Even though it is over a century since the discovery of X-rays by Wilhelm Roentgen on 8 November 1885 and in spite of the major advances in imaging techniques which are presented in subsequent sections, plain radiographs still command an important place in surgical practice. As the value of plain radiography will be illustrated extensively in specialist chapters, this section will concentrate mainly on the chest radiograph and plain films of the urinary tract.

The posteroanterior chest radiograph is still the mainstay of the standard medical examination. In hospital practice a routine film on admission will provide a baseline for later comparison, following surgery, when infection, oedema, or collapse might supervene. The lateral projection is no longer carried out routinely, but may be necessary to localize a lesion anatomically (for interventional purposes) or to obtain a view of a structure not seen on the posteroanterior view, for example the right-ventricular border, the left-atrial border, the oblique fissure, the posterior costophrenic angle, or the spine. It is also useful for the differential diagnosis of mediastinal masses.

The key to successful diagnosis of the chest radiograph is its systematic examination, which must include the soft-tissue shadows (breast, muscles, cutaneous tissues), the diaphragmatic and subdiaphragmatic areas (of great importance to the surgeon), the bony cage (ribs, clavicles, scapulae, spine, proximal humeri), the lung fields, the heart, and mediastinum. Whenever possible, bilateral and symmetrical structures must be carefully compared.

Although it is the duty of the radiographer to produce a technically perfect product, it is still imperative that the film reader checks that this is achieved. For example, positioning must be exact with both left and right costophrenic angles and apices within the film area. The scapulae must not overlap the bony cage. Penetration, as tested by the thoracic vertebrae just being visible through the heart shadow, must be assessed. Underpenetration may produce a useless white film, whereas an overpenetrated film, although looking very black, can be salvaged by the use of a bright light. Rotation with respect to the cassette, which can cause discrepancies in the appearance of the left and right lung fields, must be checked by making sure that the angles made by the clavicle with the vertical are the same on each side. Finally, the degree of inspiration must be checked by counting the number of ribs, preferably on the right side, that appear above the right hemidiaphragm. Ten posterior ribs are the norm. If more than this number can be counted and there is also flatness of the hemidiaphragms, with a decrease in the number and size of the lung markings, chronic obstructive disease may be present.

The routine view is, of course, taken in the posteroanterior position (which refers to the direction of the beam) so that the anteriorly-situated heart can be as close to the film as possible (Fig. 1) 78. This enables an accurate estimation of the so-called cardiothoracic ratio to be made (the ratio of the width of the cardiac shadow at its widest point to the diameter of the thorax at its widest point). The normal cardiothoracic ratio is less than 50 per cent.

The routine chest radiograph is still the first investigation of choice in the diagnosis of bronchial carcinoma (Fig. 2) 79,80. Either the primary tumour or one of its secondary effects or complications may be seen, or both. Among the latter is identification of metastases to the mediastinum or elsewhere.

The primary tumour may present as an opaque nodule, but tumours are not the only cause of pulmonary nodules and the differential diagnoses include abscesses or granulomata, infarctions, haematomas, focal collagen disease, retention cysts, sequestrated segments, arteriovenous malformations, and hamartomas. Also, the lesion may be pleural based, when encysted pleural effusions and fibromata are possible. Finally, the lesion may not lie within the pulmonary parenchyma itself, but on the surface of the body e.g. a large wart or mole (Fig. 3) 81.

A bronchial carcinoma often blocks the bronchus from which it arises and in this case leads to absorption collapse of the affected segments or lobes (Fig. 4) 82. Superimposed infection then also usually occurs. Unless there is another good reason for the collapse in an adult (e.g. bronchiectasis with inspissated pus, asthma with mucoid impaction, or inhaled foreign body) bronchial carcinoma must always be suspected. Cavitating lesions may be due either to tumours or abscesses, although an area of infarction can also break down (Fig. 5) 83.

A hilar mass may represent metastases to the mediastinal lymph nodes (Fig. 6) 84 and a pleural effusion may also arise as a result of a malignant tumour (Fig. 7) 85, although infection and infarction can also cause unilateral effusions. Failure of major organ systems like the heart, kidneys, and liver are also common causes of effusions, but these are usually bilateral. A hilar carcinoma or metastases to the mediastinal nodes can involve the phrenic nerve, with subsequent elevation and paresis of a hemidiaphragm (Fig. 8) 86.

In an apical or so-called ‘Pancoast’ tumour there is often lysis of the adjacent ribs. Metastases to bone in general may present as lytic or sclerotic lesions, depending on the aggressiveness of the tumour. Alternatively, they may present with pathological fractures.

The lungs are a common site for haematogenous metastases, where they often produce multiple round nodules of different sizes (Fig. 9) 87 (as opposed to granulomatous disease, where the nodules are usually small and of similar size (Fig. 10) 88). Alternatively, lymphatic spread may show a reticular, almost fibrous-looking appearance, often with septal lines and is referred to as lymphangitis carcinomatosa (Fig. 11) 89.

Lymphoma usually affects the mediastinum. Hodgkin's disease, which is the most common of the lymphomas, normally affects the paratracheal glands, leading to local enlargement and generalized widening of the superior mediastinum (Fig. 12) 90. Leukaemia and sarcoidosis can, however, lead to similar appearances, although sarcoidosis classically enlarges the hilar glands.

These usually present as diffuse, water-dense opacities (Fig. 13) 91. Lobar pneumonia is now not often seen, but when it is, the opacity usually outlines an entire lobe. If resolution is incomplete, fibrosis may appear and bronchiectasis may be seen as a late sequel. The more common bronchopneumonia gives similar densities, but they are usually more patchy and are seen mainly in the lower lobes. Pneumonitis gives a similar picture, with the opacities usually confined to one segment of a lobe.

The very common acute or chronic bronchitis may show nothing on chest radiography because bronchi are air-filled structures superimposed on an air-filled background and thus comply with the rules of radiology that a structure or an area of pathology can be seen only if its radiographic density is different from that of an adjacent tissue.

In bronchiectasis, however, the bronchi do become thick enough to be seen and so may be seen as end-on ring shadows or else small cystic areas, usually at the bases (Fig. 14) 92. Bronchography is necessary before resection is considered.

The characteristic radiographic appearance of tuberculosis in children is an area of water density with enlarged hilar glands in the affected side. It is important to remember that tuberculosis is the only infection which can enlarge hilar lymph nodes enough to make them visible on the routine chest radiograph. Alternatively the disease can present with a miliary pattern, consisting of multiple small round opacities of similar size throughout the chest (Fig. 10) 88. In adult infections, the disease has a tendency to spread to the posterior segment of the upper lobe and appear as an apical lesion which can cavitate. A mycetoma may later appear in the cavity (Fig. 16) 94,95.

In patients who are immunosuppressed for any reason, but especially as a result of AIDS, unusual opportunistic infections may occur, for example those from Pneumocystis carinii or cytomegalovirus (Fig. 17) 96.

Obstructive airways disease includes the various types of emphysema and asthma and presents radiologically as elongated, translucent lung fields with flattened diaphragms, prominent hilar shadows, and a decrease in the number and size of the lung markings. In emphysema, bullae may occur. These are translucent areas where the alveolar walls have broken down and appear as black areas which are devoid of lung markings and are delineated by fine, curvilinear markings (Fig. 18) 97.

Like tuberculosis, this disease is characterized by non-caseating granulomatous lesions which can affect the lungs, skin, eyes, and even bone. In the lungs, the disease classically presents with symmetrical, bilateral hilar, and paratracheal gland enlargement (Fig. 12) 90. If the disease progresses, the lung fields may demonstrate a nodular-reticular pattern, (Fig. 19) 98 which proceeds to fibrosis and emphysema.

This is a collective name for a group of conditions usually arising in workers from industrial enterprises such as mining where foreign substances are inhaled. These include silica, iron, tin, talc, asbestos, and beryllium. Silicosis is perhaps the most common of the pneumoconioses. In the early stages there is a widespread small-nodular pattern, which once again may proceed to fibrosis and bullous emphysema. In silicosis the fibrotic areas often occur bilaterally and symmetrically in the upper lung fields and are ‘geometric’ in shape—so-called conglomerate masses characteristic of the entity known as pulmonary massive fibrosis (Fig. 20) 99.

Pleural tumours are rare, but the malignant pleural tumour mesothelioma occurs in workers with asbestos. Such workers may also develop pleural or diaphragmatic calcification and are prone to develop asbestosis per se, which gives a characteristically diffuse reticular pattern to the lung fields.

Pleural effusions may be free or encysted ( Fig. 7 85 and 21 100 respectively). When free, they manifest as basal opacities which initially fill the costophrenic angles and then rise up the hemithorax towards the axilla, usually with a meniscus. They may be seen following infections like pneumonia or tuberculosis, infarctions, or malignancy. They are also seen as complications of cardiac failure, hypoproteinaemic states (like hepatic failure), and renal failure (the ‘uraemic lung’). Empyema, or pus in the pleural space, which was common in tuberculosis, is now rarely seen as a postpneunomic complication.

Spontaneous pneumothorax is common in young people and, although sometimes ascribed to the rupture of a bulla, its aetiology is usually unknown (Fig. 22) 101.

Pneumothorax may also be due to trauma and is often associated with rib fractures. Tension pneumothorax occurs when air continues to enter the space, but cannot escape because the tear in the pleura acts like a one-way valve. It is therefore essential to observe any shift in the mediastinal structures towards the opposite side and, if so, to equilibrate the pressures immediately.

The posteroanterior chest radiograph can yield information about the cardiac diameter, enlargement of individual chambers, and the state of the pulmonary vasculature. The cardiothoracic ratio has already been considered.

In the posteroanterior view the right heart border is formed by the right atrium with the superior vena cava entering it from above. On the left side three protuberances may be seen. The top one is the aortic knuckle, the next one the pulmonary outflow tract (opposite the left main pulmonary artery which constitutes the left hilum—normal lymph nodes and bronchi are invisible), and the lower one is the border of the left ventricle. The left atrium lies behind the heart, but occasionally the prominent auricular appendage of an enlarged left atrium will form a further protuberance between the pulmonary outflow tract and the left ventricular border. On the lateral view, the right ventricle forms the anterior border and the left atrium most of the posterior border, where it is a close relation of the invisible oesophagus.

The diagnosis of left-ventricular enlargement is made on the posteroanterior view when its border moves outwards and the apex downwards. Right-ventricular enlargement is diagnosed on the lateral view by noting that the anterior border has risen up higher behind the sternum. On the posteroanterior view, it manifests as a lateral shift of both the left and right heart borders, but with the apex tilted upwards (forming the imaginatively-named ‘boot-shaped heart’) (Fig. 23) 102. In biventricular enlargement the left and right borders are also displaced laterally, but the apex stays in its normal horizontal plane. The right-ventricular component is again observed on the lateral view, where left-ventricular enlargement shifts the lower posterior border too little for detection.

Isolated right atrial enlargement is very rare, but would shift the right-hand border laterally. Left atrial enlargement, arising mainly from mitral-valve disease, forms a double shadow behind the heart as the enlarged chamber penetrates posteriorly and towards the right, surrounded by air-filled lung which provides the contrast. It will also splay the carina, resulting in a left main bronchus pointing laterally rather than downwards towards the left costophrenic angle. The proof of an enlarged left atrium is obtained from looking at a lateral chest after the patient has swallowed some barium. The enlarged left atrium will then indent the contrast-filled oesophagus as it curves round the posterior border of the heart towards the hiatus (Fig. 24) 103.

The appearance of the lungs provides major clues to the diagnosis of heart disease. Normally the lower-zone vessels are more prominent and larger than the upper-zone vessels and the outer rim of the chest is usually free of lung markings. Because of the disposition of the left and right pulmonary arteries and bronchi, the left hilum is slightly higher than the right and as they emerge from the hila, the main right and left pulmonary arteries have a largely vertical configuration. The pulmonary veins, on the other hand, return to the left atrium, which is about 5 cm below the hila. The veins returning from the upper zones therefore run vertically, whereas those draining the lower zones run horizontally. It is, thus, not possible to differentiate between arteries and veins in the upper half of the lung fields, whereas in the lower half, arteries are vertically disposed and veins horizontally.

In pulmonary venous hypertension (the chief causes of which are mitral-valve disease and left-ventricular failure) both the vertical upper-zone and the horizontal lower-zone veins become larger. The latter are seen coming in right from the periphery, an area where there are normally no markings. As the pressure rises, pulmonary oedema will occur, which first fills the interstitial and then the alveolar spaces. The lower zones become hazy and vessel differentiation is lost. This and true upper-zone venous enlargement contribute to the characteristic ‘upper-lobe diversion’, when the upper-lobe vessels appear larger and more prominent than the lower-lobe vessels. Interstitial oedema may appear as septal lines in the costophrenic angles, but these are short-lived as water, accumulating on each side, soon obliterates these distended interlobular lymphatics. A much more certain sign is peribronchial oedema or ‘cuffing’ when the normally-invisible end-on bronchi become visible as black holes because of the surrounding fluid—a variant of the so-called ‘air bronchogram’ (Fig. 25) 104. There may be pleural effusions to a greater or lesser degree, or if no treatment is offered, full-blown perihilar alveolar oedema which presents as widespread cotton-wool-like opacities in the central areas (Fig. 26) 105.

In pure pulmonary arterial hypertension, which arises when there is either increased pulmonary blood-flow (e.g. anaemia, thyrotoxicosis, left-to-right shunts) or peripheral arterial close-down (e.g. primary pulmonary arterial hypertension, pulmonary emboli, chronic obstructive lung disease) there is so-called pulmonary plethora with an enlarged pulmonary outflow tract, left and right main pulmonary arteries, and the rest of the vertically-disposed arterial tree (Fig. 27) 106. Obviously it may also arise from pulmonary venous hypertension and the two varieties often occur together, usually in left-heart failure.

These are traditionally classified under the headings inflammatory, non-inflammatory, and malignant, and in fact the causes are very similar to those producing pleural effusions.

The common inflammatory causes are suppurative, viral, tuberculotic, and rheumatic. Non-inflammatory causes include heart-failure, uraemia, and myocardial infarction. The effusion could also be due to blood in the pericardial sac from trauma or from a ruptured aortic or left-ventricular aneurysm.

Constrictive pericarditis may be a sequel to viral or tuberculous pericarditis and is sometimes seen after haemorrhage into the pericardium or in one or two of the collagen diseases. Subsequent fibrosis of the pericardium may lead to cardiac tamponade and right-heart failure. About half of the cases lead to calcification (Fig. 28) 107.

Cardiac calcification may also be seen in the mitral and aortic valves, the coronary arteries, and in the left atrium, where it occurs as mural thrombus (Fig. 29) 108.

A lateral view is mandatory for the differential diagnosis of mediastinal opacities, the usual approach being to separate those occurring in the anterior, middle, and posterior compartments.

The normal structures in this compartment are the thymus, retrosternal lymph nodes, the ascending aorta and, occasionally, a retrosternal extension of the thyroid.

Opacities occurring in this compartment may therefore be due to thymomas (Fig. 30) 109,110, enlarged lymph nodes, aneurysm of the ascending aorta, or retrosternal goitre (Fig. 31) 111. Other possibilities are dermoid tumours, pericardiocoelomic cysts, parathyroid adenomas, and hernia of Morgagni.

Middle-mediastinal structures include the aortic arch and its branches, the pulmonary artery, the inferior and superior venae cavae, and the heart.

Anomalies may be due to a big left atrium, aortic aneurysm, bronchial cyst, enlarged hilar lymph nodes (due to lymphoma, leukaemia, sarcoidosis, tuberculosis, or metastases).

Structures normally occurring in this compartment are the trachea and bronchi, oesophagus, descending aorta, lymph nodes, vagi, spine, and nerves emerging through the intervertebral foramina.

Abnormalities include tumours of neurogenic origin (neurofibroma, ganglioneuroma, neuroblastoma, myelocele, and meningomyelocele), paravertebral abscess, aneurysm of the descending aorta, sequestrated lung segments, reduplication cysts of the oesophagus, loculated pleural effusions, corrective-tissue tumours, Zenker's diverticulum, and oesophageal lesions (achalasia (Fig. 32) 112, hiatus hernia (Fig. 33) 113, leiomyoma, and sub- or epiphrenic diverticula).

After general surgery, poor respiratory effort and retained secretions lead to local collapse, often referred to as ‘plate atelectasis’, which usually appears as horizontal lines in the lower zones. Pleural effusions are also common, but both of these entities resolve soon after surgery. General anaesthesia may lead to aspiration pneumonia or even to the full-blown adult respiratory distress syndrome. The radiographic appearances of this syndrome are indistinguishable from pulmonary oedema due to cardiac failure, fluid overload, or any form of alveolar damage. Pulmonary emboli may lead to an oligaemic area of lung with vessel cut-off, but it is usually diagnosed on pulmonary perfusion–ventilation scintigraphy. When the resulting infarction becomes established it manifests as a water-dense wedge which may cavitate.

A subphrenic collection of pus, blood, or fluid can lead to elevation of the hemidiaphragm and an associated ‘sympathetic’ pleural effusion. Air under the diaphragm is common after abdominal surgery, but it may arise from an anaerobic infection or perforation of a viscus. Occasionally it may arise from the lung or via the vagina in women.

The hallmark of a thoracotomy is a resected 4th, 5th, or 6th rib. Partial regeneration of the rib can take place. After a lobectomy or a sublobectomy resection, the remaining lung should expand to fill the volume previously occupied by the resected segment. This will be accompanied by appropriate shift of landmarks. However, in spite of drainage, pleural effusions, empyema and haemothorax can occur and it is not uncommon to see a mixture of expanded lung and organizing fluid densities (Fig. 34) 114. Poor closure of a bronchus can lead to bronchopleural fistula and early surgical emphysema in the soft tissues is a common occurrence. After pneumonectomy there is a combination of hyperinflation of the remaining lung with consequent shift of the mediastinum towards the side of the operation and the accumulation of fluid in the pneumonectomy space. Any chest operation can lead to phrenic nerve damage and elevated hemidiaphragm, but the nerve is often crushed deliberately to reduce the size of the treated hemithorax.

Open-heart surgery is done via a sternal split, radiographic evidence for which is the presence of wire sternal sutures. A widened mediastinum and associated pleural effusions are common and air may enter any of the pleura, pericardium, or peritoneum. Sudden widening of the mediastium may indicate haemorrhage or an aortic dissection. The postpericardotomy syndrome is characterized by pain, fever, and pleurisy and the cardiac outline is enlarged by a pericardial effusion visible with echocardiography.

Plain abdominal radiographs are essential before embarking upon contrast studies of the kidneys. As the perinephric fat is translucent, the kidneys are often visible lateral and parallel to the psoas lines, opposite T12, L1, and L2 and with the left kidney about 1.5 cm higher than the right. As the perirenal fat line persists after nephrectomy, the evidence for this operation is a resected rib and not an absent renal outline.

Even on plain film it may be possible to recognize an enlarged or shrunken kidney. The latter could be due to chronic pyelonephritis, chronic glomerulonephritis, or renal ischaemia, whereas enlargement may be due to hydronephrosis, a tumour, or simply to compensatory hypertrophy. Bilaterally enlarged kidneys may be due to polycystic disease or to bilateral hydronephrosis. Kidneys are also enlarged in acute situations such as acute pyelonephritis.

Calcification in the renal area is very common and usually due to renal calculi, the majority of which are opaque (Fig. 35) 115. Diffuse calcification of the parenchyma, known as nephrocalcinosis, is uncommon, but may be seen in tuberculosis, hyperparathyroidism, renal-tubular acidosis, medullary sponge kidney, and in milk-alkali syndrome (Fig. 36) 116. Renal cysts and tumours are occasionally identified by calcification in adjacent involved kidney.

Renal stones can travel down the ureters and appear in the bladder or urethra (Fig. 37) 117. Encrustations on papillary bladder tumours may be visible on the plain film (Fig. 38) 118, as can the florid calcification in the walls of the bladder and ureter in schistosomiasis.

The adrenals are nowadays usually investigated by ultrasound, CT, or radionuclide techniques. In areas where tuberculosis is common, this involves the adrenals leading to Addison's disease and calcification in the adrenal areas on the plain film. This could also arise from haemorrhage into the adrenal in infancy and theoretically in certain tumours, notably neuroblastoma.

Davidson AJ, ed. Radiology of the Kidney. Philadelphia: WB Saunders Co, 1985.

Fraser RG, Pare JAP. Diagnosis of Diseases of the Chest. 2nd edn. Philadelphia: WB Saunders Co, 1977–1979.

Grainger RG. Allison DJ, eds. Diagnostic Radiology. An Anglo-American Textbook of Imaging. Vols 1, 2, and 3. Edinburgh: Churchill Livingstone, 1986.

Sutton D. Textbook of Radiology and Imaging. 4th edn. Edinburgh: Churchill Livingstone, 1987.

Sutton D, Young JWR, eds. A Short Textbook of Clinical Imaging. London: Springer-Verlag, 1990.