Pleural lesions

The pleural membranes produce pleural fluid, which is resorbed through lymph channels in both layers. Increased production or diminished resorption leads to pathological accumulation of fluid in the pleural cavity. The pleural fluid may consist of clear transudate, serofibrinous exudate, blood or haemorrhagic effusion, or chylous exudate. With plain chest radiographs it is not possible to differentiate between the different types of pleural fluid. Pleurocentesis can be performed under guidance of imaging techniques. Pleural transudate is clear, yellow, and usually bilateral. The commonest cause of transudate is cardiac failure. Other causes may be chronic renal failure, hypoproteinaemia, or over-transfusion.

Exudates may be yellow-brown or purulent, and are caused by tuberculosis or other pulmonary or pleural infections, or by a subphrenic abscess. Other causes are lung cancer and systemic connective tissue diseases such as lupus erythematosus or rheumatoid arthritis. Blood in the pleural cavity can be caused by open or closed thoracic trauma, or haemorrhagic diseases with prolonged bleeding time. Blood-coloured pleural fluid may be found with pulmonary embolism and lung cancer. Chylothorax may be seen after thoracic trauma, or with obstruction of the thoracic duct or the bronchomediastinal lymph trunks because of malignant disease of infective conditions (filariasis).

In the upright position, small amounts of fluid will accumulate in the costophrenic angle, first posteriorly, then also laterally. The acute angle between the diaphragm and the chest wall is filled by an opacity, which, as the volume of fluid increases, gradually stretches up along the inside of the chest wall like a cloak (Fig. 27).
If one is uncertain whether there is fluid or only the remains of previous pleural pathology with pleural thickening, the diagnosis can be verified by taking a supplementary film. This is acquired with the patient in lateral decubitus position with the affected side down, and a horizontal x-ray beam (Fig. 28). Even small amounts of fluid drain by gravity along

Figure 27. Drawing of the phrenocostal sinus (cardiophrenic angle). Normal and pathological findings.

Figure 28. Standing and lateral decubitus views of the thorax.

the dependent chest wall and collect as a narrow band between the lateral chest wall and the lung. The breadth of the band of fluid increases when the film is exposed with the diaphragm elevated, i.e. on expiration. Pleural thickening may also give a band-shaped opacity in a lateral decubitus film, but the breadth of this opacity will be the same whether the patient is upright or lying down.

Large volumes of fluid may give massive opacities over the entire hemithorax, but usually some aerated lung tissue is visible at the apex. When this condition is unilateral, the mediastinum will be displaced towards the normal side, a sign that is useful in differentiating this opacity from that seen in total collapse of the lung (atelectasis) (Fig. 29 a, b).

Figure 29. Massive opacity over left hemithorax. a) Greater than normal proportion of the heart shadow is located to the right of the Vertebral column. Slight rightward displacement of the trachea. These findings indicate a left-sided expansion, as caused by a large left pleural effusion. b) The vertebral column is seen more clearly than normal along the right border of the mediastinum. The trachea is shifted to the left. This indicates left-sided reduction of volume, caused by atelectasis.

With total collapse, the mediastinum will be pulled towards the involved side. In the presence of bronchial cancer and simultaneous total collapse of the lung and large amounts of pleural fluid, the mediastinum may remain in the midline.

Sometimes pleural fluid may have a subpulmonary localization on upright films. On the left side this condition is readily recognized because of the increased distance between air in the stomach and the base of the lung. On the right side, the condition can be confused with an elevated diaphragm, as the upper surface of the accumulated fluid is misinterpreted as the diaphragm. Usually, the costophrenic angle will be rather round laterally and posteriorly and a lateral decubitus film may disclose large volumes of fluid.

The pleural fluid may also be loculated in closed pockets (loculi), which are formed by adhesions between the visceral and parietal pleura. Encapsulated fluid of this kind will not float freely on lateral decubitus films; consequently the diagnosis of fluid must be verified by CT scan or ultrasound. Thoracocentesis of loculated fluid can be guided by ultrasonography. Free pleural fluid flows into the fissures (Fig. 27) as a wedge-shaped opacity with the pointed end towards the hilum and the base peripherally. Encapsulated interlobar fluid also occurs. It usually assumes a biconvex lens shape using a tangential x-ray beam, but it may also be globular and be confused with a tumor. As the fluid is gradually

Figure 30. Empyema a) The right sinus is filled by an opacity that extends upward along the chest wall, and has an upward convex border. b) CT section at the thoracoabdominal transition showing right-sided empyema with gas bubbles. a

b

resorbed and the appearance returns to normal, this type of interlobar fluid has been called a "vanishing tumor".

In active infection with production of a large amount of pus, the pleural fluid not only flows passively up along the chest wall with a medially concave border, but may also bulge in towards the lung with a medially convex border (Figs. 27, 30 a, b). This leads one to suspect empyema, which may develop in connection with pneumonia or pulmonary abscess.

The empyema can break through the visceral pleura to communicate with aerated lung tissue and the bronchial tree. Communication like this may also occur when an infection in the lung breaks through the pleura from the lung side. The radiograph raises the suspicion of the presence of this type of bronchopleural fistula when air enters a fluid-containing

Figure 31. Development of pleural adhesions

pleural cavity, giving fluid levels in upright films, and the air is not resorbed but increases with time. When the empyema and fistula heal, a thickened pleura remains with adhesions, which may cause traction upon the heart and mediastinum. The diaphragm may be tethered upward and attached to the chest wall, with loss of diaphragmatic motion. Pleural thickening is often caused by infections and is an accompanying phenomenon in pulmonary tuberculosis. The thickening is often seen at the base, combined with adhesions in the costophrenic angle, which becomes shallow and right-angled (Fig. 31). The thickening can also be observed at the inferior extent of the fissures, where it produces linear thickening of the interlobar fissure. Tent-shaped basal opacities may represent pleural adhesions after earlier pleurisy. Above the apex of the lung, localized pleural thickening may occur, producing a downwardly concave half-moon-shaped opacity.

After tuberculous pleurisy, and after bleeding in the chest cavity, large calcified pleural plaques may be formed. In pneumoconiosis such as asbestosis, pleural thickening is also a common phenomenon, and thin, well-defined stripes of calcium in the basal part of the chest wall along the dome of the diaphragm may also be found. Calcification and pleural thickening of this kind are best seen in the tangential projection, and radiographs of the lung may be supplemented by oblique films with this type of problem. The optimal method for displaying pleural plaques and calcification is by CT.

Figure 32. Pneumothorax. A 2-3 cm broad air cap has developed after fine needle puncture of tumor (T). The arrows show the surface of the lung.

Extensive nodular pleural thickening is seen with mesothelioma, a malignant pleural tumor which occurs in connection with long-lasting exposure to asbestos. Mesothelioma often gives rise to hemorrhagic pleural fluid, which can mask the pleural tumor. Air in the pleural cavity, pneumothorax (Fig. 32), may arise spontaneously, as a result of rupture of small subpleural emphysematous cysts or larger emphysematous bullae. Air in the pleural cavity will usually be seen as a narrow, dark zone with no vascular markings along the chest wall. In check valve pneumothorax, pressure in the pleural cavity progressively increases, causing progressive collapse of the lung with contralateral mediastinal shift.

When there are adhesions, the air may be confined to encapsulated loculi, and the adhesions may partly or completely prevent collapse of the lung. CT is very useful for localizing small bullae and limited pneumothorax. Pneumothorax may also occur as a result of penetration of the chest wall, for example during tapping of pleural fluid, or after needle biopsy of lung tumors. Damage to air-filled organs in the mediastinum,

Figure 33. Stripe along the lateral chest wall (arrows) resembles pneumothorax, but some scanty vascular markings are seen peripheral to the stripe. Repeat x-ray after change in position showed normal fin dings. The stripe had been caused by a skin fold.

or damage to the diaphragm combined with rupture of part of the intestinal tract may also give rise to pneumothorax.

A very large emphysema bulla, which takes up most of the chest cavity, may be confused with a pneumothorax. Puncture of this type of bulla in order to drain it may give the patient a true pneumothorax. A small rim of air around the lung may be difficult to discover, especially in overexposed (dark) film. Expiratory films are taken routinely when pneumothorax is suspected.

In bedridden patients, who have lost weight in connection with their disease, skin folds that run parallel to the chest wall may easily be confused with pneumothorax (Fig. 33). By examining the film in bright light, it is possible to trace vascular patterns peripherally to the line caused by the skin fold, or to see that the skin fold extends outside the thorax. When in doubt, a repeat film should be performed as the lines formed by the skin folds are not reproduced after the patient has changed position.

Most cases of pneumothorax show spontaneous regression, but the patients must be checked clinically and radiologically so that a thoracic tube with suction can be introduced if the condition progresses because of a check valve mechanism, or if spontaneous improvement does not occur. In pneumothorax in a patient with pleural fluid, upright films will show a horizontal fluid level, as a sign of hydropneumothorax. When the lung is adherent to the chest wall laterally, a fluid level may be the sign that discloses the presence of pneumothorax (Fig. 34).

Figure 34. Horizontal fluid level in the right thoracic cavity (open arrow) shows that both pleural fluid and pneumothorax (hydropneumothorax) must be present. The mediastinum is pulled to the right because of atelectasis of the lower lobe. Pericardial calcification (closed arrow) after pericarditis.

Figure 35. A mass anteriorly and cranially in the mediastinum caused by calcified retrosternal goiter (s).

Alf Kolbenstvedt, Arnulf Skjennald and Charles B. Higgins