Introduction

Acute pulmonary processes present a diagnostic challenge for intensivists and radiologist alike. Only when clinical data and radiographic findings are correlated can patient care be optimized. Although many acute pulmonary process are not unique to the ICU patient, these entities often have atypical presentations in the critically ill patient. Physicians caring for ICU patients must understand the role of the in diagnosing and following such processes. Despite the decreased sensitivity and specificity of ICU chest films they are the most commonly ordered radiologic examination for inpatients. Their use stems from the fact that studies have shown that up to 65% of ICU chest films may reveal a significant or unsuspected process. Currently, the American College of (ACR) suggests that daily chest radiographs be obtained on patients with acute cardiopulmonary problems and those receiving mechanical ventilation. Otherwise, only initial chest radiographs are needed for the placement or change of indwelling lines or devices.

Indications:

1.Determining the placement of patient instrumentation- catheters, tubes, and monitoring devices. 2.To recognize the common normal and pathological appearances of portable chest x- rays in the postoperative or medically ill patient. 3.Identify complications of lines and tubes after insertion and removal.

Technique:

Routine chest films are obtained in the radiology department in a posteroanterior (PA) direction to minimize magnification of the heart. The optimal ICU chest radiograph is obtained in the anteroposterior (AP) view at a target-to-film distance of 72 inches with the patient in the upright position at maximum inspiration; alternatively a distance of 40 inches is used in the supine patient. Due to the decreased mobility of patients in the ICU, chest films are often taken while the patient is supine.

Factors affecting the appearance of the ICU CXR:

1.AP view results in –  the magnification of anterior structures such as the clavicle, sternum, and heart, often significantly  up to a 15% difference between the width of the in a 72-inch PA and a 40-inch AP view  the medial border of the scapula is projected several centimetres further into the . 2.Supine positioning-  widens the mediastinum and heart due to gravitational effects.  changes the physiology of the pulmonary vasculature, putting more flow to the upper lobes and making diagnosis of cephalisation more difficult.  make differentiating between and parenchymal processes difficult, and  may make detecting a difficult or impossible due to unusual distribution. 3.Respiration-  Incomplete inspiration can make differentiating basilar and lung oedema more difficult.  may cause significant changes in the apparent size of the heart and mediastinum.  the diameter of a patient's mediastinum may differ by up to 50% between an expiratory supine AP and a erect inspiratory PA.

Instrumentation:

1.Endotracheal Tubes- important to identify the location of the tip of the ETT. The rate of serious malposition of endotracheal tubes has been reported to be between 12-15%. The ideal position is in the midtrachea, 5 cm from the carina, when the head is neither flexed nor extended. This allows for movement of the tip with head movements. The minimal safe distance from the carina is 2 cm. The carina is often not visible. The carina can be assumed to be at the T4-T5 interspace, given that 95% of patients' carinas project over the T5, T6, or T7 vertebral bodies. Common malposition: the right main stem

CXR with Endotracheal Tube insitu

2.Thoracostomy tubes- Ideal position-all of the fenestrations in the tube must be within the thoracic cavity. The last side-hole in a thoracostomy tube is indicated by a gap in the radiopaque line. If this interruption in the radiopaque line is not within the thoracic cavity or there is evidence of subcutaneous air, then the tube may not have been completely inserted. Tubes placed within fissures often cease to function when the lung surfaces become apposed. Determining whether a tube is anterior or posterior is often difficult with a single AP chest x-ray and may need CT scan. Complications: injury to adjacent structures. Often difficult to detect with a chest x- ray alone and may require a CT scan. Also useful when the location of the tube is important and unclear on plain radiographs.

CXR showing Intercostal Catheter 3. Feeding tubes- Naso/Orogastric tubes- the tip of the tube should be below the level of the diaphragm. Malposition within the lung have serious consequences. Nasojejunal tubes-placed into the proximal small bowel, and confirmed by an abdominal film.

CXR of Nasogastric Tube

4.Central venous catheters- either through the subclavian veins or the internal jugular veins. Ideally the catheter tip should lie between the most proximal venous valves of the SVC and the right atrium as placement beyond the superior vena cava may be detrimental. Malposition: the internal jugular vein, right atrium, and right ventricle. Pneumothorax, occur in as many as 6% of cases. Damage may also be caused by guidewires causing injury to the endothelium. This may result in thrombus formation or possibly vessel perforation.

CXR showing R) sided Subclavian Central Line

5. The intraaortic counter pulsation balloon pump (IABP)- Introduced percutaneously through the right femoral artery. Ideally the catheter should be in the region of the aortic isthmus or left main bronchus and above the origins of the celiac trunk and superior mesenteric artery. During systole the balloon may appear as a fusiform air (helium) containing radiolucency.

CXR showing IABP

6.Transvenous pacemakers- Transvenous pacers are introduced through the internal jugular or subclavian vein into the apex of the right ventricle. The pacer tip should be at the apex with no sharp angulations throughout its length. The integrity of the pacer wire should be inspected along its entire length.

A CXR of an ICU patient with ETT, NGT, CVC, Vascath and ICC

The Abnormal CXR-

1.Extra-alveolar air - manifest as pulmonary interstitial emphysema, pneumothorax, , pneumopericardium or subcutaneous air. When searching for lucencies which may represent air on the chest x-ray, be aware of the Mach effect. The Mach effect is caused by lateral inhibition of light receptors in the eye. The eye enhances the contrast between objects by increasing the brightness of objects near dark borders and decreasing the brightness of dark objects near bright borders. This optical illusion can deceive a person interpreting a chest x-ray into believing that a lucent streak exists when it does not.

A.Subcutaneous emphysema: usually occurs due to an air leak from the lung into the chest cavity and out into the subcutaneous tissues. It may also result from poorly positioned chest tubes or a non-occlusive dressing around a thoracostomy site. In the absence of pneumomediastinum, patients with cervical subcutaneous emphysema should be examined for upper airway injury, especially following a difficult intubation or the placement of a new nasogastric tube.

CXR showing Subcutaneous Emphysema

B.Pneumothorax: In the erect patient, air will rise to the apicolateral surfaces of the lung. An apicolateral pneumothorax appears as a thin, white pleural line with no lung markings beyond. The presence of lung markings beyond this line, though, does not exclude pneumothorax. This is especially true in the patient with parenchymal disease which may alter the compliance of affected lobes, making their collapse more difficult to detect radiographically. Parenchymal disease may also make visualization of the pleural line more difficult or impossible. Skin folds on a patient can mimic a pleural edge and a pneumothorax. One can sometimes differentiate the two by noting that the skin fold line continues outside of the chest. In the supine patient, intrapleural air rises anteriorly and medially, often making the diagnosis of pneumothorax difficult. The anteromedial and subpulmonary locations are the initial areas of air collection in the supine patient. An apical pneumothorax in a supine patient is a sign that a large volume of air is present. Subpulmonic pneumothorax occurs when air accumulates between the base of the lung and the diaphragm. Anterolateral air may increase the radiolucency at the costophrenic sulcus. This is called the . Other signs of subpulmonic pneumothorax include a hyperlucent upper quadrant with visualization of the superior surface of the diaphragm and visualization of the inferior vena cava. Occasionally, a posterior subpulmonary pneumothorax will result in visualization of the more superior anterior diaphragmatic surface and the inferior posterior diaphragmatic surface, resulting in the double-diaphragm sign. Anteromedial pneumothoraces are differentiated into those which are superior or inferior to the pulmonary hilum. A superior anteromedial pneumothorax may result in visualization of the superior vena cava or azygos vein on the right. An inferior anteromedial pneumothorax may be evidenced by delineation of the heart border and a lucent cardiophrenic sulcus. This is the key sign of a pneumothorax as this is the highest point in the supine patient, where the air will accumulate first. A tension pneumothorax in the ICU patient is a clinical diagnosis based on ventilatory and cardiac compromise. Radiographically, a tension pneumothorax in an ICU patient can be an extremely challenging diagnosis. Parenchymal disease such as ARDS may reduce lung compliance such that total lung collapse in the face of a tension pneumothorax may not occur. is usually seen in a tension pneumothorax, but the use of PEEP may prevent this from occurring. The most reliable sign of tension pneumothorax is depression of a hemidiaphragm. Other signs of tension pneumothorax include shifting of the heart border, the superior vena cava, and the inferior vena cava. The shifting of these structures can lead to decreased venous return.

Mobile CXR showing pneumothorax

CXR showing Deep Sulcus Sign

C.Pneumomediastinum: The radiographic appearance of pneumomediastinum results from air outlining structures which are not normally visible on chest x-ray. Pathognomonic signs of pneumomediastinum include lucencies around the great vessels, the medial border of the superior vena cava, and the azygos vein. Air may also be seen outlining the aortic knob, descending aorta, or the pulmonary arteries. Patients with posteromedial pneumomediastinum (usually due to oesophageal rupture) may have dissecting air at the paraspinal costophrenic angle and beneath the parietal pleura of the left diaphragm. This is called the V-sign of Naclerio.

CXR of Pneumomediastinum

D.Pneumopericardium: an uncommon occurrence, is most often found in the post- operative cardiac patient. Radiographically, pneumopericardium appears as a lucent area around the heart extending up to the main pulmonary arteries. A lucent stripe along the inferior border of the cardiac silhouette which crosses the midline is also diagnostic for pneumopericardium.

2.Abnormal fluid collection:

A. Pleural effusions: blood, chyme, pus, transudates or . The appearance of a pleural effusion on a chest film is largely dependent on the position of the patient. Fluid in the chest cavity will accumulate in the dependent areas of the chest. This makes identifying small collections extremely difficult, especially in the supine patient. Fluid in the posterior basilar space appears as an homogenous graded increase in the density of the lung base, maximal inferiorly. The normal bronchovascular markings are not lost. As the amount of fluid increases, the diaphragmatic contour and lateral costophrenic sulcus may be obliterated. Fluid in the apex, in a supine patient, is more easily identified. A large pleural effusion may appear as a pleural cap with fluid occasionally collecting on the medial side, appearing as a widened mediastinum. Even with optimal radiographic technique, small pleural effusions are difficult to identify in the supine patient. In the erect patient fluid collects at the base of the chest. Costophrenic angle blunting and decreased visibility of the lower lobe vessels are commonly the result of pleural fluid pooling. Subpulmonic effusions are a frequent occurrence in the ICU patient. Up to a litre of fluid may collect between the diaphragm and the lung without blunting of the costophrenic angle. Radiographically, subpulmonic effusions appear as a raised diaphragm with flattening and lateral displacement of the dome. The gastric bubble and splenic flexure of the colon show displacement inferiorly. The distance between the lung and the stomach bubble will exceed 2 cm in subpulmonary effusions. The diagnosis of interlobar effusion can often be challenging, especially in the presence of incomplete pleural fissures. Another challenge can be differentiating between a loculated effusion in the minor fissure and right middle lobe atelectasis. An effusion appears as an homogenous density with biconvex edges and preservation of the minor fissure, while atelectasis appears as an inhomogenous density with concave margins and obliteration of both the right heart border and minor fissure.

CXR showing pleural effusion

CXR of same patient with pleural effusion post drainage Note R) sided pigtail catheter

B.Pericardial effusions: accumulations of fluid between the visceral (epicardium) and parietal pericardium. Blood in the pericardium (hemopericardium) may be an important clue to post operative bleeding. Radiographically, pericardial effusions appear as changes in the size and shape of the cardiac silhouette resulting a featureless, globular or "water bottle" shape. The pericardial fluid on an ICU film is generally not distinctly visible; instead it enlarges the cardiac shadow.

CXR of Pericardial and Pleural Effusion

C.Pulmonary oedema: The initial phase of cardiogenic pulmonary oedema is manifested as redistribution of the pulmonary veins. This is know as cephalization because the pulmonary veins of the superior zone dilate due to increased pressure. This diagnosis is made when the upper lobe vessels are equal to or larger in diameter than the lower lobe vessels. The diagnosis of cephalization is more difficult in the supine patient due to gravitational effects. Interstitial oedema as seen on the chest x-ray may in fact precede clinical symptoms. This is testimony to the importance of the ICU chest film. Therefore, excess fluid accumulates in the intersitial space surrounding capillary walls first. Several signs are indicative of interstitial oedema. The large pulmonary vessels may begin to lose definition and become hazy. Septal lines may begin to appear. Kerley's A lines range from 5 to 10 cm in length and extend from the hila toward the periphery in a straight or slightly curved course. They represent fluid in the deep septa and lymphatics, usually in the upper lobes. Kerley's B lines are shorter thin lines (1.5 to 2.0 cm in length) and are seen in the periphery of the lower lung, extending to the pleura (see below). These represent interlobular septal thickening. The chest x-ray in interstitial oedema may take on a diffuse reticular pattern resembling widespread interstitial fibrosis. represents interstitial oedema and appears as very thick bronchial walls. Classically, alveolar oedema appears as bilateral opacities that extend in a fan shape outward from the hilum in a "bat wing" pattern. As the oedema worsens, the opacities become increasingly homogenous. These water-density opacities may contrast with air-filled bronchi which, in normally aerated parenchyma are invisible. The visible appearance of previously imperceptible bronchi is known as air-bronchograms Typically, the radiographic appearance of pulmonary oedema includes one or more of the following: cephalization of pulmonary vessels, Kerley's B lines peribronchial cuffing, bat wing pattern, patchy shadowing with air bronchograms, and increased cardiac size. Generally, pulmonary oedema is bilateral and may change rapidly. Atypical patterns of pulmonary oedema can represent a challenge. Pulmonary oedema may be unilateral, lobar, miliary, or restricted to the lower zones of the lung. Pulmonary oedema may assume any asymmetric or unusual distribution. Although gravity as been implicate as the culprit many other theories have been devised to explain the bizarre patterns of pulmonary oedema noted. Miliary oedema is often considered a normal transitory phase in the development of full scale oedema. Lobar or lower zone oedema is found in patient suffering from chronic obstructive pulmonary disease with predominate upper lobe emphysema. One method of differentiating pulmonary oedema from other causes of lung opacities is the gravitational shift test. The patient is kept in the supine position for two hours before a chest film is taken. Then the patient is left in the decubitis position with the suspicious hemithorax in the independent position for 2 to 3 hours before a second film is taken. In 85% of patients with pulmonary oedema there is a shift in the opacity as opposed to 80% of patient without pulmonary oedema who had no shift. The patient on the left suffered from unilateral cardiogenic pulmonary oedema. This entity is unusual and thought to be the result of an enlarged left ventricle compressing the left main paradoxically shielding it from increased hydrostatic pressures. Often pulmonary oedema is difficult to differentiate from until the patient has been treated with diuretics (right). The chest film may play a role in differentiating cardiac versus non-cardiac forms of pulmonary oedema. Cardiac oedema is usually characterized by cardiac enlargement, pleural effusions, pulmonary vascular redistribution to the upper lobes, Kerley's lines, peribronchial blurring, and basal oedema. Although, there may be exceptions in patients suffering acute cardiac injury. Pulmonary oedema caused by inhaled irritants usually has a more mottled appearance and may be more peripherally distributed.

CXR of Acute Pulmonary Oedema

Cardiogenic pulmonary oedema: The chest radiograph plays an important role in distinguishing fluid overload or congestive failure causes before the onset of symptoms. Left-sided cardiac failure may be detected on a chest x-ray in 25-40% of patients in the event of an acute myocardial ischemia prior to clinical diagnosis. Under ideal situations, the chest film should be taken erect and in the PA view. Supine AP films reduce the viewer’s ability to detect cardiomegaly and redistribution of pulmonary flow. Therefore, semierect and decubitus films are recommended in patients who may have new onset congestive . As the left ventricle fails and begins to distend an enlarged cardiac silhouette is seen on x-ray, especially in patients with chronic CHF. This sign, though, is not specific; a pericardial effusion will also enlarge the cardiac silhouette. Also, AP films magnify the cardiac shadow making it difficult to determine actual cardiac enlargement. As pulmonary venous pressures rise pulmonary vessels are recruited in an attempt to normalize pressures. This phenomenon can be seen on chest x-ray as increased pulmonary vascularity with redistribution to the apex. This signs is also compromised by the typical ICU portable film. Supine position of the patient will cause redistribution of pulmonary flow even in the absence of CHF. The azygos vein may enlarge as a result of increased pressures transmitted to the venous system. This signs also depends on patient position. The more reliable signs of CHF in the ICU patient are alveolar or intersitial oedema. Pleural effusions often accompany subacute or chronic cardiogenic pulmonary oedema.

Adult respiratory distress syndrome (ARDS): While it is not always easy, it is often possible to radiographically distinguish between pulmonary oedema caused by congestive heart failure (CHF) and ARDS. Indeed, both may coexist. Although both entities may share the x-ray finding of bilateral airspace opacification or "white out", ARDS is not associated with cardiomegaly or with cephalization of pulmonary vasculature. However, cephalization may not be visible in the midst of "white out" and CHF can exist without cardiomegaly. Both of these findings may be difficult to discern in the supine patient. The patient with ARDS could also have pre-existent cardiomegaly or be fluid overloaded because of sepsis. Features that are helpful in distinguishing CHF from ARDS include the following: While cardiogenic pulmonary oedema typically begins centrally in the bilateral perihilar areas, ARDS usually causes more uniform opacification. Pleural effusions are not typical of ARDS but often present in CHF. Kerley B lines are common in CHF but not in ARDS, while air bronchograms can be found in both. Temporally, radiographic abnormalities usually closely parallel cardiogenic pulmonary oedema, while the chest radiograph in ARDS may remain unremarkable for up to twelve hours and usually stabilize after the first thirty-six hours. While radiographic findings in cardiogenic oedema may clear rapidly, ARDS typically clears slowly. Unlike cardiogenic oedema, which, once resolved, does not leave behind permanent pulmonary changes, a percentage of ARDS cases will result in some degree of permanent , characterized by increased interstitial markings depending on the severity and length of time the patient was in ARDS.

CXR of a patient with ARDS

3. Abnormal Opacities:

A. Atelectasis: It is the most frequent abnormality detected in the ICU chest film. Atelectasis in ICU patients occurs most frequently in the left lower lobe, presumably due to compression of the lower lobe bronchus by the heart, in the supine patient. Contributing to this tendency is the relatively greater difficulty of blind suctioning of the left lower lobe. Usually atelectasis is more extensive than is suggested by the radiograph. Radiographically, atelectasis may vary from complete lung collapse to relatively normal-appearing . For example, acute mucus plugging may cause only a slight diffuse reduction in lobar or lung volume without visible opacity. Mild atelectasis usually takes the form of minimal basilar shadowing or linear streaks (subsegmental or "discoid" atelectasis) and may not be physiologically significant. Atelectasis may also appear similar to (dense opacification of all or a portion of a lung due to filling of air spaces by abnormal material), making it difficult to distinguish from pneumonia or other causes of consolidation. The distinction between atelectasis and other causes of consolidation -atelectasis will often respond to increased ventilation, while pneumonia, for example, will not. Crowding of vessels, shifting of structures such as interlobar fissures towards areas of lung volume loss and elevation of the hemidiaphragm suggests atelectasis. Another key for distinguishing between atelectasis and consolidation is recognition of the typical patterns that each pulmonary lobe follows when collapsing Right upper lobe atelectasis is easily detected as the lobe migrates superomedially toward the apex and mediastinum. The minor fissure elevates and the inferior border of the collapsed lobe is a well demarcated curvilinear border arcing from the hilum towards the apex with inferior concavity. The left lung lacks a middle lobe and therefore a minor fissure, so left upper lobe atelectasis presents a different picture from that of the right upper lobe collapse. The result is predominantly anterior shift of the upper lobe in left upper lobe collapse, with loss of the left upper cardiac border. The expanded lower lobe will migrate to a location both superior and posterior to the upper lobe in order to occupy the vacated space. As the lower lobe expands, the lower lobe artery shifts superiorly. The left mainstem bronchus also rotates to a nearly horizontal position. Right middle lobe atelectasis may cause minimal changes on the frontal chest film. A loss of definition of the right heart border is the key finding. Right middle lobe collapse is usually more easily seen in the lateral view. The horizontal and lower portion of the major fissures start to approximate with increasing opacity leading to a wedge of opacity pointing to the hilum. Like other cases of atelectasis, this collapse may by confused with right middle lobe pneumonia. Atelectasis of either the right or left lower lobe presents a similar appearance. Silhouetting of the corresponding hemidiaphragm, crowding of vessels, and air bronchograms are standard, and silhouetting of descending aorta is seen on the left. It is important to remember that these findings are all non-specific, often occurring in cases of consolidation, as well. A substantially collapsed lower lobe will usually show as a triangular opacity situated posteromedially against the mediastinum. Silhouetting of the right hemidiaphragm and air bronchograms are common signs of right lower lobe atelectasis. Right lower lobe atelectasis can be distinguished from right middle lobe atelectasis by the persistence of the right heart border.

B.: The radiographic appearance of pneumonia may be difficult to differentiate from atelectasis or early ARDS. Classically, pneumonia first appears as patchy opacifications or ill-defined nodules. It is often multifocal and bilateral, occurring most often in the gravity dependent areas of the lung. This feature makes it difficult to distinguish from atelectasis or pulmonary oedema. E-coli and pseudomonas species can rapidly involve the entire lung. Their symmetric pattern often simulates pulmonary oedema. The presence of patchy air space opacities, air bronchograms, ill-defined segmental consolidation or associated pleural effusion support the diagnosis of pneumonia. Occasionally, in gram-negative pneumonias small lucencies may be found within consolidated lung which may represent unaffected acini or areas of air trapping. This is particularly likely to occur in patients with underlying COPD. However, these must be distinguished from lucencies created by cavitation and abscess formation. Complications of nosocomial pneumonias: pleural effusions, empyema, formation.

CXR showing (Klebsiella) Pneumonia

C. Aspiration . The chest film in patients that progress to pneumonitis will reveal pulmonary consolidation within the first two days. The consolidation is usually perihilar and bilateral, though asymmetric. The radiographic findings begin to stabilize or resolve by the third day. Some patients' radiographs will show worsening of the consolidation as well as findings associated with pneumonia, including pleural effusions and abscess formation. Aspiration may also cause ARDS.These events seldom proceed to pulmonary consolidation. However, aspiration of infected material may lead to pneumonia.

D.: Due to its relative lack of sensitivity, the chest x-ray in patients with suspected pulmonary embolism is usually relegated to the role of ruling out other disorders which may have a similar clinical presentation. The chest x-ray is also very useful when interpreting ventilation-perfusion scans. Though the majority of patients with pulmonary embolism in retrospect do have abnormalities on the chest x- ray, findings are usually too non-specific to be of diagnostic value. Without infarction there are few chest film signs of pulmonary emboli. These include discoid atelectasis, elevation of the hemidiaphragm, enlargement of the main pulmonary artery into what has been described as the shape of a "sausage" or a "knuckle" (Palla's sign), and pulmonary oligemia beyond the point of occlusion (Westermark's sign). Pulmonary Infarction-Multifocal consolidation of the affected lung may occur in 12 to 24 hours following the embolic event. A consolidation which begins at the pleural surface and is rounded centrally is called a Hamptom's Hump. These types of consolidation differ from pneumonia in that they lack air bronchograms. Up to 50% of patients with pulmonary embolism will also have ipsilateral or bilateral nonspecific pulmonary effusions. It is unusual for pulmonary infarctions to be diagnosed by chest although infarctions are known to occur much more frequently. Presumably infarcts are confused with or indistinguishable from atelectasis or pneumonia. Despite the low sensitivity of these signs, the chest radiograph remains an important first step in the diagnosis of pulmonary embolism, primarily to exclude other causes of and to aid in the interpretation of the ventilation/perfusion scan.