What in the world is in those lungs? A review of pulmonary patterns (Proceedings)

Before we can start begin to review abnormalities in the lungs lets first do a review of normal anatomy. In the lungs there are three main structures, the interstitium, the airways, and vessels. To differentiate between the vessels and the bronchi, remember that bronchi converge together toward the lung periphery as they taper, where as pulmonary vessels diverge. On the lateral view, the artery is always dorsal, the bronchus is in the middle, and the vein is ventral. To evaluate size of the vessels, in left lateral recumbency compare the right cranial lobar artery and vein. They should be the same diameter and each vessel should not exceed the smallest diameter of the right 4th rib. On the VD view, the artery is lateral, the bronchus again is in the middle and the vein is axial. As on the lateral view with the cranial lobar vessels, the caudal lobar pulmonary artery and vein are of similar size and in the dog the diameter of these two vessels should not exceed the diameter of the 9th rib. In the cat, we compare these vessels to the10th rib.

We need to initially look at a film and determine if it is of adequate quality to interpret. Initially we evaluate to determine if the radiograph was exposed during the inspiratory phase of respiration. The area of the lung that is caudal to the heart, cranial to the diaphragm and ventral to the caudal vena cava should be large in size on an inspiratory film. The lumbodiaphragmatic angle (where the caudal dorsal lung extends adjacent to the lumbar spine) is caudal to T12 on inspiratory films. Make sure the film is adequately exposed, as underexposure may simulate disease (non-structured interstitial pattern) while overexposure may mask disease.

Now we are onto patterns of pulmonary disease. There are three main patterns: alveolar, bronchial, and interstitial. Let us begin with alveolar. Alveolar patterns represent infiltration of lung to the point of filling of the alveoli. The roentgen signs are replacement of air with soft tissue opacity and air bronchograms. Air bronchograms represent air within all (or portions of) a bronchial lumen and the adjacent lung tissue (alveoli) is of abnormal fluid opacity. In long axis these appear tree-like, while end-on they look like "holes". You are unable to see the outside walls of the vessels or bronchi, and this is what differentiates air bronchograms from doughnuts seen with bronchial disease. The soft tissue infiltrates can be blood, pus, or water. We determine the likely etiology of the infiltrates depending on the distribution. Localized alveolar lung disease can be seen with pneumonia, hemorrhage (due to trauma), atelectasis, neoplasia, infarction, and torsion. Disseminated alveolar pattern can be seen with severe inflammatory lung disease, severe edema, hemorrhage (due to bleeding disorder), near drowning, or smoke inhalation. Edema has many etiologies, cardiogenic (concurrent cardiac enlargement is present), neurogenic (from electric cord bite, following head trauma, post ictal, and from strangulation injury or smoke inhalation. The location of alveolar infiltrates can also help us to determine etiology. Asymmetric lung infiltrate is common with hemorrhage (contusion associated with trauma), inflammatory, atypical pneumonia, foreign body pneumonia, bronchoesophageal fistula, and thromboembolism (often the history includes predisposing renal or adrenal disease). Consolidation of a lung lobe (with infiltrates) will have no loss of volume and no shift of the mediastinum. By comparison atelectasis will have loss of volume and shift of the mediastinum toward the alveolar infiltrates. With respect to atelectasis....if a patient is recumbent for at least 30 minutes or longer atelectasis will occur. If an animal is under anesthesia, positive pressure ventilation is necessary, as atelectasis will obscure visualization of pulmonary parenchyma. Accidental intubation into a single bronchus also results in atelectasis.

The histories also give clues to the etiology of the pulmonary infiltrates. Pneumonitis can occur from circulating pancreatic enzymes with pancreatitis, re-expansion pulmonary edema following chronic lung collapse (esp in cats), sepsis with secondary acute respiratory distress syndrome (ARDS), and pulmonary hemorrhage from disseminated intravascular coagulopathy (DIC).

Bronchial is the next main pulmonary pattern to discuss. Bronchial disease is caused by infiltration of airways by inflammatory cells, edema, neoplastic cells, or mineral. Chronic bronchitis can be due to allergic, parasitic, or inflammatory etiologies. Edema creating thickened bronchi is actually a peribronchial infiltrate and is caused by cardiac disease. Neoplasia such as bronchoalveolar carcinoma has a primary bronchial pattern yet can also have other patterns present. Mineralization of the bronchi can be due to age or Cushing's disease. The bronchi are increased in visualization when mineralized, but not increased in thickness. Roentgen signs of bronchial disease include tram lines and donuts.

Tram lines are thickened paired linear/ branching lines which converge as they are traced into the lung periphery. Donuts are bronchi viewed in cross section and they appear as a thick circle. Bronchiectasis is a result of end stage chronic bronchial disease and is an irreversible change seen as increased diameter of bronchi as they extend into the pulmonary periphery (compared to the normal decrease in diameter of the bronchi as they extend into the periphery). Feline bronchial lung disease is considered a syndrome. Overall there are prominent bronchial markings. However 37% of cats also have alveolar lung disease, while 10% have atelectasis of the right middle lung lobe and 10% have pulmonary hyperinflation.

Interstitial patterns have two distinct appearances. Let us discuss the structured nodular interstitial pattern first. Structured nodules may be due to neoplasia, granulomas, abscesses, or mineral. They appear most often as multiple soft tissue nodules measuring between 5 – 40mm. They can be smooth or irregularly marginated. Metastatic neoplasia is the most frequent cause of multiple soft tissue nodules. Nodules with an alveolar pattern should suggest inflammatory etiology. Solitary soft tissue masses are usually neoplastic. Bronchogenic carcinoma is the most common pulmonary neoplasia. Lung tumors rarely calcify. Multiple mineralized nodules between 1-3mm in size represent benign osseous metaplasia (aka pulmonary osteomas) and should not be confused with metastatic neoplasia (which is soft tissue opacity). A single mineralized nodule between 3 – 40mm in size are usually due to calcified granulomas. Cavitary nodules (fully or partially filled with air) with thick walls can represent an abscess or primary pulmonary neoplasia which has outgrown its blood supply. Oval shaped cavitary nodules can be caused by parasitic granuloma (i.e. Paragonimus kellicoti). Thin walled gas filled structures most often are bullae. BEWARE of artifactual causes of a structured nodular pattern, such as soft tissue nodules from engorged ticks, teats, and end-on vessels.

Finally we will talk about the nonstructured interstitial pulmonary pattern. In this pattern, the interstitium of the lung is increased in overall opacity. This results in decreased visualization of vasculature margins. Pulmonary vascular markings are obscured but not obliterated (they are obliterated in alveolar pattern). If the pulmonary pattern is not alveolar, bronchial, or structured nodular then it must be a non-structured interstitial pattern. A non-structured interstitial pattern can be described in several ways. A hazy fog-like appearance, short linear fuzzy soft tissue markings (called reticular or linear interstitial), numerous punctate dot-like opacities (called miliary interstitial) and small irregular to round very fuzzy soft tissue aggregate opacities usually seen in conjunction with short fuzzy linear markings (called reticulonodular). Diseases associated with non-structured interstitial patterns include fibrosis which is due to aging or scarring from chronic lung disease, pulmonary edema (perihilar in location with cardiac enlargement), granulomatous (fungal) pneumonia (a reticulonodular manifestation is frequent). Metastatic neoplasia such as with hemangiosarcoma, lymphosarcoma, lymphangatic spread of carcinomas can appear miliary to reticulonodular. Diagnosis often requires aspirates or biopsy of the lung.

A vascular pattern can be considered an additional pulmonary pattern by some. A vascular pattern is when the vessels are increased in visualization. Simple visualization of pulmonary vessels does not constitute a vascular pattern. Vessels can change in three ways: shape, size, and opacity. Abnormal vessel shape is usually seen as obvious tortuosity and blunting of the vessel ends (called "pruning"), common with heartworm disease. When there is increased artery size, heartworm disease is suspected due to muscular hypertrophy and intimal proliferation. Aleurostongylus (another lung parasite) could also be the etiology. Pulmonary hypertension from chronic lung disease, chronic hypoxia, and inflammatory hyperecmia (from septicemia, pancreatitis), and thromboembolic disease. When the veins are increased in size, cardiac causes and non-cardiac etiologies (such as mass at hilus, atelectic lung, and venous thrombosis are possible). Diseases such as fluid overload, left to right shunts, and combinations of left and right heart disease (mitral insufficiency with heartworm disease) should be considered. With shock, hypovolemia, Addison's disease, severe pulmonic stenosis, and right to left shunts can result in decreased size of both arteries and veins. The arteries and veins can artifactually appear small from pulmonary hyperinflation/ emphysema. Pulmonary thromboembolism (PTE) may cause oligemia in the caudodorsal lung lobes. Oligemia is the loss of visualization of pulmonary vessels in the periphery. PTE is often wedged in shape.