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180 oracic ultrasound
In most cases (98%), individuals with DPLD show a seemingly or actually thickened pleural
line, that is irregular and fragmented, sometimes enhanced by a small pleural effusion (present
in about one third of cases)
28-29, 71-72
(Fig. 24).
Figure 24 – Hypoechoic or (pseudo) anechoic retroparietal images do not always represent effusions.
They can be consolidated cortical lung or pleural thickenings. a, b, c: images of subpleural consolidation,
simulating an effusion. However, the effusion changes its thickness with the acts of breathing, and, in
these cases, the presence of air within the consolidation, is evident (arrows). In doubtful cases, the
administration of ultrasound contrast agent makes the differential diagnosis obvious, because the pleural
fluid assumes no contrast. In d: normal lung.
ese features may be due to traction by fibrotic septa, fibrous pleural surface irregularities
and superficial micronodules. e latter can produce very evident posterior enhancements,
similar to B Lines, but with nodular rather than punctiform origin. Even small alveolar consolidations can show this characteristic, inducing strong echoes directed in depth (Figs. 25-26).
e structural variation in DPLD produces an interstitial syndrome with variable concentrations of B-Lines and white lung, present in 98% of patients. is picture must be differentiated
from similar images in cases of cardiogenic pulmonary edema.
B Lines of hydrostatic edema are clear, laser-like and have, in the vast majority of cases, a
punctiform origin from mobile and linear pleura.
Comet-tail artifacts of DPLD tend to be diffuse, although they are often prevalent at the level
of the lower lobes or give preference to specific pathology related areas. With appropriate
enlargement and the use of high frequencies, the punctiform origin of DPLD B Lines may
not be maintained, resulting as a micronodular origin (Fig. 27).
Parenchymal lung patology 181
Figure 25 – Lung interstitial disease.
Figure 26 – Lung interstitial syndrome. No findings of heart failure. On the left (a) X-ray. In the
ultrasound images: presence of mild interstitial syndrome. In particular (c, d, arrows) two subpleural
nodular images. Artifacts behind them, are not B Lines, but acoustic enhancements of the nodules.
182 oracic ultrasound
Figure 27 – Idiopathic pulmonary fibrosis (UIP). a: X-ray. b, c CT. Honeycombing is evident in c to the
left. c, d, e, ultrasound scans with linear probe 10 MHz, where B Lines and irregularities/fragmentation
of the pleural line area evident. In f, on the right of the image, a spared area with A Lines, corresponds
to honeycombing. A lack of homogeneity of the interstitial disease is characteristic of UIP.
Similarly, to pulmonary edema, the origin of these artifacts, can be traced back to acoustic
microholes due to inflammatory or fibrotic thickening of the subpleural interstitium, characteristic of DPLD.
In DPLD inter- and intralobular pulmonary interstitium, is involved in almost all the pathological variants. is results in the constant representation of the white lung and variable
arrangements of B Lines. In HRCT, these anatomo-sonographic features appear as reticularnodular, smooth or irregular images, or constitute the CT findings of ground glass.
We believe that the deep honeycombing in ultrasound is not visible, being a conglomerate of
air cysts. e feature of a deep honeycombing is that of the lung cortex that covers it. In UIP,
the subpleural honeycombing is characteristic of basal regions, and may produce acoustically
impermeable interfaces. erefore, it may appear with a pseudonormal or even hypernormal
pattern (with A Lines, hypermirror) that contrast with neighboring more dense areas, contributing to the inhomogeneous pattern of pneumogenic interstitial syndrome.
Although this has not been studied yet, comments on hypernormal patterns in pulmonary
fibrosis have appeared in the literature70. In our opinion, the patchy normal/hypernormal
pattern of UIP can express a focal subpleural honeycombing that disrupts the appearance of
fibrogenic interstitial disease.
During its clinical course, idiopathic pulmonary fibrosis produces a restrictive syndrome
with reduction in vital capacity and total lung capacity. is condition may be suggested by
the association of a subpleural inhomogeneous pattern (B Lines, white lung, predominantly
basal “spared areas”) with hypomobility of the lung bases and an increase in the size of the
Parenchymal lung patology 183
diapragmatic zone of apposition (see Chapter 1 and the chapter on diaphragm pathology),
especially in subjects with slow and insidious onset of symptoms.
Among the diseases that cause secondary collagen interstitial lung diseases, scleroderma has
a prominent role. Pulmonary fibrosis affects 70% of patients with this collagen disease, and
from the anatomical point of view, a diffuse pulmonary and pleural involvement, superficial
honeycombing (with air cysts of 2-10 mm) and vascular changes characterize it. ese features
are not easily distinguishable from those of UIP in CT. In our limited experience, ultrasound
scans of the pleural plane in subjects with scleroderma do not show significant differences
compared to subjects with UIP (Fig. 28).
Figure 28 – Sclerodermic pulmonary fibrosis. a, b, c, d scans of the pleural plane with convex and
sector probes. Same pleural regions explored with 10 MHz probe. The best resolution of the pleural
plane with its irregularities and inhomogeneous interstitial syndrome is evident.
Scleroderma shows early aspects (fibrotic infiltrates with reticular, intra- and interlobular appearance), late aspects (cystic, honeycombing) and pleural involvement (fibrosis, adhesions)
(Fig. 29).
In accordance with the premise, sclerodermic pulmonary fibrosis produces an interstitial
syndrome. Its stereotyped expression concerns hyperechoic ultrasound images in the form
of B Lines and white lung. Any type of probe shows these artifacts, however, the use of the
linear probe can clearly emphasize the pleural irregularities that often have a micronodular
appearance.
Recently, the quantification of B Lines in patients with scleroderma lung fibrosis was ob-
71-72
served
. ese artifacts are more numerous in the diffuse forms of scleroderma and correlate
with the severity of fibrosis studied in HRCT (Warrick score).
We believe that, even in this case, a simple numerical estimate of the artifacts is not sufficient.
A more accurate analysis of the pleural surface is necessary.
184 oracic ultrasound
Figure 29 – Fibrosis with pleural thickenings. a: X-ray. b:interstital syndrome with uniform pleural
thickening. c: pleural fibrous lenticular plaque. d, e, f: B Lines and irregularities of the pleural surface.
Potential of echography in DPLD
Most of DPLD (idiopathic pulmonary fibrosis and non-specific interstitial pneumonia), are
diseases of the pulmonary mantle.
Echography detects interstitial anomalies through the characteristic artifactual pattern. e
increase of density of the cortical lung ensure the high sensitivity of this test, which clearly
relates the symptom (usually dyspnea) with a diffuse parenchymal disease. erefore, according
to the described diagnostic criteria, interstitial syndrome from DPLD must be distinguished
from cardiogenic and non-cardiogenic pulmonary edema.
When a fibrogenic non-edematous lung disease is identified, HRCT represents the confirmation, in many cases detecting the etiology.
However, certain ultrasound signs (similarities of AIP to ARDS, basal spared areas from
honeycombing and inhomogeneities in UIP, extended representations of white lung in NSIP)
may offer some information.
Other applications of ultrasound may include:
• Recognition of complications (pleural effusion, pneumothorax);
• Topographical diffusion of the disease;
• Identification of the most involved areas, to direct a surgical biopsy;
• Evaluation of the effectiveness of therapy (regression of interstitial syndrome);
• Recognition of a diffuse alveolar damage (i.e. clinically an acute exacerbation) in a form of
DPLD, because UIP, and primary and secondary NSIP, can show AIP-like acute changes.
Parenchymal lung patology 185
➣ Pathology of airspaces
Atelectasis
Atelectasis is defined as the lack of ventilation of the pulmonary parenchima.
On pathogenic basis, resorption (or obstructive) atelectasis and compressive atelectasis are
distinguished. Some data have already been discussed in the chapter on pleural effusions, as
parenchymal epiphenomenon of pleural hypertension.
Obstructive atelectasis are real atelectasis, characterized by obstruction at various levels, resulting in resorption of the alveolar and bronchial gas. Obstructive atelectasis may be central
(pulmonary or lobar), usually caused by intrinsic or extrinsic bronchial disease, or peripheral,
generally produced by mucus hypersecretion, inflammation or neoplastic obstruction.
Chest X-ray shows obstructive atelectasis as a consolidated area with decreased volume, which
exerts a pulling action on the neighboring structures (mediastinum, diaphragm, lobes, and
fissures). e intercostal spaces are constricted, the hemidiaphragm is elevated and the mediastinum is attracted toward the collapsed portion of the lung
Atelectasis can affect an entire lung, one or more lobes or lung segments.
In echography, compression atelectasis is typical of those parts of the lung which are im-
mersed in the pleural fluid. For this reason, when examined through radiography, the pleural
effusion usually masks it.
Compressed part of the lung appears as artifactual if it still contain air, otherwise, it take on a
solid, parenchymatous appearance. Many times a compressive atelectasis still contains air in
the form of air broncho- and bronchiolograms and, unlike true alveolar consolidations, the
border with the aerated parenchyma tends to appear blurred. If air bronchograms are visible,
unlike true (obstructive) atelectasis, during inspiration air can be seen entering within the
hepatized area. A final verification of parenchymal compression occurs with the evacuation
of the effusion and the reappearance of a normal lung pattern.
After airway obstruction, airspaces, even if not ventilated, maintain for a certain time gaseous expansion and may then seem normal in ultrasound. e physiological pleural sliding is
lost, but the lung pulse is maintained75. When alveolar gases are drastically reduced and then
disappear, the atelectasic area appears as a solid hepatized structure, similar to liver tissue.
e lung sliding is naturally absent.
In the case of complete atelectasis of the lung, the lung pulse is clearly visible. It is represented
by the perception of the cardiac activity at level of the pleural line. is sign has a sensitivity
of 93% and a specificity of 100% for complete pulmonary atelectasis75 and it has proved extremely useful in the immediate diagnosis of selective intubation of a bronchus76 (Clips 13-14).
73-74
.
Clip 13 – Selective intubation of the right main bronchus. The left lung shows
the absence of sliding and lung pulse.
Clip 14 – After repositioning of the tube into the trachea, immediate
reappearance of sliding and disappearance of lung pulse.
186 oracic ultrasound
Of course, in the stages preceding the total gaseous resorption, the ultrasound image can
appear with all possible shades between normality and hepatization, through intermediate
stages with B Lines and white lung (Clips 15-16).
Clip 15 – Atelectasis with almost total hepatization of the lung: it shows the
presence of some air bronchogram. Absence of sliding and presence of lung
pulse.
Clip 16 – Left lung completely hepatized after selective intubation of the
right main bronchus. The withdrawal of the endotracheal tube leads to an
immediate re-expansion of the lung. Parallel course of the bronchi when the
air fills them again.
Two other elements can help identify an obstructive consolidation: the lack of dynamic air
bronchograms
77-78
and the parallel course of the bronchial tree that loses it typical expanded
appearance (Fig. 30).
Atelectasis: parallel course
of the bronchi
Figure 30 – Parallel course of air bronchograms in obstructive atelectasis. This is due to the loss of lung
volume (A). In pneumonia, which leads to an increase of lung volume, the air bronchograms maintain
their treelike appearance (B).
Lobar pneumonia: the bronchi
maintain their treelike appearance
B
Unlike inflammatory consolidations, in obstructive atelectasis air bronchograms, if present,
is still (static bronchogram). erefore the evidence of dynamic air bronchograms excludes
the obstructive nature of a consolidation (Clip 17).
Clip 17 – Dynamic air bronchogram in hepatized lung area. This finding
excludes the obstructive nature of consolidation.
Parenchymal lung patology 187
Especially in non-acute obstructions, the presence of fluid bronchograms79 (tubular elements with echogenic walls and fluid content) suggests the obstructive nature of pulmonary
hepatization. e vessels are devoid of visible walls and are easily distinguishable by color
Doppler (Fig. 31).
FLUID BRONCHOGRAMS
Figure 31 – Fluid bronchograms appear as anechoic tubular structures with hyperechoic walls.
e atelectatic non-ventilated regions of a lung are predisposed to inflammatory events. If
they are colliquative, they may appear as hypoechoic areas or as fluid collections with corpuscular content.
Hypoechoic nodule or mass located deep to atelectasis may represent causative primary or
secondary neoplastic lesions.
e color Doppler shows that the atelectatic regions are richly vascularized by the pulmonary
artery (three-phase flows with a high resistance index > 0,80). is is reflected in the behavior
of atelectasis after intravenous administration of contrast ultrasound agent (CEUS low-IM),
consisting of a very early lively enhancement (about 6 seconds)
80-81
.
Ultrasound is an extraordinarily useful bedside tool for monitoring the lung re-expansion in
the course of bronchoscopy.
Clips 18-22 document the complete re-expansion, in a few minutes, of the left upper lobe
in the course of bronchoscopy.
Clips 18, 19, 20, 21, 22 – In Clip 18 an area of hepatized lung in the left
paracardiac region. The bronchoscopic aspiration of a mucus plug induces
the immediate re-expansion of the lung. This occurs in the case of interstitial
syndrome that is reduced within minutes (white lung in Clip 20, presence of
B Lines in Clip 22).
188 oracic ultrasound
Postoperative atelectasis
Ultrasound is performed easily at the bedside or in postoperative intensive care and is useful
as a diagnostic and monitoring tool in lung collapses.
Atelectasis appear in the dependent lung regions in 90% of patients undergoing general
anesthesia. ere is no doubt that prevention and early correction of atelectasis in the operated patient encourages its positive outcome, improving the oxygenation of the patient, and
decreasing pulmonary arterial pressure and the risk of lung injury.
In the anesthetized and operated subject, all mechanisms underlying atelectasis are active:
surfactant deficiency, gas absorption and compression of the lungs.
Mechanical ventilation of the lungs invariably determines an alveolar damage, which results
in inactivation of surfactant. Pulmonary surfactant, however, has a pulmonary reserve and a
large turnover, ensuring in most cases a residual function.
e resorption of alveolar gas can take place with pervious or obstructed airways. Bronchial
obstruction isolates distal air collections that are gradually absorbed. In the case of airway
patency, lung regions with discrepancy between (reduced) ventilation and maintained perfusion play a decisive role, in the moment in which oxygen is provided and therefore the tension
of the alveolar gas increases.
Finally, compressive atelectasis occurs whenever the forces that produce the alveolar collapse
are greater than those that keep the alveoli open. In anesthetized subjects, the relaxation and
the cephalic positioning of the diaphragm induces basal atelectasis (see section on diaphragm
in ultrasound). With this mechanism, pleural pressure increases more in the dependent and
supra-diaphragmatic regions of the lung, causing compression.
e position of the patient greatly influences the development of atelectasis. e simple transition from upright to supine position causes a decrease of 0.5-1 liter of functional residual
capacity (CFR) in the awake patient. In the anesthetized subject, it decreases by a further half
a liter. ese phenomena are accentuated in the Trendelenbug position and in obese subjects.
On the contrary, the prone position can increase the CFR.
Factors affecting atelectasis are also represented by the patient’s age and by the administration
of oxygen. Aging per se is not associated with a greater development of atelectasis. Instead, it
is more frequent in children (1-3 years) for the greater compliance of the rib cage and a larger
airway closing volume (the lung volume that causes the closure of small airways).
➣ Pulmonary consolidations
Generalities
When the distal lobar segmental and subsegmental lung air spaces are replaced by liquid,
semi-liquid or solid material (transudate, exudate, blood, pus, neoplastic tissue, lymph, parasites, fungi or proteinaceous material), consolidation of a normally aerated tissue develops. In
traditional radiology, a loss of parenchymal transparency, resulting in lung opacity, is obtained.
Consolidations and lung collapses (which we called atelectasis) can occur simultaneously, but
for different etiologic reasons.
Consolidations develop because of bacterial infections and the affected parenchymal volume is maintained, because airspaces distal to the terminal bronchiole are completely filled.
Atelectasis, instead, is characterized by a volume loss of the affected lung, associated with a
centripetal movement (compared to the collapsed side) of contiguous structures (see section
Parenchymal lung patology 189
on atelectasis). is occurs when a bronchus is obstructed and the lung distal to the obstruction is no longer aerated, consequently losing its volume82.
ese pathophysiologic concepts have practical implications in the interpretation of radiological images. Radiographic consolidation (usually inflammatory) has a more or less systematized morphology and its volume is normal or, rarely, expanded. Conversely, the collapse (or
atelectasis) implies an anatomic distortion, with impacts on adjacent lobes, on the chest wall
and on the mediastinum.
e ultrasound feature of lung consolidations, with or without bronchial obstruction, is
quite characteristic. e sonographic evaluation of a consolidation allows not only a generic
diagnosis of alveolar disease, but also allows an estimate of lesion’s degree of aeration83.
As already mentioned, lung consolidation is the most frequent abnormality in the majority
of lung infections, but it also relates to non-cardiogenic edema, interstitial (organizing) and
granulomatous diseases, alveolar proteinosis and others84.
e radiographic manifestations of infective lung consolidations are variable and often nonspecific, even if sometimes these appear sufficiently characteristic, as in the case of secondary
tuberculosis.
Moreover, what the radiologist sees as a lung opacity, may be due either to an alveolar process
(air space pattern), or to an interstitial or mixed process. In alveolar process, the alveoli are
filled with material not naturally present, and thus represents the pulmonary consolidation
in the proper sense of the term85. In pure interstitial disease, a minimal alveolar ventilation
is maintained, while the interlobular, intralobular and perivascular tissue participates in the
pathological process. is picture is characteristic of certain viral pneumonias86.
CT is very accurate in defining consolidations, for studying air bronchograms and to differentiate less dense radiologic opacities, defined in CT “ground glass”.
Of course, there may be situations in which the alveolar pattern merges with the interstitial
one. e most significant of these is pulmonary edema and some inflammations from virus
or mycoplasma87. ese mixed aspects are difficult to characterize by the simple chest X-ray,
but require a more detailed analysis with CT.
Ultrasound of pulmonary consolidations
88-91
In echography, the visibility below the pleural plane is permitted only by a disease, which
excludes air from the tissue. e alveolar consolidation allows, as an acoustic window, the
parenchymal expression in terms of echogenicity and echostructure, otherwise not evaluable
because of the air effects. erefore, a consolidation with bronchial obstruction and complete
resorption of the air is an acoustically perfect solid tissue.
Air within a pulmonary consolidation generates scattering and the ultrasound image is the
result of the dispersion and the shape of the air inside the consolidation. A critical ratio between air and tissue erases the tissutal image and produces an artifactual picture.
Inside the consolidation, ventilated bronchi and bronchioles may or may not be visible. ey
appear as treelike air bronchograms when the shape of the air is arborescent, otherwise they
take the form of hyerechoic spots, when the bronchiolar air acts as punctiform scatterer
77-78
(Fig. 32).
Partially consolidated areas may show only a subpleural region rich in artifacts, as it occurs in
predominantly interstitial inflammations, because the artifacts may hide the consolidation.
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