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thickening, nodules, Kerley B lines, and pleural effusion can be additional findings seen in
association with pulmonary KS. Chest CT scans can demonstrate “flame shaped” nodules with a
halo of ground glass attenuationm, bronchial wall thickening and spiculated lesions with poorly
marginated nodular infiltrates radiating out from the hilum and from bronchovascular structures
into interlobular septae, and endobronchial lesions. Interlobular septal thickening can occur with
tumor invasion and lymphatic obstruction. Hilar lymphadenopathy tends to be seen as a late
finding. Gallium scans may help to distinguish KS from infections.[547,607]
A diagnosis of KS is suggested by the finding on fiberoptic bronchoscopy of raised,
cherry-red to violaceous macular to papular endobronchial lesions averaging several millimeters
in size. This finding is often regarded by experienced bronchoscopists as diagnostic, even in the
absence of histological support, and the vascular nature of KS can produce copious bleeding with
biopsy. Transbronchial biopsy is often nondiagnostic, because of the focal distribution of the
lesions, lack of endobronchial lesions, distal lesions, and the predominantly submucosal location
with subsequent sampling error, and because of the sparse amount of tissue obtained. Pleural
biopsy and pleural fluid cytology have a very poor yield for diagnosis of KS. The non-specific
finding of increased hemosiderin-laden macrophages in bronchoalveolar lavage fluid is
suggestive of KS. Open lung biopsy has a diagnostic yield of only 50% and is rarely performed
due to potential complications.[547,617]
Grossly at autopsy, KS lesions of lung appear as firm dark red to purple nodular areas,
most often surrounding large bronchi or blood vessels for a distance of 1 to 5 mm, or as
subpleural nodules. Up to 10% of lesions can be white or tan rather than red or purple. With
extensive involvement, the lesions may become almost confluent. Nodules of KS may also
appear on bronchial or tracheal mucosal surfaces.
Microscopically, KS in lung shows infiltrates of atypical spindle cells with endothelial-
lined, slit-like spaces containing red blood cells. The pattern of KS is infiltrative into the lung
parenchyma, and the lesions of KS also tend to surround blood vessels and bronchioles or form
subpleural nodules. Extravasated red blood cells, hemosiderin, plasma cells, and lymphocytes
may also be present. When accompanied by organizing pneumonia or diffuse alveolar damage,
KS may be difficult to diagnose, and cellular atypia helps to distinguish the lesions of KS from
inflammatory or reparative changes.

MALIGNANT LYMPHOMAS.-- Pulmonary non-Hodgkin lymphoma (NHL) in patients
with AIDS will have a similar gross and microscopic appearance as elsewhere. In most cases,
the lung is secondarily involved due to widespread dissemination. NHL limited to the lung in
AIDS is very uncommon and diagnosed when there is absence of mediastinal and/or hilar
lymphadenopathy and absence of extrathoracic extension. Such primary NHL’s of lung are
typically of a high grade B cell histologic type with demonstratable Epstein-Barr virus in tumor
cells. They are not usually accompanied by pleural effusions, but they may cavitate.[639] Thus,
in the absence of an infectious cause, the presence of multiple peripheral pulmonary nodules
and/or masses without hilar or mediastinal adenopathy and without pleural effusion suggests a
primary pulmonary NHL. The best diagnostic yield comes from use of percutaneous
transthoracic needle biopsy.[640]
Malignant lymphomas can have a bronchovascular distribution (where lymphatic vessels
are found), or less commonly they may present as one or more definable mass lesions. Rarely,
they may appear only as malignant effusions (primary body cavity-based lymphomas), without a
definable mass lesion.[570]