Why all the heavy breathing? Radiography of pulmonary pathology (Proceedings)


Initially we have to review all the normal structures on a thoracic radiograph before we can begin to discuss pathology. So a review....There are three main normal structures in the lungs: the interstitium, airways, and vessels. The interstitium is the supporting structure of the lungs.

Initially we have to review all the normal structures on a thoracic radiograph before we can begin to discuss pathology. So a review....There are three main normal structures in the lungs: the interstitium, airways, and vessels. The interstitium is the supporting structure of the lungs. The bronchi are the large airways and can be seen as they taper and converge together toward the lung. These are so thin they are radiolucent when normal. Mineralization of the bronchial wall (does not cause thickening just increased visualization) can be an age related change. The vessels are thicker than the bronchi and diverge as they extend into the periphery. In a lateral view, the artery is dorsal, the bronchus is in the middle, and the vein is ventral. In left lateral recumbency, the right cranial lobar artery and vein should be the same diameter. The diameter of each vessel should not exceed the smallest diameter of the right 4th rib. On the VD view, the artery is lateral and the vein is axial. The caudal lobar pulmonary artery and vein are similar in size. In the dog, the diameter of these two vessels should not exceed the diameter of the 9th rib. In a cat the vessels are compared to the size of the 10th rib.

It is important to be able to distinguish inspiratory from expiratory radiographs because expiratory films can artifactually appear to have pathology. The post cardiac triangle (the area of the lungs that is caudal to the heart, cranial to the diaphragm and ventral to the caudal vena cava will be large if inspiratory exposure. The lumbodiaphragmatic angle (where the caudal dorsal lung extends adjacent to the lumbar spine on a lateral view) is at or caudal to T12 on an inspiratory film. The costodiaphragmatic angle (where the diaphragm meets the costal arches on a VD view) should be at or caudal to T10 on an inspiratory film. The diaphragmatic cupula will be at or caudal to T8 on an inspiratory VD view. The retrosternal lucency dorsal to the sternum on a lateral view will extend to the 5th sternal segment during inspiration. The apex of the left cranial lung lobe on a lateral view will extend cranial to the first rib on a full inspiratory film. Poor exposure can also be problematic. Underexposure will simulate disease while overexposure will mask disease.

Now onto pathology. We will start with a bronchial pattern. A bronchial pattern is caused by infiltration of the airway by inflammatory cells, edema, neoplastic cells, or mineral. Chronic bronchitis can be due to allergic, parasitic, or inflammatory etiologies. Edema from cardiac disease can cause what appears to be a bronchial pattern but it is actually a peribronchial infiltrate. With bronchoalveolar carcinoma a primary bronchial pattern is seen with concurrent interstitial and alveolar patterns as well. This is considered a mixed pattern. Mineralization of the bronchi can occur with diseases such as Cushings disease. Bronchiectasis is an increased diameter of bronchi or lack of tapering as they extend into the periphery. This represents end stage of chronic bronchial disease and can be secondary to ciliary dyskensis. Feline bronchial lung disease (a syndrome) presents with prominent bronchial markings, 37% have concurrent alveolar lung disease, 10% have collapse of the right middle lung lobe and 10% have pulmonary overinflation due to air trapping. Radiographically bronchial disease appears as "tram lines" which are thickened paired linear/ branching lines which converege as they are traced into the lung periphery or "donuts" which are thickened bronchi viewed in cross section.

There are two types of interstitial patterns. Nonstructured and structured (nodular). Nonstructured is identified as infiltration of lung with soft tissue opaque material. This results in increased pulmonary opacity and decreased visualization of pulmonary vasculature. The pulmonary vascular markings are obscured but not obliterated. This can be described in four different ways: hazy (fog-like), short linear fuzzy soft tissue pulmonary 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 which cause an interstitial pattern include 1) interstitial fibrosis – aging or scarring from chronic lung disease 2)

Interstitial pulmonary edema – perihilar in location with associated cardiomegaly and pulmonary venous congestion 3) Granulomatous (fungal) pneumonia - reticulonodular manifestation is frequent and 4)

Metastatic neoplasia (hemangiosarcoma, lymphosarcoma, lymphangatic spread of carcinomas) - miliary to reticulonodular pattern seen. Structured interstitial patterns show multiple soft tissue nodules measuring between 5mm and 4cm. Most often due to neoplasia, but also can be seen with granulomas, abscesses, or mineral. 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 an inflammatory etiology. Beware of artifactual soft tissue nodules due to by engorged ticks, teats, and end-on vessels. Solitary soft tissue masses are usually neoplasitc. Structures larger than 4cm are called a mass. Multiple mineralized nodules between 1-3mm in size represent benign osseous metaplasia (aka pulmonary osteomas). Soolitary mineralized nodule between 3mm – 4cm in size are usually due to calcified granulomas. Lung tumors rarely calcify. Cavitatary nodules are fully or partially filled with air pockets. Most are smoothly marginated. Thin walled gas filled nodules are considered bullae while thick walled gas nodules are more consistent with an abscess. Paragonimus parasitic granulomas are sometimes oval in shape.

An alveolar pattern in the lungs is due to infiltration of lung to the point of filling of the alveoli. Radiographically we see that soft tissue opacity replaces air opacity. Air bronchograms are seen when air is 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". These are not doughnuts, as the outside bronchial wall is not seen. Infiltrates can be blood, pus, or water. Differentiation depends on distribution. Localized alveolar lung disease can be caused by pneumonia, hemorrhage due to trauma, atelectasis, noeplasia, infarction, or torsion. Thromboembolism usually results due to predisposing renal or adrenal disease, and presents with consolidation of a lung lobe (with infiltrates). There is no loss of volume and no shift of the mediastinum. Disseminated alveolar patterns are seen with severe inflammatory lung disease, severe pulmonary edema, hemorrhage due to coagulopathy, atypical pneumonia, eosinophillic bronchopneumonopathy, and smoke inhalation pneumonitis.

By comparison, atelectasis will have loss of volume and a shift of the mediastinum. Recumbency occurs after at least 30 minutes or more recumbent on one side. When a single bronchus is intubated atelectasis will occur. Plmonary edema etiologies include cardiogenic, neurogenic (electric cord bite, following head trauma, post ictal (seizure), elevated intracranial pressure, near drowning, strangulation injury, smoke inhalation, pneumonitis due to circulating pancreatic enzymes, re-expansion pulmonary edema following chronic lung collapse (esp in cats), actue respiratory distress syndrome (ARDS), hypoprotienemia, and disseminated intravascular coagulopathy (DIC).

Vascular patterns. Simple visualization of pulmonary vessels does not constitute a vascular pattern.

Vessels can change in three ways 1) abnormal vessel shape is usually seen as obvious tortuosity and blunting of the vessel ends (called "pruning") 2) abnormal vessel size and 3) Increased artery size, which occurs with heartworm disease due to muscular hypertrophy and intimal proliferation. Lung parasites such as aleurostrongylus, pulmonary hypertension, chronic lung disease, chronic hypoxia (ie such as can be caused by severe tracheal collapse), inflammatory hyperemia (septicemia, pancreatitis), thromboembolic disease can cause abnormal vessel shape. Increased vein size is seen with both cardiac and non-cardiac causes. Non-cardiac causes result in resistance to venous drainage (mass at the hilus, atelectic lung, venous thrombosis). Increased size of both arteries and veins is seen with cardiac causes such as left to right shunts, iatrogenic fluid overload, cardiomyopathy, mitral insufficiency, and with heartworm disease. The veins and arteries are both decreased in size with shock, hypovolemia, Addisons disease, and cardiac causes such as severe pulmonic stenosis as well as right to left shunts. Small vessel size can be artifactual as well due to pulmonary hyperinflation/ emphysema. Oligemia is the loss of visualization of pulmonary vessels in the periphery of the lung. This is seen with pulmonary thromboembolism (PTE). PTE is usually located caudodorsally and is wedge in shape. Patterns of hyperlucency can be caused diffusely by pulmonary overinflation. You will also see a flattened and caudally displaced diaphragm, increased distance between the heart and diaphragm,ventral bowing of the caudal vena cava, and overally increased lucency of the lungs. On the lateral view the lungs can be seen extending to L1 or further caudally. Overinflation of lungs can be simulated by hypoperfusion, overexposed films, and deep chested dogs on inspiration. Causes of focal hyperlucency include congenital or traumatic bullae, a signet ring granuloma caused by Paragonimus kellicoti, or cavitary neoplasia, abscess, or granuloma.

Next is a review of common pulmonary diseases, what patterns they have, and the distribution of lesions.

1) Aspiration Pneumonia has an alveolar infiltrate that is ventral in distribution and asymmetric. 2) Pulmonary edema can be caused by both cardiogenic and non-cardiogenic etiologies. Cardiogenic pulmonary edema has an interstitial to alveolar pattern which is symmetric and perihilar in distribution.

(It is important to remember that CATS AND DOBERMANS ARE EXCEPTIONS TO THIS DISTRIBUTION!!!!) With cardiogenic pulmonary edema the pulmonary vein is larger than artery and there is left heart enlargement. With non- cardiogenic edema: neurogenic etiologies, vasculitis, and hypoprotienemia are differentials. 3) Allergic lung disease can be caused by eosinophillic bronchopneumonopathy or asthma. Roentgen signs include a diffuse mixed bronchial and interstitial patterns with air trapping (caudal displacement of diaphragm). 4) Granulomatous pneumonitis

May be caused by fungal diseases (most common: blastomycosis, histoplasmosis, coccidiomycosis). The radiographic changes identified with fungal disease include enlarged tracheobronchial lymph nodes, all pulmonary patterns may be present, and cavitary pulmonary nodules (granulomas) are often present.

5) Pulmonary hemorrhage/ contusion – trauma or coagulopathy. Appears as patchy, asymmetric irregular interstitial to alveolar infiltrates that are not perihilar in distribution. 6) Pulmonary embolism is commonly associated with heartworm disease, Cushings disease, glomerulonephritis, neoplasia, pancreatitis, and sepsis. There may be no radiographic changes visible. However oligemia, blunted arteries and a caudodorsal distribution are seen. 7) Primary pulmonary neoplasia is a focal well circumscribed mass that can be cavitary due to central necrosis. Multiple pulmonary metastasis or tracheobronchial lymph node enlargement may be present. With Metastatic pulmonary neoplasia, there are numerous nodules diffusely throughout lungs. 8) Cavitary lung disease can be due to congenital or traumatic etiologies. Caviatry lung disease may also be due to necrotic neoplasia. 9) Degenerative pulmonary disease include pulmonary fibrosis (appears as a nonstructured interstitial infiltrate diffusely throughout the lungs with concurrent bronchial mineralization (seen as increased visualization of bronchial walls), not thickened however pulmonary osteomas – less than 3mm irregularly shaped mineralized opacities in lung

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