Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5769_Библиотеки_им_академика_М_И_Перельмана
.pdf
160 oracic ultrasound
In cardiogenic edema, though with all its specific limits, radiological stages range from
congestive vascular aspects (stage 1) to alveolar and lobular flooding with diffuse confluent
opacity (stage 4) (Table 1).
Table 1 – Degree of increase in extravascular lung water on the chest radiograph
Degree 1
Degree 2
Degree 3
Degree 4
Apical flow reversal, ilar enlargement and increased density
Blurred ila, perivascular and peribronchial cuffs, Kerley’s B Lines
Patchy alveolar edema
Confluent alveolar edema, scissural effusions
e absence of flow variations, the less centrifugal tendency of the edema and the lack of
causal cardiac disease are the hallmark of the lesional edema (ARDS, for example).
Especially noticeable is the difference in incidence of patchy alveolar opacities between hydrostatic and lesional edema, respectively 13% and 58%43.
However, if in unmistakable cases with a positive history and prompt response to a specific
therapy, the radiologic diagnosis of pulmonary edema does not create difficulties, it is more
problematic in the case of initial interstitial edema. is is not always clearly distinguishable
from other interstitial diseases44, or from a very localized alveolar edema that cannot be easily
differentiated from other kind opacity or consolidations.
According to these assumptions, a subject with B Lines can have a cardiogenic pulmonary
edema. If he shows only A Lines, he has no pulmonary edema. Moreover, a bilateral and a
uniform framework of B-Lines strengthen the cardiogenic hypothesis. is picture refers to
the absence of spared areas, in which the lung has a normal appearance13.
e cardiogenic edema can show a density base/apex gradient of B Lines, but shows no
discontinuity in the interstitial pattern (for example, a basal and apical positivity and the
absence of B Lines in the medial field).
It must be emphasized that the B Lines are not pathognomonic of edema (they lack of specificity). eir evidence must suggest the differential diagnosis of pulmonary fibrosis, ARDS,
ALI, and, in the case of localized B Lines, inflammation and contusions45. Only employing
ultrasound, this may not be easy in cases with complex comorbidities.
e only categorical assumption of a sonographyc triage in dyspnea is that the absence of
interstitial syndrome excludes a parenchymal pathology. A practical consequence of the previous assumption is that if a focal pathology (pneumonia, atelectasis) is excluded, and if the
diagnosis of pleural syndrome is invalid (effusion, pneumothorax), vascular disease, asthma
and pulmonary embolism are probable hypothesis.
Figure 9 shows another flow-chart concerning the patient with acute dyspnea.
is algorithmic approach to dyspnea has recently had a clinical validation with the so-called
BLUE protocol14. Following a “step by step” procedure, an ultrasonographic approach for
dyspnea has been proposed. It essentially confirms what has already been discussed.
e basic concept is that each type of acute respiratory failure is characterized by a particular
pleuropulmonary pattern. An evident pleural sliding identifies a subpleural profile which
can be A or B type. e B profile B (with B Lines) represents interstitial syndrome and pulmonary edema. e A type is further defined by an echographic analysis of the deep veins of
the lower limbs with venous compression ultrasonography (CUS) for the detection of deep
Parenchymal lung patology 161
DYSPNEA
Physical examination, BGA, ECG,
chest X-ray, echocardiography
CHEST ULTRASOUND
Pleural eff.
Interstitial lung
Bronchopneumonia
Focal edema
Lung contusion
Consolidation at
early stage
Figure 9 – Flow-chart illustrating the role of lung ultrasound in the dyspneic patient.
Focal B Lines
Pulmonary edema
Lung interstitial dis.
Diffuse interst.
pneumonia
Pneumonia
Atelectasis
Contusion
ARDS
Diffuse
interstitial syndr.
Consolidation A Lines
PNX
Multiple small
consolidations
Normal
COPD
Bronchial asthma
Pulmonary embolism
Pulmonary embolism
Bronchopneumonia
venous thrombosis (DVT). In this context, DVT is indicative of pulmonary embolism. On
the contrary, the absence of DVT leads us to consider COPD, asthma or pneumonia (if
evidence of pleural or alveolar syndrome).
An abolished pleural sliding suggests PNX, confirmed by the presence of at least one lung
point. Conversely, a B Lines pattern excludes PNX and leads us to consider pneumonia.
Table 2 shows the sensitivity and specificity values of the lung patterns reported in the BLUE
protocol14.
In our opinion, the real value of the BLUE protocol is its educational role. On the practical
side, it is characterized by immediate applicability and speed of execution in urgent contexts.
Undoubtedly, in many cases it allows a sufficiently accurate screening (using the Occam’s
razor method) of acute respiratory failure in many settings.
However, in our experience, it is important to consider that sometimes the patient has overlapping diseases (e.g. COPD or cardiorespiratory failure in the context of chronic interstitial
162 oracic ultrasound
lung disease). Moreover complex disorders with secondary involvement of the heart (see
ARDS), require cardiac and hemodynamic monitoring for a better comprehension and a
targeted therapy. In the BLUE protocol, heart is not mentioned and there is no reference
to acute or chronic interstitial disease involving the critically ill patients, but which are not
attributable simply to cardiogenic pulmonary edema or pulmonary embolism (see sepsis
related cardiomyopathy and ARDS).
Table 2 – Sensitivity and specificity values reported in the BLUE protocol
Pleuropulmonary pattern Disease Sensitivity % Specifity %
Predominance of A Lines + lung sliding COPD, asthma 89 97
Multiple anterior B Lines + lung sliding Pulmonary edema 97 95
Normal + DVT Pulmonary
embolism
No sliding + A Lines + lung points Pneumothorax 81 100
Anterior alveolar consolidations,
diffuse anterior B Lines, anterior
asymmetrical interstitial pattern, posterior
consolidations with pleural effusion
without anterior B Lines
Pneumonia 89 94
81 99
False negativity of ultrasound in dyspnea
In the dyspneic patient ultrasound does not provide any signs in pure bronchial or bronchiolar
pathology, and in many cases of vascular disease
10,14
. All the bronchial noises have no “echographic” correspondence. e obvious consequence is that the chest auscultation maintains
a prominent role, even if ultrasound is extensively used at the bedside. Rather, auscultation
of the chest is much more significant when the subpleural fields are “dry”, that is, they have
no interstitial or alveolar signs. e differential diagnosis of the airways pathology producing
bronchial and bronchiolar noise is summarized in Table 3.
In ultrasound there is correspondence when the dynamic bronchial obstruction determines
atelectasis, hypoventilation, interstitial or alveolar syndrome, and inflammatory edema.
Ultrasound and extravascular lung water
e normal lung is made up of 80% water. e extravascular lung water is physiologically
less than 500 ml. e fluid passage in the alveolar lumen during pulmonary edema reports a
clearance fault, related to an increase in extravascular water greater than 75-100%46. It is very
important, for diagnosis, monitoring and treatment of the critical care patient, to define how
much is the increase in extravascular lung water before it becomes evident with conventional
means (chest X-ray). e ideal test should be accurate, sensitive, reproducible, practical and
economical. Currently there is no method that meets every requirement.
Table 4, modified from Lange and Shuster47, contains several existing methods aimed at
defining the extravascular lung water. Ultrasound was added later.
Parenchymal lung patology 163
Table 3 – Lung diseases with auscultatory findings and associated sonographic signs
Pathology with bronchial
auscultatory findings
Upper airways
Angioedema
Foreign body
Infections (croup, epiglottitis, tracheitis)
Lower airways
Asthma Regional hypoventilation (interstitial syndrome)
Transient hyperreactivity of the airways Atelectasis (usually segmental, lamellar) due to
Bronchiolitis Small consolidating focus (inflammatory), even
Chronic obstructive bronchopulmonary
disease
Foreign body Major atelectasis due to foreign body obstruction
Cardiovascular
Cardiac asthma Interstitial syndrome due to cardiogenic edema
ARDS Interstitial and consolidating syndrome due to ARDS
Pulmonary embolism (rare) Embolic consolidations (tardive)
Psychogenic No findings
Any “echographic” correspondence
(if complication)
Generally no findings
obstruction
multiple
Typical inflammatory consolidations
Regional or focal fibrosis (chronic forms)
(constant)
Table 4 – Methods to assess extravascular lung water
Method Target Quantification
Chest
X-ray
Chest CT Density Excellent Unknown Unknown High
MRI Total water Weak Underestimation
PET
Indicator
diluition
Ultrasound Density Excellent Nonspecific Good Excellent
*Coefficient of Variation
Density Poor Unknown Unknown Moderate
Extravascular
water
Extravascular
water
Excellent Underestimation
Good Overestimation
Accuracy
about 40%
about 15%
about 20%
Reproducibility*Sensitivity
5-10% Poor
< 5% High
4-8% Moderate
Each imaging system for this purpose considers spatial anatomical information related to
physical parameters. Each voxel (volume unit) and each pixel in the image represents a
physical unit with its features. In the case of the lung, composed largely of air, the amount of
lung tissue in each voxel is variable in relation to its degree of inflation (i.e. density). Many
methods proposed do not estimate the extravascular lung water but, based on the assumptions
164 oracic ultrasound
described above, they measure both intra- and extravascular water, introducing errors in the
pulmonary blood volume, which of course may vary.
e role of chest radiography in the definition and quantitation of pulmonary edema has
been described. It is useful to remember that the radiographic signs of edema usually appear
with increases in lung water greater than 30%48.
CT has the advantage of being able to quantify and map in cross section the densities related
to the water increase. Experimentally the CT lung density increases by 69% for gravimetric
increase of 250%49. MRI avoids the use of ionizing radiation, but it has low sensitivity and
it is not practical in critically ill patients50. PET specifically measures the extravascular lung
water. It correlates well with the gravimetric estimates and is highly reproducible. However,
this method is expensive and not readily available.
e systems that use single or double indicators, both in mean transit time and in slope volume
versions, correlate well with the gravimetric methods (r: 0.9), with values of sensitivity and
specificity, respectively 88% and 97%51. eir disadvantages are the invasiveness (need for
venous and arterial catheter) and the underestimation regarding hypoperfused lung regions.
e electrical bio-impedancemetry measures the impedance of the body or of a body area
to the passage of alternating current. It mainly reflects the total body water content or water
content in a body area. e multifrequency bio-impedancemetry may also have the advantage of calculating and distinguish between intra- and extracellular water compartments,
and has been applied on patients receiving dialysis. e estimation of water with thoracic
bio-impedancemetry shows, after suitable corrections, a correlation with the extravascular
lung water52. It is however necessary to acquire additional data before validating an extensive
use of this technique.
Some studies have suggested “lung” ultrasound as a simple, non-invasive and relatively reproducible method for estimating extravascular lung water (EVLW). ey are based on the
correlation between findings of heart failure or edema (EVLW determined by thermodilution, natriuretic peptides, pulmonary capillary wedge pressure, echocardiographic estimates)
and interstitial syndrome, expressed by B Lines
11,16,18
. According to our preliminary remarks
regarding the density related acoustic properties of the lung, it seems clear that lung edema
corresponds to an hyperdense tissue expressed by a weight increase relative to extravascular
(and, to a lesser degree, intravascular) lung water. Accordingly, the acoustic properties of the
organ may vary appropriately in order to produce artifacts (B Lines). It is also clinically (and
experimentally) evident that the density, or (in misnomer) the “number” of B Lines, correlates
with the severity of the lung edema.
Based on what has been repeatedly stated, we believe that B Lines essentially express a hyperdense non-consolidating state of the first subpleural millimeters of the explorable lung.
Edema (or the increase in EVLW) is responsible for this hyperdensity.
erefore, ultrasound indirectly estimates the intra- and extravascular lung water based on
the subpleural pulmonary density.
In conclusion:
• Ultrasound, like conventional radiography and CT, is a technique that estimates density.
• Ultrasound has a complete sensitivity for hyperdense subpleural syndromes, at present
there is no hyperdensity (or interstitial syndromes) without B Lines or white lung.
• Obviously, ultrasound is not specific for pulmonary edema, because every pathology that
varies the subpleural pattern towards a hyperdense non-consolidating state can generate
B Lines or white lung.
Parenchymal lung patology 165
• Ultrasound defines a hyperdense state due to water increase, but cannot distinguish whether
this water is intra- or extravascular.
• We believe that a total count of B Lines to assess the severity of interstitial syndrome is
not correct5. B Lines are not the expression of anatomical structures, but of density and
geometry. B Lines appear to be very different if explored with different probes. B Lines,
at least in experimental models, are angle-dependent artifacts, as it happens in reflection
phenomena. eir expression depends on how the ultrasound beam impacts on the target.
• ere is at least one study11, stating that pulmonary edema is numerically quantifiable by
means of the count of the artifacts. is may be true in broad terms, operating at relatively
low frequencies with a sector probe. In these conditions all echogenic, linear, full-screen
artifacts are considered as B Lines. Simply, “di notte tutti i gatti sono neri” (italian proverb: in
the night all cats are black). However, many of the artifacts identified by the sector probe as
B Lines are very different at pleural level using linear transducers. ey frequently are very
short or appear as acoustic enhancements that originate behind micronodular structures.
We believe that the exploration technique used (especially in terms of depth, definition
and frequencies) influences the classification systems. Many studies seem to forget this.
Wet and dry in dialysis
e subtraction of fluid is a primary goal in dialysis and the determination of the so-called
“dry weight” represents one of the major problems for the nephrologist53. e dry weight
is the weight at the end of the dialysis session, below which it is likely that the patient develops hypotension symptoms. In practice, an underestimation of the dry weight induces
hypovolemia with hypotension, and an overestimation of this parameter causes congestion
and pulmonary edema.
e clinical indices of dry weight have proved to be not very sensitive, so it is considered
important to employ other more accurate methods.
Standard chest radiographs has low accuracy for the definition of intrathoracic congestion,
which have already discussed in relation to pulmonary edema.
e behavior of the inferior vena cava has a certain interest because the diameter of this vessel
was related to the right atrial pressure and blood volume54.
e central venous pressure (considered equivalent to the right atrial pressure) physiologically
shows variations, mainly related to changes in intrathoracic pressure during the respiratory
cycle and secondarily to cardiac function.
Despite differences in methods and results, under normal conditions this pressure is 8 cm H2O,
equivalent to 6.5 mmHg.
Table 554 shows that in
normal situations, the inferior vena cava, shortly
before (2-3 cm) crossing
the diaphragm to reach
the right atrium, shows
a diameter variable between 1.5 and 2 cm in the
end expiratory phase. e
inspiration collapses the
vessel at least 50%.
Table 5 – Correlation between respiratory variations of inferior
cava vein diameter and the right atrial pressure
AP measure Inspiratory reduction PVC
< 1,5 cm Collapse 0-5 mmHg
1,5-2,0 cm > 50% 5-10 mmHg
1,5-2,0 cm 33-50% 10-15 mmHg
2,0-2,5 cm 0-33% 15-20 mmHg
> 2,5 cm Absent > 20 mmHg
Modified from Otto54.
166 oracic ultrasound
However, if the subject is ventilated with positive pressure, both PEEP (end-inspiratory pressure) and plateau pressure (PP) have an impact on the diameter of the vessel. In the course of
ventilation, a caval diameter less than 1.2 cm has a specificity of 100% in predicting a right
atrial pressure less than 10 mmHg.
e definition of the diameter and collapsibility of the inferior vena cava in ultrasound is
simple.
e convex or cardiologic probe is placed longitudinally in the right paramedian position
along the axis of the vessel, which appears as a tubular structure more or less collapsed and
collapsible, behind the liver (IV hepatic segment) and the gallbladder. e angle of the transducer upward shows the transdiaphragmatic passage of the vessel and its entrance into the
right atrium. e lack of visualization of the inferior vena cava can be caused by the almost
total depletion of the vessel or by intestinal bloating. In addition, a big right polycystic kidney
can compress the vessel.
Many authors have sought correlations between the inferior vena cava diameter and the
blood volume status in patients with renal insufficiency. In 1989, Cheriex55 has employed this
technique for the determination of the dry weight in patients on dialysis. According to this
author, the diameter of the inferior vena cava, after the dialysis session, correlated with the
right atrial pressure and the circulating blood volume. Hypervolemia was defined by a caval
diameter greater than 11 mm/m2 of body surface and an index of collapsibility (expiratory
caval diameter - caval inspiratory diameter / caval expiratory diameter x 100) of less than
40%. Hypovolemia showed a vascular expiratory diameter under 8 mm/m2 and an index of
collapsibility greater than 75%. Over time, these results have not always been reproduced,
and a certain variability of the results in relation to the population studied has appeared.
e results of this method can be affected by pathological conditions that increase central
venous pressure (cardiac tamponade, pulmonary embolism, right heart failure, valvular heart
disease, and pneumothorax).
e relationship between interstitial syndrome and lung congestion has recently drawn the
attention on B Lines and pre- and post-dialysis state.
Currently two studies
56,57
have addressed the problem. In both of them, dialysis reduced the
expression of B Lines, which therefore appear in these patients as a marker of congestion/
edema. e excess of lung water does not seem to correlate with the state of hydration, but it
is strongly dependent on the NYHA functional class and with echocardiographic parameters
of systolic and diastolic function. is suggests that cardiac performance possesses a critical
role in controlling lung water in end stage renal failure.
In conclusion, although the scarce available data, ultrasound lies in the follow-up of these
patients as a complementary, but often decisive tool to clinical examination. Ultrasound is
also a functional analysis and a multidistrictual assessment. e evaluated targets are blood
volume, cardiac function and lung density (edema). A careful analysis of these indices can
differentiate the blood volume of a nephropathic patient from a contributory cardiac mechanical cause, or a lung parenchymal contribution.
Fluid responsiveness
e hematic expansion has a definite role in the treatment of critically ill patients with hemorrhage, hypovolemia, severe sepsis and shock. Euvolemia relative to the pathophysiology is
therefore an essential target to avoid fluid overload, or, on the contrary, hypoperfusion with
ischemia.
Parenchymal lung patology 167
By “fluid responsiveness”, we mean a significant increase in cardiac output in relation to a
volume expansion, which reflects an optimal response of the heart to an increase in preload.
erefore, the hemodinamics of a responsive patient is consistent with the ascending portion
of the Frank-Starling curve.
A particularly simple technique for evaluating the response of the preload to the fluid administration is the leg-raising test. eoretically, this causes an expansion of the central blood
volume of 300-500 ml.
e behavior of the inferior vena cava resulting from the leg-raising test is an indicator of
fluid responsiveness when its collapse index is more than 18%58. See Chapter 9 for more
informations.
Acute exacerbation of chronic obstructive pulmonary disease
Exacerbations of COPD are a common cause of dyspnea, especially in old people. It is often
worsened by an intercurrent pathological event (Tab. 6). Progressive dyspnea, cough, sputum,
wheezing, increased work of breathing, up to severe respiratory failure with altered state of
consciousness are the clinical symptoms.
Table 6 – Causes of COPD exacerbation
Infectious causes
• H. influenzae, S. pneumoneae, S. viridans, B. catarralis
• mycoplasmas
• legionella
• virus
Other causes
Due to allergens
PNX
Sudden expansion of large lung bubbles
Retention of secretions with areas of atelectasis
Left ventricular failure with pulmonary stasis
Pulmonary embolism
Abandonment of therapy
Often the etiology of an acute exacerbation is not immediately understood and the therapy is practiced in
an empirical way. e chest auscultation reveals mixed findings of dry and
wet bronchial sounds, the meaning
of which can be not immediately
evident. Similarly, chest X-ray may
not be decisive59.
Even in this pathology, ultrasound
examination can play an important
role to rule out associated diseases.
e exacerbation of COPD does not
generate itself specific ultrasound images10 and the subpleural plane may
appear normal. Bronchial inflamma-
tion, bronchoconstriction and mucus
hypersecretion do not change the appearance of lung, unless they cause inflammation of the
pulmonary cortex, superficial fibrosis and hypoventilation or atelectasis.
At present, emphysema does not have an ultrasonic representation, although theoretically it
could appear as a hypermirror. We noticed that subpleural emphysematous bubbles, especially
if located in an even slightly fibrotic parenchyma, may appear as regions with strong and
dense horizontal reverberations. Otherwise, the pleura induces a strong mirror effect. ese
reverberations contrast with contiguous sectors, where an interstitial disease is rooted (Fig. 10).
Sometimes, in subjects with COPD, B Lines along the pleura may appear with an uneven
or patchy distribution. ere is not a well-defined etiology for this clinical case. It is likely
that this pneumogenic interstitial syndrome stems from secondary inflammation, marked
hypoventilation, or from concomitant or secondary chronic interstitial disease.
ese ambiguous aspects do not detract, however, the strongly predictive meaning of interstitial syndrome as a pathological aspect of the organ.
168 oracic ultrasound
Figure 10 – Hypermirror. Thick and marked horizontal reverberations in a case of panlobular
emphysema by alpha 1 antitrypsin deficiency. The pleural plane has acoustic impedance close to that of
a pure air collection (courtesy of Dr Natalia Buda, University of Gdanz-Poland).
Single or multiple areas of parenchymal consolidation appear in some cases of COPD and
usually have an infective or atelectatic origin.
A secondary PNX leads to the disappearance of the sliding sign, while the presence of diffuse
B Lines assumes, may indicate decompensate heart failure, inflammatory or fibrogenic interstitial disease. Sometimes these occurrences are quite difficult to differentiate on ultrasound.
When the pleuropulmonary analysis cannot resolve the issue, the evaluation of the cardiac
systo-diastolic function, the diameter of the inferior vena cava or the presence of pleural effusions is determinant. As a rule, the path to accurate diagnosis cannot be separated from a
multidistrictual assessment. Finally, diuretic therapy does not alter the sonographic pattern
of a diffuse interstitial lung disease, and this can be an ex adiuvantibus criterion.
➣ Diffuse parenchymal lung diseases
In 2002, the American orax Society and the European Respiratory Society60 classified diffuse parenchymal lung diseases (DPLD) in:
• DPLD from a known cause (e.g. collagen vascular diseases).
• Idiopathic interstitial pneumonias.
• Granulomatous DPLD (e.g. sarcoidosis).
• Other forms of DPLD (Fig. 11).
In 2013, the American oracic Society and the European Respiratory Society have updated
this classification, but this is irrelevant for our discussion.
Parenchymal lung patology 169
Diffuse parenchymal lung
diseases (DPLD)
DPLD from a
known cause
Idiopathic
pulmonary fibrosis
Figure 11 – Classification of DPLD60.
Idiopathic interstitial
pneumonias
Desquamative
interstitial
pneumonia
Acute interstitial
pneumonia
Nonspecific
interstitial
pneumonia
Granulomatous DPLD
Other idiopathic
interstitial pneumonias
Other forms of DPLD
(e.g. LAM, HX)
Respiratory
bronchiolitis iip
Cryptogenic
organising
pneumonia
Lymphocytic
interstitial
pneumonia
Although not Intensive Care Unit (ICU) or Emergency Department (ED) diseases, DPLD
pose important problems of differential diagnosis in ICU and ER patients with dyspnea.
Idiopathic interstitial pneumonias are a heterogeneous group of DPLD including, among
others, idiopathic pulmonary fibrosis, nonspecific interstitial pneumonia (NSIP) and acute
interstitial pneumonia (AIP). Idiopathic pulmonary fibrosis is histologically characterized
as usual interstitial pneumonia (UIP), and is the most common cause of idiopathic DPLD.
NSIP resembles idiopathic pulmonary fibrosis but, especially in its cellular form, has a better
prognosis, so it is important to differentiate it from UIP
61,62
. Acute interstitial pneumonia
63
(the
old Hamman Rich syndrome) has a rapid course, a severe prognosis and can be considered
as a form of idiopathic ARDS without multiorgan failure.
Subjects with DPLD usually have dyspnea on exertion and, in advanced cases, even at rest.
eir diagnosis involves physical examination, serological and laboratory tests, traditional
radiology, high-resolution CT (HRCT)64, pulmonary function tests, bronchoalveolar lavage
and transbronchial lung biopsy or surgery.
Chest X-ray is inaccurate for the diagnosis of DPLD. Although the majority of patients with
these disorders show an abnormal X-ray, 10% of patients with biopsy-proven interstitial disease,
has no radiographic abnormalities65. Because of the lack of specificity of conventional radiography, the correct diagnosis of the disease through X-ray occurs only for half of the patients.
Соседние файлы в папке Библиотека им академика М.И. Перельмана