CONTENTS
8.1 Introduction 121 8.2 Morphologic Changes 122 8.2.1 Acute Phase 122
8.2.2 Subacute Phase 125 8.2.3 Late Phase 125
8.3 Physiologic Changes 126 8.4 Conclusion 129
References 129
8.1 Introduction
In 1967, Ashbaugh et al. reported on 12 patients who developed acute dyspnea, tachypnea, refractory hy poxia, and diffuse bilateral infi ltrates on the chest radiograph. In each patient, symptoms had de vel oped after a major systemic insult. They coined the term
“adult respiratory distress syndrome” [sub se quent ly termed acute respiratory distress syndrome] (ARDS), a syndrome distinct from Respiratory Dis tress of the Newborn. Over the next three decades, these terms have been applied loosely and often im pre cise ly to many forms of respiratory failure in the adult and in children beyond the neonatal period.
In response to the uncertain criteria and un cer tain clinical defi nitions of ARDS, the American-Eu ro pe an Consensus Conference (AECC) more rig or ous ly defi ned the condition so that research and clin i cal studies could proceed using more uniform criteria (Bernard et al. 1994). The AECC subdivided respira- tory failure into two groups: “Acute Lung In ju ry” (ALI) and the more severe form, “Acute Res pi ra to ry Distress
8 Multidetector CT Eval u a tion of Acute Res pi ra to ry Dis tress Syn drome
L. R. Goodman and L. Gattinoni
L. R. Goodman, MD, FACR
Director, Thoracic Imaging, Medical College of Wisconsin, 9200 West Wisconsin Avenue, Milwaukee, WI 53226–3596 USA L. Gattinoni, MD, FRCP
Professor of Anesthesiology, Istituto di Anestesia e Rianima- zione, Università degli Studi di Milano, Ospedale Maggiore di Milano Italy I.R.C.C.S.
Syndrome” (ARDS). The term “Adult” was dropped in recognition of the occurrence of these conditions in children, as well. Although these changes are a signifi - cant move forward in defi ning ARDS, they are still a somewhat general defi nition and do not distinguish between the varied etiologies of ALI/ARDS, and they do not explain the varied re spons es to treatment.
According to the AECC clas si fi ca tion, a major systemic insult causing respiratory insuffi ciency is described as Acute Lung Injury (ALI), and its more severe form is termed Acute Res pi ra to ry Distress Syndrome (ARDS).
The syndrome requires the following for diagnosis:
acute onset of respiratory insuffi ciency, pulmonary artery wedge pressure of <18 mmHg (no CHF) and bilateral in fi l trates on the chest X-ray. In ALI, the PaO2/ FiO2 is >300 mmHg and in ARDS, it is >200 mmHg.
Prior to the use of CT to study ALI/ARDS, the ba sic in vivo morphologic understanding was derived from the portable radiograph, an imperfect tool un der the best of circumstances. Emphasis was placed on radiographic appearance, correlation with clin i cal parameters, and temporal progression. To para phrase Putman’s 1983 description (Putman and Ravin 1983):
1) The X-ray is usually normal at the onset of symp- toms.
2) At 24 hours, there is perihilar haze and radiat- ing linear densities consistent with interstitial edema.
3) Over the next 24 hours, the densities coalesce and resemble edema or pneumonitis.
4) Once established, the radiograph is often stable for days.
Not overtly stated, but implied by most de scrip - tions of “diffuse infi ltrate,” was the assumption that the lungs are relatively uniformly involved. Phys i o- log i cal ly, the lungs were thought to be “stiff ” (low com pli ance). Since these humble beginnings, a bet- ter defi nition of ARDS has been established and CT has provided valuable morphologic and physiologic insights, markedly changing our understanding of this often fatal condition.
When body CT was fi rst introduced in the 1970 s, there was little interest in studying ARDS. The time per axial image was long (8 to 18 seconds per image) and scanners were not readily available for this type of application. Furthermore, the lungs were thought to be homogeneously involved, and therefore CT was thought to offer little additional diagnostic or phys- i o log ic information. Pioneering articles by Maunder et al. (1986) and Gattinoni et al. (1986) showed that ARDS was surprisingly heterogeneous, not ho mo - ge neous, and scanning was now rapid enough to study the lung in different phases of respiration.
Helical CT, and now multidetector CT, provide very rapid volumetric acquisition, or repeated imaging at a giv en anatomic level in different phases of res- piration. They have and will play an increasing role in the un der stand ing of both lung morphology and phys i ol o gy in ALI/ARDS. Better temporal and spatial res o lu tion will provide better regional, as well as global, real time imaging and the potential of mea- suring perfusion changes, as well. What follows is a de scrip tion of the CT morphology of ARDS and then a de scrip tion of the functional data derived from CT. A recently published article by Gattinoni et al.
(2001a) summarizes many of these topics.
8.2 Morphologic Changes
The radiographic and CT appearance of ALI/ARDS is diffi cult to characterized succinctly, because the morphologic (i.e., pathologic) lung changes progress rapidly during the fi rst few days, the lung appearance is altered by coexistent or superimposed lung dis ease, and mechanical ventilation and other in ter ven tions change the morphologic appearance of the lung. Ther- apy may also lead to its own set of unique complica- tions. Nonetheless, some basic patterns have emerged (Goodman 1996; Gattinoni et al. 2001a; Tagliabue et al. 1994; Desai 2002; Pesenti et al. 2001).
8.2.1 Acute Phase
From the beginning, CT refuted the concept that ARDS is homogeneous. It is, in fact, usually het er o g- e neous and has a somewhat predictable distribu- tion. CT usually reveals areas of apparently normal lung, areas of ground glass opacifi cation, and areas of dense consolidation. Although the radiographic
de scrip tion “ground glass opacifi cation” has many eti ol o gies, in the setting of ALI/ARDS, it is probably due to a combination of interstitial edema, alveolar wall thickening, partial fi lling of alveoli with edema fl uid and cell debris, and diminished aeration due to atelecta sis. Areas of alveolar consolidation are more problematic. They may represent collapsed, airless lung, which are potentially re-expandable (re cruit- able), or they represent areas of complete al ve o lar fi lling (edema, pus, or blood), which are not easily expandable. Frequently, both are present.
These varied parenchymal patterns do not occur at random. In ALI/ARDS, the “normal” lung is usu al ly ventral (anterior in the supine patient), the al ve o lar consolidation is usually dorsal, and the ground glass opacifi cation most often in between (Fig. 8.1) (Gattinoni et al. 1988). In addition to the ventral/
dor sal gradient, the density of the lung increases along a craniocaudal axis (Puybasset 1998).
For years, it was assumed that all ALI/ARDS lung injuries were similar, and that similar supportive treat ment was appropriate regardless of etiol- ogy. Re cent work indicates that the etiology of the res pi ra to ry insuffi ciency may infl uence morphol- ogy, patho phys i ol o gy, and response to intervention (Goodman et al. 1999; Gattinoni et al. 1998). ALI/
ARDS may be due to direct injury to the lung from diseases such as pneumonia, aspiration, toxic inhala- tion, etc. In these instances of direct or primary lung injury (ARDSP), the imaging refl ects the local lung damage (often air space consolidation), the result- ing generalized cap il lary leak edema (often ground glass opacifi cation), and the subsequent atelectasis from prolonged su pine positioning (usually gravity- dependent) (Figs. 8.2, 8.3). Conversely, when the lung injury is sec ond ary to a systemic or extrapulmonary insult (ARDSexp), such as sepsis, hypotension, or pan- cre ati t is, the CT should show the results of the diffuse cap il lary leak edema and the dependent atelectasis (Figs. 8.1, 8.4).
Two recent studies indicate that the above mor pho - log ic dichotomy is often, but not universally, the case.
In a CT study of 22 patients with ARDS due to pulmo- nary disease (ARDSP) and 11 patients with ARDS due to extra pulmonary disease (ARDSexp), we found that approximately 20% of the lung was nor mal in both ARDSp and ARDSexp.(Goodman et al. 1999) In patients with ARDSp, the volume of ground glass opacifi cation and consolidation were ap prox i mate ly equal, whereas in ARDSexp ground glass opaci fi ca tion was the domi- nant pattern (Figs. 8.2, 8.3). In ARDSexp, airspace con- solidation tended to be in gravity-dependent caudal locations (Figs. 8.1, 8.4). Asymmetric and non-grav-
Fig. 8.1. ARDS density gradient. a Scan through the lung base shows progressive increased density from ventral to dorsal. b Color coded CT shows normally aerated lung in red, ground glass areas in blue, and gravity dependent atelectasis in green
a b
Fig. 8.2. ARDS due to community acquired pneumonia (ARDSp).
a Chest X-ray shows RLL consolidation and diffuse ground glass opacifi cation. b CT through carina shows dif fuse ground glass opacifi cation, sparing the ventral lung. There is consolidation of the superior segment of the RLL. c CT through the lung base shows right lower lobe dense con sol i da tion due to pneumonia and diffuse ground glass opaci fi ca tion due to ARDS
a
c b
Fig. 8.3. ARDSp.Dense consolidation and a small amountof ground glass opacifi cation characterizes a patient with a hos- pi tal acquired bacterial pneumonia and ARDS
ity dependent con sol i da tion was more prominent in ARDSp, usually the pri ma ry lung process. Desai et al.
(2001) found similar differences between ARDSp and ARDSexp, but did not fi nd the differences great enough to distinguish be tween the two pathologic pathways in individual pa tients. They termed ARDSexp, the pattern of ground glass opacifi cation and gravity-dependent atelecta sis, “typical” ARDS. This typical pattern was present in 72% of ARDSexp but also in 31% of ARDSp pa tients. This undoubtedly refl ects the complexity of the problem and the multiplicity of processes in the same badly damaged lung.
Conventional radiography seldom demonstrates pleural effusions in ALI/ARDS, but CT scans show small to moderate effusions in approximately half of the patients (Goodman et al. 1999). Bronchial di la ta tion is present in about two-thirds of the lobes of pa tients with ALI/ARDS. Air bronchograms are present in over 90% of patients. They tend to be more fre quent in ARDSp. In our study, more than four seg men tal air bronchograms were present in 86%
Fig. 8.4. ARDS due to extrapulmonary causes (ARDSexp). Young male with abdominal sepsis and increasing dyspnea.
a Chest X-ray after three days of increasing respiratory in suf fi cien cy, just prior to intubation. There is diffuse sym- metrical ground glass opacifi cation. The lung volumes are low.
b, c CT scans through the upper and lower thorax show dif- fuse ground glass opacifi cation, sparing the ventral lung. The dor sal and caudal lung shows more consolidation, at least in part due to atelectasis
a
c b
of ARDSp patients and in 54% of ARDSexp patients.
When high resolution CT is used to study ARDS, sep- tal lines are seen in approximately 80% of patients and lung cysts in approximately 35% of patients (De sai 2001).
Although Kerley lines are seen in many ARDS pa tients on HRCT, one should be able to distinguish ARDS from CHF. In ARDS, the pulmonary vessels re main normal in size, whereas in CHF, they increase.
The arteries are larger than the adjacent bronchi.
Peri bron chi al cuffi ng and left heart enlargement also indicate CHF. Pleural effusion is seen frequently in both (Goodman 1996).
8.2.2 Subacute Phase
After the early changes of ALI/ARDS are established, progression and resolution are variable. By the sec- ond week, overall lung density decreases, the ground glass densities become more heterogeneous, and the interstitium thickens. After several weeks, most of the ground glass opacifi cation resolves and irregular reticulation remains (Desai et al. 1999; Gattinoni et al. 1994, 2001a). Fibrosis causes interstitial dis tor tion and thickening of the bronchovascular mark ings (Fig. 8.5). The bronchi may dilate further. Be yond the fi rst week or two, emphysematous cysts or pneu- ma to ce les appear. These vary from a few mil li me ters to several centimeters and are usually as so ci at ed with prolonged mechanical ventilation (Tagli a bue et al.
1994). The cystic structures may be due to cavitation from abscess formation but are usually due to “vo lu- trau ma or barotrauma”. Abscesses should follow the
distribution of the parenchymal infection. Ven ti la tor induced cysts have several pro posed etiologies. If found in the nondependent lung, they may be due to alveolar overdistension of the relatively normal low resistance lung. If found in the mid-lung, they may be due to the shearing forces caused by opening and closing of the air spaces in the lung that is re cruit ed by PEEP during inspiration but collapses on expira- tion because the residual PEEP is insuffi cient to keep the alveoli open. Pneumatoceles may rupture, giving rise to interstitial emphysema, pneu mo me di asti num, or pneumothorax.
8.2.3 Late Phase
Within six months, the majority of patients regain normal or near normal respiratory function and a relatively normal chest X-ray. However, CT scanning shows that the majority of patients have residual parenchymal abnormalities. These abnormalities tend to be in the ventral portion of the lung. Dis- tort ed reticular densities are most frequently seen (Fig. 8.5). These are often associated with areas of traction bronchiectasis. These scarred areas cor re - spond to the areas of relatively normal lung during the acute phase, rather than the areas of consolidated lung. The degree of fi brosis correlates with the length of mechanical ventilation and with the use of inverse ratio ventilation. It is thought that the ventral lung, which is distensible with mechanical ventilation, is injured by the mechanical overdistension and col- lapse. Conversely, the densely opacifi ed lung may remain collapsed during the ventilatory cycle and
Fig. 8.5. Subacute phase. a There is residual reticular infi ltrate and lung distortion in the ventral portions of the upper lobes, six weeks into ARDSexp. b Four weeks later, there is im prove ment
a b
consequently not exposed to the trauma of me chan i cal ventilation or the high FiO2. It is therefore likely that the residual CT changes are, in part, the ia tro gen ic sequelae of mechanical ventilation (Desai et al. 1999;
Gattinoni et al. 2001a; Nobauer-Hu h mann et al.
2001). Clearly, areas of lung abscess, pneu mo nia, lac er a tion, etc., may cause local scarring.
8.3 Physiologic Changes
Over the last 15 years, numerous investigators have used CT to better understand the physiology of the lung in ALI/ARDS. Initial studies utilized 10 mm ax i al images, with images limited to 1 to 3 pre de - ter mined levels. The lung was studied at these levels under different therapeutic conditions (mechanical ventilation, prone positioning, etc.) (Gattinoni et al. 2001a). The scanning parameters were a com- pro mise between maintaining acceptable radiation lev els and achieving an adequate representation of the lung. Currently, helical CT and electron beam CT (im proved temporal resolution at the cost of spacial resolution) provide rapid information about the en tire lung but at an increased radiation dose.
Mul tide tec tor CT provides even better spatial and temporal resolution. With the 16-slice multidetector, and very high resolution images (.6 mm), the entire thorax can be scanned in less than 5 seconds. For many ap pli ca tions, a low mA (40 to 80) provides adequate in for ma tion while minimizing dosage.
Stationary sub sec ond scans can be respiratory or cardiac gated to study temporal changes in ventila- tion and fi rst pass perfusion. What follows is a very brief review of the morphologic/physiologic cor- relates elucidated by CT over the last 15 years and a look at some of the newer applications of fast CT and electron beam CT scanning. The results of mul- tidetector studies are just starting to appear as this book goes to press.
Understanding the distribution of gas in the nor- mal lung and the diseased lung, as well as the effects of mechanical ventilation and other maneuvers, rests on the measurement of lung density (Gat ti no ni et al. 1987, 1988, 2001a). If one assumes that pure air is –1000 Hounsfi eld units and water (tissue) is 0 Houn- sfi eld units, a voxel of –500 Hounsfi eld units is 50% air and 50% water (tissue). At functional re sid u al capac- ity, the lung measures approximately-700 Hounsfi eld units (70% air and 30% water). In ALI/ARDS, the average lung density is –300 Hu (30% air and 70%
water) (Fig. 8.6). Knowing the amount of water and the lung volume, one can calculate the weight of the lung. Unfortunately, the change in den si ty of a voxel does not indicate whether it is due to a change in the amount of air per measured volume or to a change in the amount of tissue per measured volume.
We can compute, for any lung region in which the total volume is known, the volume of gas, the volume of tissue, and the gas to tissue ratio. The later be comes important in understanding lung recruit- ment during mechanical ventilation. With mechani- cal ven ti la tion, an increasing gas to tissue ratio, or an increasing number of voxels in the “aerated” range, indicates recruitment of underinfl ated areas or over- in fl a tion of already infl ated areas (Figs. 8.7, 8.8). This type of analysis has led to the important re eval u a tion of the belief that the lung is rigid (non com pli ant) in ALI/ARDS. Studying lung mechanics with pres sure/
volume curves, Gattinoni et al. (1987, 1995) showed that most of the aeration occurs in the rel a tive ly normal lungs located ventrally in the su pine patient and the amount of aerated lung is strict ly cor re lat ed with compliance. The consolidated lung changes little. Therefore, the lung is not really “stiff,” but the lung is small relative to the tidal volume ap plied.
As stated earlier, in the supine ALI/ARDS patient, there is a gradient from normal, to ground glass, to consolidation, as one goes ventral to dorsal (Pelosi et al. 1994). Recruitment follows this same gradient. The level of PEEP needed for recruitment of the lung can
Fig. 8.6. Residual scarring, 11 years after ARDS from pan- cre ati t is. There is marked scarring anteriorly. The remainder of the lung show areas of mosaic attenuation and slight dis- tor tion of the interstitial markings. At the time of the ARDS, the patient was 32 years old and was not known to have pre- existing lung disease
also be estimated using CT. In the supine patient, the anterior lung weighs on the posterior lung, caus ing atelectasis (Gattinoni et al. 1998). The lung weight increases when there is increased lung water (edema, pus, etc.). This ventral dorsal gradient is a major cause of gravity dependent atelectasis in both the ICU and in general anesthesia. Moreover, the heart weight may play a role in producing com pres sion atelectasis in the supine patient (Malbouisson et al. 2000). CT has confi rmed that the level of PEEP re quired to recruit nonaerated lung is proportional to the changes along the ventral/dorsal gradient (Fig. 8.7). CT has also confi rmed that higher PEEP lev els are needed to keep recruited lung “open”. The lung in ARDSexp appears to be more easily recruited than the lung in ARDSp (Gattinoni et al. 1998). As one increases
PEEP to recruit the areas of dense con sol i da tion, one overdistends the already recruited areas, sometimes leading to barotrauma with sub se quent air leaks or tissue damage (Gattinoni et al. 2001a).
Although three lung images are helpful in un der stand ing the distribution of ventilation and re cruit ment in the lung, they do not provide the whole sto ry. Puybassat et al. (1998) looked at heli- cal whole lung scanning in healthy volunteers and patients with ALI to determine the effects of PEEP induced alveolar re cruit ment. The entire lung was scanned at functional residual capacity and 15 cm of PEEP. They found that the AP and transverse dimen- sions of the lungs were similar in patients and normal controls, but in the ALI/SRDS group, craniocaudal dimension was re duced by more than 15% and total
Fig. 8.7. The lungs in three states of infl ation. The fi rst depicts the lung at functional residual capacity (zero end expiratory pres- sure). It demonstrates the diminishing aeration of the alveoli from ventral to dorsal due to increasing su per im posed pressure (SP). The next two images indicate the effects of 5 and 10 cm of PEEP on lung infl ation. Five mm of PEEP expand the mid-lung zone, where the PEEP exceeds the stand ing pressure of the lung. Ten mm of PEEP overdistends the ventral lung, completely expands the central lung, and partially overcomes the effects of standing pressure on the dorsal lung
Fig. 8.8. Fig. 8 PEEP effects ¯ ARDSexp. A Baseline expiratory CT. B During 10 cc H2O PEEP, 700 ml tidal volume. Increased aera- tion most pronounced ventrally. Zone 1, diminished 124 Hu. Zone 2, diminished 66 Hu. Zone 3, diminished 15 Hu (Goodman 1996, with permission)
a b
lung vol ume was reduced by 27%. Upper lobe volume dif fered little from controls but the lower lobes were only 48% of the predicted value. Nonaerated lung was pre dom i nant ly juxtadiaphragmatic. Re cruit ment fol- lowed a ventral/dorsal and craniocaudal gra di ent (Fig. 8.4).
The same group (The CT Scan ARDS Study Group – Malbouisson et al. 2001) has also used the he li cal scanner to take a more detailed look at lung re cruit ment. They measured improved aeration of both ar eas of ground glass opacifi cation and con sol i da tion, rather than just consolidation alone. They showed alve- olar recruitment of approximately 500 ml and al ve o lar distension or overdistension of approximately 400 ml between expiration and 15 cm of PEEP. They found an excellent correlation (r = .76) between CT measured alveolar recruitment and the increase in PaO2.
They also revisited how lung morphology in ter acts with physiologic parameters and prognosis (Rou by et al. 2000). They defi ned three CT patterns of lung consolidation. The fi rst group (23%) showed dif fuse bilateral increased density. Most had primary ARDS, markedly abnormal respiratory mechanics, and an overall mortality rate of 75%. The second group (41%) showed patchy consolidation with in creased attenuation throughout. These patients had predominantly primary ARDS, and markedly altered mechanics, but a mortality of only 41%. The third group (36%) showed predominantly lower lobe dis ease. They were more likely to have extrapulmo- nary ALI/ARDS, less mechanical derangement, and a mor tal i ty rate of 42%. The authors developed an ARDS Severity Score, based on CT features, the de gree of hypoxia, the calculated lower infl ection point of recruitment, and the slope of the pressure volume curve (see Rouby et al. 2000).
The increased speed of the multidetector scanner provides a more accurate assessment of moment to moment lung infl ation and defl ation. A recent study of 11 ALI/ARDS patients studied changes con tin u ous ly throughout the respiratory cycle. It showed that vari- ous portions of the lung infl ate or defl ate at different rates. For the majority of the lung, the time constant of infl ation was approximately one second, but as much as 7 seconds for the rest (Yamaguchi et al. 2001).
If the patient is placed in the prone position, the lung weight gradient reverses, dorsal to ventral. In addition, the lung dorsal to the heart is no longer com pressed (Albert and Hubmayr 2000). CT dem on strates that atelectasis develops ventrally and atelecta sis diminishes dorsally (Langer et al. 1988).
Oxygenation improves in most patients. The effects of periodic prone positioning on morbidity and mor-
tal i ty during mechanical ventilation, however, appear to be limited (Gattinoni et al. 2001b; Chatte et al.
1997). It is also likely that patients with ALI/ARD- Sexp have more atelectasis and are more like ly to show gravity dependent shifts in the prone position.
Unfortunately, Papazian et al. (2002) found no mor- pho log ic CT features that would pre dict response to prone positioning.
Ultimately, gas exchange is the balance between ventilation and perfusion. CT has done well at an a - lyz ing global and regional aeration but not per fu sion.
It is clear that hypoxia is related to poor ox y gen ation of consolidated lung, but it is not totally clear how much gas exchange and perfusion occurs in the par- tially aerated (ground glass) lung.
Multidetector CT and electron beam CT now pro vide tools for assessing perfusion in local areas through out the lung. This perfusion can then be matched with ventilation maps. For example, how does perfusion change in the prone and supine pa tient? How does that relate to the ventilatory changes documented by CT? Jones et al. (2001) have con fi rmed, using contrast enhanced fi rst pass rapid CT, the already known fact that perfusion in normal sub jects is greater in the dorsal lung in the supine pa tient. When a normal person is placed prone, the gra di ent reverses. Using multiple small regions of in ter est, they demonstrated heterogeneous per fu sion throughout the lung in both positions but less so in the prone position. This type of approach may provide the regional mapping of perfusion needed to better understand local ventilation/perfusion re la tion ships.
CT can also be used to assess regional fl ow and perhaps distinguish between permeability edema and hydrostatic edema (Ullrich et al. 2002).
Hy dro stat ic edema was induced in fi ve piglets and oleic acid permeability edema was induced in seven pig lets. CT scanning was performed 90 minutes after in duc tion of edema. Regions of interest in normal, ground glass, and consolidated lung were measured.
Intravenous contrast agent was then injected and lung enhancement was measured in both groups dur ing the fi rst pass and then over time. The density of ground glass areas increased continuously in both groups for the fi rst 80 seconds. Beyond 80 seconds, lung density increased in the permeability group only. No enhancement was observed immediately, or with time, in either the normal or the consolidated lung in either group. This suggests that much of the perfusion is occurring in the ground glass areas, and capillary leak in ALI/ARDS is predominantly in the ground glass areas in early ALI/ARDS.
Schoepf et al. (2000) have used electron beam CT to study pulmonary blood fl ow and perfusion in pa tients suspected of having a pulmonary embo- lism. They studied a 7 cm volume of lung during the in fu sion of intravenous contrast. First pass mea sure - ments showed that blood fl ow in normal lung areas was approximately four times that of embolized ar eas and returned to normal after anticoagulation (Fig. 8.9). Such techniques are potentially applicable to ALI/ARDS.
In the future, multidetector and electron beam CTs will provide increasing temporal and spatial res- o lu tion. Recent technical developments suggest that four-dimensional scanning will be achievable in the near future. This will provide rapid, sequential three- dimensional images, providing a fourth di men sion
(time) and the next level of understanding in both ventilation and perfusion. Although global informa- tion about the lung and ALI/ARDS is im por tant, the marked heterogeneity of the lung disease requires local analysis of both ventilation and per fu sion.
Other imaging modalities will also contribute to our understanding. CT/PET scanning, available in a single unit will provide more precise anatomic cor re la tion between structure and function (Schuster 1998).
Similarly, MRI can be used to assess in ter paren chy mal water, capillary permeability, and blood fl ow. MRI may also be able to analyze gas dis tri bu tion using hyper- polarized helium (Eberle et al. 1999). Sophisticated computer modeling will pro vide three-dimensional spatial and fourth-di men sion al temporal resolution (Sandiford 1995; Ue mat su et al. 2001).
8.4 Conclusion
Both ventilation and perfusion in ALI/ARDS are dy nam ic processes that occur inhomogeneously through out the lung. Multidetector scanners and the next generation of four-dimensional scanners will further refi ne the insights provided by conventional and helical CT over the last 15 years.
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