Overview

The normal pulmonary parenchyma can be a challenge for interpretation. This is because of the substantial breed variations in dogs and also, the technical aspect of taking the thoracic radiograph impacts overall lung opacity and thereby may preclude accurate interpretation. It is imperative that the practitioner obtains well‐positioned, thoracic radiographs of high diagnostic quality that are made on peak inspiration. An interpretation paradigm will be used in this chapter that tries to simplify the approach to interpretation of the lungs. This paradigm should serve as a starting point for evaluating thoracic radiographs. Continued evaluation of thoracic radiographs will refine the interpretation paradigm as the practitioner grows in experience and the art of pulmonary interpretation.

Warnings and Obstacles

The infinite number of nuances of pulmonary interpretation makes it impossible to show all examples for the different radiographic presentations for each disease process.

It is important to recognize several caveats about the pulmonary parenchyma and a description of pulmonary changes. The first is that pulmonary pattern recognition is not necessarily the endgame in interpretation of the lungs. Second, pulmonary patterns do not equate with histology, although pulmonary patterns were originally ascribed to histology. This is no longer the case, as different diseases can have mixed pulmonary patterns. The pulmonary patterns represent nonspecific changes that could be caused by multiple different etiologies. However, certain etiologies do occur with certain lung patterns, thereby providing a differential diagnosis list. Third, often lung patterns are mixed, and one needs to decide the dominant lung pattern to look up a specific set of differentials.

Finally, there are descriptive terms used in veterinary medicine that have not been defined and thereby should be avoided. Additionally, when looking up differentials, these terms are not used in current veterinary textbooks for creating differential lists. The first term is infiltrate, which refers to a nonspecific increase in pulmonary opacity from many possible etiologies. The term has, in fact, been discarded from the human pulmonary radiology literature because a definition has never been agreed upon. Infiltrate is a histologic description and since radiology is not histology, it should not be used. The second term is consolidation. This has been used to describe an increased opacity that involves a portion of or an entire lung lobe without volume loss within the affected lung lobe. This term is really an act of two businesses merging to form a larger corporation and has nothing to do with the lung. The Fleishner Society has defined consolidation as just an increase in opacity within the lung, so it is also nonspecific [1]. The third term is the use of combinations such as broncho‐interstitial pulmonary pattern. Again, this term does not have a differential list associated with it in the textbooks. There are plenty of diseases that can result in both an unstructured interstitial and bronchial pulmonary pattern; however, one must choose what the dominant pattern is, as this will dictate the differential diagnosis and next steps for reaching a final diagnosis.

Anatomy and Physiology

There are six lung lobes present in the dog and cat (Figures 16.1 and 16.2) [2–15]. The pulmonary parenchyma is characterized by a background gray appearance that gets its overall opacity from the airspace within the alveoli, major and minor airways, the circulating blood, blood vessels and capillary beds of the pulmonary circulation. The blood supply to the lung is twofold, including the pulmonary circulation carrying deoxygenated blood from the right ventricle in the pulmonary arteries to the lungs, pulmonary capillaries and then returning oxygenated blood to the left atrium via the pulmonary veins. The bronchoesophageal artery (branch of the thoracic aorta at the level of the right fourth intercostal artery) carries oxygenated blood to the airways. The venous drainage of the bronchial blood supply enters the azygos vein before entering the cranial vena cava or right atrium.

The trachea extends from the larynx (Figure 16.3) through the thoracic inlet to its bifurcation into the right and left principal bronchi at the terminal trachea that is called the carina. Immediately off the right principal bronchus is the right cranial lung lobe (RB1) that extends in a cranioventral direction over the base of the cardiac silhouette [12]. The right cranial lung lobe has a dorsal and ventral aspect. The dorsal aspect is in contact with the craniodorsal mediastinal structures along its medial side. Caudally, the right cranial lung lobe is in contact with the right caudal lung lobe dorsally and the right middle lung lobe and cardiac silhouette ventrally. The ventral aspect of the right cranial lung lobe is separated from the left cranial lung lobe by the cranioventral mediastinal reflection. The right cranial lung lobe extends from the right to the left side of the thorax cranial to the cardiac silhouette (Figure 16.4). The right middle lung lobe bronchus extends from the right caudal bronchus in a ventral location and has a triangular shape. This lung lobe does not go above the carina as noted on the lateral views. The caudal border of the right middle lung lobe approximates the caudal border of the cardiac silhouette (Figure 16.5). The right caudal lobe bronchus continues caudally as seen on the lateral projections in the caudodorsal lung field. The right caudal lung lobe also has a dorsal and ventral component and meets the mediastinal structures on the medial side of the lung and the diaphragmatic surface caudally.

The accessory lobe bronchus originates from the right caudal lung lobe bronchus in a ventromedial position and extends from the right to left side of the thorax caudal to the cardiac silhouette (Figure 16.4). The accessory lung lobe wraps around the caudal vena cava at the plica vena cava. This lobe extends to the left side of the thorax. The left lateralmost extent of the accessory lung lobe is the caudoventral mediastinal reflection as seen on ventrodorsal or dorsoventral radiographs (Figure 16.6). The dorsal border of the accessory lung lobe can be seen between the esophagus and the caudal vena cava (Figure 16.6).

The left lung is smaller than the right and is made up of the left cranial and left caudal lung lobes. The left cranial lung lobe is divided into cranial and caudal subsegments. The cranial subsegment extends cranioventrally to the thoracic inlet and in some dogs can extend over to the right side of the thorax (called the lingula; Figure 16.7). The left cranial lung lobe bronchus extends ventrally from the left lobe principal bronchus at the bifurcation of the trachea. This bronchus immediately divides into cranial and caudal subsegments (Figure 16.8). Dorsally, the left lung lobes contain an impression along the medial aspect as an indentation of the descending thoracic aorta. This impression is deeper in the cranial thorax and the descending thoracic aorta continues caudal and medial to a midline position by the time the aorta enters the abdomen at the aortic hiatus of the diaphragm. In some dogs, the descending thoracic aorta is more clearly visible cranially compared to the caudal thoracic aorta (Figure 16.9).

Atelectasis

The term atelectasis implies volume loss within a given lung lobe. The degree of air volume loss correlates with the degree of atelectasis. There are physiologic and pathologic factors that result in the loss of normal air volume from an affected lung lobe. Atelectasis should be viewed as a nonspecific change that can be caused by multiple etiologies (different diseases) that affect the lungs, mediastinum, and pleural space. Acute atelectasis will result in an ipsilateral mediastinal shift of the cardiac silhouette toward the area of atelectasis (Figure 16.10). As the atelectasis becomes chronic, hyperinflation of the surrounding lung lobes may shift the cardiac silhouette back into a levocardia position, with the apex of the cardiac silhouette pointing in a leftward and caudal direction (Figure 16.10).

Common causes of atelectasis include prolonged lateral recumbency and/or anesthesia, particularly with a FiO₂ of 100% [16–18]. Plate‐like atelectasis has been reported in dogs and cats as a focal linear collapse of a portion of the lung lobe specifically localized to a sublobar fissure (Figure 16.10) [19].

Interpretation Paradigm

A systematic approach to the evaluation of the lung is necessary so that all aspects of the lung fields are evaluated. There is a normal background opacity that is a result of the blood, blood vessels, capillary beds, airways, and interstitium (supporting connective tissue; Figure 16.11). Once an abnormality is identified, one must ask whether the abnormality is an increase in opacity, a decrease in opacity or both. Increased and decreased opacity will determine which part of the decision tree one goes down in describing a specific pattern and formulating a differential diagnosis.

If decreased opacity, the first question is whether the change is focal, multifocal, or generalized (Box 16.1). If focal, is the opacity structured into a circular lesion or lobar? If circular, then differentials would include pulmonary bulla, pneumatocele, or hematocele (Figure 16.12). If lobar (triangular), then is the decreased opacity due to regional oligemia (from decreased blood flow) or trapping of gas within the pulmonary parenchyma? The most common causes of lobar decreased opacity include bullous lobar emphysema (Figure 16.13) or pulmonary thromboembolism (Figure 16.14). If multifocal, then the distribution will be random throughout the lung lobes and the appearance circular as in multiple cavitated nodules, bullae (Figure 16.15) or lobar as in pulmonary thromboembolic disease. The above reasons for decreased opacity have an uncommon prevalence. The most common reason for decreased opacity is hypovolemia regardless of the cause, which is generalized with all lung lobes being equally affected (Figure 16.16). In addition, in hypovolemic patients, the cardiac silhouette and caudal vena cava can be small (Figure 16.17).

The increased opacity decision tree also starts with distribution and specifically where the lesion is located (position in lung lobes and which lung lobes are involved). The first question is focal, multifocal, or generalized? Focal would involve one lung lobe, multifocal would involve more than one lung lobe and generalized would involve all lung lobes.

Anatomically, it is important to think of the thorax in terms of cranial and ventral opposed to caudal and dorsal distributions. A bronchopneumonia will be gravity dependent and cranioventral in distribution. Pulmonary edema (cardiogenic or noncardiogenic) will be caudodorsal in distribution. The position of the mediastinum should then be evaluated assuming the ventrodorsal/dorsoventral radiographs are straight in their positioning. An ipsilateral mediastinal shift will result in the cardiac silhouette moving toward the area of increased opacity, usually secondary to loss of air volume within the lung lobe (called atelectasis; Figure 16.18). A contralateral mediastinal shift will result in the cardiac silhouette being displaced away from the increased opacity, which typically is a mass or creates a mass effect (Figure 16.19).

Next is defining the pulmonary pattern. The easiest approach to learning pulmonary patterns is to run a list of possibilities from easiest to identify to the hardest to identify (Box 16.2). These include:

• pulmonary mass
  
• alveolar pulmonary pattern
  
• bronchial pulmonary pattern
  
• vascular pulmonary pattern
  
• structured interstitial pulmonary pattern
  
• unstructured interstitial pulmonary patterns.

One always must bear in mind that the pulmonary abnormality identified can be a combination of several pulmonary patterns and a differential list must be created for each pattern. Also, unstructured interstitial pulmonary pattern and alveolar pulmonary pattern in the same patient most likely represents different degrees of severity of the same disease process. One can progress to the other (unstructured interstitial to alveolar) as the disease process worsens and one can regress as the disease responds to treatment (alveolar to unstructured interstitial; Figure 16.20).

The easiest pattern to identify is a pulmonary mass. A mass is greater than 3 cm in diameter and has a smooth rounded border (Figure 16.21). Pulmonary masses can be cavitated and/or mineralized (Figure 16.22). The process of cavitation involves the central portion of the mass outgrowing its blood supply and becoming necrotic fluid. The mass then invades a bronchus, and the fluid drains out of the mass and is replaced by air. Pulmonary abscesses in small animals can also have a gas‐cavitated mass appearance but this is less common. Depending on the location of the mass, the mass can border efface with the cardiac silhouette or diaphragm and is usually a uniform soft tissue opacity. The most common mass in the dog is found in the left caudal lung lobe and is secondary to a primary lung tumor (bronchogenic, bronchoalveolar or squamous cell carcinomas; Figure 16.23). Masses in the right middle lung lobe in dogs have been shown to most commonly be histiocytic sarcoma (Figure 16.24). In cats, pulmonary (bronchogenic carcinoma most common) masses can occur in the hilum and obstruct a central bronchus, resulting in an atelectatic lung lobe (see Chapter 19). Additionally, lung–digit syndrome occurs where the pulmonary bronchogenic carcinoma metastasizes to the digits (see Chapter 19). Often these cats present clinically for a thoracic or pelvic limb lameness and not clinical signs related to thoracic disease. In some pulmonary interpretation paradigms, pulmonary masses are characterized as a structured interstitial pulmonary pattern. This implies that these masses originate from the interstitium, which is the least common origin for a pulmonary mass. The mass could be alveolar, bronchial, or interstitial in cell origin. Also, the term pulmonary mass is very descriptive and implies a large (greater than 3 cm), rounded and soft tissue opaque lesion.

The next pulmonary pattern that is easy to identify is the alveolar pattern (Box 16.3). There are five aspects of an alveolar pulmonary pattern: a uniform soft tissue opacity with the presence of air bronchograms (Figure 16.25), a lobar sign, border effacement of the affected lung lobe with the cardiac silhouette or diaphragm, depending on the lung lobe involved and position within the lung lobe, and border effacement of the small structures within the affected portion of the lung lobe, including the pulmonary vessels and serosal border of the bronchi. Three of the five must be present to be an alveolar pattern. Border effacement of the small structures and outer serosal wall of the bronchi must be present to represent an alveolar pulmonary pattern. Air bronchograms, although considered the hallmark of alveolar disease, do not always have to be present and in a minority of cases will not be present. Total atelectasis of a lung lobe would be considered an alveolar pattern but does not necessarily contain a central air bronchogram (Figure 16.26).

The most common lung lobe to undergo complete atelectasis is the right middle lung lobe which usually occurs in cats with feline allergic lung disease secondary to mucous plugging (Figure 16.27).

The next pulmonary pattern that could result in increased opacity is a bronchial pulmonary pattern. The hallmark feature of this disease is the presence of thickened small airways (rings and, less commonly, parallel lines; Figure 16.28). Typically, bronchial disease is a generalized disease, and the rings and parallel lines are found in the peripheral aspects (thinnest sections) of the lung parenchyma. The caveat includes the fact that the central airways are always prominent and should not be misinterpreted as a bronchial pattern. In addition, there are geriatric changes as well as disease conditions (Cushing syndrome) that might result in central bronchial mineralization (and can be quite eye catching; Figure 16.29). This should not be misinterpreted as a bronchial pulmonary pattern. The term “peribronchial” cuffing has been used in veterinary medicine, but it is extremely rare in that the increased pulmonary opacity forms a concentric separate circle surrounding a thickened bronchus centrally. When switching from analog radiographic film to a digital system, one can also see the airway walls more clearly, but this is not a bronchial pulmonary pattern.

A bronchial pulmonary pattern is determined by thickening of the airway walls and the finding of midzone and peripheral interlobar airway walls (rings and parallel lines). Inappropriate radiographic technique (such as when radiographing the abdomen) can also artefactually increase the conspicuity of the bronchi and can be misinterpreted as a bronchial pattern, falsely raising concerns for lower airway disease.

The next pulmonary pattern is the vascular pulmonary pattern. Increased opacity implies that the pulmonary arteries and/or veins are enlarged, thereby adding opacity to the lung lobes. The pulmonary artery and vein parallel each other and are equal in size. Pulmonary artery enlargement is seen in canine and feline heartworm disease (Figure 16.30). This disease process results in an endarteritis of the pulmonary arteries where the arteries will become enlarged, tortuous, and/or blunted (abruptly tapers). Enlargement of the pulmonary veins usually implies elevations of left ventricular and left atrial enddiastolic pressures and thereby increased pulmonary venous pressures (Figure 16.31). This is typically seen in dogs and cats with congestive left‐sided heart failure. Enlargement of the pulmonary arteries and veins is usually secondary to volume overload of the pulmonary circulation. This could be secondary to overcirculation from left to right intra‐ or extracardiac congenital shunts, volume overload from excessive intravenous fluids, arteriovenous fistulas, or cats with congestive left‐sided heart failure, (Figure 16.32).

A structured interstitial pulmonary pattern can be classified as nodular or miliary. Pulmonary nodules range in size from 0.5 to 3.0 cm, and are rounded and soft tissue in opacity (Figure 16.33). Fake‐outs for pulmonary nodules include centrally located end‐on pulmonary vessels (near the pulmonary hilum), ectoparasites, osteomas, degenerative costochondral junction changes, nipples, and cutaneous masses/nodules (Figure 16.34). Metastatic neoplasia is the primary differential diagnostic consideration for pulmonary nodules although other causes of nodules are not excluded (such as granulomas or abscesses). A miliary pulmonary pattern implies that there is a generalized increase in soft tissue opacity with a nodular background opacity shaped like “millet seeds” (Figure 16.35). Differentials would include fungal disease, lymphoma, or metastatic carcinoma.

The final cause of an increased opacity (essentially the left‐over back door diagnosis) is the unstructured interstitial pulmonary pattern (Figure 16.36). The features of an unstructured interstitial pattern include an increase in soft tissue opacity with partial loss of normal vascular and bronchial markings but not complete border effacement. The pulmonary changes could also obscure but not border efface the cardiac silhouette and/or the diaphragm, depending on the location of the pulmonary abnormalities. The unstructured interstitial pattern could be further classified as moderate or severe. A mild unstructured interstitial pulmonary pattern can commonly be recognized but is not worth taking into consideration given that no therapy will be administered solely based on the presence of a mild unstructured interstitial pulmonary pattern (particularly generalized) as this could just be age‐related change (pulmonary fibrosis), expiration, and underexposure. The severe unstructured interstitial pulmonary pattern is on its way to being alveolar, but air bronchograms are not yet present and one can still make out vessels in the affected pulmonary parenchyma.

Mixed pulmonary patterns include a combination of decreased and increased opacity. This include hematoceles, pneumatoceles, cavitated lung nodules or masses (neoplasia or abscess formation), and a vesicular pulmonary pattern. A vesicular pulmonary pattern is a specific term to describe the type of pattern seen in a lung lobe torsion. The right middle lobe is the most common lobe to undergo a torsion in deep‐chested dogs (Figure 16.37). Radiographic features of a lung lobe torsion are described in Box 16.4.

Airspace and Bronchocentric Disease: an Alternative Approach

A different interpretation paradigm has been proposed [20]. In this paradigm, the opacity of the lung, the degree of lung expansion, and the anatomic distribution of the alterations are utilized to prioritize differentials. Increased opacity is further characterized as being solid (consolidation) or atelectasis and as either airspace or bronchocentric in pulmonary distribution.

In this scheme, consolidation refers to a lung lobe that is soft tissue opaque with loss of intralobar structures, has not lost volume and may or may not have air bronchograms within the affected lobe. In this scenario, atelectasis implies loss of air volume of the affected lung lobe with an ipsilateral mediastinal shift toward the affected lobe. Four different types of atelectasis have been described in human medicine: relaxing, obstructive, adhesive, and cicatrizing. These terms will not be defined here as often the etiology of the atelectasis may not be determined on the thoracic radiographs.

The term airspace has been applied to the lower airways and alveoli that contain air normally. This term can be applied to lesions that have been characterized as being consolidation, ground‐glass opacity, nodules, and masses. This would correlate with alveolar, structured interstitial, unstructured interstitial, and mass pulmonary patterns in the previously described pulmonary interpretation paradigm.

Bronchocentric distribution implies thickening and abnormalities of the bronchovascular bundle (airways and corresponding blood vessels) in each of the lung lobes. This would correlate with bronchial and vascular pulmonary patterns in the previously described paradigm. At a certain level, these terms introduce an entire new level of complexity with overlap in their use and meaning, making the interpretation paradigm confusing. This interpretation paradigm, however, should not be totally discounted and has its merits. These include the same starting points with increased or decreased opacity, anatomic localization of the abnormal lung opacity, and presence or absence of a mediastinal shift being answered in both paradigms.