The Future of Continuing Education in Diagnostic Imaging

Radiographic Pathology of the Chest

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Author:  Karen Vieira, PhD, MSM

Abstract: Imaging techniques are commonly used to diagnose pathologies of the chest, including dysfunctions of the heart and lungs. Frequently used methodologies include chest X-rays (CXRs), computed tomography (CT), high-resolution CT (HRCT), magnetic resonance imaging (MRI), positron emission tomography (PET), and ultrasonography (US). As technological advances are constantly being made, continual study regarding the proper utilization of such technologies is imperative. This article provides a continuing education activity for registered technologists (R.T.) with emphasis being placed on radiographic pathology of the chest and common chest pathologies such as atelectasis, chronic obstructive pulmonary disease, congestive heart failure, and pulmonary edema.



This article was designed as a continuing education (CE) activity with focus being placed on the topic of radiographic pathology of the chest . The participants will be able to describe imaging modalities and techniques that are frequently used for the diagnosis of different pathologies of the chest. Participants will also be able to define several common chest pathologies (atelectasis, chronic obstructive pulmonary disease, congestive heart failure and pulmonary edema) that are typically diagnosed through radiographic techniques, including typical signs and symptoms associated with each of these. A technologist may benefit from improved understanding of their main features and signs. This may inform the choice of equipment, positioning, doses and technical settings that may optimize the visualisation of these.






Pathologies of the chest are some of the most common abnormalities requiring imaging for diagnostic, visualization and assessment purposes. They are most often related to disorders, conditions or injuries to the important organs contained in the thorax (or chest cavity). These are of course the heart, lungs and major vessels . The diaphragm and ribs may also be relevant to these pathologies, as these structures may be displaced or disturbed by the effects of major chest pathologies. Many cardiac pathologies are related to cardiovascular disease or disorders, which are currently prevalent in the United States. This prevalence is related to factors such as atherosclerosis, (the build-up of cholesterol plaques on arterial linings) dietary factors and lifestyle choices (e.g. smoking) [1]. Pulmonary pathology may also be related to these disorders. Alternatively, they may be associated with pulmonary disease, environmental factors or behavioral factors.


Another major factor in pulmonary pathology is trauma. Accidents such as falls from a height, and injuries such as blunt-force assault are commonly associated with the appearance of abnormalities such as atelectasis (complete or partial collapsed lung) and pneumothorax (presence of air in the pleural cavity). Some features of pathology may overlap between discrete abnormalities, or, in other words, be a symptom of multiple pathologies. The actions taken by the R.T can contribute greatly to distinguishing between pathologies, assessing features and accurately diagnosing the pathology in question.


Anteroposterior (AP) Chest X-rays (CXRs) may be more useful for conditions in which the silhouette of the heart requires improved enhancement. Lateral decubitus positions are useful for assessing the volume and extent of anomalies such as pleural effusion, and gravity-dependent subtypes of other pathologies such as a pulmonary edema. The supine (AP) position results in flattened images of the pulmonary vasculature, which may actually be less useful in certain circumstances. For example, supine AP CXRs may not adequately show the differences in size between lobes, as the position may 'equalize' (or flatten) these. This may make conditions such as pulmonary edema and lobar alectasis (further described later) more difficult to detect. In addition, pneumothorax may be missed by an AP CXR Although this information may seem a review for radiologic technologists, as X-rays are so often the first line of thoracic medical diagnosis, consistent re-education regarding the basics of its delivery may be beneficial.


Developments in Imaging and their Impact on Analysis


The diagnosis of a condition featuring pathology of the chest can depend largely on an image such as a CXR. In fact, this is often the only visualization technique carried out in assessing an individual case [3]. However, technologists may enhance this through the optimization and refinement of the image once captured. These are known as radiographic techniques, modalities and/or image processing. The processing of an image involves modulating or transforming aspects of the image that may be under the control of the technologist.


Imaging Modalities/Techniques


For the purpose of diagnosing various pathologies, a CXR is still quite often the first line of imaging technology that is used. Additional modalities such as CT or HRCT scans, an MRI, PET, or US have become increasingly utilized modes of modern radiology. For example, up to 50% of the less common forms of atelectasis may not be detected by using a standard CXR [4]. Accordingly, a CT may detect distinct subtypes of chronic obstructive pulmonary disease, such as some forms of emphysema [5]. Some researchers have also concluded that HRCT will further enhance this differential detection [6]. Currently, single-photon emission computed tomography (SPECT) is increasingly recommended for the detection of pulmonary embolism [7].


CXR quality, optimization and enhancement depends on a number of image-processing variables a technologist may be able to manipulate to a considerable degree (which may depend on experience, skill and the equipment available). These include dynamic range. This is the gradient between the highest and lowest intensity that may be distinguished by a detector. Dynamic range may be regarded as inversely proportional to the size and complexity of the structure(s) under investigation (i.e. the field of view) and the penetration of the X-rays into the structure(s) in question [3]. The chest as a structure is liberally endowed with these factors. In other words, it is large, complex and susceptible to the uneven distribution of any radiation type [3]. The technologist may compensate for dynamic range by enhancing other variables, such as contrast, brightness, image noise and sharpness [3]. The advantage of this is that it may correct for discrepancies in radiological penetration and intensity, resulting in (for example) an unclear mediastinum [8].


The analysis of chest radiography may be also enhanced through image processing. These may be divided into some basic categories, including:


  • Feature-based processing
  • Intensity-based processing


Feature-based processing is an approach that identifies image displacements by finding features or structures that are well localized in two dimensions. The structures can also be tracked as the frames change, allowing the structure of interest to be visualized in two or more successive images. If performed properly, feature-based processing reduces the workload and also has the ability to enhance the understanding of the image detection.


Intensity-based processing requires the specification of a pair of images, an optimizer, a transformation type, and a metric. The metrics define image similarity and allows for evaluation accuracy by producing a scalar value of the paired images. The optimizer regulates the minimization or maximization of the scalar value and the transformation type aligns a misaligned image or moving image with a reference image known as a fixed image. This form of image processing is commonly used for histogram equalization and contrasted stretching. Histogram equalization may be further subdivided into categories such as [3]:


  • Bi-histogram equalization (Bi-HE): Histogram equalization (HE) is used in a variety of settings to enhance contrast [9]. It does this by making the distribution of intensity in an image more constant (or uniform). A cumulative distribution of this is then calculated, which is then applied as a transformative function [9]. This 'flattens' and 'stretches' the dynamic range [10]. In other words, this form of processing remaps gray levels based on the probability distribution of these levels from the original input. However, this 'flattening' effect may result in significant detriments to brightness [9]. Bi-HE is the use of separate histograms over two sub-images, which are derived from an original image using its mean [9]. Bi-HE may have a 'saturating' effect, i.e. some gray levels may appear to be disproportionately or 'artificially' enhanced [10]. This may be solved using a further processing adaptation called brightness-preserving bi-histogram equalization (BBHE). This splits the original histogram into two and then performs an equalization on each of these [10].


  • Multi-peak histogram equalization (MPHE): This form of HE is also regarded as effective in conserving brightness [11]. MPHE detects each individual peak of a histogram (rather than the histogram of each sub-image) and equalizes these [11]. This produces uniform intensity without affecting the mean brightness of an image [11]. Some researchers assert that this form of HE is superior as it allows for higher peak signal-to-noise ratios.


  • Multi-histogram equalization: This form of HE divides the histogram of an image into multiple sub-histograms and performs equalization on each of these [12]. This is thought to retain brightness and the features of the image [12]. However, some researchers conclude that it is less efficient in terms of contrast enhancement compared to other types of HE [13]. This may be improved on by splitting the histogram, identifying segments with narrower ranges within each of these, allocating full dynamic range to these segments and then applying equalization to the sub-histograms [13].


  • Adaptive histogram equalization (AHE): This relatively basic form of HE divides an image into multiple separate sub-images (that do not overlap) and performs equalization on each of these. This is thought to best suit the contrast of each separate part of the original image [10]. Some forms of AHE calculate these histograms separately, then modify them according to the mean pixel value of the sub-image and also certain variables of the cumulative function of distribution for the image [14]. This may allow discrete regions in a CXR to be optimized according to differences in contrast [14].


  • Contrast limited adaptive histogram equalization: (CLAHE) This is a variation of AHE developed to enhance images with low contrast [9]. AHE splits up the image and performs HE on these, as above. It then re-assembles the whole image, using bi-linear interpolation to remove the borders of the sub-images. However, CLAHE also incorporates an upper limit on the maximum slope of the transformative function, which also limits the sample number per bin. This allows uniform re-distribution based on the cumulative function (as above) [9]. This limit, also known as a 'clip limit' is thought to minimize saturation [9]. Saturation is associated with high histogram peaks in a subdivision of an image due to a disproportionate amount of pixels falling into the same range of gray [9].



Common Chest Pathologies


In the following section, several common chest pathologies will be outlined and reviewed. The review will include the typical signs and symptoms associated with each of the pathologies as well as their structural, functional, and descriptive classifications (where applicable). Factors to consider that may affect the detection of the pathologies will also be discussed. Furthermore, examples of rare forms of typical pathologies will also be described.




Atelectasis is a particularly common anomaly that can be observed through thoracic imaging, but may still be challenging to diagnose [15]. It may be regarded as a total or partial impairment of lung expansion, or, in other words, a 'lung collapse'. A patient with atelectasis may not be able to expand the lung as normal (i.e. through inspiration) and find independent breathing difficult due to the impairment of gaseous exchange.


Structural Classification of Atelectasis


This abnormality may be divided into several main categories based on their anatomical location or the part of the lung affected. These categories include:


  • Sub-segmental atelectasis: These may appear as linear or semi-linear opacities [16]. Sub-segmental atelectasis may be related to disorders such as pneumonia or ascites [16]. These collapses may also be associated with microemboli. Sub-segmental microemboli account for up to 17% of all pulmonary emboli, but may not always present as atelectasis (and vice-versa).
  • Segmental atelectasis: This may often be related to an obstructive central or bronchial mass. Such a feature may be demonstrably apparent on a CT image [17]. Other findings that may indicate segmental atelectasis related to a hilar or bronchial tumor may include bronchial mucus [17].
Atelectasis (arrows) seen on axial CT image of the thorax
  • Lobar atelectasis: This is often associated with endobronchial lesions, such as a tumor or build-up of mucus [18]. The lesions may be characterized by the Luftsichel sign, a translucent feature caused by the intrusion of the apex of a lower lobe between a collapsed upper lobe and the mediastinum [19]. This sign is typically much more common in the left upper lobe than the right.
  • Whole-lung atelectasis: This form of collapse involves all or nearly all of an affected lung. Some rare cases of this may feature considerable torsion of the collapsed lung toward the hilum [20].


More than one main type of atelectasis may also be present in some cases. Examples of this include combined lobar atelectasis and combined lobar and whole-lung atelectasis [21]. The most common form of combined lobar atelectasis is middle-lobe and lower-lobe atelectasis, which is often related to a bronchal obstruction [21]. Combined upper-lobe and middle-lobe, or upper-lobe and lower-lobe atelectases are less common [21]. A report describing 15 cases of combined upper-lobe and middle-lobe collapses found that two were related to infective diseases (e.g., pneumonia and tuberculosis) and the othe

rs were related to malignant growths [22]. In addition, combined lobar atelectasis may be due to infiltrations by tumors from one lobe to another, compression of the bronchus intermedius by a tumor in an upper lobe, or tumors (malignant or benign) in two separate locations [22]. 


Indicators of atelectasis include [15]:


  • Air bronchogram crowding: Air bronchograms are clearly-defined bronchi made apparent by inflammation or fluid build-up of the surrounding alveoli. This results in the bronchus as a darker line against (often-increased) opacity.
  • Fissure displacement: The fissures of the lung (particularly the major fissures) may be pushed upward in some cases of atelectasis [23].
  • Vascular crowding: Pulmonary vessels may become crowded or compressed in the course of atelectasis. This is due to the reduction in volume of the organ. The vascular damage resulting from this feature may be visible as a 'comet-tail sign' on a chest CT [23].




Atelectasis of right lung showing increased density


Atelectasis may also exhibit radiographic signs such as [15]:


  • Costal approximation: This is a shifting of the rib(s) over the site of atelectasis. It may result in a distorted, flattened or distended appearance of these bones on a CXR.
  • Fissural, mediastinal, and/or tracheal shift, usually in the direction of the collapse. This is a feature similar to fissural displacement, in which these structures appear to have moved in relation to the extent of atelectasis.
  • Hilar displacement; upper lobe collapses usually result in hilar elevation, whereas lower lobe collapses tend to lead to hilar depression
  • Hyperinflation of the surrounding lobes (e.g., to compensate for the collapse)
  • Opacification; although this is not always present. Opacification indicates increased density, which as outlined above is a common CXR feature of atelectasis. Whole-lung atelectasis often appears as a whole-lung opacification. Lobar collapses may also appear as opacities.
  • Upward displacement (which is also referred to as 'elevation' or 'tenting') of the diaphragm



Oberlappenatelektase links seitlich

Figure 3. Atelectasis of the left upper lobe showing some increased density on both PA & Lateral and a mediastinal shift in the direction of the collapse on the PA (arrows). Courtesy: "Oberlappenatelektase links seitlich" by Hellerhoff - Own work. Licensed under CC BY-SA 3.0 via Wikimedia Commons -



Descriptive Classification of Atelectasis


Atelectasis may also appear as a number of distinct shapes. These include:


  • Discoid: These are collapses that may result in a disc- or band-like appearance on a CXR.


  • Linear: This form of atelectasis appears as a straight line or line on a CXR.


  • Platelike: These are atelectases that have a tapered, band-like appearance. This type is sometimes regarded as another form of discoid atelectasis.


  • Round: These collapses may result in roughly spherical or oval opacities on a CXR.



Functional Classification of Atelectasis


Atelectasis may be classified according to the underlying factors that are likely to be associated with certain subtypes of this pathology. These may include [15]:


  • Adhesive atelectasis: this may arise from the loss of surfactant, or possibly, from pre-existing inflammation
  • Cicatricial atelectasis: this is related to conditions such as pulmonary fibrosis where tissue becomes damaged and scarred
  • Compressive atelectasis: this form appears to be associated with abdominal distention, compressive intrathoracic masses, or tension pneumothorax (progressive build-up of air within the pleural space)
  • Gravity-dependent atelectasis: this form, as the name suggests, is most often associated with gravity-dependent changes in alveolar volume
  • Passive atelectasis: this type is most often related to straightforward disorders such as diaphragmatic dysfunction, pneumothorax, or hypoventilation
  • Resorptive atelectasis: this type may be associated with the resorption of alveolar air distal to obstructive airway lesions


Factors that may affect the diagnosis of atelectasis include changes in hilar vascularity [17]. In addition, not all CXRs will necessarily show fissures, or will show very subtle shifts [18]. The absence of air bronchograms may indicate lobar or segmental atelectases related to tumors. Opacity, while a good indication of atelectases, may mimic solid masses [24]. The orientation of the collapse, as the direction and final position of the collapse, may affect the appearance or opacity on a CXR, e.g., a left upper-lobe atelectasis may result in a 'veil-like' opacification. In some cases, the lung may re-establish expansion to a certain degree. This can change the image of an atelectasis, or even make features such as air bronchograms clearer. Volume loss may be subtle or exaggerated, making CT detections of lobar atelectasis more difficult [17, 18, 24, 25].


Rare Form(s) of Atelectasis and Their Detection


Round atelectasis (also known as Blesovsky syndrome or 'folded lung') is a less common form of this pathology. It tends to be associated with pleural damage, and may often be misdiagnosed as carcinoma [23]. The fact that it often occurs in conjunction with lung cancer may make it even more difficult to detect [4]. Approximately 80% of cases are seen in men [23]. Round atelectasis is associated with dust and asbestos inhalation, but may also be caused by diseases including tuberculosis or pneumonia, and it is also seen in sarcoidosis [23, 26]. This form of lung collapse may cause the organ to 'curl' or 'fold up' on itself, thus giving a rounded appearance. The reasons for this are not clear, but may be related to pleural irritation, the development of adhesions, or the build-up of fluid in the pleura. Many cases of round atelectases are asymptomatic and are detected in CXRs carried out for other reasons [23]. They tend to be well-defined peripheral opacifications on CXRs, and as dense masses on CT scans [21]. More specifically, CT scans shows these masses as round or oval lesions, likely to present with air bronchograms, compressed bronchi, and vessels as they travel into the lesion. These compressions are known as 'comet tail' signs, and are a common characteristic of round atelectasis [23].



MRI (T1) scans may enhance some features (e.g. pleural folding) of the atelectasis, but is not regarded as superior for the visualization of these lesions in comparison with CT or HRCT [4]. Round atelectases may be associated with pleural thickening, but only if they are related to a history of asbestos exposure [21].


These lesions are often difficult to distinguish from lung carcinoma, especially if it manifests as singular tumors. However, round atelectasis is associated with reductions in lung volume, whereas cancer is not typically associated with this symptom [23]. However, lung volume may change if the tumor causes atelectasis via bronchial obstruction. Supplying vessels may also be visible in cases of cancerous lesions [23]. FDG-PET may also distinguish round atelectases from malignant lesions, but not from benign growths [4].


An important difference between round atelectasis and carcinomas are changes over time. Atelectases typically do not increase in size, and may even remit spontaneously over time in rare cases. They may actually remain stable in terms of size and shape over a year or more of follow-up scans [4]. Malignant tumors, on the other hand, are likely to change in size, and possibly in shape, over time. They also tend to be irregular and off-centre in pulmonary angiogram scans, and may also metastasize. 


Chronic Obstructive Pulmonary Disease


Chronic obstructive pulmonary disease (COPD) may be defined as pulmonary obstruction that is not resolved over time [27]. COPD is usually detected using quantitative CT and comparative follow-up CT [27].



Spirometry, an alternative assessment of lung function that depends on the flow and volume of inspiration and exhalation, is also used in the assessment of COPD, but CT is regarded as a superior technique in the detection of structural changes [28]. CXR may detect some general signs of COPD, such as tracheal saber-sheathing (figure 4), which is identified as a decrease in lateral diameter and an increase in anterior to posterior diameter of the trachea within the intra-thoracic area.


Saber Sheath Trachea

Figure 4. Courtesy of Dr Andrew Ho, From the case Saber sheath trachea



Some researchers argue that an MRI may deliver an effective and radiation-free alternative for the assessment and analysis of COPD. A trial regarding this modality compared 24 patients with COPD and twelve non-smoking healthy controls using two 1.5T MRI examinations and spirometry. Mean qS0 (quantitative equilibrium signal) was significantly reduced, and relative lung area (RA0.20) was significantly increased, in patients with COPD compared to controls. RA0.20 and qS0 moderately correlated with common spirometry parameters of forced expiratory volume of 1 (FEV1 ) second/forced vital capacity (FVC) and percentage-predicted FEV1. The COPD group also underwent chest CT scans. This supplied measurements analogous to the MRI values (e.g., RA-950). RA0.20, mean and 15th-percentile qS0 were strongly correlated with both of these modalities [29].


Structural Classification of Chronic Obstructive Pulmonary Disease


COPD is a syndrome that may be associated with many diseases or disorders. More specifically, it may be caused by inflammation of the airways, obstruction of the bronchioles, parenchymal damage or structural changes of the bronchi and/or trachea



Descriptive Classification


COPD may also be described in terms of the physical characteristics or symptoms exhibited by the patient. The symptoms may not directly affect imaging, but in some cases, recording patient symptoms and relaying them to the Radiologist may be useful in assisting diagnosis a specific underlying cause. Descriptive or phenotypic classifications of COPD include airway hyper-responsiveness. This is a disorder in which the probability and frequency of airway constriction is disproportional to a stimulus [33].


Phenotypic classification may be complicated in that it may extend to the type of disease that may be the underlying cause of the COPD [33]. This, on the other hand, may be more accurately referred to as functional classification.


Functional Classification


COPD may also be classified based on the specific disorder or disease that is causing the obstruction. These include bronchial dilation, bronchial wall thickening, centrilobular nodularity, gas-trapping, large airway disease, small airway disease, mosaic attenuation and emphysema. Emphysema may be subdivided further based on the distinct types of this disorder, or the structure it affects. These include bullous emphysema (in which alveoli become progressively enlarged until they rupture [34]), centrilobular emphysema (alveolar damage centred around the bronchiole of a secondary lobule (alveolar damage typically located close to the septal lines [35]).


CXR of a patient with COPD

Figure 5. CXR of a patient with COPD, showing a lung bulla (the result of bullous emphysema, circled). Courtesy: James Heilman, MD (Own work) [CC BY-SA 3.0 ( or GFDL (], via Wikimedia Commons


In addition, some forms of emphysema are strongly associated with genetic disposition. These include the basal predominant panlobar form of the disorder, which as mentioned above may be detected on CT based on its unique characteristics.


The functional imaging of COPD may be enhanced with SPECT, especially as patients exhibiting this pathology tend to be more susceptible to pulmonary cancer and other co-morbid conditions [7].



Figure 6. Label E Demonstrates severe COPD in right upper lobe. Labels B and D led to false-positive pulmonary embolism diagnosis. Courtesy : This research was originally published in JNM.  Reinartz P, et al. Tomographic imaging in the diagnosis of pulmonary embolism: a comparison between V/Q lung scintigraphy in SPECT technique and multislice spiral CT. J Nucl Med. 2004 Sep;45(9):1501-8. © by the Society of Nuclear Medicine and Molecular Imaging, Inc.



 Factors that may affect a diagnosis of COPD may include:


  • Patient age: More senior patients who present with complaints related to pulmonary obstruction are more likely to be diagnosed with COPD [36]. However, this is likely to be based on clinical as well as non-clinical signs and may not be dependent on imaging [36]. Chest radiography in geriatric patients has also been shown to result in a significantly higher probability of pathology [36].
  • Quantitative analysis: Some researchers argue that more qualitative analysis may be feasible for certain cases of COPD. Quantitative analysis may adequately detect emphysema associated with genetic factors, but qualitative analysis may be superior in detecting other functional signs such as airway thickening [6]. Furthermore, some mild forms of emphysema, such as centrilobar emphysema, may not meet the quantitative threshold for this disorder [5].
  • Bronchial wall thickening: This sign may have considerable variability in COPD patients, especially when compared to that of other conditions such as asthma [5]. The segmental and sub-segmental bronchi may show particular variability, in thickness as well as dilation and shape [5].
  • Severity and progression of COPD: In general, observers are more likely to detect signs in advanced or severe COPD in comparison to the newer-onset or milder cases of the disease.
  • Low attenuation area (%): A study including CT scans from over 1500 patients found that this factor was significantly correlated to visual emphysema scoring [37].
  • Gas trapping: This may be mistaken for low attenuation areas in patients with emphysema [37].
  • Emphysema type: Detection and scoring of this disorder may depend heavily on the subtype of emphysema that is present.
  • Inspiratory/expiratory scans: A review and meta-analysis of 79 articles found that there was a stronger correlation between airway obstruction and expiratory scans in comparison to inspiratory scans [28]. Inspiration or expiration may also affect the assessment of other features such as lobar air trapping. This may be accounted for using the air-trapping ratio (ATR). Some researchers assert that newly-developed indices, such as the attenuation-volume index (AVI), which refers to the increase in mean value of lung attenuation/volume decrease ratio, is subject to less variation than relative volume change and correlates comparably to FEV1/FVC [38]. The inspiratory/expiratory ratio of plain radiographs has also demonstrated some use in detecting airflow reductions as well as significant correlations with pulmonary function [39]. However, these ratios in GOLD (a classification of COPD severity based on some variables of spirometry, including FEV1) stages III and IV ('severe' and 'very severe' respectively) were not significantly different, indicating that they may not be of use in distinguishing between these symptoms [39].
  • Smoking: This is a factor that has demonstrable effects on COPD severity, air trapping, and emphysema. A study on the effects of nicotine dependence, as determined by polymorphisms in CHRNA3/5, found that there was no association between this factor and the severity of emphysema, but concluded that nicotine dependence may influence CT density due to increases in inflammation [40].

Congestive Heart Failure

Congestive Heart Failure


This is a condition particularly prevalent in emergency medicine. CHF may be detected using first-line CXR, but some researchers assert that the standard heart and lung US is more useful [41].





Basic signs that are associated with CHF include increases in heart size (e.g., cardiomegaly). It is detected based on symptoms such as:


  • Occlusion of the hilum
  • Interstitial fluid accumulations
  • Kerley A-lines and B-lines in the lower lung. Kerley lines are very thin, linear opacities on CXRs, commonly associated with conditions such as CHF. They are associated with interstitial damage and fluid accumulation [42]. Kerley-A lines are usually longer, and extend from the hilum toward the edges of the lungs. Kerley-B lines are short, often occur in small parallel groups and are more likely to be found in the periphery of the lung [42].



CXR showing intersittial infiltration

Figure 9.  CXR showing interstitial infiltration with Kerley-B lines and pleural effusion. Courtesy: Wan-Hsiu, L., L. Sheng-Hsiang, and W. Tsu-Tuan, High-resolution computed tomography illustrating pulmonary lymphangitic carcinomatosis in a patient with advanced pancreatic cancer: a case report. Cases Journal, 2009. 2: p. 7428.



  • Peribronchial and perivascular 'cuffing' with blurring and widening of their margins. Peribronchial 'cuffing' is the build-up of mucus or fluid in an airway, causing a cuff-like band of opacity across it (i.e. from the point of view of an individual viewing a CXR). Perivascular cuffing are similar signs on an X-ray which may be caused by the accumulation of inflammatory material or fluid around a pulmonary vessel [43].
  • Pulmonary interlobar fissures with subpleural fluid accumulation
  • Vascular opacity extending towards the upper lobes
  • Vascular distention: This is an increase in the size of the pulmonary vessels, particularly the artery, which is associated with adverse cardiac events [44]. Changes in the ratio of the size of a pulmonary artery and that of the aorta may be an indicator of vascular disease [44].


Most of these are often clearly visible on a CXR.


Factors that may affect the diagnosis of CHF include:


  • The loss of definition in pulmonary vessels: visualizing this feature on a CXR often indicates heart failure, but may also indicate pulmonary edema. However, these two disorders may also co-exist. Cardiogenic edema may be difficult to distinguish from non-cardiogenic edema (see below).
  • Pleural effusion: This often occurs in cases of CHF, but is also present in other pathologies.
  • Gravitational dependence: The position and visibility of the edema may depend on the position the patient is in during the CXR. In addition, the occlusion of hilar and perihilar structures may differ between supine and standing positions [41]. However, it may be difficult from a practical standpoint to obtain different positions (e.g., decubitus) to assess a gravity-dependent edema in a patient with CHF, which indicates importance of recording patient position at time of imaging if not standard (e.g. semi-erect, supine, etc.).
  • Types of heart failure: A myocardial infarction or mitral dysfunction may result in asymmetrical edema that may be mistaken for a noncardiogenic edema [41].



Pulmonary Edema


A pulmonary edema is defined as the accumulation of fluid in the parenchyma and airspaces, involving alveolar cells and the interstitium [45]. It has a complex etiology, involving interactions between hydrostatic, oncotic, and interstitial pressure [46]. It may also involve other factors such as osmotic forces and lymphatic drainage [47].


Types of Pulmonary Edema


There are two main types of pulmonary edema. These are:


  • Cardiogenic edema
  • Non-cardiogenic edema


Cardiogenic edema is generally related to increased hydrostatic pressure in the pulmonary capillaries [48]. However, it is often associated with left-ventricle-related heart failure. Non-cardiogenic edema is typically associated with changes in the permeability of capillary membranes or oncotic pressure [46]. It may also be linked to several additional factors which include [49-51]:


  • Acute respiratory distress syndrome (ARDS)
  • Acute lung contusion or trauma
  • Advanced sepsis
  • Allergic alveolitis
  • Aspiration
  • Increased altitude
  • Near-drowning or choking
  • Oxygen therapy
  • Pharmaceutical toxicity
  • Pulmonary contusion
  • Renal disorder
  • Resuscitation
  • Toxic inhalants
  • Transfusions


Other factors that may play a role in the development of acute pulmonary edema may include diving, exercising, and swimming [46]. In addition, an acute edema is a complication of pregnancy in some cases. This may be associated with pre-eclampsia, but may also be related to hypertension, airway obstruction, or aspiration [52]. Rare causes of acute edema may include severe venomous attacks by marine creatures [53]. Furthermore, edema resulting from acute lung injury may be related to factors such as traumatic brain injuries [54].


A noncardiogenic edema is thought to be related to damage of epithelial and endothelial barriers. Some research indicates that other cardiac signs, such as increased right ventricular volume, may be an important indicator of abrupt changes in the hydrostatic pressure of the capillaries [46].


Descriptive Classification


Pulmonary edema may appear as an extensive, bilateral diffuse opacification on the CXR, that obscures conventional signposts such as the cardiac silhouette and possibly even the entire diaphragm. This may recede in a number of days. Cardiogenic edema may be described as a 'batwing' configuration. Edema may also be diagnosed using US through the detection of Kerley B-lines [55].



CXR demonstrating pulmonary edema with plural effusions bilaterally

Figure 10. CXR demonstrating pulmonary edema with plural effusions bilaterally. Courtesy: By James Heilman, MD (Own work) [CC BY-SA 3.0 ( or GFDL (], via Wikimedia Commons


Functional Classification


Both types of edema may show interstitial infiltrates, alveolar flooding and air bronchograms [48, 56]. However, cardiogenic edema is more likely to be associated with signs such as [57]:


  • Increased heart size
  • Increased width of the vascular pedicle. This consists of the vessels in the mediastinum at the level of the aortic knuckle (or arch), roughly bordered by the superior vena cava on the right and the subclavian artery on the left [58]. Increases in the width of this feature (between where the superior vena cava crosses over the right main-stem bronchus and where the left subclavian artery leaves the aortic arch) are associated with pulmonary edema [59].
  • Kerley B-lines
  • Peribronchial 'cuffing'
  • Pleural effusion


Pulmonary edema is often easy to distinguish from other conditions. However, differentiating cardiogenic edema from the non-cardiogenic form may be more challenging [60]. An obvious factor in spotting cardiogenic edema is a history of recent cardiovascular events, and the cardiac cues (e.g., changes in heart size) as mentioned above [48]. Other forms of evaluation, such as laboratory evaluation of biomarkers such as troponin or brain natriuretic peptide levels, may be alternative methods of distinguishing cardiac from non-cardiac pulmonary edema [48]. Additional input from techniques such as electrocardiography may be necessary to distinguish a condition such as acute respiratory distress syndrome (ARDS) from cardiogenic edema [60]. Some conditions, such as drug-related infiltrative lung disease, may also be misdiagnosed as a pulmonary edema [59].


Rare Form(s) of Pulmonary Edema and Their Detection


Re-expansion pulmonary edema is a rare, but often-described complication associated with thoracentesis. It is usually unilateral, and may be related to the draining of a pneumothorax or hemothorax in the ipsilateral (same) lung [61]. However, several cases of bilateral re-expansion edema have been reported [61]. Re-expansion pulmonary edema is characterized by diffuse opacity on a CXR, bronchial 'cuffing' and Kerley B-lines [61]. Kerley B-lines may also be seen in lung US. The incidence of unilateral re-expansion edema may be up to 6.5%, whereas bilateral forms of this pathology are even rarer [61]. Most cases are not of traumatic origin (e.g., related to pleural effusion, etc.), but a recent report described the case of bilateral re-expansion edema that was the result of a 1.5 meter fall [61]. Some isolated cases may occur after unilateral lung ventilation, without the detection of pleural effusion or other disorders with a CT scan [62].





The role of imaging in the diagnosis of pathologies of the thorax is demonstrably consistent. It is relatively convenient, well-validated and standardized across many healthcare providers. Chest X-rays are often the first line in visualization-assisted assessment. This indicates the importance of the role of technologists who deliver radiographic services to modern medicine.


A major concern linked to the use of imaging dependent on radioactive particles is the exposure to these. However, modern CT is associated with decreasing doses and exposure to radiation. The exposure to standard X-rays may be controlled by technologists to a certain degree without reducing overall image quality. These strategies in reducing dose may be preferable to having the patient submit to a repeat exam.


This article has also outlined some major pathologies of the heart and lungs. Different types of these may exhibit similar signs and features. Close inspection of these, coupled with familiarity with their descriptive and functional characteristics, may aid in distinguishing one from another. Based on the material in this article, it could be argued that these abnormalities can be diagnosed using imaging alone. However, other diagnostic tools and criteria may aid in the accurate detection of a certain anomaly. These may include genetic analysis. Conversely, there are situations in which imaging (e.g. quantitative CT) may accurately diagnose pathology (e.g. emphysema) associated with certain mutations. The factors that may affect the appearance of some pathological features (e.g. atelectasis, see above) have the potential to impact the use of a radiological image. Vigilance for these may be useful.


Furthermore, in addition to understanding how to properly perform the basic techniques, the delivery of optimal radiological services has become increasingly dependent on the continued development and progression of radiology equipment as well as additional technologies that are incorporated into most modern-day facilities. Technologists who seek out ways to consistently expand their knowledge regarding radiographic modalities will be able to secure their future in this ever-growing field.






  1. Ritchey, M.D., et al., Million hearts: prevalence of leading cardiovascular disease risk factors--United States, 2005-2012. MMWR Morb Mortal Wkly Rep, 2014. 63(21): p. 462-7.
  2. Omar, H.R., et al., Anteroposterior chest radiograph vs. chest CT scan in early detection of pneumothorax in trauma patients. International Archives of Medicine, 2011. 4: p. 30-30.
  3. Alavijeh, F.S. and H. Mahdavi-Nasab, Multi-scale Morphological Image Enhancement of Chest Radiographs by a Hybrid Scheme. J Med Signals Sens, 2015. 5(1): p. 59-68.
  4. Stathopoulos, G.T., et al., Rounded atelectasis of the lung. Respir Med, 2005. 99(5): p. 615-23.
  5. Lynch, D.A., et al., A combined pulmonary -radiology workshop for visual evaluation of COPD: study design, chest CT findings and concordance with quantitative evaluation. COPD, 2012. 9(2): p. 151-159.
  6. Patel, B.D., et al., Airway wall thickening and emphysema show independent familial aggregation in chronic obstructive pulmonary disease. Am J Respir Crit Care Med, 2008. 178(5): p. 500-5.
  7. Jögi, J., et al., The added value of hybrid ventilation/perfusion SPECT/CT in patients with stable COPD or apparently healthy smokers. Cancer-suspected CT findings in the lungs are common when hybrid imaging is used. International Journal of Chronic Obstructive Pulmonary Disease, 2015. 10: p. 25-30.
  8. McAdams, H.P., et al., Histogram-directed processing of digital chest images. Invest Radiol, 1986. 21(3): p. 253-9.
  9. Yeong-Taeg, K. Quantized bi-histogram equalization. in Acoustics, Speech, and Signal Processing, 1997. ICASSP-97., 1997 IEEE International Conference on. 1997.
  10. Jeong, C.B., et al., Comparison of Image Enhancement Methods for the Effective Diagnosis in Successive Whole-Body Bone Scans. Journal of Digital Imaging, 2011. 24(3): p. 424-436.
  11. Wongsritong, K., et al. Contrast enhancement using multipeak histogram equalization with brightness preserving. in Circuits and Systems, 1998. IEEE APCCAS 1998. The 1998 IEEE Asia-Pacific Conference on. 1998.
  12. Shakeri, M., et al. Image contrast enhancement using optimum sub-histograms modification and preserving brightness levels mean without losing image specification. in Computer and Knowledge Engineering (ICCKE), 2014 4th International eConference on. 2014.
  13. Khan, M.F., E. Khan, and Z.A. Abbasi, Segment dependent dynamic multi-histogram equalization for image contrast enhancement. Digital Signal Processing, 2014. 25(0): p. 198-223.
  14. Sherrier, R.H. and G.A. Johnson, Regionally adaptive histogram equalization of the chest. IEEE Trans Med Imaging, 1987. 6(1): p. 1-7.
  15. Woodring, J.H. and J.C. Reed, Types and mechanisms of pulmonary atelectasis. J Thorac Imaging, 1996. 11(2): p. 92-108.
  16. Page, J.E. and A.G. Wilson, Linear opacities as a feature of pneumocystis pneumonia. Br J Radiol, 1990. 63(752): p. 597-601.
  17. Woodring, J.H., Determining the cause of pulmonary atelectasis: a comparison of plain radiography and CT. AJR Am J Roentgenol, 1988. 150(4): p. 757-63.
  18. Woodring, J.H. and J.C. Reed, Radiographic manifestations of lobar atelectasis. J Thorac Imaging, 1996. 11(2): p. 109-44.
  19. Webber, M. and P. Davies, The Luftsichel: an old sign in upper lobe collapse. Clin Radiol, 1981. 32(3): p. 271-5.
  20. Irie, M., et al., Spontaneous whole-lung torsion after massive pleural effusion and atelectasis. Ann Thorac Surg, 2014. 97(1): p. 329-32.
  21. Lee, K.S., et al., Combined lobar atelectasis of the right lung: imaging findings. AJR Am J Roentgenol, 1994. 163(1): p. 43-7.
  22. Chiang, C.S. and C.D. Chiang, Combined atelectasis of right upper and middle lobes: a clinical study of 15 cases. Zhonghua Yi Xue Za Zhi (Taipei), 1991. 48(5): p. 359-68.
  23. Sobocińska, M., et al., Rounded atelectasis of the lung: A pictorial review. Polish Journal of Radiology, 2014. 79: p. 203-209.
  24. Ashizawa, K., et al., Lobar atelectasis: diagnostic pitfalls on chest radiography. Br J Radiol, 2001. 74(877): p. 89-97.
  25. Salati, U., A. Smyth, and C.A. Wall, Lifting the veil: a case of lobar atelectasis. BMJ Case Reports, 2010. 2010: p. bcr0120102691.
  26. Tetikkurt, C., et al., Round atelectasis in sarcoidosis. Multidiscip Respir Med, 2011. 6(3): p. 180-2.
  27. Coxson, H.O. and R.M. Rogers, Quantitative computed tomography of chronic obstructive pulmonary disease. Acad Radiol, 2005. 12(11): p. 1457-63.
  28. Xie, X., et al., Morphological measurements in computed tomography correlate with airflow obstruction in chronic obstructive pulmonary disease: systematic review and meta-analysis. Eur Radiol, 2012. 22(10): p. 2085-93.
  29. Zhang, W.J., et al., MR Quantitative Equilibrium Signal Mapping: A Reliable Alternative to CT in the Assessment of Emphysema in Patients with Chronic Obstructive Pulmonary Disease. Radiology, 2015: p. 132953.
  30. Scichilone, N., et al., Clinical implications of airway hyper-responsiveness in COPD. International Journal of Chronic Obstructive Pulmonary Disease, 2006. 1(1): p. 49-60.
  31. George, C., W. Zermansky, and J.R. Hurst, Frequent exacerbations in chronic obstructive pulmonary disease. Vol. 342. 2011.
  32. Congleton, J., The pulmonary cachexia syndrome: aspects of energy balance. Proc Nutr Soc, 1999. 58(2): p. 321-8.
  33. Friedlander, A.L., et al., Phenotypes of chronic obstructive pulmonary disease. Copd, 2007. 4(4): p. 355-84.
  34. Ruiz Izquierdo, J., J. Ramos Lázaro, and I. González Prieto, Hydropneumothorax in a Patient With Bullous Emphysema. Archivos de Bronconeumología (English Version), 2014. 50(05): p. 204-204.
  35. Thurlbeck, W.M. and N.L. Müller, Emphysema: definition, imaging, and quantification. American Journal of Roentgenology, 1994. 163(5): p. 1017-1025.
  36. Karadeniz, G., et al., Differences in evaluation between geriatric and adult patients requiring pulmonary consultation. Z Gerontol Geriatr, 2015.
  37. Gietema, H.A., et al., Quantifying the extent of emphysema: factors associated with radiologists' estimations and quantitative indices of emphysema severity using the ECLIPSE cohort. Acad Radiol, 2011. 18(6): p. 661-71.
  38. Nagatani, Y., et al., A new quantitative index of lobar air trapping in chronic obstructive pulmonary disease (COPD): Comparison with conventional methods. Eur J Radiol, 2015.
  39. Kinoshita, T., et al., Paired maximum inspiratory and expiratory plain chest radiographs for assessment of airflow limitation in chronic obstructive pulmonary disease. Eur J Radiol, 2015. 84(4): p. 726-31.
  40. Kim, D.K., et al., Epidemiology, radiology, and genetics of nicotine dependence in COPD. Respir Res, 2011. 12: p. 9.
  41. Cardinale, L., et al., Effectiveness of chest radiography, lung ultrasound and thoracic computed tomography in the diagnosis of congestive heart failure. World Journal of Radiology, 2014. 6(6): p. 230-237.
  42. Wan-Hsiu, L., L. Sheng-Hsiang, and W. Tsu-Tuan, High-resolution computed tomography illustrating pulmonary lymphangitic carcinomatosis in a patient with advanced pancreatic cancer: a case report. Cases Journal, 2009. 2: p. 7428.
  43. Lowe, K., et al., Perivascular fluid cuffs decrease lung compliance by increasing tissue resistance. Critical care medicine, 2010. 38(6): p. 1458-1466.
  44. Wells, J.M. and M.T. Dransfield, Pathophysiology and clinical implications of pulmonary arterial enlargement in COPD. International Journal of Chronic Obstructive Pulmonary Disease, 2013. 8: p. 509-521.
  45. Demling, R.H., C. LaLonde, and K. Ikegami, Pulmonary edema: pathophysiology, methods of measurement, and clinical importance in acute respiratory failure. New Horiz, 1993. 1(3): p. 371-80.
  46. MacIver, D.H. and A.L. Clark, The Vital Role of the Right Ventricle in the Pathogenesis of Acute Pulmonary Edema. Am J Cardiol, 2015.
  47. Nowakowski, J.F., Acute alveolar edema. Emerg Med Clin North Am, 1983. 1(2): p. 313-43.
  48. Murray, J.F., Pulmonary edema: pathophysiology and diagnosis. Int J Tuberc Lung Dis, 2011. 15(2): p. 155-60, i.
  49. Schmickl, C.N., et al., Comparison of Hospital Mortality and Long-term Survival in Patients With Acute Lung Injury/ARDS vs Cardiogenic Pulmonary Edema. Chest, 2015. 147(3): p. 618-25.
  50. Bhagi, S., et al., Positive Association of D Allele of ACE Gene With High Altitude Pulmonary Edema in Indian Population. Wilderness Environ Med, 2015.
  51. Belice, T., et al., Noncardiac Pulmonary Edema induced by Sitagliptin Treatment. Journal of Family Medicine and Primary Care, 2014. 3(4): p. 456-457.
  52. Dennis, A.T. and C.B. Solnordal, Acute pulmonary oedema in pregnant women. Anaesthesia, 2012. 67(6): p. 646-59.
  53. Berling, I. and G. Isbister, Marine envenomations. Aust Fam Physician, 2015. 44(1): p. 28-32.
  54. Chen, G.S., et al., Thaliporphine derivative improves acute lung injury after traumatic brain injury. Biomed Res Int, 2015. 2015: p. 729831.
  55. Al Deeb, M., et al., Point-of-care ultrasonography for the diagnosis of acute cardiogenic pulmonary edema in patients presenting with acute dyspnea: a systematic review and meta-analysis. Acad Emerg Med, 2014. 21(8): p. 843-52.
  56. Shigematsu, H., M. Yoneda, and Y. Tanaka, Negative pressure pulmonary edema associated with anterior cervical spine surgery. Asian Spine J, 2014. 8(6): p. 827-30.
  57. Hammon, M., et al., Improving diagnostic accuracy in assessing pulmonary edema on bedside chest radiographs using a standardized scoring approach. BMC Anesthesiology, 2014. 14: p. 94.
  58. Rice, T.W., et al., Vascular pedicle width in acute lung injury: correlation with intravascular pressures and ability to discriminate fluid status. Crit Care, 2011. 15(2): p. R86.
  59. Bonniaud, P., et al., [Drug-induced interstitial lung diseases]. Rev Prat, 2014. 64(7): p. 951-6.
  60. Schmickl, C.N., et al., Decision support tool for differential diagnosis of Acute Respiratory Distress Syndrome (ARDS) vs Cardiogenic Pulmonary Edema (CPE): a prospective validation and meta-analysis. Critical Care, 2014. 18(6): p. 659.
  61. de Wolf, S.P., et al., Case Report: Bilateral reexpansion pulmonary edema following treatment of a unilateral hemothorax. F1000Research, 2014. 3: p. 318.
  62. Sugiyama, Y., et al., Severe Re-expansion Pulmonary Edema Induced by One-Lung Ventilation. Respir Care, 2015.