Chest Radiography.pdf

Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211

Chest radiography Betty J. Tsuei, MDa,*, Peter E. Lyu, DDSb a

Department of General Surgery, College of Medicine, University of Kentucky, 800 Rose Street, Room C-221, Lexington, KY 40536, USA b Division of Oral and Maxillofacial Surgery, College of Dentistry, University of Kentucky, 800 Rose Street, Room D-508, Lexington, KY 40536, USA

One of the most commonly performed imaging procedures is the plain chest radiograph, accounting for up to 50% of studies obtained in some radiology practices. Currently, radiographic evaluation of the chest is utilized in many routine settings. Preoperative radiographs are often used to screen for underlying pulmonary and cardiovascular diseases. Pleural effusions and cardiac enlargement suggestive of heart failure may be present. In the febrile patient, the chest radiograph is useful for visualizing pulmonary sources of fevers, such as atelectasis, viral and bacterial pneumonias, and lobar collapse. In addition, the chest radiograph is an important diagnostic tool in the evaluation of the traumatically injured patient in which concomitant head, neck, and facial injuries may be present. Rib fractures, hemothorax, pneumothorax, and pulmonary contusions, and acute respiratory distress syndrome (ARDS) are commonly seen, and the hallmarks of these injuries should be readily identifiable. Finally, thoracic imaging can also detect injuries and infections that originate in the head and neck. With the many pulmonary, cardiac, esophageal, and mediastinal diseases, it is not surprising that countless volumes of radiology textbooks have been dedicated solely to thoracic imaging. This article touches on a few of the conditions noted previously and is intended to outline some basic findings in chest radiography. Although the article reviews clinical symptoms and treatment, it is not meant to be a definitive dissertation on thoracic diseases—collaboration with not only radiologists but also pulmonologists, cardiothoracic surgeons, and trauma and critical care specialists will succeed in providing accurate and timely diagnosis and appropriate medical care.

Atelectasis Frequency/incidence The incidence of postoperative atelectasis is approximately 80%, but only about 20% of cases are clinically significant [1]. In a review of chest radiographs of 200 consecutive patients in the surgical ICU, 18 cases of lobar collapse were diagnosed in 17 patients (8.5%). Most cases involved the left lower lobe (66%), but collapse of the right lower lobe (22%) and the right upper lobe (11%) was also noted [2]. Signs and symptoms Patients may present with low-grade fever, mild leukocytosis, and mild tachypnea. In mild atelectasis, alterations in oxygenation and ventilation may not be seen. In atelectasis resulting from bronchial obstruction with significant loss of pulmonary parenchyma, patients may exhibit marked tachypnea and hypoxia. * Corresponding author. E-mail address: [email protected] (B.J. Tsuei). 1061-3315/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 6 1 - 3 3 1 5 ( 0 2 ) 0 0 0 0 6 - 9

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Etiology/pathophysiology Atelectasis is defined as a decrease in lung volume and can arise from several causes. Obstructing lesions, caused by a foreign body, mucus plugging, or endobronchial tumors may result in distal air resorption and atelectasis. Compressive atelectasis is caused by the compression of normal lung by an adjacent space-occupying lesion, such as a large peripheral lung tumor or bullous or lobar emphysema. Pneumothorax and pleural effusion may also result in atelectasis. One of the most common forms of atelectasis occurs when the intraluminal surfaces of alveoli collapse and adhere together. This is usually caused by a decreased tidal volume during spontaneous respirations. Poor inspiratory volumes are common in postoperative patients as a result of sedation, anesthetic, pain, or immobility. Atelectasis can also be caused by scarring and fibrosis in the interalveolar and interstitial space, decreasing lung compliance and reducing lung volumes. Image of choice The preferred imaging modality is a standard chest radiograph, although atelectasis may also be seen as an incidental finding on chest computed tomography (CT). Image hallmarks Hallmarks of atelectasis primarily consist of an increased opacity in the anatomic area of collapse. In postoperative atelectasis (Fig. 1A), this occurs primarily at the lung bases and is a bilateral process. Elevation of the diaphragm and displacement of the pulmonary hilum may also been seen. In cases of lobar collapse, more marked anatomic delineation is seen, such as the left upper lobe collapse (Fig. 1B). In addition to increased lobar opacity, there is often displacement of the adjacent fissure and compensatory overinflation of the normal lung. In severe cases, cardiac rotation and mediastinal shift can occur. Management Treatment of atelectasis includes aggressive pulmonary toilet to expand the collapsed portions of the lung. Deep breathing, forced coughing, and use of spironometry can be employed in the cooperative patient. Nebulizer treatments and nasotracheal suction to induce coughing, or positive pressure masks, may also be beneficial. In cases of lobar collapse, more aggressive measures, such as bronchoscopy to eliminate the cause of obstruction and positive pressure ventilation, may be required. Fig. 1C shows resolution of the left upper lobe collapse within 24 hours with vigorous pulmonary toilet.

Pleural effusion Frequency/incidence Pleural effusion is usually a secondary effect from a primary disease state, and as such, the incidence varies depending on the underlying cause. In patients with congestive heart failure, the incidence of pleural effusion may be as high as 58% to 88% [3]. Effusions may also be present in 67% of patients with pericardial disease [4]. Cirrhosis and ascites are also associated with pleural effusion (6%), and as many as 11% of patients with bacterial pneumonia may exhibit concomitant pleural effusion [5]. Signs and symptoms Patients with pleural effusion may be asymptomatic if the effusion is mild. Generally, they exhibit symptoms of the underlying cause of the effusion—for example, congestive heart failure or ascites (see following subsection). Large effusions can cause respiratory compromise with

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Fig. 1. Atelectasis. (A) Postoperative. Characteristic bibasilar platelike atelectasis (arrows). (B) Lobar collapse. Note the increased density which demarcates the left upper lobe. (C) Resolution of lobar collapse. Re-expansion of the left upper lobe collapse seen in figure 1b after 24 hours of vigorous pulmonary toilet.

dyspnea, tachypnea, and hypoxia. Decreased basilar breath sounds may be found on physical examination.

Etiology/pathophysiology Excess pleural fluid can be attributed to the increased transport of pulmonary interstitial fluid from the mesothelium into the pleural space. Congestive heart failure is the most common cause of transudative pleural effusion, although other disease states in which intravascular volume is

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Fig. 1 (continued)

elevated, such as renal failure, nephrotic syndrome, and cirrhosis may also cause effusion. Sympathetic effusion, resulting from disease in an adjacent organ—cardiac (pericarditis), upper abdomen (pancreatitis, splenic disease)—is also common. Infectious agents, such as bacterial pneumonia, tuberculosis, and fungal or viral infections, usually cause exudative pleural effusions. Malignancies, particularly breast and lung cancers, may also cause pleural effusion.

Image of choice Although pleural effusion may be seen on supine chest radiography, the imaging modality of choice is an upright or lateral chest radiograph.

Image hallmarks The most common manifestation of pleural effusion on upright radiograph is a fluid level in the hemithorax. Small amounts of pleural fluid may be manifest as a meniscus that blunts the costophrenic angle on the PA projection (Fig. 2A). Small effusions may also be visualized in the posterior sulcus on the lateral film. At least 175 mL of fluid is needed for the effusion to be visualized on plain radiograph, whereas a large pleural effusion may completely opacify the hemithorax. If the patient is unable to tolerate an upright film, a lateral decubitus film with the affected side down may reveal dependent layering of fluid in the hemithorax, suggesting the presence of pleural effusion. In a supine patient, the effusion is generally seen as a diffuse opacification of the affected hemithorax (Fig. 2B). Atelectasis of a lobe can also be present with pleural effusions.

Management Treatment of the underlying cause of the pleural effusion often results in resolution of the effusion. In general, pleural effusion is not treated unless the patient is symptomatic. Methods of treatment in the symptomatic patient include thoracentesis or drainage with thoracostomy tube.

Fig. 2. Pleural effusion. (A) Left pleural effusion on upright chest radiograph, demonstrating characteristic blunting of costophrenic angle and visible fluid level. (B) Right pleural effusion on supine chest film, demonstrating the diffuse increase in density through the right hemithorax.

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Viral pneumonia Frequency/incidence Viral infections are common and often cause more morbidity and mortality than do bacterial infections. Most viral pneumonias occur in children and adults who are relatively immunocompromised. Infants are particularly susceptible during the ages of 2 months to 2 years, with boys affected twice as often as girls [6]. One study indicated that 90% of influenza-related fatalities occurred in patients older than 65 years. Individuals residing in nursing homes are also particularly susceptible, with a mortality rate of 30% from viral pneumonia [7]. Infection rates of viruses depend on the immune status of the individual. Patients with immune suppression (chemotherapeutic agents, transplant patients, HIV) may become infected with viruses, which are usually not pathogenic (eg, cytomegalovirus). Signs and symptoms Respiratory symptoms of viral pneumonia may include cough and nonpurulent sputum. Low-grade fever, chills, headache, conjunctivitis, myalgia, anorexia, and malaise are also common. Severely affected patients show rapid progression of tachypnea, dyspnea, cyanosis, and hypoxemia. Etiology/pathophysiology Most viruses causing pneumonia travel from the upper to the lower respiratory tract. Common viral agents include influenza virus, respiratory syncytial virus, measles, picornavirus, coxsackievirus, enterocytopathogenic human orphan virus, and rhinovirus. The pathologic changes induced in the lung are similar for all viruses. Necrosis and sloughing of epithelium lead to loss of normal mucosal surface. Mucous production increases, leading to bronchiolar plugging, and the alveoli are often filled with fluid and leukocytes. The diagnosis of viral pneumonia is often one of exclusion. It is based on the absence of purulent sputum production, failure to culture a pathogenic bacterium, a relatively benign clinical presentation, or a white blood cell count that is normal or only slightly elevated. Image of choice The preferred imaging modality is a chest radiograph. Image hallmarks Image hallmarks can be nonspecific and depend on the extent of the disease; findings range from mild interstitial prominence (Fig. 3A) to significant air space disease (Fig. 3B), especially if bacterial superinfection occurs. Areas of patchy consolidation, air trapping, and perihilar infiltrates may also be seen [8]. Management Supportive therapy is the main course of treatment. Cell culture, serology, and detection of viral antigens can aid with diagnosis but are usually not employed, because the disease is usually self-limited with complete clinical recovery in 2 to 3 weeks. Antiviral agents, usually reserved for immunocompromised patients, include ganciclovir, acyclovir, ribavirin, amantadine, and rimantadine. The respiratory tract may become secondarily infected and result in a superimposed bacterial pneumonia, which should be treated with the appropriate antibiotics (see following section).

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Fig. 3. Viral pneumonia. (A) Mild diffuse interstitial changes seen in viral pneumonia. (B) Significant air space disease (right lower lobe) may be present in advanced pneumonia, or if bacterial superinfection occurs.

Bacterial pneumonia Frequency/incidence There are 2 to 3 million cases of pneumonia in the United States per year. Many patients with bacterial pneumonia can be treated on an outpatient basis. The mortality rate from community-acquired pneumonia in patients who require hospitalization is 14%, and increases up to 50% in patients who require admission to the ICU [9]. Among hospitalized patients,

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pneumonia is the second most common and most frequently fatal nosocomial infection [10]. With mechanical ventilation, the risk of acquiring a nosocomial infection increases five to ten fold. Among mechanically ventilated patient in an ICU, the incidence of nosocomial pneumonia is 18% to 58%, with a mortality rate of 38% [11].

Signs and symptoms Patients with pneumonia may present with fever, new or increased cough, purulent sputum production, or dyspnea. Clinical findings on physical examination can include fever, tachypnea, tachycardia, rales, dullness to percussion, or decreased breath sounds. Unfortunately, some studies have indicated that these signs are only 50% specific for the diagnosis of pneumonia [12]. Nosocomial pneumonia can be more difficult to diagnose, especially in ventilated patients in the ICU. In these cases, fever, leukocytosis, sputum gram stain and culture, infiltrate on chest radiograph, and presence of purulent sputum are used for diagnosis. At least three of these findings should be present for the diagnosis of pneumonia to be made.

Etiology/pathophysiology Infectious agents gain entry to the lung either directly by inhalation of 0.5 to 1.0 lm aerosolized particles or after respiration of oropharyngeal secretions. If the inoculum is unable to be cleared by the pulmonary tree, bacterial multiplication results in development of pneumonia. Because of virulence factors, certain microorganisms are more capable of avoiding pulmonary clearance mechanisms, resulting in rapid replication and damage to host tissues. Common organisms that cause community–acquired pneumonia include S. pneumoniae, H. influenza, and K. pneumoniae. These organisms can often be treated with single agent or oral antibiotics. Atypical pneumonia may result from Mycoplasm or Legionella species. Aspiration pneumonia may be multibacterial, and is more likely to contain anaerobic species. Hospital-acquired pneumonia usually results from more virulent bacteria, such as Pseudomonas, Enterobacter, Acinetobacter, and Staphylococcus species. These organisms may require double antibiotic coverage, or exhibit unusual resistance patterns.

Image of choice The preferred imaging modality is a PA and lateral chest radiograph. The infiltrate seen on radiograph may take several weeks to resolve. Therefore, serial radiographs are not necessary as long as the clinical picture shows improvement. A follow-up radiograph should be taken to document resolution of the infection.

Image hallmarks The hallmark of bacterial pneumonia is a discreet pulmonary infiltrate. Loss of discreet pulmonary borders, such as the diaphragm or cardiac silhouette, indicates an increased density in the adjacent pulmonary region. Whereas lower lobe infiltrates are the most common, aspiration pneumonia often results in an infiltrate in the right upper lobe. Fig. 4 shows the characteristic infiltrate in the right upper lobe.

Management The treatment of bacterial pneumonia consists of antibiotic therapy and supportive care. Specific pharmacologic intervention is dictated by the pathogen. Community-acquired pneumonias may often be treated with single or oral antibiotic agents, whereas nosocomial pulmonary

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Fig. 4. Bacterial pneumonia resulting in right upper lobe infiltrate.

infections often involve more virulent organisms. In these instances, multiple antibiotics may be required, and development of drug resistance is common. Sputum cultures, microbial susceptibility, and hospital and specific unit-based bacterial biograms may be beneficial in determining the antimicrobial agent of choice. In certain cases, hospitalized patients with nosocomial pneumonia may require respiratory isolation to prevent spread of the organism.

Rib fractures Frequency/incidence Rib fractures are a common injury resulting from trauma to the chest wall, and are less common in children because of the elasticity of the cartilage and flexibility of the bone. Isolated rib fractures have an overall incidence of approximately10%; however, 90% of patients with multisystem injuries have rib fractures. Commonly associated pulmonary injuries include pneumothorax or hemothorax (32%) and pulmonary contusion 26%. Rib fractures and other pulmonary injuries can result in significant hospital morbidity: one study noted that 35% of patients with rib fractures developed a pulmonary complication, with an overall mortality rate of 12% [13]. Signs and symptoms Pain is the most common symptom of rib fractures. The complications of rib fracture, such as pulmonary contusion and pneumonia, are considered more significant than the injury itself. Associated underlying pulmonary contusion, especially in patients with flail segments, can cause pulmonary compromise, with resultant tachypnea, dyspnea, and respiratory failure. Etiology/pathophysiology Trauma is by far the most common cause of rib fractures. In traumatic injuries, direct blows to the rib cage will create an inward fracture, potentially damaging the pleura and parenchyma

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of the lung. Pneumothorax, hemothorax, and pneumohemothorax are frequent concomitant findings. The specific location of the injuries can relay some important information about the direction and force of impact. Rib fractures of the first, second, or third ribs can be associated with injuries to the aortic, spine, or airway. Trauma to the lower rib cage (tenth, eleventh, or twelfth ribs) often is associated with upper abdominal trauma, such as injury to the spleen, kidneys, or liver. Multiple segmental rib fractures involving two or more contiguous ribs constitutes a flail chest. In patients with underlying bone disease, such as tumors and osteoporosis, even minor trauma, such as coughing, may precipitate rib fractures. Image of choice The preferred imaging method for rib fractures is an upright chest radiograph. Although there are specific rib films that may be obtained, these are not often performed because the diagnosis is largely clinical and the treatment supportive. Image hallmarks Rib fractures are classically seen as an irregularity of the bony contour, especially of the rib border (Fig. 5). These findings can be quite pronounced, with overlap of the ends of the ribs and significant chest wall deformities, or they can be very subtle and easily overlooked. Clinical correlation with point tenderness of the chest wall can often confirm the diagnosis. Associated findings may include subcutaneous emphysema, pneumothorax, hemothorax, and pulmonary contusion. Management The complications of rib fracture are considered more important than the injury itself. Significant underlying pulmonary contusion should be treated with respiratory support and mechanical ventilation, if necessary. Pain control is an important part of treatment, because limited inspiratory efforts can result in atelectasis, collapse, and secondary pneumonia. Oral or intravenous narcotics are often utilized but can cause respiratory compromise. Epidural catheter

Fig. 5. Rib fractures (arrows) after blunt thoracic trauma.

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placement for pain control can be quite efficacious. Aggressive pulmonary toilet often is necessary as well.

Pneumothorax Frequency/incidence Traumatic injury is one most common cause of pneumothorax. As many as 35% to 40% of patients with blunt traumatic injuries will develop some form of pneumothorax, with the incidence depending largely on the severity of the trauma [14]. About 40% of these pneumothoraces are occult, meaning they are apparent on CT but not on chest radiographs [15]. Primary spontaneous pneumothorax, which commonly occurs in patients with underlying pulmonary disease, accounts for about 9000 cases of pneumothorax each year. Signs and symptoms Symptoms of pneumothorax depend on the degree of lung collapse, and small pneumothoraces may be asymptomatic. Chest pain and dyspnea are the two main symptoms associated with the development of pneumothorax. Hypoxia may occur if the pneumothorax is large, and development of tension pneumothorax (see section on tension pneumothorax) may be lethal. Etiology/pathophysiology Spontaneous pneumothorax usually results from rupture of a subpleural emphysematous bleb, which is usually located in the apex of the lung. Blebs are present in 75% of cases of primary spontaneous pneumothorax, and are especially common in patients with emphysema or other underlying pulmonary diseases. Another group of patients that appears to be at risk are young, thin, male athletes. Pneumothorax can also be iatrogenic in origin. Central line placement, either via subclavian or jugular approach, can cause puncture of the lung parenchyma with resultant pneumothorax. Operations of the neck, such as tracheostomy and thyroidectomies, can also cause pneumothorax, although this is rare. Violation of the pleura and pneumothorax is a common finding in trauma patients who sustain rib fractures. Image of choice The preferred imaging method for detection of pneumothorax is a PA chest radiograph taken during exhalation. Exhalation may enhance the appearance of pneumothorax by increasing the density of the lung, which increases contrast between the trapped air. Image hallmarks The hallmark of pneumothorax on chest radiograph is a lucent space between the pleural line and the chest wall. This lucency, where there is a notable absence of lung parenchymal markings, is most readily apparent in the apex of the lung, especially on an upright film (Fig. 6A). Close examination may be needed to visualize the pleural line (Fig. 6B). Increased opacity of the affected lung may also be visible. Subcutaneous air may also be visualized, especially in cases of traumatic pneumothorax. Management Management of pneumothorax depends on its size and on the presentation of the patient. Small pneumothoraces may be observed and resolve spontaneously. Supplemental oxygen and incentive spirometry may be beneficial. If expectant management is undertaken, close patient monitoring and serial chest radiographs should be employed. If there is significant increase

Fig. 6. Pneumothorax. (A) Right pneumothorax seen on chest radiograph. (B) Inset from above, with pleural line indicated (arrows). Note the absence of lung parenchymal markings lateral to the pleural line.

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in the size of the pneumothorax between films, therapeutic intervention may be required because spontaneous resolution is less likely. A large pneumothorax may require decompression with tube thoracostomy and suction. In cases of prolonged unresolved pneumothorax, thoracostomy with a Heimlich valve or pleural sclerosis may be required.

Hemothorax Frequency/incidence Trauma is by far the most common cause of hemothorax. One study found that 44% of patients with multiple traumatic injuries had associated hemothorax [16]. Another review found that as many as 75% of patients who sustained severe blunt or penetrating chest trauma had significant hemothorax [17]. Hemothorax usually results from injury to the lung parenchyma or, on occasion, to the intercostal or great vessels. Iatrogenic causes are less common and include venous catheter placement, thoracocentesis, lung or pleural biopsy, or thoracic surgery. Signs and symptoms The clinical significance of hemothorax depends on the degree of blood loss. Symptoms can range from the asymptomatic presentation to profound hypovolemic shock. Patients may complain of dyspnea or shortness of breath. Physical examination findings are decreased breath sounds and dullness to percussion on the injured side. If significant respiratory compromise is present, decreased arterial saturations and hypoxia may be seen. Hemothorax may also be present in conjunction with significant pneumothorax (see section on hemopneumothorax), and the clinical presentation may consist of aspects of both respiratory and circulatory compromise. Etiology/pathophysiology Hemothorax usually results from injury to the chest wall or lung parenchyma. Other less common but more serious causes are hemorrhage from one of the great vessels, intercostals, internal mammary arteries, or the heart. Image of choice Plain radiograph is the preferred diagnostic imaging modality, and clinical correlation is often used to confirm the diagnosis. Image hallmarks Images of hemothorax may mimic pleural effusion, because both entities consist of fluid between the lung parenchyma and the chest wall (see section on pleural effusion). Unlike the fluid present in effusion, however, the blood present in hemothorax will coagulate, preventing free flow in the chest cavity. For this reason, hemothorax may be seen as a generalized density over the entire hemithorax, especially in a supine chest radiograph (Fig. 7). Other manifestations of hemothorax include the presence of a visible pleural line, with increased density between the lung parenchyma and chest wall. Because most cases of hemothorax arise after trauma, the clinical presentation and index of suspicion differentiate hemothorax from effusion. Management Management of hemothorax consists of measures to clear the pleural space of blood. Large caliber tube thoracostomy is often employed to accomplish this. Despite these maneuvers, clotted hemothorax can be difficult to evacuate, and in some situations, thoracoscopy or thoracotomy may be warranted. If associated infection is present (eg, pneumonia), the pleural blood is at risk for becoming an empyema through secondary infection.

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Fig. 7. Left hemothorax presenting with diffusely increased density throughout the hemithorax.

Hemopneumothorax Frequency/incidence Trauma is the most common cause for hemopneumothorax, which occurs less frequently than an isolated pneumothorax or hemothorax. The incidence of hemopneumothorax is 21.6%, which was reported in one retrospective study analyzing blunt trauma [18]. The incidence increases with penetrating trauma (35%–38%) [19,20]. Signs and symptoms Patients can present relatively asymptomatic or with hypovolemic shock, depending on the volume of blood loss. Patients may initially complain of dyspnea or shortness of breath. Physical examination findings are decreased breath sounds and unilateral percussive dullness with areas of hyperresonance on the injured side. If significant respiratory compromise is present, decreased arterial saturations and hypoxia may be seen. Because a hemothorax is present in conjunction with significant pneumothorax, the clinical presentation may consist of aspects of both respiratory and circulatory compromise. Etiology/pathophysiology Bleeding into the pleural space is usually due to chest wall injury or parenchymal laceration. Other more serious causes are hemorrhage from one of the great vessels, one of the intercostals or internal mammary arteries, or the heart. This condition is further complicated by pneumothorax, which usually results from trauma to the lung parenchyma. Image of choice The preferred imaging modality for detection of hemopneumothorax is a PA chest radiograph. Exhalation may accentuate the appearance of the pneumothorax component of this entity.

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Image hallmarks Signs of both pneumothorax and hemothorax will be seen on chest radiograph (Fig. 8A). The pneumothorax component can been seen as a distinct pleural line (Figs. 8A and 8b, white arrow) with absence of peripheral lung parenchymal markings. On an upright film, the pleural blood may be seen at the base of the lung, and an air-fluid level may be visualized if the blood has not coagulated (Fig. 8A, black arrow). In Fig. 8A, note the presence of rib fractures (outlined arrow), which are likely responsible for the hemopneumothorax. On a supine film, only the hemothorax may be clearly visible. Management Management of pneumohemothorax consists of measures to clear the pleural space of blood and reexpand the collapsed portion of lung. Large-caliber tube thoracostomy is usually employed to accomplish this. Despite these maneuvers, clotted hemothorax can be difficult to evacuate, and in some situations, thoracoscopy or thoracotomy may be warranted. If associated infection is present (eg, pneumonia), the pleural blood is at risk for becoming an empyema through secondary infection.

Fig. 8. Hemopneumothorax. (A) Hemothorax and pneumothorax seen on upright chest radiograph. Black arrow indicates fluid level and blunting of costophrenic angle from hemothorax. White arrow indicates pleural line and apical pneumothorax. Outlined arrows indicate the presence of multiple rib fractures which are likely the cause of the hemopneumothorax. (B) Inset of left lung apex from above, illustrating the presence of the pleural line (white arrow) and the apical pneumothorax.

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Fig. 8 (continued)

Tension pneumothorax Frequency/incidence The major cause of tension pneumothorax is trauma. The incidence of tension pneumothorax from trauma is approximately 10% in severe blunt thoracic injuries. Approximately 5% of patients who present with simple pneumothorax develop a tension pneumothorax when placed on positive pressure mechanical ventilation [21].

Signs and symptoms Tension pneumothorax is a life-threatening entity, and a high degree of clinical suspicion must be employed, especially in patients with traumatic injuries or after procedures in which pneumothorax may occur. Unilateral decreased breath sounds and contralateral tracheal deviation may be present but are usually late findings. Progressive dyspnea, tachycardia, and hypotension can occur, and the patient’s clinical condition may deteriorate rapidly to the point of cardiorespiratory arrest.

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Etiology/pathophysiology Tension pneumothorax occurs when the pleural injury causes air to enter the pleural cavity during inspiration and a one-way valve effect prevents this air from escaping. With progressive inspiration, the pneumothorax increases in size, and this can cause significant mediastinal shift with impaired cardiac venous return and hemodynamic collapse. Image of choice The diagnosis of tension pneumothorax should ideally be made from clinical evaluation, because even a minor delay (such as obtaining a chest radiograph) may be lethal. Nonetheless, tension pneumothorax can be readily visualized on chest radiograph. Image hallmarks Significant collapse of the pulmonary parenchyma is clearly seen (Fig. 9). Shift of the trachea (arrow) and mediastinal structures to the contralateral side may be present. In severe cases, the entire mediastinum may be shifted into the contralateral hemithorax. Management Immediate needle decompression of tension pneumothorax can be life saving. Thoracostomy tube placement should then be instituted, and further management of the pneumothorax should be undertaken when the patient is stable (see section on pneumothorax).

Fig. 9. Left tension pneumothorax. Note the complete collapse of the left lung parenchyma with tracheal deviation to the right (arrow).

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Pulmonary contusion Frequency/incidence Pulmonary contusion is a frequent sequela of blunt chest trauma, and usually is evident on radiographic examination within 6 hours of the initial trauma. It is most often associated with rib fractures, flail chest, and sternal fractures and can occur in up to 56% to 70% of patients with severe blunt chest trauma [14]. Signs and symptoms The most common symptoms of pulmonary contusion are usually related to the associated chest injuries. Thus, pain from rib fractures, sternal fractures, or soft tissue contusions may be the initial symptoms. Patients may also present with dyspnea and tachypnea. Physical examination findings may include ecchymosis over the involved chest wall, point tenderness of the rib cage from associated bony injuries, and decreased breath sounds on the injured side. In cases of severe pulmonary contusion, hypoxemia and significant alveolar-arterial gradient on arterial blood gas examination may also be present. Etiology/pathophysiology The initial traumatic event leads to leakage of blood and edema fluid into the interstitial and alveolar spaces. This leads to alveolar collapse and extravasation of blood and plasma into the alveoli. Inadequate ventilation of the injured lung parenchyma can lead to significant ventilation-perfusion mismatch and arterial hypoxemia. Image of choice The preferred imaging modality for detection of pulmonary contusion is a chest radiograph. Image hallmarks The hallmark of pulmonary contusion is an increased density of the affected lung parenchyma, which results from the alveolar and interstitial edema (Fig. 10). The presence of associated chest trauma, such as rib fractures, is common and is generally located in the proximity of the pulmonary contusion. These findings are usually present within 1 hour of injury; however, in as many as 30% of patients, radiographic evidence of pulmonary contusion may not be apparent until several hours later. Management The management of pulmonary contusion largely consists of respiratory support. Supplemental oxygen, pulmonary toilet, and adequate pain control are some initial measures that can be utilized. Significant pulmonary contusion may require intubation and mechanical ventilation. Ventilatory maneuvers to treat hypoxia are similar to those methods used to treat ARDS (see following section). Pain management issues may be especially important in cases where rib fractures are present (see section on rib fractures). Acute respiratory distress syndrome (ARDS) Frequency/incidence ARDS is a subset of acute lung injury (ALI), a pathophysiologic syndrome with a range of severity and outcomes rather than a single disease. The exact incidence of ARDS is difficult to determine; however, there are distinct risk factors (see Etiology/pathophysiology), which

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Fig. 10. Right upper lobe pulmonary contusion.

predispose patients to the development of ARDS, and in these patients, the incidence of ARDS may be as high as 40% with associated mortalities of up to 90% in some studies [22–24]. Signs and symptoms Most patients demonstrate similar clinical and pathologic features, irrespective of the etiology of ALI. During the acute phase (first 24 hours), there are limited signs and symptoms of ARDS, with a relatively normal physical examination and chest radiograph. During the next 48 hours (latent period), there is often an observable increase in the work of breathing and minor abnormalities on physical examination and chest radiograph. After a few days have passed, acute progressive respiratory failure is common, with decreases in oxygenation and lung compliance and the development of the characteristic diffuse infiltrates on chest radiograph. Finally, in severe cases of ARDS, marked severe hypoxemia refractory to standard ventilatory management, increased intrapulmonary shunting, and associated organ dysfunction may be present [24]. Etiology/pathophysiology There are many associated risk factors for the development of ARDS, including aspiration, sepsis, shock, massive hemorrhage, and large-volume transfusion of blood products. Trauma-associated injuries, such as long bone fractures, fat embolism, pulmonary contusion, head injury, and multiple transfusions, are also risk factors for the development of ARDS. Other less common risks for ARDS include inhalation of smoke or toxic gases, near drowning, and drug ingestions. The pathophysiology behind the development of ARDS is increased alveolarcapillary membrane permeability, which causes acute interstitial and alveolar edema. Although the exact mechanisms of these permeability changes are not known, the marked increase in extravascular lung water results in a picture of ‘‘noncardiogenic’’ pulmonary edema, which is a hallmark of ARDS. As the syndrome progresses, aggregates of plasma proteins, cellular debris, and fibrin adhere to the denuded alveolar surface, forming hyaline membranes, and the alveolar septum thickens over the next 3 to 10 days as it is infiltrated by proliferating fibroblasts, leukocytes, and plasma cells. Eventual fibrosis of the alveolar septa and hyaline membranes can occur. Although these histologic changes are characteristic of ARDS, not all patients with the

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syndrome progress through this entire pathologic process. Some patients will recover within several days and never develop fibrosis, while others progress to end-stage fibrotic lung disease.

Image of choice The most common imaging modality used to assess patients with respiratory distress is the plain radiograph.

Image hallmarks Findings of ARDS can be difficult to distinguish from other causes of respiratory compromise, primarily cardiogenic pulmonary edema. In general, however, bilateral diffuse infiltrates extending to the periphery of the lung fields are ARDS hallmarks (Fig. 11). The absence of findings that are characteristic of cardiogenic edema, such as enlarged heart size or central edema, may also support the diagnosis of ARDS. Nonetheless, many of these radiographic findings will overlap, and clinical correlation is necessary. Management Underlying causes of ARDS, such as infection, shock, or traumatic injury, should be identified and treated. The remainder of treatment largely consists of supportive ventilatory care. One cornerstone of therapy is the use of positive end-expiratory pressure, which results in a decrease in physiologic shunt fraction and recruits unventilated tissue into the well-aerated zone. Commonly accepted ventilatory techniques used in the treatment of ARDS include minimizing tidal volumes and peak pressures in an effort to recruit dependent, collapsed alveoli while avoiding overdistension and the repeated opening and closing of airways [23]. Changes in the ventilatory mode, such as the use of pressure-controlled ventilation and prone positioning, are other techniques that may also be beneficial in the treatment of ARDS.

Fig. 11. Acute respiratory distress syndrome (ARDS). Note the presence of bilateral diffuse infiltrates which are a hallmark of this disease.

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Mediastinitis Frequency/incidence Acute suppurative infection of the mediastinum, regardless of the cause, is associated with great mortality. The most common cause of acute mediastinitis is esophageal perforation. Currently, 77% of these esophageal perforations arise from endoscopic procedures, with only a small percentage occurring after vigorous emesis (Boerhaave syndrome). The mortality rate from esophageal disruption is 10% to 50%, and can be higher if the injury is not immediately diagnosed and treated [25]. Other forms of mediastinal infection can originate in the oropharynx and descend into the mediastinum, and mortality rates for descending necrotizing mediastinitis are greater than 50% [26]. Less common causes of mediastinal infections include penetrating trauma and postsurgical infections. Signs and symptoms Classic symptoms of esophageal injury consist of severe chest pain, often acute, occurring after esophageal instrumentation or an episode of severe emesis. This pleuritic chest pain may be exacerbated by breathing or coughing, and can be associated with dysphagia, fever, and varying degrees of airway obstruction resulting from dissection of large amounts of air and acute inflammation within the mediastinal fascial planes. Patients with mediastinitis arising from infection in the oropharynx present with dysphagia, limitation of motion, and insidious neck pain. Other symptoms include fever, mild leukocytosis, neck stiffness, anorexia, odynophagia, regurgitation, nasal obstruction, swelling of glands, snoring, and dyspnea. Because the mediastinal fascial planes are contained, infection spreads rapidly causing stridor and respiratory obstruction. Within hours, signs of systemic toxicity, including fevers, chills, and hypotension, may be present. Etiology/pathophysiology Infectious agents can gain entry into the mediastinal space through violation of the esophagus, tracheobronchial tree, or chest wall. Because the fascial planes of the mediastinum are well developed, infection can spread rapidly in these compartments, causing rapid systemic toxicity and clinical deterioration. Posterior involvement of the mediastinum can suggest tuberculous or pyogenic spinal infections. Postoperative complications after cardiac intervention are often related to poor flap construction and sternal instability. Descending necrotizing mediastinitis arises from oropharyngeal infections (eg, odontogenic, peritonsillar, or retropharyngeal), which spread through the retropharyngeal space and other fascial planes to enter the mediastinal space. Image of choice There are several images that can be useful in the detection of mediastinitis. In cases where esophageal perforation is suspected, an upright chest radiograph may show signs of mediastinal air. Gastrograffin swallow may also confirm the diagnosis and delineate the extent of injury. In cases of mediastinitis where an oropharyngeal source is suspected, CT scan of the neck may be useful in determining the location of the original infection and the extent of mediastinal violation. Image hallmarks Hallmarks of mediastinitis on plain radiograph include the presence of air in the mediastinum (Fig. 12). Mediastinal widening and air-fluid levels may be seen, and pneumothorax or hydropneumothorax may be present, especially if the infection has entered the pleural cavity. Extravasation of contrast on swallowing study is seen with esophageal perforation. A CT scan of the neck and chest may show mediastinal air, fluid, or soft tissue stranding, which suggests inflammation.

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Fig. 12. Mediastinal air (arrows) seen in a patient with esophageal perforation.

Management Broad-spectrum aerobic and anaerobic antibiotic therapy should be started immediately, but surgical treatment of the underlying factors is usually necessary, especially in cases of severe infections. For infections that are located above the fourth thoracic vertebra, standard transcervical mediastinal drainage may be adequate. When the infection is extensive, an aggressive combination of transcervical, subxiphoid, or transthoracic drainage is indicated. In the face of airway compromise, a tracheostomy should be performed if the patient displays signs of respiratory distress. References [1] Brooks-Brunn JA. Postoperative atelectasis and pneumonia: risk factors. Am J Crit Care 1995;4:340–9. [2] Shevland JE, Hirleman MT, Hoang KA, et al. Lobar collapse in the surgical intensive care unit. Br J Radiol 1983;56:531–4. [3] Mattison LE, Coppage L, Alderman DF, et al. Pleural effusions in the medical ICU: prevalence, causes, and clinical implications. Chest 1997;111:1018–23. [4] Gotsman I, Fridlender Z, Meirovitz A, et al. The evaluation of pleural effusions in patients with heart failure. Am J Med 2001;111:375–8.

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