- •Chest Imaging
- •Foreword
- •Preface
- •Educational Support and Funding
- •Acknowledgments
- •Contents
- •Fundamentals > Chest Primer Presentation
- •Chest X-Ray Interpretation Self-Study Instructions
- •Using the RoboChest Website
- •Decision Tree Algorithms to Help Solidify Concepts
- •References
- •Comprehensive Review of Search Patterns
- •Search Pattern Mnemonic
- •Interpretive Approach to CXR
- •Applying the Mnemonic to the Search Pattern
- •Chest Primer Presentation
- •References
- •Introduction and Terminology
- •Chest Imaging Terminology
- •Mach Effect on CXR
- •Trachea and Lungs on CXR
- •Mediastinal Anatomy on CXR
- •The Hilum (Plural: Hila)
- •Pulmonary Arteries and Veins
- •Normal Lung Markings
- •Vessel Size
- •Quiz Yourself: Mediastinum Lines, Edges
- •Shoulder Anatomy
- •Reference
- •Abnormal Lung Parenchyma
- •Mass
- •Mass Considerations
- •Size
- •Mass Characteristics
- •Malignancy
- •Case 4.1
- •Metastatic
- •Case 4.2
- •Bronchial Carcinoid
- •Radiological Signs
- •Case 4.3
- •Granulomatous Disease
- •Infectious Granulomatous Disease
- •Case 4.4
- •Non-infectious Granulomatous Disease
- •Benign Neoplasm
- •Hamartoma
- •Case 4.6
- •Congenital Abnormality
- •Pulmonary Arteriovenous Malformations
- •Case 4.7
- •Consolidation
- •Consolidative Radiological Findings/Distribution
- •Consolidative Model
- •Blood (Hemorrhage)
- •Case 4.8
- •Pus (Exudate)
- •Case 4.9
- •Case 4.10
- •Water (Transudate)
- •Pulmonary Edema
- •Case 4.11
- •Case 4.12
- •Protein (Secretions)
- •Case 4.13 (see Figs. 4.38 and 4.39)
- •Cells (Malignancy)
- •Interstitial
- •Radiological Signs
- •Linear Form: Lines
- •Case 4.14
- •Nodular Form: Dots
- •Case 4.15
- •Reticulo-Nodular Form
- •Pneumoconiosis
- •Case 4.16
- •Case 4.17
- •Destructive Fibrotic Lung
- •Case 4.18
- •Langerhans Cell Histiocytosis
- •Case 4.19
- •Vascular Pattern
- •Normal Pulmonary Vascular Anatomic Review
- •Radiological Signs in the Vascular Pattern
- •Mechanism
- •Vascular Examples
- •Pulmonary Arterial Hypertension (PAH)
- •Case 4.20
- •Pulmonary Venous Congestion
- •Pulmonary Venous Congestion: Edema
- •Emphysema
- •Airway (Bronchial) Patterns
- •Complete Obstruction
- •Lobar Atelectasis (Collapse)
- •Signs
- •Lobar Atelectasis Patterns
- •Complete Obstruction: Case Study
- •Partial Obstruction
- •Radiological Signs
- •Bronchial Wall Thickening
- •Bronchial Wall Thickening Causes
- •Bronchial Wall Thickening Model
- •Bronchiolar
- •Case 4.21
- •References
- •Pleural Effusion
- •Case 5.1
- •Technique and Positioning Revisited
- •Case 5.2
- •Comparison of Effusions over Time
- •Loculated Fluid/Pseudotumor
- •Case 5.3
- •Case 5.4
- •Thickening
- •Pneumothorax
- •Fluid and Air
- •Analogous Model
- •References
- •Anterior Mediastinal Mass
- •Case 6.1
- •Middle Mediastinal Mass
- •Posterior Mediastinal Mass
- •Case 6.2
- •Mediastinal Enlargement
- •Case 6.3
- •Reference
- •Case 7.1
- •Lines and Tubes
- •References
- •Appendix
- •Appendix 1: Glossary and Abbreviations
- •Appendix 2: Sources and Additional References
- •Text Sources
- •Image Sources
- •Additional References
- •Chest Imaging References
- •Chest Imaging Online References
- •Index
Airway (Bronchial) Patterns |
89 |
Forms
•Complete airway obstruction: Opacity and decreased volume
•Partial obstruction: Lucency and increased volume
•Wall thickening: Tram tracks, central cystic spaces or circles
For the differential diagnosis, look for the following.
•Opacities: Endobronchial malignancies; granulomas; inflammatory, benign or congenital masses; mucous plugs; foreign bodies potentially causing complete obstruction
•Lucencies: Chronic obstructive pulmonary disease (COPD), cysts, blebs, pneumatoceles
•Thickening: Bronchiectasis, chronic bronchitis
Complete Obstruction
Obstruction of a bronchus or airway results in complete obstruction.
Radiological Signs
•Direct Signs: Displacement of interlobar fissures
•Indirect Signs: Opacification, mediastinal shift (ipsilateral), hilar displacement, elevation of hemidiaphragm, crowded vasculature, compensatory hyperinflation of unaffected lung, “shifting” granuloma sign and juxtaphrenic peak
The four main types of mechanisms of obstruction and resultant atelectasis are as
follows:
1.Resorptive/Obstructive: This type is caused by a complete bronchial obstruction. If there is no flow, then air becomes absorbed from the lung. Oxygen gets absorbed much more rapidly than ambient air. (E.g., a ventilator patient on 100% oxygen will collapse within minutes to hours.)
2.Passive/Compressive: This type is caused by extrinsic pressure from air, fluid, or mass (tumors, bullae, or abscesses). A large pleural fluid collection or pneumothorax could produce virtual complete collapse of the lobe.
3.Cicatricial: Areas of pulmonary fibrosis can cause reduced alveolar volume. It can be focal or diffuse. When focal, it is generally associated with old granulomatous infection, typically TB. However, it may be diffuse, as seen typically in idiopathic pulmonary fibrosis.
4.Adhesive: This type occurs in association with surfactant deficiency and subsequent microatelectasis. Type II pneumocytes can be injured from inhaled anesthetic agents, ischemia, or radiation, therefore, causes include general anesthesia, adult respiratory distress syndrome, hyaline membrane disease, and acute radiation pneumonits.