Figure 37.1. Hemoptysis: chest x-ray 1.

    The differential diagnosis of a pulmonary cavity includes tuberculosis, bacterial lung abscess, lung cancer, and pulmonary vasculitis (e.g., granulomatosis with polyangiitis). The upper lobe location and associated volume loss are suggestive of mycobacterial disease such as tuberculosis. Which of the four clinical histories might fit with this x-ray appearance? Our choice is case history 3, the patient with subacute to chronic purulent sputum production with blood admixed plus night sweats, fever, and weight loss. The chest x-ray together with this brief history raises high the suspicion of cavitary tuberculosis, with multifocal spread of infection in both lungs. Consider the initial evaluation and treatment in this patient: have the patient wear a face mask; if hospitalized, request a negative-pressure isolation room; send sputum on at least three occasions for mycobacterial (acid-fast bacilli or AFB) culture and smear; and probably soon initiate antituberculous therapy with three or four drugs.

    The second chest x-ray in this series (Figure 37.2) has two major left-sided abnormalities notable as one inspects the normal contours of the hilar and mediastinal structures and of the diaphragms and pleural surfaces. There is a large, rounded opacity that at its top begins at the level of the arch of the aorta and then obliterates both the aortopulmonary recess and the left hilar shadows. It looks like a large mass. In addition, the left hemidiaphragm is raised cephalad several centimeters above its usual position. A third finding of note is the hazy fanlike opacity with sharp medial border that extends “northeast” from the hilar area into the region of the left upper lobe. It is this appearance that is particularly worth remembering: the image of left upper lobe collapse. Unlike the right upper lobe, which collapses as an opacity that fills the right apex, the left upper lobe collapses anteriorly (its apex still tethered at the hilum), allowing aerated left lower lobe tissue to fill the left apex.

    As in any lobar atelectasis, there must be adjustment of other structures to compensate for the volume loss—cephalad movement of the ipsilateral diaphragm, shifting of mediastinal structures (sometimes including the heart) toward the side of collapse, and overexpansion of the remaining ipsilateral lobe(s) of the lung. In this example the left hemidiaphragm has shifted dramatically upward, perhaps in compensation for left upper lobe collapse, perhaps also due to phrenic nerve injury with hemidiaphragmatic paralysis.

    What is the cause of left upper lobe collapse in this case? It is likely the result of proximal obstruction of the left upper lobe bronchus by the large medial mass. In a patient with hemoptysis, we would strongly suspect a neoplasm, probably a lung cancer. Case history 1 seems the best fit: a cigarette smoker with symptoms of chronic bronchitis (daily early morning cough) and weight loss, whose physical examination indicates (among other likely findings) clubbing of the digits. Evaluation of this patient with hemoptysis might include further imaging (chest computed tomography [CT]), sputum for cytology, and probable bronchoscopy for visualization of the airway obstruction and tissue sampling. Treatment will depend on the type of neoplasm and the anatomic extent of tumor involvement (both within and outside the thorax) but might include external beam radiation, chemotherapy, and possibly endobronchial approaches to opening the left upper lobe bronchus.

    The third chest x-ray to consider (Figure 37.3) has diffuse parenchymal opacities bilaterally, left more than right. Especially in the left lung, the appearance is that of diffuse “ground-glass” opacities. This ground-glass appearance is uniform in its “texture,” not so dense (like consolidation) that one cannot see aerated lung throughout, and not linear and nodular (like an interstitial process). It reminds one of the glass door of a shower stall made opaque by grinding the surface of the glass. The pathologic correlate of this radiographic pattern is partial or incomplete airspace filling, sometimes with edema fluid (e.g., congestive heart failure), sometimes with inflammatory material (e.g., Pneumocystis pneumonia), and sometimes with blood (e.g., diffuse alveolar hemorrhage).

    In our patient with hemoptysis, this radiograph raises a relatively limited differential diagnosis. Diffuse alveolar hemorrhage (in the absence of severe coagulopathy and/or platelet disorder) makes one think of a pulmonary vasculitis, and if we add in the “dark-colored urine and serum creatinine of 2.5 mg%” of case history 2, it specifically focuses us on pulmonary-renal hemorrhage syndromes. Diagnostic considerations include Goodpasture syndrome, granulomatosis with polyangiitis (Wegener’s granulomatosis), and collagen-vascular disorders, especially systemic lupus erythematosus. To establish a specific diagnosis we may rely on serologic information, such as anti-glomerular basement membrane (anti-GBM) antibody, antinuclear cytoplasmic antibody (ANCA), and antinuclear antibody (ANA), or we may obtain tissue for histologic analysis via lung or kidney biopsy. In fact, in this patient the finding on chest x-ray of free air under the right diaphragm (extra credit for all who noticed this finding!) suggests that a renal biopsy may have recently been performed. Treatment of hemoptysis in this patient is likely to involve high-dose systemic corticosteroids with potential addition of other modalities such as cyclophosphamide or rituximab (for granulomatosis with polyangiitis) or plasmapheresis (for Goodpasture syndrome).

    By process of elimination we can match the fourth chest x-ray in this series with case history 4, a patient with hemoptysis and pleuritic chest pain 3 days after a surgical procedure. Based on the history alone, the possibility of pulmonary embolism jumps to mind. Other potential causes might include pneumonia, perhaps upper airway bleeding following intubation, or postsurgical bleeding following thoracic surgery—but pulmonary embolism is the potentially fatal etiology that we will not want to miss. The chest x-ray that we obtain (Figure 37.4) has opacity at the left base. There is “blunting” of the left costophrenic angle consistent with a small pleural effusion (a lateral chest film would be helpful here for confirmation) and loss of the normal silhouette along the medial portion of the left hemidiaphragm, perhaps due to pleural effusion and perhaps due to a component of subsegmental atelectasis causing the left hemidiaphragm to be raised up slightly and higher than the right hemidiaphragm (the reverse of normal).

    A small pleural effusion and minor subsegmental atelectasis are common findings following cardiothoracic and upper abdominal surgery and are nonspecific. And that’s the point, here. The findings of pulmonary embolism on plain chest radiography are typically none (a normal chest film) or nonspecific (with pleural effusion and minor atelectasis being the most common abnormalities). Only very rarely in pulmonary embolism will one find the dramatic pleural-based, wedge-shaped consolidation with rounded apex (so-called “Hampton’s hump”; Figure 37.5) that is characteristic of pulmonary infarction. Were one to wait to see this plain film manifestation of pulmonary embolism, one would miss a lot of pulmonary emboli!

    For our last patient with hemoptysis, then, evaluation will likely involve either a ventilation-perfusion lung scan or chest CT angiogram. If a diagnosis of pulmonary embolism is confirmed, then treatment of this patient with hemoptysis will be, paradoxically, anticoagulation.

CHRONIC INTERSTITIAL LUNG DISEASES

Alveolar walls and their constituents (epithelial lining cells, macrophages, collagen, elastin, and other matrix proteins, and pulmonary capillaries) make up the pulmonary interstitium. As discussed elsewhere in this volume, a broad collection of chronic inflammatory lung diseases affect primarily the pulmonary interstitium. Common categories include idiopathic pulmonary fibrosis, sarcoidosis, hypersensitivity pneumonitis, pneumoconiosis, and “other.” The plain film radiographic hallmarks of these interstitial pulmonary processes are linear and nodular opacities. As shown in the accompanying cartoon (Figure 37.6), this pattern is made up of some combination of opaque lines of varying length and thickness and dots (nodules) of varying size. The combination of linear shadows and dots gives a lacelike pattern generally readily distinguishable from consolidation (dense white opacity) or ground-glass appearance (as discussed above). High-resolution chest CT imaging (HRCT) has proved very useful in distinguishing distinctive patterns of interstitial inflammation, helping further to identify specific diseases or disease patterns within this broad category. Obtaining an HRCT is the appropriate next step in the radiographic evaluation of most instances of chronic interstitial lung disease.

    Often the finding of diffuse linear and nodular opacities on chest film is nonspecific. A specific etiologic diagnosis will require additional history, further chest imaging (HRCT), and perhaps lung biopsy (either bronchoscopic or thoracoscopic). However, on occasion the history and characteristic chest x-ray appearance will point to a specific diagnosis or limited group of diagnoses, as illustrated by the following examples (figures 37.7–37.10). Four brief case histories follow (to be matched to the four accompanying chest x-rays). Each of these four patients presented with nonproductive cough and progressive dyspnea on exertion of several months’ duration.

•  Case 1. Inoperable gastric cancer

•  Case 2. Work as a stonecutter in a quarry for 20 years, now retired for 10 years

•  Case 3. Prior episodes of erythema nodosum and uveitis

•  Case 4. Work cleaning and insulating boilers for 30 years

    The first chest x-ray in this series (Figure 37.7) has fairly subtle parenchymal opacities, left lower lung zone more than right, with what appear to be fine nodular opacities. Most striking is an ancillary finding: large hilar shadows bilaterally. The lobulated appearance suggests enlarged hilar lymph nodes. Bilateral hilar adenopathy can often be confirmed on lateral chest x-ray with the so-called “doughnut” or “bagel” sign: a ring of opacification surrounding the major bronchi at the distal end of the tracheal air column (Figure 37.11, right-hand panel). On the posteroanterior chest film one can probably make out bilateral mediastinal adenopathy as well: an enlarged azygous node along the right margin of the inferior portion of the trachea and aortopulmonary adenopathy suggested by blunting of the normal recess between the aortic arch and the upper margin of the left main pulmonary artery.

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