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Lung assessment 

Lung assessment
Chapter:
Lung assessment
Author(s):

Andrew Walden

DOI:
10.1093/med/9780198749080.003.0016
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date: 06 December 2021

Introduction

This chapter describes the US appearances of common pathology involving the lung parenchyma. The features of consolidation and atelectasis are described and differentiated. The alveolar-interstitial syndrome is outlined, and the US characteristics that allow ARDS and cardiogenic pulmonary oedema (CPO) to be differentiated are listed. The advanced section describes the use of US to assess diaphragmatic function.

Limitations of clinical assessment of the lung

Clinical assessment of the lung parenchyma in critically ill patients is notoriously difficult. Patients are typically managed semi-recumbent and cannot be sat forward or make large inspiratory efforts to command, rendering the standard system of respiratory examination near impossible. Similarly, chest X-ray has been shown to be insensitive when trying to determine the causes of acute respiratory failure and even worse than clinical examination alone. This is problematic, given the incidence of respiratory problems in the critically ill. Undoubtedly, the reference imaging standard is CT. However, this requires the transfer of unwell patients and is associated with significant costs and morbidity and cannot be repeated too frequently due to significant exposure to ionizing radiation.

Historically, it was felt US was of no value in the assessment of lung parenchyma due to the low acoustic impedance of air. However, as the lung becomes diseased, the changes in acoustics lead to characteristic appearances. Indeed US has demonstrated excellent diagnostic accuracy in determining the causes of respiratory failure both in patients within the emergency department as well as those within ICU on mechanical ventilation. With the increasing availability of smaller and more powerful machines, LUS is becoming the primary tool in the assessment of respiratory failure in this patient group. LUS has distinct advantages over other imaging modalities in that it can be performed rapidly at the bedside and be repeated frequently without any risk of ionizing radiation exposure.

Ultrasound of the lung parenchyma

While US cannot replace CT (and, in rare cases, histology), it has high sensitivity and specificity at recognizing common causes of acute respiratory failure. These can be categorized according to their ultrasonographic appearances into alveolar conditions (lung consolidation and atelectasis) and alveolar-interstitial conditions such as ARDS, pulmonary oedema, and interstitial pneumonia (Table 16.1).

Table 16.1 Ultrasound classification of pulmonary pathology

Condition

Examples

Alveolar

Pneumonic consolidation

Atelectasis

Alveolar-interstitial

Acute respiratory distress syndrome

Cardiogenic pulmonary oedema

Atypical pneumonia

Predominantly interstitial

Inflammatory pneumonia

Lymphangitis carcinomatosis

Healthy lung has high air content and very low acoustic impedance, which results in 99% of US waves being reflected, preventing any useful US imaging below the pleural line. In disease, elements of the lung parenchyma may change their fluid and air content, allowing either direct visualization of structures with high water content or the creation of characteristic artefacts such as B-lines and lung rockets due to increases in the fluid content of subpleural structures. These changes are now well described and have been validated against CT scanning, demonstrating excellent diagnostic accuracy. This can help both in terms of understanding the underlying diagnosis as well as identifying new problems that develop as part of the patient’s stay on ICU.

Alveolar conditions

Alveolar conditions are those where the content of air within the lungs changes, such that it is possible to directly visualize parts of the lung with US. The main two clinical entities responsible for this pattern are pneumonic consolidation and atelectasis. The differentiation of these two conditions can be difficult. This section will try to explain the common findings in each condition and then will consider how best to differentiate the two conditions.

Consolidation

LUS is very useful at identifying consolidation. Ninety-eight per cent of lung consolidation abuts the pleura, and the pathological changes in the air/fluid content of the lung result in characteristic features. Where the consolidation is translobar, the lung develops a solid tissue-like pattern whereby it takes on the appearance of the liver. This is also called ‘hepatization’ as a pure descriptive term (Figure 16.1).


Figure 16.1 Consolidated lung: hepatization.

Figure 16.1 Consolidated lung: hepatization.

Where consolidation is not translobar, the lung develops the ‘shred’ sign. This is another descriptive term characterizing the loss of normal lung pattern at the pleural line. There is an irregular border of normally aerated lung and consolidated lung which has a higher fluid content. There are often comet tail artefacts emanating from the irregular border of the consolidated lung (Figure 16.2).


Figure 16.2 Shred sign of consolidated lung.

Figure 16.2 Shred sign of consolidated lung.

In both translobar and non-translobar consolidation, air/fluid bronchograms may be identified (Figure 16.3). However, these are also features that may be found in atelectatic lung. Indeed, distinguishing translobar consolidation from atelectasis may be one of the limitations of LUS.


Figure 16.3 Air bronchogram in consolidated lung.

Figure 16.3 Air bronchogram in consolidated lung.

Atelectasis

Lung collapse in critically ill patients is often multifactorial. Patients on positive pressure ventilation can suffer from derecruitment as a consequence of inadequate doses of PEEP or following disconnection from the mechanical ventilator. In addition, inspissation of secretions can lead to airway blockage, leading to atelectasis, as can inadvertent one-lung intubation and ventilation. Another consideration in longer-term critically ill patients is the development of large-volume pleural effusions, which is common (Chapter 15).

The predominant aetiology may often lead to more characteristic patterns of lung collapse. In the situation where pleural effusion is the main reason for collapse, the lung collapses to a point with smooth edges and becomes a sylph-like structure (Figure 16.4 and Video 1.12.1 Lung assessment). This has previously been described as the ‘jellyfish’ sign.


Figure 16.4 ‘Jellyfish sign’: atelectatic lung in pleural effusion.

Figure 16.4 ‘Jellyfish sign’: atelectatic lung in pleural effusion.

Where collapse occurs mainly due to derecruitment or secretion retention, the lung can often take on a picture similar to consolidation with the presence of air bronchograms and a lung which becomes similar in homogeneity to the underlying liver or spleen. There can still be pleural effusion present, but often not to the same degree. The differentiation can be difficult.

A fairly unique situation occurs following endotracheal intubation when the endotracheal tube is inserted in the right main bronchus. Due to the sudden lack of ventilation in the left lung, there are none of the features of volume loss or altered homogeneity described previously. However, there will be absence of pleural sliding due to a lack of ventilation, with the presence of the lung pulse to the pleural line as cardiac pulsations are transmitted through the motionless lung (Video 1.12.2 Lung assessment).

Differentiating atelectasis from consolidation

Table 16.2 summarizes the features that distinguish consolidation from atelectasis. One pathognomonic sign of consolidation is the dynamic air/fluid bronchogram (Video 1.12.3 Lung assessment). In a portion of consolidated lung when there is free movement of air and fluid, it is possible to see a shifting pattern of air and fluid moving during the respiratory cycle. In atelectatic lung which is obstructed or derecruited, this movement of air and fluid does not occur. The dynamic air bronchogram has a very high positive predictive value for consolidation, but a poor negative predictive value.

Table 16.2 Ultrasound features of consolidation and atelectasis

Consolidation

Atelectasis

Tissular pattern

Yes

Yes

Shred sign

Yes

No

Air bronchograms

Yes

Yes

Fluid bronchograms

Yes

Rare

Dynamic bronchograms

Yes

No

Pleural sliding

Diminished

Greatly diminished

Lung pulse

Present but diminished

With absent pleural sliding highly likely

Pleural effusion

Evidence of septation

Free-flowing effusion

Other—dynamic effect of recruitment

Little change with recruitment

Increased size and aeration with recruitment

In contrast, atelectatic lung will increase in size during a recruitment manoeuvre and will lose its tissular pattern as aeration increases, often taking on the appearance of normal lung, but with multiple lung rockets or B-lines.

Alveolar-interstitial conditions

The alveolar-interstitial syndrome describes a group of conditions where both the alveolar tissues and the interstitium are involved and may be broadly categorized into those conditions that mainly affect the alveoli, such as ARDS or CPO, and those that predominantly affect the interstitium such as interstitial pneumonia or lymphangitis carcinomatosis. The common US finding that links all these conditions is the presence of B-lines (Figure 16.5).


Figure 16.5 B-lines: arising from the pleural line. Multiple B-lines may be termed lung rockets.

Figure 16.5 B-lines: arising from the pleural line. Multiple B-lines may be termed lung rockets.

The mechanism of B-line artefacts is key to understanding the pathophysiology of alveolar-interstitial conditions. The usual US pattern of the lung in health is regularly spaced A-lines, a normal reverberation artefact (Figure 16.6). When the US beam reaches the normal pleura/air interface, the marked change in acoustic impedance results in most of the US waves being reflected to the probe, which is processed to show the presence of the pleural line. However, some of the returning beam is reflected back from the probe to the pleural line where the same change in acoustic impedance leads to further reflection back to the probe, resulting in the generation of a second deeper, but artefactual, pleural line. This process of reverberation between the US probe and the pleural line may be repeated a number of times, resulting in the generation of multiple regularly spaced A-lines (Figure 16.7).


Figure 16.6 A-lines: repeating horizontal lines that are the same distance apart and are reverberations of the pleural line.

Figure 16.6 A-lines: repeating horizontal lines that are the same distance apart and are reverberations of the pleural line.


Figure 16.7 Mechanisms of A- and B-line artefacts.

Figure 16.7 Mechanisms of A- and B-line artefacts.

Reprinted from The American Journal of Cardiology, 93, 10, Jamrik et al., ‘Usefulness of ultrasound lung comets as a non radiological sign of extravascular lung water’, pp. 1265–1270. Figure 7. Copyright © 2004 Excerpta Medica Inc. All rights reserved., with permission from Elsevier.

In alveolar-interstitial disorders, subpleural structures become thickened and engorged. This leads to a change in the acoustic impedance of these structures, such that the US beam is repeatedly reflected within them, and each time a signal is sent back to the probe, a small line is generated. This leads to multiple small lines concertinaed on top of each other, which gives the sense of a line emanating from the pleural line to the edge of the screen (Figure 16.7).

The distance between each B-line may represent the underlying pathophysiology. Ultrastructurally, subpleural lymphatics are much more closely aligned, such that conditions that tend to cause predominantly lymphatic engorgement, such as pulmonary oedema, lead to a spacing much closer together than in conditions such as pulmonary fibrosis which predominantly affects the septa. Indeed case series have shown that where the spacing of B-lines is <3 mm, the aetiology is likely to be due to high levels of extravascular lung water, such as ARDS or pulmonary oedema (Figure 16.8 and Video 1.12.4 Lung assessment), whereas a spacing of >7 mm would favour pulmonary fibrosis or an inflammatory pneumonia (Figure 16.9 and Video 1.12.5 Lung assessment).


Figure 16.8 Confluent B-lines in pulmonary oedema.

Figure 16.8 Confluent B-lines in pulmonary oedema.


Figure 16.9 Interstitial pattern B-lines.

Figure 16.9 Interstitial pattern B-lines.

B-lines are frequently observed in ICU patients, usually as a consequence of pulmonary oedema, with the number seen in each rib space examined correlating with measurements of extravascular lung water. US assessment has been shown to be more sensitive than chest radiography in identifying pulmonary oedema. Furthermore, B-lines will appear and disappear in a time frame that closely matches the course of pulmonary oedema and can be used to monitor therapy. It has been proposed that LUS can be used to monitor fluid resuscitation, with the appearance of B-lines during resuscitation as a sign of adequate fluid filling.

Not all B-lines are pathological. A few B-lines may be visible in the dependent regions of normal lungs, while B-lines in the non-dependent anterior regions are nearly always significant.

Differentiating acute respiratory distress syndrome from cardiogenic pulmonary oedema

ARDS and CPO are two of the more common conditions encountered in critically ill patients. They are both characterized by generalized increases in extravascular lung water. Both therefore lead to bilateral B-line patterns on US examination. Table 16.3 summarizes the differences that may help to distinguish ARDS and CPO.

Table 16.3 Ultrasound features of acute respiratory distress syndrome (ARDS) and cardiogenic pulmonary oedema (CPO)

ARDS

CPO

Bilateral B-lines

Yes

Yes

Homogenous B-lines

No

Yes

Subpleural irregularities

Yes

No

Reduced B-line in response to diuresis

No

Yes

Higher density posteriorly

Variable

Always

Pleural sliding

Diminished

Greatly diminished

Lung pulse

Present but diminished

With absent pleural sliding highly likely

Pleural effusion

Evidence of septation

Free-flowing effusion

Other—dynamic effect of recruitment

Little change with recruitment

Increased size and aeration with recruitment

Advanced ultrasonography

Ultrasound assessment of diaphragmatic function

The diaphragm is the most important muscle for respiration, and its function can be impaired during critical illness. Trauma, post-operative damage, specific neuromuscular conditions, and atrophy from prolonged periods of misuse can all impair diaphragmatic function and result in prolonged weaning from mechanical ventilation and increased ICU length of stay. Fluoroscopy, CT scanning, MRI, transdiaphragmatic pressure measurements, and electromyography (EMG) have all been used to determine diaphragmatic function. However, in the critically ill population, these are either impractical or unnecessarily invasive. There is accumulating evidence that US of the diaphragm provides both a good assessment of function but also may help to predict those patients who may struggle to breathe spontaneously. This information may help to guide weaning strategies and the decisions on tracheostomy tube placement.

Standard scanning technique and measurements

There are two main views of the diaphragm that are used. Using a curvilinear 3.5–5 MHz probe placed cranio-caudally in the subcostal area in the mid-clavicular line, with the probe angled 30–45°, allows visualization of the diaphragm, using the liver as a window (Figure 16.10a and b). With 2D mode, it is possible to look at the overall function and movement of the hemidiaphragm. However, more accurate and reproducible information can be gleaned by placing an M-mode line through the diaphragm (Figure 16.10c). It is essential that the line of M-mode is kept perpendicular to the line of the diaphragm, either by adjusting the probe position or, where this is not possible, by using compass M-mode. It is then possible to measure the excursion of the diaphragm during quiet breathing and following a deep inspiration (Figure 16.11). The following parameters can be measured to assess diaphragmatic function: the peak excursion distance a in centimetres, the time to peak excursion b in seconds, and the velocity of diaphragm movement (a/b) in centimetres per second.


Figure 16.10 2D and M-mode assessment of diaphragm movement.

Figure 16.10 2D and M-mode assessment of diaphragm movement.


Figure 16.11 M-mode assessment of diaphragm movement during maximal inspiration.

Figure 16.11 M-mode assessment of diaphragm movement during maximal inspiration.

The second point of measurement is the zone of apposition where the diaphragm inserts into the lower chest wall. By using a curvilinear or linear probe in the mid-axillary line between rib spaces 8 and 10, it is possible to see the three layers of the muscular portion of the hemidiaphragm. Using M-mode, it is possible to measure the thickness of the hemidiaphragm (tdi) as well as fractional thickening during inspiration. This is calculated by subtracting the thickness at the end of expiration from the thickness at the end of inspiration and dividing the product by the thickness at the end of expiration.

Assessment of diaphragmatic weakness or paralysis needs to be undertaken during spontaneous breathing, as there will be passive normal movement during controlled mechanical ventilation, independent of diaphragmatic function. US evaluation needs to be undertaken during a brief period of unsupported spontaneous breathing.

Diaphragmatic paralysis or weakness

There are several situations in which diaphragmatic paralysis or weakness may be present in critically ill patients. Damage to the phrenic nerve can follow thoracic trauma or can be a post-operative complication following cardiothoracic or upper gastrointestinal surgery. Trauma to the higher cervical spine can lead to bilateral diaphragmatic weakness. Medical causes include acute polyneuropathies such as Guillain–Barré syndrome, degenerative conditions such as motor neurone disease, or primary myopathic problems such as myasthenia gravis.

The hallmark of complete paralysis of a hemidiaphragm is paradoxical movement in inspiration as a result of the other respiratory muscles generating a negative pressure and pulling the flaccid hemidiaphragm cephalad. This paradoxical movement is best demonstrated from M-mode in the subcostal view. Where there is weakness, rather than paralysis, the features may be more subtle. A reduction in the tdi at the zone of apposition is a feature of atrophy of the diaphragm. A thickness of <2 mm is seen in patients with motor neurone disease. However, this measurement varies with height and weight and so is not as useful as fractional thickening.

Chapter 16

MCQs

Questions

1. The following are US signs of atelectasis:

  1. A Absent pleural sliding with a lung pulse Air A

  2. B Lung that looks like solid tissue

  3. C Dynamic air bronchograms

  4. D A-lines

  5. E Air bronchograms

2. Considering B-lines:

  1. A They are reverberation artefacts arising within thickened subpleural lymphatics

  2. B If present, they exclude a pneumothorax

  3. C The number correlate with measures of extravascular lung water

  4. D Are always pathological

  5. E Homogenous distribution suggests ARDS

Answers

1. The following are US signs of atelectasis:

  1. A TRUE. The presence of a lung pulse rules out a pneumothorax. It is also seen over the non-ventilated lung following endobronchial intubation.

  2. B TRUE. This is known as hepatization.

  3. C FALSE. This is a sign of consolidation.

  4. D FALSE. These are seen in normal aerated lung.

  5. E TRUE. Static air bronchograms may be seen in both lung consolidation and atelectasis, so they cannot be used to differentiate between the two conditions.

2. Considering B-lines:

  1. A TRUE. Multiple B-lines indicate pulmonary interstitial syndrome.

  2. B TRUE. B-lines are reverberation artefacts arising from below the visceral pleura and therefore can only occur if the pleural layers are in apposition.

  3. C TRUE. B-lines will appear and disappear in a time frame that closely matches the course of pulmonary oedema and can be used to monitor therapy.

  4. D FALSE. One to two can be seen in normal subjects, particularly in the dependent regions.

  5. E FALSE. Homogenous distribution suggests CPO. In ARDS, a heterogenous distribution is described associated with subpleural irregularities.

Further reading

Lichtenstein D, Goldstein I, Mourgeon E, et al. Comparative diagnostic performances of auscultation, chest radiography, and lung ultrasonography in acute respiratory distress syndrome. Anesthesiology 2004;100:9–15.Find this resource:

Lichtenstein D, Mezière G. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the Blue Protocol. Chest 2008;134:117–25.Find this resource:

Matamis D, Soilemezi E, Tsagourias M, et al. Sonographic assessment of the diaphragm in critically ill patients. Technique and clinical applications. Intensive Care Medicine 2013;39:801–10.Find this resource:

Mayo PH, Doelken P. Pleural ultrasonography. Clinics in Chest Medicine 2006;27:215–27.Find this resource: