Diseases that are primarily hematogenous in origin, such as miliary infections or hematogenous metasta-ses, give rise to nodules that are randomly distributed throughout the secondary lobule, with the greatest profusion in the lung bases (Fig 3). These patterns are clearly separate from nodules that result from inhalational disorders such as occur in patients with endobronchial spread of infection or hypersensitivity pneumonitis (HP), in which nodules are predominantly centrilobular in distribution, sparing the lobular periphery (Fig 4, 5).
This includes assessing a number of characteristics including whether nodules are as follows: uniform or variable in size; sharply or poorly marginated; solid or subsolid in density (so-called ground-glass opacities) [Fig 5]; or have a so-called tree-in-bud appearance (Fig 4). Additionally, nodules may either be calcified, as occurs in fungal disease, or cavitary, as is seen, for example, in patients with septic emboli, metastatic disease, or Langerhans cell histiocytosis (LCH). It should be emphasized that many of these characteristics are best evaluated on high-resolution CT scan images. With the introduction of multidetector CT scanners, it is now possible to routinely, prospectively reconstruct both thick and thin sections through the lungs after a single breathhold, provided that the initial data are acquired using appropriately thin collimation. This approach also enables the use of high-definition, multiplanar reconstructions, the use of which may be of value in further characterizing lung nodules.
The use of this algorithm begins by dividing CT scans into two broad arms based on the presence (group 1) or absence (group 2) of pleural or perifis-sural involvement (Table 1).
Figure 3. Random nodules. A diagrammatic representation of the characteristic distribution of randomly distributed nodules in patients with lymphohematogenous disease. Note that in distinction with patients having predominantly perilymphatic disease, random nodules may been seen adjacent to all secondary lobular structures. Some nodules may also appear to be attached to pulmonary arterial branches (so-called feeding vessels). Random nodules are most commonly due to metastatic disease, and may vary considerably in size and edge characteristics. The differential diagnosis most importantly includes miliary infection. Lym-phangitic carcinomatosis, while hematogenous in origin, is easily distinguished from random metastatic nodules by the presence of characteristically thickened interlobular septae, preferentially involving the lung bases, and usually associated with asymmetric hilar adenopathy and pleural effusions.
Figure 4. Bronchiolar disease. A diagrammatic representation of the typical appearance of bronchiolar inflammation resulting in so-called tree-in-bud opacities. These characteristically result in clusters of ill-defined nodules “attached” to adjacent branching or tubular structures due to extensive bronchiolar mucoid impaction. Most importantly, note that, unlike the situation in patients with either perilymphatic disease or random nodules, mucoid impacted bronchioles do not extend to the pleural, fissural, or septal surface. This pattern is nearly always due to infected secretions resulting from virtually any cause of acute or subacute bronchiolar infection.
Figure 5. Centrilobular disease. A diagrammatic representation of the distribution of diseases that predominantly affect the centrilobular portion of secondary lobules, excluding those diseases that result in predominantly mucoid impaction due to infected secretions. The most common cause of diffuse centri-lobular disease is subacute HP. This characteristically results in poorly defined, poorly marginated ground-glass opacities. Similar to tree-in-bud opacities, these rarely involve the pleural or fissural surfaces. While a number of different entities may result in predominantly centrilobular opacities, the differential diagnosis most often includes RB/RB-lLD. In distinction with subacute HP, RB in particular is less extensive, typically upper lobe in distribution, and almost always occurs in smokers.
Table 1—HRCT Algorithm for Multinodular Disease