Abstract

707 ocal or diffuse lesions of the central airways are produced by a variety of diseases. The etiology includes infection, malignancy, trauma, aspiration, collagen vascular disease, and idiopathic entities such as sarcoidosis, amyloidosis, or tracheopathia osteochondroplastica. Even though patients may present with significant symptomatology, these airway abnormalities are frequently not apparent or are overlooked on chest radiographs. Thus, diagnosis is often delayed. If there is a clinical or radiographic suspicion of tracheobronchial abnormality, further evaluation on CT is warranted. In particular, helical CT permits excellent multiplanar reconstructions, which are especially useful for surgical planning. This pictorial essay concentrates on CT techniques useful in central airway evaluation and on the diseases that cause focal airway abnormalities. We recognize that the distinction of focal and diffuse airway abnormalities is somewhat arbitrary and is complicated by the fact that many diseases can cause either focal or diffuse airway narrowing. For purposes of this review, however, we will discuss the diseases that most commonly affect the airway in a focal manner, and we will discuss the diseases that often result in long-segment or multifocal disease in a separate review. Imaging Techniques CT is the imaging modality of choice for radiologic evaluation of the central airways [1, 2]. Helical CT is preferred because it eliminates slice misregistration and respiratory motion artifacts, thus producing excellent axial images of tracheobronchial anatomy. Thin slices (2–3 mm) are preferred because weblike stenosis can easily be missed or underestimated with thicker slices. With single-detector row CT, a collimation of 2to 3-mm with a pitch of 1.5–2.0 is used, whereas with multidetector row CT, a 2.5mm collimation with an effective pitch of up to 6.0 is used with at least 30% overlap in reconstruction. Because a continuous volume data set Focal Abnormalities of the Trachea and Main Bronchi Edith M. Marom 1 , Philip C. Goodman, H. Page McAdams

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