| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Guest Access | Sign In via User Name/Password
|
|
|
|||||||
Guest Access | Sign In via User Name/Password |
|||||||||
Dr. Matthay is Professor of Medicine and Anesthesia and Senior Associate of the Cardiovascular Research Institute at the University of California at San Francisco.
Correspondence to: Michael A. Matthay, MD, FCCP, Cardiovascular Research Institute, University of California, San Francisco, 505 Parnassus Ave, M917, Box 0624, San Francisco, CA 94143-0624; e-mail: mmatt{at}itsa.ucsf.edu
Pulmonary edema is an important cause of acute respiratory failure in critically ill patients. In patients with acute myocardial infarction or with exacerbations of chronic left heart failure, pulmonary edema is often a major complication, leading to arterial hypoxemia and the need for treatment in an ICU setting. In some patients, assisted ventilation is required either with noninvasive ventilation or with positive-pressure ventilation via an endotracheal tube. Pulmonary edema also is a cardinal feature of clinical acute lung injury (ALI) and ARDS, resulting from an increase in lung vascular permeability with exudation of protein-rich edema fluid into the interstitium and distal air spaces of the lung.1
Pulmonary edema can be detected on physical examination by the presence of rales and can be confirmed through chest radiography by the presence of bilateral pulmonary opacities. However, it has been difficult to quantify the extent of pulmonary edema based on chest radiography or any other noninvasive measures.2 In the experimental setting, a quantitative assessment of pulmonary edema can be made by the gravimetric measurement of extravascular lung water in lungs that have been removed from experimental animals.3
Approximately 20 years ago, Lewis and colleagues4 proposed that extravascular lung water could be measured in patients with a thermal-green dye indicator dilution. Several experimental and clinical studies evaluated the potential utility of this method. Although the method has considerable accuracy in the presence of hydrostatic pulmonary edema,5 there has been concern that in the setting of ALI the heterogeneity of perfusion to portions of the lung makes the accuracy of the method less reliable.6 7 Recently, a large clinical study8 established that patients with ARDS have a high dead space fraction (58%) within a few hours of the diagnosis of ARDS, thus confirming the likelihood that there are several ventilated lung units that are poorly perfused. Thus, there has been concern that the thermal dilution method would not be sufficiently accurate in the clinical setting of pulmonary edema from ALI/ARDS.
In this issue of CHEST (see page 2080), an interesting study by Sakka and colleagues reports the results of extravascular lung water measurements with a transpulmonary double indicator (thermal-dye) dilution technique. Each patient required a thermal artery sheath through which a 4F flexible catheter with an integrated thermistor and fiber-optic device was advanced into the infradiaphragmatic aorta. The study was carried out in 373 critically ill patients, and the data were analyzed retrospectively to determine whether there was any prognostic value in measuring extravascular lung water by this method in critically ill patients. The authors report that the maximum level of extravascular lung water was higher in nonsurvivors (14.3 mL/kg) than in survivors (10.2 mL/kg). When the data were analyzed in a univariate logistic regression model, extravascular lung water at baseline, acute physiology scores, and acute physiology and chronic health evaluation scores were significant predictors of mortality, although the r value was relatively low. As would be expected, patients with ARDS had a significantly higher extravascular lung water level (14.9 mL/kg) than other patients. When the authors used a cutoff approach for statistical analysis, they found that the mortality rate was approximately 65% in patients with an extravascular lung water level > 15 mL/kg, whereas the mortality rate was approximately 33% in patients with an extravascular lung water level < 10 mL/kg. Also, a subgroup analysis indicated that, in patients with sepsis, nonsurvivors had a significantly higher extravascular lung water level than survivors.
There are some limitations to the current study. The study was retrospective, and all of the measurements were not made at the same time point, for example, within the first 24 h after admission to the ICU. Also, a careful analysis of all other physiologic parameters including pulmonary hemodynamic variables was not done, although the authors did evaluate the predictive value by comparing the extravascular lung water level to standard severity-of-illness scores.
Is measurement of extravascular lung water useful for research purposes or for the clinical management of patients with pulmonary edema? Mitchell and his colleagues9 from the Washington University in St. Louis reported that the use of extravascular lung water measurements to guide the management of patients with cardiac and noncardiac pulmonary edema (ARDS) resulted in a reduction in the duration of mechanical ventilation. There was also some evidence that the extravascular lung water-guided treatment reduced mortality in patients with both cardiac and noncardiac pulmonary edema, although there was no significant effect when patients with ARDS alone were analyzed.
The fundamental question is whether an aggressive approach to reducing the amount of extravascular lung water, when guided by the measurement of extravascular lung water or by other clinical parameters, can reduce mortality in patients with pulmonary edema. In patients with cardiogenic pulmonary edema, clinical treatments are already directed toward reducing pulmonary vascular pressures with diuretics, vasodilators, and other treatments designed to enhance cardiac performance. The potential benefit of reducing the amount of extravascular lung water with a lower intravascular filling pressure in patients with ARDS is being studied in a large multicenter prospective clinical study that is underway in the United States and Canada. This clinical trial, which is supported by the National Institutes of Health, is comparing a fluid-conservative approach vs a fluid-liberal approach in patients with clinical ALI. Patients are randomized to receive either a central venous catheter or a pulmonary artery catheter to guide whichever fluid strategy they have been randomized to in the protocol. The results of this trial will be available in approximately 2 years. The goal is to enroll 1,000 patients, and 400 patients have been enrolled so far. We hope that the results of this trial will answer the question of whether reducing pulmonary vascular pressures with diuresis and fluid restriction will improve clinical outcomes in patients with ARDS.
If the results of the current NIH trial demonstrate that an aggressive approach to diuresis is beneficial, then there might be reason to consider the use of the thermal method to measure extravascular lung water in patients with ALI. At this time, however, the use of the thermal-dye method remains useful for selected clinical research studies but is not necessary for standard clinical management. While awaiting the results of the NIH clinical trial of ARDS, investigators who are interested in using the thermal method for measuring extravascular lung water should consider carrying out these studies prospectively and should focus on groups of patients in whom an increase in extravascular lung water is likely to be a major determinant of outcome. Thus, patients with ARDS and sepsis would seem to be the most valuable groups to evaluate. Sequential measurements over the first 3 days could provide particularly valuable information. For example, a comparison of extravascular lung water levels in patients with ARDS could be carried out in a group of ARDS patients who had received ventilation with two different types of lung-protective ventilatory strategies or in patients who had received treatment with two different types of vasodilator strategies. In this way, investigators could generate potentially useful information regarding the effects of these therapies on extravascular lung water accumulation and the resolution of ARDS.
References
This article has been cited by other articles:
|
|
 |
|
  N. Kurimoto, T. Miyazawa, S. Okimasa, A. Maeda, H. Oiwa, Y. Miyazu, and M. Murayama Endobronchial Ultrasonography Using a Guide Sheath Increases the Ability To Diagnose Peripheral Pulmonary Lesions Endoscopically Chest, September 1, 2004; 126(3): 959 - 965. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Michard, V. Zarka, S. Alaya, S. Sakka, and M. Klein Better Characterization of Acute Lung Injury/ARDS Using Lung Water Chest, March 1, 2004; 125(3): 1166 - 1167. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
