The Core Curriculum: Cardiopulmonary Imaging, 1st Edition (2004)

Chapter 10. Thoracic Imaging in the Critically Ill

Imaging of the thorax in critically ill and/or intensive care unit (ICU) patients has an important role in successful patient management. Portable chest radiography is the mainstay for evaluation of the thorax in these patients. Chest radiographs are either performed as daily routine examinations or are performed as urgent or immediate examinations due to abrupt changes in clinical status or the manipulation of indwelling diagnostic, therapeutic or monitoring lines, tubes, and devices. The latter are covered in detail in Chapter 11. Performing daily routine portable chest radiographs on ICU patients has been shown to detect unexpected problems, with subsequent alterations in the diagnostic approach or treatment after nearly 40% of “routine” examinations and after nearly two-thirds of all portable chest radiographs on ICU patients (1,2,3). Although routine testing faces considerable scrutiny by health care facilities and third-party payers facing constant pressure to reduce costs, such imaging for critically ill intensive care unit patients may be justified as an effective method to discover unexpected problems that may be a source of morbidity or mortality. Guidelines for portable radiography can be developed successfully by multidisciplinary teams, so that imaging is appropriate (4,5).

Daily routine portable radiographs in ICU patients commonly reveals significant findings.

Important elements of acute care radiology include not only the timely performance and accurate interpretation of examinations, but prompt communication of abnormalities to the ordering physician. Daily radiology rounds between radiologists and the ICU team, including physicians, nurses, and respiratory therapists, promotes quality patient care. Bitetti and Zimmerman (6) described the concepts of such a team, indicating the positive benefits of improved diagnostic information, facilitated sequencing of studies, and decreased hospital length of stay.

In the last decade, computed tomography (CT) has played a greater role in the imaging of critically ill ICU patients (7,8,9,10,11). Clinical indications for CT in this setting include distinguishing between pleural and parenchymal disease (Fig. 10.1) and evaluating pleural fluid collections, including empyema (Chapter 17), lung abscess (Fig. 10.2), mediastinal abnormality, abnormal or unusual fluid or air collections (Fig. 10.3), and pulmonary embolism (Chapter 21). CT may also be used for CT-guided percutaneous drainage and fluid aspiration (12). CT for ICU patients generally requires the transportation of ill and often medically unstable patients to the radiology department, with careful attention to the logistical difficulties of maintaining life support systems during transportation. Physiologic changes are common during transportation, as frequently occurs when these patients are in the ICU. In one study, 39% of all patients transported to radiology had a change in management within 48 hours of the diagnostic examination; for abdominal CT examinations, that number was even higher, at 51% (13). At our institution the transportation of adult ICU patients to radiology is done by a specialized team of six registered nurses with critical care training, called the SWAT team (Smiling,Willing, Able and Technical), a concept developed at the University of Missouri (14). Up to two SWAT nurses and a respiratory therapist usually transport the ICU patients, depending on their clinical status. Use of specially trained nursing staff has been shown to reduce adverse outcomes associated with intrahospital transportation of critically ill patients (14).

Figure 10.1 Empyema confused for lung consolidation on chest radiograph. A. Posteroanterior and (B) lateral chest radiographs demonstrate ill-defined opacity over the mid-lower left lung, seen over the spine on the lateral view (asterisk), without sharp borders.C. Computed tomography demonstrates a loculated left pleura fluid collection, heterogeneous in attenuation, with pleural thickening and enhancement.

Mobile or portable CT scanners are also available to use in or adjacent to the ICU (15,16). In general, image quality is poorer than the modern fast helical CT scanners that are prevalent today. Portable CT scanners are not technically capable of performing fast CT angiographic examinations, as required to evaluate for suspected pulmonary embolism or vascular emergencies. They are capable of basic evaluation of the lungs, pleural spaces and mediastinum, abdomen, and intracranial structures. In one series, the physicians who ordered portable CTs cited that patient severity of illness, use of extracorporeal life support, and cardiovascular instability were the most common indications for the study; when faced with a situation in which the portable CT scanner was not available, 67% of physicians ordered fixed helical CTs requiring transportation to the radiology department (15). In contrast to CT, ultrasound examinations may be performed at the bedside and are particularly useful for the evaluation of pleural fluid collections, both for diagnosis and percutaneous ultrasound-guided intervention (Chapter 22) (17,18).

Figure 10.2 Right middle lobe lung abscess secondary to methicillin-resistant Staphylococcus aureus (MRSA) with pericardial effusion.A. Posteroanterior chest radiograph demonstrates a mass-like opacity in the right middle lobe and a large cardiac silhouette. B.Computed tomography demonstrates the mass to be a fluid and air-filled lung abscess with a moderately sized pericardial fluid collection that required a surgical pericardial window for drainage.

Figure 10.3 Negative pressure pulmonary edema. Computed tomography image after traumatic intubation for thoracoscopic thoracic duct ligation demonstrates ground glass opacities predominantly in the central and anterior aspect of the lungs.

Radiologic Approach

Comprehensive and systematic assessment of chest radiographs in critically ill patients includes evaluation of lung parenchymal abnormalities, pleural disease, mediastinum, cardiovascular structures, and physiologic parameters. The visualized portion of the abdomen should also be evaluated for signs of disease processes that are often silent clinically in intubated, sedated, and/or paralyzed patients. It is important to look at the musculoskeletal structures as well. The correct position of all diagnostic, therapeutic, and monitoring devices should be confirmed, as detailed to a greater extent in Chapter 11. The use of computed radiography with soft-copy interpretation of images on workstations by radiologists improves the delivery of portable chest images and facilitates the initiation of clinical actions, without any reduction in diagnostic quality, when compared with conventional film-screen radiography (19,20). As a by-product, the use of computed radiography also reduces consultation with radiologists.

Table 10.1: Lung Parenchymal Opacification in the ICU Setting

ARDS
Edema (cardiogenic and noncardiogenic)
Pneumonia
Aspiration
Hemorrhage
Underlying lung disease

ICU, intensive care unit; ARDS, acute respiratory distress syndrome.

The interpretation of portable chest radiography is made more difficult by the limited power output of portable equipment and subsequent inconsistency of filming technique. The latter can be overcome in many cases by the use of computed radiography, which allows manipulation of image parameters at a computer workstation to optimize evaluation of the thorax. Patient factors also contribute to reduced image quality and include the inability to position patients fully upright, the inability to obtain images free of respiratory motion at full inspiration in intubated and often medically paralyzed patients, and the superimposition of the internal and external components of lines, tubes, and devices.

Causes of lung parenchymal abnormality are discussed here, including acute respiratory distress syndrome (ARDS), acute interstitial pneumonitis (AIP), infection (Chapters 5 and 6), atelectasis, aspiration, and both cardiogenic and noncardiogenic pulmonary edema (Table 10.1). Abnormal air collections are then discussed, including pneumomediastinum, pneumopericardium, pneumatoceles, and interstitial emphysema. Pneumothorax is discussed briefly here in the setting of barotrauma and in greater detail in Chapters 12 and 17.

Pulmonary Parenchymal Opacification

Acute Respiratory Distress Syndrome

Definition

Previously termed adult respiratory distress syndrome, the modern definition of acute respiratory distress syndrome (ARDS) was reported in 1967 by Ashbaugh et al. (21). Today, ARDS is defined as the onset of acute respiratory failure, accompanied by severe and persistent hypoxemia despite the administration of high concentrations of inspired oxygen (ratio of arterial partial pressure of oxygen-to-fraction of inspired oxygen less than 200 mm Hg), pulmonary capillary wedge pressure (PCWP) less than 18 mm Hg, and the absence of elevated left heart filling pressures, with consolidation in three or four quadrants of the lungs on the chest radiograph. This definition was reported by a joint American–European Consensus Conference on ARDS (22). The definition had previously included diffuse pulmonary opacity, shunt physiology, increased dead space, and decreased lung compliance in the absence of increased left-sided filling pressures (23). Systemic inflammatory response syndrome may be a precursor to or trigger acute lung injury, ARDS, and multiple organ system failure (24). Systemic inflammatory response syndrome is defined as a systemic inflammatory response to a variety of clinical insults and is manifested by two or more of the items listed in Table 10.2 (24). There are many potential proinflammatory and antiinflammatory mediators of acute lung injury, and it is the balance between these factors that culminates in the clinical manifestations of acute lung injury and ARDS. The former includes platelets and white blood cells, cytokines, endorphins and histamine, endotoxins, and vasoactive neuropeptides. The latter includes interleukins, epinephrine, leukotriene B4 receptor antagonist, and lipopolysaccharide binding protein.

Table 10.2: Systemic Inflammatory Response Syndrome (Defined as Two or More of the Items Below)

Temperature >38°C or <36°C
Heart rate >90 beats/min
Respiratory rate >20 breaths/min
WBC count
   >12,000/mm3 or
   <4,000/mm3 or
   >10% immature forms

WBC, white blood cell.

Clinical Presentation and Risk Factors

ARDS is a clinical syndrome and is diagnosed clinically not radiographically. Patients with ARDS usually present acutely with rapidly progressive dyspnea, tachypnea, and respiratory distress. The risk factors for ARDS are listed in Table 10.3, with sepsis accounting for up to 35% of cases (25). Risk factors are synergistic, with more risk factors further increasing the risk of ARDS. The mortality of ARDS remains high, between 40% and 60%, despite advances in treatment and understanding of the pathophysiology of ARDS. There has been a gradual reduction in mortality. In general, mortality from ARDS is lower in patients less than 60 years of age and in patients with ARDS secondary to sepsis (26).

ARDS is a clinical syndrome, not a radiographic diagnosis.

Radiography and Phases

Although the diagnosis of ARDS is based primarily on clinical findings, the chest radiograph may provide additional diagnostic information concerning the effectiveness of treatment, complications, and prognosis. Bachofen and Weibel (27) described the three pathologic phases of ARDS lung injury and response in 1977: the acute exudative phase/stage, a fibroproliferative phase, and a fibrotic phase or healing stage. The acute phase, represented pathologically by diffuse endothelial cell injury with alveolar capillary leak of proteinaceous fluid and neutrophils, manifests radiologically as diffuse ill-defined alveolar opacities predominantly in the lung periphery (Fig. 10.4A) (28). As capillary leak progresses, with greater extravasation of fluid from the intravascular space into the alveoli, widespread pulmonary opacification and complete “white-out” of the lungs occurs radiographically (Fig. 10.4B) (29). Grossly, the lungs are heavy and wet. Other microscopic pathologic features include platelet microthrombi and white blood cells in the capillary lumen, swelling of capillary endothelial cells, infiltration by polymorphonuclear leukocytes, and hyaline membrane formation within the alveoli. Injury to alveolar epithelial cells results in decreased surfactant production and therefore decreased lung compliance, reflected on radiographs as small lung volume and atelectasis (27).

Table 10.3: Risk Factors for Acute Respiratory Distress Syndrome

Sepsis
Systemic inflammatory response syndrome
Disseminated intravascular coagulation
Prolonged hypotension
Gastric acid aspiration
Near drowning
Trauma, lung contusion, fat embolism
Burn injury
Pancreatitis
Multiple emergency transfusions
Post-cardiopulmonary bypass

Figure 10.4 Progression of acute respiratory distress syndrome on serial chest radiographs in a patient on extracorporeal life support over 12 days. A. Diffuse alveolar opacity. B. Dense bilateral alveolar opacity with extensive air bronchograms. Little to no alveolar air filling, only air within the bronchial tree.

Figure 10.5 Acute respiratory distress syndrome with pneumatoceles in a patient with late-stage acute respiratory distress syndrome, day 19 after clinical diagnosis of acute respiratory distress syndrome. A. Chest radiograph and (B) computed tomography demonstrate bilateral thin walled lucencies (arrows) representing pneumatoceles on a background of ground glass and reticular lung opacities.

Table 10.4: Radiologic Manifestations of Barotrauma

Pneumothorax
Pneumomediastinum
Pneumopericardium
Pulmonary interstitial emphysema
Pneumoperitoneum
Pneumoretroperitoneum

In general, during the acute exudative phase, the alveolar opacities of ARDS progress over several days on chest radiographs, until there is diffuse or near diffuse opacification of the lungs. Subsequently, the appearance changes very slowly from day to day. The alveolar edema of ARDS is not associated with widening of the vascular pedicle, cardiomegaly, or altered pulmonary blood flow distribution, which is in contrast to cardiogenic, uremic, and hypervolemic pulmonary edema. Because capillary leak occurs directly into the alveolar spaces, septal lines are usually absent on chest radiographs in ARDS. Although the pulmonary vessels are generally not visible through the alveolar opacities, when seen they may be vasoconstricted. In the subacute phase, which occurs over the next 5 to 10 days after the acute phase, the pathologic findings are proliferation of epithelial cells and fibroblasts, together with collagen deposition. This produces the radiographic findings of progressive lung destruction and a transition from alveolar to combined alveolar and interstitial opacities (Fig. 10.5). Findings of barotrauma (Table 10.4), including pneumothorax and pneumatocele formation, are frequent during this fibroproliferative phase, during which fibrosis has developed and the lungs become stiff and noncompliant (30,31). Although some patients recover from ARDS with no pulmonary function deficit, other patients eventually enter the chronic phase several weeks after the initial lung injury, manifested by fibrosis and focal emphysema on chest radiographs.

ARDS generally changes slowly on radiographs from day to day.

Early recognition of barotrauma in ARDS patients is important to minimize potentially serious complications, such as tension pneumothorax.

Computed Tomography

CT of ARDS was first reported in the early-to-mid 1980s and has been studied extensively since that time. Much of the work has been performed by Gattinoni and colleagues (32,33,34). What was once thought to be a disease process that homogeneously involved both lungs based on chest radiography is now recognized to be a more heterogeneous process based on CT investigations. The CT appearance varies with the etiology of ARDS, mechanical ventilation, patient position, and time. For example, in ARDS secondary to direct lung injury, such as pneumonia or aspiration, the radiologic appearance is more patchy and multifocal. In contrast, in ARDS with indirect lung injury, such as sepsis or sustained hypotension, lung injury is more diffuse (Fig. 10.6) (35). CT is clinically useful in patients with ARDS who are not improving or are deteriorating clinically, by identifying pleural effusions, lung abscess, lobar atelectasis, barotrauma, and malpositioned lines and tubes more accurately than chest radiographs (36,37).

Ground glass opacity, consolidation, and a reticular pattern are the hallmarks of ARDS on CT. The ground glass opacity is believed to represent active inflammation in lung interstitium and alveolar wall, coupled with incomplete alveolar filling by inflammatory cells, cellular debris, and edema. Consolidation is due to either complete filling of the alveolar spaces with fluid and debris, and/or atelectasis, referred to as the collapse of potentially recruitable lung units. If a patient were to be placed prone, the potentially recruitable lung units may reexpand and fill with air, thereby improving gas exchange. This has lead to the theory that patients with ARDS should be rotated regularly, with changes in the distribution of lung abnormality demonstrated on CT with changes in position (34,38). The reticular pattern may be seen both acutely, secondary to edema or inflammation, or in the chronic phase of ARDS, representing fibrosis. During the acute phase of ARDS, the anterior or most nondependent lung may be normal or near normal, whereas the mid-third of the lungs in the ventral to dorsal direction is ground glass in attenuation, with consolidation in the dorsal or most dependent lung, creating a ventral to dorsal gradient of lung attenuation. A cranial-to-caudal gradient is also noted, being more consolidated in the lower lungs than at the apices.

Figure 10.6 Computed tomography of acute respiratory distress syndrome demonstrates dense bilateral alveolar consolidation, more severe in the dependent (posterior) regions of the lungs than the nondependent (anterior) regions. Scattered small lucencies within the consolidation are pneumatoceles.

If ARDS resolves within 1 week, there are usually few if any radiologic sequelae. With a more protracted course of ARDS, the exudated fluid is reabsorbed from the lung and the fibroproliferative organizing phase sets in. Lung attenuation improves, whereas signs of fibrosis, including distortion of the normal bronchovascular architecture, may be found. Subpleural cysts, also known as pneumatoceles, varying in size from a few millimeters to a few centimeters, develop in both the dependent and nondependent lung.

Follow-up high resolution CT of the lungs after ARDS demonstrates fibrosis in most patients (39,40). The extent of fibrosis correlates with the severity of ARDS, the duration of mechanical ventilation using high peak inspiratory pressures, and a higher fraction of inspired oxygen. The location of the fibrosis is predominantly in the ventral or nondependent lung in the supine position, suggesting that it may be secondary to the high peak inspiratory pressures and oxygen therapy used to treat ARDS rather than to the ARDS itself. The collapsed dependent lung may be spared from this injury, protected by the failure to ventilate this region of the lung. Partial liquid ventilation is an experimental treatment for ARDS, in which perfluorocarbon is instilled into the airway with continuous gas ventilation through the endotracheal tube. Perfluorocarbon is a clear odorless liquid that is radiopaque (41). It distributes within the lungs in a gravity-dependent distribution, which matches the distribution of the most severely consolidated lung in ARDS, where it reduces alveolar surface tension and keeps the alveoli distended to facilitate gas exchange (Fig. 10.7).

Figure 10.7 Partial liquid ventilation with perfluorocarbon. Computed tomography images photographed on (A) bone and (B) soft tissue windows settings demonstrate the gravity dependent distribution of the high attenuation perfluorocarbon.

Acute Interstitial Pneumonitis

AIP is an idiopathic form of acute lung injury, characterized by rapidly progressive cough and dyspnea leading to severe hypoxemia and respiratory failure over days. This short duration is in contrast to other chronic idiopathic interstitial pneumonias, such as usual and nonspecific interstitial pneumonitis that have a more insidious disease onset (Chapter 14). AIP was formerly referred to as Hamman-Rich syndrome. In 1935 Hamman and Rich (42) described five patients with acute lower respiratory tract illness, four of whom died after hospital stays of up to 6 months; one died within days. At autopsy, organizing diffuse alveolar damage and diffuse interstitial fibrosis was present in all cases (42). In 1986 Katzenstein and colleagues (43) coined the phrase “acute interstitial pneumonia” to reflect the acuity of the disease and distinguish it from other chronic interstitial pneumonias. Others later reviewed the autopsy material of the original 1935 cases and compared them with current cases of AIP, confirming that the pathologic lesion of AIP was identical to that described by Hamman and Rich (44).

AIP is acute diffuse alveolar damage of unknown etiology.

AIP should be suspected in patients diagnosed initially with severe diffuse bilateral community-acquired pneumonia that does not respond to broad-spectrum antibiotics and from whom no infectious organism is isolated (45). It is distinguished from ARDS by the absence of a known cause of ARDS and the lack of systemic involvement or multisystem organ failure. Surgical lung biopsy in AIP demonstrates organizing diffuse alveolar damage, the same pathologic lesion seen in the fibroproliferative phase of ARDS (45). Similar to ARDS, the chest radiographic manifestations of AIP are bilateral, patchy, alveolar opacities that may progress to extensive diffuse consolidation. Reported survival in AIP ranges from 26% to 67%; however, the higher numbers likely reflect case series contaminated by ARDS and the lower figure is from a series of well-documented biopsy-proven cases. The number of pathologically confirmed AIP cases is small, and the impact of treatment, such as corticosteroids or cytotoxic drugs that are used for other forms of interstitial pneumonitis, is unclear.

Infection

Pulmonary infections are covered extensively in Chapters 5 and 6. Aspects of infection as they relate to ICU patients are discussed here. The radiographic hallmark of pneumonia is airspace consolidation with air bronchograms, which may be segmental, lobar, or diffuse in distribution. New or progressing consolidation, together with two or more of the following, should raise suspicion for pneumonia: fever, hypothermia, peripheral leukocytosis or leukopenia, purulent respiratory secretions, and worsening respiratory failure (22). In critically ill patients the diagnosis of pneumonia may be delayed or unrecognized, because fever and leukocytosis may be absent. Fever may also be present in at least 50% of patients with atelectasis and no pneumonia, making it a poor clinical sign of infection (46,47). Pneumonia is difficult to diagnose in the setting of ARDS, with a high false-negative rate, as high as 29% (27). In a series by Mock et al. (48), the clinical variables and radiographic findings of 80 patients with positive sputum cultures were reviewed. One point each was given for the presence of new airspace “shadows,” air bronchograms, segmental infiltrates, asymmetric infiltrates, infiltrates in nondependent lung, ipsilateral pleural effusion, and for the absence of volume loss, cardiomegaly, and hilar enlargement on chest radiographs. Clinical symptoms of fever, leukocytosis, respiratory failure, and mortality did not correlate with the radiographic findings. Patients with high radiographic scores, ranging from 4 to 10, were more likely to have positive blood and fluid cultures, polymicrobial cultures, multisystem organ failure, Escherichia coli or Pseudomonas infection, and improvement on antibiotics.

Clinical signs of pneumonia are often absent in critically ill patients.

Table 10.5: Risk Factors for Nosocomial Pneumonia in the Intensive Care Unit

Prolonged mechanical ventilation
Depressed consciousness
Massive gastric aspiration
Prophylactic antimicrobial therapy
Histamine 2 receptor blockers
Continuous enteral feeding
Corticosteroid use

Nosocomial infections in the ICU setting are of particular concern, both in surgical and medical ICUs. They occur in 20% to 40% of patients, increasing morbidity, mortality, and costs (49,50,51,52). For example, in one series of trauma ICU patients, mortality was 43.5% in the patients with nosocomial pneumonia compared with 18% in the patients without nosocomial pneumonia (49). Risk factors for nosocomial infection are listed in Table 10.5. Prolonged mechanical ventilation is a major risk factor. Endotracheal tubes bypass natural host defenses, allow leakage of bacteria and secretions around the cuff into the airway, damage the ciliated tracheal epithelium, reduce bacterial clearance from the trachea, and direct bacteria into the lungs through tube manipulation and airway suctioning. It has been estimated that for each day of mechanical ventilation, the risk of nosocomial pneumonia increases by 1% (53). The organisms responsible for the infection and the rate of infection may vary from hospital to hospital and even from ICU to ICU within the same hospital (54). CT may be useful in ICU patients with sepsis of unknown origin, identifying the source of fever within the thorax or abdomen in nearly 20% of patients (55).

The risk of nosocomial pneumonia increases by 1% for each day intubated.

Another form of thoracic infection that should be considered in ICU patients is septic pulmonary emboli. ICU patients are at risk due to indwelling vascular catheters for combined underlying infection or nosocomial infection. When patchy bilateral lung parenchymal opacities or wedge-shaped nodularity develops, often subpleural in distribution, the possibility of septic pulmonary emboli should be raised (Figs. 21.24and 21.25). Although the lung abnormality usually increases slowly, in some cases progression can be quite rapid. The nodules are usually less than 3 cm in size and may cavitate (56). CT is more sensitive than plain radiography for diagnosing septic emboli and may yield a diagnosis before it is clinically or radiographically suspected (56,57,58)

Patchy subpleural alveolar or nodular opacities should raise the suspicion of septic pulmonary emboli.

Aspiration and Aspiration Pneumonia

Critically ill patients are at increased risk of aspiration and aspiration pneumonia. Predisposing reasons for this are given in Table 10.6. Aspiration should be suspected when chest radiographs demonstrate the sudden appearance of new focal alveolar opacities (Fig. 10.8).

Unless occurring acutely related to manipulation of airway or esophageal tubes, episodes of aspiration are often unrecognized by caretakers. Aspiration can be divided into three categories, according to the type of fluid aspirated and subsequent lung reaction: toxic, bland, and infectious (Table 10.7) (59).

Table 10.6: Factors that Contribute to Aspiration in Intensive Care Unit Patients

Tracheal and esophageal intubation
Depressed cough reflex
Impaired mucociliary function
Increased secretions
Supine position
Cardiopulmonary resuscitation events

Figure 10.8 Aspiration in an intubated intensive care unit patient manifesting as new bibasilar consolidation. The chest radiograph was normal the previous day and returned to normal 5 days later.

Acute focal or multifocal alveolar opacities, particularly at the lung bases or in superior segments of lower lobes, should raise the suspicion of aspiration, which is often clinically silent.

Toxic aspiration occurs with the aspiration of acidic gastric contents with an acidic pH of less than 2.5 or water-soluble radiographic contrast material. In toxic aspiration, severe bronchospasm and chemical pneumonitis may develop within minutes of aspiration, manifesting radiographically as noncardiogenic pulmonary edema. When massive, toxic aspiration may result in immediate apnea, hypotension, and shock. Half of these patients will subsequently develop fever and leukocytosis, in the absence of infection, confounding the caretakers into diagnosing pneumonia. In milder forms, there may be mild bronchiolitis. The radiographs may also mimic pneumonia; however, unlike pneumonia, the alveolar opacities gradually improve over 1 to 2 days, which is faster than bacterial pneumonia.

When bland fluid, such as water, blood, or fluid, is aspirated, the radiograph may be normal unless a large volume of fluid is aspirated. Transient respiratory distress usually improves after airway suctioning, and there is usually no significant inflammatory lung response. If either toxic or bland fluid is aspirated in conjunction with solid foreign material such as food, the radiographs will demonstrate airway obstruction with distal atelectasis and frequently subsequent pneumonia.

The aspiration of infected material, such as pharyngeal or airway secretions colonized by multiple organisms, results in radiographic findings of pneumonia, with persistent alveolar consolidation. The location of the abnormality is related to patient position during the aspiration event. When supine, the superior segments of the lower lobes, particularly on the right, are most common, followed by the posterior segments of the upper lobes (60). When upright, the basilar segments of the lower lobes are usually involved (Fig. 5.20). If the patient is prone, as is common when using a rotational bed, the abnormality may be located in the anterior segments of the upper or lower lobes, the middle lobe, or lingula. Aspiration occurring when in a decubitus position may involve multiple or even all segments of the dependent lung and completely spare the nondependent lung. Aspiration of infected contents in hospitalized patients or patients with poor oral hygiene may cause necrotizing pneumonia due to anaerobic organisms, often accompanied by cavitation and empyema. The most commonly implicated organism is Pseudomonas aeruginosa.

The location of opacities due to aspiration depends on patient position during the aspiration event.

Table 10.7: Categories of Aspiration

Toxic
Bland
Infectious

Atelectasis

In contrast to the hazy increased lung parenchymal opacity of pulmonary edema, diffuse atelectasis can often be recognized by secondary signs of volume loss, including low lung volumes and crowding of the bronchovascular structures and ribs. In intubated patients, chest radiographic exposure should be timed to peak inspiration of the ventilatory cycle after tidal volume has been delivered, because images at end-expiration will suffer from diffuse atelectasis and therefore be suboptimal for the evaluation of lung disease. Focal bibasilar subsegmental atelectasis is more common and often transient. After cardiac surgery, the left lower lobe is a common location for both atelectasis and pneumonia, secondary to stretching and cold-induced injury of the phrenic nerve (61). Angulation of the x-ray beam is important. With as little as 10 degrees of lordotic angulation the beam is no longer tangential to the apex of the hemidiaphragm, creating pseudo-opacity in the left retrocardiac region that may be interpreted as atelectasis or consolidation behind the heart (62).

Intubated patients are at increased risk of mucous plugging of the airway due to decreased ciliary function, depressed cough reflex, and increased secretions. Mucous plugging may be a source of acute respiratory decompensation. Whenever acute lobar collapse or even whole lung collapse is identified radiographically, mucous plugging should be suspected. Suctioning of the airway usually results in radiographic and clinical improvement (Fig. 10.9). Atelectasis without air bronchograms is more responsive to suctioning than atelectasis with air bronchograms because of the presence of occlusive secretions within the airway that are amenable to removal (63).

Acute partial or complete lung collapse in an intubated patient is most commonly due to a mucous plug in the airway.

Figure 10.9 Acute lobar collapse secondary to a mucous plug in an intensive care unit patient. A. Initial radiograph demonstrates normal lungs. B. Radiograph a few hours later demonstrates acute left lower lobe collapse with retrocardiac and left lower lung opacity (asterisk) obscuring the left hemidiaphragm, slight shift of the heart toward the left, crowding together of the left posterior ribs compared with the right side, and leftward positioning of the esophagus compared with A as demonstrated by the esophageal tube.

Evaluation of Cardiovascular Status

Circulating blood volume (CBV), central venous pressure (CVP), pulmonary blood volume (PBV), pulmonary arterial pressure (PAP), capillary wedge pressure, and systemic extravascular water are indications of cardiovascular status that can be evaluated with chest radiographs (64,65,66,67). The radiographic findings of these cardiovascular status indicators are listed in Table 10.8 and have been shown to correlate with both clinical symptoms and physical examination findings.

Circulating Blood Volume

CBV, also known as systemic blood volume, is defined as the total volume of blood within the systemic circulation, including the heart, arteries, veins, and capillaries and excluding the pulmonary circulation. The vascular pedicle width across the superior mediastinum can be used to evaluate CBV (64,66,68,69). The term vascular pedicle width was introduced in the 1970s by Eric Milne, to whom a great deal of our understanding of physiology as it relates to chest radiography interpretation is credited (64,68,70). The right margin of the vascular pedicle is formed by the lateral aspect of the right brachiocephalic vein and the superior vena cava. The left margin is formed by the lateral aspect of the left subclavian artery and the aortic arch. The thoracic vessels that make up the borders of the vascular pedicle are distensible and respond to changes in CBV. The right border of the vascular pedicle is made up entirely of venous structures that are more distensible than the arterial structures that make up the left border; therefore, the right border changes more readily in response to changes in systemic blood volume.

Vascular pedicle width is used to evaluate circulating blood volume.

Changes in the vascular pedicle width on radiographs obtained with consistent positioning indicate changes in CBV and fluid status (66,69,71). Changes in the vascular pedicle width are more important than an absolute measurement and have been shown to have a greater correlation with CBV. The normal vascular pedicle width is 4.8 cm ± 5 mm, acknowledging that in general larger people have a wider pedicle than thin people (66). The vascular pedicle should be measured from two points. On the right side, it should be measured from where the upper border of the right main bronchus crosses the superior vena cava. On the left side, it should be measured from the aortic arch at the left subclavian artery origin (Figs. 10.10 and 10.11). A line is drawn vertically down from the left point to meet a line drawn horizontally from the right point. The meeting point of the two lines to the right point is the vascular pedicle width. The supine position increases the width of the vascular pedicle by increasing venous return. Expiration increases the width of the mediastinum relative to the width of the thorax but has little effect of the vascular pedicle, because expiration is accompanied by increased intrathoracic pressure and pumping of blood out of the thoracic vessels (70).

Changes in vascular pedicle width are more important than a single measurement at one point in time.

Table 10.8: Measures of Cardiovascular Status that Can Be Evaluated on Radiography

Parameter

Indicators

Circulating blood volume

Vascular pedicle width
Transverse cardiac diameter
Azygos vein diameter
Pulmonary blood volume

Central venous pressure

Azygos vein diameter
Vascular pedicle width

Pulmonary blood volume

Pulmonary artery-to-bronchus ratio
Pulmonary vascular recruitment

Pulmonary arterial pressure

Central vs. peripheral pulmonary artery diameter
Vessel tortuosity
Increased pulmonary artery: vein diameter

Capillary wedge pressure (LV function)

Pulmonary vascular cephalization
Interstitial edema
Alveolar edema

Systemic extravascular water

Chest wall thickness

LV, left ventricular.

Figure 10.10 Measuring the vascular pedicle. Step 1: right side (dotted horizontal line): measure from where the upper border of the right main bronchus crosses the superior vena cava to midline (1). Step 2: left side (solid horizontal line): measure from the aortic arch at the left subclavian artery origin to midline (2). Step 3: add measurements from steps 1 and 2 above.

The transverse diameter of the heart, the azygos vein diameter, and PBV also change with CBV but are less predictable than the vascular pedicle width. Unequivocal radiographic change in left ventricular chamber size occurs reproducibly only with a 66% increase in volume (67). Changes in the distance from the right heart border to midline correlate better with changes in CBV than the total transverse cardiac diameter.

Figure 10.11 The vascular pedicle and azygos vein in a patient with alcohol- and cocaine-induced cardiomyopathy. A. Normal vascular pedicle (lines) and azygos vein (arrow). B. Enlarged vascular pedicle (lines), enlarged azygos vein (arrow), and increased heart size.

Central Venous Pressure

CVP is the pressure of blood returning to the right side of the heart, in either the superior or inferior vena cava, immediately adjacent to the heart. CVP reflects right ventricular function, fluid balance, and peripheral vascular resistance. CVP can be invasively and directly measured using a CVP catheter placed into the superior vena cava, usually through either a subclavian vein or internal jugular vein or through the proximal port of a pulmonary arterial catheter (a.k.a. Swan-Ganz catheter). Because there is no valve between the superior vena cava and the right atrium, the pressure is the same. In the absence of tricuspid valve disease, CVP reflects right ventricular end-diastolic pressure, as measured when the tricuspid valve is open. The catheter is attached to either a transducer/monitor system or a manometer set to 0 when held at bedside at the level of the right atrium. Normal CVP measures 4 to 12 mm Hg. CVP is commonly monitored in evaluating the need and effectiveness of fluid replacement or resuscitation. Trends in CVP are more important than an absolute single measurement.

Noninvasively, the azygos vein diameter can be used as an indicator of CVP. On a frontal radiograph, the azygos vein is seen end-on just above the right main bronchus in the right tracheobronchial angle in approximately 85% of chest radiographs (Fig. 10.11) (72). The azygos vein is a distensible structure that responds directly to changes in right atrial pressure (64). It also responds to changes in CBV, paralleling changes in the vascular pedicle width, but less consistently. The azygos vein increases in diameter 7% for every 1% increase in the vascular pedicle width. If the azygos vein is disproportionately large, it should prompt evaluation for causes of inferior vena cava obstruction, acquired or congenital, such as azygos continuation of the inferior vena cava. Normal azygous vein diameter is usually 1 cm or less. Changes in the relative width of the azygos vein on serial chest images can be used as an indicator of CVP. When switching from a posteroanterior to an anteroposterior chest view, there will be a slight increase in the azygos vein diameter. Clinical evidence of elevated CVP includes neck vein distension, peripheral edema, and hepatomegaly.

Azygos vein diameter is used to evaluate CVP.

Causes of elevated and reduced CVP are listed in Table 10.9. Left ventricular failure and mitral valvular disease can both cause increased pressure in the left atrium, subsequently extending into the pulmonary veins, pulmonary arteries, and right heart, resulting in an elevated CVP. Constrictive pericarditis and cardiac tamponade both impair systemic venous return and thereby increase CVP. Peripheral vasoconstriction and the Trendelenburg position both increase CVP by increasing systemic venous return. Chronic lung disease resulting in decreased lung compliance results in increased pulmonary resistance and elevated CVP. Low cardiac output associated with decreased venous return decreases CVP. Similarly, low CBV, as may be seen in trauma or surgery patients with blood loss or with a large gastrointestinal bleed, also reduces CVP (73). Positive pressure ventilation, pneumothorax, abdominal distension, atrial fibrillation, complete heart block, and tricuspid valve disease all lead to inaccurate falsely elevated CVP readings.

Table 10.9: Causes of Abnormal Central Venous Pressure

Increased

Reduced

Right ventricular failure
Left ventricular failure
Pulmonary arterial hypertension
Increased circulating blood volume
Mitral valve disease
Constrictive pericarditis
Cardiac tamponade
Peripheral vasoconstriction
Chronic lung disease
Trendelenburg position
Tricuspid valve disease
Pneumothorax
Atrial fibrillation/complete heart block
Abdominal distension
Pregnancy

Low cardiac output
Low circulating blood volume

Pulmonary Blood Volume and Flow Distribution

The pulmonary circulation is a high capacity low resistance system positioned between the right and left sides of the heart. Normal PBV is the total amount of blood within the pulmonary vascular circulation. PBV is much smaller than the total pulmonary vascular bed capacity by approximately 30% to 50%, allowing the accommodation of changes in cardiac output that occur physiologically between rest and exercise (resting cardiac output, 6 L/min; exercise cardiac output, up to 16 L/min). PBV varies with patient size, position, respiration, and fluid status. For example, intrathoracic pressure decreases with inspiration, increasing PBV; the reverse occurs with expiration, resulting in the pumping of blood in and out of the pulmonary circulation. Larger patients have larger PBV than smaller patients (74). Overhydration increases PBV, whereas dehydration decreases it. Causes of altered generalized PBV are listed in Table 10.10. The excess pulmonary vascular capacity allows for acute or chronic increases in PBV without an increase in right ventricular or PAP (75). Pathologic changes in the pulmonary vascular bed, as seen with primary pulmonary arterial hypertension and chronic mitral stenosis, and primary lung diseases, such as emphysema and fibrosis, decrease the total capacity of the pulmonary vascular bed, with resultant increase in pulmonary arterial and right ventricular pressures.

Pulmonary vascular capacity is almost twice as large as PBV.

PBV can be estimated by examining the relative diameter of pulmonary vessels to each other and to the adjacent bronchi. The ratio of the diameter of adjacent pulmonary arteries and bronchi seen on end, the A:B ratio, aids in determining whether vessels are abnormally enlarged (64,68). The ratio can be easily estimated on a frontal radiograph by looking at the end on anterior segmental artery and bronchus of the upper lobes (Fig. 10.12). The normal A:B ratio is 1:1 or less. It is closer to 1:1 in the supine position and 0.6 to 0.8:1 when upright. Normally, the A:B ratio is smaller in the upper lobes, 0.6 to 0.8:1, and equal in the lower lobes, because the upper lobes are relatively oligemic. Changes in PBV change both the A:B ratio and the balance of that ratio throughout the lungs. An increase or decrease in the A:B ratio throughout the lungs indicates a generalized increase or decrease in PBV, respectively (64). As PBV increases, the ratio in the upper and lower lungs may become balanced at 1:1 throughout the lungs as all the pulmonary vessels dilate. This is referred to as pulmonary vascular recruitment of additional pulmonary vascular bed capacity (Fig. 10.13). Regional changes in PBV and flow may also be seen. For example, there may be a focal increase in the A:B ratio associated with partial anomalous venous return or pulmonary sequestration or a focal decrease with pulmonary embolism, focal emphysema or bulla, or bronchial occlusion/mucous plugging; the latter are associated with a mosaic perfusion pattern on CT (Chapters 14 and 21).

The artery-to-bronchus ratio, the A:B ratio, is used to evaluate pulmonary blood flow.

Table 10.10: Causes of Altered Generalized Pulmonary Blood Volume

Increased

Decreased

Inspiration

Expiration

Fluid overload

Fluid deficiency

   Overhydration

   Dehydration

   Renal failure

Third spacing

Increased right ventricular output
   Left-to-right cardiac shunt
   Arteriovenous malformations

Cardiac tamponade

Anemia

Addison disease

Thyrotoxicosis

Hypothyroidism

Fever
Pregnancy
Exercise

Positive pressure ventilation

Figure 10.12 The pulmonary artery-to-bronchus ratio (A:B) on coned down views of the anterior segmental pulmonary artery and bronchus in the upper lobes. A. Normal ratio in the right upper lobe, with artery (arrow) slightly smaller than the bronchus (arrowhead). B. Abnormal ratio in the left upper lobe, with artery (arrow) larger than the bronchus (arrowhead).

Figure 10.13 Pulmonary vascular redistribution, also known as cephalization, on a portable chest radiograph.

Putting Circulating Blood Volume, Central Venous Pressure, Pulmonary Blood Volume, and Heart Size Together

By evaluating all the indicators of cardiovascular status described above, conclusions can be drawn from chest images regarding fluid status and underlying disease processes. For example, an increase in vascular pedicle width, transverse cardiac diameter, and PBV indicates fluid overload. A wide vascular pedicle accompanied by decreased PBV should suggest cardiac tamponade; the decreased PBV is due to reduced right ventricular output and the wide vascular pedicle due to obstructed central venous return. Finally, increased PBV with normal or decreased systemic blood volume suggests a left-to-right shunt such as a septal defect or acquired rupture of the ventricular septum after myocardial infarction.

Pulmonary Arterial Pressure

The normal PAP is 15 to 30 mm Hg systolic, 6 to 12 mm Hg diastolic, and 14 to 18 mm Hg mean. Causes of elevated PAP include primary pulmonary vascular disease, pulmonary thromboembolic disease, cardiac disease, and chronic lung disease (Chapter 21).

The pressure in the pulmonary arterial circulation can be estimated by comparing the diameter of central and peripheral pulmonary arteries (64,68). Unfortunately, these observations do not distinguish acute variations in PAP that occur in unstable ICU patients but predict a range of pressures in the steady state usually due to chronic increased vascular resistance. With a mild increase of PAP up to 40 mm Hg, there may be mild enlargement of the central pulmonary arteries and suggestion of increased tortuosity of the peripheral pulmonary arteries. These findings are consistently seen with elevations of PAP over 40 mm Hg. Pruning of arteries immediately beyond the hilum may be seen with elevations over 60 mm Hg and is more consistently seen with PAP over 80 mm Hg (76,77). As PAP increases, there is also a gradual increase in the pulmonary artery-to-vein ratio, which can reach 3 or more with elevations in PAP of more than 80 mm Hg. Initially, right ventricular hypertrophy develops in response to elevated PAP, with right ventricular chamber enlargement occurring later and often rapidly once the right ventricle begins to fail.

Central and peripheral pulmonary artery size can be used to evaluate pulmonary arterial pressure.

Left Ventricular Function

An assessment of left ventricular function can be made by analyzing the pulmonary vessels and the lung interstitium. In upright normal individuals, the diameter of the lower lobe vessels is larger than in the upper lobes (and therefore the A:B ratio is larger in the lower lungs) with preferential blood flow to the lung bases due to gravity; vessel margins are sharply delineated. In this normal state, total extravascular lung water is approximately 50 mL/L at total lung capacity (64,65). PCWP is used to reflect left-sided heart function. It is a surrogate measurement of left ventricular end-diastolic pressure, as when the mitral valve is open during diastole the pressure between the left ventricle, left atrium, and valveless pulmonary veins equilibrates. PCWP as a reflection of left ventricular function will be invalid in the setting of mitral valve disease; for example, with mitral stenosis PCWP will be artificially elevated. More details about how PCWP is measured can be found in Chapter 11. With elevations in PCWP, changes in both blood vessel size and distinctness occur (78,79). These abnormalities can be divided into three stages: cephalization or pulmonary vascular redistribution (Fig. 10.13), interstitial edema (Fig. 10.14), and alveolar edema (Fig. 10.15).

PCWP estimates left ventricular end-diastolic pressure.

Normal PCWP is 6 to 12 mm Hg. As PCWP rises above normal, vessel diameter in upper and lower lung zones first equalizes, with an A:B ratio of 1 throughout the lungs. With further increases in PCWP, redistribution of pulmonary blood flow to the upper lungs occurs, with both an increase in upper lung vessel diameter and a decrease in lower lung vessel diameter (Fig. 10.13). This is recognized radiographically as larger vessels in the upper lungs compared with lung bases and is often referred to as “cephalization” of pulmonary blood flow. A word of caution is in order when using this sign of elevated PCWP: It can only be applied when the patient is fully upright, has taken sufficient inspiration for the lungs to be near total lung capacity, and when the lung bases are normal. When there is basilar lung disease, such as atelectasis or pneumonia, cephalization will occur secondary to these disease processes to maintain ventilation-perfusion matching and gas exchanged. During this stage there is microscopic interstitial edema that is not yet visible radiographically but is enough to reduce gas exchange. The microscopic edema occurs in a gravity-dependent distribution, resulting in basilar vasoconstriction and shunting of blood flow to the upper lobes to preserve gas exchange and matching of ventilation and perfusion.

Normal PCWP is 6 to 12 mm Hg.

Figure 10.14 Interstitial edema. A. Portable chest radiograph demonstrates a large heart. B. New interstitial edema with Kerley B lines, indistinct pulmonary vessels, peribronchial cuffing, and subpleural edema manifesting as a thick minor fissure, in addition to pulmonary vascular redistribution.

Elevated PCWP leads to cephalization, interstitial edema, and alveolar edema.

Figure 10.15 Alveolar pulmonary edema with bilateral alveolar opacity. Abnormality is more diffuse in the left lung and spares the subpleural aspect of the right lung.

As PCWP rises further to 18 to 25 mm Hg, it exceeds the normal colloid osmotic pressure of blood, and a fluid transudate develops in the lung interstitium edema. The interstitium of the lungs has both a central compartment that surrounds the bronchovascular bundles and a peripheral compartment that includes the interlobular and intralobular septa. Interstitial fluid in the central compartment results in indistinct vessel margins and peribronchial cuffing. Fluid in the interlobular septa creates linear opacities that extend to the pleural surface, known as Kerley B lines, and fluid in the intralobular septa creates finer basilar reticular opacities, known as Kerley C lines (Fig. 10.14). Kerley A lines are longer and more central. At this stage, total lung water is approximately 60 to 100 mL/L measured at total lung capacity (78,79).

Kerley B lines are a classic finding in interstitial edema.

When PCWP reaches 25 mm Hg or greater, fluid transudates collect in larger amounts within both the interstitium and alveoli, producing alveolar pulmonary edema. Radiographically, this manifests as diffuse, symmetric, bilateral, ill-defined, or fluffy lung opacity, often in a perihilar and basilar predominant distribution edema (Fig. 10.15). When alveolar edema begins to appear, lung water is estimated to be 110 to 130 mL/L, increasing to 160 mL/L or more with widespread edema (78,79).

Hemodynamic measurements reflect a moment in time. In contrast, the movement of water in and out of the extravascular compartment may take hours to days. For example, the resorption of fluid from the lung and clearance of lung opacity on radiographs may lag behind normalization of PCWP by hours to a day. There may be a discrepancy in the estimate of left ventricular failure evident on chest radiographs and the measured PCWP. For example, in one series 38% of patients with left ventricular end-diastolic pressures greater than 20 mm Hg had no radiographic evidence of left heart failure (80). Others have noted discrepancies in the estimation of PCWP in patients with acute myocardial infarction or acute left ventricular power failure (80,81). Possible explanations for these discrepancies include preexisting lung disease (emphysema or interstitial lung disease) or poor inspiration on the radiograph. Furthermore, many of the radiographic estimations described above were made on nonportable radiographs, which are technically superior to ICU portable radiographs performed an sick patients. On such portable radiographs, estimation of blood flow in the upper versus the lower lungs cannot be made because critically ill patients are often imaged in a semiupright position, and the vessel diameter measurements described above were done in fully upright patients. Woodring (82) attempted to circumvent this by studying the relationship of pulmonary artery diameter to the adjacent bronchus in supine and upright patients. When supine, hydrostatic differences occur from the dorsal to ventral aspect of the lungs rather than from the lung bases to apices. Under normal conditions, the A:B ratio is equalized throughout the lungs. When PCWP is elevated, the ratio increases throughout the lungs, allowing distinction between left ventricular failure and normal physiology. This ratio cannot distinguish increased PBF (cardiac shunt) from left ventricular failure, because both produce an increase in the A:B ratio. However, in practice this comparison is often limited by the inability to identify adjacent end on arteries and bronchi.

Systemic Extravascular Water

Total fluid balance is a combination of intravascular and extravascular components. Changes in systemic extravascular water, or soft tissue water, can be estimated by changes in chest wall thickness on chest images obtained with consistent patient position. On a frontal radiograph, a useful location for measurement is between the lateral-most rib and the overlying skin. On a lateral view, the distance from the anterior border of the sternum to the skin may be used. A retrospective study correlating changes in chest wall thickness with body weight in renal failure patients showed good correlation (64).

Chest changes in wall soft tissue thickness are used to evaluate systemic extravascular water.

Cardiogenic Edema versus Noncardiogenic Edema versus Other Causes of Lung Opacity

As described already, there are many etiologies of lung parenchymal opacity in the critically ill patients, including pulmonary edema, atelectasis, pneumonia, and ARDS. It may be difficult to distinguish between these on a single chest radiograph, particularly if the abnormality is diffuse bilateral alveolar opacity. A predominantly perihilar “batwing” or “butterfly” appearance to the opacity is characteristic of pulmonary edema (Fig. 10.16) and atypical for ARDS or pneumonia. On serial chest radiographs, cardiogenic edema usually changes over hours to a day or so (Fig. 10.17), as the etiology of left ventricular failure is clinically identified, whereas ARDS gradually progresses over several days to complete opacification of the lungs.

Cardiogenic edema usually changes quickly on several radiographs, over days if not hours.

Causes of pulmonary edema are listed in Table 10.11 and include both cardiac and noncardiac causes. The etiologies of noncardiogenic pulmonary edema are varied (83). For example, high-altitude pulmonary edema is a potentially fatal condition that occurs with rapid ascent (84). It has been estimated that as many as three of four climbers may have subclinical high-altitude pulmonary edema after a modest climb, whereas 15% in one prospective series had either rales or interstitial edema on radiographs after ascent (85). High-altitude pulmonary edema is believed to be secondary to altered permeability of the alveolar-capillary barrier due to intense pulmonary vasoconstriction, resulting in fluid in the lungs of climbers with a high-protein content, in the absence of inflammatory cells. Life-threatening edema may develop secondary to airway obstruction. For example, negative pressure pulmonary edema may occur as a consequence of postintubation laryngospasm due the generation of high negative intrathoracic pressures against a closed airway (86). This characteristically occurs in young men with well-developed thoracic musculature (Fig. 10.3).

Neurogenic pulmonary edema may develop within hours of a neurologic insult, such as stroke, subarachnoid hemorrhage, or traumatic injury, in association with elevated intracranial pressure, systemic and pulmonary arterial hypertension, and elevated left ventricular pressure (87). Patients with subarachnoid hemorrhage have been shown to have abnormal left ventricular wall motion and myocardial enzyme release; in severe cases reduction in cardiac output may further exacerbate cerebral ischemia due to ongoing vasospasm (88). In one series, 21% of patients with subarachnoid hemorrhage had moderate or severe cardiac injury and 29% had mild cardiac injury, whereas half had no cardiac injury. The mechanism by cardiac impairment develops is poorly understood and may include endothelial injury with increased pulmonary capillary permeability and hydrostatic changes with increase left atrial pressure and pulmonary venous constriction due to increased sympathetic tone.

Figure 10.16 Batwing or butterfly acute alveolar pulmonary edema on chest radiograph in a patient who has undergone coronary artery bypass graft surgery in the past.

Figure 10.17 Rapid changes in pulmonary edema on serial portable chest radiographs. A. Normal chest radiograph. B. Alveolar edema with new mid and lower lung alveolar opacities 37 hours later. C. Extensive alveolar edema with diffuse lung opacification 4 hours afterB. D. Only interstitial edema remains 33 hours after C.

There are many toxic substances that when inhaled may cause pulmonary edema. Examples include chlorine-containing bleaching agents; sodium hypochlorite found in disinfectants and spot remover; petroleum distillates or mineral spirits found in furniture polish, wood stain, and varnish; car wax and polish; motor oil and gasoline; selenium found in hazardous waste sites; and ash from burning coal or metal industries (89,90). Detail on the effects of specific toxic agents can be found at the website for the Agency for Toxic Substances and Disease Registry (ATSDR), an agency of the U.S. Department of Health and Human Services, at http://www.atsdr.cdc.gov. Some ingested drugs also cause pulmonary edema, such as freebase cocaine (91).

Table 10.11: Causes of Pulmonary Edema

Left ventricular failure
   Myocardial infarction
   Cardiomyopathy
   Aortic or mitral valve disease
Noncardiogenic
   Fluid overload
   Renal failure
   Hepatic failure
   Brain injury
   Near drowning
   Acute respiratory distress syndrome
   High altitude
   Drug reaction
   Drug overdose (cocaine)
   Carbon monoxide toxicity
   Radiation therapy
   Negative pressure pulmonary edema
      Postextubation laryngospasm
      Acute airway obstruction
   Reexpansion pulmonary edema

It is important to recognize atypical manifestations of pulmonary edema (Table 10.12). Because pulmonary edema changes with gravity and therefore patient position, a patient in the Trendelenburg position may have more severe edema in the upper lobes (Fig. 10.18) compared with an upright patient, and a patient who preferentially lies on their right side will develop more severe edema in the right lung than in the nondependent left lung. Patients with severe upper lobe predominant emphysema preferentially have most of their pulmonary artery blood flow going to the lower lobes at baseline to maintain gas exchange. When left ventricular failure occurs, pulmonary edema may manifest as bibasilar alveolar consolidation, radiographically mimicking pneumonia or aspiration. The reverse is true in patients with α1-antiprotease deficiency and lower lobe predominant emphysema. Similarly, patients with either pulmonary embolism or tumor occluding a pulmonary artery will not develop edema in the lung parenchyma supplied by the occluded vessel. Because venous thromboembolism usually involves the lower lobes to a greater extent that the upper lobes, because of the greater distribution of blood flow to the lower lungs, patients with chronic pulmonary embolism may develop bilateral upper lung edema when left ventricular failure occurs (Fig. 10.19). Unilateral pulmonary edema may develop after the rapid drainage of pleural fluid or air and is referred to as reexpansion pulmonary edema (Fig. 10.20). Lobar sparing of pulmonary edema may be seen if the pulmonary artery to that lobe is occluded by tumor, such as with bronchogenic carcinoma or a lobar artery embolus.

Pulmonary edema is common. Atypical manifestations of common diseases are more common than typical manifestations of rare diseases.

Table 10.12: Causes of Atypical Pulmonary Edema Distribution

Location

Etiology

Unilateral

Persistent decubitus position
Rapid drainage of large pleural effusion
Rapid drainage of large pneumothorax

Bibasilar

Upper lobe predominant emphysema

Biapical

Lower lobe predominant emphysema
Chronic pulmonary embolism

Spares a lobe

Artery occluded by tumor or thromoembolism

Figure 10.18 Gravitational shift in pulmonary edema distribution with changes in patient position. A. Initial chest radiograph demonstrates bilateral upper lung edema when the patient was imaged after being in the Trendelenburg position. B. Within 24 hours another radiograph taken after upright positioning demonstrates edema that is now more severe in the lower lungs.

Figure 10.19 Upper lobe distribution of pulmonary edema in a patient with chronic pulmonary emboli occluding blood flow to the lower lobes, manifesting as bilateral upper lung consolidation on posteroanterior chest radiograph.

Figure 10.20 Reexpansion pulmonary edema. A. Initial posteroanterior chest radiograph demonstrates a large left pneumothorax (asterisk) with complete collapse of the left lung. B. After chest tube placement with rapid reexpansion of the left lung, there is new diffuse alveolar opacity throughout the left lung.

Abnormal Air Collections

There are many locations of abnormal thoracic air collections, as listed in Table 10.13. Some air collections arise as a complication of barotrauma in patients with stiff noncompliant lungs, such as patients with advanced ARDS. Some air collections are iatrogenic, such as after central venous or pulmonary arterial catheter placement (Chapter 11). Other air collections may be a clue to injury or a disease process, such as pneumomediastinum and pneumothorax in the setting of traumatic airway rupture (Chapter 12), or small pockets of air within a pleural fluid collection secondary to infection with gas-forming organisms. In many cases the air collection itself is of little consequence; rather, it is the reason for the development of the air collection that is important. However, in some circumstances the air itself can be a cause of morbidity and even mortality. For example, a tension pneumothorax may result in collapsed lung and even impaired systemic venous return to the heart due to the compression of the superior vena cava. The latter is more common with a right tension pneumothorax than a left one, because the large low-pressure venous structures of the mediastinum are right sided. Many causes of these air collections are discussed in greater detail in chapters related to the specific disease or underlying anatomy. (See Chapter 8 with regard to metastases; also Chapters 11121417, and 22.) A review of the air collections themselves and etiologies to consider for each are discussed here.

A right tension pneumothorax impairs central venous return more than a left tension pneumothorax.

Table 10.13: Abnormal Thoracic Air Collections

Pneumothorax
Pneumomediastinum
Pneumopericardium
Pneumatoceles
Pulmonary interstitial emphysema
Subcutaneous emphysema

Pneumothorax

A pneumothorax is defined as “the presence of air or gas in the pleural space” (92). Because of the elastic recoil of the lung, the alveolar pressure is always greater than pleural pressure. When a communication between lung and pleural space develops, air flows from the lung into the pleural space until equilibrium occurs. The larger the pneumothorax, the smaller the lung becomes. As the lung becomes smaller in size, vital capacity of the lung becomes smaller. Symptoms are usually acute ipsilateral chest pain that is exacerbated with breathing and dyspnea. This may be accompanied by tachypnea and hypoxia and even tachycardia, hypotension, and cyanosis when severe. For individuals with normal lungs, symptoms may be minimal even with what may be considered a large pneumothorax (Chapter 12Fig. 12.14). However, in patients with underlying lung disease with already reduced lung function, this additional reduction can be a cause of significant respiratory distress (Fig. 10.21). Also, a large pneumothorax may cause mediastinal shift and impaired venous return to the heart due to compression of the superior vena cava and inferior vena cava. This is more common on the right side, where these venous structures are located, than on the left side. This is referred to as a tension pneumothorax and should always be suspected when mediastinal shift accompanies a pneumothorax (Fig. 10.22) (Fig. 12.20). Treatment of pneumothorax depends on size and patient stability and ranges from observation to aspiration, chest tube placement, and even surgical treatment in the setting of recurrent bleb rupture or bronchopleural fistula (93)

Causes of pneumothorax are listed in Table 10.14 (94). Air combined with fluid is a hydropneumothorax, with pus is a pyopneumothorax, and with fecal material, as has been reported on the setting of traumatic diaphragmatic rupture, is a fecopneumothorax (95,96).

Figure 10.21 Acute respiratory distress syndrome with diffuse lung alveolar opacity and a left pneumothorax on a portable chest radiograph.

Figure 10.22 Acute respiratory distress syndrome with diffuse lung alveolar opacity and bilateral pneumothoraces on a portable chest radiograph.

Table 10.14: Causes of Pneumothorax

Primary
   Ruptured bleb or bulla
Secondary
   Trauma
      Penetrating (knife, gunshot)
      With rib fracture(s)
      Biopsy/aspiration (lung, pleura, transbronchial, breast, abdominal)
      Iatrogenic (central venous access)
      Ex vacuo (space-occupying process removal and stiff lung)
      Cardiopulmonary resuscitation
      Acupuncture
      Surgery (thoracic, abdominal, neck)
   Interstitial lung disease
      Fibrosis
      Sarcoidosis
   Obstructive lung disease
      Emphysema
      Bronchiectasis
      Langerhans cell histiocytosis
      Lymphangioleiomyomatosis
      Bronchiolitis obliterans/graft-versus-host disease
   Cavity metastases
      Squamous
      Sarcoma
   Increased intrathoracic pressure
      Barotraumas (mechanical ventilation)
      Blunt abdominal trauma
   Other
      Catamenial

A primary spontaneous pneumothorax is usually due to the rupture of an apical bleb (Fig. 10.23); it more commonly occurs in tall individuals and is six times more common in men than women (97). These blebs are actually intrapleural, that is, they are located within the visceral pleural lining of the lung that is made up of a layer of mesothelial cells and submesothelial connective tissue. On imaging studies we recognize blebs as discrete air collections with a well-defined thin wall, usually at the lung apices. Another common location to look for blebs that rupture is the superior segments of the lower lobes, which can be thought of as the apex of the lower lobes. An acute elevation in intrathoracic pressure, as may be seen in trauma or weight lifting, may lead to bleb rupture. Secondary spontaneous pneumothorax is due to underlying lung disease, such as fibrosis, emphysema, or malignancy (98,99), particularly metastatic sarcoma (Fig. 8.24). Trauma is an important cause of pneumothorax, including both blunt and penetrating trauma, as well as iatrogenic pneumothorax secondary to central venous access. Catamenial pneumothorax occurs in synchrony with the menstrual cycle (Fig. 17.19) (100).

Apical blebs that cause spontaneous pneumothorax are actually within the pleural lining.

Figure 10.23 Apical blebs in a patient that later developed a spontaneous right pneumothorax. A. Chest radiograph demonstrates thin apical lines representing the walls of blebs, seen in more detail on (B) computed tomography.

Figure 10.24 Bilateral balanced pneumothoraces on computed tomography with no mediastinal shift.

Although in most cases a small pneumothorax resolves without treatment, in patients with ARDS a small pneumothorax is evidence of barotraumas and may rapidly enlarge, further reducing oxygenation. Bilateral pneumothoraces usually occur in patients with underlying lung disease and are usually balanced by the pressure across the thorax (Fig. 10.24) (101). Patients with underlying lung disease have a higher mortality with secondary pneumothorax than patients with primary pneumothorax. In patients with chronic obstructive pulmonary disease, the mortality risk is 3.5 times higher. Another important consideration in patients with ARDS and stiff noncompliant lungs is an ex vacuopneumothorax that may occur with the drainage of pleural fluid because of the inability of the small collapsed lung to reexpand into the space previously occupied by the fluid that has been removed (Fig. 10.25). This phenomenon may also be observed when there is rapid lobar collapse due to acute bronchial obstruction (101).

Figure 10.25 Ex vacuo pneumothorax in a patient with acute respiratory distress syndrome and stiff noncompliant lungs. A. Initial radiograph demonstrates a large right pleural effusion (asterisk). B. After chest tube drainage there is a large pneumothorax (asterisk) conforming to the location of the prior pleural effusion.

Radiographically, pneumothorax appears as a thin white line (the visceral pleura) surrounded by lucency (air) in the pleural space on one side and the lung on the other side. Air in the pleural space is found in the most nondependent portion of the thorax. In an upright patient this will be at the apex of the lung. Care should be taken in interpreting semiupright and supine radiographs for pneumothorax, common positions of trauma or ICU chest radiographs, because the location of the pneumothorax will be different. When supine, air collects in the basilar aspect of the pleural space and may be seen between the hemidiaphragm and the lower edge of the lung, at the cardiophrenic angles, and at the lateral costophrenic angle that appear expanded caudally; the latter is known as the deep sulcus sign (Figs. 12.17 and17.13). It is not uncommon to find a pneumothorax on CT in trauma patients that was not visible on a supine portable chest radiograph. In the decubitus position, air will collect adjacent to the lateral rib margins (Fig. 17.11). Uncommonly, air may be located within a fissure (Figs. 17.14 and 17.15).

Always “hot light” or magnify the lung apices when looking for a pneumothorax in an upright patient.

In a supine position, pneumothorax collects anteriorly at the lung base.

Expiratory radiographs are of limited value. On expiration, the lung becomes smaller whereas the pneumothorax is unchanged; hence, the relative size of the pneumothorax is larger. Careful study of this has shown that the odds of missing a small pneumothorax on inspiratory or on expiratory radiographs is equal and likely related to where the thin visceral pleural edge fortuitously overlies the ribs. An expiratory radiograph should be reserved for patients with a normal inspiratory radiograph when there is a high clinical suspicion for pneumothorax and should not be used routinely (102). Ultrasound can identify pleural air and may be particularly useful in ICU patients by bringing the machine to the patient bedside. Pleural air can be recognized as the absence of lung sliding toward the chest wall with separation of the normal lung–chest wall interface, usually viewed anteriorly through the intercostal spaces (103).

Pneumomediastinum

Pneumomediastinum is defined as “escape of air into mediastinal tissues, usually from interstitial emphysema or from a ruptured pulmonary bleb” (104). The sources of air in pneumomediastinum include the lung, airway, esophagus, neck, and abdomen. Excessive intraalveolar pressure, as may be seen when ventilating stiff noncompliant lungs in ARDS or from blunt trauma with compression of the thorax, results in the rupture of alveoli along the bronchovascular bundles with air dissecting into the adjacent connective tissue (known as the central or axial interstitium of the lung) and then into the mediastinum. Air can subsequently extend from the mediastinum into the neck and then into the body wall soft tissues, manifesting as subcutaneous air and intramammary air (Figs. 10.2610.27, and 10.28). Air may also extend caudally from the mediastinum into the retroperitoneum, extraperitoneal compartments, and even the peritoneal cavity. Similarly, air in the neck or retroperitoneal soft tissue can dissect into the mediastinum, as may be seen with neck trauma or surgery or with bowel rupture into the retroperitoneum. Uncommonly, a pneumomediastinum can lead to a pneumothorax, usually when mediastinal pressure rises abruptly or when there is massive pneumomediastinum.

Figure 10.26 Pneumomediastinum manifesting as lucency along both heart borders on a chest radiograph of a patient with acute respiratory distress syndrome. Note the subcutaneous air in the chest wall bilaterally.

Figure 10.27 Pneumomediastinum on computed tomography. Two axial computed tomography images, A and B, demonstrate lucency throughout the mediastinum, with intervening strands of opacity caused by mediastinal fat, small neurovascular structures, and lymph nodes.

Figure 10.28 Extensive subcutaneous air, intramammary air, and pneumomediastinum due to Munchausen syndrome, as seen on (A)posteroanterior chest radiograph and (B) computed tomography. Air was self-injected into the chest wall.

The air in the mediastinum itself is usually of little consequence, and patients often have no symptoms. When present, symptoms include substernal chest pain that is exacerbated by deep breathing, coughing or the supine position, dyspnea, dysphagia, and dysphonia. These may be accompanied by crepitus from subcutaneous emphysema and the Hamman sign (precordial crunching sound with each heart beat). More important than the air is the cause of the air. Causes of pneumomediastinum are listed in Table 10.15 and are generally related to conditions in which there is an acute elevation of thoracic pressure, as may be seen with an acute asthmatic attack or severe coughing or trauma. In the setting of blunt chest trauma, alveolar rupture and dissection of air along the central interstitium into the mediastinum is known as the Macklin effect, first described in 1939. In one series it was responsible for 39% of the cases of pneumomediastinum in patients with severe blunt chest trauma (105). Pneumomediastinum secondary to Boerhaave syndrome, esophageal rupture in the setting of extensive or violent vomiting, carries a high mortality. Pneumomediastinum secondary to traumatic airway or esophageal rupture also carries a high mortality rate, particularly if the diagnosis is not recognized early.

Whereas the radiographic appearance of pneumomediastinum may be dramatic, the air causes little problems. The cause of pneumomediastinum is more important.

Table 10.15: Causes of Pneumomediastinum

Asthma
Trauma
   Airway rupture
   Esophageal rupture
   Oropharynx trauma
   Blunt chest trauma
Barotrauma (mechanical ventilation)
Substance abuse
   Smoking marijuana
   Inhalation of cocaine
Athletic competition
Respiratory tract infection
Child birth
Emesis
Severe cough
Seizures
Valsalva maneuver

Radiographically, pneumomediastinum appears as thin lucent lines or bubbles of gas along the mediastinal contours, such as the heart, aorta, and superior vena cava, and as streaks of lucency in the superior mediastinum extending toward the neck (Fig. 10.27) (106). On the lateral view, attention should be paid to the retrosternal region when searching for pneumomediastinum and to gas surrounding the aorta and pulmonary artery. Air can also be seen to surround the aortic knob, central pulmonary arteries, airway, and esophagus on radiographs; however, this is usually more appreciated on CT. Air around the right pulmonary artery is known as the ring around the artery sign on the lateral radiograph (Fig. 12.18). Mediastinal gas may insinuate between the parietal pleura and either lung apex or diaphragm, external to the parietal pleura. CT is more sensitive than radiography for the presence of mediastinal gas and for delineating the location of that gas (Fig. 10.27) (Fig. 12.21). The V sign of Naclerio is seen when mediastinal gas is located between parietal pleura and left hemidiaphragm (107). The continuous diaphragm sign with air outlining the central tendon of the diaphragm is seen when mediastinal gas is located between the heart and the diaphragm (108). Changes in position, such as being placed decubitus or supine, does not usually change the distribution of air in the mediastinum, which is in contrast to air in the pleural and pericardial spaces or peritoneal cavity.

Changes in position usually do not change the appearance of pneumomediastinum radiographically.

Pneumopericardium

Pneumopericardium is defined as the “presence of gas in the pericardial sac” (109). Pneumopericardium is much less common that pneumothorax or pneumomediastinum. Causes of pneumopericardium are listed in Table 10.16. It is usually secondary to trauma, often penetrating trauma, or may be seen after cardiac surgery (Fig. 10.29) (110,111,112). Pneumopericardium may also be spontaneous, although this is less common (113), and may also be a cause of cardiac tamponade (114). The latter should be suspected whenever the heart becomes small in the setting of pneumopericardium. Rarely, in Boerhaave syndrome there may be rupture of the esophagus into the pericardial sac, resulting in pneumopericardium. Lung disease may erode into the pericardium, such as bronchogenic carcinoma or invasive aspergillosis. Even cocaine abuse, laparoscopy, ruptured gastric ulcers, and amebic liver abscesses have been reported to cause pneumopericardium (110,115).

Table 10.16: Causes of Pneumopericardium

Trauma
   Penetrating trauma
   Surgery
Infection with gas-forming organism
Increased intrathoracic pressuer
   Asthma
   Barotrauma
   Valsalva maneuver
Lung disease
   Bronchogenic carcinoma
   Lung infection
Esophageal rupture (severe emesis, Boerhaave syndrome)
Other
   Forceful coughing
   Cocaine abuse
   Gastric perforation (ulcer, tumor)
   Liver abscess
   Pancreatic pseudocyst
   Postpartum

Figure 10.29 Pneumopericardium after bilateral lung transplantation. A. Coned down posteroanterior and (B) lateral radiograph demonstrate lucency conforming to the pericardial sac that does not extend above the aortic knob. Lucency extending above the aortic knob would indicate a pneumomediastinum.

Radiographically, pneumopericardium appears as lucency confined to the pericardial sac (Figs. 10.29 and 20.33). It should not extend above the aortic knob, because that is the cephalad aspect of the pericardial space. This can be used to distinguish pneumopericardium from pneumomediastinum. On echocardiography, pneumopericardium has the distinct appearance of swirling echogenic bubbles (116).

Pneumopericardium should not extend above the aortic knob.

Pneumatoceles and Interstitial Emphysema

Pneumatoceles and interstitial emphysema are abnormal air collections within the lung. A pneumatocele is defined as “an emphysematous or gaseous swelling” and “a thin-walled cavity within the lung, one of the characteristic sequelae of staphylococcal pneumonia” (117). Most pneumatoceles secondary to staphylococcal pneumonia are found in children. They may be seen with other infections, includingStreptococcus pneumoniaeHaemophilus influenzaeE. coli, group A streptococci, Serratia marcescens, Klebsiella pneumoniae, tuberculosis, and adenovirus and also with trauma, barotrauma, or hydrocarbon inhalation (Figs. 5.15 and 5.16) (118). In the setting of trauma, rapid compression of the lung creates shearing forces due to the negative intrathoracic pressure upon decompression, with rupture of normal lung architecture to create air-filled cyst-like spaces (Figs. 10.5 and 12.16). In infection, peribronchial abscesses may create a ball–valve phenomenon, obstructing a bronchial lumen, with distal hyperexpansion into an air-filled cyst-like space. Pneumatoceles may rupture and are associated with pneumothorax.

Interstitial emphysema is defined as “the presence of air in the pulmonary tissues consequent upon rupture of the air cells; presence of air or gas in the connective tissue” (119). It is commonly referred to as pulmonary interstitial emphysema (PIE). Interstitial emphysema is more commonly seen in neonates with lung disease than in adults. Noncompliant lungs and the use of positive pressure ventilation are both associated with PIE in premature infants requiring mechanical ventilation for respiratory distress syndrome, meconium aspiration, infection, or amniotic fluid embolism (120). Two percent to 3% of all neonatal ICU patients and up to 30% of premature neonatal ICU patients develop PIE. On radiographs, air in alveolar spaces and air in the interstitium are indistinguishable unless there is abnormality of the intervening lung to provide sufficient contrast to detect the interstitial emphysema. Small rounded or linear lucencies are usually seen along the bronchovascular bundles but may also involve the peripheral or septal interstitium and the subpleural connective tissue. PIE ranges from a single focus to diffuse pulmonary involvement and is associated with the subsequent development of pneumomediastinum, pneumothorax, pneumopericardium, and pneumoperitoneum. In neonates, interstitial emphysema may be extensive and change quickly, as in the example given in Fig. 10.30 of a neonate with respiratory distress syndrome.

Figure 10.30 Pulmonary interstitial emphysema in a neonate with respiratory distress syndrome (RDS) changing in appearance within a few days. A. Portable chest radiograph demonstrates diffuse ground glass opacity of RDS throughout the right lung and diffuse round lucencies representing extensive pulmonary interstitial emphysema throughout the left lung. B. Portable chest radiograph 5 days later shows RDS throughout the left lung and diffuse round lucencies representing extensive pulmonary interstitial emphysema throughout the right lung.

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