Chest Radiography

Chest radiography

Betty J. Tsuei, MDa,*, Peter E. Lyu, DDSb

aDepartment of General Surgery, College of Medicine, University of Kentucky,

800 Rose Street, Room C-221, Lexington, KY 40536, USAbDivision 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, ac-

counting 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 car-

diac enlargement suggestive of heart failure may be present. In the febrile patient, the chest ra-diograph 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 di-

agnostic 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 pulmo-

nary 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 ra-diology 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 radiog-

raphy. Although the article reviews clinical symptoms and treatment, it is not meant to be a de-

finitive 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 in-

volved the left lower lobe (66%), but collapse of the right lower lobe (22%) and the right upperlobe (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 � 2002, Elsevier Science (USA). All rights reserved.

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

Etiology/pathophysiology

Atelectasis is defined as a decrease in lung volume and can arise from several causes. Ob-

structing lesions, caused by a foreign body, mucus plugging, or endobronchial tumors may re-sult 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 sponta-

neous 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 fib-

rosis in the interalveolar and interstitial space, decreasing lung compliance and reducing lungvolumes.

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 col-

lapse. In postoperative atelectasis (Fig. 1A), this occurs primarily at the lung bases and is a bi-

lateral 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, car-

diac rotation and mediastinal shift can occur.

Management

Treatment of atelectasis includes aggressive pulmonary toilet to expand the collapsed por-

tions 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 ven-tilation, 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

190 B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211

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

examination.


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

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.

191B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189–211

elevated, such as renal failure, nephrotic syndrome, and cirrhosis may also cause effusion. Sym-

pathetic effusion, resulting from disease in an adjacent organ—cardiac (pericarditis), upper ab-

domen (pancreatitis, splenic disease)—is also common. Infectious agents, such as bacterial

pneumonia, tuberculosis, and fungal or viral infections, usually cause exudative pleural effu-sions. 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 vi-sualized on plain radiograph, whereas a large pleural effusion may completely opacify the hemi-

thorax. 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 pres-

ence of pleural effusion. In a supine patient, the effusion is generally seen as a diffuse opacifica-

tion 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. 1 (continued)


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.

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 immunocom-

promised. 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 partic-

ularly susceptible, with a mortality rate of 30% from viral pneumonia [7]. Infection rates of vi-

ruses depend on the immune status of the individual. Patients with immune suppression

(chemotherapeutic agents, transplant patients, HIV) may become infected with viruses, whichare 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.


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 plug-

ging, and the alveoli are often filled with fluid and leukocytes. The diagnosis of viral pneumoniais 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 infil-

trates 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 reservedfor immunocompromised patients, include ganciclovir, acyclovir, ribavirin, amantadine, and

rimantadine. The respiratory tract may become secondarily infected and result in a super-

imposed bacterial pneumonia, which should be treated with the appropriate antibiotics (see

following section).


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,

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.


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 find-

ings should be present for the diagnosis of pneumonia to be made.


Infectious agents gain entry to the lung either directly by inhalation of 0.5 to 1.0 lm aerosol-

ized 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 or-

ganisms 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. Atyp-

ical pneumonia may result from Mycoplasm or Legionella species. Aspiration pneumonia maybe 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 pul-

monary 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 pneumo-

nias may often be treated with single or oral antibiotic agents, whereas nosocomial pulmonary


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 deter-

mining the antimicrobial agent of choice. In certain cases, hospitalized patients with nosocomialpneumonia 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 com-

mon 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 multi-

system injuries have rib fractures. Commonly associated pulmonary injuries include pneumotho-

rax or hemothorax (32%) and pulmonary contusion 26%. Rib fractures and other pulmonaryinjuries 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. As-

sociated underlying pulmonary contusion, especially in patients with flail segments, can cause

pulmonary compromise, with resultant tachypnea, dyspnea, and respiratory failure.


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

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


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, ortwelfth ribs) often is associated with upper abdominal trauma, such as injury to the spleen, kid-

neys, 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. Althoughthere 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 corre-lation 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 lim-ited inspiratory efforts can result in atelectasis, collapse, and secondary pneumonia. Oral or in-

travenous narcotics are often utilized but can cause respiratory compromise. Epidural catheter

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


placement for pain control can be quite efficacious. Aggressive pulmonary toilet often is neces-

sary 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 inci-

dence 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 spon-

taneous 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 pneumothora-ces 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 devel-

opment of tension pneumothorax (see section on tension pneumothorax) may be lethal.


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 pri-

mary 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 place-

ment, either via subclavian or jugular approach, can cause puncture of the lung parenchyma

with resultant pneumothorax. Operations of the neck, such as tracheostomy and thyroidecto-

mies, can also cause pneumothorax, although this is rare. Violation of the pleura and pneumo-thorax 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 mark-

ings, 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 ofthe 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 pa-

tient 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.

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 pa-

tients 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 hadsignificant 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 in-

clude 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 com-plain 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. Hemothoraxmay also be present

in conjunction with significant pneumothorax (see section on hemopneumothorax), and the clin-

ical presentation may consist of aspects of both respiratory and circulatory compromise.


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, in-

ternal 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 be-

tween 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 ofhemothorax 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 clin-

ical 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 tho-

racotomy may be warranted. If associated infection is present (eg, pneumonia), the pleural blood

is at risk for becoming an empyema through secondary infection.


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. Phys-

ical examination findings are decreased breath sounds and unilateral percussive dullness with

areas of hyperresonance on the injured side. If significant respiratory compromise is present, de-

creased arterial saturations and hypoxia may be seen. Because a hemothorax is present in con-

junction with significant pneumothorax, the clinical presentation may consist of aspects of bothrespiratory and circulatory compromise.


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 intercostalsor internal mammary arteries, or the heart. This condition is further complicated by pneumo-

thorax, 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.

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


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 bloodmay 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 he-

mothorax 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 em-

ployed to accomplish this. Despite these maneuvers, clotted hemothorax can be difficult to evac-

uate, 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.


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 pa-

tients 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 suspicionmust be employed, especially in patients with traumatic injuries or after procedures in which

pneumothorax may occur. Unilateral decreased breath sounds and contralateral tracheal devi-

ation may be present but are usually late findings. Progressive dyspnea, tachycardia, and hypo-

tension can occur, and the patient’s clinical condition may deteriorate rapidly to the point of

cardiorespiratory arrest.

Fig. 8 (continued)



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 shiftwith 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).


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 exami-

nation 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.


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 ventila-

tion-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 parenchy-

ma, 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 thepulmonary 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. Supple-

mental oxygen, pulmonary toilet, and adequate pain control are some initial measures thatcan be utilized. Significant pulmonary contusion may require intubation and mechanical venti-

lation. 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


predispose patients to the development of ARDS, and in these patients, the incidence of ARDSmay 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 etiol-

ogy 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 mi-nor 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 com-

pliance and the development of the characteristic diffuse infiltrates on chest radiograph. Finally,

in severe cases of ARDS, marked severe hypoxemia refractory to standard ventilatory man-

agement, increased intrapulmonary shunting, and associated organ dysfunction may be

present [24].


There are many associated risk factors for the development of ARDS, including aspira-

tion, 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 alveolar-

capillary membrane permeability, which causes acute interstitial and alveolar edema. Althoughthe exact mechanisms of these permeability changes are not known, the marked increase in extra-

vascular lung water results in a picture of ‘‘noncardiogenic’’ pulmonary edema, which is a hall-

mark 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, leuko-

cytes, and plasma cells. Eventual fibrosis of the alveolar septa and hyaline membranes can oc-

cur. Although these histologic changes are characteristic of ARDS, not all patients with the

Fig. 10. Right upper lobe pulmonary contusion.


syndrome progress through this entire pathologic process. Some patients will recover within sev-

eral 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 compro-

mise, 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 find-

ings will overlap, and clinical correlation is necessary.

Management

Underlying causes of ARDS, such as infection, shock, or traumatic injury, should be identi-

fied 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 decreasein physiologic shunt fraction and recruits unventilated tissue into the well-aerated zone. Com-

monly 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 tech-

niques 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.


Mediastinitis

Frequency/incidence

Acute suppurative infection of the mediastinum, regardless of the cause, is associated withgreat mortality. The most common cause of acute mediastinitis is esophageal perforation. Cur-

rently, 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 maybe exacerbated by breathing or coughing, and can be associated with dysphagia, fever, and vary-

ing 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 in-

fection in the oropharynx present with dysphagia, limitation of motion, and insidious neck pain.

Other symptoms include fever, mild leukocytosis, neck stiffness, anorexia, odynophagia, regur-

gitation, nasal obstruction, swelling of glands, snoring, and dyspnea. Because the mediastinal

fascial planes are contained, infection spreads rapidly causing stridor and respiratory obstruc-

tion. Within hours, signs of systemic toxicity, including fevers, chills, and hypotension, maybe present.


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 de-veloped, 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 re-

lated 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 mediasti-

num (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.


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 in-

fections. For infections that are located above the fourth thoracic vertebra, standard transcer-

vical 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 res-piratory 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.

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


[5] Marel M, Zrustova M, Stasny B, et al. The incidence of pleural effusion in a well-defined region. Epidemiologic

study in central Bohemia. Chest 1993;104:1486–9.

[6] Glezen WP, Denny FW. Epidemiology of acute lower respiratory disease in children. N Engl J Med 1973;288:

498–505.

[7] Bradley SF. Influenza in the elderly: prevention is the best strategy in high-risk population. Postgrad Med

1996;99:138–9, 143–9.

[8] Gharib AM, Stern EJ. Radiology of pneumonia. Med Clin North Am 2001;85:1461–5.

[9] Marston BJ, Plouffe JF, File TMJ, et al. Incidence of community-acquired pneumonia requiring hospitalization.

Results of a population-based active surveillance study in Ohio. The Community-Based Pneumonia Incidence Study

Group. Arch Intern Med 1997;157:1709–18.

[10] Centers for Disease Control and Prevention . Guidelines for prevention of nosocomial pneumonia. MMWR Morb

Mortal Wkly Rep 1997;46:1–79.

[11] Jimenez P, Torres A, Rodriguez-Roisin R, et al. Incidence and etiology of pneumonia acquired during mechanical

ventilation. Crit Care Med 1989;17:882–5.

[12] Metlay JP, Kapoor WN, Fine MJ. Does this patient have community-acquired pneumonia? Diagnosing pneumonia

by history and physical examination. JAMA 1997;278:1440–5.

[13] Ziegler DW, Agarwal NN. The morbidity and mortality of rib fractures. J Trauma 1994;37:975–9.

[14] Gaillard M, Herve C, Mandin L, et al. Mortality prognostic factors in chest injury. J Trauma 1990;30:93–6.

[15] Winchell RJ. Trauma, definitive care phase: chest injuries. In: Greenfield LJ, Mulholland MW, Oldham KT,

Zelenock GB, Lillemoe K (editors). Surgery, scientific principles and practice (3rd edition). Philadelphia: JB

Lippincott; 2001 p. 320–33.

[16] Kulshrestha P, Iyer KS, Das B, et al. Chest injuries: a clinical and autopsy profile. J Trauma 1988;28:844–7.

[17] Light RW, Broaddus VC. Pneumothorax, chylothorax, hemothorax, and fibrothorax. In: Murray J, Nadel J,

Mason R, Boushey H (editors). Textbook of respiratory medicine (3rd edition). Philadelphia: WB Saunders; 2000

p. 2501–66.

[18] Shorr RM, Crittenden M, Indeck M, et al. Blunt thoracic trauma. Analysis of 515 patients. Ann Surg 1987;206:

200–5.

[19] Madiba TE, Thomson SR, Mdlalose N. Penetrating chest injuries in the firearm era. Injury 2001;32:13–6.

[20] Vasquez JC, Castaneda E, Bazan N. Management of 240 cases of penetrating thoracic injuries. Injury 1997;28:45–9.

[21] Light RW. Tension pneumothorax. Intensive Care Med 1994;20:468–9.

[22] Fowler AA, Hamman RF, Good JT, et al. Adult respiratory distress syndrome: risk with common predispositions.

Ann Intern Med 1983;98:593–7.

[23] Hudson LD, Milberg JA, Anardi D, et al. Clinical risks for development of the acute respiratory distress syndrome.

Am Rev Respir Crit Care Med 1995;151:293–301.

[24] Foner BJ, Norwood SH, Taylor RW. The acute respiratory distress syndrome. In: Civetta JM, Taylor RW, Kirby

RR, editors. Critical care. 3rd edition. Philadelphia: Lippencott-Raven; 1997. p. 1825–39.

[25] Craddock DR, Logan A, Mayell M. Traumatic rupture of the esophagus and stomach. Thorax 1968;23:657–62.

[26] Lalwani AK, Kaplan MJ. Mediastinal and thoracic complications of necrotizing fasciitis of the head and neck.

Head Neck 1991;13:531–9.


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