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We have already seen how disease can consolidate or collapse a segment or lobe. We now look at other patterns of diffuse and focal lung disease. The lung reacts to disease in a limited number of ways. The interstitium can thicken or thin and the alveoli can fill with fluid or extra air. These changes may be focal or diffuse. They may be acute or chronic. This leads to 16 possible combinations: (interstitium = thick/thin), (alveoli = fluid/air), (location = focal/diffuse), and (time = acute/chronic). Relax. We will concentrate only on the most common combinations. These four basic variables help us analyze the chest x-ray and form our differential diagnosis.
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Air sacs form acini, and several acini form a secondary pulmonary lobule. Review Figs. 9.1A and 9.1B . | ||
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Most lung diseases result in increased radiodensity of the lung. If the interstitium thickens, it can be seen more peripherally on the x-ray or computed tomography (CT) scan. If the interstitial thickening is generalized, the pattern is linear (reticular, Fig. 9.2A ). If the thickening is discrete, it forms multiple nodules ( Fig. 9.2B ). If the alveoli fill with fluid, the fluid-filled area becomes radiodense and the interstitium is enveloped in the dense white lung and is not visible ( Fig. 9.2C ). | ||
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In your mind's eye (whatever that is), fuse the patterns in Fig. 9.2 with those in Fig. 9.3 to evaluate these x-ray patterns. | ||
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At the same time, the alveoli still remain aerated. The basic appearance is one of aerated lung but with too many “markings.” | ||
CLINICAL PEARL: Most diffuse interstitial lung disease is chronic and usually caused by fibrosis. Acute diffuse interstitial lung disease is usually caused by pulmonary edema and viral/mycoplasmal pneumonia. | ||
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If the lung markings are sharp (well defined) and distorted (i.e., angular, irregular, bowed), the disease is probably chronic. | ||
CLINICAL PEARL: The most reliable method of distinguishing acute from chronic is by viewing past films or, heaven forbid, taking a history. Neither is cheating. It is synthesizing information to arrive at the best possible answer for the patient. | ||
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In Fig. 9.5B , the CT scan shows distorted and sharp interstitium from interstitial fibrosis. The rest of the lung is aerated. | ||
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Fig. 9.6B also shows prominent interstitium that is not well defined or distorted. Note that the bronchial walls are thick, suggesting active disease. Figs. 9.6A and 9.6B are due to acute nonbacterial (interstitial) pneumonia. | ||
Another form of fibrosis is “honeycombing.” The fibrosis forms multiple small “cysts,” often stacked up one on another, adjacent to the pleura. Figs. 9.7A and 9.7B show an x-ray and CT scan with honeycombing. | ||
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We have just learned that most diffuse interstitial lung disease is chronic. Most alveolar disease whether focal, multifocal, or diffuse, is acute. With alveolar disease, the airspaces are filled with fluid (e.g., edema, blood, mucus, pus, or cells), making the lung appear airless. The alveolar pattern may be relatively homogeneous (a lobe or segment) or patchy and scattered throughout the lung. | ||
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Note the consolidation in Fig. 9.8A is not uniform in the left lower lobe. The mid lung is consolidated and the lower lung shows groundglass opacifcation. In Fig. 9.8B , the CT scan shows the two patterns | ||
In alveolar disease, an air bronchogram is visible if the airways are open. In interstitial disease, unless very severe, the bronchi are still surrounded by aerated lung. | ||
Fig. 9.9 shows multifocal airspace consolidation. The right upper lobe has an air bronchogram (arrows) and a silhouette sign of the upper heart and mediastinum—three important signs of alveolar filling disease. There is also focal consolidation of the right lower lobe without a visible air bronchogram or silhouette sign. | ||
CLINICAL PEARL: The most frequent causes of acute diffuse alveolar disease are bacterial pneumonia and severe pulmonary edema. The most frequent cause of acute focal alveolar consolidation is also infection. Subacute alveolar consolidation is often granulomatous infection (tuberculosis, fungal). | ||
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History is helpful but less reliable. | ||
To make life difficult, some diseases have alveolar consolidation and interstitial thickening. There is also an intermediate density called “ground glass” opacification (think frosted shower door glass). It increases lung density without obscuring the vessels. This pattern is nonspecific and can be due to partial alveolar filling or extreme interstitial thickening. (See Fig. 9.8B ; the posterior lung shows ground glass disease.) | ||
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CLINICAL PEARL: An important form of focal alveolar consolidation is the mass or nodule (the famous “spot on the lung”). If a very focal area of consolidation has well-defined borders and measures greater than 3 cm, it is referred to as a mass. If it is less than 3 cm, it is called a nodule. | ||
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In Fig. 9.12A , the smaller opacity (B) measures 1.2 cm and is termed a nodule. | ||
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CLINICAL PEARL: In young patients, chronic alveolar consolidation, nodules, and masses are most often due to indolent infection or inflammatory lung disease. In patients older than age 40, cancer becomes a major concern. | ||
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Fig. 9.13A shows a cavitary mass (white arrow), a cavitary nodule (black arrow), and a noncavitary mass, all from lung metastasis. Fig. 9.13B is an infectious cavity (abscess). | ||
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This is because the x-ray beam is perpendicular to air-fluid level on supine images. | ||
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In Fig. 9.14B , the cup margin ( arrow ) is very sharp, but the water margin ( arrowhead ) is less sharp. The top of the water column is wider than the bottom, so one is looking down at two edges not quite superimposed. | ||
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Fig. 9.15A shows an air-fluid level ( arrow ) in a cavitary right mid lung pneumonia. Fig. 9.15B shows air-fluid level in a right middle lobe abscess. Compare with Fig. 9.13 , where there is no fluid in the cavities. | ||
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Fig. 9.16B shows the same granuloma on CT. | ||
CLINICAL PEARL: Heavy calcification is an important sign of benign disease in the lung. Healed tuberculosis and histoplasmosis are the most frequent causes of lung granulomas. Fig. 9.16B also shows a calcified lymph node, difficult to see on the x-ray. | ||
Few conditions cause the lung to be more radiolucent. If the lung is hyperinflated, it becomes hyperlucent because a fixed amount of tissue is spread over a larger volume. If the interstitium is destroyed, such as in bulla formation, the lung becomes more hyperlucent because there is less tissue to absorb radiation. Bullae or sparse markings replace normal branching vessels ( Fig. 9.17 ). Cavities and air cysts cause focal hyperlucencies. | ||
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The anteroposterior diameter is increased (i.e., barrel chest). | ||
The combination of hyperinflation and bullae (sparse or distorted markings or lung destruction) indicates emphysema. In Figs. 9.17C and 9.17D , note the cystic spaces and distortion caused by the thin walled bullae. On Fig. 9.17A , note the sparse upper lobe marking due to bulla. | ||
CLINICAL PEARL: Asthma may also hyperinflate the lung, but there are no bulla present. A very tall, thin, normal person may also appear to have “long lungs” (pseudohyperinflation). | ||
In real life, these nice neat patterns of lung disease often overlap. However, this approach provides a way of organizing your descriptions to form a differential diagnosis. | ||
Anagram: Snooze alarms = _____________. |
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No quiz – Below are some illustrations that will help you master the interstitial patterns better. |
Note that the pulmonary vessels are the only structures seen within the air-filled lung. They branch, taper, and are barely visible as they reach the pleura. Bronchi are barely visible beyond the inner half of the lung.
This is like looking at the anatomy through a frosted shower door. The lung is an intermediate shade of gray, but the pulmonary vessels are visible within the gray areas. The diminished aeration may be due to (1) decreased air in the alveoli caused by partial alveoli filling, (2) decreased air in the alveoli caused by thickened interstitium encroaching on the alveoli, or (3) decreased air in the alveoli due to hypoventilation and atelectasis.
atelectasis
aspiration pneumonitis
infection, such as pneumocystis
edema, acute respiratory distress syndrome (ARDS)
pulmonary hemorrhage
idiopathic (e.g., desquamative interstitial pneumonitis, chronic organizing pneumonia)
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