CONVENTIONAL CHEST RADIOGRAPHY

The views of the chest most frequently performed in the ambulant patient are the erect posteroanterior (PA) and lateral projections, taken with the patient breath-holding at total lung capacity. While portable or mobile chest radiography, as undertaken on an ICU, has the obvious advantage that the examination can be done without moving the patient from the ward, there are many disadvantages. These include:

DIGITAL CHEST RADIOLOGY

In the ICU, digital chest radiographs may be obtained utilising conventional X-ray generators, but the image is captured on a reusable photostimulable plate instead of conventional film. The digital information is then manipulated, displayed and stored in whatever format is desired. Traditional systems suffer greatly from the large day-to-day variations in the density of the radiograph due to small differences in exposure. Digital radiographic systems are able to capture and display a standard density image from a much wider range of exposures (Figure 35.1).

Figure 35.1 Digital radiograph. The image has been edge-enhanced, which makes the multiple chest drains, Swan–Ganz catheter and endotracheal tube position more conspicuous. Note that two of the chest drain side holes lie within the soft tissues of the chest wall (arrows).

COMPUTED TOMOGRAPHY

CT relies on differing absorption of X-rays by tissues with constituents of differing atomic number, so slight differences in X-ray absorption can be interpreted to produce a cross-sectional image. The components of a CT scanner are an X-ray tube, which rotates around the patient, and an array of X-ray detectors opposite the tube. The speed with which a CT scanner acquires an image depends upon the time it takes to rotate the anode around the patient. Modern CT machines have tube rotation times of as little as 0.33 seconds.

Spiral (also known as volume or helical) scanning entails sustained patient exposure by the rotating X-ray tube during continuous movement of the examination couch through the CT gantry aperture. In this way a continuous data set or ‘spiral’ of information may be acquired in a single breath-hold. The information is reconstructed into axial sections, perpendicular to the long axis of the patient, identical to conventional CT sections. Three-dimensional reconstructions of complex anatomical areas can also be produced.

When short rotation times are coupled with the ability to acquire multiple spirals simultaneously (currently up to 64 slices), the speed of these systems is now so great that breath-holding or suspended ventilation is no longer necessary for high-quality imaging. Furthermore, the detector thickness that determines the minimum slice width of the reconstructed images is now commonly less than 1 mm. Thus a 64-channel scanner can acquire almost 200 submillimetre images per second.

CLINICAL APPLICATIONS OF HRCT IN THE ICU PATIENT

HRCT is increasingly being used to confirm the impression of an abnormality seen on a chest radiograph. HRCT may also be used to achieve a histospecific diagnosis in some patients with obvious but non-specific radiographic abnormalities. Furthermore, HRCT has provided a number of useful insights into chest disease in the severely ill patient in an ICU setting.

HRCT in uncomplicated acute respiratory distress syndrome (ARDS):¹

• reveals that the apparently homogeneous opacification apparent on the chest radiograph has an anterior-to-posterior graded increase in density – an appearance referred to as a gravitational gradient (Figure 35.2)

• demonstrates early dilatation of the smaller airways within areas of ground-glass density, an appearance that suggests development of fibrosis, and may prompt anti-inflammatory treatment

• demonstrates that a shift from the supine to the prone position results in redistribution of the previously dependent dense parenchymal opacification to the now dependent anterior lung, a phenomenon that may be accompanied by improvements in patient oxygenation

Figure 35.2 Computed tomography of a patient with acute respiratory distress syndrome. Note the marked anterior-to-posterior density gradient. The anterior lung is of almost normal density, becoming of ground-glass attenuation in the mid-part of the lung before fading into consolidation posteriorly. There are also moderate-sized bilateral pleural effusions.

HRCT of complications of ARDS2,3

• Infection is common in ARDS. Diagnosis may be difficult. Radiographically there may be a lack of specific findings, often due to superimposition of changes attributable to ARDS. This is a particular problem in the critically ill patient when the usual indicators of pneumonia are also unreliable. Although the diagnosis may still be in question following HRCT, associated pneumonic changes such as abscess formation, empyema and mediastinal disease, as well as development of non-dependent areas of consolidation, are all useful pointers to superadded infection (see Figure 35.2).

• Barotrauma – mediastinal and interstitial emphysema, as well as pneumothorax, are all increasingly common at higher levels of peak end-expiratory pressure (PEEP). The incidence of barotrauma has been reported to be as high as 50%.

• HRCT delineates early change and allows exact location of loculated air collections to be defined.

THE MEDIASTINUM, CENTRAL AIRWAYS AND HILAR STRUCTURES

Appreciation of abnormality requires a sound grasp of normal radiological anatomy. The mediastinum is delimited by the lungs on either side, the thoracic inlet above, the diaphragm below and the vertebral column posteriorly. Because the various structures that make up the mediastinum are superimposed on each other on the chest radiograph, they cannot be separately identified. Nevertheless, because a chest radiograph is usually the first imaging investigation, it is necessary to have an appreciation of the normal appearances of the mediastinum, together with variations due to the patient’s body habitus and age. Key points include:

THE PULMONARY FISSURES, VESSELS AND BRONCHI

The two lungs are separated by the four layers of pleura behind and in front of the mediastinum. The resulting posterior and anterior junction lines are often visible on chest radiographs as nearly vertical stripes, the posterior junction line lying higher than the anterior. The junction lines are not invariably seen and their presence or absence is not usually of significance (Figure 35.3).

Figure 35.3 (a) Close-up of the mediastinum of a patient in whom both the anterior and posterior junction lines are evident. The anterior junction line is more inferior and slants from right to left (short arrows), whereas the posterior junction line is more vertical, superior and is delineated by the arrowheads. (b) Computed tomography scan through the upper mediastinum demonstrating the anterior (arrowheads) and posterior (arrows) junction lines in a different patient.

The upper and lower lobes of the left lung are separated by the major (or oblique) fissure. The upper, middle and lower lobes of the right lung are separated by the major fissure and the minor (horizontal or transverse) fissure. The minor fissure is visible in over half of normal PA chest radiographs. The major fissures are not visible on a frontal radiograph and are inconstantly identifiable on lateral radiographs. In a few individuals, fissures are incompletely developed; a point familiar to thoracic surgeons performing a lobectomy, because of incomplete cleavage between lobes. Accessory fissures are occasionally seen.

All of the branching structures seen within normal lungs on a chest radiograph represent pulmonary arteries or veins. It is often impossible to distinguish arteries from veins in the lung periphery. On a chest radiograph taken in the erect position, there is a gradual increase in the diameter of the vessels, at equidistant points from the hilum, travelling from lung apex to base; this gravity-dependent effect disappears if the patient is supine or in cardiac failure.

THE DIAPHRAGM AND THORACIC CAGE

The interface between aerated lung and the hemidiaphragms is sharp and the highest point of each dome is normally medial to the mid-clavicular line. The right dome of the diaphragm is higher than the left by up to 2 cm in the erect position unless the left dome is elevated by air in the stomach (Figure 35.4).

Figure 35.4 Erect chest radiograph of a patient with a pneumoperitoneum demonstrating the normal thickness in position of the hemidiaphragms. The right lies slightly higher than the left.

Filling-in or blunting of these costophrenic angles usually represents pleural disease, either pleural thickening or an effusion.

POSITIONING OF TUBES AND LINES⁴

CENTRAL VENOUS CATHETERS (CVC)

The end of a CVC needs to be intrathoracic, and is ideally in the superior vena cava. CVCs may be introduced via an antecubital, subclavian or jugular vein. Subclavian venous puncture carries a risk of pneumothorax and mediastinal hematoma. Rarely, perforation of the subclavian vein leads to fluid collecting in the mediastinum or pleura. All catheters have a potential risk of coiling, misplacement, knotting and fracture (Figure 35.5). The tip should not abut the vessel wall at an obtuse angle.

Figure 35.5 Intensive care unit patient with multiple tubes and lines in place. The endotracheal tube tip position is satisfactory, and there are sternotomy wires, an intra-aortic balloon pump (radiopaque tip) and a prosthetic heart valve. The central line inserted into the left internal jugular vein passes into the right internal jugular vein. The Swan–Ganz catheter, which has been inserted via the right internal jugular vein, loops into the left brachiocephalic vein, before taking a satisfactory course through the cardiac chambers (black arrows).

NASOGASTRIC TUBES

These should reach the stomach but may coil in the oesophagus or occasionally are inserted into the tracheobronchial tree (Figure 35.6).

Figure 35.6 Misplaced nasogastric tube. (a) The tip of the tube is in the bronchus intermedius. (b) The tube is looped in the oesophagus (black arrowheads) before passing into the trachea, as demonstrated on this lateral spine view. Note the anterior wedge fracture of C5. (c) The tube is coiled in the oesophagus without passing into the stomach. Note the bullet projected over the left upper zone and the adequately positioned Swan–Ganz catheter (white arrow).

ENDOTRACHEAL TUBES

Extension and flexion of the neck may make the tip of an endotracheal tube move by as much as 5 cm. With the neck in neutral position the tip of the tube should ideally be about 5–6 cm above the carina. A tube that is inserted too far usually passes into the right bronchus, with the risk of non-ventilation or collapse of the left lung (Figure 35.7).

Figure 35.7 Endotracheal tube inserted into the right main bronchus as demonstrated on computed tomography. This image, obtained in expiration, demonstrates air trapping in the left lung.

PLEURAL TUBES

These are used to treat pleural effusions and pneumothoraces. A radiopaque line usually runs along pleural tubes, and is interrupted where there are side holes. It is important to check that all the side holes are within the thorax. Tracks may remain on the chest X-ray following removal of chest tubes, causing tubular or ring shadows. When doubt remains about tube position, then CT scanning should be considered (Figure 35.1 and 35.8).

Figure 35.8 Computed tomography scan demonstrating loculated pneumothoraces in a patient with acute lung injury. The posteromedial pneumothorax on the left is not being drained by the multiple chest tubes.

INTRA-AORTIC BALLOON PUMP

These are used in patients with cardiogenic shock, often following cardiac surgery. The ideal position of the catheter tip is just distal to the origin of the left subclavian artery (Figure 35.9). If the catheter tip is advanced too far it may occlude the left subclavian artery, and if it is too distal the balloon may occlude branches of the abdominal aorta. The intra-aortic balloon pump may only be visible by its radiopaque tip (see Figure 35.5).

Figure 35.9 Intra-aortic balloon pump. Two chest radiographs in the same patient demonstrating the balloon pump during the inflated (a) and deflated (b) phases. The tip of this balloon pump will be impinging upon the origin of the left subclavian artery and is slightly too high.

PACEMAKERS

These may be permanent or temporary (Figure 35.10). Temporary epicardial wires are sometimes inserted during cardiac surgery, and may be seen as thin, almost hair-like metallic opacities overlying the heart. Temporary pacing electrodes are usually inserted transvenously via a subclavian or jugular vein. If a patient is not pacing properly, a chest X-ray may reveal that the position of the electrode tip is unstable, or a fracture in the wire may be seen.

Figure 35.10 There is a fracture in the now redundant pacing wire on the right side. The functioning pacing wire is sharply kinked as it passes over the first rib and is at increased risk of subsequent fracture.

CONSOLIDATION

Consolidation, or synonymously air space shadowing, is due to opacification of the air-containing spaces of the lung, usually without a change in volume of the affected area. It is not possible to tell what the air space filling is due to in the absence of a clinical history, except perhaps for shadowing due to cardiogenic alveolar oedema, when there will be associated signs of cardiac failure. Typical features of all forms of consolidation (Figure 35.11) include:

Figure 35.11 Close-up view of an area of consolidation adjacent to the right heart border, which is obscured. Air bronchograms can be identified passing through this area. A chest tube is in situ.

When an area of consolidation undergoes necrosis, either due to infection or infarction, then liquefaction may result, and if there is either a gas-forming organism or communication with the bronchial tree, then an air–fluid level may develop in addition to cavity formation.

COLLAPSE

When there is partial or complete volume loss in a lung or lobe this is referred to as collapse or atelectasis, implying a diminished volume of air in the lung with associated reduction of lung volume. There are several different mechanisms for lung or lobar collapse, for example relaxation or passive collapse, when fluid or air accumulates in the pleural space, cicatrisation collapse when volume loss is associated with pulmonary fibrosis, adhesive collapse as in ARDS, or resorption collapse, as in bronchial obstruction.

The radiographic appearance in pulmonary collapse depends upon a number of factors. These include the mechanism of collapse, the extent of collapse, the presence or absence of consolidation in the affected lung and the pre-existing state of the pleura. This latter factor includes the presence of underlying pleural tethering or thickening and the presence of pleural fluid.

The direct signs of collapse include:

The indirect signs of collapse include:

COMPLETE LUNG COLLAPSE

Complete collapse (Figure 35.12) will cause complete opacification of the hemithorax, with displacement of the mediastinum to the affected side and elevation of the hemidiaphragm. Compensatory hyperinflation of the contralateral lung with herniation across the midline may be apparent. Herniation may occur in the retrosternal space, anterior to the ascending aorta, or may be posterior to the heart.

Figure 35.12 Complete lung collapse. The left hemithorax is opaque and the mediastinum has shifted to that side, together with deviation of the trachea. There was an obstructing tumour in the left main stem bronchus.

INDIVIDUAL OR COMBINED LOBAR COLLAPSE

In any situation, some or all of the signs may be present.

Right upper lobe collapse(Figure 35.13)

• horizontal fissure moves upwards and medially towards the superior mediastinum

• trachea deviates to the right

• compensatory hyperinfiation of the right middle and lower lobes

Figure 35.13 Right upper lobe collapse. The horizontal fissure has become elevated and the right upper lobe has become a wedge-shaped density extending from the hilum to the right lung apex. There is evidence of volume loss with shift of the trachea to the right side.

Middle lobe collapse(Figure 35.14)

• horizontal fissure and lower half of the oblique fissure move towards each other – best seen on the lateral projection

• frontal radiograph changes may be subtle, with obscuration of the right heart border

• indirect signs of volume loss are rarely obvious

Figure 35.14 Middle lobe collapse. The horizontal fissure is depressed and demarcates the collapsed middle lobe as a wedge-shaped density best demonstrated on the lateral (arrows).

Right lower lobe collapse

• partial depression of the horizontal fissure

• triangular opacity of the collapsed lower lobe on the frontal projection, usually obscuring the diaphragm but preserving the right heart border

• eventually a completely collapsed lower lobe may be so small that it flattens and merges with the mediastinum, producing a thin, wedge-shaped shadow

Left lower lobe collapse(Figure 35.15)

• collapsed lobe may be obscured by the heart and a penetrated view may be required

• mediastinal structures and the diaphragm adjacent to the non-aerated lobe are obscured

• extreme volume loss may cause the lobe to be so small as to be invisible as a separate opacity

• loss of lower lobe artery silhouette at the hilum

Figure 35.15 Left lower lobe collapse. The left lower lobe has become a wedge-shaped density behind the heart forming a double left heart border (arrows). The left hilar vessel to the lower lobe has disappeared as a result of collapse.

Lingula collapse

• often involved in collapse of the left upper lobe

• may collapse individually

• radiographic features are similar to those of middle lobe collapse

Left upper lobe collapse (Figure 35.16)

• Lateral view demonstrates anterior displacement of the entire oblique fissure, oriented almost parallel to the anterior chest wall, demarcating the posterior surface of the upper lobe as an elongated opacity extending from the apex almost reaching the diaphragm and lying anterior to the hilum.

• Eventually the upper lobe retracts posteriorly and loses contact with the anterior chest wall.

• Frontal radiograph demonstrates an ill-defined hazy opacity in the upper, mid and sometimes lower zones, with loss of hilar clarity.

• Hilum is often elevated, and the trachea deviated to the left.

Figure 35.16 Left upper lobe collapse. A hazy opacity extends from the hilum towards the left lung apex. It is sharply demarcated inferiorly and laterally (white arrows) due to the presence of a large tumour at the left hilum which is obstructing the left upper lobe bronchus. Note the signs of volume loss, particularly the elevation of the left hemidiaphragm.

UNILATERAL INCREASED TRANSRADIANCY

The commonest causes are technical and include:

Pathological causes include:

When there is relative increased transradiancy of one hemithorax for which there is no obvious cause then the possibility of generalised increase in radiopacity of the opposite side should be considered – for example, the posterior layering of a pleural effusion in a supine patient. Usually hypertransradiancy due to technical factors can be identified by comparison of the soft tissues around the shoulder girdle, and particularly over the axillae.

ABNORMALITIES OF THE MEDIASTINUM

Pneumomediastinum or mediastinal emphysema is the presence of air between the tissue planes of the mediastinum (see section on injuries to the mediastinum, below). Chest radiography may show vertical translucent streaks in the mediastinum, representing air separating the soft-tissue planes. The air may extend up into the neck and over the chest wall, causing subcutaneous emphysema, and also over the diaphragm. The mediastinal pleura may be displaced laterally and then be visible as a thin stripe alongside the mediastinum.

Acute mediastinitis is usually due to perforation of the oesophagus, pharynx or trachea and chest radiograph usually shows widening of the mediastinum and pneumomediastinum.

Mediastinal haemorrhage may occur from venous or arterial bleeding (Figure 35.17). The mediastinum appears widened, and blood may be seen tracking over the lung apices. It is imperative to identify a life-threatening cause such as aortic rupture.

Figure 35.17 Aortic rupture. (a) There is opacification of the left hemithorax due to a large haemothorax which is layering posteriorly in this supine patient. There is widening of the mediastinum due to mediastinal haemorrhage. (b) Arch aortogram demonstrating widening of the descending thoracic aorta due to the aortic wall rupture. The point of return to normal calibre is demarcated by the arrows. (c) Computed tomography angiography of a different patient demonstrating a penetrating ulcer resulting in an aorto-oesophageal fistula that caused massive haematemesis. Note the local irregularity in the otherwise smooth anterior aortic wall on this oblique sagittal reformat.

PLEURAL FLUID

The most dependent recess of the pleural space is the posterior costophrenic angle and this is where a small effusion will tend to collect. As little as a few millilitres of fluid may be detected using decubitus views with a horizontal beam, ultrasound or CT. Larger volumes of fluid eventually fill in the costophrenic angle on the frontal view, and with increasing fluid a homogeneous opacity spreads upwards, obscuring the lung base (Figure 35.18). The fluid usually demonstrates a concave upper edge, higher laterally than medially, and obscures the diaphragm. Fluid may track into the fissures. A massive effusion may cause complete opacification of a hemithorax with passive atelectasis. The space-occupying effect of the effusion may push the mediastinum towards the opposite side, especially when the lung does not collapse significantly. Effusions in a supine patient redistribute into the paravertebral sulcus and produce an even increased density throughout that hemithorax.

Figure 35.18 A large right pleural effusion is present in this patient. There is a typical configuration of its upper border, a meniscus extending up the lateral chest wall.

Lamellar effusions are shallow collections between the lung surface and the visceral pleura, sometimes sparing the costophrenic angle, and occur early in heart failure.

Subpulmonary effusions accumulate between the diaphragm and undersurface of a lung, mimicking elevation of the hemidiaphragm, altering the diaphragmatic contour so the apex moves more laterally than usual. When left-sided, there is increased distance between the gastric air bubble and lung base.

Fluid may become loculated in the interlobar fissures and is most frequently seen in heart failure. Loculated interlobar effusions may disappear rapidly and are sometimes known as pulmonary pseudotumours.

Differentiation between a simple effusion and a complicated parapneumonic effusion or an empyema usually requires thoracentesis. Loculation is best demonstrated with ultrasound.

PNEUMOTHORAX

In an erect patient, air will usually collect at the apex (Figure 35.19). The lung retracts towards the hilum and on a frontal chest film the sharp white line of the visceral pleura will be visible, separated from the chest wall by the radiolucent pleural space, which is devoid of lung markings. This should not be confused with a skin fold, which mostly occurs in supine or recumbent patients. The lung usually remains aerated, although perfusion is reduced in proportion to ventilation and therefore the radiodensity of the partially collapsed lung remains relatively normal. A large pneumothorax may lead to complete retraction of the lung, with some mediastinal shift towards the normal side. Because it is a medical emergency, tension pneumothorax is often treated before a chest radiograph is obtained. However, if a radiograph is taken in this situation it will show marked displacement of the mediastinum. Radiographically the lung may be squashed against the mediastinum, or herniate across the midline, and the ipsilateral hemidiaphragm may be depressed. A supine pneumothorax may produce increased transradiancy towards the diaphragm, and a deep sulcus sign.

Figure 35.19 Pneumothorax. (a) This patient, with underlying lung abnormality, has developed a pneumothorax. The fine white line that represents the visceral pleura delineates the edge of the lung. (b) Close-up of the pleural line. Note how there are no vascular markings beyond this point.

COMPLICATIONS OF PNEUMOTHORAX

Pleural adhesions may limit the distribution of a pneumothorax and result in a loculated or encysted pneumothorax (see Figure 35.8). The usual appearance is an ovoid air collection adjacent to the chest wall, and it may be radiographically indistinguishable from a thin-walled subpleural pulmonary cyst or bulla. Pleural adhesions are occasionally seen as line shadows stretching between the two pleural layers, preventing relaxation of the underlying lung. Rupture of an adhesion may produce a haemopneumothorax. Collapse or consolidation of a lobe or lung in association with a pneumothorax is important because they may delay re-expansion of the lung.

Since the normal pleural space contains a small volume of fluid, blunting of the costophrenic angle by a short fluid level is commonly seen in a pneumothorax. In a small pneumothorax this fluid level may be the most obvious radiological sign. A larger fluid level usually signifies a complication and represents exudate, pus or blood, depending on the aetiology of the pneumothorax. A hydropneumothorax is a pneumothorax containing a significant amount of fluid (Figure 35.20). On a radiograph obtained with a horizontal beam, a fluid level is evident. A hydro- or pyopneumothorax may arise as a result of a bronchopleural fistula, and may be a complication of surgery, tumour or infection.

Figure 35.20 Hydropneumothorax developing in a patient who has had a previous pneumonectomy on the right for carcinoma. Spontaneous development of a bronchopleural fistula has occurred.

PULMONARY EMBOLISM

CT diagnosis of pulmonary embolism is becoming routinely available, and depends upon the ability to acquire, within a single breath-hold, a volume of data large enough to include the entire thorax. This rapid acquisition allows excellent contrast opacification of the pulmonary arterial tree for the duration of the scan, revealing any thrombus within the central pulmonary vessels (Figure 35.21). There are numerous studies evaluating helical and electron beam CT in the diagnosis of acute pulmonary embolus, with excellent reported sensitivity and specificity for the detection of clot down to the segmental level.^5–8 Most of these studies also allow other diagnoses to be made that explain the symptoms of chest pain or dyspnoea, even when no pulmonary embolism is present.

Figure 35.21 (a) Large pulmonary embolus in the right lower lobe pulmonary artery demonstrated by spiral computed tomography scanning. Both pulmonary arteries are outlined by contrast except for the embolus itself. (b) Coronal reformat in the same case, domonstrating thrombus in the lower lobe artery.

SKELETAL INJURY⁹

Following trauma rib fractures are common and may be single, multiple, unilateral or bilateral. In cases of chest trauma, the chest X-ray is more important in detecting a complication of rib fracture than the fracture itself. Fracture of one of the first three ribs is often associated with major intrathoracic injury, and fracture of the lower three ribs may be associated with important hepatic, splenic or renal injury. Complications of rib fracture include a flail segment, pneumothorax, haemothorax and subcutaneous emphysema. A flail segment is usually apparent clinically and radiologically. The fractured ends of ribs may penetrate underlying pleura and lung and cause a pneumothorax, haemothorax, haemopneumothorax or intrapulmonary haemorrhage. Air may also escape into the chest wall and cause subcutaneous emphysema. Fractures of the sternum usually require a lateral film or CT for visualisation. Fractures of the thoracic spine may be associated with a paraspinal shadow, which represents haematoma. Fractures of the clavicle may be associated with injury to the subclavian vessels or brachial plexus, and posterior dislocation of the clavicle at the sternoclavicular joint may cause injury to the trachea, oesophagus, great vessels or nerves of the superior mediastinum.

DIAPHRAGMATIC INJURY¹⁰

Laceration of the diaphragm may result from penetrating or non-penetrating trauma to the chest or abdomen. Rupture of the left hemidiaphragm is encountered more frequently in clinical practice than rupture on the right (Figure 35.22). The typical plain film appearance is of obscuration of the affected hemidiaphragm and increased shadowing in the ipsilateral hemithorax due to herniation of stomach, omentum, bowel or solid viscera, although such herniation may be delayed. Ultrasound may demonstrate diaphragmatic laceration and free fluid in both the pleura and peritoneum. Barium studies may be useful to confirm herniation of stomach or bowel into the chest.

Figure 35.22 Ruptured left hemidiaphragm. Previous trauma resulted in rupture of the hemidiaphragm. A chest radiograph obtained some months later demonstrates herniation of the stomach into the left hemithorax.

PLEURAL INJURY^9,11

Pneumothorax may be a complication of rib fracture, and is then usually associated with a haemothorax. If no ribs are fractured, pneumothorax is secondary to a pneumomediastinum, pulmonary laceration or penetrating chest injury. Pneumothorax due to a penetrating injury is liable to develop increased pressure, resulting in a tension pneumothorax, which may require emergency decompression. Haemothorax may also occur with or without rib fractures, and is due to laceration of intercostal or pleural vessels. If a pneumothorax is also present a fluid level will be seen on a horizontal-beam film. Pleural effusion may also result from trauma. Open injuries to the pleura are prone to infection and development of an empyema.

INJURIES TO THE LUNG^12–14

Pulmonary contusion is due to haemorrhagic exudation into the alveoli and interstitial spaces and appears as patchy, non-segmental consolidation within the first few hours of penetrating or non-penetrating trauma. There is usually improvement within 2 days and clearance within 3–4 days. Pulmonary lacerations may be obscured by pulmonary contusion, but, as this resolves, the laceration will become evident. If filled with blood it appears as a homogeneous round opacity, and if partly filled with blood it may show a fluid level. Such pulmonary haematomas or blood cysts gradually decrease in size, but may take a few months to resolve completely. Fat embolism is a rare complication of multiple fractures, with poorly defined nodular opacities throughout both lungs, which resolve within a few days.

INJURIES TO THE TRACHEA AND BRONCHI^13,15

Laceration or rupture of a major airway is an uncommon result of severe chest trauma. Fracture of the first three ribs and mediastinal emphysema and pneumothorax may also be evident. The injury is usually in the trachea just above the carina, or in a main bronchus just distal to the carina. If the bronchial sheath is preserved there may be no immediate signs or symptoms, but tracheostenosis or bronchiectasis may occur later. CT may be helpful in diagnosis, but bronchoscopy is the best diagnostic method in the acute stage.

INJURIES TO THE MEDIASTINUM¹⁶

Pneumomediastinum and mediastinal emphysema, discussed above, are the presence of air between the tissue planes of the mediastinum. Air may reach here as a result of pulmonary interstitial emphysema, perforation of the oesophagus, trachea or bronchus, or from a penetrating chest injury. Pulmonary interstitial emphysema is a result of alveolar wall rupture due to high intra-alveolar pressure, and may occur during violent coughing, severe asthma or crush injuries, or be due to positive-pressure ventilation. Air dissects centrally along the perivascular sheath to reach the mediastinum. Rarely, air may dissect into the mediastinum from a pneumoperitoneum. A pneumomediastinum may extend beyond the thoracic inlet into the neck, and over the chest wall. Pneumothorax is a common complication of pneumomediastinum, but the converse rarely occurs. Pneumomediastinum usually produces vertical translucent streaks in the mediastinum. This represents gas separating and outlining the soft-tissue planes and structures of the mediastinum. Gas shadows may extend up into the neck, or dissect extrapleurally over the diaphragm, or extend into the soft-tissue planes of the chest wall, causing subcutaneous emphysema. The mediastinal pleura may be displaced laterally, and become visible as a linear soft-tissue shadow parallel to the mediastinum. If mediastinal air collects beneath the pericardium the central part of the diaphragm may be visible, producing the ‘continuous diaphragm’ sign. Mediastinal haemorrhage may result from penetrating or non-penetrating trauma, and be due to venous or arterial bleeding. Many cases are probably unrecognised, as clinical and radiographic signs are absent. Important causes include automobile accidents, aortic rupture and dissection, and introduction of CVCs. There is usually bilateral mediastinal widening, but a localised haematoma may occur.

ACUTE AORTIC INJURY

Aortic rupture (see Figure 35.17)¹⁷ is usually the result of an automobile accident. Most non-fatal aortic tears occur at the aortic isthmus, the site of the ligamentum arteriosum. Only 10–20% of patients survive the acute episode, but a small number may develop a chronic aneurysm at the site of the tear. The commonest acute radiographic signs are widening of the superior mediastinum, and obscuration of the aortic knuckle. Other radiographic signs include deviation of the left main bronchus anteriorly, inferiorly and to the right, and rightward displacement of the trachea, a nasogastric tube or the right parasternal line. A left apical extrapleural cap or a left haemothorax may be visible. Although aortography is the definitive investigation, CT, transoesophageal echocardiography or magnetic resonance imaging may be diagnostic. In everyday practice, many departments will have emergency access to a CT scanner, but will not be centres of cardiothoracic surgery. A properly conducted CT scan demonstrating a normal mediastinum has a very high negative predictive value for aortic rupture. However, if CT is equivocal or shows a mediastinal haematoma then generally angiography will be required prior to surgery.

CARDIAC INJURY¹⁸

This is rare but may result from penetrating or blunt trauma. Penetrating injuries are usually rapidly fatal but may cause tamponade, ventricular aneurysm or septal defects. Blunt trauma may cause myocardial contusion and infarction and may be associated with transient or more permanent rhythm disturbance.

OESOPHAGEAL RUPTURE¹⁹

This is usually the result of instrumentation or surgery, but occasionally occurs in penetrating trauma, and is rarely spontaneous and due to sudden increase of intraoesophageal pressure (Boerhaave syndrome). Clinically there is acute mediastinitis; radiographically there are signs of pneumomediastinum, with or without a pneumothorax or hydropneumothorax, which is usually left-sided. The diagnosis should be confirmed by a swallow. This should initially be with water-soluble contrast medium in order to avoid the small risk of granuloma formation in the mediastinum that has been described following barium leakage. Chylothorax due to damage to the thoracic duct may become apparent hours or days after trauma. Thoracic surgery is the commonest cause.

THORACIC COMPLICATIONS OF GENERAL SURGERY

THORACIC COMPLICATIONS OF CARDIAC SURGERY

Most cardiac operations are performed through a sternotomy incision, and wire sternal sutures are often seen on the postoperative films. Mitral valvotomy is now rarely performed via a thoracotomy incision, but this route is still used for surgery of coarctation of the aorta, patent ductus arteriosus, Blalock–Taussig shunts and pulmonary artery banding.

Widening of the cardiovascular silhouette is usual, and represents bleeding and oedema. Marked or progressive widening of the mediastinum suggests significant haemorrhage (Figure 35.23). Some air commonly remains in the pericardium following cardiac surgery, so that the signs of pneumopericardium may be present.

Figure 35.23 Following cardiac surgery (a) the postoperative chest radiograph appears satisfactory. A few hours later (b) the mediastinum has widened considerably, due to mediastinal haemorrhage.

Left basal shadowing is almost invariable, representing atelectasis. This shadowing usually resolves over a week or two. Small pleural effusions are also common in the immediate postoperative period.

Pneumoperitoneum is sometimes seen, due to involvement of the peritoneum by the sternotomy incision. It is of no pathological significance (see Figure 35.4).

Violation of left or right pleural space may lead to a pneumothorax. Damage to a major lymphatic vessel may lead to a chylothorax or a more localised chyloma. Phrenic nerve damage may cause paresis or paralysis of a hemidiaphragm.

Surgical clips or other metallic markers have sometimes been used to mark the ends of coronary artery bypass grafts. Prosthetic heart valves are usually visible radiographically, but they may be difficult to see on an underpenetrated film.

Sternal dehiscence may be apparent radiographically by a linear lucency appearing in the sternum and alteration in position of the sternal sutures on consecutive films. The diagnosis is usually made clinically and may be associated with osteomyelitis. A first or second rib may be fractured when the sternum is spread apart. The importance of this observation is that it may explain chest pain in the postoperative period.

Acute mediastinitis may complicate mediastinal surgery, although it is more commonly associated with oesophageal perforation or surgery. Radiographically there may be mediastinal widening or pneumomediastinum, and these features are best assessed by CT scan.