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Thoracic Imaging |
1 From the Department of Radiology, Medical College of Wisconsin, 9200 W Wisconsin Ave, Milwaukee, WI 53226-3596 (L.R.G.); the Departments of Anesthesia and Intensive Care (L.R.G., R.F., P.T., A.P.) and Radiology (M.T.), and the Institute of Biomedical Sciences (M.F.), University of Milan, Monza, Italy; and the Department of Anaesthesia and Intensive Care, Ospedale Maggiore Di Milano IRCCS, Milan, Italy (L.G.). Received October 23, 1998; revision requested January 5, 1999; revision received February 16; accepted June 8. Address reprint requests to L.R.G.
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Abstract |
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MATERIALS AND METHODS: Thirty-three patients, 22 with ARDSP and 11 with ARDSEXP, underwent helical CT shortly after intubation. Two readers evaluated images for the type, extent, and distribution of pulmonary opacities; secondary findings; and correlation with survival and physiologic parameters.
RESULTS: In both ARDSP and ARDSEXP, approximately 80% of the lung was abnormal. In ARDSP, ground-glass opacification and consolidation were equally prevalent, whereas in ARDSEXP ground-glass opacification was dominant. Ground-glass opacification was evenly distributed, whereas consolidation tended to be dorsal and caudal. ARDSP often caused asymmetric consolidation, whereas ARDSEXP caused symmetric ground-glass opacification. Air bronchograms were almost universal. Pleural effusions were present in one-half of the patients, and Kerley B lines and pneumatoceles were uncommon. Lung consolidation correlated with the ratio of mean partial pressure of arterial oxygen to fraction of inspired oxygen, shunt fraction, and pulmonary arterial pressure. The patients who died tended to have more consolidation and asymmetric disease.
CONCLUSION: ARDSP tends to be asymmetric, with a mix of consolidation and ground-glass opacification, whereas ARDSEXP has predominantly symmetric ground-glass opacification. In both groups, pleural effusions and air bronchograms are common, and Kerley B lines and pneumatoceles are uncommon.
Index terms: Computed tomography (CT), helical, 60.12115 • Lung, consolidation • Lung, CT, 60.12111, 60.12115 • Lung, diseases, 60.21, 60.413 • Respiratory distress syndrome, adult (ARDS), 60.413
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Introduction |
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A major reason for this variability is the very broad definition of ARDS (12–15). The 1992 American-European Consensus Conference (12) defined ARDS as a clinical syndrome of acute persistent respiratory failure characterized by severe hypoxia (partial pressure of arterial oxygen to fraction of inspired oxygen [PaO2/FIO2] ratio, < 200 mm Hg), bilateral pulmonary infiltrates, and no evidence of congestive heart failure. The conference recognized that ARDS may be due to direct or indirect lung damage. "In general, it is useful to think of the pathogenesis as consisting of two pathways: (a) the direct effects of an insult on lung cells and (b) the indirect result of an acute systemic inflammatory response" (12). There was no mention of how this dual classification might affect the radiographic and CT appearances. Many researchers (4,16) recognize that experimental ARDS due to pulmonary vascular injury and ARDS due to direct lung injury are not identical. Gattinoni et al (16) also found that the respiratory mechanics in patients with ARDS due to direct pulmonary disease (ARDSP) and those in patients with ARDS due to extrapulmonary disease (ARDSEXP) differ substantially. The retrospective nature of most CT studies of ARDS, in which most patients are examined for specific clinical problems, also adds confusion. The majority of patients examined have late-stage disease (2,6,10,17,18).
There may be clinical and imaging advantages to distinguishing ARDSP from ARDSEXP. In this prospective study, 33 patients with ARDS in the early course of the disease underwent CT scanning. The scans were graded for morphologic appearance, disease severity, regional disease distribution, and secondary features. The imaging findings in patients with direct pulmonary injury (ie, ARDSP) and indirect lung injury (ie, ARDSEXP) were analyzed separately. After the CT scores were correlated with key physiologic parameters, the results were reanalyzed, and the survivors were compared with the nonsurvivors. This study was performed to assess the differences between ARDSP and ARDSEXP and determine whether pulmonary and systemic insults contribute to its variable appearance.
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MATERIALS AND METHODS |
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CT Scanning
CT scanning was performed with a Tomoscan SR-7000 spiral CT unit (Phillips Medical Systems, Best, the Netherlands). Ten-millimeter-collimation helical scans were obtained from the apex of the lung to the diaphragm during controlled ventilation (tidal volume [± SD], 590 mL ± 240.5; respiratory rate, 17.5 breaths per minute ± 4.7; positive-end expiratory pressure, 5–15 cm of water [average, 11.6 cm ± 3.2]). The scans were obtained by using 120 kV, 250 mA, and a 1:1 pitch. The lungs were viewed at a window width of 1,500 HU and level of -600 HU. Three patients underwent scanning (one helical, two nonhelical) at outside institutions.
CT Evaluation
The scans were evaluated at three representative levels: the apex (top of the upper aortic arch), the hilum (first section below the carina), and the base (2 cm above the highest diaphragm). Each transverse scan was divided into three sections: an anterior third (sternal), posterior third (vertebral), and middle third (central). The left and right lungs were analyzed individually. The final analysis consisted of 18 anatomic locations: three transverse levels (apex, hilum, and base), each of which was analyzed at three positions (sternal, central, and vertebral) in the left and right lungs.
Two experienced chest radiologists (L.R.G., M.T.) read the CT scans jointly without knowledge of the clinical or radiologic data. They were aware of the patient's age, sex, and diagnosis of ARDS. At each of the 18 locations, the lung was scored as follows: normal lung (NL), ground-glass opacification (GG) (mild increased attenuation, visible vessels), and consolidation (CO) (markedly increased attenuation, no visible vessels). For each location, a 0 was assigned when the morphologic features were essentially absent; 1, when the morphologic features occupied one-third or less of the subsection; 2, when the morphologic features occupied one- to two-thirds of the subsection; and 3, when the morphologic features occupied more than than two-thirds of the subsection. The sum for each subsection had to equal three (eg, NL = 2, GG = 1, CO = 0). A representative case is shown in Figure 1.
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The entire CT scan of the lung (all transverse levels) was also scored for secondary abnormalities.
1. Segmental air bronchograms were scored as absent (none or one per lung), few (two to four per lung), or numerous (more than four per lung).
2. Pleural effusion less than 1 cm was considered to be small, and that greater than 1 cm was considered to be large (unilateral or bilateral).
3. Pneumothorax was scored as absent or present (unilateral or bilateral).
4. Pneumomediastinum was scored as present or absent.
5. Kerley B lines (visible interlobular septa) were scored as absent, at the apex only, or at the lung base (unilateral or bilateral).
6. Pulmonary vessel size and distribution were rated subjectively as normal, diminished, increased (enlarged relative to adjacent bronchi), or not visible because of lung disease.
7. Bullae (homogeneous focal areas of hypoattenuation) were counted, assigned to one of three levels of the lung—the apical third, basal third, or middle third—and then located in one of three lung positions—the sternal, central, or vertebral third.
Clinical and Physiologic Assessment
The cause of ARDS was determined by a senior intensive care physician (R.F.) by using all clinical, biochemical, radiologic (but not CT), and bacteriologic data and American-European Consensus Committee guidelines (12). No patient had evidence of left-sided heart failure at admission. To be as inclusive as possible, a cause was assigned on the basis of the best available data. A specific pulmonary cause was assigned in 21 of 22 patients with ARDSP. None of the patients with ARDSEXP had historical or laboratory evidence of acute lung disease at admission; however, they all presented with an obvious major nonpulmonary disease known to cause ARDS.
Basic demographic data were collected and compared in both groups. In addition, the patient's overall condition was evaluated with a Simplified Acute Physiology Score, version II (SAPS II) at admission and a Murray score on the day of CT. All patients had a pulmonary arterial Swan-Ganz catheter in place to assess pulmonary hemodynamics and to draw mixed venous blood for shunt fraction determination. Arterial and mixed venous gases were analyzed within 4 hours of the CT examination by using an ABL 330 radiometer. Invasive hemodynamic and ventilatory parameters were recorded on a Sirecust 1281 unit (Siemens, Uppsala, Sweden). To normalize the arterial oxygenation relative to the FIO2 concentration, the PaO2/FIO2 ratio was adopted to express the degree of oxygenation derangement (19). The intrapulmonary shunt fraction (Qs/Qt) was computed according to the following formula: Qs/Qt = (Ccap - Cart)/(Ccap - Cven), where Ccap equals capillary concentration of oxygen; Cart, arterial concentration of oxygen; and Cven, venous concentration of oxygen. Finally, the various clinical, CT, and physiologic parameters were compared between the survivors and nonsurvivors.
Statistical Analysis
The normal distributions of the radiologic composite scores (total NL, total GG, total CO) and the physiologic variables were assessed by means of the Shapiro-Wilk statistic (20). Because the null hypotheses were not rejected for all of these variables, parametric statistics were primarily considered for the reported analysis. The differences in mean values between the patients with ARDSP and those with ARDSEXP and between the survivors and nonsurvivors were assessed by using the Student t test for unpaired data. First-moment Pearson correlation coefficients were used to assess the association between variables. Nonparametric statistics were computed (Wilcoxon rank sum and Kendall 
rank tests), but, as expected, they did not show any differences from the parametric test results or any increase in power. Taking into consideration the small sample size, .05 was chosen as the indication of statistical significance. The data were analyzed by using the SAS statistical package (SAS/Stat User's Guide, version 6, 4th ed; SAS Institute, Cary, NC).
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RESULTS |
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TOPAbstractIntroductionMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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Types of Parenchymal Abnormality
In ARDSEXP, ground-glass opacification was more than twice as extensive as consolidation (mean total GG, 45.6 ± 15.4; mean total CO, 19.3 ± 9.2 [P = .002]). This contrasted markedly with ARDSP, in which there was an even balance between ground-glass opacification and consolidation (mean total GG, 32.5 ± 14.2; mean total CO, 30.5 ± 14.6 [P nonsignificant]) (Fig 2).
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In ARDSP, ground-glass opacification was evenly distributed in both the craniocaudal and sternal-vertebral directions. Consolidation tended to favor the middle and basal levels, but it favored the vertebral position significantly (mean total CO sternal, 4.1; mean total CO central, 9.7; mean total CO vertebral, 16.8 [P < .01]).
The total lung disease was almost evenly distributed between the left and right lungs in 10 of 11 patients with ARDSEXP and in 16 of 22 patients with ARDSP. Grossly asymmetric disease (greater than 50% difference in total lung disease between the left and right lungs) was always due to asymmetric consolidation.
The following observations were made with regard to the total lung rather than to the three transverse levels.
1. Air bronchograms were seen in 21 (95%) of the 22 patients with ARDSP and in 10 (91%) of the 11 patients with ARDSEXP. More than four air bronchograms were present in at least one lung in 19 (86%) of the 22 patients with ARDSP and in six (54%) of the 11 patients with ARDSEXP. On a lung-by-lung basis, 43 (65%) of the 66 lungs showed four or more air bronchograms at CT.
2. Pleural effusion could not be evaluated in 11 of the 66 hemithoraces because of an indwelling chest tube (five in the right lung, six in the left lung; six in patients with ARDSP, five in patients with ARDSEXP). Nine small and 22 large (>1-cm) effusions were present in 31 (56%) of the 55 remaining pleural cavities (in 21 [55%] of 38 with ARDSP, in 10 [59%] of 17 with ARDSEXP) (Figs 1, 3–5).
3. Pneumothorax was found in seven hemithoraces (in four with ARDSP, in three with ARDSEXP), all of which were known and drained at the time of CT.
4. Pneumomediastinum was present in five patients (four with ARDSP, one with ARDSEXP). In three of these five patients, concurrent pneumothoraces were drained. In the two without pneumothorax, the pneumomediastinum was first discovered at CT.
5. Kerley B lines were seen in 11 patients (seven with ARDSP, four with ARDSEXP). However, only one patient had bilateral lower lobe Kerley B lines. Three had unilateral, basilar Kerley B lines, and seven had upper lobe Kerley B lines only. Four of the 33 patients had wedge pressures greater than 18 mm Hg (range, 18–21 mm Hg) at the time of CT. The wedge pressure was greater than 18 mm Hg in only two of the 11 patients with Kerley B lines, both of which were in the apex. The wedge pressure was greater than 18 mm Hg in two of the 22 patients who did not have Kerley B lines. (Note: All wedge pressures were below 18 mm Hg at the time of intubation.) The distribution of ground-glass opacification in the four patients with elevated wedge pressures was generalized in one, sternal in one, and predominantly unilateral in two patients.
6. The pulmonary vessels could not be evaluated in 36 (54%) of the 66 lungs because of surrounding pulmonary parenchymal density. In the remaining 30 lungs, the pulmonary vessels were believed to be enlarged in only one patient, who had ARDSP. This is the previously mentioned patient with bilateral lower lung Kerley B lines. She had a wedge pressure of 16 mm Hg at the time of CT.
7. Bullae were present in 15 (23%) of the 66 lungs. The total number of bullae in each patient ranged between zero and 18. The average number of bullae was almost identical in the ARDSP and ARDSEXP groups (2.5 for ARDSP vs 2.3 for ARDSEXP). There was no discernible regional pattern or dominance of initial cause.
Survivors versus Nonsurvivors
Six of the patients with ARDSP died, whereas none of those with ARDSEXP died. All six patients who died had ARDSP due to lung infections, but none had AIDS. In the following analysis, the patients who died were compared with all of the survivors. The mean Murray scores of the survivors and nonsurvivors were similar (2.9 ± 0.44 in survivors vs 3.0 ± 0.42 in nonsurvivors [P nonsignificant]). The survivors had a lower mean SAPS II score (32.4 ± 7.9 vs 40.3 ± 7.2 [P = .02]).
The survivors and nonsurvivors had similar mean total disease scores (64.9 ± 13.6 in survivors vs 58.6 ± 14.8 in nonsurvivors [P nonsignificant]). The specific parenchymal patterns, however, showed definite differences. The survivors had twice the ground-glass opacification (mean total GG, 40.6 ± 17.2 vs 20.5 ± 11.6 [P = .01]) and one-third less consolidation (mean total CO, 24.2 ± 12.4 vs 38.1 ± 14.2 [P = .02]). In the survivors, ground-glass opacification and consolidation were symmetrically distributed between the right and left lungs (mean total GG right, 17.7 ± 10.4 vs mean total GG left, 19.6 ± 9; mean total CO right, 14.8 ± 10 vs mean total CO left, 12.9 ± 7.7 [P nonsignificant]). In the nonsurvivor group, however, consolidation was grossly asymmetric, being greater in the right than in the left lung (mean total CO right = 24.4 ± 9 vs mean total CO left = 13.8 ± 7.6 [P = .02]). In three (50%) of the six patients who died, there was a greater than 50% difference in consolidation scores between the left and right lungs, whereas only four (15%) of the 27 survivors had such asymmetry. The sternal-vertebral distribution of disease was similar in both groups.
Numerous air bronchograms (more than four per lung) were seen in 11 (92%) of 12 lungs in the nonsurvivors but in only 32 (59%) of 54 lungs in the survivors. Both the patients with pneumothorax and those with pneumomediastinum survived.
Physiologic Correlations
The mean measurements of the hemodynamic and blood gas parameters are reported in Table 3. As expected, we did not find any statistically significant differences between ARDSP and ARDSEXP. When the population was subdivided according to outcome, survivors had significantly higher arterial oxygenation and lower pulmonary arterial pressure (mean PaO2, 174.0 mm Hg ± 95.9 vs 75.0 mm Hg ± 15.5 [P < .01]; mean pulmonary arterial pressure, 27.1 mm Hg ± 4.69 vs 33.0 mm Hg ± 7.29 [P < .01]).
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DISCUSSION |
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TOPAbstractIntroductionMATERIALS AND METHODSRESULTSDISCUSSIONReferences |
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The CT scans in the majority of patients with ARDSP have areas of consolidation that are presumably due to the initial direct lung injury and areas of ground-glass opacification that are presumably due to either less direct injury, atelectasis, or edema from the systemic effects of the lung injury (eg, septicemia from pneumonia) (6,21). The consolidation is often asymmetric, and, in our study, it was more often in the right lung and in a vertebral-basal location. Not surprisingly, the scans in the patients who died showed more consolidation and less ground-glass opacification, because consolidation indicates more profound physiologic effects.
Conversely, the typical CT scan in a patient with ARDSEXP shows multiple areas of ground-glass opacification, which are usually symmetric and somewhat homogeneous. Consolidation is frequently in the vertebral-basal area of the lung and usually caused by atelectasis due to the weight of the overlying lung (22). Crowded air bronchograms and displaced fissures may help to distinguish atelectasis from infection. Secondary evidence supports our belief that most consolidation in the vertebral and caudal areas of the lung is due to atelectasis rather than infection. Winer-Muram (23) found that these areas seldom represent pneumonia. Langer et al (24) and Pelosi et al (25) found that turning a patient from the supine to the prone position decreases the dorsal consolidation and increases the ventral consolidation within minutes. This dramatic shift must be due to shifting atelectasis, because neither edema nor inflammatory infiltrate should redistribute so rapidly.
Although many of the CT differences between ARDSP and ARDSEXP described above are statistically significant, it is important to emphasize that there is a moderate amount of overlap between the groups. Not every patient with ARDSP has marked asymmetric consolidation. In our study, some had diffuse, ground-glass opacification and consolidation interspersed. Conversely, a few patients with ARDSEXP had extensive, non–gravity dependent areas of consolidation. The reasons for this overlap are numerous. Our initial ARDSP and ARDSEXP classification may have been in error, or some patients may have had both pulmonary and extrapulmonary conditions. Consolidation due to parenchymal disease and that due to non–gravity dependent, airless lung may have similar CT appearances. Very severe capillary leak in ARDSEXP may totally flood the alveoli and appear as consolidation.
We limited our study to the 1st week of intubation because the features that might distinguish alveolar damage (ie, ARDSP) from capillary damage (ie, ARDSEXP) are most likely to be present early in the course of disease (2–4,6,11,17,18). Iatrogenic problems (eg, nosocomial infection, pulmonary infarction) should also be minimal during the 1st week. Nonetheless, the time between intubation and CT varied from 0 to 7 days. Undoubtedly, this added some heterogeneity to our results. A CT examination in the first 24 hours would have been ideal. Intubation was chosen as the reference point because it is reproducible and understandable, whereas the precise time of onset of ARDS is subjective and may vary with the cause. This study also addressed various secondary issues in the imaging of ARDS:
1. Air bronchograms were very common, regardless of the cause of ARDS (8,10,11,17). The majority of lungs had two or more visible segmental air bronchograms. Not surprisingly, they tended to be more frequent in patients with ARDSP and in those who died; both of these groups had more extensive lung consolidation.
2. Pleural effusions have long been held to be uncommon in ARDS and to point one toward an alternative diagnosis of congestive heart failure or local disease (2,7,8,11,17). In fact, CT findings demonstrate that modest pleural effusions are found in the majority of patients, but portable radiography is insensitive for detecting them (26).
3. Kerley B lines are said to be uncommon in ARDS, and, on the basis of our study results, they are (7,8). Bilateral, lower lobe Kerley B lines were visible in only one patient. That patient had enlarged blood vessels and a wedge pressure of 16 mm Hg, all of which indicated mild, left-sided heart failure at the time of CT. In several patients, interlobular septa were seen at the lung apices. Not surprisingly, these did not correlate with the wedge pressure because visible septa are not infrequent in the apices of healthy patients (27–29). The data from our study suggest that by using published criteria (28,29) for CT of left ventricular failure, one might be able to distinguish ARDS from left-sided heart failure or from ARDS with left-sided heart failure. It is likely that thin-section CT would demonstrate more Kerley B lines than did our CT examinations with 10-mm sections.
4. Focal areas of hypoattenuation were seen in only 15 (23%) of 66 lungs. It is not clear whether these represented preexistent bullae or disease-related pneumatoceles (infection or barotrauma). Prior CT studies have shown that pneumatoceles in ARDS are usually seen later in the course of the disease (11,17).
As expected, the hemodynamic and gas exchange values were similar in the ARDSP and ARDSEXP groups. The morphologic ratings used in this study are different from those used in our prior reports (17,30) in which the distribution of CT attenuation (in Hounsfield units) was compared with the physiologic data. In the current series, a correlation between consolidation (ie, total CO) and PaO2/FIO2 and between consolidation and pulmonary arterial pressure was found, confirming our densitometric data. The lack of correlation with most of the physiologic parameters is disappointing, but it reflects the complexity of the syndrome. There was no correlation between total disease (total GG + total CO) and physiologic data. This may have been due to our scoring system, in which total CC and total GG are not independent variables. They are inversely related: The higher the total CO score, the lower the total GG score because they are evaluating the same tissue. Considering consolidation as the main determinant of oxygen impairment and that total CO and total GG are inversely related, one would expect a small correlation with total GG. Similarly, the total disease score is a combination of the total CO and total GG scores. When the population is divided into the two subgroups, ARDSP and ARDSEXP, the relationship with the physiologic parameters is still present in the direct injury population, but it is lost in the indirect injury population. This confirms that total CO, which is more extensive in ARDSP than in ARDSEXP, is the main factor that influences the PaO2, shunt fraction, and mean pulmonary arterial pressure.
One can only speculate on the differences in CT appearance between the patients who survived and those who died, because our sample size was small. The total amount of lung disease was similar between the patients who died and those who survived, but consolidation was more extensive and ground-glass opacification was less extensive in those who died. In our limited series, very extensive ground-glass opacification was not associated with increased mortality, but moderately extensive consolidation was. Perhaps survival is dependent on the amount of normal and mildly abnormal lung (ie, ground-glass opacification) rather than on the overall amount of disease (30,31).
This study also improved our understanding of the distribution and types of pulmonary patterns and perhaps explains why response to mechanical ventilation in ARDS varies from patient to patient. Gattinoni et al (22,30) and Maunder et al (31) emphasized that ARDS is nonhomogeneous and that in early-stage ARDS, the lung can be considered as having three basic compartments: normal lung, edematous and/or atelectatic lung, and consolidated lung. With mechanical ventilation, the CT-based normal lung is thought to be easily distensible—potentially overdistensible—and vulnerable to volutrauma. Ground-glass opacification has many causes, but in the setting of early-stage ARDS, it probably represents a combination of edema, atelectasis, or early hyalin membrane formation. Ground-glass opacification is thought to be pliable, potentially inflatable with positive pressure ventilation, and probably the area most responsible for improved gas exchange. The consolidated lung, which is basically due to alveolar injury or severe alveolar flooding, is not distensible and responds minimally to mechanical ventilation. Perhaps a lung that has predominantly consolidated and normal tissue requires an approach to mechanical ventilation that is different from that for the lung that has predominantly ground-glass opacification and normal tissue.
There were several additional limitations to our study. Our results were, in part, influenced by the mix of patients. Although our intensive care unit is fairly typical and the patient demographics and physiologic parameters in this study were typical for moderate to severe respiratory failure, the patient population was somewhat unusual in that none of the 11 patients with ARDSEXP died, whereas six (27%) of the 22 patients with ARDSP did. For ethical and medical reasons, some of the patients at highest risk could not be moved to the CT suite; this eliminated the sickest patients. It is possible that the four patients with mildly elevated wedge pressures had mild cardiac heart failure, which influenced our results. A review of these cases showed that three of these four patients had ARDSP, but the distribution of ground-glass opacification did not suggest cardiogenic edema.
It is possible that three transverse images do not give a true sample of the lung. However, Tagliabue et al (32) compared three transverse sections with all the transverse sections in five patients with ARDS and found a correlation coefficient r of 0.944 (32). Finally, the patients in our study were examined during the mechanical ventilation cycle. Keeping the patient in forced inspiration or expiration (ie, positive end-expiratory pressure) would have created its own artifacts. The effects of scanning through the respiratory cycle may have caused a slight overestimation of the total GG (ie, blurring). If so, this effect should have been randomized throughout our subjects.
The results of this study demonstrate the differences in CT findings between ARDSP and ARDSEXP. In future imaging and clinical studies, both cause and temporal changes must be considered when characterizing this syndrome.
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Acknowledgments |
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Footnotes |
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Author contributions: Guarantors of integrity of entire study, L.R.G., R.F.; study concepts, R.F., P.T., L.R.G., L.G.; study design, R.F., M.F., P.T., A.P., L.R.G.; definition of intellectual content, L.R.G., R.F.; literature research, L.R.G.; clinical studies, L.R.G., M.T., R.F., P.T.; data acquisition, R.F., P.T.; data analysis, M.F., M.T., R.F., P.T., L.R.G.; statistical analysis, M.F.; manuscript preparation, L.R.G., R.F.; manuscript editing and review, P.T., M.T., L.G., A.P.
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 B. Trotman-Dickenson Radiology in the Intensive Care Unit (Part 2) J Intensive Care Med, September 1, 2003; 18(5): 239 - 252. [Abstract] [PDF]
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 P. Pelosi, D. D'Onofrio, D. Chiumello, S. Paolo, G. Chiara, V.L. Capelozzi, C.S.V. Barbas, M. Chiaranda, and L. Gattinoni Pulmonary and extrapulmonary acute respiratory distress syndrome are different Eur. Respir. J., August 1, 2003; 22(42_suppl): 48s - 56s. [Abstract] [Full Text] [PDF]
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P. Pelosi, L. Brazzi, and L. Gattinoni Prone position in acute respiratory distress syndrome Eur. Respir. J., October 1, 2002; 20(4): 1017 - 1028. [Abstract] [Full Text] [PDF]
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 L Tomlinson and G. Bellingan Trauma and acute lung injury Trauma, July 1, 2002; 4(3): 147 - 157. [Abstract] [PDF]
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D. M. Hansell Acute Interstitial Pneumonia: Clues from the White Stuff Am. J. Respir. Crit. Care Med., June 1, 2002; 165(11): 1465 - 1466. [Full Text] [PDF]
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 A. S. Arbab, S. Aoki, K. Toyama, N. Miyazawa, H. Kumagai, T. Umeda, T. Arai, T. Araki, H. Kabasawa, and Y. Takahashi Quantitative Measurement of Regional Cerebral Blood Flow with Flow-Sensitive Alternating Inversion Recovery Imaging: Comparison with [Iodine 123]-Iodoamphetamin Single Photon Emission CT AJNR Am. J. Neuroradiol., March 1, 2002; 23(3): 381 - 388. [Abstract] [Full Text] [PDF]
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L. GATTINONI, P. CAIRONI, P. PELOSI, and L. R. GOODMAN What Has Computed Tomography Taught Us about the Acute Respiratory Distress Syndrome? Am. J. Respir. Crit. Care Med., November 1, 2001; 164(9): 1701 - 1711. |
