Multiple Lucent Lesions

Infection

As in solitary cavities, infection is the most common cause of multiple pulmonary cavities (see Fig. 24.1 ). Acute pyogenic infections are radiologically characterized by areas of air space consolidation, a clinical course of elevated temperature, and often diagnostic laboratory findings, including elevation of the white blood cell (WBC) count with an associated shift to the left and positive sputum cultures. The development of multiple lucencies in the midst of an acute pneumonia (see Fig. 24.2, A and B ) is the expected appearance of necrotizing pneumonias. Peripheral cavities from necrotizing pneumonias and septic emboli are at high risk for rupture into the pleural space with bronchopleural fistulas causing pneumothorax. (Answer to question 1 is e .) Other causes of lucent spaces in the consolidations caused by pneumonia include the following: (1) resolution of the process with intervening normal lung; and (2) pneumatoceles. The pathogenesis of these processes was considered in Chapter 23 . Clinical correlation is extremely valuable in making this distinction. When the patient appears to be recovering from illness, the holes likely represent normal aerated lung or pneumatoceles. The radiologic observation of a round, sharply defined lucency with a discrete smooth wall suggests that the lucencies represent pneumatoceles. Ill-defined lucencies without a distinct margin are more typical of reaerated lung. The development of air-fluid levels in the midst of an area of consolidation indicates the development of spaces in the lung parenchyma that are most probably the result of tissue necrosis and abscess formation.

Air-fluid levels are not encountered in normally aerated lung or pneumatoceles; they are likely to appear when the patient is profoundly ill. In such cases, they are diagnostic of a virulent necrotizing pneumonia. The most common organisms to result in such a process include Staphylococcus, Klebsiella, Pseudomonas , anaerobes, and mixed gram-negative organisms ( Chart 24.2 ). (Answer to question 2 is d. ) As emphasized earlier, it is exceptional for pneumococcal pneumonia, Mycoplasma pneumonia, or viral pneumonias to cavitate, but cavitary Mycoplasma has been reported. 338, 540

Septic emboli ( Fig. 24.4, A and B ) are another cause of necrotizing pulmonary infection that may result from infection with some of the same organisms that cause necrotizing pneumonia, especially staphylococcus and, more recently, methicillin-resistant Staphylococcus aureus (MRSA). ⁴¹¹ Septic emboli may result from any cause of systemic sepsis. Bacterial endocarditis of the right heart is a complication of intravenous (IV) drug abuse that places the patient at high risk for MRSA septic emboli. ³¹² Other sources of septic emboli include long-term indwelling vascular lines, pacemaker wires, septic thrombophlebitis, and organ transplants. ⁴⁹¹

Tuberculous cavities may be distinctive with apical cavities and associated reticular or nodular scarring. The clinical findings and radiologic patterns of chronic tuberculosis are substantially different from that of the acute necrotizing pneumonias, but reactivation of tuberculosis may be more difficult to distinguish from a bacterial pneumonia and the air space consolidations may obscure the cavities on the chest radiograph ( Fig. 24.5, A - C ). Reactivation of tuberculosis may cause cavities, air space consolidations, and clusters of small nodules from transbronchial spread of the infection.

Histoplasmosis, blastomycosis, coccidioidomycosis, and tuberculosis are frequently radiologically indistinguishable. The chronic cavities from these granulomatous infections may be associated with considerable parenchymal reaction, but the parenchymal reaction is often a reticular or reticulonodular reaction and is usually distinctive when compared with the consolidations of acute necrotizing pneumonias (see Fig. 24.2, A and B ). The marked tendency to apical distribution is likewise characteristic but is not absolutely diagnostic of these infections. In tuberculosis and histoplasmosis, cavities may develop months to years after the primary infection. There is, however, a rare form of tuberculosis—primary progressive tuberculosis—in which there is progression from primary air space consolidation to cavitary tuberculosis over a short period without an asymptomatic interval between the two phases of the disease.

Blastomycosis and coccidioidomycosis, in contrast to histoplasmosis and tuberculosis, are more difficult to define in terms of primary and secondary disease. ⁴⁵⁰ The cavities of blastomycosis may be apical and mimic the appearance of postprimary tuberculosis, but the cavitation may occur during the acute alveolar exudative phase of the disease with an appearance more like that of a necrotizing pneumonia. The radiologic course of such cases of blastomycosis is more protracted than that of necrotizing pneumonia, and the clearing of the exudate sometimes requires 2 to 3 months. The clinical course is also more indolent than that of the necrotizing pneumonias, with characteristic low-grade temperatures.

Coccidioidomycosis (see Fig. 24.3 ) is known for producing very thin-walled cavities that may lack the surrounding parenchymal reaction that is expected in the other granulomatous infections. The radiologic presentation of thin-walled cavities occurs as a late sequela of the infection. (Answer to question 3 is c. ) In the early stages of the process, cavities may occur in areas of air space consolidation. This early acute cavitation results from central necrosis and liquefaction of parenchyma. As the infection is contained, there is organization with circumscription of the opacity. The radiologic sequence may thus be that of a process that begins with an air space consolidation followed by cavitation, leading to the appearance of a thick-walled cavity. When air is trapped in the cavity, it expands under tension. As the surrounding inflammatory response resolves, the characteristic thin-walled cavity appears. The cavities of coccidioidomycosis are also much less likely to follow the characteristic apical distribution of tuberculosis or histoplasmosis. The combination of a typical radiologic presentation of multiple thin-walled cavities and a definite history of exposure to Coccidioides , with positive serologic studies, frequently makes possible a precise diagnosis.

Neoplasms

Multiple cavities are not rare in patients with pulmonary metastases. This radiologic appearance makes the diagnosis of primary lung cancer less likely, but lucent cystic lesions have been described as so-called “pseudocavitation” and reported as a possible presentation of invasive mucinous adenocarcinoma of the lung. 621, 623 The diagnosis of metastasis is frequently aided by knowledge of a distant primary tumor. The typical radiologic appearance is that of sharply circumscribed multiple opacities with some having central lucencies ( Chart 24.3 ). These cavities frequently have thick nodular walls, although occasionally the wall may be very thin and smooth. Wall characteristics are not reliable for distinguishing metastases from other causes of multiple cavities. Approximately two-thirds of cavitating metastases are of the epidermoid variety. Squamous cell tumors of the head and neck, esophagus, and uterine cervix are best known for producing cavitary metastases, but as many as one-third of cavitary metastases may be from adenocarcinoma. Even malignant melanoma and osteosarcoma have been reported to cavitate. Lymphoma is an infrequent cause of cavitary pulmonary nodules. The exact pathologic mechanism for the cavitation of metastases is not always easily determined, but most cavitating metastases seem to represent tumors that have undergone central necrosis.