Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4534_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •Contents
- •1.1.9 Laryngeal Atresia
- •1.1.10 Laryngeal Webs
- •1.1.11 Congenital Subglottic Stenosis
- •1.1.12 Laryngeal Cleft
- •1.1.13 Tracheoesophageal Fistula
- •1.1.14 Tracheal Bronchus
- •1.2.2 Mesenchyme Development
- •1.2.4 Lung Development
- •1.2.4.1 Embryonic Stage
- •1.2.4.2 Pseudoglandular Stage
- •1.1.1 Oral Cavity
- •1.1.2 Nasal Cavity
- •1.1.3 Palate
- •1.1.4 Primitive Pharynx
- •1.1.5 Upper Airway Anomalies
- •1.1.6 Cleft Lip/Palate
- •1.1.7 Choanal Atresia
- •1.1.8 Laryngomalacia
- •1.2.4.3 Canalicular Stage
- •1.2.4.4 Saccular Stage
- •1.2.4.5 Alveolar Stage
- •1.2.5 Congenital Respiratory System Defects
- •1.2.5.1 Tracheal Agenesis
- •1.2.5.2 Congenital Tracheal Stenosis
- •1.2.5.3 Lung Agenesis
- •1.2.5.4 Lung Hypoplasia
- •References
- •2.1 Introduction
- •2.2 Nasal Cavity
- •2.2.1 Vestibule
- •2.2.2 Respiratory Mucosa
- •2.2.3 Olfactory Mucosa
- •Supporting Cells
- •Basal Cell
- •Olfactory Receptor Cell (Bipolar Neuron)
- •Brush Cell (Microvillar Cell)
- •2.2.3.2 The Lamina Propria
- •2.2.3.3 Olfactory Glands (Bowman’s Glands)
- •2.3 Paranasal Sinuses
- •2.4 Pharynx
- •2.5 Larynx
- •2.6 Trachea
- •2.6.1.1 Ciliated Columnar Cells
- •2.6.1.2 Goblet Cells
- •2.6.1.3 Brush Cells
- •2.6.1.4 Basal Cells
- •2.6.1.5 Enteroendocrine System Cells (Kulchitsky Cells or DNES Cells)
- •2.6.2 Lamina Propria
- •2.7 Lungs
- •2.7.1 Pleura
- •2.7.2 Bronchi
- •2.7.3 Bronchioles
- •2.7.3.1 Terminal Bronchioles
- •2.7.3.2 Respiratory Bronchioles
- •2.7.4 Ductus Alveolaris
- •2.7.5 Alveoli
- •2.7.5.2 Type II Alveolar Cell (Septal Cell, Large Alveolar Cell)
- •References
- •3.1.1.3 Nerves
- •Ophthalmic Division
- •Maxillary Division
- •Parasympathetic Nerve Supply
- •3.1.1.4 Bony Anatomy
- •3.1.1.5 Cartilaginous Pyramid
- •3.1.1.6 Structure
- •External Nasal Anatomy
- •Internal Nasal Anatomy
- •3.1.2 Nasal Physiology
- •3.1.2.1 Nasal Airflow
- •3.1.2.2 Abnormal Nasal Physiology
- •3.2.1 Larynx Anatomy
- •Cricoid Cartilage
- •Thyroid Cartilage
- •Epiglottis
- •Arytenoid Cartilages
- •Corniculate Cartilages
- •Cuneiform Cartilages
- •Extrinsic Ligaments
- •Intrinsic Ligaments
- •Laryngeal Cavity
- •Piriform Recesses
- •Cricothyroid Muscles
- •Posterior Cricoarytenoid Muscles
- •Lateral Cricoarytenoid Muscles
- •Transverse Arytenoid Muscle
- •Thyroarytenoid Muscles
- •Superior Laryngeal Nerve
- •Arteries
- •Veins
- •Lymphatics
- •Swallowing
- •Respiration
- •Phonation
- •3.2.2.1 Reflex Glottic Closure
- •References
- •4.1 Introduction
- •4.2.1 Choanal Atresia
- •4.2.2 Pyriform Aperture Stenosis
- •4.2.3 Cleft Lip Nasal Deformity
- •4.2.4 Nasolacrimal Duct Cysts
- •4.2.5 Encephaloceles
- •4.3 Craniofacial Anomalies
- •4.3.1 Pierre Robin Syndrome
- •4.3.2 Treacher-Collins Syndrome
- •4.3.3 Crouzon Syndrome
- •4.3.4 Down Syndrome
- •4.3.5 Apert Syndrome
- •4.4.1 Thyroglossal Duct Cyst
- •4.4.2 Laryngomalacia
- •4.4.3 Vocal Fold Paralysis
- •4.4.5 Subglottic Stenosis
- •4.4.6 Subglottic Hemangioma
- •4.4.7 Laryngeal Cysts
- •4.4.8 Laryngeal Cleft
- •4.5 Conclusion
- •References
- •5.1 Innate Immunity
- •5.2 Adaptive Immunity
- •References
- •6.1 Introduction
- •6.2 Innate Immunity
- •6.3 Adaptive Immunity
- •References
- •7.1 Introduction
- •References
- •8: Respiratory Microbiome
- •8.1 Introduction
- •8.2.1 Childhood Asthma
- •8.2.2 Asthma Exacerbation
- •8.3 Bacteriome
- •8.4 Virome
- •8.5 Mycobiome
- •References
- •9.1 Introduction
- •References
- •10.1 Introduction
- •10.3.3 The Appointment Process, Explained
- •10.3.5 Parental Involvement
- •10.4 Coordinating Care When Your Child Is Ill
- •10.4.3 Exhibit Cohesion
- •10.6 Conclusion
- •References
- •11.1 Introduction
- •11.2 Nasal Cavity
- •11.2.1 Choanal Atresia
- •11.2.2 Rhinosinusitis
- •11.2.4 Juvenile Nasopharyngeal Angiofibroma
- •11.3 Pharynx
- •11.4 Nasopharynx
- •11.4.1 Adenoid Hypertrophy
- •11.4.2 Nasopharyngeal Carcinoma
- •11.5 Oropharynx
- •11.5.1 Thyroglossal Duct Cyst
- •11.6 Hypopharynx
- •11.6.1 Retropharyngeal Abscess
- •11.6.2 Lymphatic Malformation
- •11.6.4 Lymphoma
- •11.6.5 Rhabdomyosarcoma
- •11.7 Larynx
- •11.7.1 Subglottic Stenosis
- •11.7.2 Laryngotracheal Papillomatozis
- •11.7.3 Croup
- •11.7.4 Epiglottitis
- •11.7.5 Foreign Body Aspiration
- •References
- •12.2.1 Plain Radiography
- •12.2.1.1 The Thymus
- •Tracheal Buckling
- •Hilum
- •Diaphragm
- •Mediastinal Borders
- •Lung Opacities
- •Cystic Lung Diseases
- •Pulmonary İnterstitial Emphysema (PIE)
- •Unilateral Hyperlucent Lung
- •12.2.2 Fluoroscopy
- •12.2.3 Ultrasound
- •12.2.4 Computed Tomography
- •12.2.5 Magnetic Resonance Imaging (MRI)
- •12.2.6 Angiography
- •12.2.7 Positron Emission Tomography (PET)
- •12.3 Conclusion
- •References
- •13.1 Introduction
- •13.2 Nasal Diagnostic Procedures
- •13.2.1 Indications
- •13.2.2 Contraindications
- •13.2.3 Anatomical Features
- •13.2.4 Technical Considerations
- •13.2.5 Technique
- •13.2.5.1 First Pass
- •13.2.5.2 Second Pass
- •13.2.5.3 Third Pass
- •13.3 Flexible Laryngoscopy
- •13.4 Direct Laryngoscopy
- •13.5 Video Laryngoscopy
- •13.5.1 Indications
- •13.5.2 Contraindications
- •13.5.3 Outcomes
- •13.5.4 Equipment
- •13.5.5 Approach Considerations
- •References
- •14.1 Upper Airways
- •14.2.3 Laryngeal Pathologıes
- •References
- •15.1 Introduction
- •15.2 Airway Measurements
- •References
- •16.1 Introduction
- •16.2 Background
- •References
- •17: Allergen Testing: Purpose, Procedure, Interpretation
- •17.1 Introduction
- •17.2 Tests
- •17.2.1 Skin Tests
- •17.2.3 Component Resolved Diagnosis (CRD)
- •17.2.4 Tryptase
- •17.2.5 Basophil Activation Test (BAT)
- •17.2.6 Provocation Tests
- •17.2.7 Nasal sIgE
- •17.2.8 Nasal Smear Eosinophilia
- •17.2.9 Eosinophilic Cationic Protein (ECP)
- •References
- •18: Smell Testing: Purpose, Procedure, Interpretation
- •18.1 Introduction
- •18.2 Possible Olfactory Disorder Diagnosis
- •18.2.1 Conductive Defects
- •18.2.3 Inherited Disorders
- •18.2.3.1 Hormonal Disturbances
- •18.4 Odor Threshold Tests
- •18.8.1 Butanol Threshold Test
- •18.8.1.1 The Penn State University Odor Identification Exam
- •18.8.2 Cross-Cultural Smell Identification Test
- •18.8.3 Sniffin’ Sticks
- •References
- •19: Taste Testing: Purpose, Procedure, Interpretation
- •19.1 Introduction
- •19.2 Definitions
- •19.2.1 Taste Dysfunction Abnormalities
- •19.4.1 Taste Dysfunction
- •19.4.2 COVID-19
- •19.5 Taste Disorder Diagnosis
- •19.6.2 Magnitude Matching
- •19.6.3 Spatial Test
- •References
- •20.1 Introduction
- •20.2 Primary Otalgia Causes
- •20.2.1 Auricle
- •20.2.1.1 Infections
- •20.2.1.2 Trauma
- •20.2.1.3 Allergic Angioedema
- •20.2.1.4 Thermal Damage
- •20.2.2 External Auditory Canal
- •20.2.2.1 Otitis Externa
- •20.2.2.2 Malignant Otitis Externa
- •20.2.2.3 Eczematous Dermatitis
- •20.2.2.4 Furunculosis
- •20.2.2.5 Foreign Body
- •20.2.2.6 Cerumen Impaction
- •20.2.2.7 Tumors
- •20.2.3 Middle Ear
- •20.2.3.1 Acute Otitis Media
- •20.2.3.3 Eustachian Tube Dysfunction
- •20.2.3.4 Cholesteatoma
- •20.2.3.5 Trauma
- •20.3 Secondary Otalgia Causes
- •20.3.1 Oropharyngeal Infections
- •20.3.2 Dental Causes
- •20.3.3 Auricular Lymphadenitis
- •20.3.4 Neck Abscess
- •20.3.5 Parotitis
- •20.3.6 Temporomandibular Joint Dysfunction
- •20.3.7 Sinusitis
- •20.4 Differential Diagnosis
- •References
- •21.1 Introduction
- •21.2 Bacterial Otitis Externa
- •21.3 Acute Otitis Media
- •21.4 Chronic Suppurative Otitis Media
- •21.5 Foreign Body
- •21.5.1 Cerumen
- •21.5.2 Tympanostomy Tube Drainage
- •21.5.3 Traumatic Cerebrospinal Fluid Otorrhea
- •21.5.5 Necrotizing Otitis Externa (Malignant External Otitis)
- •21.5.6 Neoplasms
- •21.5.7 Polyps
- •21.5.8 Otomycosis
- •21.5.9 First Branchial Cleft Cysts
- •21.5.10 Cholesteatoma
- •21.5.11 Spontaneous Cerebral Spinal Fluid Otorrhea
- •References
- •22.1 Introduction
- •22.4 Congenital Causes
- •22.4.1 Choanal Atresia
- •22.4.2 Pyriform Apertura Stenosis
- •22.4.3 Nasal Midline Congenital Masses
- •22.4.3.1 Nasal Dermoid Cyst
- •22.4.3.2 Nasal Glioma
- •22.4.3.3 Encephalocele (Encephalo-Meningocele)
- •Differential Diagnosis
- •22.4.3.4 Nasolacrimal Duct Cyst (Dacryocystocele)
- •22.5 Infectious Causes
- •22.5.1.1 Rhinitis Etiology
- •22.5.2 Neonatal Rhinitis
- •22.5.3 Bacterial or Viral Rhinitis
- •22.5.4 Iatrogenic Rhinitis
- •22.5.5 Infectious Rhinitis (Rhinosinusitis)
- •22.6 Adenoid Hypertrophy
- •22.7 Inflammatory Causes
- •22.7.1 Allergic Rhinitis
- •22.7.2 Nonallergic Rhinitis
- •22.7.3 Eosinophilic Nonallergic Rhinitis (NARES)
- •22.7.4 Nasal Polyp
- •22.7.5 Antrochoanal Polyp
- •22.7.6 Inferior Turbinate Hypertrophy
- •22.8 Neoplasia
- •22.8.1 Benign Tumors (Juvenile Nasopharyngeal Angiofibroma)
- •22.8.2 Malignant Tumors
- •22.9 Systemic Causes
- •22.9.1 Cystic Fibrosis
- •22.9.2 Primary Ciliary Dyskinesia
- •22.10 Trauma/Iatrogenic Causes
- •22.10.1 Nasal Trauma-Septal Hematoma
- •22.10.2 Septum Deviation
- •22.10.3 Nasal Foreign Bodies
- •References
- •23.1 Introduction
- •23.2 Pathophysiology
- •23.3 Allergic Rhinitis
- •23.4 Non-allergic Rhinitis
- •23.5 Infectious Rhinitis
- •23.6.1 Vasomotor Rhinitis
- •23.7 Evaluation
- •23.8 Diagnosis
- •23.9 Treatment
- •23.10 Prognosis
- •23.11 Conclusion
- •References
- •24.1 Introduction
- •24.2 Pathogenesis
- •24.3 Diagnosis
- •24.3.1 History
- •24.3.2 Examination
- •24.4 Differential Diagnoses
- •24.5 CSF Rhinorrhea
- •24.5.1 CSF Physiology
- •24.5.1.1 Pathogenesis
- •24.6 Diagnosis
- •24.6.1 Chemical Diagnosis
- •24.6.2 Imaging Diagnosis
- •24.7 Treatment
- •24.7.1 Surgical Technique
- •References
- •25.1 Introduction
- •25.1.1 Waldeyer Ring
- •25.3 Anatomy
- •25.3.1 Lymphatic Drainage
- •25.3.1.1 Nerve Supply
- •25.6 Tonsillary Hypertrophy
- •25.7 Physical Examination
- •25.8.1 Obstructive Sleep Apnea
- •References
- •26.1 Introduction
- •26.5 Halitosis Physiopathology
- •26.6.1 Oral Halitosis (Intraoral Halitosis, Oral Malodor)
- •26.6.1.1 Periodontal Infections
- •26.6.1.2 Tongue Oriented Halitosis
- •26.6.1.3 Peritonsillar Abscess
- •26.7 Paranasal Sinus Diseases
- •26.8 Adenoid Vegetation
- •26.9 Chronic Pharyngitis
- •26.10 Chronic Tonsillitis
- •26.11 Tonsillolith
- •26.12 Non-Oral Halitosis
- •26.13 Gastroesophageal Reflux
- •26.14 Diagnosis
- •26.14.1 Organoleptic Measurement
- •26.14.2 Sulfur Monitoring
- •26.14.2.1 Indirect Methods
- •26.14.2.3 Ammonia Monitoring
- •26.14.2.4 Polymerase Chain Reaction (PCR)
- •26.15 Physical Examination
- •References
- •27.1 Introduction
- •27.2 Epidemiology
- •27.4 Diagnosis
- •27.5.1 Clinical Assessment
- •27.6 Treatment
- •27.6.1 Voice Therapy
- •27.7 Phonosurgery
- •References
- •28.1 Introduction
- •28.2 Epidemiologic Characteristics
- •28.3 Swallowing Physiologic Phases
- •28.3.1.1 Prematurity
- •28.3.1.2 Neuromuscular
- •28.3.1.5 Cardiopulmonary Disease
- •28.4 Symptoms
- •28.5 Clinical Feeding Assessment
- •28.7 Flexible Endoscopic Swallowing Evaluation
- •28.8 Imaging
- •28.9 Endoscopic Assessments
- •28.9.1 High-Resolution Manometry
- •28.10 Medical Management
- •28.11 Surgical Management
- •28.11.1 Ankyloglossia
- •28.11.2 Laryngomalacia
- •28.11.3 Laryngeal Cleft
- •28.12 Conclusions
- •References
- •29.1 Introduction
- •29.2 Reactive Lymph Node Enlargements
- •29.3 Vaccines
- •29.4 Acute Suppurative Lymphadenitis
- •29.6 Granulomatous Lymphadenitis
- •29.6.1 Mycobacterial Infection
- •29.6.2 BCG Vaccine
- •29.6.3 Cat-Scratch Disease
- •29.6.4 Sarcoidosis
- •29.6.5 Kikuchi-Fujimoto Disease
- •29.7 Malignancies
- •29.8 Diagnosis
- •References
- •30.1 Introduction
- •30.2 Upper Airway Cough Syndrome
- •30.3 Chronic Rhinosinusitis
- •30.5 Otogenic Cough
- •30.6 Laryngeal Clefts
- •30.7 Conclusion
- •References
- •31.1 Introduction
- •31.5.1 Vocal Cord Disfunction (VCD)
- •31.5.2 Obstructive Sleep Apnea Syndrome (OSAS)
- •31.5.3 Allergic or Non-Allergic Rhinitis
- •31.6 Conclusion
- •References
- •32.1 Introduction
- •32.2.1 Non-massive Hemoptysis
- •32.2.2 Massive Hemoptysis
- •32.4 Diagnostic Evaluation
- •32.4.1 History
- •32.4.1.1 Infection Warning Signs
- •32.4.1.2 Choking
- •32.4.1.3 Exposures
- •32.4.1.4 Underlying Medical Problems
- •32.4.2 Physical Examination
- •32.4.3 Laboratory Evaluation
- •32.4.4 Imaging
- •32.5.1 Respiratory Illness
- •32.5.3 Trauma
- •32.5.4 Hemoptysis Mimics
- •References
- •33.1 Introduction
- •33.6 Conclusion
- •References
- •34: Pediatric Allergic Rhinitis: Otolaryngology Perspective
- •34.1 Introduction
- •34.2 Epidemiology
- •34.2.1 Prevalence
- •34.2.2 Risk factors
- •34.3.1 Classical Pathway
- •34.3.2 Nasal Pathway
- •34.4.2 Physical Examination
- •34.4.3 Diagnostic Tests
- •34.4.4 Nasal Cytology
- •34.4.5 Imaging
- •34.5.1 Adenoid Hypertrophy
- •34.5.2 Nasal Septal Deviation
- •34.5.3 Chronic Rhinosinusitis
- •34.5.4 Turbinate Hypertrophy
- •34.5.5 Nasal Foreign Body
- •34.5.6 Other Clinical Conditions
- •34.6.1 Saline Irrigation (Douching)
- •34.7 Treatment
- •34.7.1 Oral Antihistamines
- •34.7.2 Intranasal Steroids
- •34.7.3 Leukotriene Inhibitors
- •34.7.5 Oral Steroids
- •34.7.6 Intranasal Antihistamines
- •34.7.7 Immunotherapy (Sublingual-Subcutaneous)
- •34.8 Conclusion
- •References
- •35: Allergic Rhinitis: Pediatric Pulmonologist Perspective
- •35.1 Introduction
- •35.2.1 Epidemiological Relationship
- •35.2.4 Immunopathology
- •35.2.7 Non-pharmaceutical Treatment Method
- •35.2.8 Pharmaceutical Medication Policy
- •35.2.9 Immunotherapy Against Allergens
- •35.6 Conclusion
- •References
- •References
- •37.1 Introduction
- •37.2 Adenoid Hypertrophy
- •37.7 Preoperative Evaluation
- •37.8 Contraindications
- •37.9 Complications
- •37.9.1 Bleeding
- •37.9.2 Hypernasality
- •37.9.3 Surgical Traumas
- •37.9.4 Torticollis
- •37.9.5 Otitis Media
- •37.9.6 Psychological Trauma
- •37.9.7 Nasopharyngeal Stenosis
- •37.9.8 Recurrence
- •37.10 Postoperative Care
- •37.11 Surgery
- •37.12.1 Adenoiditis
- •References
- •38.1 Introduction
- •38.2 Anatomy
- •38.2.1 Palatine Tonsils (Faucial Tonsils)
- •38.2.2 Lingual Tonsil
- •38.2.3 Adenoids (Pharyngeal Tonsil)
- •38.2.4 Tubal Tonsils
- •38.5.1 Viral Tonsillitis
- •38.5.2 Bacterial Tonsillitis
- •38.5.3 Candida
- •38.6.1 Suppurative Complications
- •38.6.1.1 Peritonsillar Abscess (Quincy Tonsil)
- •Lemierre’s Syndrome
- •38.6.2 Nonsuppurative Complications
- •38.6.2.1 Acute Rheumatic Fever
- •38.6.2.2 Poststreptococcal Glomerulonephritis
- •38.6.2.3 Scarlet Fever
- •38.6.2.6 Palmoplantar Pustulosis (PPP)
- •38.6.2.7 IgA Nephropathy
- •38.7 Clinical Manifestation
- •38.7.1 Infection
- •38.7.2 Obstruction
- •38.7.3 Neoplasia
- •38.8 Diagnosis
- •38.8.2 Physical Examination
- •38.8.3 Laboratory
- •38.8.4 Imagining
- •38.8.5 Polysomnography
- •38.9 Treatments
- •38.9.1 Medical Treatment
- •38.9.2 Surgery
- •38.9.2.2 Tonsillectomy
- •38.9.3.1 Intraoperative Complications
- •38.9.3.4 Postoperative Long-Term Complications (>weeks)

156
cd
S. Taşar and R. Savaş
ab
Fig. 12.5 The appearance of normal thymus tissue on chest X-ray, ultrasonography, CT, and MRI
in a 2-year-old patient. Ultrasonographically, scattered hyperechoic foci resembling a starry sky
are observed in a homogeneous background
Fig. 12.6 Normal
rightward displacement of
the trachea; tracheal
buckling

ab
12 Radiologic Evaluation ofLower Respiratory System
diaphragms. In case of increased aeration, the diaphragms are bilaterally attened,
the distance between the ribs is widened, and the anterior-posterior diameter is
increased on the lateral radiograph. Increased aeration in children is more common
in viral infections. It may be a sign of excessive ventilator pressure in an intubated
child. If there is asymmetric lobar overination, advanced examination methods are
used to detect possible underlying bronchial compression (e.g., mediastinal bronchogenic cyst), an anomaly (congenital lobar emphysema), or a mass causing partial obstruction in the bronchus (endobronchial granuloma) (Fig.12.7).
Sometimes the diaphragm of the dense hemithorax is observed high in cases
such as pulmonary aplasia. In these cases, the mediastinum is displaced toward the
157
c
Fig. 12.7 In a newborn diagnosed with congenital lobar emphysema, focal lucency in the upper
zone of the right lung on the chest X-ray (a), attening in the diaphragm on the lateral radiograph
(b), and a hypodense area in the upper lobe due to air trapping on the CT examination (c) are
observed

158
ab
S. Taşar and R. Savaş
dense hemithorax because of volume loss. Other causes of asymmetrical lung volumes include diaphragmatic paresis/paralysis and a large abdominal mass. The diaphragm may also be elevated, apparently secondary to a collection of subpulmonic
uid. Diaphragm contours in the neonatal period should be evaluated for possible
congenital diaphragmatic hernia (Fig.12.8).
Mediastinal Borders
The normal structure of the mediastinum should always be reviewed. On the left
side, you should look for the thymus, aortic arch, pulmonary conus, hilus, and left
c
Fig. 12.8 In the bilateral chest radiograph, there is an appearance secondary to intestinal and
herniation in the left hemithorax posterior (a, b). With CT, herniation of the intestinal loops into
the hemithorax from the defective area in the diaphragm was demonstrated (c)

12 Radiologic Evaluation ofLower Respiratory System
159
heart border; on the right side, you should consider the thymus, azygos vein, hilus,
and right heart border. The thymus may be misleading in young children, but it
should be checked that the posterior paraspinal section can be easily observed since
the thymus is located anteriorly. Disturbances in the paraspinal lines or increased
opacity at the apex suggest posterior mediastinal masses (meningocele, neuroenteric cyst, duplication cyst, neurogenic tumor, and infection). Erosions in adjacent
bone tissues are caused by infection or suggest malignancy. Any abnormal appearance of the thymus suggests an anterior mediastinal mass lesion (thymic hyperplasia, germ cell tumor, T-cell lymphoma, and thymoma). The other mass lesion in the
mediastinum usually originates from the middle mediastinum. In young children,
this mass is usually a congenital abnormality such as a bronchogenic cyst or duplication cyst. An older child may have enlarged lymph nodes secondary to infective
and neoplastic processes.
Lung Opacities
The contours of the mediastinum are used to locate the localization of opacities in
the lungs. The differential attenuation of two adjacent structures denes the silhouette sign. For example, the loss of the upper mediastinal outline indicates upper lobe
opacication, the loss of the heart borders is the result of right middle lobe or lingular opacication, and the loss of diaphragmatic denition is caused by lower lobe
pathology.
Atelectasis and consolidations cause the lung to appear opaque. Volume loss in
atelectasis and volume increase in consolidations with air bronchograms are distinctive. In volume loss, mediastinal shift toward the ipsilateral hemithorax, elevation of
the diaphragm, and convergence of the ribs are observed. The hilum may be displaced toward the atelectasis, and noncollapsed lung may show compensatory overination. In acute atelectasis, a displaced endotracheal tube, foreign body aspiration,
or mucus occlusion are causes that should not be considered rst. In chronic atelectasis, extrinsic airway obstruction (bronchogenic cyst, mediastinal lymphadenopathy, neoplasia), or chronic infection (e.g., tuberculosis) are more likely causes.
Consolidation is the replacement of air in terminal airspaces. It is the uptake of uid,
mucus, or cellular material. Clinical history, accompanying lymphadenopathy, or the
presence of pleural effusion is important for differential diagnosis. Bilateral pulmonary edema presents as perihilar patchy consolidation with pleural uid.
Ground-glass change describes increased attenuation of the lung with preserved
bronchial and vascular signs. It is a nonspecic nding with a wide etiology, including infection, and interstitial and alveolar diseases.
CT/MRI is needed to elucidate the underlying cause of focal and multifocal lung
opacities other than pneumonia. The cause of a solitary parenchymal lesion may be
congenital malformations such as sequestration, congenital pulmonary adenomatoid malformation, and vascular anomaly. Also, a lung abscess may have no apparent gas-uid level and can be observed as a round mass.
In multifocal lesions, infective (tuberculosis, fungal, septic embolism), inammatory (LCH) processes, common interstitial lung diseases, and metastasis form the
priority diagnosis list.

160
cc
S. Taşar and R. Savaş
In children, lower respiratory tract infections remain a major cause of morbidity
and mortality. Various pathogens such as viruses, bacteria, bacteria-like organisms,
mycobacteria, fungi, and parasites, either alone or in combination, may affect the
peripheral airways (bronchiolitis) or the alveoli (pneumonia).
Pneumonia can cause morbidity in children, with the potential development of various acute and chronic complications. Medical imaging is used to conrm or exclude
the presence of pneumonia. However, it is also useful in the detection of underlying
anomalies in recurrent infections and the evaluation of complications (Fig.12.9).
Cystic Lung Diseases
Cystic sequelae lesions can be observed in necrotizing pneumonia, infective processes with cavitation (Staphylococcus aureus, tuberculosis, fungus), and abscesses.
A lung abscess usually includes both liquid and gas. With the CXR, the gas-liquid
ab
Fig. 12.9 There is an increase in opacity in the middle-lower zone of the right lung on the chest
X-ray (a). Contrast-enhanced thorax CT examination reveals dense cystic lesions (b). After medical treatment, there was still a cystic mass in the right lung (c). The patient was operated on, and
the pathological diagnosis was CPAM. Control chest X-ray shows postoperative changes after
surgery (d)

12 Radiologic Evaluation ofLower Respiratory System
161
level can be overlooked, sometimes appearing as nodular opacity. Multifocal, multicystic parenchymal lesions may be congenital cystic adenomatoid malformation,
Langerhans cell histiocytosis nodules at the cavitating stage, granulomatosis with
polyangiitis, or necrotizing vasculitis.
Pulmonary İnterstitial Emphysema (PIE)
PIE is a complication that can occur when high ventilator pressures are used. Rarely,
it can be seen spontaneously in babies who have never been ventilated. It is the
escape of air into the intestinal tract as a result of alveolar leakage. It is in the form
of lace-like linear lucency extending from the pulmonary hilum toward the periphery. If complicated, pneumothorax or pneumomediastinum also develops.
Unilateral Hyperlucent Lung
(a) Chest Wall Abnormality: Poland syndrome is a congenital unilateral aplasia of
the pectoralis muscles. The characteristic radiographic ndings include unilateral hyperlucency of the lung related to the lack of soft tissues in the chest wall.
(b) Pneumothorax
Pneumothorax is the presence of air between the leaves of the pleura. It often
develops spontaneously or after chest trauma in pediatric patients. It is caused
by the transthoracic pressure difference in newborns. Pneumothorax can be
fatal if not diagnosed and treated promptly. The main feature of pneumothorax
on a chest radiograph is the white visceral pleural line. In most cases, a nonvascular hyperlucent pneumothorax area is also observed adjacent to the visceral
pleura. CT is generally used in complicated cases. A progressive pneumothorax
may present as a life-threatening tension pneumothorax that causes the mediastinal contralateral shift, increased intercostal distance, and the appearance of a
attened hemidiaphragm.
(c) Lung Parenchymal Abnormality
– Bronchial atresia is a congenital anomaly that results from the focal oblit-
eration of a proximal segmental or subsegmental bronchus. The develop-
ment of the distal airways is normal. However, preserved ventilation via
collateral pathways leads to air trapping and hyperination. The atretic bron-
chus becomes lled with secretions and forms a bronchocele. The radio-
graphic appearance of bronchial atresia is a round or oval branching opacity
representing the bronchocele with an associated area of hyperlucency in the
adjacent lung parenchyma (Fig.12.10).
– Congenital lobar emphysema is characterized by progressive hyperination
of a lobe. The most likely cause is thought to be air trapping with a check
valve mechanism as a result of ineffective expiration secondary to malaise or
stenosis in the bronchial cartilage.
– Congenital pulmonary airway malformations are multicystic masses of seg-
mental lung tissue with disorganized hamartomatous and adenomatoid pro-
liferation that communicate with the bronchial tree. The diagnosis is usually
made on antenatal ultrasound in the neonatal period [4]. If large, they may
cause pulmonary hypoplasia, with resultant respiratory distress syndrome.

162
S. Taşar and R. Savaş
a
Fig. 12.10 The CT scans show a bronchocele appearance, which indicates a mucus-lled atresic
bronchus with an air trapping area around it, located in the posterior of the upper lobe of the left
lung, as observed in the parenchymal window on both axial (a) and coronal (b) sections
b
– Swyer-James Syndrome usually develops during childhood as a sequela of
postinfectious bronchiolitis obliterans. It is generally characterized by uni-
lateral small lung with hyperlucency and air trapping and diminished vascu-
larity. It can be unilateral or bilateral, also be lobar and segmental, and
subsegmental involvement with a pathy distribution [5].
(d) Pulmonary Vasculature Abnormality
In conditions such as pulmonary agenesis and proximal interruption of the
pulmonary artery, herniation secondary to compensatory hyperination in the
contralateral lung and a unilateral hyperlucent lung occur.
In pulmonary artery sling, an aberrant course of the left pulmonary artery
may cause impingement of the right main bronchus that can lead to right-lung
air trapping and hyperination.
In Scimitar syndrome, also known as venolobar syndrome or hypogenetic
lung syndrome, a hyperlucent appearance occurs in the contralateral lung sec-
(e) Central Airway Abnormality
– Foreign Body Aspiration
– Foreign body aspiration is the most common cause of intraluminal airway
abnormalities in children aged 6months to 3years. Most of the aspirated
foreign bodies are nonradiopaque foodstuffs. The typical clinical picture is
acute cough and wheezing. Foreign body aspiration should also be suspected
in a child without a history of asthma presenting with recurrent lobar pneu-
monia. The radiographic appearance depends on the size, location, duration,
and nature of the aspirated material. Radiopaque foreign bodies can be eas-
ily identied on radiographs. Obstructive lobar or segmental hyperination
or atelectasis may be observed in the aspiration of a nonradiopaque foreign
body. Inspiration-expiratory radiographs are evaluated with uoroscopy to
better evaluate air trapping. In case of clinical suspicion, bronchoscopy and
CT can be performed if necessary. Foreign body can be directly identied

12 Radiologic Evaluation ofLower Respiratory System
163
with CT, as well as secondary changes such as retained secretions, hyper-
aeration, atelectasis, and consolidation.
– The right main bronchus is shorter and wider than the left, making a narrow
angle with the trachea; therefore, foreign bodies are more likely to escape
into the right main bronchus in children.
– Endobronchial Tumors
Endobronchial tumors are rare in the pediatric population but should be considered in the differential diagnosis when no other abnormality is present. This list
includes carcinoid tumor, papilloma, adenoid cystic carcinoma, mucoepidermoid carcinoma, myobroblastic tumor, and metastasis.
12.2.2 Fluoroscopy
Fluoroscopy can be used to evaluate dynamic large airway and lung abnormalities,
such as airway obstruction, air trapping, and diaphragmatic paralysis. Use of uoroscopic techniques and equipment should be optimized to minimize radiation
exposure.
Fluoroscopy, a dynamic method, is used to evaluate diaphragm movements and
mediastinal displacement in patients with air trapping, especially in cases of foreign
body aspirations. Paradoxical movement is investigated with uoroscopy in diaphragmatic paralysis or eventration. Nowadays, diaphragmatic movements are
often evaluated with ultrasound (US), especially in pediatric patients.
12.2.3 Ultrasound
Evaluation of the lungs with ultrasound is typically performed with the patient in
the supine or upright position. The lateral decubitus view or the supraclavicular and
suprasternal notch view may be benecial in some selected patients. Ultrasound is
a valuable and common imaging modality used in the evaluation of the thorax in
pediatric patients. It is easy to apply, cost-effective, noninvasive, and does not
expose patients to radiation. It has many advantages, such as being portable and
providing real-time imaging.
Lung and Mediastinum: US can be used to characterize lesions that present as
peripheral opacities on chest X-rays (atelectasis, consolidation, lung necrosis, lung
abscess, congenital lung lesions, and masses). Vascular structures in cases of pulmonary sequestration or blood ow in cases involving a neoplasm can also be evaluated with Color Doppler US (Fig.12.11).
Pleura: It indicates whether the opaque appearance on the chest X-ray is due to
pleural uid or parenchymal lesion. Additionally, ultrasound can visualize the internal debris, septations, and pleural thickening often associated with parapneumonic
collections (Fig.12.12).
It is used to determine whether the pleural effusion is loculated or free by positioning the patient and as a guide imaging method in interventional procedures such

164
ab
S. Taşar and R. Savaş
c
Fig. 12.11 In the US and Doppler US, examination performed while the patient is in the prone
position, sequestered lung tissue (star), whose systemic artery (arrow) is selected, is observed in
the posterobasal region of the left lung lower lobe (a, b). The presence of sequestered tissue (star)
and the feeding artery (arrow) was conrmed in the noncontrast coronal plan MRI performed with
mild sedation (c)
as thoracentesis. It may be more sensitive than radiography in the evaluation of
pneumothorax in supine patients [6]. CT is insufcient to differentiate between
pleural effusion and empyema. Effusion content and septa can be evaluated better
with ultrasonography. For this reason, it is necessary to evaluate with ultrasound
after a plain X-ray.
In the neonatal intensive care unit (NICU), lung ultrasound (LUS) can be used to
diagnose the etiology of neonatal respiratory distress. These diseases include HMD
(hyaline membrane disease), transient neonatal tachypnea, neonatal pneumonia,
pneumothorax, neonatal pulmonary atelectasis, and congenital anomalies
(Fig.12.13).
In Pneumothorax, the rst diagnostic method is plain radiography. However, an
anteriorly located pneumothorax may be difcult to detect in neonates or infants,
especially in the supine position. In the NICU, we can also use the US to detect
pneumothorax.

ab
12 Radiologic Evaluation ofLower Respiratory System
c
165
Fig. 12.12 Almost all of the right hemithorax is opaque in the chest X-ray, and the diaphragm line
and heart contour cannot be distinguished (a). In the US examination, dense pleural uid (arrowhead) compatible with empyema is observed adjacent to the consolidated lung tissue (star) and
visceral pleura (arrow) (b). In this complicated pneumonia patient, the empyema border cannot be
distinguished from the consolidated tissue in the noncontrast CT examination (c)
The change or disappearance of artifacts observed in normal lungs gives us clues
about some parenchymal diseases. Among these, “A lines” denote pleural reverberation artifacts, and “B lines” denote vertical short sheen. Normally, there are 2–3
B lines at most in each intercostal space. An increase in the B lines represents
increased alveolar or interstitial uid retention. We suspect pneumothorax if the B
lines converge and cast a shadow as a single beam, and we do not see the sliding
movement of the lung on the dynamic US (Fig.12.14).
12.2.4 Computed Tomography
CT is currently the most sensitive way of imaging the lungs due to its high spatial
resolution. With the widespread use of multidetector row CT scanners (MDCT),
there has been a signicant increase in the number of CT exams. As a result of rapid
technological developments in radiology, the duration of the examination has considerably shortened. Completing the exam within seconds is particularly important
in pediatric patients who may not be able to follow breath-hold commands.
Соседние файлы в папке Библиотека им академика М.И. Перельмана
