IAP Textbook of Pediatric Radiology Anoop Verma, M Zulfikar Ahamed, TM Ananda Kesavan, S Venkateswaran, G Vijayalakshmi, Anand S Vasudev, TK Nandakumaran, TU Sukumaran
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Respiratory SystemCHAPTER 1

S Venkateswaran
Know the normal chest X-ray first?
A good pediatrician must be able to recognize normal roentgenographic chest before attempting to explore the radiopathology. It is more of identifying the normal shape, contour and densities of visualized structures in the chest. It is mainly comparing the whiteness and darkness of one half with that of other half.
Chest Posteroanterior View: The norms to be observed
Whether the film is taken with the required norms?
  • Whether it is anteroposterior (AP) or posteroanterior (PA) view?
  • Whether it is taken in deep (full) inspiration or expiration?
  • Whether positioning is correct or tilted?
  • Whether side marking is given?
  • Whether all required anatomic parts are included in the film?
How to Differentiate between AP and PA Film of the Chest?
In AP view (Fig. 1.1)
  • The lung volume is reduced
  • The lung appears rectangular because of horizontally placed diaphragmatic leaflet and inwardly placed scapular margin
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    Fig. 1.1: Chest AP view The lung volume appears to be reduced and the heart appears to be increased in size which are all because of inwardly turned scapulae and elevated diaphragm
  • The heart appears increased in size because of elevated diaphragm
  • The costophrenic and cardiophrenic angles give false appearance of pleural effusion.
In PA view (Fig. 1.2)
  • The anatomical shape of the lung is visualized
  • Well aerated clear lungs are seen
  • Lateral chest wall margin is well delineated
  • Diaphragmatic leaflets with its normal curvature is well distinguished
  • Costophrenic and cardiophrenic angles are clearly seen.
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Fig. 1.2: Chest PA view The entire area of the lung and all the margins including the diaphragmatic leaflets are well delineated
How to Order for a Chest X-ray
  • Order by chief complaint
  • Order the correct view
  • Posteroanterior view: standard frontal chest film
  • Lateral view: marked by which side of chest is against the film
  • Order the correct position:
    • Lying vs upright
    • Right vs left.
What is to be Observed Before Interpreting a Film?
  • Make sure it is the right patient
  • Know the patient's detail
  • Have older films if available
  • Place the film on the view box as though you are facing the patient.
Go for Systematic Interpretation
Suggested routines:
Look for label and other data base
  1. Name: Since the names can be shared by others, check for the hospital number if any.
  2. Date: Important for comparing prior exams. Serial images to be numbered.
  3. Position markers: Right (Rt) vs Left (Lt)
  4. Position of the patient:
    • AP
    • AP supine
    • PA view
    • Lateral (Lt/Rt) for anatomy reading
    • Lordotic view for apical region
    • Lateral decubitus (Lt/Rt) for effusion or thickening
    • Oblique (Rt/Lt; postr/Antr): eliminate superimposed lesion.
  5. Quality of the film: One should be able to see the outlines of the vertebral bodies within the heart shadow.
  6. Rotation: Should be minimal. It can be assessed by comparing the medial ends of clavicle to the margins of vertebral body at the same level. This should be at equidistance on either side.
Systematic Interpretation
Systematic interpretation is done with a search for pathology.
Reading a chest X-ray requires systematic approach. It is tempting to leap to the obvious findings but failure to be systematic can lead to missing pathologies, over looking more subtle lesions, drawing false conclusions, based on a film that is technically poor. This may lead on to wrong management on an inaccurate interpretation.
The best way of learning how to spot abnormalities on a chest X-ray is to look lot of them repeatedly both normal and abnormal.
This reduces the chances of missing and difficult to see features.
General Principles
  • Read X-ray yourself
  • Be systematic
  • Be aware of common artifacts
  • Serially compare
  • Observe symmetry
  • Believe you missed a finding until you confirm that your review is clear.
Reading Order of a Chest X-Ray
One of the commonly used method is given below
  1. General review
  2. Centering of the film
  3. Trachea
  4. Mediastinum
  5. Hilum
  6. Diaphragm
  7. Heart
  8. Lung
  9. Soft tissues, skeleton and artifacts.
Pathological Search
  1. General review
    Is the film well penetrated and symmetrical?
  2. Centering of the film
    Is the image centered? – Inner clavicular ends should be at the same distance from the midline.
  3. Trachea
    Is the trachea central?
    Rotation is the most common cause for inequality in the translucency of the lungs and needs to be differentiated from increased transradiancy from other causes.
  4. Mediastinum
    Are there any bumps that should not be there?
    What might they be?
    • Masses
    • Lymph nodes
    • Thymus
    • Thymoma.
  5. Hilum
    How is the hila?
    • Normal relationship
    • Size.
  6. Diaphragm
    • Does the lowest part of the heart shadow meet the diaphragm at a sharply defined angle? If not why?
    • Does the dome of the diaphragm have a normal sweep? If not why?
    • Does the outer edge of the diaphragm meet the pleura at a sharp acute angle? If not why?
    • Look for any pathological variations in relation to diaphragm
      • Air under diaphragm
      • Flattened diaphragm
      • Loss of diaphragm definition
      • Elevated hemidiaphragm
      • Tenting of diaphragm.
  7. Heart
    • Right border: Edge of right atrium
    • Left border: (L) ventricle + (L) atrium
    • Anterior border: Right ventricle
    • Posterior border: Left ventricle
    Assess for the size, shape and position of the heart and pulmonary circulation.
    The cardiothoracic ratio (CT ratio) is usually about 50% but can be more in the first year of life and a large thymus can make assessment difficult as with a film in poor inspiration. As with adults, one-third should be to the right of center and two-third to the left.
    Assessment of pulmonary circulation can be important in congenital heart disease but can be very difficult in routine practice. Heart appears water dense seen usually with the apex to the left, occupies about 50% of chest width at widest point. Aortic knob may be seen through thymus on left.
    Pulmonary vessels can be seen in hila, best on lateral view. The vessels are seen extending to midlung tapering gradually.
  8. Lungs
    1. Assess the lung volume: Count down the anterior rib ends to the one that meets the middle of the hemidiaphragm. A good inspirating film should have the anterior end of 4the 5th or 6th rib meeting the middle of the diaphragm. More than six anterior ribs show hyperinflation. Fewer than five indicates an expiratory film or under inflation. With under inflation as in expiratory film, the third or fourth rib crosses the diaphragm. This makes normal lungs appear opaque and a normal heart appears enlarged (Figs 1.3 and 1.4).
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      Fig. 1.3: Chest PA view in expiration Because of the elevated diaphragm in expiration the lung volume appears reduced with a pseudo appearance of bilateral basal congestion and enlarged heart
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      Fig. 1.4: Chest PA view in full inspiration Fully expanded lung showing maximum lung volume, clear outlines and well delineated diaphragmatic leaflets
    2. Lung density: Lungs are uniformly aerated and they appear black on most films. Divide the lungs arbitarily into upper, middle and lower zones and compare the two sides for size and density.
      Evaluate pulmonary vascular pattern and compare the upper to lower lobe, right to left, normal tapering to periphery.
    3. Pleura: Follow the pleura around the rib cage. Look for major and minor fissures if seen. Compare the hemidiaphragms, which must curve downwards and that the costophrenic and cardiophernic angles should be sharp and clear and not blunted.
  9. Soft tissues, skeleton and artifacts
    Breast shadow especially in an adolescent girl may show slightly increased density and look for symmetrical shadows.
    Look for scapula, humerus, shoulder joint, clavicle and ribs for their symmetry. Review spine and rib cage for alignment, disc space narrowing, lytic and blastic regions, etc.
    Recognize the artefacts such as skin folds which may mimic pneumothorax. In girls, either plaited or dressed with ornaments may cause a variety of artefacts usually projected over the upper lobe and mediastinum.
  10. The other way of looking into the chest
    A – B – C – D – E – F – G – H approach to interpretation of chest X-ray.
    Lung Field
    Gastric bubble
5How a normal chest should look like?
The basic principle in AP or PA view is a matter of comparing the shape and densities of the various structures visualized (Fig. 1.5).
  • Both lungs should have equal but relatively darker density because of aeration
  • Heart as a whole should have uniform density of opaqueness, as it is due to water density
  • Both hilar regions should be of relatively equal density
  • Cardiac silhouette to either side of the spine should be of about the same density
  • The juxtapositioned margins of the heart and diaphragmatic leaflet in a normally aerated lung should be crisp and distinct.
Lateral View
  • Identify the sternum anteriorly and spine posteriorly
  • Divide the space vertically as retrocardiac and retrosernal
  • In retrosternal space, the superior half is always radiolucent because of normally aerated upper lobe of the lung
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    Fig. 1.5: Chest PA view-normal All regions and borders, lung volume on either side, both hilar regions and both diaphragmatic leaflets appear normal
  • Rarely in infancy, due to normal thymus the radiolucency is replaced by radiodensity or whiteness
  • The retrosternal lower half is opaque due to cardiac shadow
  • The retrocardiac superoposterior region is relatively opaque than the lower half due to the soft tissues of the upper chest wall, axillae and shoulder.
  • The lower half of retrocardiac space is characteristically radiolucent due to normally aerated superimposed lower lobe.
The two important characters of right diaphragmatic leaflet are (Figs 1.6 and 1.7)
  1. Its position is slightly higher than the left
  2. Usually seen in its entirety, right upto its insertion on to the anterior chest wall.
The third but rare character of right diaphragmatic leaflet is that inferior vena cava being right sided blends with the right diaphragmatic leaflet.
The characteristic features of the left diaphragmatic leaflet are (Fig. 1.8)
  1. Its level is little lower than that of right
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    Fig. 1.6: Chest lateral view Lateral view showing increasing radiolucency from top to bottom of the retrocardiac space
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    Fig. 1.7: Chest lateral view Normal lower lobe pulmonary vessels mimicking pulmonary infiltrate
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    Fig. 1.8: Localisation of the diaphragmatic leaflet The right diaphragmatic leaflet is higher than the left and is seen in its entirety while the left one blends with the posterior aspect of the cardiac silhoutte
  2. Usually is seen up to the posterior cardiac wall and at this point it blends with the cardiac silhouette
  3. The gastric bubble mostly lies under this leaflet.
Note: All of these findings and relationships may not be evident in every lateral chest film, but enough of them are usually present.
The Viral Spectrum
Any viral infection of the lower respiratory tract can produce roentgenographically patterns ranging from the infiltrate free lungs of bronchiolitis to the diffusely infiltrated lungs seen with widespread parenchymal pneumonitis. Any one of these or of the entire spectrum is demonstrable especially during viral epidemic. Most of the viral infection being tracheobronchial in nature the predominant feature is that of “parahilar peribronchial infiltrate”.
The important pathological changes that occur in viral respiratory infections are:
Tracheobronchial inflammation, the inflammatory thickening and edema of bronchial and peribronchial predisposes to airway narrowing with tendency for air trapping and parahilar infiltrate (Fig. 1.9).
In the one end of the spectrum of viral lower respiratory tract infection (LRTI) is the young infant with bronchiolitis. The incidence peaks around 6 months, but it is common up to 2 years of age or so. It may roentgenographically appear as over aeration and in 3 types of form.
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Fig. 1.9: Viral parahilar peribronchial infiltrate with adenopathy
Bronchiolitis with Relatively Clear Lungs
Posteroanterior View (Fig. 1.10)
  • Considerable over aeration
  • Complete absence of peripheral infiltrates
  • Minimal parahilar infiltrate.
Lateral View (Fig. 1.11)
  • Marked over aeration
  • Characteristically bell-shaped chest
  • Markedly depressed and flattened diaphragmatic leaflets.
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    Fig. 1.10: Bronchiolitis with relatively clear lungs Hyperaerated hyperlucent lung
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    Fig. 1.11: Bronchiolitis, lateral view Classic bell-shaped chest due to overaeration
Bronchiolitis with Parahilar, Peribronchial Infiltrate
Posteroanterior View
  • Marked over aeration of both lungs
  • Some parahilar peribronchial infiltrate (Fig. 1.12).
Lateral View (Fig. 1.13)
  • Marked depression and flattening of the diaphragmatic leaflet, secondary to over aeration
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    Fig. 1.12: Bronchiolitis with parahilar peribronchial infiltrate
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    Fig. 1.13: Lateral view in a bronchiolitis Overaeration depressing the diaphragmatic leaflets and lifting the thymus
  • 8In the upper retrosternal area thymus gland is separated from heart due to over aeration.
Viral LRTI with Atelectasis Mimicking Pneumonia
Segmental atelectasis, single or multiple, unilateral or bilateral, because of combined effect of mucosal inflammation, endobronchial secretions and mucus plugs may result in bronchial obstruction and may have a propensity to mimic pneumonia. But a clue for viral diagnosis, due to rapid clearing of respiratory distress symptoms usually in less than 24 hours could be kept in mind, as it is often due to rapid dislodging of mucus plug.
This child presented with acute onset of fever of 102°F, marked respiratory distress and mild cyanosis.
Overaeration: There is generalized overaeration
  • Peribronchial infiltrate (Fig. 1.14)
  • Patchy consolidation at right lower lobe.
Next day:
  • Pneumonic patch disappeared
  • Peribronchial infiltrate persists (Fig. 1.15).
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    Fig. 1.14: Viral LRI, first admission day picture Viral LRI with atelectasis mimicking pneumonia
  • Such a rapid clearing is not possible with bacterial pneumonia.
Hilar adenopathy: A varying degrees of hilar adenopathy from nil to well circumscribed lymphnode, further accentuating the parahilar density (Figs 1.16 and 1.17).
Pneumonitis: Inflammatory extension and mucus exudation may cause either alveolar or interstitial pneumonitis (Fig. 1.18).
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Fig. 1.15: Viral LRI, second admission day picture Fastest resolution of lower lobe lesion is possibly of resolving atelectasis following mucus plug dislodging
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Fig. 1.16: Viral parahilar infiltrates and hilar adenopathy Prominent hilar adenopathy with parahilar peribronchial infiltrate
9The interstitial pattern is characterized by streaky or reticular infiltrate coursing through the lungs or radiating from the prominent hilar regions into the parenchyma presenting at times typically as “shaggy heart” appearance (Fig. 1.19). Alveolar infiltrate can be nodular, fluffy, patchy or consolidative and at times it may be difficult to differentiate from similar infiltrates produced by bacterial infections (Fig. 1.20).
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Fig. 1.17: Lateral view Prominent hilar region partly due to adenopathy and partly due to peribronchial inflammation
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Fig. 1.18: Viral interstitial pneumonia There are streaky infiltrates radiating from the parahilar region into the parenchyma of the lung giving the typical “shaggy heart”appearance
These patients in spite of obvious roentgenographic patterns are clinically less ill.
There may be even gross discrepancy between the patients clinical condition and the X-ray findings (Fig. 1.21).
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Fig. 1.19: Hazy lungs of viral interstitial pneumonitis Diffuse haziness of the lungs and some reticulation in the lung bases
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Fig. 1.20: Viral alveolar pneumonia Bilateral ill-defined fluffy infiltrate in the upper lobes and consolidation in the right middle lobe and a round infiltrate in the right lower lobe behind the heart
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Fig. 1.21: Viral alveolar pneumonitis Right upper lobe consolidation—a rare pattern of alveolar infiltration
Posteroanterior View
  • Fluffy, ill-defined parenchymal infiltrate in the right and left upper lobes.
  • A consolidation in the right middle lobe.
  • Round infiltrate in the right lower lobe behind the heart.
Atelectasis and obstructive emphysema: Thick, viscid, inflammatory mucus plugging may present with varying degrees of distal atelectasis.
These children may present with cough, tachypnea, fever, coryza and sinus congestion. The cough may be even croupy. On auscultation the findings could be either a transmitted upper airway sound or true rales, rhonchi and even wheezes can be heard. More commonly these sounds may change its character from time to time.
Obstructive Emphysema
When a major bronchus plugged by mucus, the entire lobe collapses or becomes emphysematous. This because of air trapping and the resultant hyperaeration are best seen during expiration, because the air will be emptied on the uninvolved side and the diaphragmatic leaflet will also be elevated on that side. But on the involved side air is trapped and diaphragm remains static or become flattened and the lung on that side appears hyperlucent.
This is another aeration disturbance commonly seen with LRTI especially with isolated lower lobe involvement. In such cases, the uninvolved and normal remaining lobe tends to be over aerated on inspiration and appears blacker.
Compensatory Emphysema
There is an infiltrate and partial atelectasis of the left lower lobe and because of this there is compensatory inspiratory over distension and greater radiolucency of the left upper lobe (Fig. 1.22). Also note the level of right diaphragmatic leaflet.
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Fig. 1.22: Compensatory emphysema vs obstructive emphysema Compensatory emphysema of the left upper lobe with an infiltrate and partial atelectasis of the left lower lobe
Obstructive Emphysema
This film (Fig. 1.23) taken during expiration in which air is emptied from the right lung but on the left it is trapped in the left upper lobe. There is an infiltrate in the left lower lobe behind the left side of the heart.
The clinical note to realize in such situations is that these occurrences are temporary and that given enough time the findings will disappear.
  • Radiographic images of viral respiratory infections are of bizarre in nature
  • Roentgenographically so called “parahilar peribronchial” infiltration results in prominent and “dirty parahilar regions”
  • Interpretation of viral respiratory radiography at times is subjective and will vary from viewer to viewer
  • Most of the viral respiratory chest images are temporary and are likely to be changing from time to time.
Bacterial Spectrum
Clinically, patients with bacterial pneumonias often present with abrupt onset of fever, lassitude, malaise and cough with chest pain.
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Fig. 1.23: Compensatory emphysema vs obstructive emphysema Obstructive emphysema of the left upper lobe in an expiratory film showing normal air expulsion in the right lung but trapped air in the left side
As opposed to viral infections auscultatory localization of decreased air entry into involved area are usually clearly apparent in bacterial pneumonia.
Before interpreting bacterial pneumonias following practical aspects should be kept in mind for wide and variant approaches.
Clinically Evident Symptomatic Pneumonias with Normal Chest X-Ray
The patient who obtains his/her chest roentgenograms early in the course of the disease, and because of the usual delay period of up to 12 hours from the onset of symptoms to the appearance of a roentgenographically demonstrable infiltrate the chest X-ray can be normal.
Negative Auscultation with Positive Chest Image
It is important to note that it is not uncommon for auscultation to fail to detect a well developed lobar pneumonia which turns out to be startlingly present roentgenographically. These cases represent instances of advanced consolidation and most likely breath sounds from the adjacent normal lung are so well transmitted through the consolidated lobe that it sounds normal on casual auscultation.
Subtle Pneumonia
Posteroanterior view: There is unilateral increase in density in the right apical region, which is likely to be missed as a normal soft tissue density (Fig. 1.24).
Lateral view: Lateral view clearly demonstrates pneumonia in the posterior segment of the right upper lobe (Fig. 1.25).
Picking up Subtle Pneumonias
Early or minimal infiltrate are so subtle that they are totally overlooked or simply misinterpreted as fortuitous conglomerations of rib and bronchovascular densities.
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Fig. 1.24: Hiding right apical pneumonia A unilateral increased focus of density over the right apex
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Fig. 1.25: Hiding right apical pneumonia Lateral view brings out the pneumonia in the posterior segment of the right upper lobe
The only way to diagnose such pneumonias is to be suspicious of and then methodically substantiate any focal area of increased density either by lateral chest film or by applying “Felson's silhouette sign”.
Subtle Early Infiltrate
  • There is a vague area of focal infiltration in the upper lung field lateral to the left hilar region (arrows) (Fig. 1.26).
  • Lateral view: Substantiates the presence of this infiltrate as there is corresponding area of focally increased density in the posterior chest, superimposed over the spine (Fig. 1.27).
Lateral Chest Film
The value of the lateral chest views cannot be overstated in diagnosing early pneumonias.
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Fig. 1.26: Subtle early infiltrate There is a vague area of focal infiltration in the left upper lung field, just lateral to the left hilar region
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Fig. 1.27: Subtle early infiltrate Lateral view brings out the focally increased density superimposed over the spine
The usefulness of lateral view will be more 13evident and also one may be totally surprised at how well a pneumonia is visible on the lateral view, and yet how poorly demarcated it is on the frontal projection. Never neglect to get a lateral view.
Value of the Lateral Chest Film
  • The infiltrate is so subtle on this view which needs close inspection and one might note that the left diaphragmatic leaflet is slightly indistinct and slightly elevated due to secondary splinting (Fig. 1.28).
  • Lateral view: Clearly bring out the left lower lobe pneumonia just behind the left major fissure (Fig. 1.29).
Applying Felson's Silhoutte Sign
When two structures of equal roentgenographic density are juxtaposed the interphase between them becomes obliterated. For example:
The heart with a water density with aerated lung having air density which is normally juxtaposed, the cardiac edge is clearly demarcated.
But when the heart with water density is juxtaposed against another water density of pulmonary infiltrate then the interphase becomes indistinct or frankly obliterated and this is called “positive silhouette sign” due to adjacent pneumonic consolidation.
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Fig. 1.28: Value of a lateral chest film Only subtle indistinct left diaphragmatic leaflet and a little higher than normal
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Fig. 1.29: Value of a lateral chest film A clearly visualized left lower lobe pneumonia, just behind the left major fissure
  • Lower two-third of right cardiac border is indistinct and obliterated. The left cardiac border is sharp (Fig. 1.30).
  • Lateral view: confirms the presence of right middle lobe consolidation antero-inferiorly (Fig. 1.31).
Left Diaphragmatic Leaflet Silhouette Sign
  • The clue to the suspicion is indistinct left diaphragmatic leaflet against the clearly visualized gastric air bubble (Fig. 1.32)
  • Lateral view confirms the left lower lobe pneumonia posterior to the major fissure (Fig. 1.33)
  • Positive silhouette sign in the right diaphragm (Fig. 1.34)
  • Lateral view confirms right lower lobe pneumonia (Fig. 1.35)
Unfortunately, the silhouette sign also occurs under some normal situation. This normal variation occurs most often along the right cardiac border.
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Fig. 1.30: Right middle lobe silhoutte sign Obliterated and indistinct right cardiac border by an adjacent pneumonia in the medial segment of right middle lobe
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Fig. 1.31: Right middle lobe silhoutte sign Lateral view confirms the right middle lobe pneumonia
Normal Variation of Right Middle Lobe Silhouette Sign
Posteroanterior view: Poor inspiration and normal clustering of the bronchovascular markings adjacent to the right cardiac border causes obliteration of right heart border. This could be misinterpreted for a right middle lobe, medial segment, pneumonia (Fig. 1.36).
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Fig. 1.32: Silhoutte sign, left diaphragmatic leaflet A strong clue for the presence of an infiltrate in the lower left lung field is indistinct left diaphragmatic leaflet
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Fig. 1.33: Silhoutte sign, left diaphragmatic leaflet Lateral view confirms the left lower lobe pneumonia
Lateral view (Fig. 1.37): There is no infiltrate in the right middle lobe.
Pseudofocal Pneumonia
Due to right parahilar peribronchial infiltrate.
  • The film taken in lordotic view, by virtue of the ribs appear horizontal posteriorly and slanted downwards anteriorly. With the clustering of bronchovascular markings and parahilar peribronchial infiltrate with obliterated right heart border right middle lobe, medial segment pneumonia was suggested (Fig. 1.38)
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    Fig. 1.34: Silhoutte sign of right diaphragmatic leaflet Positive silhoutte sign of right diaphragm
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    Fig. 1.35: Silhoutte sign of right diaphragmatic leaflet Lateral view confirms the right lower lobe pneumonia lying posterior to the major fissure
  • The lateral view rules out right middle lobe pneumonia (Fig. 1.39).
The reasons for such variations are:
  • Blending of prominent bronchovascular markings with the right cardiac border
  • Film taken in partial inspiration
  • When the film is obtained with the patient in partial lordotic position
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    Fig. 1.36: Right middle lobe silhoutte sign—normal variation Normal clustering of bronchovascular markings due to poor inspiration obliterating the cardiac silhoutte, suggesting right middle lobe, medial segment pneumonia
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    Fig. 1.37: Right middle lobe silhoutte sign—normal variation On lateral view there is no infiltrate in the right middle lobe
  • Merging of clustered bronchovascular markings with viral inflammatory parahilar peribronchial infiltrate with that of right cardiac border.
Looking for Hiding Pneumonias
There are certain areas which are notorious for hiding early pulmonary infiltrates. Unless one becomes thoroughly familiar with these hiding places, pulmonary infiltrate can be totally missed.
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Fig. 1.38: Pseudofocal pneumonia Hilar clustering of the right bronchovascular markings due to lordotic position of the chest film, suggesting right middle lobe medial segment pneumonia
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Fig. 1.39: Pseudofocal pneumonia Lateral view is found to be normal and the PA view lesion is more of a positional default
The favorite hiding places are:
  • Behind the left side of the heart in the lower lobe extending into the costophrenic angle
  • Behind the right side of the heart in the right lower lobe extending into costophrenic angle
  • Behind the hilar regions in the superior segments of either lower lobe
  • Deep in the posterior costophrenic sulcus behind the stomach, spleen or left lobe of liver
  • High in the upper lobes
  • Deep in the lateral costophrenic sulcus.
Hiding Left Lower Lobe Pneumonia, behind the Heart
  • Vague area of increased density behind the left side of heart (arrows) (Figs 1.40 and 1.41).
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    Fig. 1.40: Hiding left lower lobe pneumonia behind the heart Large area of increased density behind the left side of the heart
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    Fig. 1.41: Hiding left lower lobe pneumonia behind the heart Lateral view showing the pneumonia in the left lower lobe
  • 17Lateral view: Pneumonia to be the left lower lobe deep in the costophrenic recess (arrows) (Fig. 2.41).
Hiding Pneumonia behind the Right Side of the Heart
  • Focal area of increased density behind the heart with the positive cardiac silhouette (Fig. 1.42)
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    Fig. 1.42: Hiding pneumonia behind the right side of the heart There is a focal area of increased density projected through the right side of the cardiac silhoutte
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    Fig. 1.43: Hiding pneumonia behind the right side of the heart Lateral view confirms the presence of a right lower lobe pneumonia
  • Confirmation of right lower lobe pneumonia behind the heart (Fig. 1.43).
Hiding Pneumonia behind the Left Hilum
  • Left hilum is slightly denser and larger than the right (arrows) (Fig. 1.44).
  • Lateral view: Confirms the pneumonia to be in the superior segment of the left lower lobe (Fig. 1.45).
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    Fig. 1.44: Hiding pneumonia behind the left hilum Denser and larger left hilum than the right
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    Fig. 1.45: Hiding pneumonia behind the left hilum Lateral view shows the retrocarinal position of the superior segment of the left lobe pneumonia
Hiding Pneumonia behind the Right Hilum
  • Right hilum is slightly denser and larger than the left hilum (Fig. 1.46)
  • Lateral view confirms the pneumonia to be in the superior segment of right lower lobe (Fig. 1.47).
Hiding Pneumonia behind the Liver and Right Diaphragmatic Leaflet
  • Focal area of opacification behind the medial aspect of liver silhouette (Fig. 1.48)
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    Fig. 1.46: Hiding pneumonia behind the right hilum Large right hilum with increased density suggesting unilateral adenopathy
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    Fig. 1.47: Hiding pneumonia behind the right hilum Lateral view showing the retrocarinal position of lesion to be due to superior segment pneumonia
  • Lateral view confirms it to be in deep position in the posterior costophrenic recess (Fig. 1.49).
Hiding Pneumonia behind the Left Diaphragmatic Leaflet
There is an area of increased density projected through the left diaphragmatic leaflet, lying in the posterior costophrenic sulcus (Fig. 1.50).
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Fig. 1.48: Focal pneumonia, right lower lobe behind the liver There is a focal area of increased density projected through the medial aspect of the liver silhoutte
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Fig. 1.49: Focal pneumonia, right lower lobe behind the liver Lateral view showing the pneumonia lying deep in the posterior costophrenic sulcus
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Fig. 1.50: Subtle focal pneumonia behind left diaphragmatic leaflet A vague area of increased density projected through the left diaphragmatic leaflet, a consolidation of left lower lobe deep in the posterior costophrenic sulcus
Miscellaneous Pneumonias
Though bilateral dense diffuse haziness are more often seen with viral pneumonias similar infiltrates can be seen with Pneumocystis carinii pneumonia, lipoid pneumonitis and on chronicity in pulmonary hemosiderosis, the Hamman-Rich syndrome and pulmonary alveolar proteionosis.
Adenovirus infection when they prone to produce chronic lung damage may develop into Swyer-James lung.
Desquamative interstitial pneumonias are though rare in children, the picture may range from normally appearing lung with one of the lung showing parahilar peribronchial infiltrate to diffuse interstitial haziness or reticularity.
Varicella and infectious mononucleosis especially in adolescents that to in an immunologically suppressed children may present with primary pulmonary pneumonia.
Mycoplasma pneumonia may present ranging from clearly looking acute lobar consolidation or diffuse nodular infiltrate and to any number of intervening roentgenographic patterns.
Bacterial pneumonias such as those due to Staphylococcus aureus, Haemophilus influenzae type B and Streptococcus pneumoniae may at times be associated with empyema and pleural effusion.
When pneumonia occurring in sickle cell anemia we have to give importance to Pneumococcal pneumonia, Haemophilus influenzae type B and Mycoplasma pneumoniae.
Lobar consolidation in Friedlander's pneumonia may tend to expand the lobe and bulge the surrounding pictures outward.
Fungal infections of the lung are though rare in children, but may be so common in the so called fungus belt and the findings are so variable ranging from diffuse fluffy pulmonary infiltrate to those mimicking all forms of primary pulmonary tuberculosis.
Tuberculous Pneumonias
This being one of the commonest problem, the most common confronted picture is that of unilateral hilar or paratracheal adenopathy. The other type of presentations are lobar or segmental consolidation, lobar or segmental atelectasis, lobar emphysema, pulmonary infiltration and pleural effusion.
So, the rule of thumb for suspecting primary pulmonary tuberculosis is “unilateral hilar or paratracheal adenopathy alone, with or without parenchymal change of any type should be presumed tuberculous in origin until proven otherwise”.
The clinical types of pleural fluid collections are:
  • Pus: empyema or pyothorax
  • Serous fluid: hydrothorax
  • Blood: hemothorax
  • Chylous: chylothorax.
Organisms: In the order of occurrence
  1. Staphylococcus aureus
  2. Haemophilus influenzae Type B
  3. Streptococcus pneumoniae
  4. Klebsiellae.
Clinical clues: Empyema is usually due to underlying pneumonia. Hence there will be features suggestive of pneumonia with features of fluid in the chest.
Clues for Staphylococcus Empyema
  • Rapidly developing pleural fluid (pus) collection in less than 24 hours
  • Development of pyopneumothorax
  • Development of multiloculated empyema with or without loculated air pockets.
  • Focal infections such as
    • Pustules
    • Pyodermas
    • Abscess
    • Chronic suppurative otitis media
    • Osteomyelitis of rib and spine
    • Pyogenic arthritis in an infant
    • Infected BCG wound
    • Subdiaphragmatic infections such as hepatic or subphrenic abscess.
Though the most prevailing cause for empyema is Staphylococcus aureus, at times Haemophilus influenzae and Streptococcus pneumoniae may be responsible for empyema.
Rapidly Developing Staphylococcal Empyema
  • Vague opacification on the left lower lobe (Fig. 1.51).
  • Repeat picture taken after 24 hours because of rapidly increasing respiratory distress shows developing empyema and more consolidating lower lobe pneumonia (Fig. 1.52).
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Fig. 1.51: Staphylococcal empyema Vaguely defined infiltrate on the left, partially hidden by the heart
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Fig. 1.52: Staphylococcal empyema Within 24 hours there was rapidly developing empyema
Massive Empyema
Massive opacification of left side with shift of mediastinum (Fig. 1.53).
Clinical clues to rule out pleural effusion and consolidations are:
  • Seriously ill, febrile and toxic child
  • Younger the age, especially infants
  • Any extrapulmonary focal infections
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    Fig. 1.53: Massive empyema There is typical contralateral mediastinal shift and downward displacement of the left diaphragmatic leaflet and stomach
  • Possibility of consolidation of entire lung on one half is extremely rare.
  • Air-fluid levels with massive opacification (Fig. 1.54)
  • Multiseptated air pockets and air-fluid levels (Fig. 1.55).
Hydrothorax: Simple Pleural Effusion
Possible Causes
  • Same organisms that produce empyema
  • Viruses
  • Tuberculosis
  • Mycoplasma
  • Renal—Nephritis and nephrotic syndrome
  • Abdominal tumors—Neuroblastoma and lymphosarcoma
  • Subphrenic or hepatic inflammations
  • Chest wall or spine lesions
  • Pancreatitis
  • CCF
  • Collagen vascular diseases.
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Fig. 1.54: Pyopneumothorax Multiple septated fluid levels on the right characteristic of staphylococcal infection
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Fig. 1.55: Pyopneumothorax Same findings (as in Fig. 1.54) in the lateral view
Radiographic Types
Early or subtle pleural effusion
The earliest sign of minimal or subtle pleural effusion is that of blunting of costophrenic angle with wedge like menisci extending upward along the lateral border of chest wall. In the lateral view the same can be seen as 22curved or sloping menisci in the posterior costophrenic angle. Layering of fluid can also be seen at times on the retrosternal area.
Major or minor fissure opacification, other than a case of primary tuberculosis should invite attention to look for lateral layering as it often true to be due to pleural effusion.
Subtle or early or minimal effusion
  • Fluid along the lateral chest wall (Fig. 1.56): Right minor fissure opacification
  • Lateral view: Thin layers of fluid in all the interlobar fissure. Layer of retrosternal fluid extension (Fig. 1.57).
  • Right lateral decubitus: shifts the fluid down to lateral chest wall and confirms the pleural fluid (Fig. 1.58).
Subtle effusion as vertical fissure opacification
  • When the fluid accumulates in the major fissure it can be seen as sloping vertical line either on the right or on the left
  • Atelectasis of right upper lobe also present (Fig. 1.59).
Subtle interlobar fissure opacification
  • Parahilar peribronchial infiltrate (Fig. 1.60)
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    Fig. 1.56: Early, subtle pleural effusion Thin layering of fluid in the right lateral chest wall and an indistinct extension into the minor fissure
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    Fig. 1.57: Early, subtle pleural effusion Lateral view showing in all the interlobar fissure and a layer of fluid retrosternally
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    Fig. 1.58: Early, subtle pleural effusion Right lateral decubitus view shows the real accumulated amount of fluid
  • Left lower lobe infiltrate
  • Right hilum appears dense.
Lateral view shows triangular wedge-like opacification with posterior tapering running into minor fissure due to fluid accumulation (Fig. 1.61).
Massive Pleural Effusion
Massive pleural effusion is usually not missed. They are characterized by:
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Fig. 1.59: Vertical fissure effusion Accumulation of fluid in the lowermost portion of the major fissure gives an appearance of sloping vertical opacification. There is also an associated right upper lobe atelectasis
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Fig. 1.60: Small interlobar fissure effusion There is a viral left lower lobe infiltration with dense right hilum
  • Massive opacification occupying not less than 1/3 of lung volume
  • Obliteration of costophrenic and cardiophrenic angles
  • Shift of the mediastinum to the opposite side.
  • At times accompanied by
    • Lateral layering extending into the apex
    • Encircling type of accumulation.
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Fig. 1.61: Small interlobar fissure effusion Triangular dense small anterior fissure effusion and posterior tapering as a wedge-like configuration as it runs along the minor fissure
Subpulmonic Effusion Depressing the Diaphragmatic Leaflet
  • Massive opacification occupying left half of the lung (Fig. 1.62)
  • Lateral layering
  • Encircling shadow extending into the apex and paraspiral gutter
  • Shift of the mediastinum to the opposite side.
Mediastinal or Paraspinal Gutter Effusion
They often elude detection. Posteriorly they are seen as long, tapering, triangular or wedge-like paraspinal configuration.
Anteriorly they may look like mass like or triangular shadow.
Mediastinal effusion: There is a triangular, right paramedian shadow with extension into minor fissure (Fig. 1.63).
Pleural Effusion with Pneumonia
There is a double opacified shadow with varying density (Fig. 1.64).
  • Lower lobe consolidation seen as a slightly lesser in density
  • Lateral vertical opacification with slightly increased density due to pleural fluid.
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Fig. 1.62: Massive pleural effusion with large subpulmonic component Massive left sided effusion encircling the aerated lung with a large subpulmonic effusion depressing the stomach
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Fig. 1.63: Mediastinal effusion Triangular configuration of fluid in the mediastinum and it's extension into the minor fissure confirms the effusion
Large Pleural Effusion Mimicking Lobar Consolidation
Radiographic clues
  • The images may be round, oval, spindle-shaped or mass-like configuration
  • Some may appear as irregular shadows
  • Characteristic tapering ends when it involves the fissures.
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Fig. 1.64: Pneumonia with pleural effusion There is an opacification in the right lower lobe due to consolidation and an additional layering in the lateral chest wall due to pleural effusion
Radiographic confirmation is by lateral decubitus view.
Pleural effusion mimicking lobar pneumonia
  • Curved elevation of opacification in the right lower half (Fig. 1.65)
  • Lateral layering of fluid
  • Minor fissure opacification.
Loculated Pleural Effusion
These groups of effusion may mimic consolidation and on lateral view the effusion could be confirmed.
  • Large oval mass-like opacification on the right side sparing costophrenic and cardiophrenic angles (Fig. 1.66)
  • Lateral view shows opacification in the axis of major fissure which confirms loculated effusion (Fig. 1.67)
Loculated Effusion with Irregular Configuration
  • Posteroanterior view shows opacification mimicking consolidation or segmental atelectasis (Fig. 1.68)
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    Fig. 1.65: Pleural effusion mimicking lobar pneumonia The fluid along the right lateral chest wall and some fluid extending into the minor fissure confirms it to be pleural effusion
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    Fig. 1.66: Large loculated empyema Large, loculated, perfectly oval, mass-like lesion of staphylococcal empyema
  • Lateral view confirms the axis of opacification loculated in the minor fissure (Fig. 1.69).
Loculated Effusion in the Lateral Chest Wall
Oval-shaped effusion with adjacent consolidation possibly empyema in the resolving stage (Fig. 1.70).
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Fig. 1.67: Large loculated empyema Lateral view showing mass-like lesion conforms to the axis of the major fissure
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Fig. 1.68: Loculated pleural effusion PA view of the chest showing loculated effusion mimicking pneumonic consolidation
Subpulmonic Effusions
They are difficult to detect unless otherwise one is aware of various radiographic clues consistent to the diagnosis. It may even mimic elevation of diaphragm. The possible radiographic clues are (Fig. 1.71):
  • Unusual flatness of the apparently high diaphragmatic leaflet
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    Fig. 1.69: Loculated pleural effusion Lateral view showing pleural effusion loculated in the right minor fissure
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    Fig. 1.70: Loculated effusion (lateral chest wall) Pneumonia evolving into empyema loculated laterally
  • A sharp drop-off of the lateral edge of the diaphragmatic leaflet
  • Obliteration of the adjacent portion of the cardiac silhouette
  • Increased density of the posterior costophrenic recess
  • Paraspinal collections of fluid, especially on the left
  • Peculiar bumps and humps of the apparently high diaphragmatic leaflet
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    Fig. 1.71: Subpulmonic effusion Apparently elevated left diaphragmatic leaflet with triangular strip of fluid in the paraspinal gutter with obliterated vascular markings through the left diaphragmatic leaflet
  • An increase in the space between the top of the apparently elevated diaphragmatic leaflet and stomach air bubble.
Loss of visualization of the normal blood vessels of the lung through the upper most part of the apparent diaphragmatic leaflet.
The adenopathy in lungs are mostly inflammatory in origin. They can be unilateral or bilateral. The common causes of unilateral hilar or paratracheal adenopathy are:
  • Viral LRTI
  • Primary pulmonary tuberculosis.
At times adenopathy due to primary pulmonary tuberculosis may be associated with parenchymal infiltrate, atelectasis and obstructive emphysema. A good rule of thumb to follow is that, “unilateral hilar or paratracheal adenopathy with or without associated changes in the lungs, should be considered tuberculous in origin until proven otherwise”. The causes for bilateral adenopathy are commonly extra pulmonary 27such as sarcoidosis, histoplasmosis, histiocytosis, lymphoma and leukemia. Parahilar peribronchial infiltrate with hilar adenopathy–typical of viral LRTI (Fig. 1.72).
  • Unilateral paratracheal and hilar adenopathy of tuberculosis (Fig. 1.73)
  • Unilateral hilar adenopathy with suspected atelectasis (Fig. 1.74)
    • Lateral view confirms both atelectasis and paracarinal position of adenopathy (Fig. 1.75)
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      Fig. 1.72: Viral parahilar infiltrate mimicking hilar adenopathy Parahilar peribronchial infiltrate with hilar adenopathy–typical of viral LRTI
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      Fig. 1.73: Unilateral paratrachealadenopathy in tuberculosis Extensive paratracheal adenopathy on the right
  • Unilateral hilar adenopathy due to pulmonary tuberculosis (Fig. 1.76)
  • Unilateral hilar adenopathy with obstructive emphysema on the left side (Fig. 1.77)
  • Hilar adenopathy to differentiate from pneumonitis:
    • Hilar adenopathy with central paracarinal position of opacification confirms the diagnosis (Figs 1.78 and 1.79)
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      Fig. 1.74: Hilar adenopathy in tuberculosis hidden by atelectasis Barely visible hilar adenopathy on the right hidden by right middle lobe atelectasis
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      Fig. 1.75: Hilar adenopathy in tuberculosis hidden by atelectasis Lateral view clearly shows the triangular dense atelectatic right middle lobe
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      Fig. 1.76: Unilateral hilar adenopathy on the right due to tuberculosis
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      Fig. 1.77: Tuberculous adenopathy with obstructive emphysema The expiratory film showing left sided adenopathy and obstructive emphysema of the lung
    • The frontal hilar shadow on lateral view is located retrocarinal consistent with consolidation of superior segment of lower lobe (Figs 1.80 and 1.81)
Atelectasis is a common X-ray finding and it can involve a small segment or one lobe or entire lung.
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Fig. 1.78: Hilar adenopathy There is a massive unilateral left hilar adenopathy in this patient with primary pulmonary tuberculosis
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Fig. 1.79: Hilar adenopathy Lateral view shows typical central, paracarinal location of hilar adenopathy
The common causes are asthma, viral LRTI, primary tuberculosis or foreign bodies.
Certain radiographic rules to be followed in identifying atelectasis are:
  • In obstructive emphysema, the large, hyperlucent lung will show ill-defined pulmonary vascularity
  • An obstructed emphysematous lung cannot compress upon the other lung to the point of total opacification
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    Fig. 1.80: Hilar adenopathy vs Superior segment lower lobe pneumonia This picture at first might suggest bilateral hilar adenopathy or a posterior mediastinal mass
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    Fig. 1.81: Hilar adenopathy vs Superior segment lower lobe pneumonia In this lateral view the retrocarinal position of the lesion is in favor of bilateral superior segment lower lobe pneumonia
  • If a small totally opaque lung is seen it must be total atelectasis or agenesis of the lung
  • In a large, unobstructed emphysematous, hyperlucent lung the pulmonary vascularity is either normal or engorged
  • The atelectatic lung will not change its size with phases of respiration
  • The atelectatic segment or lobe in one view may be faintly visualized or non-visualized and is clearly visualized in other view.
Segmental Atelectasis
They are often confused with pulmonary infiltrates or interlobar fissure effusion. Segmental atelectasis are often seen as “plate-like” or “disc-like”. Segmental discoid atelectasis could be either single or multiple, vertical, horizontal or oblique.
  • Segmental discoid atelectasis in the left upper lobe (Fig. 1.82)
  • Vertical discoid atelectasis of left lower lobe (Fig. 1.83)
  • Bilateral extensive multiple oblique discoid atelectasis (Fig. 1.84).
Total Lung Atelectasis
The features are:
  • Total opacification of entire hemithorax
  • Ipsilateral shift of mediastinum
  • Heart hides into the atelectatic lung.
Total atelectasis of lung (Figs 1.85 and 1.86):
  • Marked loss of volume on the left side
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    Fig. 1.82: Discoid or “plate-like” atelectasis Segmental discoid atelectasis in the left upper lobe
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Fig. 1.83: Vertical discoid atelectasis Segmental collapse occurring in vertical direction
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Fig. 1.84: Multiple discoid atelectasis Bilateral multiple oblique densities representing multiple areas of segmental discoid atelectasis
  • Marked shift of mediastinum to the left.
The pulmonary vascularity in the right lung is normal (compensatory emphysema).
Lobar Atelectasis of Right Side
Right Upper Lobe Atelectasis
The common classical features are (Fig. 1.87):
  • Upper lobe is dense and triangular
  • Minor fissure is elevated
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    Fig. 1.85: Total lung atelectasis Hyperlucent, retained vascularity on the right and loss of volume and mediastinal shift to the left due to mucus plugging in the left major bronchus
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    Fig. 1.86: Total lung atelectasis Another patient with complete atelectasis of the left lung and pronounced compensatory emphysema of the right lung
  • Slight mediastinal shift to the right—may or may not.
Lateral view shows characteristic wedged V-shaped configuration in between major and minor fissure (Fig. 1.88).
Atypical Right Upper Lobe Collapse
The radiographic features are (Figs 1.89 and 1.90)
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Fig. 1.87: Right upper lobe atelectasis —classic configuration
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Fig. 1.88: Right upper lobe atelectasis Lateral view of right upper lobe atelectasis demonstrating characteristic V–shaped configuration
  • Compressed towards apex
  • Minor fissure becomes indistinct but elevated
  • Over aeration of middle and lower lobe.
Right Middle Lobe Collapse
The features are:
  • Focal area of opacification along the lower right cardiac border
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    Fig. 1.89: Atypical right upper lobe atelectasis Atelectatic right upper lobe compressed towards the apex of the right hemithorax and minor fissure is elevated
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    Fig. 1.90: Atypical right upper lobe atelectasis Lateral view shows atypically collapsed right upper lobe in the apex of the heart
  • Elevation of the right diaphragmatic leaflet
  • Depression of right hilum
  • On lateral view: typical inverted “V”-shaped opacification
  • Slight shift of mediastinum to right (Figs 1.91 and 1.92) presents with the all above features.
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Fig. 1.91: Right middle lobe atelectasis Classical findings are an area of increased density just to the right of the lower cardiac border, obliteration of the adjacent portion of the cardiac border, elevation of the diaphragmatic leaflet and depression of the right hilum
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Fig. 1.92: Right middle lobe atelectasis Lateral view shows the typical V-shaped configuration of the collapsed right middle lobe
Right Upper and Middle Lobe Atelectasis
  • Linear and diffuse opacification of medial portion of right lung
  • Positive silhouette sign
  • Smaller volume right hemithorax when compared to left
  • Slight mediastinal shift to the right
  • Mild elevation of right diaphragmatic leaflet
  • Lateral view shows anterior displacement of major fissure with extended opacification in the region of upper and middle lobe with the lower most opacification is inverted “V” shape.
Right Lower Lobe Atelectasis
Dense triangular opacification starting retrocardialy at about the hilar level extending as curved outline beyond the right cardiac border merging with the right diaphragmatic leaflet
  • Slight elevation of right diaphragmatic leaflet
  • Positive silhouette sign of right cardiac and right diaphragmatic border.
  • Lateral view clearly visualized left diaphragmatic leaflet and obliterated right leaflet with retrocardiac posterior most density.
Right Middle and Lower Lobe Atelectasis
Posteroanterior view: Dense triangular configuration starting at suprahilar level with straight sloping line towards the right costophrenic angle (Fig. 1.93).
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Fig. 1.93: Right lower lobe atelectasis Dense triangular configuration of the collapsed right lower lobe with obliterated and elevated right diaphragmatic leaflet and a slight shift of the mediastinum to the right
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Fig. 1.94: Right lower lobe atelectasis Lateral view shows a vague area of increased density
Lateral view: Large area of increased density behind and over the heart (Fig. 1.94).
Left Lung Atelectasis
Left Upper Lobe Atelectasis
Since there is no minor fissure the lingula functions as part of left upper lobe and atelectasis is seen as vague area of increased density and usually there will be associated secondary changes such as shift of the mediastinum and elevation of diaphragm.
Posteroranterior view: Left upper lobe and lingular atelectasis.
  • Mediastinal shift to the left (Fig. 1.95)
  • Positive silhouette sign by obliteration of left cardiac border
  • Ill defined, vague, diffuse haziness over the left upper central lung field.
Lateral view: Collapsed lung with anterior displacement of major fissure (Fig. 1.96).
Left Lower Lobe Atelectasis
Classically it produces a triangular area of increased density, more or less confirmed to the area behind the left side of the heart.
There is a triangular area of opacification retrocardialy and adjacent to the spine (Fig. 1.97).
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Fig. 1.95: Left upper lobe atelectasis Left upper lobe and lingular atelectasis:shift of the mediastinum to the left an obliteration of the entire left cardiac border. There is a diffuse central haziness of the left lung field
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Fig. 1.96: Left upper lobe atelectasis Lateral view shows the classic configuration of the collapsed upper lobe and lingula. The major fissure is displaced anteriorly
As a general rule the pattern of atelectasis may vary from individual to individual depending upon the degree of atelectasis. Because of this, the familiarity with accessory signs such as displacement of hilum, shift of the mediastinum and elevation of diaphragmatic leaflet will help us to arrive at a convincing conclusion.
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Fig. 1.97: Left lower lobe atelectasis Classical triangular area of increased density behind the left side of the heart adjacent to the spine
This may be either generalized or lobar. The cause for generalized emphysema is central obstructing lesions.
They are commonly
  • Tracheal foreign bodies
  • Paratracheal masses
  • Vascular rings
  • Viral or thermal induced injury with air trapping
  • Asthmatic bronchospasm
  • Cystic fibrosis
  • Rarely alpha-1 antitrypsin deficiency.
Radiographic clues:
  • Over distended, over aerated lungs
  • Abnormal tracheal deviation
  • Right-sided aortic arch with the possibility of aortic vascular ring
  • Mediastinal mass.
Endotracheal Opaque Foreign Bodies
Lateral view (Fig. 1.98):
  • Over distended chest
  • Typical bell-shaped configuration.
Posteroanterior view (Fig. 1.99):
  • Over aerated hyperlucent lungs
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    Fig. 1.98: Obstructive emphysema Lateral view of emphysematous lung with increased AP diameter assuming bell shape and flat diaphragmatic leaflets
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    Fig. 1.99: Obstructive emphysema Thermal injury induced bronchiolitis due to smoke inhalation behaving as obstruction leading to emphysematous overaeration
  • Extremely depressed diaphragm with a sloping sweep.
Lobar Emphysema
  • Usually congenital since birth
  • May become symptomatic by adulthood
  • May present as RDS after or at the time of simple respiratory infection
  • Commonly seen in the left upper lobe
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    Fig. 1.100: Congenital lobar emphysema Hyperlucent left upper lobe and small triangularly collapsed lower lobe
  • Can also occur in right upper lobe and middle lobe
  • Lower lobe involvement is very rare
  • May mimic congenital cystic adenomatoid malformation.
Congenital Left Upper Lobe Emphysema
  • Hyperlucent left upper lobe (Fig. 1.100)
  • Small triangular collapsed left lower lobe
  • Mediastinal shift to the right.
  • Thin-walled air-filled cyst
  • Variable in size
  • Fluid free
  • Single or multiple
  • Some may rapidly change in size to rupture and produce pneumothoraces
  • Some may remain static for extended periods of time.
  • The common cause is staphylococcal pneumonia.
Rarely may be due to viral LRTI, tuberculosis, hydrocarbon pneumonia, closed or blunt chest trauma.
  • Large pneumatocele with adjacent small pneumatocele in the right lower lobe (Fig. 1.101).
  • Seven days later numerous and larger size pneumatoceles are found since not responding to antibiotic (Fig. 1.102).
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    Fig. 1.101: Staphylococcal pneumonia with pneumatocele Medial large pneumatocele with a small superior pneumatocele
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    Fig. 1.102: Pneumatocele The picture was taken seven days after the first picture (Fig. 1.101) evolving into a larger pneumatocele and many other small pneumatocele adjacent to it. There is a mild shift of the mediastinum to the left
Pulmonary Abscess
They are commonly due to complications of pneumonias or chronic bronchial obstruction with suppuration. The features are:
  • Thick-walled lesions
  • Regular or irregular in outline
  • Round or oval in shape
  • Air fluid levels are significant
  • PA – Thick walled, irregular appearing cavity in the left lower lobe (Fig. 1.103)
  • Air fluid level is seen (Fig. 1.104).
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    Fig. 1.103: Pulmonary abscess Rounded pus filled abscess in the left lung with air fluid level in the bottom of the abscess
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    Fig. 1.104: Pulmonary abscess Thickwalled irregular appearing abscess in the left lower lobe with air-fluid level in the bottom of the abscess
Air Trappings in the Chest
The causes of air trappings in the chest are:
  • Closed or penetrating chest trauma
  • Asthma
  • Pulmonary infections
  • Obstructing lesions of the airway such as:
    • Foreign bodies
    • Vascular rings
    • Mediastinal cysts
    • Masses.
  • Central in location
  • Occupies various shapes and sizes
  • Usually outlines the mediastinal structures such as thymus, aorta and pulmonary artery
  • Free air can extend upwards to outline the great vessels and soft tissues of the superior mediastinum and neck
  • At times it may outline the heart.
May get collected subpleurally along the diaphragm producing “continuous diaphragm sign”.
  • Air outlining the mediastinal structures such as thymus and heart (Fig. 1.105).
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    Fig. 1.105: Pneumomediastinum Pneumomediastinal air surrounding the small triangular thymus, extending in linear sheaths into the neck and superior mediastinum and extending along the lower left cardiac edge
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    Fig. 1.106: Pneumomediastinum Pneumomediastinal air outlining the thymus on the left and clearly and continuously visible diaphragm producing the “continuous diaphragmatic sign”
  • Entire width of diaphragm is seen from side to side lifting the heart slightly above (Fig. 1.106).
Radiographic clues
  • Increased size and lucency of the involved hemithorax
  • Contralateral shift of the mediastinum
  • Increased sharpness of the ipsilateral mediastinal edge
  • Lateral or decubitus view in suspected doubtful cases show air occupying the top most column
  • Unaltered volume and lucency of the affected chest on expiration
  • Absent vascular markings on the involved side
  • Subtle or small pneumothorax on careful scrutinization over its apex or costophrenic angle delineates the small air pockets.
    • In the apex it is seen as a slender, radiolucent apical cap.
    • In the costophrenic angle typical, laterally pointing v-shaped air fluid level is seen.
Usually following a history of penetrating type of chest wall injury the pneumopericardium may occur. It is an ectopic gas in the pericardium producing a halo of free air all around the heart and ends superiorly as the pericardium inserts at the origin of great vessels. This gives appearance as though the heart is floating at the center of a gas bubble. This is to be differentiated from pneumomediastinum by following features.
Pneumopericardium does not outline the thymus with gas.
Pneumopericardium does not extend superiorly beyond the origin of the great vessels.
  • A halo of free air around the heart (Fig. 1.107)
  • Air extending along the aorta.
Pulmonary congestion and edema can rise from a number of cardiac and non-cardiac causes.
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Fig. 1.107: Traumatic pneumoperitoneum A halo of free air around the heart also extending along the aorta
In arriving at a radiographic diagnosis of pulmonary edema one must keep in mind certain basic anatomical and hemodynamic 38events which helps pediatrician to have a precise approach.
The most important point in differentiation between viral LRTI, parahilar pneumonitic infiltrate with that of pulmonary edema is cardiomegaly.
Pneumonia Versus Pulmonary Congestion
  • Parahilar peribronchial infiltrate of viral LRTI without cardiomegaly (Fig. 1.108)
  • Cardiomegaly with pulmonary congestion (Fig. 1.109).
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Fig. 1.108: Pneumonitis Parahilar peribronchial infiltrate with normal heart due to viral pneumonitis
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Fig. 1.109: Pulmonary congestion Parahilar pulmonary congestion with enlarged heart due to heart disease
They are of two types:
  1. Active congestion
  2. Passive congestion
Active congestion in a L—R shunt usually of congenital heart disease results in more blood flow into the lungs and, hence, the arteries enlarge and tortuous and visualized upto the periphery.
On the other hand passive congestion is mainly due to left heart failure, and so flow into the lungs are not significant but the increased pulmonary venous pressure leads to distension of pulmonary veins and capillaries, followed by oozing out of fluid into the perivascular interstitium (fuzzy appearance of vessels and Kerley's A and B line) and finally leading to alveolar accumulation of fluid. This alveolar fluid collection when it occupies the parahilar region, produces typical ‘butterfly’ configuration with clear periphery or may produce pulmonary consolidation either nodular or lobar type. The causes for such type of passive congestion are:
  • Obstructing lesions in aortic stenosis and coarctation of aorta
  • Myocardial dysfunction such as myocarditis, endocardial fibroelastosis and rheumatic fever
  • Acute glomerulonephritis
  • Iatrogenic fluid over load
  • Smoke or hot air inhalation
  • Noxious fume inhalation
  • Near drowning
  • Rheumatic pneumonia
  • Collagen vascular disease
  • Massive aspiration
  • Fat embolism
  • Allergic pneumonitis
  • Neurogenic pulmonary edema secondary to increased intracranial pressure
  • Shock lung syndrome
  • 39Poisoning by heroin, methadone, librium, carbon monoxide and parathion.
Interstitial Stage
First development of interstitial stage radiographically is streaky or reticular white lines in the chest, followed by increasing generalized opacity or haziness of the lungs and commonly are referred to as Kerley “A” and “B” lines. The “B” lines are the small, transverse lines located in the costophrenic sulci and the “A” lines are the longer lines, generally running outward from the hilar regions.
Alveolar Stage
After saturation of interstitium with the fluid, it oozes out into the alveolar space producing consolidation like picture of nodular or diffuse haziness. When it accumulates in parahilar region with the clear periphery it gives “butterfly” appearance.
In many of the cases edema results from the damaging of the capillaries with the resultant increased permeability and extravasations of fluid into the interstitial and alveolar spaces. In increased intracranial pressure due to associated bradycardia and low cardiac output, there is elevated pulmonary venous and arterial pressure. This increased hydrostatic pressure leads to capillary extravasation of fluid into the surrounding lung.
In near drowning it is mainly direct aspiration of liquid into the lung parenchyma that produces edema.
In smoke and noxious fume inhalation, bronchiolar epithelial injury initially causes air trapping and later replaced by non-specific infiltrates as a result of microatelectasis secondary to pulmonary microembolization. Necrotizing bronchiolitis is one another mechanism which leads to rapid development of pulmonary edema with the resultant fatality.
In rheumatic pneumonia, the streptococcal toxin by damaging and increasing the pulmonary capillary permeability, the pulmonary edema develops.
In fat embolism, it is trapping of the fat droplets in the microcirculation of pulmonary vessels those results in pulmonary edema.
In shock lung due to profound hypoxia and hypotension neurogenic pulmonary edema occurs.
Pulmonary Edema–Interstitial Stage
  • A case of acute glomerulonephritis (AGN) with white streaky lines radiating from the hilum - Kerley “A” lines (Fig. 1.110).
  • A case of cardiac failure due to aortic stenosis with extensive reticular pattern (Fig. 1.111).
  • A case of AGN, with extensive reticulation in the lung with Kerley “B” lines in the costophrenic angle (Fig. 1.112).
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    Fig. 1.110: Pulmonary edema—interstitial stage Radiating streaky white lines from hilum—Kerley “A” lines in a patient with acute glomerulonephritis
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    Fig. 1.111: Pulmonary edema—interstitial stage Extensive reticular pattern of pulmonary interstitial edema in a patient with cardiac failure
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    Fig. 1.112: Pulmonary edema—interstitial stage More extensive pronounced reticulation due to severe interstitial edema with Kerley “B” lines
Pulmonary Edema–Alveolar Stage
  • Bilateral extensive, atypical patchy confluent pulmonary edema (Fig. 1.113)
  • Prominent parahilar “butterfly” type pulmonary edema sparing the apices and costo and cardiophrenic angles (Fig. 1.114).
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Fig. 1.113: Pulmonary edema—alveolar stage Bilateral extensive patchy areas of confluent pulmonary alveolar edema
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Fig. 1.114: Pulmonary alveolar edema Parahilar and mid lung field pulmonary alveolar edema and apical sparing gives an appearance of typical “butterfly”configuration
Diagnosing asthma is not a challenging one and does not always warrant X-ray chest. It is the complication and differentiating asthma mimicking situations are more important than diagnosing classical clinical asthma. 41The underlying pathogenetic mechanisms are bronchospasm, mucosal edema and increased viscid mucosal secretions with impending mucosal plugging.
The spectrum of radiographic images are
  • Typical baseline asthmatic chest
  • Atelectasis mimicking pneumonia in asthma
  • Pneumomediastinum
  • Pneumothorax
  • Obstructive emphysema
  • Compensatory emphysema
  • Prominent pulmonary artery
  • Transient peripleural focal atelectasis.
Typical Baseline Asthmatic Chest
The presentation are widespread over aeration, parahilar peribronchial prominence, bronchial cuffing with or without hilar adenopathy. The picture may almost mimic that of viral LRTI and the only clue is recurrence of episodes and occurrence at times may be without fever.
  • Over aeration of lung (Fig. 1.115)
  • Prominent parahilar peribronchial infiltration
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    Fig. 1.115: Typical baseline asthmatic chest Moderately overaerated lung with parahilar peribronchial infiltrate, bronchial cuffing and hilar adenopathy
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    Fig. 1.116: Typical baseline asthmatic chest Overdistended chest and pushed away heart from the sternum
  • Bronchial cuffing
  • Hilar adenopathy.
Lateral View (Fig. 1.116)
  • Over-distended chest
  • Increased retrosternal depth with the heart.
Atelectasis Mimicking Pneumonia in Asthma
Wheezing episodes at time may be associated with LRTI, but more often it is viral than bacterial. Certain significant clinical observations are:
  • Viral infections are more common than bacterial
  • Increase in wheezing is more common inviral than bacterial
  • Bacterial infections are usually parenchymal and viral are peribronchial.
Though the possibility for bacterial infections is there in an asthmatic child, it is the viral, inflammatory mucus plugging with transient segmental atelectasis is more common than that of bacterial in origin. For the same reason obstructive and compensatory emphysemas are also common in asthmatic child.
Pneumomediastinum Complicating Asthma
  • Pneumomediastinal air outlining the aorta and pulmonary artery (Fig. 1.117)
  • Lateral view: Thymus gland is surrounded by pneumomediastinal air (Fig. 1.118).
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Fig. 1.117: Asthmatic pneumomediastinum Pneumomediastinal air outlining the aorta (A), pulmonary artery (P) and a slender left thymic lobe (arrow)
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Fig. 1.118: Asthmatic pneumomediastinum Lateral view in an asthmatic patient showing a small thymus surrounded by pnemomediastinal air
Obstructive Emphysema
Inspiratory Film (Fig. 1.119)
  • Hyperaerated lung
  • Over distension of lung by virtue of low placed diaphragm.
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Fig. 1.119: Mucous plug causing unsuspected obstructive emphysema Inspiratory film showing bilateral overaeration tempting to interpret as normal
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Fig. 1.120: Mucus plug causing unsuspected obstructive emphysema Expiratory film showing shift of the mediastinum to the left with the possibility of mucus plug obstruction
43Expiratory Film (Fig. 1.120)
  • Partial emptying of lung
  • Shift of mediastinum to the left
  • Unaltered right lung
Hence, there is an obstructive emphysema on the right side.
Compensatory Emphysema
Inspiratory Film (Fig. 1.121)
  • Marked mediastinal shift to the right
  • Over aeration of left lung.
Expiratory Film (Fig. 1.122)
  • Left lung is emptied
  • Heart replaced partially to the left
  • Unaltered right lung.
Hence there is possibility of mucus plug obstructing on the right with the compensatory emphysema on the left.
Prominent Pulmonary Artery
Prominent pulmonary artery possibly due to acute pulmonary hypertension (Fig. 1.123).
Elongated Small Heart
  • Bilateral over aeration of lung (Fig. 1.124)
  • Long thin cardiac silhouette.
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Fig. 1.121: Mucus plug with distracting contralateral compensatory emphysema Inspiratory film showing mediastinal shift to the right and compensatory overaeration of left lung
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Fig. 1.122: Mucus plug with distracting contralateral compensatory emphysema Expiratory film shows emptied lung on the left and maintaining the same position on the right possibly due to mucus plug on the right
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Fig. 1.123: Prominent pulmonary artery in asthma
Foreign Bodies in the Lower Airway
Small infants by virtue of their habit of taking anything on their way into the mouth are highly prone for foreign body aspiration into the airway.
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Fig. 1.124: Elongated small heart in asthma
Whenever a child who is just previously normal in all aspect suddenly develops violent coughing, gagging and vomiting and varying degrees of respiratory distress and at times even cyanosis, one must strongly suspect foreign body aspiration.
Some times all the clinical symptoms may quickly resolve with or without vomiting the foreign body even then one must not be distracted away from evaluation, because undetected foreign body may go in for recurrent pneumonias or wheezing suggestive of asthma. Of course, sudden onset of wheezing in a previously unknown history should be considered due to foreign body or another obstructing lesion such as vascular ring until proven otherwise.
The most important thing in foreign bodies evaluation is, once you start suspecting, you must proceed working up which must be immediate and thorough until you prove or disprove it.
The radiographic features may vary from normal lung to one that of pneumomediastinum and pneumothorax. One another problem that we encounter is radiolucent foreign body which evades evaluation. So it is the indirect evidences which may mimic lot of other conditions like pneumonia, atelectasis and asthma and a skillful pediatrician must be alert enough to correlate the clinical events and radiography. The sincere follow up is equally important in clinching the diagnosis.
The spectrum of radiographic pictures could be:
  • Opaque foreign body anywhere in the respiratory tract
  • Normal lung
  • Obstructive emphysema
  • Compensatory emphysema
  • Atelectasis
  • Air trapping such as pneumothorax and pneumomediastinum
  • Pneumonitic patches (acute and recurrent)
  • Bronchiectasis (in neglected cases).
The most common radiographic picture encountered is obstructive emphysema. Most of the time, physiologic dilatation of bronchus during inspiration and ball valve effect of foreign bodies allows the air to be trapped in the distal lung. With the ongoing respiratory cycle there is eventual accumulation of air and the affected side lung appears larger and hyperlucent. Ultimately pulmonary blood flow is also compromised.
Inspiratory Film (Fig. 1.125):
  • Obstructive emphysema due to foreign body in the left mainstem bronchus
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    Fig. 1.125: Foreign body – inspiratory film
  • 45Large hyperlucent right lung
  • Oligemia of the right lung
  • Mediastinal shift to the left
  • Downward displacement of left diaphragmatic leaflet.
Expiratory Film (Fig. 1.126)
  • All the above features are accentuated
  • Significant shift of the mediastinum to the left
  • Normal left lung has partially emptied the air and, hence, significantly deflated.
Foreign Body Mimicking Pneumonia
  • Infiltrate in the left lower lobe (Fig. 1.127)
  • Compensatory emphysema of left upper lobe.
Next day film (as the symptoms worsened)
  • Features of obstructive emphysema (Fig. 1.128)
  • Underlying peanut fragments were removed).
Right Lower Lobe Atelectasis (Fig. 1.129)
Compensatory emphysema of right upper lobe and entire left lung
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Fig. 1.126: Foreign body – expiratory film
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Fig. 1.127: Foreign body disguised as pneumonia
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Fig. 1.128: Foreign body disguised as pneumonia
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Fig. 1.129: Foreign body producing right lower lobe atelectasis
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Fig. 1.130: Foreign body producing right lower lobe atelectasis
Expiratory Film (Fig. 1.130)
  • Partial to near emptying of normal right upper lobe and entire left lung
  • No air trapping anywhere.
Persistence of atelectasis of right lower lobe (A tack was identified and removed).
Foreign Body with Pneumomediastinum
  • Extensive free air in the mediastinum, soft tissues of the neck and chest (Fig. 1.131)
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    Fig. 1.131: Foreign body with mediastinal and interstitial air
  • Right lung is slightly emphysematous
  • Air trapping is to be suspected because of FB in the right main bronchus.
Aspiration Problems
By virtue of ignorance and immaturity during the period of infancy, the aspiration of various substances may occur accidentally. The aspirations may be substance related or defect related events.
Substances: The common substance which may induce chemical pneumonitis even with few drops are hydrocarbons which include furniture polish, kerosene, gasoline, etc. The other substances aspirated may be milk, food and for that matter any liquid that is taken by the child.
Defects: The anatomical and physiological defects such as swallowing mechanism defect, tracheoesophageal fistulae, seizures, GE reflux with or without underlying hiatus hernia.
Radiographic Features
This could be pneumonia which can be focal or widespread and the findings depend on the volume of the fluid aspirated and the position of the patient at the time of aspiration. Certain radiographic features which are often seen are:
  • In small infants, who are fed in lying posture are prone for right upper lobe involvement
  • Aspiration in the upright position leads to medially positioned lower lobe infiltrates which may mimic hydrocarbon aspiration
  • Massive aspiration may mimic those of pulmonary edema or extensive bacterial pneumonia
  • Chronic and recurrent aspiration problems may lead on to fibrosis, bronchitis and even bronchiectasis
  • 47Chronic lipid aspiration often leads to very dense, hazy lungs
  • In hydrocarbon aspiration, the pulmonary changes are absent for the first 6–12 hours. After that local effects of lipid dissolution and cell membrane destruction occur rapidly and hyperemia, edema, bronchial and bronchiolar necrosis, peribronchial edema, small vessel thrombosis and necrotizing bronchopneumonia soon develop. The hydrocarbon being lipid solvent, destroys surfactant and leads to microatelectasis of the alveoli.
Radiographically infiltrates develop in the lung bases medially and may range from minimal fluffy infiltrates to dense streaky nodular or confluent infiltrates involving a good portion of the lungs bilaterally.
In few cases as a severe form of injury may develop into focal emphysema, pleural effusion and pneumatocele.
Right Upper Lobe Atelectasis (Fig. 1.132)
  • Collapsed upper lobe is dense and triangular
  • Minor fissure is elevated
  • Minimal mediastinal shift to the right.
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Fig. 1.132: Right upper lobe atelectasis Classic configuration of triangularly collapsed upper lobe and elevated minor fissure collapse
This can occur in infants with aspiration in lying posture.
Lateral view (Fig. 1.133): V-shaped configuration of the collapsed right upper lobe. The collapsed lobe is delineated anteriorly by minor fissure and posteriorly by major fissure.
Hydrocarbon pneumonitis in upright position (Red furniture polish).
  • Two hours after ingestion (Fig. 1.134): Radiographically normal lung.
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    Fig. 1.133: Right upper lobe atelectasis Lateral view of classic configuration as V-shaped
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    Fig. 1.134: Hydrocarbon pneumonia At the end of 2 hours of aspiration of furniture polish
  • 48By 12 hours (Fig. 1.135): Extensive bilateral typical infiltrates in the lung bases medially.
Chronic Lipoid Aspiration
Dense, diffuse, hazy infiltrates in both lungs secondary to lipid aspiration (Fig. 1.136).
Over Aerated Lung with Microcardia
Hyperinflated lung with stretched out heart may occur in so many clinical conditions.
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Fig. 1.135: Hydrocarbon pneumonia After 12 hours, typical bilateral extensive basal medial infiltrate
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Fig. 1.136: Lipoid aspiration pneumonia Bilateral dense hazy infiltrate
The commonest being dehydration with acidosis. Here, because of hyperventilation in an acidodic child in an attempt to blow off carbon dioxide, the lungs are over aerated, which depresses the diaphragmatic leaflet and stretches out the heart and the lungs are under vascularized. This occurs in dehydration following acute gastroenteritis.
Over aeration in a dehydrated child (Fig. 1.137):
  • Lungs are over distended
  • Lungs are over aerated and so hyperlucent
  • Diminished vascularity
  • Depressed diaphragmatic leaflet
  • Slightly elongated heart (microcardia).
Lateral view showing emphysematous lungs.
Over distended lung with microcardia can also occur in acute large blood volume loss (Fig. 1.138). Some other causes of microcardia are Addison's disease, anorexia nervosa, long thin normal asthenic individual and long standing debilitating diseases such as malignancy, malnutrition, severe burns and chronic infections.
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Fig. 1.137: Hyperlucent over aerated lung in a child with diarrheal dehydration
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Fig. 1.138: Lateral view also showing hyperaeration without expansion of AP diameter unlike in a bronchiolitis
Allergic Pneumonitis
The lung involvement due to allergy can occur in two important situations. It may be either toxic substance inhalation or cytotoxic drug ingestion (especially following cancer therapy). The resultant infiltrates may be focal or generalized depending upon the amount of the substances either inhaled or ingested. They are usually waxing and waning in nature especially with steroid therapy.
Bilateral extensive hazy infiltrate following leukemic therapy (Fig. 1.139). 24 hours after administration of steroids the lungs became clear.
Lung and Hemoptysis
Though not common, hemoptysis may occur in:
  • Hemangiomas of airway
  • Foreign bodies in the airway
  • Bronchial adenomas
  • Intrathoracic gastroenteric cysts
  • Chronic pulmonary infections
  • Pulmonary hemosiderosis.
Radiographic presentations could be anything from miliary like nodules, discrete cystic masses, fluffy bilateral infiltrates to nonspecific consolidative lesions.
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Fig. 1.139: Bilateral extensive hazy infiltrate following leukemic therapy with cytotoxic drugs
Pulmonary hemosiderosis: Radiological findings include fluffy, asymmetric infiltrate resembling widespread pneumonias or even pulmonary edema and rarely diffuse miliary infiltrate.
Delayed Diaphragmatic Hernia
Classically the diaphragmatic hernia occurs as an acute newborn emergency with respiratory distress. Very rarely in older children one of the causes of acute respiratory distress could be due to delayed herniation of stomach or intestinal contents either through an existing congenital diaphragmatic defect or through an acquired defect following blunt abdominal trauma either on an acute or delayed basis.
Very often it is misinterpreted as large pneumothorax or cystic mass, unless one is concentrating on the continuity of bowel shadows into the thorax or confirming by barium meal series.
  • Large hyperlucent mass in the left hemithorax
  • Mediastinal shift to the right (Fig. 1.140)
  • Absence of stomach air bubble
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    Fig. 1.140: Delayed presentation of a diaphragmatic hernia in an older child mimicking cyst like lesion
  • Continuation of bowel gas shadow in to the involved thorax.
Chest Masses
The most important things to be kept in mind to evaluate radiologically for intrathoracic mass or cysts are:
  • Clinically chest pain, respiratory distress, wheezing or asthma like symptoms
  • Possible rapid expansion with accentuation of clinical symptoms
  • Non-response to conventional management
  • The size of the lesion is relatively larger than commonly seen.
Some of the common masses are mediastinal lymphomas, thymus gland infiltrated with leukemic cells and pulmonary cysts.
  • Large mediastinal mass presenting as superior mediastinal widening—clinically presenting as wheezing. Biopsy proven lymphoma (Fig. 1.141)
  • Clinically asthma like (Fig. 1.142)
    • Large mass in the left hemithorax with calcification
    • Biopsy proven teratoma
  • Clinically respiratory distress (Fig. 1.143)
    • Large mass on the right side with air pockets
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      Fig. 1.141: Rapidly expanding mass This large mass which was interpreted as pneumonia was found to be a case of rapidly expanding mass of lymphoma
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      Fig. 1.142: Teratoma Note a large mass with calcification in the left chest who was screened for asthma like symptoms
    • Biopsy proven infected bronchogenic cyst.
Normal Lung Casting Abnormal Shadows and Causing Problems
Fallacy of Expiratory Film
In the expiratory film the lungs may appear infiltrated, heart as enlarged and draping of thymus may appear either as hilar adenopathy or mediastinal mass.
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Fig. 1.143: Large infected bronchogenic cyst Bronchogenic cyst compressing the trachea and right bronchus
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Fig. 1.144: Technical error Expiratory view making the lungs to be appeared infiltrated and the heart enlarged with the thymus gland draped over the right cardiac silhoutte
Expiratory Film (Fig. 1.144)
  • Lungs appear to be infiltrated
  • Heart appears to be enlarged
  • Thymus gland drapes along the superior cardiac silhouette with an appearance to be hilar adenopathy or mediastinal mass.
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Fig. 1.145: Technical error Same infant (Fig. 1.144)with the deep inspiration gives a normal appearance
Inspiratory Film of the Same Infant (Fig. 1.145)
  • Lungs appear clear
  • Heart appears to be normal in size
  • Thymus is hidden in the superior mediastinum
  • Diaphragm is at seventh intercostal space.
Rotation of the chest may also give false appearance of infiltrates in the lung and shift of mediastinum. Normal center position to be assessed by equidistance of medial ends of clavicle from midspinal level.
Lordotic position as is evidenced by the horizontal positioning of the posterior ribs is downward pointing anterior ribs may result in clustering of hilar vessels and bronchus with accentuation of vascular markings in the upper lobe.
Normal Thymus Gland
The normal thymus gland is notorious for mimicking pathology. The various radiographic appearances are
  • Covering the superior aspect of the heart like an umbrella and blends imperceptibly with the cardiac silhouette
  • 52Triangular in shape producing the so called “Sail Sign”. This sail sign on slight rotation may mimic pneumonic consolidation of upper lobe
  • With the blending to the cardiac silhouette it may appear as mediastinal mass.
Commonly, radiographically the thymus appears upto 2–3 years of age. Normal thymus at times may be visualized up to 10–12 years of age. The picture is so altered that it may produce tumor like superior mediastinal widening or prominence.
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Fig. 1.146: Normal thymus-notch sign The normal thymic silhoutte blends with the cardiac silhoutte with a notch at it's interface
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Fig. 1.147: Normal thymus Lateral view showing normal thymus with it's undulating lower edge
Blending of thymus with cardiac silhouette. Faint notch is seen at the junction of ribs (Fig. 1.146).
Lateral view: Normal position of the thymus in the anterior, superior mediastinal compartment with its undulating lower edge (Fig. 1.147).
Pseudopneumonia appearance of thymus with its “Sail Sign” (Fig. 1.148).
Rotation in another infant gives an appearance of right upper lobe pneumonia by normal thymus (Fig. 1.149).
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Fig. 1.148: Thymus “sail” sign Typical sail sign of normal thymus
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Fig. 1.149: “Pseudopneumonia sign” of normal thymus Rotation to right causes normal thymus to appear as though a case of consolidating pneumonia of right upper lobe
53Bilaterally appearing normal thymus in the superior mediastinum giving mass like configuration (Fig. 1.150).
Large right-sided thymus obliterating cardiac silhouette with mass like appearance (Fig. 1.151).
Superior mediastinal widening due to normal thymus (Fig. 1.152).
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Fig. 1.150: Mass-like configuration of normal thymus gland Bilateral superior mediastinal fullness caused by normal thymus
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Fig. 1.151: Mass-like configuration of normal thymus gland Large right thymic lobe suggesting a mass
In a 10-year-old with fever
  • 10-year-old while screening for pneumonia, suggested to be right-sided mass (Fig. 1.153).
  • Right anterior oblique view for barium swallow, showed it to be a normal thymus gland and because of that there is no pressure effect over the esophagus (Fig. 1.154).
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Fig. 1.152: Mass-like configuration of normal thymus gland Peculiar superior mediastinal widening secondary to incomplete descent of normal thymus gland due to lordotic positioning
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Fig. 1.153: Normal thymus in an older child A 9-year-old child when X-ray was taken to rule out pneumonia was interpreted as a case of mediastinal mass
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Fig. 1.154: Normal thymus in a older chid An oblique view with barium enema demonstrates the same mass was found to be normal thymus
Chest Traumas
Chest traumas whether penetrating or nonpenetrating need lot of careful assessment and skillful scrutinization and vigilant survey of entire thorax. By virtue of structures like thoracic cage, cardiovascular structure, pleural space and pulmonary parenchyma being the areas for scrutinization, a superficial careless assessment is likely to miss various important subtle findings. At the same time, the examination should be quick, careful and thorough.
A systematic and quick screening is likely to give better results. The various structures to be scrutinized are:
Thoracic Cage
  • Subtle rib fractures are likely to be missed in the initial films
  • Indirect evidences for subtle fractures are:
    • Subpleural hematoma
    • Pneumothorax
    • Hemothorax
  • Evidence for more serious intrathoracic or intra-abdominal injuries due to rib fracture is to search for by.
  • Anterior or lateral lower thoracic rib fracture, look for splenic or liver trauma.
  • Low posterior rib fractures—look for renal trauma.
  • Fractures of first three ribs—search for great vessel injury and blood collections over the apex of the lung.
  • Fractures of sternum are best visualized in lateral view.
    • Look for retro and post-sternal soft tissue injury
    • Look for cardiac injury.
Pulmonary Parenchymal Injuries may Manifest as:
Pulmonary contusion
  • May manifest as pneumonia like areas of homogenous or nodular infiltrate
  • Gets enlarged and denser in the first 24–48 hours of injury
  • May give an appearance of mass
  • Clears slowly.
Pulmonary hematomas
  • Appear like round or oval densities
  • Resolves slowly
  • May cavitate during the course of resolution.
Traumatic pneumatoceles:
  • Commonly following blunt chest traumas
  • May be seen in the pulmonary parenchyma or in the mediastinum
  • Usually develops within minutes or hours of the injury
  • May manifest along with other forms of pulmonary injuries
  • May appear as round, oval, single or multiple or may contain blood
  • Generally thin walled air cysts which may enlarge rapidly
  • The lesion in mediastinum may appear elongated and paraspinal in position as they are located in the inferior pulmonary ligament
  • 55Relatively innocuous
  • Mostly, small slowly progressive and smaller and disappear over 2–3 weeks period.
Catastrophic injuries to respiratory system
They are bronchial or tracheal tear or fracture and torsion of the lung.
Bronchial fracture: is characterized by
  • Massive atelectasis should be presumed to be secondary to bronchial fracture until proven otherwise.
  • Massive pneumothorax:
    • When lung is completely detached the upright view will show the lungs to fall to the bottom of the hemithorax
    • In other forms of bronchial fracture
    • The air column in the proximal portion of the fracture bronchus may appear tapered or bevelled
    • The air may be seen tracking along the bronchial wall itself
    • If bleeding fluid will be seen in the hemithorax.
With tracheal tear:
  • Pneumomediastinum is more common than pneumothorax
  • With bleeding mediastinum appears widened.
Torsion of lung:
  • Lung makes 180° turn around its hilus and so the vascular pattern of upper lobe is inverted
  • With subsequent infarction radiographic diagnosis becomes difficult.
Cardiovascular manifestations of blunt chest injury:
  • Bloody or serous pericardial effusion
  • Myocardial contusion
  • Traumatic aneurysm of heart
  • Traumatic aneurysm of aorta
  • Aortic or great vessel injury, radiographically may appear as progressively developing superior mediastinal widening or the collecting of blood in the apex of the left lung.
Pulmonary contusion:
  • Diffuse nodular infiltrate in the right lung and more in the apex (Fig. 1.155)
    • Left pneumothorax with superimposed left apical lung contusion
  • After few hours both the contused areas became more consolidated (Fig. 1.156).
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Fig. 1.155: Pulmonary contusion Note the diffuse nodular infiltrate in the right lung and more confluent in the upper lobe. Also note the pneumothorax and lesser contusion in the left apex
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Fig. 1.156: Pulmonary hemaotoma with cavitation Note a mass-like lesion in the right upper lobe
56Pulmonary hematoma with cavitation:
  • Mass-like lesion in the right upper lobe due to hematoma (Fig. 1.157)
  • A few days later a cavity developed in the hematoma (Fig. 1.158)
  • More than a month, a thin walled cavity remained (Fig. 1.159).
Traumatic pneumatocele:
  • Two spherical thin-walled pneumatocele in the contused left lung (Fig. 1.160)
  • Large post-traumatic pneumatocele on the right (Fig. 1.161)
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    Fig. 1.157: Pulmonary hematoma with cavitation A few days later, note that a cavity is developing in this hematoma
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    Fig. 1.158: Pulmonary hematoma with cavitation More than a month later, a thin-walled cavity remains
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    Fig. 1.159: Traumatic lung with paramediastinal pneumatocele A thin-walled pneumotocele remained even after one month of injury
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    Fig. 1.160: Traumatic pneumatocele Note two spherical thin-walled pneumatocele in the contused left lung
  • Traumatic pneumatocele with air and fluid level due to blunt (Fig. 1.162).
Traumatic pneumatocele in inferior pulmonary ligament:
Characteristically elongated, paraspinal air collection in the inferior pulmonary ligament with air and fluid level (Figs 1.163 and 1.164).
  • Pneumothorax on the right
  • Widened mediastinum
  • Tube is in the normal position.
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Fig. 1.161: Large post-traumatic pneumatocele on the right
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Fig. 1.162: Traumatic pneumatocele Arrows—air and fluid level due to air and blood in the pneumatocele
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Fig. 1.163: Traumatic pneumatocele in interior pulmonary ligament Small arrow elongated, paraspinal air collection in the inferior pulmonary ligament. Inferior arrow–air and fluid level
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Fig. 1.164: Widened superior mediastinum and pleural fluid but no traumatic aneurysm: Pneumothorax on the right; Widened mediastinum; Tube is in the normal position