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1 Department of Radiology, St. Marianna University School of Medicine, 2-16-1
Sugao, Miyamae-Ku, Kawasaki City, 216-8511 Japan.
2 Present address: Department of Radiology, Dokkyo University School of
Medicine, Mibu, Shimotsuga-gun, Tochigi, 321-0293 Japan.
3 Department of Radiology, University of California San Francisco, 505 Parnassus
Ave., San Francisco, CA 94143-0628.
Received August 3, 2001;
accepted after revision November 14, 2001.
Address correspondence to H. Arakawa.
Abstract
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SUBJECTS AND METHODS. Forty-one consecutive patients with suspected pulmonary embolism underwent expiratory CT followed by helical CT angiography. After excluding 12 patients who had airway disease or were smokers, we divided the patients into two groups: those with (n = 15) and without (n = 14) pulmonary embolism. For each patient, six expiratory images were evaluated for the presence of air trapping, and the corresponding six images from CT angiography were evaluated for the presence of mosaic perfusion. Clot locations were assessed on CT angiography and were correlated with the presence of air trapping and mosaic perfusion.
RESULTS. In patients with pulmonary embolism, mosaic perfusion was identified in 32 areas (seven patients, 46.7%), and air trapping was identified 68 areas (nine patients, 60%). Of the 32 areas of mosaic perfusion, 23 areas (71.9%) showed air trapping on expiratory CT scans. Of the 68 areas with air trapping on expiratory scans, 23 areas (33.8%) showed mosaic perfusion on inspiratory scans, and 44 areas (64.7%) had clots in the arteries leading to them. Clots were more frequently identified in areas of lower attenuation on inspiratory CT scans and air trapping (21/23) than in those of normal attenuation on inspiratory CT scans and air trapping (23/45) (p < 0.005). Only one patient without pulmonary embolism had air trapping (p < 0.005).
CONCLUSION. Air trapping is common in pulmonary embolism and may be the cause of mosaic perfusion. Air trapping can be seen distal to vessels not showing pulmonary embolism.
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Patients with suspected pulmonary embolism underwent chest CT as the initial screening test, followed by ventilation—perfusion radionuclide scanning, and, in selected cases, pulmonary angiography. The diagnosis of pulmonary embolism was made in 23 patients on the basis of high-probability ventilation—perfusion radionuclide scans (n = 18) or abnormal findings on pulmonary angiography (n = 5). Eight of the patients with pulmonary embolism were excluded because they had a history of pulmonary parenchymal disease or were smokers. Thus, our study included 15 patients with pulmonary embolism who neither were smokers nor had a history of pulmonary disease (seven men and eight women; age range, 18-76 years; mean age, 52.7 years). In these 15 patients, the diagnosis of pulmonary embolism was established on the basis of high-probability ventilation—perfusion radionuclide scanning (n = 11) or abnormal findings on pulmonary angiography (n = 4). Five patients had deep vein thrombosis confirmed by venography of the lower extremities; one patient had vasculitis; one patient had protein C deficiency; and in the remaining eight patients, the pulmonary embolism had no identifiable cause.
Nine patients were considered to have acute pulmonary embolism, two had chronic pulmonary embolism, and four had acute and chronic pulmonary embolism. Angiographic criteria for the diagnosis of acute pulmonary embolism included complete or partial filling defects as the sole abnormalities or as observed in association with arterial cutoffs, perfusion defects, or both [13]. On CT, emboli were considered acute if they completely or partially occluded the arterial lumen. The diagnosis of chronic pulmonary embolism was suggested by historic and clinical features and was confirmed by combined results from perfusion lung scanning, pulmonary angiography, echocardiography, and or helical CT angiography. Angiographic criteria for the diagnosis of chronic pulmonary embolism were pouching defects, webs or bands, intimal irregularities, abrupt vascular narrowing, compete vascular obstruction, or any combination of these findings [14]. On CT, the diagnosis of chronic pulmonary embolism required at least one of the following: emboli eccentric and contiguous with the vessel wall, evidence of recanalization, arterial stenosis or web, or reduction of more than 50% of the overall arterial diameter [15]. Acute pulmonary embolism in patients with chronic pulmonary embolism was suspected on the basis of clinical features of an acute episode of chest pain, dyspnea, or hemoptysis in patients with chronic pulmonary embolism and was confirmed by the presence of acute clots on CT (n = 3) or newly developed perfusion defects on perfusion scanning (n = 1).
Eighteen of the 41 patients studied were considered not to have pulmonary embolism because of concordant negative findings on helical CT angiography and ventilation—perfusion scintigraphy and negative findings at clinical follow-up of at least one month. Of the 18 patients without pulmonary embolism, 14 patients had no known airway disease, and they served as a control group (seven men and seven women; age range, 19-67 years; mean age, 49.5 years).
The diagnostic workup was performed by one of the authors and another staff radiologist at our institution. Discordance was resolved by the opinion of a third staff radiologist.
CT Technique
Helical CT angiography was performed from above the aortic arch to the
diaphragm at deep inspiration during a single breath-hold. CT scans were
obtained in all patients using X-Vigor or X-Vision CT scanners (Toshiba,
Tokyo, Japan). A bolus of 100 mL of iodinated contrast material (iopamidol
61%, Iopamiron; Nihon Schering, Osaka, Japan) was injected through the
antecubital vein at a rate of 3 mL/sec with a scan delay of 15 sec. Scanning
parameters included a 3-mm collimation, a 5-mm/sec table speed, and
reconstruction at 3- or 1.5-mm intervals.
We also obtained expiratory high-resolution CT scans at the time of helical CT pulmonary angiography. Expiratory high-resolution CT was performed at deep exhalation (expiratory scans) using a 2-mm collimation. Scans were obtained at six evenly spaced levels from lung apices to bases. In general, scans were obtained at the following levels: above the aortic arch, between the aortic arch and the tracheal carina, at the tracheal carina, between the tracheal carina and the confluence of pulmonary veins, at the confluence of pulmonary veins, and near the diaphragm.
Both mediastinal window images (window width, 300-500 H; level, 30-50 H) and lung window images (window width, 1200 H; level, -750 H) were obtained. Lung window scans were reconstructed using a high-spatial-frequency algorithm.
Image Analysis
CT scans were interpreted by consensus of two radiologists. In the first
session, reviewing both the hard copy and the monitor image, clot location was
recorded in the main, lobar, or segmental arteries in the right or left lung.
When obvious arterial changes suggestive of chronic embolism (e.g., arterial
stenosis or web, reduction of > 50% of the overall arterial diameter) were
identified, we recorded the artery as having a clot even if a low-attenuation
embolus was not clearly identified. If multiple clots were identified in both
the proximal and distal portions of the artery, only the clot in the proximal
portion was recorded. For example, when a clot was identified in the right
interlobar artery, those clots in the lobar and segmental arteries of right
lower and middle lobes were not recorded. Identification of segmental arteries
on CT images required an analysis of both mediastinal and lung window
settings; bronchi were used to accurately identify specific segmental
arteries. Opacification of pulmonary arteries was analyzed at mediastinal
window settings. While viewing on a workstation, we changed lung window widths
and levels when contrast material in the pulmonary artery was considered
sufficiently dense to mask a clot.
In the second session, lung parenchyma was evaluated on hard copy that was photographed with lung window settings, and attention was paid to any lung attenuation abnormalities. Lung window images were reviewed in a session separate from the one dedicated to searching for the clot; the interval between the two sessions was 6 months. We selected inspiratory scans on lung windows that corresponded to the same levels as those of expiratory high-resolution scans, and the presence and location of mosaic perfusion were recorded as defined by areas of decreased lung attenuation with or without reduced vessel size in a lobe [16]. Because we obtained six expiratory slices of each patient, only six inspiratory levels corresponding to the six expiratory levels were selected.
When reviewing expiratory scans, we recorded the presence and location of air trapping. Air trapping was considered present if areas of lung showed a less than normal increase in attenuation after expiration or showed little change in the cross-sectional area [10]. Because air trapping can be seen in isolated secondary pulmonary lobules even in healthy subjects [17], we excluded areas of air trapping seen in a single secondary pulmonary lobule. One area each of mosaic perfusion and air trapping was determined as an area of homogeneously lower attenuation in a lobe on inspiratory and expiratory images, respectively. The extent and location of mosaic perfusion on an inspiratory scan and air trapping on the corresponding expiratory scan were compared and were related to the presence and location of the clot. If one area of air trapping on an expiratory scan involved more than two areas of mosaic perfusion on the corresponding inspiratory scan, the area of air trapping was divided and counted as the same number of areas of mosaic perfusion.
Statistical Analysis
The difference in prevalence of air trapping between patients with
pulmonary embolism and patients without pulmonary embolism was assessed using
the chi-square test. Among the areas with air trapping, the difference in the
prevalence of clots was assessed between the areas of lower attenuation and
those of normal attenuation on the corresponding inspiratory scan levels using
the chi-square test. We considered a p value greater than 0.05 a
statistically significant difference.
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In the second session, seven expiratory slices were excluded because of poor exhalation (four slices in two patients) or mismatch between inspiratory and expiratory scan levels (three slices in two patients). Among 15 patients with pulmonary embolism, nine patients (60.0%) were considered to have air trapping (four with acute pulmonary embolism, one with chronic pulmonary embolism, and four with acute and chronic pulmonary embolism). In distinction, among 14 patients without pulmonary embolism, only one patient showed air trapping (p < 0.005). Air trapping was identified in 68 areas from nine patients with pulmonary embolism, and mosaic perfusion was identified in 32 areas from seven patients (four with acute pulmonary embolism and three with acute and chronic pulmonary embolism). These seven patients also had air trapping. Areas of air trapping were identified in the right upper lobe (n = 18), left upper lobe (n = 13), right middle lobe (n = 4), right lower lobe (n = 19), and left lower lobe (n = 14). Areas of mosaic perfusion were identified in the right upper lobe (n = 5), left upper lobe (n = 10), right middle lobe (n = 3), right lower lobe (n = 9), and left lower lobe (n = 5).
Thirty-two areas showed decreased lung attenuation on the inspiratory scan, and 20 of these areas (62.5%) showed reduced vessel size as a sign of mosaic perfusion (Fig. 1A,1B,1C). Clots were identified on helical CT angiography in 29 arteries (90.6%) proximal to the areas of decreased attenuation. Of the 32 areas of decreased attenuation on the inspiratory scans, 23 areas (71.9%) in seven patients showed air trapping on the expiratory scans. Of the nine areas with decreased attenuation not associated with air trapping, eight (88.9%) of the areas had clots in the proximal arteries.
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In 68 areas with air trapping, clots were identified on helical CT angiography in 44 arteries (64.7%) proximal to those areas (Figs. 2A,2B,2C and 3A,3B,3C). However, in the remaining 24 areas, no clot was identified (Fig. 4A,4B,4C). Forty-five areas (66.2%) showed normal attenuation on the inspiratory scans, and 23 of these areas (51.1%) showed clots in the arteries proximal to them. Twenty-three (33.8%) of the 68 areas that showed air trapping on the expiratory scans showed decreased attenuation on the inspiratory scans, and 21 of these areas (91.3%) had clots in the arteries proximal to them. The prevalence of clots in the proximal artery was significantly higher in areas of air trapping with mosaic perfusion (mosaic perfusion due to air trapping) than in areas of air trapping with normal lung attenuation on inspiratory scanning (p < 0.005).
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It has been suggested that air trapping may be seen on expiratory high-resolution CT in patients with pulmonary embolism, and that it is responsible for the areas of low attenuation [12]. Worthy et al. [12] reported that two of four patients with vascular disease in their study showed air trapping on expiratory scans. Asthmalike wheezing is reported to occur in patients with acute pulmonary embolism and is attributed to bronchoconstriction in those patients [25,26,27,28]. Initially, Gurewich et al. [26] reported seven patients with acute pulmonary embolism who showed evidence of bronchoconstriction on spirometry. One of their patients presented with expiratory wheezing. This bronchoconstriction was relieved by IV administration of heparin in four patients. In a subsequent larger series, Sasahara et al. [25] studied 72 patients with acute pulmonary embolism and confirmed the presence of bronchoconstriction on spirometry in most of their patients. The bronchoconstriction in their series also showed improvement after IV administration of a bolus of heparin. The proposed mechanism of bronchoconstriction in acute pulmonary embolism includes bronchoactive amines such as serotonin and prostaglandins that are released from platelet aggregations in the thrombus, as has been shown in canine lungs [29], or a change in parasympathetic nervous system tension, which controls the bronchial smooth-muscle tension [30].
Our study, using expiratory CT, showed that air trapping is not rare in patients with pulmonary embolism and that air trapping was associated with areas of mosaic perfusion in 71.9% of the patients we studied. In these areas, the cause of mosaic perfusion was attributed to air trapping. Air trapping on expiratory CT was seen not only in areas with pulmonary embolism (64.7%) but also in areas without embolism (35.3%). In a report of experimentally induced unilateral pulmonary embolism in dogs, Austin and Sagel [30], using 24-hr-old human venous thrombi as embolic material, observed that bronchial narrowing did not differ quantitatively between the ipsilateral and contralateral lungs. They concluded that bronchial narrowing is a generalized response, mediated by humoral factors or the parasympathetic nervous system. Our results also support this conclusion.
Furthermore, our study showed that the presence of a clot was more frequently associated with areas of mosaic perfusion due to air trapping than with areas of normal attenuation with air trapping on inspiratory scans. Because lung attenuation is determined by the amount of air in the alveoli, pulmonary interstitium, and pulmonary blood volume, lower attenuation in areas distal to the artery with pulmonary embolism can be attributed to increased air content, reduced blood volume, or both. We think that bronchoconstriction might be more severe in areas with pulmonary embolism than in areas without pulmonary embolism. It is possible that both the direct reduction of pulmonary blood volume by a clot and air trapping contribute to the lower lung attenuation on inspiratory CT, although findings in the experimental studies of Im et al. [23] and Kim et al. [24] suggest that this is not likely to be the case.
In acute pulmonary embolism, the presence of mosaic perfusion is considered uncommon. Coche et al. [21] compared lung parenchymal findings of 88 patients with suspected acute pulmonary embolism who underwent helical CT pulmonary angiography. Those researchers found mosaic perfusion in 12% of patients with acute pulmonary embolism and in 10% of patients without this finding. Shah et al. [18] evaluated parenchymal findings in 28 patients with acute pulmonary embolism and found only 7% with mosaic perfusion. However, in our series, we found mosaic perfusion in four (44.4%) of nine patients with acute pulmonary embolism—a higher frequency than expected. This high frequency in our series may result from a variability of patient selection and our special attention to changes in lung attenuation.
In our series, air trapping was observed in a patient with chronic pulmonary embolism despite the fact that air trapping is rarely reported in the literature [12]. Im et al. [23] reported that they found a patient with air trapping in a chronic pulmonary embolism who had Takayasu's arteritis. Remy-Jardin et al. [31] reported progressive cylindric dilatation of bronchi in 21 of 33 patients with chronic pulmonary embolism who were followed up with CT, and they suggested possible airway changes in this disease. Pulmonary function—test results in their series showed a normal range of mean forced expiratory volume in 1 sec, but they found that the mean value of the maximum expiratory flow between 25% and 75% of the forced vital capacity was reduced. They speculated that morphologic and functional derangements occurred in the small airways in their patients as a result of chronically absent pulmonary arterial perfusion [31]. We think that air trapping in our patient with chronic pulmonary embolism is likely the result of airway changes caused by chronic pulmonary artery obstruction, as suggested by Remy-Jardin et al., although our patient had no identifiable bronchial dilatation. Another possible mechanism of air trapping in patients with chronic pulmonary embolism may be repeated undiagnosed acute embolization.
Our study has several limitations. First, helical CT angiography was used in most of the patients to determine the presence of clots and their location. The diagnostic accuracy of helical CT angiography is comparable to that of conventional angiography in the diagnosis of both acute and chronic pulmonary embolism involving the proximal arteries [32,33,34]. However, small clots in the peripheral arteries may be missed on helical CT angiography [35]. Second, the inspiratory scans used for comparison in most patients were obtained after injection of contrast material. As a result, we could not measure lung density differences between inspiratory scans and expiratory scans, and our observation of air trapping was based solely on the subjective visual assessment of lung attenuation. Only those areas showing obvious low attenuation or no change of cross-sectional area after expiration were considered to show air trapping. Third, our study included a relatively small number of patients.
In conclusion, air trapping occurred in 60% of patients in our study with the CT finding of pulmonary embolism. Air trapping was associated with mosaic perfusion in 71.9% of lung regions and occurred not only in areas distal to visible clots but also in areas that were well perfused. In an appropriate clinical setting, pulmonary embolism should be considered in the differential diagnosis of diseases associated with mosaic perfusion and air trapping.
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