3.chest Radiography PDF

Chest radiography
Betty J. Tsuei, MD
a,
*
, Peter E. Lyu, DDS
b
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, 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 eusions 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 identiable. 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 ndings in chest radiog-
raphy. Although the article reviews clinical symptoms and treatment, it is not meant to be a de-
nitive dissertation on thoracic diseasescollaboration 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 signicant [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 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 signicant loss of pulmonary parenchyma, patients may exhibit
marked tachypnea and hypoxia.
* Corresponding author.
E-mail address: btsue@uky.edu (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) 189211
Etiology/pathophysiology
Atelectasis is dened 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 eusion 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 b-
rosis 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 nding 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 ssure and compensatory overination 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 benecial. 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 eusion
Frequency/incidence
Pleural eusion is usually a secondary eect 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 eusion may be as high as 58% to 88% [3]. Eusions may also be present
in 67% of patients with pericardial disease [4]. Cirrhosis and ascites are also associated with
pleural eusion (6%), and as many as 11% of patients with bacterial pneumonia may exhibit
concomitant pleural eusion [5].
Signs and symptoms
Patients with pleural eusion may be asymptomatic if the eusion is mild. Generally, they
exhibit symptoms of the underlying cause of the eusionfor example, congestive heart failure
or ascites (see following subsection). Large eusions can cause respiratory compromise with
190 B.J. Tsuei, P.E. Lyu / Atlas Oral Maxillofacial Surg Clin N Am 10 (2002) 189211
dyspnea, tachypnea, and hypoxia. Decreased basilar breath sounds may be found on physical
examination.
Excess pleural uid can be attributed to the increased transport of pulmonary interstitial uid
from the mesothelium into the pleural space. Congestive heart failure is the most common cause
of transudative pleural eusion, 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 gure 1b after 24 hours of vigorous pulmonary toilet.
elevated, such as renal failure, nephrotic syndrome, and cirrhosis may also cause eusion. Sym-
pathetic eusion, resulting from disease in an adjacent organcardiac (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 eu-
sions. Malignancies, particularly breast and lung cancers, may also cause pleural eusion.
Image of choice
Although pleural eusion 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 eusion on upright radiograph is a uid level in
the hemithorax. Small amounts of pleural uid may be manifest as a meniscus that blunts the
costophrenic angle on the PA projection (Fig. 2A). Small eusions may also be visualized in the
posterior sulcus on the lateral lm. At least 175 mL of uid is needed for the eusion to be vi-
sualized on plain radiograph, whereas a large pleural eusion may completely opacify the hemi-
thorax. If the patient is unable to tolerate an upright lm, a lateral decubitus lm with the
aected side down may reveal dependent layering of uid in the hemithorax, suggesting the pres-
ence of pleural eusion. In a supine patient, the eusion is generally seen as a diuse opacica-
tion of the aected hemithorax (Fig. 2B). Atelectasis of a lobe can also be present with pleural
eusions.
Management
Treatment of the underlying cause of the pleural eusion often results in resolution of the
eusion. In general, pleural eusion 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 eusion. (A) Left pleural eusion on upright chest radiograph, demonstrating characteristic blunting of
costophrenic angle and visible uid level. (B) Right pleural eusion on supine chest lm, demonstrating the diuse
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
aected twice as often as girls [6]. One study indicated that 90% of inuenza-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, 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 aected 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 inuenza 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 lled with uid 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 nonspecic and depend on the extent of the disease; ndings range
from mild interstitial prominence (Fig. 3A) to signicant air space disease (Fig. 3B), especially if
bacterial superinfection occurs. Areas of patchy consolidation, air trapping, and perihilar inl-
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 reserved
for 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 diuse interstitial changes seen in viral pneumonia. (B) Signicant 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 ve 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 ndings 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% specic for the diagnosis of pneumonia
[12]. Nosocomial pneumonia can be more dicult to diagnose, especially in ventilated patients
in the ICU. In these cases, fever, leukocytosis, sputum gram stain and culture, inltrate on chest
radiograph, and presence of purulent sputum are used for diagnosis. At least three of these nd-
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 communityacquired pneumonia include S. pneumoniae, H. inuenza, 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 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 inltrate 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 inltrate. 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 inltrates are the most common, aspiration
pneumonia often results in an inltrate in the right upper lobe. Fig. 4 shows the characteristic
inltrate in the right upper lobe.
Management
The treatment of bacterial pneumonia consists of antibiotic therapy and supportive care.
Specic 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 specic unit-based bacterial biograms may be benecial in deter-
mining 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 com-
mon in children because of the elasticity of the cartilage and exibility 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 pulmonary
injuries can result in signicant 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 signicant than the injury itself. As-
sociated underlying pulmonary contusion, especially in patients with ail 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 inltrate.
of the lung. Pneumothorax, hemothorax, and pneumohemothorax are frequent concomitant
ndings. The specic location of the injuries can relay some important information about the
direction and force of impact. Rib fractures of the rst, 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, kid-
neys, or liver. Multiple segmental rib fractures involving two or more contiguous ribs constitutes
a ail 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 specic rib lms 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 ndings can be quite pronounced, with overlap of the ends of the ribs and
signicant chest wall deformities, or they can be very subtle and easily overlooked. Clinical corre-
lation with point tenderness of the chest wall can often conrm the diagnosis. Associated ndings
may include subcutaneous emphysema, pneumothorax, hemothorax, and pulmonary contusion.
Management
The complications of rib fracture are considered more important than the injury itself.
Signicant 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 eorts 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 ecacious. 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 nding 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 lm (Fig. 6A).
Close examination may be needed to visualize the pleural line (Fig. 6B). Increased opacity of
the aected 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 benecial. If expectant management is undertaken, close pa-
tient monitoring and serial chest radiographs should be employed. If there is signicant 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 lms, 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 had
signicant 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 signicance 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 ndings are decreased breath
sounds and dullness to percussion on the injured side. If signicant respiratory compromise is
present, decreased arterial saturations and hypoxia may be seen. Hemothorax may also be present
in conjunction with signicant 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 conrm the diagnosis.
Image hallmarks
Images of hemothorax may mimic pleural eusion, because both entities consist of uid be-
tween the lung parenchyma and the chest wall (see section on pleural eusion). Unlike the uid
present in eusion, however, the blood present in hemothorax will coagulate, preventing free
ow 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 clin-
ical presentation and index of suspicion dierentiate hemothorax from eusion.
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 dicult 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 ndings are decreased breath sounds and unilateral percussive dullness with
areas of hyperresonance on the injured side. If signicant respiratory compromise is present, de-
creased arterial saturations and hypoxia may be seen. Because a hemothorax is present in con-
junction with signicant pneumothorax, the clinical presentation may consist of aspects of both
respiratory 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 intercostals
or 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 PAchest radiograph.
Exhalation may accentuate the appearance of the pneumothorax component of this entity.
Fig. 7. Left hemothorax presenting with diusely 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 lm, the pleural blood
may be seen at the base of the lung, and an air-uid 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 lm, 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 dicult 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 uid 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 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 devi-
ation may be present but are usually late ndings. Progressive dyspnea, tachycardia, and hypo-
tension can occur, and the patients 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 eect prevents this air from escaping. With progressive
inspiration, the pneumothorax increases in size, and this can cause signicant 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
Signicant 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, ail 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 ndings 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 signicant alveolar-arterial gradient on arterial
blood gas examination may also be present.
The initial traumatic event leads to leakage of blood and edema uid 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 signicant 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 aected 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 the
pulmonary contusion. These ndings 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 that
can be utilized. Signicant 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 dicult
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 ARDS
may be as high as 40% with associated mortalities of up to 90% in some studies [2224].
Signs and symptoms
Most patients demonstrate similar clinical and pathologic features, irrespective of the etiol-
ogy of ALI. During the acute phase (rst 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 diuse inltrates 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. Although
the 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 brin adhere to the denuded alveolar surface, forming hyaline membranes, and the alveolar
septum thickens over the next 3 to 10 days as it is inltrated by proliferating broblasts, leuko-
cytes, and plasma cells. Eventual brosis 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 brosis, while others progress to end-stage brotic 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 dicult to distinguish from other causes of respiratory compro-
mise, primarily cardiogenic pulmonary edema. In general, however, bilateral diuse inltrates
extending to the periphery of the lung elds are ARDS hallmarks (Fig. 11). The absence of
ndings 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 nd-
ings will overlap, and clinical correlation is necessary.
Management
Underlying causes of ARDS, such as infection, shock, or traumatic injury, should be identi-
ed 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. Com-
monly accepted ventilatory techniques used in the treatment of ARDS include minimizing tidal
volumes and peak pressures in an eort 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 benecial in the treatment of ARDS.
Fig. 11. Acute respiratory distress syndrome (ARDS). Note the presence of bilateral diuse inltrates which are a
hallmark of this disease.
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. 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 may
be 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
inammation 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 stiness, 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, may
be 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 ap 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. Gastrogran swallow may also conrm 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-uid 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, uid, or soft tissue stranding, which suggests
inammation.
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;4:3409.
[2] Shevland JE, Hirleman MT, Hoang KA, et al. Lobar collapse in the surgical intensive care unit. Br J Radiol
1983;56:5314.
[3] Mattison LE, Coppage L, Alderman DF, et al. Pleural eusions in the medical ICU: prevalence, causes, and clinical
implications. Chest 1997;111:101823.
[4] Gotsman I, Fridlender Z, Meirovitz A, et al. The evaluation of pleural eusions in patients with heart failure. Am J
Med 2001;111:3758.
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 eusion in a well-dened region. Epidemiologic
study in central Bohemia. Chest 1993;104:14869.
[6] Glezen WP, Denny FW. Epidemiology of acute lower respiratory disease in children. N Engl J Med 1973;288:
498505.
[7] Bradley SF. Inuenza in the elderly: prevention is the best strategy in high-risk population. Postgrad Med
1996;99:1389, 1439.
[8] Gharib AM, Stern EJ. Radiology of pneumonia. Med Clin North Am 2001;85:14615.
[9] Marston BJ, Ploue 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;157:170918.
[10] Centers for Disease Control and Prevention . Guidelines for prevention of nosocomial pneumonia. MMWR Morb
Mortal Wkly Rep 1997;46:179.
[11] Jimenez P, Torres A, Rodriguez-Roisin R, et al. Incidence and etiology of pneumonia acquired during mechanical
ventilation. Crit Care Med 1989;17:8825.
[12] Metlay JP, Kapoor WN, Fine MJ. Does this patient have community-acquired pneumonia? Diagnosing pneumonia
by history and physical examination. JAMA 1997;278:14405.
[13] Ziegler DW, Agarwal NN. The morbidity and mortality of rib fractures. J Trauma 1994;37:9759.
[14] Gaillard M, Herve C, Mandin L, et al. Mortality prognostic factors in chest injury. J Trauma 1990;30:936.
[15] Winchell RJ. Trauma, denitive care phase: chest injuries. In: Greeneld LJ, Mulholland MW, Oldham KT,
Zelenock GB, Lillemoe K (editors). Surgery, scientic principles and practice (3rd edition). Philadelphia: JB
Lippincott; 2001 p. 32033.
[16] Kulshrestha P, Iyer KS, Das B, et al. Chest injuries: a clinical and autopsy prole. J Trauma 1988;28:8447.
[17] Light RW, Broaddus VC. Pneumothorax, chylothorax, hemothorax, and brothorax. In: Murray J, Nadel J,
Mason R, Boushey H (editors). Textbook of respiratory medicine (3rd edition). Philadelphia: WB Saunders; 2000
p. 250166.
[18] Shorr RM, Crittenden M, Indeck M, et al. Blunt thoracic trauma. Analysis of 515 patients. Ann Surg 1987;206:
2005.
[19] Madiba TE, Thomson SR, Mdlalose N. Penetrating chest injuries in the rearm era. Injury 2001;32:136.
[20] Vasquez JC, Castaneda E, Bazan N. Management of 240 cases of penetrating thoracic injuries. Injury 1997;28:459.
[21] Light RW. Tension pneumothorax. Intensive Care Med 1994;20:4689.
[22] Fowler AA, Hamman RF, Good JT, et al. Adult respiratory distress syndrome: risk with common predispositions.
Ann Intern Med 1983;98:5937.
[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;151:293301.
[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. 182539.
[25] Craddock DR, Logan A, Mayell M. Traumatic rupture of the esophagus and stomach. Thorax 1968;23:65762.
[26] Lalwani AK, Kaplan MJ. Mediastinal and thoracic complications of necrotizing fasciitis of the head and neck.
Head Neck 1991;13:5319.

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