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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)

502
D. D. Keskin et al.
Tonsillectomy has been proposed as a treatment for PANDAS, but the evidence is
limited, and the condition is poorly understood. A recent comprehensive study
showed no recommendations for or against tonsillectomy as a treatment for
PANDAS [30, 31].
38.6.2.5 Periodic Fever, Aphthous Stomatitis, Pharyngitis,
andAdenopathy Syndrome (PFAPA)
PFAPA syndrome (periodic fever, aphthous stomatitis, pharyngitis, and cervical
adenitis) is a recurrent febrile condition primarily affecting children aged 2–6, with
a minor male predisposition. The sudden onset of fever, pharyngitis, tender cervical
lymphadenopathy, or aphthous ulcers characterizes it [13, 32, 33]. Clinical criteria
are used to make a diagnosis. Despite research that shows a hereditary origin, the
genetic origins, and etiology of PFAPA syndrome remain unknown. The cornerstone of treatment is corticosteroids. However, tonsillectomy has also been shown
to induce remission and/or minimize the severity of episodes [32, 33]. Although
there have been isolated reports of sporadic cases in adults, they become less common after age 10 [13].
38.6.2.6 Palmoplantar Pustulosis (PPP)
Palmoplantar pustulosis (PPP) is dened by the recurrence of sterile pustules on the
palms and soles, accompanied by scaly and erythematous skin that might ssure
[34, 35]. PPP patients have an intraepidermal aggregation of neutrophils in the
upper dermis and a mixed perivascular, diffuse inltrate with inammatory cells.
Molecular investigations of PPP reveal that CD4-positive T cells in the tonsils and
peripheral blood detect streptococcal antigens and exhibit increased levels of immunological markers such as beta-1integrin and CCR6in PPP patients. Immune complexes, antikeratin antibodies, and inammatory cytokines (IL-6, IFN-, and TNF-)
were found to be elevated in PPP patients, and changes in these levels following
tonsillectomy were found to be closely connected with the prevalence of skin lesions
[34, 36]. As a result, tonsillectomy appears to decrease the number of autoreactive
cells. Tonsillectomy has effectively improved PPP skin lesions in several studies
[34–36].
38.6.2.7 IgA Nephropathy
The most frequent type of glomerulonephritis in the world is IgA nephropathy.
Progress takes 10–20years and can lead to end-stage renal failure. It is caused by
immunoglobulin A (IgA) protein deposits inside the kidney’s lters (glomeruli) [36,
37]. Upper respiratory infections, such as tonsillitis, frequently manifest with mac-
roscopic hematuria in IgAN patients. There is a link between tonsillar immunity and
pathophysiology, according to clinical data. Tonsillar immunity is a type of mucosal
immunity in which antigen-presenting cells, such as macrophages, form the starting
point for B cells and plasma cells to make antibodies, including IgA, when exposed
to pathogens (e.g., bacteria and their constituents) [38]. Hotta etal. were the rst to
propose that for IgAN patients, a tonsillectomy combined with steroid pulse therapy
will reduce hematuria/proteinuria and increase remission rates [36–39].

38 Meeting Organ forENT andPediatric Pulmonology: Tonsils
503
38.7 Clinical Manifestation
The most prevalent upper respiratory tract disorders are recurrent acute tonsillitis
(RT) and obstructive diseases induced by tonsillar hyperplasia (TH). Although the
severity of frailty varies, many patients suffer from chronic and recurrent medical
conditions that have an impact on their physical and mental health, as well as their
educational performance and healthcare costs [40].
38.7.1 Infection
Acute tonsillitis is a clinical diagnosis. It can be challenging to distinguish between
bacterial and viral causes, but it is necessary to avoid antibiotic overuse. To differentiate between viral and bacterial tonsillitis, data such as the patient’s history, clinical
symptoms, and laboratory data are required [17, 41]. In 70–95% of patients, viral
infection causes acute tonsillitis [41]. Epstein-Barr virus (EBV), rhinovirus, enterovirus, inuenza, and adenovirus are viral infections that frequently cause acute tonsillitis [1, 13]. The most prevalent bacterial etiology is Group A beta-hemolytic
streptococcus (GABHS) [1, 4, 13, 17]. Different pathogen spectrums are detected
depending on age [17, 41]. Streptococcal pharyngitis affects people of all ages,
though it is most frequent in children and teenagers—the infection peaks between the
ages of 3 and 14. Although the disease is more common in the winter and early
spring, it can strike any time of year. The incubation period is between 2 and 5days
[41]. Both aerobic and anaerobic microorganisms can cause bacterial tonsillitis.
Histologically, a necrotic crypt epithelium, leukocytes within the crypts (empyema), and numerous bacterial colonies are all signs of acute bacterial tonsillitis.
Chronic inammation, on the other hand, is dened by larger and activated germinal
centers, as well as a signicant rise in IgG production. Crypts are dilated and frequently include debris, bacteria, and calcication (tonsillithiasis).
38.7.2 Obstruction
In the pediatric population, obstructive sleep apnea is the most common reason for
tonsillectomy [1]. Sleep apnea syndrome (SAS) is a common disorder characterized
by snoring and partial or intermittent obstruction of the upper airway during sleep.
It is estimated to occur in 1–3% of children with a peak age of 2–5years. Common
symptoms include chronic snoring, difculty breathing during sleep, restlessness,
and witnessed apnea. The most prevalent related condition in otherwise healthy
children is adenotonsillar hypertrophy, but cranial-facial deformities, neuromuscular disorders, and obesity are risk factors. Excessive daytime sleepiness, growth
failure, school failure, behavioral issues, cor pulmonale, and even death can be signicant neurobehavioral and cardiorespiratory consequences of severe
OSAS.Diagnosis is based on data from the history, physical exam, and laboratory
studies that conrm the presence and severity of the upper airway obstruction.

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The diagnostic tool of choice has been polysomnography. The severity of the
symptoms, as well as the underlying anatomic and physiologic abnormalities, determine treatment options. Because adenotonsillar hypertrophy is generally present in
children with OSAS, most cases can be treated surgically [1, 42–45].
Snoring should be monitored in all children and adolescents. If polysomnography is unavailable, alternative diagnostic testing or referral to a specialist for a complete assessment should be considered in children/adolescents with snoring and
symptoms/signs of OSAS.Patients with adenotonsillar hypertrophy should receive
adenotonsillectomy as a rst-line treatment. If adenotonsillectomy is not performed
or if OSAS persists after surgery, continuous positive airway pressure is indicated
as a therapy. In patients who are overweight or obese, weight loss is shown in addition to other treatments. Intranasal corticosteroids are an option for children with
minor OSAS who are not candidates for adenotonsillectomy or who have minor
OSAS after surgery [45].
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38.7.3 Neoplasia
Tumors in the oropharynx are most commonly found in the anterior tonsillar pillar
and the tonsil. Lesions on the anterior tonsillar most widely manifest as regions of
leukoplakia or erythroplakia and are often asymptomatic. Exophytic or ulcerative
lesions, predominantly in the tonsillar fossa, are more common. Tonsil lesions are at
a signicant risk of spreading to regional lymph nodes due to lymphatic drainage.
They may also be the unobvious primary site when carcinoma appears in the lymph
nodes with no known place of origin in the pharynx. Lymphoma, Hodgkin’s disease, and tonsil cancer have been the most prevalent lesions [19]. Asymmetric tonsil
enlargement is uncommon and may indicate the necessity for tonsillectomy to conrm the diagnosis [1, 4, 15, 19]. Patients with concomitant symptoms suggestive of
a malignant process, such as adenopathy over 3cm, dysphagia, night sweats, and
fevers, may consider tonsillectomy for tonsil asymmetry [46].
38.8 Diagnosis
38.8.1 Symptoms andSigns
The most prevalent upper respiratory tract disorders are recurrent acute tonsillitis
(RT) and obstructive infections caused by tonsillar hyperplasia (TH) [40]. Children
who have tonsillar diseases present variably. Fever, tonsillar exudates, sore throat,
odynophagia, halitosis, and sensitive anterior cervical chain lymphadenopathy are
common symptoms of infection [1, 13, 25, 47]. Patients may also have dysphagia
secondary to tonsillar swelling. A complete history and physical exam should be
performed rst, and the results can be used to calculate a Centor Score or McIsaac
score (modied Centor score) [17, 48]. According to national and international
guidelines, the McIsaac Score for clinical assessment of the possibility of GABHS

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tonsillitis is still recommended as the preferred clinical screening technique.
According to McIsaac, the modied Centor score is correct for age and may thus be
utilized in both adults and children [17, 48]. Both methods were created to determine the likelihood that streptococcal bacteria and guiding treatment cause pharyngitis. A rapid test or culture should only be considered if the patient scores 3 or
above (Centor or McIsaac). This is not recommended for people with a score of 2 or
less unless they have a persistent illness or a unilateral nding [17, 48].
38.8.2 Physical Examination
There have been no standard recommendations for the clinical assessment of the
tonsils. To prevent gagging, a tongue depressor is softly placed on the anterior twothirds of the tongue in front of the circumvallate papillae [4]. The palatine tonsils
can often be seen in a pediatric child by steadily depressing the posterior oral tongue
using a tongue depressor. Conversely, involution may make the palatine tonsil less
visible in the adult patient [4, 13].
Brodsky and colleagues developed a tonsillar hypertrophy assessment scale [4].
38.8.3 Laboratory
Acute tonsillitis is a clinical diagnosis. Acute tonsillitis will be diagnosed clinically.
To distinguish between viral and bacterial tonsillitis, information such as the
patient’s history, clinical symptoms, and test data are required [17].
GABHS can be detected using throat culture alone or with rapid antigen testing.
It is vital to remember that while rapid antigen testing is specic (88–100%), it is
not sensitive (61–95%); false negatives are possible. Clinicians should consider
acquiring pharyngeal swabs for gonorrhea, chlamydia, and HIV in the appropriate
clinical situation. When the Ebstein-Barr virus is suspected, a mononucleosis spot
test may be considered [25].
The sampling technique is essential for the diagnostic quality of the pharyngeal
swab [49]. The tongue should be forced down, and the swab should be wiped across
both tonsils and the posterior pharyngeal wall in a rotating motion. The intraoral
mucosa and saliva should not be touched [49]. If the rapid test ndings are negative
and there is a strong suspicion of bacterial pharyngeal infection, a microbiological
culture should be used to identify the bacteria [17, 48, 49]. Mostly, microbiological
culture is less expensive than rapid test procedures. However, one disadvantage of
culturing is the time required until the test result is available [17]. Multiplex PCR
can offer molecular genetic conrmation of viral (tonsillitis) infections. Rapid tests
or multiplex PCR for virus identication are nearly always unimportant in the clinical routine for different viruses (e.g., adenoviruses) due to the lack of therapeutic
signicance [25].
The human antibody production against such streptococcal antigens is measured
by antistreptolysin O titer (ASLO titer) values. An acute b-hemolytic streptococcal

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infection could trigger the development of antibodies. The ASLO titer and all other
currently known human antibody titers against b-hemolytic streptococci (e.g., antihyaluronidase, and anti-DNase B) do not provide valid diagnostic criteria for the
diagnostics. An increased antibody response to streptococci (e.g., an increased ASL
titer) does not indicate protection from acute streptococcal infections, nor does it
imply an increased risk of acute streptococcal disease, nor does it indicate an
increased risk of purulent or immunogenic streptococcal secondary illness [17, 50].
38.8.4 Imagining
A lateral neck lm can occasionally help identify the tonsils’ inferior extension;
however, this modality cannot precisely evaluate the tonsils’ relative airway size
[4, 51].
A more thorough examination may be required in complicated infections, such
as those involving patients with unstable vital signs, toxic appearance, difculties
swallowing, inability to accept oral intake, or trismus. CT imaging of the neck with
intravenous contrast can rule out dangerous conditions such as abscess, Lemierre
disease, and epiglottitis [25]. Imaging with head and neck magnetic resonance
imaging (MRI) or computed tomography (CT) is appropriate if abscessing is suspected beyond the peritonsillar region. A CT scan can conrm the diagnosis of
peritonsillar abscess with a sensitivity of up to 100% and a specicity of up to 75%,
and it can also identify additional abscessing and is nearly always available and
cost-effective. Because MRI enables higher soft tissue resolution and visualization
of vessels without exposing patients to radiation, it is highly suggested for children
[17, 51].
38.8.5 Polysomnography
According to the American Academy of Pediatrics, the gold standard tool for diagnosing OSAS in children is overnight, attended, in-laboratory polysomnography
[45, 52]. Video recording, electro-encephalogram; electrooculogram, submental
and leg electromyogram, oronasal airow; abdominal and chest wall movements;
pulse oximetry, and end-tidal or transcutaneous partial pressure of carbon dioxide
(PCO2) should all be recorded during polysomnography (PSG) [1, 4, 45, 51, 52].
Despite its high cost and scheduling challenges, PSG is still the gold standard for
objectively correlating ventilatory problems with sleep-disordered breathing (SBD).
Other evaluation procedures, such as audiotaping, videotaping, and home PSG,
have generated promising ndings but need more research [46]. Abbreviated PSG
(i.e., nocturnal oximetry or nap PSG) has been demonstrated to have a high positive
predictive value and a low negative predictive value, indicating that patients with
negative results may require further testing [46]. When polysomnography is unavailable, nocturnal pulse oximetry is a low-cost, easy-to-use diagnostic method for
detecting OSAS in children with SDB symptoms. Oximetry results can facilitate

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treatment decisions and help predict immediate major respiratory complications
postadenotonsillectomy [52].
PSG avoids unnecessary or ineffective surgery in children with primarily nonobstructive events or central apnea [43]. Before performing tonsillectomy, the clinician should refer children with sleep-disordered breathing (SDB) for PSG if they
exhibit any of the following: obesity, Down syndrome, craniofacial abnormalities,
neuromuscular disorders, sickle cell disease, or mucopolysaccharidoses [43]. When
the need for surgery is uncertain or when there is a discrepancy between tonsillar
size on physical examination and the reported severity of SDB, the doctor should
advocate for PSG before tonsillectomy for SDB in children without any of the
comorbidities described earlier [43]. Provide a baseline PSG for comparison after
surgery. Persistent SDB or OSA, despite surgery, is more common in high-risk
patients than in otherwise healthy children [43].
38.9 Treatments
38.9.1 Medical Treatment
An acute episode of tonsillitis, with or without a documented GABHS infection,
usually has a self-limiting clinical course. Because viral etiologies are so common,
supportive care, such as analgesics and hydration, is the basis of treatment for acute
tonsillitis; patients rarely require hospitalization. NSAIDs, for example, can help
with symptom relief [4].
Antibiotics are frequently used in treating patients at high risk of bacterial pharyngitis based on Centor or McIsaac criteria and antigen testing or throat culture.
Patients with streptococcal pharyngotonsillitis should be treated with an antibiotic
in the proper dosage for the duration required to eradicate GABHS from the pharynx once diagnosed. Inadequate administration of antibiotic therapy may result in
bacterial resistance. Penicillin and amoxicillin are recommended as rst-line antibiotics for those not allergic to them.
In patients allergic to penicillin, treatment for streptococcal pharyngotonsillitis
should include (except for cross-reactions) a rst-generation/second-generation
cephalosporin for 10 days (5–6 days for a third generation) clarithromycin for
10 days, or azithromycin for 5 days, erythromycin for 5 days recommended for
patients with demonstrated IgE-mediated allergy to beta-lactam. In most cases, treatment of the carrier state is not necessary [13, 15, 17, 18, 53]. Most patients, particularly adolescents and adults, are symptom-free within 48h of receiving appropriate
treatment. Except in patients with risk factors (such as a history of ARF), there is no
need to do a pharyngeal swab following antibiotic medication [17]. Antibiotic-treated
patients are no longer contagious after at least 24h. It can reduce purulent complications. Immunogenic secondary diseases such as acute rheumatic fever (ARF) or
acute post-streptococcal glomerulonephritis (APSGN) are potentially avoided [17].
Increased antibacterial resistance, GI distress, diarrhea, Clostridium difcile infection, and cost are among the risks associated with antibiotic use [17].

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38.9.2 Surgery
Recurrent throat infections and obstructive sleep-disordered breathing (SDB), which
can signicantly impact a child’s health and quality of life, are two of the most common reasons for surgery [30]. With the decline of infection as a reason for surgery in
children, the prevalence of obstructive sleep-disordered breathing (oSDB) as a primary reason for surgery has risen, particularly in children under three [30, 54, 55].
Although tonsillectomy has advantages, it can also have complications, such as
throat pain, postoperative nausea and vomiting, dehydration, delayed nutrition,
speech problems (e.g., velopharyngeal incompetence), bleeding, and death [30, 56].
The criteria for surgical management decision-making are outlined by the
American Academy of Otolaryngology, Head, and Neck Surgery and updated 2011
guidelines in 2019 for tonsillectomy [30].
1. Clinicians should recommend watchful waiting for recurrent throat infections if
there have been <7 episodes in the past year, <5 episodes per year in the past
2years, or 3 episodes per year in the past 3years.
2. Clinicians may recommend tonsillectomy for recurrent throat infection with a
frequency of at least 7 episodes in the past year, at least 5 episodes per year for
2years, or at least 3 episodes per year for 3 years with documentation in the
medical record for each episode of sore throat and >1 of the following: temperature >38.3°C (101°F), cervical adenopathy, tonsillar exudate, or positive test for
group A beta-hemolytic streptococcus.
3. Clinicians should evaluate children with recurrent throat infections who do not
fulll the criteria for tonsillectomy, have multiple antibiotic allergies/intolerance, PFAPA, or have a history of more than one peritonsillar abscess.
4. Children with obstructive sleep-disordered breathing (SDB), should be referred
for polysomnography (PSG) if they are <2years old or have any of the following: obesity, Down syndrome, craniofacial abnormalities, neuromuscular problems, sickle cell disease, or mucopolysaccharidoses.
5. Tonsillectomy should be recommended for children who have obstructive sleep
apnea (OSA), as evidenced by overnight polysomnography (PSG).
6. Children undergoing tonsillectomy should not be given or prescribed periopera-
tive antibiotics.
7. For pain relief following tonsillectomy, doctors should prescribe ibuprofen, acet-
aminophen, or both. After tonsillectomy in children under 12, clinicians must
not provide or prescribe codeine or any drug-containing codeine.
8. If children <3years old or have severe obstructive sleep apnea (OSA; apnea-
hypopnea index [AHI] >10 obstructive events/hour, oxygen saturation <80%, or
both), clinicians should arrange for overnight hospital monitoring after
tonsillectomy.
9. Children undergoing tonsillectomy should receive a single intraoperative dose of
intravenous dexamethasone. They reduced postoperative nausea and vomiting
(PONV) up to 24h after tonsillectomy, shorter time to rst oral intake, and less

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pain, as evaluated by lower pain scores and longer latency times to painkiller
administration.
Chronic tonsillitis, febrile seizures, mufed (“hot potato”) speech, halitosis, malocclusion of teeth, tonsillar hypertrophy, cryptic tonsils, and chronic pharyngeal
carriage of GABHS are among the poorly validated indications for tonsillectomy
that have not been assessed in any controlled trials or case series. When considering
tonsillectomy for one of these conditions, there is a signicant role for shared decision-making with caregivers, with individualized decisions considering the severity
of the illness and quality of life [30].
38.9.2.1 Tonsillotomy (Partial Tonsillectomy, Intracapsular
Tonsillectomy)
Tonsillotomy is the partial intracapsular removal of tonsil tissue instead of tonsillectomy, which is the complete extracapsular removal. Tonsillotomy, partial tonsillectomy, tonsil ablation, intra-capsular tonsillectomy, radiofrequency-induced
thermotherapy (RFITT) of the tonsils, and subtotal tonsillectomy are some of the
terms used in the literature to describe the partial removal of tonsils. Tonsillotomy
has been performed with several surgical devices, including CO2-Laser, diathermy,
radiofrequency, microdebrider, coblation, bipolar, and cold-steel tonsillectomy.
Tonsillotomy is usually done under general anesthesia. However, it can also be done
with local anesthesia. Tonsillotomy is mainly used in pediatric obstructive sleep
apnoea syndrome (pOSAS) children and is performed under general anesthesia [57].
38.9.2.2 Tonsillectomy
The surgical removal of the palatine tonsils, known as a tonsillectomy, is one of the
most common surgical procedures in the head and neck area. Tonsillectomy is a
surgical operation that completely removes the tonsil, including its capsule, by dissecting the peritonsillar space between the tonsil capsule and the muscle wall, with
or without adenoidectomy [30].
Tonsillotomy has shown to be as successful as tonsillectomy in treating tonsillar
hypertrophy. Conversely, tonsillotomy reduces the risk of subsequent bleeding by
79%, reduces the severity of postoperative pain, and allows earlier return to regular
diet and exercise [1, 57–61]. After tonsillectomy, postoperative hemorrhages were
more common; tonsillotomy may lower the risk of bleeding that necessitates a hospital visit (tonsillotomy: 2/1000; tonsillectomy: 14/1000) [57, 58]. Furthermore, the
changing trends from tonsillectomy to tonsillotomy reduced the need for and
expense of healthcare services. Only 1.5% of patients required resurgery following
tonsillotomy [59, 61].
There was no difference in postoperative discomfort and bleeding in the tonsillotomy between the microdebrider and the coblator. No substantial infection was
observed despite the possibility of tonsillar remaining following tonsillotomy.
Regarding sleep disturbance and quality of life, there is no benet to utilizing tonsillotomy versus tonsillectomy [60, 61].

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38.9.3 Complications ofTonsil Surgery
One of the most common operations performed by otolaryngologists is tonsillectomy. The number of complications associated with tonsillectomy has decreased
dramatically due to meticulous surgical techniques and technological advances in
modern anesthesiology [1].
38.9.3.1 Intraoperative Complications
Within the rst 24h, primary complications develop intraoperatively or soon after
tonsillectomy. Complications from anesthesia are a signicant worry. Intraoperative
complications include atlantoaxial subluxation, temporomandibular joint dislocation, loose teeth dislodging, accidental extubation, or kinking of the endotracheal
tube. To reduce the danger of laryngospasm and aspiration after extubation, secretions, or blood in the hypopharynx must be suctioned. One of the most severe complications of tonsillectomy is bleeding, which can happen at any time during the
perioperative period. Intraoperative bleeding may be related to an underlying coagulopathy or possibly to major arterial damage in severe cases. With the use of electrocautery, intraoperative bleeding is substantially less common. Detecting
underlying coagulation problems through history and physical ndings, as well as
preoperative screening in carefully selected individuals, can help avoid severe intraoperative blood loss. Suction cautery or ligation, or even the implantation of a pack
in the tonsillar fossa and over-suturing of the tonsillar pillars to give continual compression of the fossa, are all options for controlling signicant intraoperative hemorrhage. Ligating larger arteries through an open-neck exploration may be necessary
in severe cases. However, this should be an extremely uncommon step [1, 56].
38.9.3.2 Postoperative Early Complications (<24h)
Most patients have nausea, vomiting, oropharyngeal pain, or referred otalgia in the
early postoperatively period. Dehydration can arise due to poorly controlled pain,
intractable nausea, and vomiting, which is frequently caused by the use of narcotic
painkillers. One of the most severe complications of tonsillectomy is bleeding,
which can happen at any time during the perioperative period. Pulmonary edema
may occur. After a long-standing upper airway obstruction, the removal of the tonsils and an increase in intrathoracic pressure can rapidly increase pulmonary hydrostatic pressure, resulting in uid transudation into the pulmonary interstitium.
Patients with a long history of obstructive sleep apnea, as demonstrated by polysomnography and cor pulmonale, should be closely monitored with pulse oximetry
in a monitored setting following surgery. Patients with prolonged hypercapnia may
require planned mechanical breathing after surgery until their Pco2 levels return to
normal [1, 56].
38.9.3.3 Postoperative Late Complications (>24h–2weeks)
Pharyngitis can occur in dehydrated patients and necessitates the use of systemic
antibiotics. Atelectasis or aspiration of loose teeth, blood, or tissue can cause lung
infections. The most common manifestation of postoperative bleeding is delayed

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hemorrhage, which occurs between days 5 and 10 after surgery due to premature
eschar separation, which causes retraction of small surface arteries and the creation of an overlaying clot. If the surgeon is unsure whether active bleeding is
occurring, the lump should be suctioned to allow for a more thorough examination. Blood clots can hide bleeding veins and, as a result of brinolysis, can inhibit
proper coagulation. Patients with a blood clot in the tonsillar fossa and a delayed
hemorrhage who are not actively bleeding should be admitted for at least overnight observation. It is necessary to get a coagulation prole and a hematocrit
measurement [1, 56].
38.9.3.4 Postoperative Long-Term Complications (>weeks)
Eagle syndrome (ossication of the stylohyoid ligament) is a rare condition with a
poorly known pathophysiologic basis for its symptoms. Patients with face pain or
dysphagia may present months or years following tonsillectomy [56].
38.9.4 Immunological Effects ofTonsil Surgery
Due to the limited availability of sequential studies, these have yet to be thoroughly
investigated, the fact that any immunological deciency could have existed prior to
surgery should be taken into consideration. However, there is evidence of a reduction in the number of activated B cells and a decrease in secretory IgA and other
immunoglobulins, but only to the lower end of the normal range [1, 11]. The number of lymphocytes in children’s tonsils is higher than in adults’ tonsils, and the
number of helper and cytotoxic T lymphocytes is higher in sick tonsils. Also, the
persistent antigenic stimulation from infected tonsils causes increased levels of
immunoglobulins throughout the pretonsillectomy interval. It was found that following tonsillectomy, the immune response was decreased and that the greater levels of immunoglobulin in the preoperative period were related to bacterial activation
of lymphocytes [62].
Tonsillar lymphocytes can become so overstimulated by antigenic stimulation
that they lose their ability to respond to other antigens. When this immunologic
impairment develops, the tonsil can no longer provide adequate local protection or
reinforce the upper respiratory tract’s secretory immune system. As a result, removing recurrently sick tonsils has a therapeutic benet [30]. Some studies, however,
found minimal changes in Ig concentrations in the serum and surrounding tissues
after tonsillectomy. Nonetheless, no research has shown that tonsillectomy has a
signicant clinical inuence on the immune system [30].
After tonsillectomy and adenoidectomy, children who had previously been
immunized orally with live poliovirus vaccine saw their titers decline three- to fourfold. Attempts to vaccinate seronegative children who had tonsillectomy and adenoidectomy resulted in delayed and reduced nasopharyngeal secretory immune
responses, as evaluated by poliovirus IgA antibodies [1, 11].
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