ABSTRACT
I. Introduction 454
II. Plain Radiography Findings 454
III. Computed Tomography Findings 455
A. CT Morphology of Emphysema/A1AD 455 B. Other CT Characteristics of Emphysema 456
C. CT Quantitation of Emphysema 457
D. CT Quantitation of Emphysema by
Densitometric Parameters 458
E. CT Monitoring of the Progress of
Emphysema 460
F. CT Findings in Small Airways
Disease 460
IV. Scintigraphy Findings 462
A. Lung Scintigraphy in Emphysema/A1AD 462 B. Radio-Aerosol Scintigraphy in Emphysema/A1AD 462 C. Drug Deposition 463
D. Mucociliary Clearance 465
E. DTPA Lung Clearance 466
V. Magnetic Resonance Imaging Findings 467
VI. Conclusion 468
References 468
I. Introduction
Anatomically, emphysema is defined as abnormal permanent enlargement of the
airspaces distal to the terminal bronchioles, accompanied by destruction of their
walls, without obvious fibrosis (1). The underlying cause of emphysema is
believed to be an imbalance in the activities of proteolytic and antiproteolytic
enzymes in the lung tissue, resulting in destructions of lung elastin and collagen.
Cigarette smoke has been shown to increase this destruction and is the major
cause of emphysema worldwide. Another cause is alpha-1 antitrypsin deficiency
(A1AD), which was discovered as a cause of emphysema in 1963 (2). This
enzyme normally inactivates the neutrophil elastase in the lung. Owing to
insufficient quantities of the enzyme, the abundance of activated neutrophil
elastase causes destruction of alveolar walls and panacinar emphysema with
lower lobe predominance. This is most typical in patients with homozygote
phenotype (PiZZ). The gene frequency in white individuals of this phenotype
varies among countries, but in the Scandinavian countries and the UK it is
2-3% (3).
