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Invited Commentary |
1 Department of Radiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico
The term pulmonary edema is not much more specific than the term dropsy, which it was fashionable to use a century ago to describe excess serous fluid within tissues. Simply defined, pulmonary edema is the abnormal accumulation of extravascular lung water that occurs when normal clearance mechanisms in the lung are overwhelmed. Ever since Ashbaugh et al (1) described ARDS over 30 years ago, pulmonary edema has been divided into hydrostatic edema and increased permeability pulmonary edema (ie, ARDS) (1). During the intervening years, it has become apparent that the clinical and radiologic characteristics of many diseases do not fit neatly into either category. Investigators have begun to uncover the basis for these variations.
Hydrostatic edema is more complex than was previously thought. Pulmonary blood flow is not governed by cardiac output alone but also by other factors such as reflex vasospasm and atrial natriuretic peptide (2). Sufficient increases in hydrostatic pressure in the lung can cause structural damage to both the alveolar epithelium and endothelium (stress failure) (3). This may account for the apparent presence of components of both hydrostatic and increased permeability edema in some disease processes. The degree of damage to the alveolar endothelium and epithelium is probably also variable in ARDS. Typical ARDS is accompanied by DAD with extensive epithelial damage. However, ARDS may also occur with only limited damage to the alveolar epithelium and may have a different clinical and radiologic course (4).
Some of the variations in the radiologic appearance of pulmonary edema result from these structural changes in the alveolar epithelium and endothelium. Unusual forms of pulmonary edema are also caused by underlying lung or cardiac disease and their effects on the pulmonary interstitium and vasculature. Gluecker et al (5) present an excellent pictorial review of both classic and atypical pulmonary edema. The authors show how CT can better demonstrate the relation of edema distribution to changes in the lung parenchyma (emphysema) or vasculature (chronic pulmonary embolism). They also show how the use of CT in ARDS demonstrates that the inhomogeneity in lung opacity is often not the result of inhomogeneous lung injury but of exaggerated dependent atelectasis of edematous lung tissue (6). In cases in which there is no gravity-dependent increased lung attenuation, lung disease may be the result of direct injury such as pneumonia rather than a systemic inflammatory response (7). This may have significant clinical ramifications because recent work suggests that these entitiesARDS from direct lung injury and ARDS from systemic mediator releaserequire different ventilator management (8).
Unfortunately, there is much about pulmonary edema that CT does not tell us. Although there are some pathologic and experimental data to suggest that the alveolar epithelium is better preserved in more rapidly resolving ARDS, clinical corroboration is limited. I agree with Gluecker et al that heroin-induced pulmonary edema and pulmonary edema caused by IL-2 or tumor necrosis factor infusions probably improve more rapidly than typical ARDS because of better preservation of the alveolar epithelium. At present, we can only speculate about the actual extent of alveolar damage, and histologic data are unlikely to become available due to the relatively benign natural history of these diseases. Nuclear medicine can aid in the evaluation of epithelial integrity by measuring clearance of aerosolized technetium-99m diethylenetriamine pentaacetic acid. It can also help assess endothelial leakage with a variety of methods, most of which involve use of a dual isotope technique in which technetium-labeled red blood cells serve as a marker for pulmonary blood volume and a second protein-bound agent is used to measure extravascular leakage (9). However, these studies are not widely performed and to my knowledge have not yet been used to study permeability edema from a variety of causes.
A much larger issue also looms regarding the imaging of pulmonary edema. Over the past decade, there has been considerable progress in the understanding of systemic inflammatory response syndrome, which is often the physiologic process that leads to ARDS. Numerous drug trials are currently underway to determine if antagonists of specific inflammatory mediators (eg, agents directed against platelet activating factor and IL-8) can prevent or ameliorate permeability edema (10,11). It is likely that for any of these agents to be used successfully, they will need to be administered early in the course of the disease.
In the near future, thoracic radiologists may be faced with a challenge similar to that confronted by neuroradiologists with the advent of early thrombolytic therapy for acute stroke. Once early therapeutic intervention proved to be successful, it became essential to diagnose cerebral infarctions within a few hours of onset. Neuroradiology has risen to this challenge with use of diffusion-weighted and perfusion magnetic resonance imaging. The early diagnosis and treatment of ARDS will require different but similarly ingenious methods of detection.
References
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