with the evaluation of cough frequency and severity as the primary outcome measures. At the conclusion of the trial period, a notable enhancement in both measures
was seen in comparison to the placebo group [11]. A cohort of individuals presenting with a persistent cough and concurrent eosinophilic bronchitis, commonly
referred to as atopic cough, was studied. A noteworthy reduction in cough symptoms was observed after 1week of treatment with non-sedating antihistamines [12].
It is postulated that the development of UACS may be attributed to many variables,
including postnasal drip, persistent inammation of the airway, and heightened sensitivity of the sensory nerves. Further research is required to distinguish the effects
of distinct factors within, including thermal, mechanical, or chemical stimuli, on the
development of chronic cough [5, 13]. The use of targeted therapy directed at particular receptors, such as transient receptor potential vanilloid 1 (TRPV1), has the
potential to enhance symptom relief in individuals who exhibit resistance to conventional antihistamine and decongestant treatments [13].
30.3 Chronic Rhinosinusitis
Chronic rhinosinusitis is characterized by the presence of two or more symptoms,
including purulent rhinorrhea, nasal obstruction, cough or face pressure/pain, persisting for a minimum duration of 3months. Additionally, the condition is diagnosed based on the observation of mucosal edema, purulent discharge, or nasal
polyps by endoscopic examination, and/or the identication of ostiomeatal complex
or sinus edema using computer tomography (CT) scan imaging [14, 15]. The etiology of CRS in pediatric patients remains incompletely understood. Acute rhinosinusitis is predominantly caused by infection, but CRS encompasses a range of
disorders that can be inuenced by concomitant medical illnesses, infection, and
environmental factors.

30 Chronic Cough inChildren: Upper Respiratory Tract Related Etiologies
395
The inuencing factors exhibit variation across different age groups, wherein
adenoiditis emerges as a relatively signicant trigger among younger children,
while allergic rhinitis assumes greater importance among older children [16].
Furthermore, the presence of cystic brosis, primary ciliary dyskinesia, asthma, and
GERD augments the prevalence of CRS.Young children have the potential to experience a range of 3–8 viral upper respiratory tract infections annually. The prevalence of acute bacterial rhinosinusitis as a complication of upper respiratory tract
infections is estimated to range from 0.5% to 5%. Additionally, a subset of these
cases may further proceed into CRS [17]. CRS is inuenced by several environmental variables, such as exposure to smoking, industrial pollutants, and the commencement of formal education. The blockage of the ostiomeatal complex is caused by
multifactorial inammation of the sinus mucosa, whereas the impedance of the
sinus ostia is a result of edema. This edema contributes to the reduction in secretions, a decrease in ciliary function, and the development of persistent bacterial
infection [17, 18].
The utilization of nasal endoscopy allows for the direct observation of the nasal
cavity, making it an optimal method for diagnosing CRS.Doing nasal endoscopy in
children might pose difculties, recommendations suggest that it should be considered as the rst step in diagnosing CRS [14, 15]. According to the recommendations
of guidelines, CT is the preferred rst imaging modality for assessing chronic rhinosinusitis. CT is considered to be an optimal imaging modality due to its ability to
assist with surgical navigation and its high sensitivity in detecting mucosal inammation [15, 19]. Magnetic resonance imaging (MRI) is recommended in cases when
there is suspicion of intracranial or intraorbital problems associated with sinusitis,
since it offers superior vision of soft tissue, as per the established standards.
According to the guidelines, the use of plain radiographs is not suggested due to
their limited connection with CRS [14, 15]. A study which evaluated 6-year results
of maxillary sinus punctures of children with CRS detected that the predominant
bacterial species present were alpha-hemolytic Streptococcus, Haemophilus inuenza, Streptococcus pneumonia, coagulase-negative Staphylococcus,
Staphylococcus aureus, and anaerobic bacteria [20]. Guidelines advocate for the
acquisition of cultures exclusively in cases when patients have exhibited no response
to empiric therapy within a 72-h timeframe, possess notable comorbidities, or suffer
from a serious sickness. Maxillary sinus aspiration is recommended as the rst
choice because of the high probability of microorganism isolation in culture.
However, the invasiveness of the operation and the requirement for anesthesia have
limitations on their applicability within the children [15].
The utilization of saline irrigations has been shown to enhance the elimination of
pathogens in the nasal passage and reduce the presence of inammatory mediators.
The use of saline irrigation is supported by recommendations for the treatment of
CRS due to its relative efcacy and low risk. Saline irrigation can be used as a standalone treatment or as an additional therapy in the management of children (especially under 6years old) with CRS [14, 15].
The usage of nasal steroids is prevalent due to the prevailing notion that steroids
possess the capacity to effectively diminish inammation [21]. Although there is a

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T. Ramasli Gursoy and L. Gochicoa-Rangel
scarcity of research specically targeting the pediatric population, current recommendations advocate for the use of daily topical steroid spray as the primary therapeutic approach for children patients diagnosed with CRS, regardless of the presence
or absence of nasal polyposis [14, 15].
In light of the established advantages associated with nasal saline irrigations,
some researchers postulate that intranasal antibiotic irrigations might potentially
offer the therapeutic effectiveness of antibiotics while circumventing the systemic
adverse effects commonly associated with oral or intravenous administration of
antibiotics [22, 23]. An examination of the existing literature pertaining to adult and
pediatric populations reveals that the utilization of antibiotic nasal irrigations may
be particularly advantageous when employed subsequent to endoscopic sinus surgery in the management of refractory CRS [23]. Nevertheless, due to the scarcity of
information encompassing aspects such as medicine dosage and the potential for
ototoxicity, it is challenging to provide denitive recommendations for pediatric
patients [14].
The existing body of evidence regarding the efcacy of oral antibiotics for CRS
is limited. Given the scarcity of data, the selection of antibiotics is frequently determined by treatment protocols for acute rhinosinusitis. The recommendations advocate amoxicillin for the rst choice. Amoxicillin/clavulanate and cephalosporins
can serve as viable options in cases when there is a perceived risk of encountering
beta-lactamase generating bacteria [15]. The use of clindamycin is warranted in
cases when anaerobic bacteria are detected. According to the guidelines set out by
the Infectious Disease Society of America (IDSA), the preferred choice of medication is amoxicillin/clavulanate rather than amoxicillin due to the prevailing prevalence of beta-lactamase generating bacteria [24]. Consideration may be given to
dual treatment with a third-generation cephalosporin and either clindamycin or
levooxacin in those who have documented allergies to penicillin [25]. The optimal
length of antibiotic therapy remains undetermined due to the little information
available in the existing literature. The guidelines recommend a prolonged course of
treatment [14, 15].
There is a limited body of research examining the advantages of intravenous (IV)
antibiotics in the pediatric chronic CRS population. While there is evidence showing therapeutic advantages, it is challenging to determine the effectiveness of IV
antibiotics in isolation due to the presence of simultaneous surgical procedures and
the absence of a comparison group [26, 27]. Based on the existing constraints in
available data, the recommendations do not endorse the utilization of IV antibiotics
as a standard practice for chronic rhinosinusitis [15]. Nevertheless, it is recommended to administer IV antibiotics in cases when there is suspicion of an intraorbital or intracranial complications arising from rhinosinusitis [14, 15].
Surgery may play a valuable role in cases whose symptoms do not improve adequately with medical treatment. Adenoidectomy is considered the primary surgical
intervention for CRS.In certain instances, it is possible to integrate antral irrigation
of the maxillary sinuses or balloon dilatation as complementary procedures.
Endoscopic sinus surgery is a viable option for children who have had treatment
failure and are aficted with nasal polyps. The presence of foreign bodies is a rare
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