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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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410 oracic ultrasound
highlighting some of the acute complications of HMD, such as pneumothorax, pneumomediastinum, interstitial emphysema, and pneumopericardium, secondary to alveolar rupture.
Pulmonary hemorrhage is another complication frequently associated with surfactant therapy,
which appears with areas of density.
e radiological picture improves dramatically within a few hours after intratracheal administration of surfactant.
Lung ultrasound in HMD
In HMD ultrasound shows extremely compact B Lines, spreading throughout the lungs in a
symmetrical and bilateral way2. e compactness of the artifacts gives a diffusely and homogeneously echogenic appearance to the lung (echographic white lung) (Fig. 11).
APEX
APEX
Figure 11 – HMD: compact B Lines, homogeneously present throughout the lung field (bilateral white
lung).
Small hypoechoic subpleural consolidations are very frequent. ey are probably an expression of atelectatic areas (Fig. 12) (Clips 7-10).
Clips 7, 8, 9,10 – HMD: ultrasound image prior to treatment with exogenous
surfactant. Bilateral white lung. Clip 7 shows a moderate consolidation with
fluid bronchograms.
Pleural and lung ultrasound in the neonatal period and in childhood 411
Hypoechoic subpleural areas
Figure 12 – HMD: small hypoechoic subpleural areas secondary to alveolar collapse.
A
Alterations in the pleural line
B
Granular appearance of the pleural line
Figure 13 – HMD: the pleural line appears less echogenic, thickened, less defined and with a grainy
look. (A, B, C)
C
Granular appearance of the pleural line
e presence of compact B Lines at the apex and the bases is an important element that
differentiates the echography of HMD from TTN. Another important difference concerns
the alterations in the pleural line that appears constantly and diffusely thickened, not welldefined, irregular and with finely granular appearance (Fig. 13).
412 oracic ultrasound
e sonographic feature of the pleural line is therefore different from that observed in TTN
(Fig. 14).
Figure 14 – HMD: different features of the pleural line in HMD and TTN.
It is important to emphasize that the echographic images, unlike chest X-ray, doesn’t change
substantially after treatment with surfactant. is suggests that the clearance of lung liquid
is not affected by such therapy.
is supposition is confirmed by experimental studies on animal models21 that have confirmed
the effect of surfactant on the alveolar stabilization, but have shown that the total pulmonary
water does not change in the six hours after administration of surfactant (Fig. 15). is might
indicate that HMD is not only caused by deficiency of surfactant, but also by the immaturity
of the interstitial matrix on which the effect of surfactant seems to be of little relevance.
Figure 15 – Ratio over time of wet/dry lung (W/D) in preterm rabbits treated with surfactant (●),in
preterm rabbits not treated (▲) and in full-term rabbits (▼). As you can see, the ratio W/D remains
unchanged in preterm rabbits treated with surfactant or not.
e clinical improvement coincides with a reduction in the compactness of B lines and the
disappearance of the pleural line abnormalities, that occur over several days or weeks (Fig. 16).
Regarding some of the acute complications of HMD, lung ultrasound is not able to detect
pneumomediastinum or interstitial emphysema, but it highlights, more accurately than radiography, pulmonary haemorrhage and pneumothorax (see relevant chapters).
Pleural and lung ultrasound in the neonatal period and in childhood 413
Figure 16 – HMD: improvement after 3 weeks.
➣ Bronchiolitis
Bronchiolitis is an acute infectious seasonal disease of the upper and lower respiratory tracts,
which causes an obstruction of the small airways. It can affect all ages, but in adults the
diameter of the airways is larger and the mucosal edema is better tolerated than by younger
children, who show considerably more serious respiratory symptoms. In 85% of cases, two
subtypes of bronchiolitis (A and B syncytial viruses) are responsible
6 months, requiring hospitalization, respiratory syncytial virus is present in 80% of cases.
Other viruses are less frequent (adenovirus 11%, parainfluenza virus, enterovirus, influenza
virus, rhinovirus and Mycoplasma pneumoniae).
e infection causes necrosis of the epithelial cells resulting in proliferation of mucus
producing cells, with the secretion of mucus excess. e epithelial regeneration with nonciliated cells makes the removal of mucus even more difficult. is results in obstruction of
the bronchioles causing hyperinflation, increased airways resistance and alteration of the
ventilation-perfusion ratio.
e physical examination often detects the presence of otitis media, tachypnea, tachycardia,
fever (38-39°C), inspiratory retractions, fine crackles and diffuse bronchospasm.
Hypoxemia is the most important element for predicting the severity of the disease, and it
correlates closely with tachypnea. In the acute stages of the disease, 18-20% of children who
22-23
. In children aged under
414 oracic ultrasound
are hospitalized develops apnea, often requiring intubation and mechanical ventilation24.
is event is most common in premature and newborns who have not yet reached 44 weeks
of life and it is typical of infections with respiratory syncytial virus.
A few laboratory tests are needed when the age, the season and the physical examination are
compatible with the clinical diagnosis of bronchiolitis. A number of immunological tests
that can be performed on nasal swab are available, and allow to quickly and cost effectively
identify the syncytial virus related cases.
Chest radiography is more useful to rule out other medical conditions or congenital abnormalities than to confirm the diagnosis. Hyperinflation is the most common finding and in
20-30% of cases chest X-ray detects the presence of lobar infiltrates and/or atelectasis.
ese findings are not specific and can also be observed in asthma, in viral or atypical pneumonia and in aspiration. Chest X-ray should not, however, be part of the diagnostic work up.
Lung ultrasound in bronchiolitis
Ultrasound images of bronchiolitis are characterized by abnormalities constantly affecting
both lungs.
ere are typically areas of normal lung adjacent to areas with subpleural consolidations
related to atelectasis. ey are ranging in size, and are surrounded by B Lines that can be
extended and compact. Consolidations, when isolated, have a typical enhancement of the
rear wall, probably caused by exudate contained in the alveoli. In correspondence with the
most extended consolidations, a marked attenuation of echogenicity of the pleural line is
observed (Fig. 17) (Clip 11). Limited areas with several B Lines are also observed both sides.
Sometimes the atelectatic areas can be related to pleural effusions (Clips 12-13).
Clip 11 – Bronchiolitis: subpleural consolidation with marked attenuation of
echogenicity of the pleural line. Enhancement of the rear wall and presence
of B Lines.
Clip 12 – Bronchiolitis: parenchymal consolidation surrounded by compact
B Lines. Loculated pleural effusion.
Clip 13 – Bronchiolitis: left costophrenic angle scan that highlights atelectatic
triangular area of a few millimeters and minimum pleural effusion.
e clinical situation generally reveals the abnormalities detected by a lung ultrasound.
Recently Caiulo and coll. published a paper25 which confirms our observations and demon-
strates that ultrasound makes the execution of the chest radiograph useless.
Finally, not published observations by Basile and coll. report that, in early bronchiolitis,
pulmonary paravertebral areas are affected by the appearance of B Lines and small subpleural
consolidations.
Pleural and lung ultrasound in the neonatal period and in childhood 415
A C
Subpleural consolidation
Subpleural consolidation
B
with vertical compact artifacts
Subpleural consolidation
with vertical compact artifacts
Figure 17 – Bronchiolitis: small subpleural
consolidations, some of them with enhancement of
the posterior wall and compact B lines. (A, B, C)
➣ Pulmonary hemorrhage
e neonatal pulmonary hemorrhage (PH) is usually considered as a complication of other
neonatal lung diseases such as pneumonia, inhalation of meconium, HMD (after treatment
with surfactant)26, sepsis27, persistence of the ductus arteriosus
ous and prolonged hypoxia.
PH may occur in both preterm and born at term infants, prevailing in the latter26. It is often
the first striking symptom of a neonatal disease still evolving (sepsis is typical). Its onset is
acute with a characteristic emission of bright red blood from the upper respiratory tract or
with the issue of blood from the endotracheal tube (if the infant is intubated).
It may be a dramatic event with intense anemia, or simply a prolonged emission of frothy
bright red blood. Coagulation is usually not altered, even if some therapies (topical and
systemic) with coagulants have been employed
30-31
.
28-29
, severe and acute, or insidi-
416 oracic ultrasound
PH is a secondary cause of deficiency of endogenous surfactant and it can cause severe
respiratory failure32. e presence of alveolar blood leads to inactivation of endogenous
surfactant. erefore the treatment of PH is based not only on mechanical ventilation but
also on bronchoalveolar lavage and administration of exogenous surfactant33. is therapy
apparently contrasts with the association of pulmonary hemorrhage and exogenous surfactant
administration, that is limited to cases of HMD.
e radiological appearance of PH is not typical, as it is often confused with the underlying
lung disease. It shows diffuse, irregular, and sometimes unilateral consolidations, that can be
easily related to hemorrhage only because the clinics is obvious.
Lung ultrasound in pulmonary hemorrhage
In PH lung ultrasound is characteristic, especially for its dynamic and evolutive features.
In the early stages of PE only an extensive compact alveolar-interstitial syndrome with B
Lines may be evident. In the later stages, subpleural (first small and subsequently more large)
consolidations are detected. When the consolidations are larger, they are hypoanechoic, with
irregular and fragmented boundaries. Punctiform hyperechoic spots indicating air contained
in the bronchi are also detected. Consolidations are constantly surrounded by compact B
Lines (Fig. 18) (Clips 14-15).
Clip 14 – Pulmonary hemorrhage: extensive alveolar-interstitial syndrome.
Clip 15 – Pulmonary hemorrhage: triangular pulmonary consolidation of
considerable size in the context of an alveolar-interstitial syndrome.
Subpleural consolidation
Figure 18 – Pulmonary hemorrhage: initial phase. Presence of small subpleural consolidation. An
extensive alveolar-interstitial syndrome and hyperechoic spots are detected.
In a more advanced phase, extended pulmonary consolidations appear and the lung echogenicity becomes similar to that of the liver (lung hepatization). Large acoustic windows allow to
Pleural and lung ultrasound in the neonatal period and in childhood 417
detect bronchial fluid mixed with air within the bronchi as dynamic air bronchogram34. e
air moves into the bronchi synchronously to breaths with a typical movement of “coming
and going” (Clips 16-17). Whenever an extensive pulmonary hepatization exists, the presence of lung pulse is clearly evident. is sign has already been described as pathognomonic
of complete pulmonary atelectasis. It consists in the finding of pulsation of the pleural line
synchronous with the cardiac activity35 (Clip 18). In the context of extensive pulmonary
hepatization, color Doppler allows to easily highlight the pulmonary vessels (Clip 19). At this
point the presence of pleural effusion, detectable even in the fissures, is constant (Clips 20-21).
ese aspects can be bilateral or unilateral.
A very interesting finding seen in PE consolidations is that the air reaches the bronchi, but it is
not able to expand the lung because of the alveolar collapse due to the surfactant inactivation
(Clip 22). Lung inflation does not occur even at higher pressures or volumes. erefore, in
PH the lung hepatization does not depend on airway obstruction, as in the case of obstructive
atelectasis, but on alveolar collapse that is not recruitable.
In our experience, treatment with surfactant leads to a regression of the echographic condition in less than 24 hours (Clips 23-26).
Clips 16, 17 – Pulmonary hemorrhage: lung hepatization with dynamic
air bronchograms.
Clip 18 – Pulmonary hemorrhage: extensive lung hepatization with lung
pulse.
Clip 19 – Pulmonary hemorrhage: visualization of the pulmonary vessels
with color Doppler in the context of lung hepatization.
Clip 20 – Pulmonary hemorrhage: longitudinal scan of the right lung: in the
second intercostal space, on the left of the clip, the fissure between the middle
and lower lobe occupied by liquid is evident. An extensive hepatization of
the two lobes is observed.
Clip 21 – Pulmonary hemorrhage: longitudinal scan at the base of the left
lung: pleural effusion in the costophrenic angle in which the collapsed lung
is floating.
418 oracic ultrasound
Clips 22, 23 – Pulmonary hemorrhage: longitudinal scan. The lung is
completely hepatized. Synchronously to the movements of the respirator, the
air fills the bronchi in the absence of expansion of the lung parenchyma due
to alveolar collapse. Evidence of lung pulse.
Clips 24 – Pulmonary hemorrhage: longitudinal scan of the right lung after
18 hours. An extensive alveolar-interstitial syndrome remains, but alveolar
collapse and pleural effusion have regressed (compared with Clip 16).
Clip 25 – Pulmonary hemorrhage: longitudinal scan at the base of the
left lung after 18 hours. No more evident pleural effusion (compared with
Clip 17). Re-expansion of the lung with alveolar-interstitial syndrome.
Clip 26 – Pulmonary hemorrhage: after 36 hours clear regression of the
alveolar-interstitial syndrome.
➣ Meconium aspiration syndrome (MAS)
Meconium is the first substance eliminated from the gastrointestinal tract in the perinatal
36-37
period
secretions (bile salts, pancreatic and liver enzymes), solids (vernix, lanugo, squamous cells),
blood, minerals and lipids (fatty acids).
e passage of meconium in the amniotic fluid is a physiological event, but in many situations it may occur in response to fetal hypoxemia and acidosis. It probably requires nerve
stimulation of a mature gastrointestinal tract. In fact, this event does not occur when intestinal
peristalsis and anal sphincter relaxation are absent. is may explain why it is very rare to
find meconium in the amniotic fluid before 34 weeks of gestation.
MAS almost always concerns infants born at term and post-term, and it occurs when the
baby inhales meconium contained in the amniotic fluid. In addition to airway obstruction,
meconium aspiration involves an inflammatory response of the lung resulting in chemical
pneumonitis. It is still not completely clear which components of meconium stimulate the
inflammatory response, but bile and liver enzymes are considered among the responsible
agents. Finally, the meconium may determine the inactivation of surfactant.
Meconium pneumonitis determines the appearance of pulmonary infiltrates on chest radiography. Mortality and morbidity are high: about 5% of babies require oxygen therapy up
to one month of life, and there is a high incidence of respiratory infections. In the neonatal
period the mortality rate is around 3-5% and increases to 20% when pulmonary involvement
is severe with pulmonary hypertension. Other acute complications are represented by pneumomediastinum, pneumothorax, pneumopericardium, interstitial emphysema, pulmonary
hemorrhage and pulmonary hypertension.
. It is a sterile mixture of water (75-95%), mucopolysaccharides, gastrointestinal
Pleural and lung ultrasound in the neonatal period and in childhood 419
In MAS meconium does not always reach the alveoli. ree classes of alveoli have been
described:
• Unventilated alveoli due to complete obstruction (atelectatic);
• Alveoli downstream of partially obstructed bronchi;
• Alveoli downstream of open bronchi.
It is believed that the alveoli with partially obstructed bronchi trap the air. During inspiration
the alveoli expand, but the air can not be exhaled in expiration for the bronchial diameter
reduction. e ventilation of these infants is extremely critical for the barotraumatic risk
related to hyperinflated distal airways.
MAS is suspected in newborns with respiratory distress, whenever the amniotic fluid is
meconium-stained at birth. e differential diagnosis considers transient tachypnea of the
newborn, neonatal pneumonia and HMD.
Chest radiograph is considered the best imaging technique for detecting MAS. Hyperinflation
with inhomogeneous lung opacity is typically evident. ese findings are due to the presence
of mixed atelectatic and hyperinflated areas.
Chest x-ray may highlight the presence of pneumomediastinum, pneumopericardium, interstitial emphysema and pneumothorax. Sometimes there is pleural effusion. Often the radiological appearance of MAS is quite comparable to severe transient tachypnea of the newborn.
Lung ultrasound in the meconium aspiration syndrome
Ultrasound experience in MAS is very limited. Our data show that lung ultrasound diagnostic
power is dependent on the severity of the syndrome. In the early stages, however, an interstitial
syndrome is always evident. It may be followed by more or less voluminous consolidations
and an important involvement of the pleural line (Fig. 19) (Clips 27A-29A).
Figure 19 – Meconium aspiration: localized interstitial syndrome.
Clips 27A, 28A, 29A – Meconium aspiration: ultrasound shows a severe
interstitial syndrome with subpleural consolidations.
In one case the interstitial syndrome was limited to the right upper lobe where the chest X-ray
showed a pulmonary infiltrate (Fig. 20).
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