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View All Books >> Differential Diagnosis in Computed Tomography >> Chapter 14 : Pleura, Chest Wall, and Diaphragm >> Pleura, Chest
Wall, and Diaphragm

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On CT a 1- to 2-mm thick line is normally seen on the periphery of the lung connecting the visualized rib Image
segments. This line consists of the visceral and parietal pleura, extrapleural fat, endothoracic fascia, and Figure 14.1
the innermost intercostal muscle. The latter is absent in the paravertebral region medial to the most
Figure 14.2 a
posterior rib, resulting in an even thinner or invisible line. The most posterior rib is also the lowest in the
thoracic cage with each more anterior rib arising at a higher level. A thicker than 2-mm pleural line may be Figure 14.3 a
found in obese patients due to excessive extrapleural fat. This condition can usually be differentiated from Figure 14.4
pleural disease by its perfect symmetry. Figure 14.6
Figure 14.7 b
A pneumothorax ( Fig. 14.1 ) is readily diagnosed by CT even in the presence of extensive soft-tissue Figure 14.8
emphysema. Air collections such as subpleural blebs, pneumopericardium, and mediastinal emphysema Figure 14.9
can easily be differentiated from an adjacent loculated pneumothorax with CT. Pleural effusions Figure 14.10
(transudative, exudative, and chylous) have a homogeneous, near-water density and cannot be
Figure 14.11
differentiated by CT. An acute hemothorax on the other hand is often inhomogeneous, with a CT density
Figure 14.12
greater than water, especially in its most dependent locations.
Figure 14.13
Figure 14.14
Pleural fluid initially collects in the most dependent portion of the pleural space, which is posteromedial and
caudal to the lung base in the supine position. The fluid assumes a crescent or lenticular shape. Small Figure 14.16
pleural effusions may be difficult if not impossible to differentiate from pleural thickening despite an overall Figure 14.17
higher CT density of the latter. In these cases, freely mobile fluid can be diagnosed by obtaining images in Figure 14.18
the prone or lateral decubitus position. Furthermore, after intravenous contrast medium administration, a Figure 14.19
thickened, inflamed, or neoplastic pleura enhances, whereas a purely fibrotic pleural thickening and pleural Figure 14.20
fluid do not. Larger pleural effusions extend toward the lateral chest wall and may enter the major fissure,
Figure 14.21
where the fluid tapers medially and produces a characteristic “beak” appearance. A large pleural effusion
compresses the lower lobe and displaces it anteriorly, giving the appearance that the collapsed lower lobe
floats on the pleural fluid. The airless posterior edge of the lower lobe may be mistaken for the diaphragm
with pleural fluid posteriorly and peritoneal fluid anteriorly. Similarly, inversion of a hemidiaphragm by a
massive pleural effusion may also simulate intra-abdominal fluid. However, the correct diagnosis can easily
be made by analyzing both fluid collection and the lower lobe, as well as their relationship in sequential,
more cephalad images.

Both pleural and peritoneal fluid present as an arcuate or semilunar density displacing liver and spleen
away from the adjacent chest wall ( Figs. 14.2 and 14.3 ). Differentiation of those fluid collections is
possible by CT using a variety of different criteria. Fluid outside (peripheral to) the diaphragm is pleural,
whereas fluid inside the diaphragm is peritoneal. Pleural fluid may surround the lung, while peritoneal fluid Purchase a hardcopy of
may be surrounded by the lung bases. In the posterior costophrenic angle, a pleural fluid collection is this book from Thieme.
posterior to the diaphragm and causes anterolateral displacement of the crus. Posterior peritoneal fluid is
anterior to the diaphragm. Pleural fluid gradually decreases in size on more caudal images, whereas
peritoneal fluid increases in size and progressively extends lateral to the liver and spleen on more caudal
images. Fluid seen posterior to the liver is within the pleural space, since the peritoneal space does not
extend into this region because the bare area of the liver is not covered by peritoneum. The interface of
pleural fluid with the liver or spleen is hazy, whereas with peritoneal fluid it is sharp.

Unilateral or bilateral pleural effusions not associated with any other signs of intrathoracic disease are most
often tuberculous in young patients and neoplastic in the elderly. Neoplastic effusions are found with
metastases, lymphoma, and leukemia and in the Meigs–Salmon syndrome: nonmalignant pleural effusion
and ascites with benign or malignant ovarian tumors, or occasionally with a uterine leiomyoma. Besides
tuberculosis, viral and mycoplasma infections may present with pleural effusions as the sole finding. Of the
collagen vascular diseases, both rheumatoid disease and systemic lupus erythematosus (primary and
drug-induced) may present with pleural effusion as the only intrathoracic manifestation. Congestive heart
failure is the most common cause of pleural effusions, but an enlarged cardiac silhouette and other signs of
cardiac decompensation are usually associated. In Dressler's syndrome, effusions usually develop 2 to 3
weeks after myocardial infarction or pericardial surgery, but may occasionally occur months or even years
after the causative episode. Pulmonary thromboembolic disease presenting with pleural effusions as the
sole manifestation is highly unusual.

Traumatic and postsurgical pleural effusions are common, but both history and associated findings are
usually diagnostic. Patients with asbestos exposure occasionally present with pleural effusion alone. A
variety of abdominal diseases such as pancreatitis, subphrenic abscess, ascites of any etiology, renal
failure, and cirrhosis are frequently associated with pleural effusions, but the primary cause is readily
identified by CT in these conditions. Myxedema, familial Mediterranean fever (familial paroxysmal
polyserositis), and primary lymphedema are rare inherited conditions presenting with pleural effusions as
the only intrathoracic abnormality.

Empyema is a purulent pleural infection usually secondary to a bacterial pneumonia. Other less frequent
extrapulmonary sources include bacteremia, subphrenic abscess, spondylitis, thoracotomy, and
penetrating chest trauma. An empyema has to be differentiated from a parapneumonic effusion, which is
an uninfected (sympathetic) serous exudate in pneumonias that resolves spontaneously. It results from
increased permeability of the inflamed visceral pleura. Pulmonary infections that frequently extend beyond
the pleural space into the chest wall include actinomycosis and nocardiosis, and occasionally tuberculosis,
blastomycosis, and coccidioidomycosis.

A loculated empyema ( Fig. 14.4 ) has a lenticular shape conforming to the pleural space that may appear
elliptical or round in cross section. Its outer margin is sharply demarcated from the pulmonary parenchyma
and it forms obtuse angles with the chest wall. The neighboring lung is compressed by a large empyema,
resulting in gradual displacement and bowing of the adjacent pulmonary vessels and bronchi. The wall of
the empyema consists of the inflamed visceral and parietal pleura and appears relatively thin, smooth, and
of uniform thickness. After intravenous contrast medium administration, the wall of the empyema enhances
so that the visceral and parietal pleural layers separated by pus become clearly visible (“split pleura sign”).
The shape of an empyema as well as the length of any possibly contained air–fluid level change when the
patient is moved from supine to the prone or decubitus position. In an organizing empyema the walls may
become thickened and eventually even calcified. Demonstration of fluid collections within the thickened
pleural peel, even at this stage, suggests that the infection is still ongoing and active.

An empyema has to be differentiated from a peripheral lung abscess abutting the pleural surface ( Fig. 14.5
). A lung abscess tends to be spherical without change in shape and with equidimensional air–fluid level
when the patient is scanned in different positions. The walls of a lung abscess are irregular and poorly
defined and may contain several areas of cavitation. The lesion characteristically forms an acute angle with
the chest wall. Pulmonary vessels and bronchi appear to enter the abscess rather than being displaced by
it. After intravenous contrast material administration, the irregularly enhanced periphery contrasts with the
necrotic low-density material in the center.

Pleural thickening is caused by fibrosis and neoplasia. Pleural fibrosis is a common sequela of hemothorax,
empyema, tuberculosis, and exposure to asbestos and talc. In all these conditions, focal to extensive
pleural calcifications are frequent, and, with the exception of asbestos and talc inhalation, the pleural
fibrosis predominantly affects the visceral pleura. Other less common causes of nonneoplastic pleural
thickening include fungal diseases, rheumatoid disease, radiation therapy, organizing pleural effusions of
other etiologies, sarcoidosis, and splenosis (post-traumatic implantation of splenic tissue on the left pleura).
Neoplastic pleural thickening is associated with mesotheliomas (benign and malignant), metastasis,
lymphoma and local invasion from bronchogenic carcinomas (especially Pancoast tumors), and malignant
thymomas.
Extensive pleural thickening caused by fibrosis may result in encasement of the lung, causing restriction
and loss of volume. A thickened layer of extrapleural fat often becomes visible in this stage, separating the
parietal pleura, which may be calcified, from the rib cage.

Asbestos-related pleural disease ( Figs. 14.6, 14.7 ) is almost invariably bilateral. Pleural plaques (smooth
focal thickening of the parietal pleura) are characteristically visible adjacent to the inner surfaces of the
sixth to tenth ribs posteriorly and laterally, whereas the pleura between these ribs is often not affected
(“skip lesions”). Diffuse, more or less uniform pleural thickening in the lower hemithorax is another slightly
less frequent manifestation. Focal visceral pleural fibrosis also occurs and may cause interlobar fissural
thickening, occasionally simulating a pulmonary nodule or inducing a round atelectasis. Calcifications are
common and range from punctate, nodular, and linear densities to complete encirclement of the lower
portions of the lung. Pleural plaques with or without calcifications frequently occur in the diaphragmatic
pleura, but typically spare the costophrenic angles. CT demonstration of diaphragmatic plaques may,
however, be hampered if they lie in the scanning plane. Mediastinal and paravertebral pleural plaques and
thickening are also common findings on CT.

Benign (fibrous) mesotheliomas ( Fig. 14.8 ) usually arise from the visceral pleura. They present as a
localized, sharply defined soft-tissue mass, sometimes with slightly lobulated margins, ranging from 2 to 14
cm in diameter. Smaller lesions are homogeneous on CT, whereas larger lesions may have an
inhomogeneous appearance, especially after contrast enhancement, since necrosis, hemorrhage, cyst
formations and calcifications can occur. A small pleural effusion is occasionally also associated.

Malignant mesothelioma ( Figs. 14.9, 14.10 ), is a highly malignant neoplasm with an extremely poor
prognosis. The majority of cases occur in patients with asbestos exposure. It presents as diffuse nodular or
plaque-like pleural thickening that eventually encases the entire lung. Hemorrhagic pleural effusions are
commonly associated and may mask the irregular, nodular pleural thickening caused by the malignancy.
CT scans obtained in different positions (e. g., prone or lateral decubitus) may be useful to separate pleural
fluid collection from mesothelioma. Large effusions associated with mesothelioma are frequently not
accompanied by a significant mediastinal shift to the contralateral side, probably because of tumor
encasement of the affected hemithorax. Significant contrast enhancement of mesotheliomas may be
helpful to differentiate the tumor from both asbestos-related pleural thickening and loculated pleural
effusions. The tumor spreads by local invasion into the fissures and adjacent structures such as the
ipsilateral lung, mediastinum, pericardium, diaphragm, lateral chest wall, and contralateral hemithorax.
Hematogenous metastases are less common.

Pleural metastases ( Figs. 14.11, 14.12 ) presenting with nodular pleural thickening and effusions are often
indistinguishable from malignant mesothelioma. Bilateral involvement and the absence of both asbestos-
related pleural disease and pulmonary asbestosis favor metastatic disease. Besides bronchogenic
carcinoma (especially Pancoast tumor) and malignant thymoma, both of which invade the pleura by
contiguous spread, hematogenous pleural metastases most frequently originate from carcinoma of the
breast, kidney, ovary, and gastrointestinal tract. Pleural lymphoma may present as a localized, broad-
based pleural mass, usually associated with pleural effusion, but is rarely the initial manifestation of the
disease.

An apical cap with or without a superior sulcus lesion may be caused by a variety of conditions. Pleural
fluid tends to accumulate over the pulmonary apex, especially in the supine position. Apical pleural
thickening not associated with a soft-tissue mass results most often from chronic tuberculosis (usually
bilateral, but often asymmetric) or from a healed empyema, hemothorax, or radiation therapy. An irregular
soft-tissue mass with involvement of the brachiocephalic plexus and vessels and/or invasion of the
adjacent ribs and vertebral bodies indicates a malignant neoplasm. The most common superior sulcus
malignancy is a Pancoast tumor ( Fig. 14.13 ), but metastases (e. g., from breast carcinoma; Fig. 14.14 )
and rarely lymphoma can present in a similar fashion. Benign tumors are rare and may be of neural (e. g.,
neurofibroma and schwannoma) or mesenchymal origin (e. g., fibroma, desmoid, and lipoma). Hematomas
and hemorrhages in the superior sulcus are associated with rib, clavicle, and spine fractures, or are
secondary to aortic and great vessel rupture, or are iatrogenic (catheter perforation). Both atelectasis of the
upper lobe and normal variants such as excessive periapical fat and vascular anomalies (e. g., elongation
or dilatation of the subclavian artery) may also produce apical densities that are all easily diagnosed by CT
because of their characteristic features.

Extrapleural chest wall lesions commonly originate from the ribs and intercostal soft tissues including
vessels and nerves. These lesions displace the overlying parietal and visceral pleura centrally, thereby
forming an obtuse angle between the lesion and the chest wall ( Fig. 14.15 ). Associated chest wall
abnormalities (e. g., rib destruction) further support the extrapleural origin. Rib lesions are most commonly
caused by traumatic, neoplastic, and infectious processes and do not differ from their presentation in other
skeletal locations. Common rib lesions include healing fractures, metastases ( Fig. 14.16 ), multiple
myeloma ( Fig. 14.17 ),osteomyelitis (bacterial, tuberculous, fungal), and benign conditions such as fibrous
dysplasia, bone cyst, enchondroma, osteochondroma, eosinophilic granuloma, brown tumors, and
extrameduallary hematopoiesis ( Fig. 14.18 ).

The axillary space is bordered by the pectoralis major and minor muscles anteriorly; the latissimus dorsi,
teres major, and subscapularis muscles posteriorly; the chest wall and serratus anterior muscle medially;
and the coracobrachialis and biceps muscles laterally. When the patient is scanned with the arms above
the head, the axilla is open laterally.

The axilla contains the axillary artery and vein, branches of the brachial plexus, and a large number of
lymph nodes all embedded in fat. The axillary vein lies usually anterior and caudad to the axillary artery,
whereas the brachial plexus is located cephalad and posterior to the artery. Axillary lymph nodes normally
measure up to 1 cm in diameter, but occasionally slightly larger lymph nodes are found in healthy subjects.
Lymph nodes measuring between 1.5 and 2 cm suggest inflammation (reactive hyperplasia) or early
neoplastic disease, whereas lymph nodes exceeding 2 cm in diameter are indicative of metastatic or
lymphomatous disease. Both axillary and parasternal (internal mammary) lymph nodes are the primary
regional nodes of breast carcinomas and are exquisitely evaluated by CT ( Fig. 14.19 ). Similarly, CT is
also effective in the evaluation of tumor recurrence in mastectomy patients.

The diaphragm is a large, dome-shaped muscle that incompletely divides the thorax from the abdomen.
The diaphragmatic crura are tendinous structures arising from the anterolateral surface of the upper lumbar
spine. The right crus is larger and longer than the left crus and originates from the first three lumbar
vertebral bodies, whereas the left crus arises from the first two lumbar vertebrae. The diaphragmatic crura
may have a nodular appearance that should not be mistaken for enlarged retrocrural lymph nodes.
Normally these nodes are quite small and do not exceed 6 mm in cross-sectional diameter.

Diaphragmatic hernias may be congenital or acquired. Hiatal hernia (herniation of the stomach through the
esophageal hiatus) is by far the most common type and does not require CT for diagnosis. Bochdalek
hernias ( Fig. 14.20 ) are commonly left-sided and occur anywhere along the posterior costodiaphragmatic
margin. They tend to be rather large and may contain omental or retroperitoneal fat, bowel, spleen, liver,
kidney, stomach, and pancreas. Morgagni hernias occur through an anteromedial parasternal defect and
contain liver, omentum, or bowel. They are rare and usually right-sided, tend to be small, and may be
associated with a pericardial defect.

Traumatic diaphragmatic hernias ( Fig. 14.21 ) are found with both blunt and penetrating trauma, but may
be asymptomatic for months and even years. Over 90% are located on the left side, usually in the central
or posterior portion of the diaphragm. Omentum, stomach, bowel, spleen, and kidney may all herniate
through the ruptured diaphragm. Strangulation is a common complication.

A diaphragmatic eventration is caused by a congenitally weak diaphragm with cephalad displacement of

the corresponding abdominal content. The eventration occurs more frequently on the right side, where it
involves the anteromedial portion of the diaphragm. In this case the liver is displaced superiorly and should
not be confused with a peripheral pulmonary or pleural mass. On the left side the eventration usually
involves the entire hemidiaphragm and mimics diaphragmatic paralysis.

Information courtesy of Thieme .

© 1996 Georg Thieme Verlag

View All Books >> Differential Diagnosis in Computed Tomography >> Chapter 14 : Pleura, Chest Wall, and Diaphragm >> Pleura, Chest
Wall, and Diaphragm

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