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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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200 oracic ultrasound
Figure 43 – Lung abscess adjacent to the chest wall. A: CT image, the arrow indicates the abscess.
B: corresponding ultrasound image, the abscess is readily identifiable and drainable.
Figure 44 – Pulmonary abscess. A: CT appearance. B:The ultrasound image accurately shows the
compressed lung contiguous to the collection (small arrow) and the purulent collection (large arrow).
Figure 45 – Lung abscess. The ultrasound image (left) shows the inhomogeneous abscess. The
inhomogeneity of the fluid content is more evident by ultrasonography compared to CT (same patient,
right).
Parenchymal lung patology 201
Figure 46 – Necrotizing pneumonia and pleural empyema. a: pleural effusion and compressed lung
(thin arrow) with residual punctiform (bronchiolar) aeration. b: the pleural effusion shows echogenic
strands, that tend to set a complex arrangement. c: compact pulmonary area, devoid of air (thin arrow)
with relatively hypoechoic central colliquative focus. d: better evidence of necrosis (large arrows) and
Figure 47 – Pneumonia with pleural empyema. a: complex septated (or areolar) pleural effusion,
typical of empyema. b: compact parenchymal consolidation. c: better evidence (calipers) of the
colliquation focus, which is confirmed in CT (d). In these situations the use of ultrasound contrast agents
can facilitate the diagnosis.
202 oracic ultrasound
Figure 48 – Left lower lobar pneumonia. On the left, consolidation free of air. On the right, after a
week of treatment, air in the form of bright punctiform bronchograms announces its healing.
Bronchograms
PNEUMONIA
AIR BRONCHOGRAMS
Figure 49 – Lobar pneumonia. a: left upper lobar consolidation with air bronchograms. c: ultrasound
image, with segmental air bronchograms. The peripheral parenchyma is completely hepatized. b:
X-ray of the same subject after seven days of effective antibiotic treatment. Significant reduction with reaeration of the lesion. The ultrasound, as well (d) shows a clear reduction of the consolidation just with
small air bronchiolograms.
e sensitivity of lung ultrasound for pneumonic consolidations extrapolated from existing
studies is very high (80-97%)
79,90,97-98
. Ultrasound localization of a consolidation is accurate
if the sonographer knows the skin landmarks that indicate the major and accessory scissurae
(Table 15). Figure 50 shows the projection of the lung lobes on the chest wall.
Parenchymal lung patology 203
Table 15 – Lobar and segmental subdivision of the lungs
Right lung Left lung
Upper lobe Upper lobe
Anterior segment Apex
Apical segment (2) •Anteriorsegment(1)
Posterior segment (3) •Apicalsegment(2)
Middle lobe •Posteriorsegment(3)
Anterior-internal segment (4) Lingula
Posterior-external segment •Inferior-externalsegment(4)
Lower lobe •Superior-externalsegment(5)
Apical segment (6) Lower lobe
Internal segment (7) Apical segment (6)
Basal pyramid Basal pyramid
•Anteriorsegment(8) •Anteriorsegment(7)
•Externalsegment(9) •Externalsegment(8)
•Externalsegment(10) •Externalsegment(9)
Figure 50 – A: projection of the lung lobes on the anterior chest wall. B: posterior. C: left lateral.
D: right lateral.
204 oracic ultrasound
Pneumonia typically has a rapid, intense and homogeneous enhancement after a period of
5-7 seconds, compatible with an inflow through the pulmonary artery (Clip 31). A delay
in the acquisition of contrast agents can occur in cases of lobar or late pneumonia, for the
vasoconstriction induced by hypoxia. Clear defects of contrast enhancement appear within
the consolidation when there is a necrotic or colliquative evolution.
e behavior after administration of contrast agent in peripheral tumors (primary or secondary)
is quite different. Tumors have a mainly bronchial arterial supply, variable and inhomogeneous.
e most obvious consequence is therefore a relative delay in the acquisition of the contrast
agent, which reaches the lesion after about 18-20 seconds (Clip 32).
Finally, hemorrhagic lesions, embolic consolidation and pulmonary infarcts show a very low
or absent enhancement. In other cases, only a peripheral bronchial enhancement is observed.
Ultrasound contrast agents have a role in delineating the true extent of an effusion (which
does not capture the contrast), whereas the compressed and hypoechoic lung parenchyma
is contrasted. ey also can discover a deep obstructive lesion (assuming a late contrast) as a
cause of atelectasis (which shows a rapid acquisition of contrast).
Clip 31 – Left pneumonia. Contrast enhanced sonography (CEUS).
After intravenous administration of sulfur hexafluoride microbubbles, the
enhancement of the consolidation is rapid (after 8 seconds) and bright
(similar to that of the spleen), without colliquation.
Clip 32 – Left paracardiac consolidation. CEUS with administration of
sulfur hexafluoride microbubbles. The enhancement of the right heart cavity
is evident after 8 seconds. And the left heart cavity after approximately
15 seconds. The contrast outlining large and abnormal arterial vessels in
the lesion goes through bronchial arteries (16-20 seconds after injection).
Peripheral pulmonary neoplasm.
➣ Lung disease in the critically ill patient
In the patient in the ICU, the clinical and instrumental evaluation of the chest has a fundamental role to detect significant problems and complications (acute dyspnea, fever, pain,
definition of optimal PEEP, early diagnosis and follow-up in ARDS, individuation of collapsed
regions)
One of the most important problems is the diagnosis and monitoring of the diffuse alveolar
damage typical of adult respiratory distress syndrome (ARDS).
Since the first definition of ARDS by Ashbaugh
Even today the accepted criteria for ARDS are bilateral radiographic infiltrates associated with
“refractory” hypoxemia and altered respiratory mechanics (stiff lungs). e absence of clinical or instrumental findings of increased pulmonary capillary pressure is the prerequisite
107-110
. e approach to these situations is not sufficiently defined.
109
, chest X-ray has characterized this disease.
110
.
Parenchymal lung patology 205
In ARDS, chest X-ray is usually performed with mobile devices, sometimes with a daily
frequency, but this practice has not a clear demonstration of efficacy. It has been shown
111-112
that up to 65% of these X-rays show new and unsuspected significant anomalies, conditioning
changes in therapy. Against this background, the diagnostic accuracy of chest radiography
in the intensive care unit is not high. For example, its sensitivity and its specificity toward
nosocomial pneumonia are, respectively, 62% and 28%. As already stated, chest X-ray, if it is
technically not perfectly executed, has a low sensitivity and specificity towards parenchymal
density, effusion and pneumothorax, that are clearly visible with ultrasound.
e definition of the true nature of a radiographic consolidation is particularly difficult. A
hyperdensity at chest X-ray can be atelectasis, interstitial or intracinar edema, or alveolar consolidation. e specificity of chest X-ray in quantifying and categorizing inflammatory edema,
which is the marker of ARDS, is particularly controversial, and an accurate differentiation of
cardiogenic from non-cardiogenic edema is generally questionable
113
.
Computed Tomography (CT) is a cross sectional method. In critically ill patients, it is very
accurate for analyzing overlapping structures and for quantifying parameters of volume and
density of the pathological lung
114-117
.
However, chest CT is expensive and biologically invasive. It cannot be performed at the bedside
and therefore exposes the patient to the risks of a transfer from a protected environment to the
hall of diagnostic radiology. e impracticality of CT therefore greatly affects the diagnostic
work up of the critically ill patients and every innovation in this context is very interesting.
In critical care, CT has changed the view of ARDS. In the eighties, it was shown that ARDS
has an uneven distribution in the lungs, and the major radiographic densities are distributed
in a dependent position. Quantitative analysis showed or confirmed important aspects of
the pathophysiology of ARDS, which had implications in the ventilation methods used at
that time.
e main evidence for pulmonary involvement in ARDS concerns the distribution of the
pulmonary lesions. In CT, involved lung compartments are areas of different radiological
and physical density, related to different aeration, which generally follow a gravity gradient. In supine position, the highest density is in dorsal regions. ese compartments can
be hyperexpanded, normally expanded, hypoexpanded or completely collapsed. e great
advantage of CT is to quantify them in terms of volume and number (Hounsfield units). e
practical implication is therefore to reopen the collapsed airway without further damaging
the normally- or already hyperexpanded regions.
It has already been seen how CT can be accurate in the definition of interstitial diseases and
for detecting single or multiple infective consolidations, both in normal and in immunocompromised subject.
e distinction of infective mono- or multifocal consolidations from ARDS is therefore
facilitated by this means, even if ARDS can follow septic events with pulmonary genesis.
➣ Echography in lung diseases of the critically ill patient
Generalities
In critically ill patients, heart failure and cardiogenic pulmonary edema occur with a noninterrupted (without spared areas) interstitial syndrome, characterized by multiple and
bilateral B Lines. e pleural line, if not already affected by other diseases, is regular and
relatively mobile.
206 oracic ultrasound
B Lines can assume a septal appearance (separated by an adequate distance compared to
normal interlobular septa), or be particularly dense or even confluent. Alveolar consolidations
are unusual and always very soft13. ere may be pleural effusions and heart shows changes
in systolic or diastolic function with high values of capillary wedge pressure.
Parenchymal consolidations from various causes can be represented in ultrasound, as already
seen. is is logical since the alveolar consolidations typically reach the pleural surface and
water, which is abundant in the exudate, acts as an excellent means of ultrasound transmission.
e sensitivity of ultrasound in this specific field is about 90%, while its specificity is 98%
118
Nosocomial pneumonias in intubated patients have a frequency between 12% and 29% and a
mortality rate between 27% and 33%
119
. Its diagnosis, not easy, must differentiate pneumonia
from cardiogenic pulmonary edema, ARDS, atelectasis and aspiration syndrome.
Ultrasound can distinguish atelectasis from non-obstructive inflammatory consolidations,
based on the presence of air bronchograms and the visualization of their dynamics.
A colliquated consolidation strongly suggests an infectious etiology. ARDS will be described
in detail in the following paragraph.
Aspiration pneumonia
120
is a chemical pneumonia with possible evolution in infectious
consolidation. e aspiration most commonly affects the right bronchial system and, in the
supine patient, the posterior lung regions. If not complicated by infection, its resolution is
usually rapid. Ultrasound can show the consolidations, their degree and, most of all, their
aeration trend over time. Complications of aspiration, such as abscess and pleural effusion
have a representation in basic ultrasound, and in LCEUS
121
.
e aspiration of solid material induces distal hyperinflation or atelectasis, demonstrable, and
especially differentiable, with ultrasound.
e incidence of barotrauma in intubated patients varies between 4% and 11%, but in patients with ARDS it may be 60%. Among the effects of barotrauma
122
, pneumothorax is easily
diagnosed by ultrasound. In this setting, pneumothorax is particularly at risk of becoming
hypertensive during mechanical ventilation. Moreover, in the presence of a stiff and irregularly consolidate lung, the tissue may collapse in inhomogeneous way, and pneumothorax
can be located in unusual position. Although located in atypical regions, in critical care patient the typical appearance of the subpleural plan facilitate the diagnosis of pneumothorax.
Demonstration of B Lines and white lung is incompatible with PNX. In these circumstances
lung points are particularly evident.
.
➣ ARDS
ARDS is the extreme of a spectrum of acute lung injuries due to a lesion of the alveolarcapillary membrane, caused by a uniform inflammatory mechanism, regardless of etiology.
Of this spectrum, the initial edematous stages are less easily recognizable
Beyond the histopathological differences between pulmonary and extrapulmonary ARDS
recent studies performed with CT have shown that ARDS (and its earlier stages) are inhomogeneous processes. Moreover, their morphology may vary with causes, type of ventilation
used and the patient’s position.
Some data show that the pathophysiology and radiographic expression of extrapulmonary
ARDS may look different from pulmonary ARDS, but there are significant overlaps between
the two.
123
.
124-125
,
Parenchymal lung patology 207
For example, a ventrodorsal density gradient is not always present in extrapulmonary ARDS
and, vice versa, not every pulmonary ARDS shows asymmetric consolidations and ground glass.
Nevertheless, a bilateral evolution of a unilateral lung inflammation is a prognostically unfavorable event. e inhomogeneous involvment of the lung is the hallmark of ARDS and
it differentiates ARDS from pulmonary hydrostatic edema13. is patchy involvement is not
well recognized by X-ray, but it is found with CT. Ultrasound is very sensitive for detecting
subtle subpleural densities, therefore, in our opinion chest sonography has a definite monitoring role in ICU.
Ground glass areas and alveolar consolidations represent the characteristic pulmonary alterations detected by CT in the acute stages of ARDS (during the first week of disease)
126
.
eir pathogenesis is linked to inflammation and dysventilation, with the contribution of the
lung and heart weigh and of the transdiaphragmatic effect of the abdominal hypertension.
Ultrasound interrogation of ARDS takes into account these considerations, particularly the
relationships between edema, interstitium and air, which characterize every echographic
representation, and the uneven distribution of the pathology.
Although sonography of ARDS is actually only a technique for investigating the acoustics of
the pleural and subpleural plane, the biophysical conditions that support US imaging are very
suggestive. If we consider ultrasound as a tool for detecting the subpleural tissue in terms of
density, ultrasound, in its essential terms, is very similar to a surface CT
127
.
Ultrasound in ARDS
13,127
In our experience, ARDS is expressed early with an interstitial syndrome. Its severity is correlated to a significant reduction or abolition of the pleural sliding, probably due to an acute
decrease in lung compliance (the stiff lung). However, the relatively still pleura reveals a typical
pulsatility synchronous with the cardiac systole.
erefore, a heavy and stiff lung shows the lung pulse, but ARDS mainly expresses an inhomogeneous pattern of B Lines, white lung and small subpleural consolidations, that can
evolve into large alveolar consolidating syndrome.
A pathologic ventrodorsal gradient of parenchymal density clearly appears. Its typical feature
is a ventral interstitial syndrome, an intermediate preconsolidating white lung, and posterior
gravitational consolidations.
e pleural line is involved. It is irregular and frequently interrupted above micronoduations
or consolidation. ese aspects are accentuated in the late phase and especially in fibrotic
evolutions.
“Normal” areas of the lung surface can be seen (spared areas), and are typical features of
ARDS. is picture contrasts with the cardiogenic edema that never shows spared areas and
generally show linear pleura.
Oleic acid injected in pigs to induce ARDS has provided interesting observations. In this
experimental setting, the appearance of interstitial syndrome confirming an increase in extravascular lung water preceded hypoxemia
128
.
e precocity of ultrasound in understanding changes and providing a greater amount of
details compared to X-ray, suggests interesting future prospects (Figs. 51-53) (Clips 33-37).
208 oracic ultrasound
Figure 51 – ARDS. Radiographical evolution. a: patient before the disease. b, c: clinically expressed
disease. d: resolution. Evidence of bilateral lung consolidations during the disease. CT (e) shows with
greater evidence the inhomogeneous and gravitational aspects of the parencymal disease (above).
Figure 52 – Same patient of Figure 53. Echo images before the disease (left) and during the disease
(right). 10 MHz linear probe. What looks like ground glass in CT, appears as a particularly dense
interstitial syndrome in echography. The pleura is irregular.
Parenchymal lung patology 209
Figure 53 – After healing, there are still pleural fibrotic irregularities (right: image with 10 MHz probe).
Clip 33 – ARDS: extended interstitial syndrome. Reduction of the pleural
sliding.
Clip 34 – ARDS: presence of lung pulse, reduction of the pleural sliding in
a white lung area.
Clip 35 – ARDS: thickening and irregularity of the pleural line with no
sliding. Millimetric subpleural consolidation.
Clip 36 – ARDS: coexistence of areas with pleural sliding and with no sliding.
The dynamical changes of the pleural line are more evident in relation to the
entity of the interstitial syndrome.
Clip 37 – ARDS: lung areas with normal pattern (spared area). Left: clear
edge of white lung area.
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