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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5769_Библиотеки_им_академика_М_И_Перельмана
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170 oracic ultrasound
HRCT is particularly diagnostic in these diseases. It identifies the fine structure of the lung
parenchyma at submillimetric level. Its sensitivity is about 94% with a very low rate of false
positives66.
Table 7 – DPLD with a characteristic
CT appearance
Idiopathic pulmonary fibrosis (UIP, NSIP)
Sarcoidosis
Hypersensitivity pneumonia
Lymphangitic carcinomatosis
Histiocytosis with Langerhans cells
Lymphangioleiomyomatosis
Alveolar proteinosis
e diagnostic criteria obtainable with HRCT have been well described
Many studies have reported that HRCT can
make diagnosis of specific DPLD, especially
of UIP. is is possible because of the basal
honeycombing and the spatial and temporal
heterogeneity that characterizes UIP. Grenier
and his colleagues66 have argued that HRCT
can make specific diagnosis in 61-80% of
cases. Particularly interesting is the possibility
of a differential diagnosis between UIP and
NSIP, given the distinctly different prognosis
of the two diseases. Table 7 lists the cases of
DPLD with a characteristic CT framework67.
67-69
.
From the echographic point of view, we consider three points:
• e pathology expressed in the perilobular and in the intralobular interstitium. In fact, a
certain correlation between the perilobular interstitium and ultrasound septal syndrome,
and between the “white lung” and the ground glass seen with Computed Tomography
(CT) exists.
• e tomographic and topographic expressions of the pathology. is point is relative to the
apico-basal and lateral distribution of the pathology, as well as to the depth of the disease
compared to the pleural plane.
• e presence of micro/macronodules (from few mm to 1 cm and beyond), and of an
airspace filling pattern. ey are visible in ultrasound only if appearing on the surface and
if the surface is explored with the appropriate frequencies (Fig. 12).
Figure 12 – HRCT surface reconstructions of UIP and NSIP. In these diseases high-frequency ultrasound
“reads” the surface of the lungs with its irregularities and (acoustic) inhomogeneities (courtesy of
prof. Mario Maffessanti).
Parenchymal lung patology 171
Leslie68 has described different anatomical patterns of interstitial lung disease. Table 8 illustrates them with some details.
Table 8 – Anatomical patterns in interstitial lung diseases
Pattern 1: ALI Diffuse alveolar damage with hyaline membrane (as in ARDS)
Pattern 2: fibrosis
Pattern 3: cellular
interstitial infiltrates
Pattern 4: airspace filling
Pattern 5: nodules
Pattern 6: almost normal
lung
Permanent structural remodeling of the interstitium by collagen
(idiopathic interstitial fibrosis)
In the alveolar walls there are lymphocytes, plasmacells and
macrophages (hypersensitivity pneumonia)
Cells or other material that fills the alveoli (organizing pneumonia,
pneumocystis pneumonia, alveolar proteinosis, diffuse pulmonary
haemorrhages, desquamative interstitial pneumonia)
Wegener’s granulomatosis (large nodules), miliaria, sarcoidosis,
histiocytosis Langerhans tumors
Vascular and airway diseases (small airway disease,
lymphangioleiomyomatosis, pulmonary hypertension)
Table 9 shows the correlations between DPLD pathology as seen with HRCT and with
ultrasound. For detecting subtle pleural and subpleural alteration the use of a linear probe
with appropriate frequencies (7-13 MHz) is recommended (Fig. 13).
Figure 13 – The characteristic features in CT, such as interstitial disease and consolidation are clear
even in ultrasound. a: interstitial syndrome with compact B Lines and irregular pleural profile. b, c, d:
subpleural microconsolidations.
172 oracic ultrasound
Table 9 – DPLD: correlations between HRCT and ultrasound findings
Presentation CT Echo Prevailing pathology
Interstitial: septal
pattern
Interstitial: reticular
pattern
Interstitial: ground
glass pattern
Interstitial: nodular
and reticular
pattern
Airspace Single or multiple
Mixed interstitial
and airspace
Thickening of
interlobular septa
(Kerley A and B
Lines)
Intralobular and
interlobular linear
opacities
Opacity non
associated to lack
of visualization of
the vessels
Interstitial nodules,
with or without
linear opacities
opacities with
little or no
recognition of
vascular structures.
Bronchograms
and air
bronchiolograms
Mixed CT pattern
B Lines separate 1 cm
or more (mean 0.7 cm),
with punctiform origin,
full screen, no fusion
between them
Close B Lines < 1 cm Hydrostatic edema
Close B Lines consolidated
up to confluence and
white lung
The ultrasonographic
evidence of nodules is
related to their size (> 1 mm
with linear probe) and
their subpleural location.
The interstitial component
is manifested by B Lines
and white lung
Consolidations
or subpleural
microconsolidations
with air and fluid
bronchograms and
bronchiolograms. The
posterior enhancement of
the small consolidations
produces large vertical
reverberations, similar to
B Lines but with nodular
origin
Mixed echo pattern with
possible underestimation
of the airspace component
(consolidation) due to
interstitial covering (B Lines)
Hydrostatic edema
Lymphangitic
carcinomatosis
Viral pneumonias
Pulmonary fibrosis
Severe edema,
particularly that of ARDS
Acute interstitial
pneumonia
Allergic alveolitis
Miliary TB and fungina
Silicosis and other
pneumoconiosis
sarcoidosis
allergic alveolitis
Pneumonia
Hemorrhage
Suction
Edema (especially ARDS)
Many of the diseases
mentioned occur with
interstitial and alveolar
components
e septal (perilobular) and intralobular interstitial enlargement have already been discussed
as producer of more or less confluent B Lines and of white lung.
Parenchymal lung patology 173
Ultrasound DPLD characterization has never been proposed in the literature, however,
in our experience some differential diagnostic aspects deserve attention. Among the many
pathological expressions of DPLD, subpleural micro/macro nodulations and consolidations
(airspace filling diseases) may have a differential diagnostic potential during an ultrasound
examination of the pleural line.
Subpleural nodules are frequent on the ultrasound of patients with diffuse interstitial diseases,
and sometimes are wrongly defined “cysts” for their posterior acoustic enhancement70. Indeed,
they are solid and the posterior enhancement is simply the interface between the nodule
and the deep aerated lung tissue. Of course, ultrasound cannot see air cysts because they
are specular. erefore, there are no known ultrasound representations of real sonographic
simple cysts, clustered cysts or honeycombing. It is likely that cystic air collections appear
on ultrasound as specular pleura that may conflict with the neighboring interstitial pattern,
creating inhomogeneities.
In diffuse lung interstitial diseases, nodules vary in size from 2-3 mm and 1 cm that is such
as to be contained within or on the periphery of the secondary lobules. Above a centimeter,
they are more properly macronodules or real consolidations.
Inside of lobular units they can be located centrally, random or in the interlobular septa.
In a centrilobular position, they do not intercept the pleural surface and they cannot be seen
by ultrasound. Centrilobular nodulations characterize hypersensitivity pneumonia, Langerhans
cell histiocytosis, lymphocytic interstitial pneumonia and respiratory bronchiolitis ILD.
When nodules are randomly arranged, silicosis, miliary tuberculosis and metastasis occur.
Subpleural nodules often characterize the perilymphatic (or perilobular) arrangement.
Sarcoidosis and lymphocytic interstitial pneumonia appear this way.
At present, there is no controlled experience on the use of high frequency (12-18 MHz) to
define pleural and subpleural nodules for the purposes of a differential diagnosis of DPLD,
but theoretically, this is a viable way15.
An alveolar pattern (or DPLD with alveolar consolidations) is characterized by mixed
interstitial and air-space hyperdensities and is constituted by lesions that
appear as white lung and real consolidations. It is characteristic of many
interstitial lung diseases, including
hypersensitivity pneumonia, ARDS
and acute interstitial pneumonia,
Pneumocystis carinii pneumonia,
pulmonary alveolar edema, chronic
eosinophilic pneumonia, pulmonary
alveolar proteinosis, bronchoalveolar
carcinoma, desquamative interstitial
pneumonia, organizing pneumonia, drug toxicity, alveolar hemorrhages of Wegener’s granulomatosis
Figure 14 – An example of diffuse lung disease with
consolidations. In organizing pneumonia, air (arrows) is
so rare and fragmented that it does not significantly affect
the production of real ultrasound images.
(Fig. 14).
Ultrasonography of ARDS is de-
scribed elsewhere. In our numerically
reduced experience, the sonographic
174 oracic ultrasound
Table 10 – DPLD with nodular or alveolar features: diffusion and distribution
Disease Distribution Vertical diffusion Lateral diffusion Pattern
Silicosis Bilateral Mid-superior areas
Miliary TB
Metastasis
Sarcoidosis Bilateral, patchy Mid-superior areas
Lymphocytic
interstitial
pneumonia
Pneumocystis
carinii
pneumonia
Alveolar
hemorrhages
Acute interstitial
pneumonia
Acute
hypersensitivity
pneumonia
ARDS
Pulmonary
alveolar edema
Chronic
eosinophilic
pneumonia
Alveolar
proteinosis
Bronchoalveolar
carcinoma
Desquamative
interstitial
pneumonia
Organizing
pneumonia
Drug toxicity
Bilateral,
symmetrical
Bilateral,
symmetrical
Diffuse evenly Mid-inferior areas Uniform
Bilateral,
symmetrical,
patchy or diffuse
Bilateral, diffuse
or patchy
Bilateral,
symmetrical,
patchy or diffuse
Bilateral, patchy More often basal Uniform Acute alveolar
Bilateral,
symmetrical,
patchy
Bilateral,
symmetrical,
patchy or diffuse
Bilateral, patchy Mid-superior areas
Bilateral, diffuse
or patchy
Uni- or bilateral,
asymmetrical,
patchy
Bilateral,
symmetrical,
patchy
Bilateral, patchy Basal
Bilateral,
symmetrical,
patchy
Uniform Uniform
Basal prevalence
Mid-superior areas Often perihilar Acute alveolar
Variable
Variable
More intense
when basal
Basal prevalence
Variable Variable
Variable
Basal
Basal Peripheral
Posterior
predominance
Possible subpleural
localization
Perihilar, dorsal and
subpleural regions
Parahilar or diffuse,
not peripheral
Peripheral, gravitydependant
Gravitational Acute alveolar
Subpleural, gravitydependant
Peripheral and
subpleural
Often peripheral
and subpleural
Subpleural but also
diffuse
Peripheral but also
peribronchial
Nodular,
random
Nodular,
random
Nodular,
random
Perilymphatic
nodular
Perilymphatic
nodular
Acute alveolar
Acute alveolar
Acute alveolar
Chronic
alveolar
Chronic
alveolar
Chronic
alveolar
Chronic
alveolar
Chronic
alveolar
Chronic
alveolar
Parenchymal lung patology 175
appearance of acute interstitial pneumonia (formerly known as Hamman Rich syndrome)
is similar to that of ARDS.
Table 10 summarizes these nodular and alveolar cases in relation to their topography and
diffusion in the organ.
Echography of DPLD
In DPLD the pleural level is constantly involved. erefore, ultrasound with high-frequency
probes (10-12 MHz, set depth to 3-4 cm) is the best method for defining these diseases. e
only way to explore interstitial lung diseases is to characterize the pleural plane, its artifacts
and its nodulations, together with the homogeneity of the pleural involvement, and the
apico-basal and lateral distribution of the pathology (Figs. 15-17).
A
C D
Figure 15 – Three examples of dense lung tissue in preconsolidating phase, capable of producing an
interstitial syndrome. A: pulmonary fibrosis (NSIP); B: pulmonary fibrosis (UIP); C: normal deflated lung
(at a density of approximately 0.6 g/ml); D: normal lung at a density of approximately 0.4 g/ml. In A,
B and C an increased interstitial component is evident, in absolute (A and B) and in relative terms (C),
compared to normal lung.
A
B
B
Figure 16 – Histology of diffuse alveolar damage (B). A minor “porosity” (or an increase in density) is
evident compared to normal lung (A). A denser lung is more permeable to ultrasound.
176 oracic ultrasound
A B
Figure 17 – Microscopic images of a lung with diffuse alveolar damage (A) and of a normal deflated
lung in preconsolidating phase (B). The tissue density is similar: in a pathological lung this is caused
by an increased fluid and cellular part of the lung, in the normal lung, there is a decrease of the air
component. Within certain terms of acoustic interaction, however, there is equivalence between the two
lungs.
e pleural differentiable ultrasound appearances in DPLD are indicated in Table 11
(Figs. 18-21).
Table 11 – Pleural features in chest ultrasound
Real hypoechoic or calcific thickening (not an increase
in reflection) of the parietal or visceral pleura, often not
Pleural thickening
Irregularities of the pleural
plane
Pleural nodules
Consolidations
Subpleural honeycombing
distinguishable from small effusion or thin atelectasis of the
lung (in this case the use of ultrasound contrast agent is
useful)
“Cobblestone” appearance of the pleural plane, quantifiable
by the tangent method
Micro- and macro- hypoechoic nodules with posterior
acoustic enhancement. In micronodules (< 1 cm) it can be
elongated in depth and resemble a B Line
Consolidations that emerge on the pleura with or without air
broncho/alveolograms
It may be the cause of subpleural regions with A Linesappearance (pseudonormal), i.e. inhomogeneity or skip areas
of interstitial disease
Parenchymal lung patology 177
Right
Left
Figure 18 – Pulmonary fibrosis (NSIP). On the left, three-dimensional CT reconstruction of the surface.
The ground glass is prevalent, honeycombing is not represented significantly, and the lesions are
relatively homogeneous. The histology (top right) shows a fibrosis, that does not seriously subvert the
structure, with relative homogeneity of the air spaces. The coronal reconstruction confirms these aspects
(courtesy of prof. Mario Maffessanti).
Right
Left
Figure 19 – Pulmonary fibrosis (UIP). On the left, three-dimensional CT reconstruction of the surface.
The septal fibrosis is prevalent with significant honeycombing (arrows), the overall picture is spatially
and temporally inhomogeneous. Spared areas are observed. The histology (top right) shows a fibrosis
with fibroblastic foci, structural disruption and air cysts. The coronal reconstruction confirms these aspects
(courtesy of prof. Mario Maffessanti).
178 oracic ultrasound
Figure 20 – Pulmonary fibrosis (NSIP). On the left, CT reconstruction of the surface. The prevailing
homogeneity of the anatomy and the ground glass expressions are highlighted in echo (right) by the
prevalence of white lung aspects, with a homogeneous pattern and diffuse pleural irregularities.
Figure 21 – Pulmonary fibrosis (UIP). On the left, CT reconstruction of the surface. The surface is
unevenly affected by honeycombing. In ultrasound these aspects are translated into a inhomogeneous
expression of the interstitial syndrome, inconstant pleural irregularities, especially where honeycombing
justifies pseudonormal subpleural patterns (right). The arrows illustrate the anatomical-echographic
correlations.
Parenchymal lung patology 179
Pathologies that do not profoundly alter structure, homogeneity and symmetry of the
subpleural airspaces (Leslie’s pattern 1), and show ground glass on HRCT, tend to express
predominantly as white lung (e.g. acute interstitial pneumonia and NSIP). However, there
are no demonstrations based on analysis of large groups of subjects.
Aspects with variously coalescing B Lines tend to be associated with pleural abnormalities,
micronodules and/or non-homogeneous geometry of distal air spaces, as it typically occurs
in cases with Leslie’s pattern 2 (idiopathic pulmonary fibrosis, UIP) (Figs. 22-23).
Figure 22 – Tomographic pictures of septal syndrome, ground glass and consolidations and
corresponding ultrasound scans. Pulmonary fibrosis.
Figure 23 – Tomographic pictures of normal lung, septal fibrosis and honeycombing (left). Respective
aspects in ultrasound scans in the same patient. Pulmonary fibrosis (UIP). Scans on areas of superficial
honeycombing can generate a large septal syndrome or even mirror (normal) effect.
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