Severe acute respiratory syndrome (SARS) is an infectious condition caused by the SARS-associated coronavirus (SARS-CoV), a new member in the family Coronaviridae. To evaluate the lung pathology in this life-threatening respiratory illness, we studied postmortem lung sections from 8 patients who died from SARS during the spring 2003 Singapore outbreak. The predominant pattern of lung injury in all 8 cases was diffuse alveolar damage. The histology varied according to the duration of illness. Cases of 10 or fewer days' duration demonstrated acute-phase diffuse alveolar damage (DAD), airspace edema, and bronchiolar fibrin. Cases of more than 10 days' duration exhibited organizing-phase DAD, type II pneumocyte hyperplasia, squamous metaplasia, multinucleated giant cells, and acute bronchopneumonia. In acute-phase DAD, pancytokeratin staining was positive in hyaline membranes along alveolar walls and highlighted the absence of pneumocytes. Multinucleated cells were shown to be both type II pneumocytes and macrophages by pancytokeratin, thyroid transcription factor-1, and CD68 staining. SARS-CoV RNA was identified by reverse transcriptase-polymerase chain reaction in 7 of 8 cases in fresh autopsy tissue and in 8 of 8 cases in formalin-fixed, paraffin-embedded lung tissue, including the 1 negative case in fresh tissue. Understanding the pathology of DAD in SARS patients may provide the basis for therapeutic strategies. Further studies of the pathogenesis of SARS may reveal new insight into the mechanisms of DAD.
Thin-section CT scores correlated with clinical and laboratory parameters in patients after SARS. Although ground-glass opacity and interstitial opacity resolve over time, air trapping persists.
Fibrosing mediastinitis is a rare benign disorder caused by proliferation of acellular collagen and fibrous tissue within the mediastinum. Although many cases are idiopathic, many (and perhaps most) cases in the United States are thought to be caused by an abnormal immunologic response to Histoplasma capsulatum infection. Affected patients are typically young and present with signs and symptoms of obstruction or compression of the superior vena cava, pulmonary veins or arteries, central airways, or esophagus. There may be two types of fibrosing mediastinitis: focal and diffuse. The focal type usually manifests on computed tomographic (CT) or magnetic resonance (MR) images as a localized, calcified mass in the paratracheal or subcarinal regions of the mediastinum or in the pulmonary hila. The diffuse type manifests on CT or MR images as a diffusely infiltrating, often noncalcified mass that affects multiple mediastinal compartments. CT and MR imaging play a vital role in the diagnosis and management of fibrosing mediastinitis.
Organization, characterized by fibroblast proliferation, is a common and nearly universal response to lung injury whether it is focal or diffuse. Despite the vast range of injurious agents, the lung's response to injury is quite limited, with a similar pattern of reaction seen radiologically and histologically regardless of the underlying cause. Although there is a tendency to divide organization into distinct entities, the underlying injury to the alveolar epithelial basement membrane is a uniting factor in these processes. This pattern of lung injury is seen in the organizing phase of diffuse alveolar damage, organizing pneumonia (OP), acute fibrinous and organizing pneumonia, and certain types of fibrotic lung disease. In addition, although organization can heal without significant injury, in some instances it progresses to fibrosis, which can be severe. When fibrosis due to organization is present, other histologic and imaging patterns, such as those seen in nonspecific interstitial pneumonia, can develop, reflecting that fibrosis can be a sequela of organization. This article reviews the histologic and radiologic findings of organization in lung injury due to diffuse alveolar damage, OP, and acute fibrinous and organizing pneumonia and helps radiologists understand that the histologic and radiologic findings depend on the degree of injury and the subsequent healing response.
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