Radiographic Diagnosis of Pulmonary Disease
Norman Ackerman, DVM, DACVR
Veterinary Radiology Consulting
Huntsville, Al, USA
Radiographic diagnosis requires classification of pulmonary abnormalities based on 1. Lesion distribution (focal or multifocal versus diffuse or disseminated); 2. Pulmonary pattern (alveolar, interstitial, bronchial or vascular); 3. Appearance of other thoracic structures (heart, lymph nodes, mediastinum, ribs).
Lesion distribution is the most important and is either focal (multifocal) or diffuse (disseminated). Focal (multifocal) lesions involve a single or multiple lung lobes with an uneven or asymmetric distribution. They involve the left cranial but not the right cranial lung lobe or are more severe in one or more lung lobes. This reflects a lobar spread of disease or a vascular spread in an uneven fashion. Diffuse (disseminated) diseases affect the entire lung and are similar on the right and left sides. This reflects bronchial, vascular or lymphatic spread.
Pulmonary patterns may be classified as alveolar, interstitial, bronchial and vascular. Nodular patterns or masses are a special distinct category.
Alveolar pattern results from flooding of the end air spaces (acini) with fluid (pus, blood, edema) only rarely with cellular material. As individual acini become filled the fluid spreads to adjacent ones through the interalveolar pores. This results in the typical radiographic pattern of a poorly margined ("fluffy") density. The densities may spread and their borders coalesce. This may progress until all acini within a lung lobe are filled. There may be a sharp border at the edge of a lung lobe due to the pleura blocking further spread of the fluid into the adjacent lung lobe. As the number of fluid filled adjacent acini increases, the air filled, large and medium sized bronchi become evident as linear radiolucent branching structures (air bronchogram). The air-filled bronchi are surrounded by a fluid density and the bronchial wall and adjacent vessel are not seen. When a bronchus branches perpendicular to the x-ray beam it will be seen as a round radiolucent dot.
Recognition of an alveolar pattern identifies the abnormal density as being within the air space rather than within the interstitial space, pleural space, mediastinum, or outside the thoracic cavity, indicates the infiltrate's fluid nature and suggests that an aspirate via the airways (transtracheal or bronchoalveolar lavage) will yield diagnostic material. Interstitial pattern has been described as linear, reticular, or nodular. This produces either a fluid dense haze which obscures or obliterates vessels, distinct linear densities or distinct nodules. Interstitial infiltrates produce bronchial wall thickening but do not produce air bronchograms.
The fine linear pattern may be due to the presence of fluid or cells (neoplastic or inflammatory) within the supporting tissues of the lung. Many linear and branching densities may be evident and these viewed in summation can produce a net-like or reticular pattern. Where these linear densities converge, small tissue dense dots may become evident as a nodular pattern. The nodular pattern is also caused by aggregations of cells within the supporting tissues of the lung in association with neoplastic or granulomatous diseases.
Interstitial patterns may be classified as chronic or active according to their radiographic appearance. An active pattern is characterized by poorly defined, wide linear densities with blurring of vascular margins. As the disease becomes chronic, or resolves, the interstitial densities become thinner and better defined and the vascular borders become more clearly visible.
Recognition of an interstitial pattern is important because it identifies the abnormal density as being within the supporting tissues of the lung rather than within the end air spaces, pleural space, mediastinum, or outside the thoracic cavity. It indicates the infiltrate's cellular rather than fluid nature and that aspiration via the airways will not yield diagnostic material. Direct sampling (fine needle aspirate or biopsy) is more likely to be successful.
Bronchial pattern results from fluid or cells within the bronchial wall or peribronchial and perivascular connective tissue. Bronchial wall thickening and delineation of bronchial structures not normally identified results. Bronchial structures may be seen as lines that converge slightly and branch in pairs. These paired lines are thinner and do not taper like pulmonary vessels maintaining a fairly uniform width throughout their length. They have been described as "railroad or tram tracks" because they converge slightly as they extend toward the lung periphery. When they branch perpendicular to the x-ray beam they produce a tissue dense circle or "doughnut". With this pattern aspirating material via the airways will be rewarding.
Bronchiectasis represents a specific bronchial pattern that may be tubular or saccular. Tubular bronchiectasis consists of bronchial dilation and loss of the normal tapering as the bronchus progresses distally. Saccular bronchiectasis consists of focal bronchial dilations. Both forms are associated with chronic inflammation.
Vascular patterns are produced by a change in size, shape and/or number of pulmonary arteries or veins. Arteries and veins have a similar size. Evaluation of pulmonary vascular size is subjective. Vessels appear as linear, tapering, branching, soft tissue dense structures with smooth distinct margins. When vessels branch perpendicular to the x-ray beam they produce distinct round solid densities with the same or a slightly smaller diameter than the parent vessel. Vascular patterns are usually observed in cardiac disease. Increased vascularity is usually diffuse and results from left to right shunts (PDA, VSD, AV Fistula) or left heart failure. Decreased lung perfusion may be focal or diffuse and is most often associated with right to left cardiac shunts (Tetralogy of Fallot), decreased pulmonary blood flow (pulmonic stenosis; pericardial fluid or tamponade) or decreased circulating blood volume (hypovolemia). Focal reduction in perfusion is usually due to pulmonary thrombosis. This can produce uneven vascular diameters, unequal sized pulmonary arteries (right and left lung lobes are compared), a small pulmonary vein when compared to the adjacent pulmonary artery, absence of vascular shadows within a normal sized lung lobe, an enlarged central pulmonary artery with abrupt reduction in diameter, right sided cardiomegaly with or without main pulmonary artery enlargement and pleural fluid.
Other thoracic structures can be used to narrow the differential diagnosis. The presence or absence of cardiac, lymph node, tracheal, esophageal, diaphragm, rib, or chest wall lesions influences the probability of a specific diagnosis. In many cases only a ranking of differential diagnoses is possible.
Multiple patterns may be observed however the predominant pattern should be used. Various patterns occur during the disease course. In the early stage of congestive heart failure an increased vascular pattern is present followed by an interstitial pattern with loss of vascular outlines. This may progress to a diffuse alveolar pattern with loss of both vascular and bronchial wall shadows, coalescing opacities and air bronchograms.
Typical patterns occur. Bacterial pneumonia usually presents with a focal alveolar pattern when first seen although interstitial patterns will be visible early in the disease and when the infiltrate has nearly resolved. Recognition of the pattern and its distribution may suggest certain diagnoses, eliminate others and narrow the list of probable diagnoses. It is a strong clue as to the next logical diagnostic test. Diseases with infiltrates in the bronchi or end air spaces may be amenable to diagnosis by transtracheal aspiration or bronchoscopy while those with infiltrates confined to the pulmonary interstitium usually require either open biopsy or fine needle aspiration.
Radiographic Patterns of Pulmonary Abnormalities
A. Focal or Multifocal
B. Disseminated or Diffuse
2. Interstitial Pattern
4. Vascular Pattern
Norman Ackerman, DVM, DACVR