## 4 Acoustic Behavior of the Diseased Pleura  
The pleura and the lung are strictly linked and share many pathologic conditions. Inflammatory and hydrostatic edema can involve the thin layer of connective tissue underneath the mesothelial cells [29]. This tissue is continuous with the sub-pleural lung interstice. Therefore, a sub-pleural edema is highly interconnected with the underlying interstitial lung tissue. Pleural fibrosis can be the result of many inflammatory processes such as rheumatoid pleurisy, bacterial empyema, asbestos exposure, malignancy, retained hemothorax, and drugs. In all these situations, a clear separation between sub-mesothelial and superficial interstitial fibrosis is impossible [27]. The fibrotic remodeling in Idiopathic Pulmonary Fibrosis (IPF) begins in the basal sub-pleural regions and progresses toward the lung apices over time [30]. In patients with IPF, High Resolution CT (HRCT) scan morphometric analysis shows a complex and connected reticulum of fibrous tissue extending from the pleura into the underlying lung tissue (lobular fibrosis). Partially or completely scarred lobules, devoid of alveolar spaces, microcysts, honeycomb and fibroblast foci are features of IPF histopathology which determine a high disordered sub-pleural morphology [31; 32]. Based on the above premises, the difference between a healthy and a diseased pleura (in the hyperdense non-consolidated range of the lung pathology) resides in the presence of regions with different acoustic characteristics along the surface of the pleural plane, normally acting as an acoustic reflector. Because of this anatomic re-configuration, and in particular because of the presence of residual air spaces, local arrangements may exist where the energy of the acoustic pulses, which are transmitted by the probe, is partially trapped (acoustic traps) (Figure 3) [13; 28]. An acoustic trap is characterized by a transonic access (likely from 0.1 to 1 mm and beyond) to the sub-pleural enlarged interstitial tissue, with a variable shape and content (water, cells, and connective tissue), and that is surrounded by residual air. Such a volume is the core of the trap, since the multiple-scattering phenomena happening within the trap act as an ultrasound source and can explain the genesis of the vertical artifacts [28; 33]. A diseased pleura, covering a hyperdense non-consolidated lung, shows a variable number of irregularities and acoustic traps on its surface which are able to break its physiological acoustic reflectivity, thus generating and opening a variety of paths (channels) through which ultrasound can be captured. Finally, it is worth noting that when we speak of a distribution of structures with variable morphology and acoustic properties along a diseased pleura, we implicitly introduce a concept of relative order or disorder of these structures [31]. For example, we can consider as cases of relatively ordered patterns of acoustic traps the early pulmonary edema and the so-called white lung. Instead examples of pathologically disordered pleura, in terms of full and empty spaces, are likely represented by idiopathic pulmonary fibrosis, Adult Respiratory Distress Syndrome (ARDS) and other pathological conditions able to subvert the sub-pleural architecture [4; 28; 33] (Table 1). The distribution of air under the pleural plane in patients with early cardiogenic pulmonary edema is characterized by the presence of thickened but anatomically intact interlobular septa. In cardiogenic edema there is an expansion of the large interstitial connective tissue space caused by transudative fluid. This fluid may be confined to the large interstice and periarterial sheaths [29]. Therefore, interlobular septa enlargement can anticipate the expansion of alveolar wall interstitial space, and swollen connective tissue planes may be seen next to essentially normal alveoli.