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At some time during the course of their disease, almost all patients develop a pleural effusion, and it is typically unilateral. Only 10% of patients develop bilateral effusions. The reported percentage of patients presenting with pleural effusion ranges from 30% to 80% (50). At initial presentation, the effusion may be too small to be detected on standard PA and lateral radiographs (50). These effusions may obscure underlying pleural thickening or masses until thoracentesis is performed (50).
Although mediastinal shift to the contralateral side is usually seen in association with massive pleural effusions, it is not a common finding in patients with MPM, which grows by encasing the lung and invading fissures and freezes the hemithorax. Instead, there may be evidence of volume loss on the affected side, with narrowing of the intercostal spaces, elevation of the hemidiaphragm, and ipsilateral shift of the mediastinum (Figure 13a). Alternatively, the mediastinum may be fixed in the midline; if the tumor bulk is massive, the mediastinum may be shifted toward the contralateral side (Figure 13b). Scoliosis with convexity away from the affected side may be present (12,50).
Diffuse, unilateral pleural thickening occurs in up to 60% of patients with MPM (Figure 14). Sheetlike or lobulated pleural thickening may encase the lung, grow into the fissures, and create a pleural rind. This thickened, fixed pleura can limit diaphragmatic excursion and mediastinal shift and thus may compromise ventilation of the lung (50).
Discrete pulmonary masses may be obscured by effusion in the early stages of the disease. Although solitary masses may occur, multiple masses are more common (Figure 15). The masses are typically large, with diameters of 5 cm or more, and they often invade the chest wall or mediastinum (50).
A hilar mass on the affected side may suggest spread of MPM to hilar lymph nodes but more likely represents direct extension of the tumor into the mediastinum. Similarly, mediastinal widening may represent direct tumor invasion or, less commonly, metastatic lymphadenopathy (50). Neoplastic involvement of the hilar and mediastinal lymph nodes is present in approximately 40%-45% of patients with MPM examined at autopsy (51).
Invasion of the chest wall occurs in far-advanced disease. Radiographically, it may manifest as periosteal reaction along the ribs, rib erosion, or complete rib destruction. Soft-tissue masses of the chest wall may be seen. Chest wall invasion is identified on chest radiographs in approximately 20% of cases (50).
Hematogenous metastases to the lung are very uncommon and manifest radiographically as multiple pulmonary nodules or masses (Figure 16). These parenchymal lung nodules may be difficult to distinguish from pleural masses or rounded atelectasis on chest radiographs. Diffuse lung involvement is very rare, and only one case report of MPM manifesting as diffuse, bilateral, miliary disease has been reported (46,50).
Rarely, lymphangitic spread may occur in advanced cases; it is visible on plain radiographs as a coarse, interstitial pattern. Diffuse, bilateral lymphangitic spread of MPM has been reported as the predominant radiographic finding in at least one case (49).
Extrathoracic lymph node groups are uncommon sites for the spread of MPM. Axillary and supraclavicular nodes, seen as soft-tissue masses on radiographs, are affected in less than 1% of patients. In addition, approximately 8% of patients have metastases to abdominal lymph nodes (51).
Massive hepatic calcifications shown on radiographs may result from dystrophic calcification within foci of metastatic malignant mesothelioma in the liver. This is a rare occurrence in patients with MPM, but in the two reported cases, the hepatic calcifications were identified before the primary pleural tumor (52).
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