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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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250 oracic ultrasound
Table 3 – Distinctive characteristics between bilateral and monolateral diaphragmatic paralysis
Clinical features Bilateral paralysis Monolateral paralysis
Hystory Neuromuscular disease,
prolonged mechanical
ventilation, critical illness,
neck injury
Symptoms Unexplained dyspnea,
dyspnea at rest, dyspnea
when bending, dyspnea in
supine position, dyspnea
when entering water,
respiratory failure.
Inspection Abdominal paradox No abdominal paradox
Vital capacity (%of predicted value) < 50 > 70
Decline in supine vital capacity 30-50% 10-30%
Complications Hypoventilation during sleep,
atelectasis, pneumonia,
respiratory failure.
Diaphragmatic motion bilaterally absent controlateral
Inspiratory diaphragmatic thickening bilaterally absent controlateral
Neck and shoulder pain,
trauma, chest or neck
surgery, mediastinal
symptoms or pathology
No symptom, unexplained
mild dyspnea, exercise
dyspnea
Supradiaphragmatic
hypoventilation
Diaphragmatic hernias
Hiatus hernia is a disease in which the stomach is displaced into the thorax through a defect
or weakness of the esophageal hiatus within the diaphragm. e use of ultrasound for diagnosing hiatus hernias is rarely described in literature and is uncommon. A widening of the
alimentary tract at the diaphragmatic iatus greater than 16 mm and the non visualization of
gastro-esophageal junction have a 100% positive predictive value for sliding hiatus hernia
(Fig. 9). ere exist no reports of paraesophageal hiatus hernia in literature
1,17
.
Congenital diaphragmatic hernias are complex and often life threatening lesions, frequently
associated with additional anatomic malformations and genetic anomalies18. e commonest
(70%) hernia involves the posterolateral diaphragm (Bochdalek hernia). Morgagni hernia
(25-30%) is located in the anterior diaphragm. A hernia rarely involves the central diaphragmatic region (2-5%). Ultrasound has been the mainstay of prenatal diagnosis of Bochdalek
hernia for many years and its sensitivity is up to 87%, according the gestational age (the
sensitivity improves beyond 18 weeks)19. e sonographic features of a left Bochdalek hernia
are the intrathoracic position of the stomach, left lobe of the liver and bowel loops with a
right mediastinal shift. e fetal lung is displaced but it is sonographically similar to the liver
and difficult to distinguish from it. e position of the gallbladder is a useful landmark. In
the postnatal period, sonography with Color Doppler is helpful in detecting stomach, liver,
portal vein and small bowel inside the thorax. Atelectatic lung and displaced heart may be
discovered20.
Unlike posterolateral hernias, Morgagni hernia often has a well defined hernia sac located
in the low anterior mediastinum, containing omentum, bowel loops, liver and spleen. e
majority of Morgagni hernias are present in older children and adults as incidental findings21.
Pathology of the diaphragm 251
Figure 9 – The distal segment of the esophagus in longitudinal scan through the left liver lobe. The
diameter is within the limits and the esophagogastric junction (arrow) is well below the diaphragmatic
hiatus.
Eventration
Diaphragmatic eventration is characterized by defective diaphragmatic muscularisation. It
is a focal cephalic displacement of one leaf of the intact diaphragm as a result of paralysis,
aplasia or muscular atrophy. In the area of eventration, the normal muscle fibers are replaced
by a thin layer of connective tissue22. e differential diagnosis between congenital hernias
and eventration is difficult because the displaced diaphragm is very thin. Eventration is often
associated with pleural and pericardial effusions.
Diaphragmatic dysfunctions
Diaphragmatic dysfunctions are diseases that mainly determine functional alterations of the
organ, which maintains its anatomical integrity. e morphological changes of the diaphragmatic dysfunctions are represented by atrophy or by abnormalities of position and movement
of the hemi-diaphragms. All neuromuscular diseases that affect the diaphragm are included in
this chapter
8,14
. ese diseases are highly interesting because the sonographer can take advantage
of some essential characteristics of ultrasound, such as dynamic assessment and repeatability.
Diaphragmatic dysfunctions may be primary (with neuromuscular origin) or secondary to
contiguous or systemic, unilateral or bilateral diseases
23,24
.
252 oracic ultrasound
Table 1 illustrates the main causes of diaphragmatic dysfunction. In addition to neuromuscular diseases, in which the diaphragm is involved as a primary aspect of the pathology, many
clinical situations alter the function of this muscle. ese conditions concern high percentage
of critically ill patients, and intensive care25.
Critical Care polyneuropathy and myopathy are frequent causes of diaphragmatic dysfunction
and ventilatory dependency in the intensive care26. Diaphragmatic weakness and atrophy is
a precocious event (after 2-3 days) during mechanical ventilation27. Paralyzing agents act as
cofactors of muscle dysfunction. Metabolic, endocrine and electrolytic abnormalities, malnutrition and sepsis can contribute to diaphragmatic dysfunction prolonging the ventilator
dependency in a vicious cycle. Finally, the association of diaphragmatic weakness and any process increasing the work of breathing (pneumonia, atelectasis, edema, ARDS, bronchospasm,
hyperinflation), can overwhelm the patient’s physiologic reserve, contributing to prolonged
mechanical ventilation
8,14,25
.
Diaphragmatic paralysis
Sonography is a useful alternative method for detecting diaphragmatic paralysis and for
repeated or prolonged examinations of the patient.
B-Mode images and M-Mode trace of a paralyzed hemidiaphragm show the absence of movements or a paradoxical motion
1,12,28
(Fig. 10).
Figure 10 – Right hemidiaphragm paralysis (A and B). The maximum inspiratory effort causes only a
minimal displacement (B). Normal side images. (Courtesy of Dr. Americo Testa. S. Maria delle Grazie
Hospital, Velletri, Rome)
is is the passive cranial motion of the diaphragm during inspiration, by the negative pressure generated by the other respiratory muscles. In diaphragmatic paralysis, the inspiratory
thickening of the muscle is absent and the area of apposition to the rib cage of the diaphragm
Pathology of the diaphragm 253
is long and fixed. Diaphragmatic thickness at Functional Residual Capacity (FRC) of < 2 mm
combined with < 20% increase in thickness during inspiration can provide discrimination
between paralyzed and normal diaphragm. When the paralysis is long lasting the diaphragm
is atrophic and its thickness is reduced to 1 mm
1,29
. Pulmonary base is high and subdiaphragmatic organs may be displaced cranially. Finally, pulmonary lower lobes often shows findings
of sonographic interstitial syndrome, or marginal atelectasia, caused by lung compression.
Diaphragmatic weakness
During the inspiratory effort, in patients with diaphragmatic weakness, a reduced diaphragmatic caudal movement is observed (Fig. 11).
Figure 11 – Above, subject with amyotrophic lateral sclerosis. Evident weakness of the diaphragm with
minimum inspiratory excursions. Below, subject with diaphragmatic weakness. Maximum breathings
cause a diaphragmatic movement comparable with quiet breathing. (Courtesy of Dr. Americo Testa.
S. Maria delle Grazie Hospital, Velletri, Rome)
e evaluation of the diaphragmatic thickness is informative, because a value less than 2 mm
of the muscle in the apposition zone is indicative of serious damage with atrophy1 (Fig. 12).
A dynamic estimation of diaphragmatic function can be made by calculating the inspiratory
diaphragmatic thickening (%)
29,30,31
according to the formula:
∆dt =(dtT LC − dt F RC)/dt T LC × 100
Where ∆dt is the change of diaphragmatic thickness, dt TLC is diaphragm thickness at total
lung capacity and dt FRC is diaphragm thickness at functional residual capacity.
254 oracic ultrasound
Figure 12 – In the subject with diaphragmatic weakness the diaphragmatic thickness is less than 2 mm
and the muscle shows a reduced inspiratory thickening (B).
All patients with a paralyzed diaphragm show less than 20% thickening of the diaphragm at
total lung capacity. e assessment of the fractional diaphragmatic thickening during inspiration is a useful tool for monitoring diaphragmatic dysfunctions in many settings, and for
estimating subsequent recovery31.
Ultrasound guided weaning procedures and
diaphragm ultrasound in ICU
Recent applications of sonography concern patients during partial or total ventilatory support.
An important feature of the movement of the diaphragm in M-Mode is its correspondence
with the trace of the pressure variations detected by an intra-esophageal catheter. During
inhalation, the lowering of the diaphragmatic dome detected in ultrasound, corresponds to
the lowering of intraesophageal pressure. erefore, it is possible to demonstrate ultrasonographically and noninvasively the beginning and the end of the respiratory effort of a patient,
which is useful for the evaluation of his interaction with the ventilator25.
About 20% to 30% of patients are difficult to wean from invasive mechanical ventilation32.
Weaning failure is defined as the failure to pass a spontaneous-breathing trial or the need for
reintubation within 48 hours following extubation. Weaning the patient from the ventilator
requires a careful evaluation of the relationship between lung function load and ventilatory
capacity of the patient
33,34
. For example, a ventilatory capacity sufficient for a patient with
normal lung parenchyma may be insufficient to wean a patient with residual non-cardiogenic
or cardiogenic pulmonary edema. Ultrasound allows not only a morphofunctional estimate
of the biggest respiration muscle, but also a rapid bedside assessment of pleural structures,
parenchymal acoustics (interstitial syndrome), presence of pulmonary consolidations and
cardiac function (Tab. 4). We believe that even in this context, the full integration of the
potential of ultrasound may have a high predictive value for weaning a patient from mechanical ventilation.
Recognition of the pulmonary, cardiac or mixed origin of weaning failure is a fundamental
issue for successful discontinuation of mechanical ventilation.
Interstitial pattern at lung sonography showed 69% sensitivity but low specificity for diagnosing weaning failure, whereas an ultrasound pattern consistent with increase extravascular lung
water, associated with left ventricular diastolic failure, probably represents a more complete
index35.
Pathology of the diaphragm 255
Table 4 – Factors impacting on the ability to wean a patient from mechanical ventilation
Factors impacting with weaning Etiology
Respiratory load Increased work of breathing, wrong
ventilatory settings, elevated intra-abdominal
pressure, pneumonia, cardiogenic edema,
ARDS, pulmonary hemorrhage, diffuse
interstitial diseases, increased resistive load,
bronchoconstriction, airway secretions, glottic
edema, central airways problems.
Cardiac load Cardiac pathology, sepsis, pulmonary embolism,
pericardial disease, dynamic hyperinflation,
increased metabolic demand.
Metabolic Metabolic disturbances, acid base and
electrolytic disturbances, hyperglycaemia.
Neuromuscular Mechanical ventilation, metabolic alkalosis,
medications, depressed central drive, paralyzing
agents.
Miscellaneous Anemia, malnutrition, overweight,
corticosteroid, ventilator induced diaphragm
dysfunction, delirium, anxiety, depression.
Modified from: Boles JM, Bion J, Connors A, Herridge M, Marsh B, Melot C, Pearl R, Silverman H, Stanchina
M, Vieillard Baron A, Welte T. Weaning from mechanical ventilation.
Eur Respir J
2007;29:1033-1056.
However, in our opinion
36,37
, diffuse, bilateral symmetrical interstitial syndrome is a general
feature of increased lung density (or decreased lung aeration), and not a specific sign of increased extravascular lung water. erefore, lung ultrasound could be an accurate predictor of
postextubation distress by detecting a high lung aeration defect immediately before weaning
and/or by evidencing significant lung derecruitment during the spontaneous breathing test.
In this setting lung ultrasound perfectly complements diaphragmatic and cardiac ultrasound
in a comprehensive approach.
Lung and cardiac ultrasound addressing for spontaneous breathing test (SBT) failure and
post-extubation distress was assessed by Soummer et al38.
Four ultrasound aeration patterns have been defined (Fig. 13): 1) normal aeration: presence
of lung sliding with A lines or fewer than two isolated B lines; 2) moderate loss of lung aeration: multiple, well-defined B lines; 3) severe loss of lung aeration: multiple coalescent B
lines and 4) lung consolidation, the presence of a tissue pattern characterized by dynamic air
bronchograms. Basal LUS score was similar in patients with SBT success and SBT failure.
Loss of lung aeration during successful SBT was observed only in patients affected by postextubation distress. Bedside lung ultrasound provided critical information about aeration
during and at end of the trial, and such information were highly relevant for predicting
respiratory complications.
Diaphragm sonography is an important monitoring tool for weaning the patient from mechanical ventilation. Patients with adequate spontaneous tidal volume but low diaphragmatic
excursion failed a breathing trial compared to patients with adequate tidal volume and normal
256 oracic ultrasound
diaphragmatic movements
39,40
. Probably the first type of patients can maintain adequate
volumes recruiting accessory muscles, while the latter use their diaphragm in a coordinated
manner. According to Kim et al.40 a vertical excursion of the diaphragm less than 1 cm or
paradoxical movement of the diaphragm are indicators of dysfunction and of a prolonged
time of weaning from the ventilator.
Figure 13 – Ventilatory patterns. A: Mirroring with good ventilation. B: Presence of B lines. C: White
lung before consolidation. D: Consolidation.
An alternative approach to the function of the diaphragm, which is useful to determine the
timing of weaning, is the measurement of the thickness of the diaphragm in the zone of apposition to the rib cage, and especially its fraction of inspiratory thickening. A diaphragm
thickness less than 2 mm is a feature of muscle atrophy. Diaphragm thickening during inspiration reflects diaphragm shortening and is analogous to an ‘ejection fraction’ of the heart.
According to recent studies, the combined sensitivity and specificity of ∆tdi% ≥ 30-36% for
extubation success is 82-88% and 71-88%, respectively. e positive predictive value and
negative predictive value are 91-92% and 63-75%, respectively41.
Diaphragmatic dysfunction after surgery
Upper abdominal and thoracic surgery have adverse effects on the respiratory system, such
as pain, restrictive physiology, increased work of breathing, airway problems and pulmonary
and diaphragmatic dysfunctions (Fig. 14). ese effects increase the risk of postoperative
pulmonary complications and respiratory failure. Diaphragmatic dysfunction is a major factor in the etiology of postoperative pulmonary complications.
In a study of Lerolle et al.42, ultrasonographic-based determination of hemidiaphragm excursions in patients requiring prolonged mechanical ventilation after cardiac surgery identified
those with and without severe diaphragmatic dysfunction as defined by the Gilbert index. e
Pathology of the diaphragm 257
greatest hemidiaphragmatic excursion during maximal inspiratory effort was lower in patients
with diaphragmatic dysfunction. A diaphragmatic excursion < 25 mm had a positive likelihood ratio of 6.7 and a negative likelihood ratio of 0 for having a pathologic Gilbert index.
Figure 14 – Patients after abdominal surgery. Diaphragmatic weakness. A: small respiratory excursions
of the muscle in M-Mode. B: quiet breathing with low value of the diaphragmatic excursion in M-Mode.
There is pleural effusion. Ascending subcostal scans. C: Two-dimensional representation of inadequate
diaphragmatic excursion in the presence of pleural effusion. The lack of inspiratory openness of the
costophrenic angle is evident. Semi-coronali intercostal scans. D: an open costophrenic angle.
In a recent prospective observational study performed in 35 patients undergoing open liver
lobectomy43, diaphragmatic movements were assessed by right intercostal M-mode sonography after a pulmonary function test on preoperatively and on postoperative days. After liver
lobectomy, diaphragmatic inspiratory amplitude during deep breathing and vital capacity
showed significant reductions of 60% from their preoperative values. Sonography showed
a linear correlation with vital capacity measured by spirometry. e best cutoff values of
diaphragmatic inspiratory amplitude for detecting 30% and 50% decreases of VC from
preoperative values were 3.61 and 2.41 cm, with sensitivity of 94% and 81% and specificity
of 76% and 91%, respectively. e Authors concluded that M-mode sonographic technique
at the bedside represents a practical way to investigate postoperative diaphragmatic dysfunction44, and may also be an effective bedside screening method for diaphragmatic paralysis.
Diaphragm and COPD
Chronic obstructive pulmonary disease (COPD) is characterized by increased resistance to
air flow, air trapping and lung hyperinflation. As lung volume increases, the diaphragm is
passively shortened and placed at a mechanical disadvantage by altered length-tension relationships. For this reason, patients with COPD may have a lower transdiaphragmatic pressure
generating capacity than healthy subjects
45,46
.
258 oracic ultrasound
Muscle strength is regarded as a limiting factor in diaphragm performance in patients with
COPD. However, chronic exposure to lung hyperinflation may result in physiological adaptations to preserve inspiratory muscle strength and perhaps obviate the development of
diaphragmatic fatigue
47,48
.
Conventionally, lung hyperinflation is said to exist when the total lung capacity (TLC) is
>120% of the predicted value.
oracic hyperinflation
13,49,50
in patients with COPD can be detected by physical examination.
Recognized clinical features of severe hyperinflation include the inward motion of the lower
lateral ribcage during inspiration, and paradoxical inward motion of the anterior abdominal
wall in synchrony with inspiratory flow.
Chest radiography represents the initial imaging tool for assessing COPD. Common findings
of hyperinflation are a widened retrosternal space, attenuation of the pulmonary branching
pattern, focal pulmonary lucencies and flattening of the domes of the hemidiaphragms.
Although chest X-ray is useful for the exclusion of other diagnosis such as pneumonia, cancer, congestive heart failure, pleural effusion, and pneumothorax, it is neither sensitive nor
specific for diagnosing COPD.
Radiological evaluation of diaphragm mobility has traditionally been performed through
fluoroscopy, but several methods have been used to quantify the diaphragmatic mobility using
chest radiographs, computed tomography scan, and dynamic magnetic resonance imaging.
Despite mixed results in the literature, it is generally believed that in subjects with COPD,
the diaphragm becomes flatter and shorter
51,52,53
(28-40% shorter than normal). Some studies
have also documented a reduction in the area and weight of the diaphragm, correlated with the
degree of emphysema, while the thickness of the muscle was normal, increased or decreased13.
Ultrasonography has many advantages over fluoroscopy, including lack of risk from ionizing
radiation, equipment portability, and direct quantitative information.
Flattening, motion, inspiratory and expiratory time of the diaphragm may be evaluated by
subcostal or semicoronal intercostal sonography, by M-Mode or B-Mode imaging54. In our
practice we prefer the subcostal approach to determine the coronal movements and to estimate
the position of the hemi-diaphragms (see Chapter 4) (Fig. 15).
Movements and thickness of the diaphragm can be measured with a linear ultrasound probe
in the zone of apposition of the muscle against the chest wall (see Chapter 4). e costal
origin of the diaphragm is identified when the subject breaths to total lung capacity (TLC)
(Fig. 16), where the length of the zone of apposition approaches zero with active inspiration.
e distance between the costal origin of the diaphragm and the point where the diaphragm
peels away from the chest wall gives the length of the zone of apposition at any lung volume.
Finally, at any lung volume, the thickness of the muscle is easily measured.
A reduction in diaphragm mobility has been identified in patients with chronic obstructive
pulmonary disease (COPD) and has been associated with a decline in pulmonary function
parameters
45,55
. In addition, some result show that reduced diaphragmatic mobility is associated with hypercapnia56, airway obstruction and pulmonary hyperinflation. e main cause
of the reduction in diaphragmatic mobility is the shortening of the apposition zone resulting
from the absence of the piston-like movement of the diaphragm. erefore, a strong relation between the reduction in diaphragm mobility and length of the apposition zone of the
diaphragm exists.
Recent studies have demonstrated that reduction in diaphragm mobility correlates with airway
obstruction, pulmonary hyperinflation and ventilator capacity. In particular, COPD patients
Pathology of the diaphragm 259
Figure 15 – A: dyspneic patient with radiographic doubt. The ultrasound shows a basal posterolateral
loculated effusion. B: diaphragmatic failure in M-Mode. Quiet breathing with diaphragmatic excursion
of about 1 cm. C: B Mode images of the diaphragmatic apposition zone to the right wall. During
maximum inspiration the insufficient muscle contraction is evident, with non-opening of the costophrenic
angle for adhesions.
Lung curtain
Length of apposition zone
Liver
Figure 16 – During normal maximum inspiration there is maximum reduction of the apposition zone
of the diaphragm to the wall.
had less ultrasound detected diaphragm mobility than did healthy subjects, mainly due to air
trapping and not influenced by respiratory muscle strength
57,58
.
Diaphragm motion in forced expiration can be analyzed using M-Mode ultrasound in an
anterior subcostal approach. Maximum expiratory diaphragmatic excursion and forced
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