Transcutaneous contrast-enhanced sonography of peripheral lung lesions.

OBJECTIVE: Transpulmonary sonography contrast agents, in conjunction with contrast-specific imaging techniques, are increasingly accepted in clinical use for diagnostic imaging of several organs. Anatomically, the lung is characterized by dual blood sources, supplied from both the pulmonary and bronchial arteries. Contrast-enhanced sonography enables us to determine whether the pulmonary or the bronchial arteries are the source of blood to lung lesions, depending on the time to enhancement and the extent of enhancement after contrast agent application. CONCLUSION: This article reports our first experience with transcutaneous contrast-enhanced sonography for the diagnosis and differential diagnosis of peripheral lung lesions.

Contrast-enhanced sonography of the lung for differential diagnosis of atelectasis.

OBJECTIVE: Because of the absence of air in atelectatic tissue, sonography allows visualization of lung atelectasis and may characterize pulmonary and bronchial arterial vascularity by contrast-enhanced sonography (CES). METHODS: Thirty consecutive patients with obstructive atelectasis (OA) (n = 17) and compression atelectasis (n = 13) were retrospectively studied by CES using a second-generation sulfur hexafluoride contrast agent (SonoVue [BR1]; Bracco SpA, Milan, Italy). The following CES parameters were evaluated: (1) time to enhancement (TE) of the contrast agent after intravenous application was determined and classified as short TE and delayed TE (short TE, < or =6 seconds; versus delayed TE, >7 seconds); and (2) extent of enhancement (EE) was evaluated during the arterial phase (2-30 seconds) and the parenchymal phase (1-5 minutes): the EE of pleural lesions was determined in comparison with splenic enhancement and classified in reduced EE versus marked EE. RESULTS: All 13 patients with compression atelectasis had a short TE and a marked EE during arterial and parenchymal phases. In the remaining 17 patients with OA, 10 patients had a short TE and 7 patients had a delayed TE. The EE during both phases was reduced in 5 patients and marked in 3. Nine of 17 patients with OA had different EE during arterial and parenchymal phases. CONCLUSIONS: Compression atelectasis is characterized by CES with a short TE and a marked EE, indicating patent pulmonary arterial vascularization. In patients with OA, a variable CES pattern is found. With regard to only the TE, a delayed TE implies OA. This indicates a shifting of pulmonary vascularization to bronchial arterial vascularization in these patients.