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Original Research: Critical Care |

Comparison of Hospital Mortality and Long-term Survival in Patients With Acute Lung Injury/ARDS vs Cardiogenic Pulmonary EdemaSurvival After ARDS vs Cardiogenic Pulmonary Edema FREE TO VIEW

Christopher N. Schmickl, MD, MPH; Michelle Biehl, MD; Gregory A. Wilson, RRT; Ognjen Gajic, MD, FCCP
Author and Funding Information

From M.E.T.R.I.C. (Multidisciplinary Epidemiology and Translational Research in Intensive Care) (Drs Schmickl, Biehl, and Gajic and Mr Wilson), Division of Pulmonary and Critical Care Medicine, and the Department of Pulmonary and Critical Care Medicine (Drs Biehl and Gajic), Mayo Clinic, Rochester, MN; and the University Witten-Herdecke (Dr Schmickl), Witten, Germany.

CORRESPONDENCE TO: Christopher N. Schmickl, MD, MPH, Schnieglingerstrasse 225, 90427 Nuremberg, Germany; e-mail: christopher.schmickl@mail.harvard.edu


FUNDING/SUPPORT: The authors have reported to CHEST that no funding was received for this study.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;147(3):618-625. doi:10.1378/chest.14-1371
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BACKGROUND:  Early differential diagnosis of acute lung injury (ALI) vs cardiogenic pulmonary edema (CPE) is important for selecting the most appropriate therapy, but the prognostic implications of this distinction have not been studied. Accurate prognostic information is essential for providing appropriate informed consent prior to initiation of mechanical ventilation.

METHODS:  This is a long-term follow-up study of a previously established population-based cohort of critically ill adult patients with acute pulmonary edema admitted at a tertiary-care center during 2006 to 2009, in which post hoc expert review had established ALI vs CPE diagnosis. Using logistic and Cox regression, hospital mortality and long-term survival were compared in patients with ALI vs patients with CPE.

RESULTS:  Of 328 patients (ALI = 155, CPE = 173), 240 patients (73%) died during a median follow-up of 160 days. After adjusting for confounders, patients with ALI were significantly more likely to die in the hospital (OR = 4.2, 95% CI = 2.3-7.8, n = 325, P < .001), but among hospital survivors the risk of death during follow-up was the same in both groups (hazard ratio = 1.13, 95% CI = 0.79-1.62, n = 229, P = .50). Independent predictors of mortality included age and APACHE (Acute Physiology and Chronic Health Evaluation) III score. Results were similar when restricting patients with ALI to the subset with ARDS (Berlin definition). In post hoc analyses, the mortality rate in hospital survivors compared with the general US population was significantly higher during the first 2 years but essentially converged by year five.

CONCLUSIONS:  Although hospital mortality is higher in patients with ALI/ARDS compared with patients with CPE, long-term survival is similar in hospital survivors from both groups.

Figures in this Article

Acute hypoxic respiratory failure with pulmonary edema is a common syndrome in the ICU,1 but distinguishing between the main differential diagnoses, noncardiogenic (ARDS,2 previously known as acute lung injury [ALI]3) and cardiogenic pulmonary edema (CPE), is often challenging in the early stages of illness.4 Recently, several efforts have been made to aid with the early distinction of ALI/ARDS vs CPE,59 which may facilitate early enrollment into research studies and improve clinical management of these patients.1013

Accurate prognostic information is essential for clinical decision-making and for providing appropriate informed consent before initiation of aggressive measures of resuscitation, such as invasive mechanical ventilation. Although several studies evaluated mortality in patients with acute respiratory failure from any cause1 and in patients with ALI/ARDS,1419 the outcomes of patients with CPE have been less well characterized20 and, to our knowledge, have not yet been compared with patients with ARDS.

To assess if early differential diagnosis of ALI/ARDS vs CPE has prognostic implications, our primary aim was to compare mortality (overall, during hospitalization, and after hospital discharge) between patients with ALI/ARDS and patients with CPE. Secondary aims were to identify (1) independent predictors of mortality and (2) subgroups among patients with ALI/ARDS and patients with CPE whose survival differs.

For this retrospective observational study we used a previously described population-based cohort of 332 adult patients with acute pulmonary edema admitted to the ICU of a tertiary-care center between 2006 and 2009, who had been classified as having ALI vs CPE vs ALI + CPE based on post hoc expert review (gold standard diagnosis), described in detail elsewhere.7 In brief, two critical care experts reviewed patients’ records after hospital discharge or death and classified them as CPE or ALI (American-European Consensus Conference definition3) based on the presence or absence of left atrial hypertension, respectively. Markers of left atrial hypertension included clinical (jugular venous pressure), echocardiographic (ejection fraction, E/E′ ratio), ECG (signs of ischemia), radiographic (cardiothoracic ratio, vascular pedicle width), and laboratory (brain natriuretic peptide, troponin) findings as well as invasive measures of filling pressures (central venous and pulmonary wedge pressure). Experts also took into account response to therapy (eg, diuretics). Patients with mixed results were classified as both (ALI + CPE). Disagreements were resolved by a third expert.

Patients were followed from onset of acute pulmonary edema (defined as the time when patients first had a Pao2/Fio2 < 300 on arterial blood gas analysis and “pulmonary edema” or “bilateral infiltrates” on the chest radiograph as read by radiologists, both within a 24-h period)7 up until January 1, 2014. The only exclusion criteria were withdrawal of research authorization (since initial recruitment) and immediate loss to follow-up after hospital discharge (ie, zero follow-up time). This study was approved by the Mayo Clinic Institutional Review Board, waiving the need for informed consent (IRB# 08-003560).

Using a previously validated database, which feeds from hospital-wide data,21 we obtained patients’ date of death or last date of follow-up (for right-censored patients), age, sex, BMI, APACHE (Acute Physiology and Chronic Health Evaluation) III score on admission, level of positive end-expiratory pressure (PEEP), ICU/hospital length of stay, and year of admission. ALI/CPE risk factors, smoking, and alcohol abuse were assessed by manual chart review.7

Statistical Analysis

Patient characteristics were summarized and compared using the Wilcoxon rank-sum test and the χ2 test for continuous and categorical variables, respectively. Patients with ALI + CPE were treated as ALI in all analyses unless noted otherwise.

Patients with ALI vs patients with CPE were compared in terms of (1) long-term survival (from onset of acute pulmonary edema until end of follow-up) using Kaplan-Meier log-rank test, (2) hospital mortality using logistic regression, and (3) long-term survival (from hospital discharge until end of follow-up) among hospital survivors based on Cox regression and Kaplan-Meier methodology. To adjust for potential confounding and to identify independent predictors of mortality, regression models were built in a stepwise fashion (P value to enter = .1; P value to leave = .25) using clinical judgment. Potential confounders/predictors were chosen on clinical grounds, including patient demographics, ALI/CPE risk factors, APACHE III score, and hospital length of stay (for long-term survival analysis). For all regression models, we assessed the need for nonlinear modeling of continuous covariates (as restricted cubic splines with three knots) and tested if the effect of diagnosis on mortality was modified by any of the candidate variables (by adding interaction terms and main effects as appropriate). The validity of the proportional hazards assumption was checked with the Cox proportional hazards test based on weighted residuals (using P < .01 to judge significant violation).22 Patients with missing data on any of the covariates were omitted from regression analyses.

To test robustness of results, a propensity score for ALI vs CPE diagnosis was created accounting for all initially considered potential confounders and entered into regression models as a covariate. Further sensitivity analyses were performed comparing (1) patients with ALI exposed to a PEEP ≥ 5 cm H2O within 12 to 72 h of onset of acute pulmonary edema (ie, patients meeting criteria for ARDS as per Berlin definition)2 vs patients with ALI and vs patients with CPE, respectively; and (2) ALI + CPE against patients with ALI and patients with CPE, respectively.

In a post hoc analysis, the probability of death was estimated for each of the first 5 years after hospital discharge for all hospital survivors (irrespective of diagnosis) and compared against the general US population (matched by age and sex) using exact binomial tests.23

Analyses were performed in JMP (version 9.0.3; SAS Institute Inc) and R (version 3.0.3; The R Foundation for Statistical Computing). Two-sided P values < .05 were used to judge statistical significance unless noted otherwise.

The final cohort comprised 328 patients (ALI = 155 including 25 ALI + CPE; CPE = 173) (Fig 1).7 Patients with ALI were significantly younger, sicker (higher APACHE III score), and more likely to abuse alcohol and to be admitted at earlier stages of the study and had a lower BMI than patients with CPE. As expected, ALI and CPE risk factors were significantly associated with ALI and CPE, respectively. Further, compared with patients with CPE, those with ALI stayed longer in the ICU and hospital, and their hospital mortality was higher. Data on covariates were near complete (Table 1).

Figure Jump LinkFigure 1 –  Study flowchart. ALI = acute lung injury; CPE = cardiogenic pulmonary edema.Grahic Jump Location
Table Graphic Jump Location
TABLE 1 ]  Patient Characteristics

Data are presented as median (interquartile range) or % (No.). ALI = acute lung injury; APACHE = Acute Physiology and Chronic Health Evaluation; CAD = coronary artery disease; CPE = cardiogenic pulmonary edema; na = not applicable; PEEP = positive end-expiratory pressure.

Two hundred forty patients (73%) died during the follow-up period (median follow-up = 160 days, maximum follow-up = 7.8 years). Long-term survival (after onset of acute pulmonary edema) was significantly lower in patients with ALI vs patients with CPE (P = .01), but visually this difference was fully explained by a higher mortality rate among patients with ALI at the beginning (approximately 50-100 days) of the follow-up period (Fig 2).

Figure Jump LinkFigure 2 –  Kaplan-Meier plot: long-term survival in patients with ALI (solid black line) vs patients with CPE (dotted gray line) after the onset of acute pulmonary edema. Visually, patients with ALI died faster than patients with CPE (diverging survival curves) during the first 50 to 100 d, after which the mortality rate appeared to be similar (parallel survival curves).Grahic Jump Location
Hospital Mortality

During hospitalization, 95 patients (29%) with acute pulmonary edema died. Crude hospital mortality was significantly higher in patients with ALI than patients with CPE (OR = 3.7, 95% CI = 2.2-6.2, P < .001) and did not change when adjusting for potential confounders (OR = 4.2, 95% CI = 2.3-7.8, P < .001) (Table 2). Age (P = .02) and APACHE III score (P < .001) were independent predictors of mortality, with a trend toward higher mortality in patients who had a history of coronary artery disease (CAD) (P = .15) or received chemotherapy (P = .06) in the 6 months prior (Table 3).

Table Graphic Jump Location
TABLE 2 ]  Risk of Death in Patients With ALI vs Patients With CPE During and After Hospitalization

HR = hazard ratio. See Table 1 legend for expansion of other abbreviations.

a 

Adjusted for age, APACHE III score, history of coronary artery disease, and chemotherapy.

b 

Adjusted for age, smoking, and chemotherapy.

Table Graphic Jump Location
TABLE 3 ]  Independent Predictors of Hospital and Long-term Mortality (in Hospital Survivors)

See Table 1 and 2 legends for expansion of abbreviations.

a 

After adjusting for ALI vs CPE diagnosis.

There was no evidence that continuous covariates required nonlinear modeling or that the effect of diagnosis on hospital mortality was modified by any of the candidate variables. Results were similar when adjusting for potential confounding by the propensity score and when comparing ARDS and ALI + CPE vs CPE, respectively (Table 4). Hospital mortality in ARDS and ALI + CPE subgroups was higher than in other patients with ALI, respectively, but without reaching statistical significance (Table 4).

Table Graphic Jump Location
TABLE 4 ]  Sensitivity Analyses

See Table 1 and 2 legends for expansion of abbreviations.

Long-term Survival Among Hospital Survivors

Of 233 patients who survived the hospital stay, four were immediately lost to follow-up after hospital discharge. Thus, the long-term survival analyses among hospital survivors were based on 229 patients (ALI = 88, including 13 ALI + CPE; CPE = 141), of whom 145 patients (63.3%) died during the follow-up period (median follow-up = 790 days).

After hospital discharge, there was no difference between patients with ALI and patients with CPE regarding overall survival (hazard ratio [HR] for ALI vs CPE = 0.89, 95% CI = 0.64-1.25, P = .50) (Fig 3). Results did not change when adjusting for potential confounders (HR for ALI vs CPE = 1.13, 95% CI = 0.79-1.62, P = .50) (Table 2). Independently of diagnosis, risk of death significantly increased with age and was higher among smokers and patients who previously received chemotherapy, but without reaching statistical significance (Table 3).

Figure Jump LinkFigure 3 –  Kaplan-Meier plot: long-term survival after hospital discharge in patients with ALI (solid black line) vs patients with CPE (dotted gray line). Log-rank test P = .50.Grahic Jump Location

There was no evidence that continuous covariates required nonlinear modeling, that the proportional hazards assumption was violated, or that the effect of diagnosis on long-term survival was modified by any of the candidate variables. There was no difference between patients with ARDS or ALI + CPE compared with those with ALI not meeting these criteria, respectively, and results were not altered by any of the other sensitivity analyses (Table 4).

Among all hospital survivors (ie, in patients with ALI and patients with CPE combined), median survival time was 913 days (95% CI = 641-1,198 days), and estimated survival probability decreased from 63% (95% CI = 57%-69%) at 1 year to 35% (95% CI = 28%-41%) at 5 years of follow-up vs 97% and 79% in the general population, respectively (e-Fig 1). Compared with the general population, the rate of death in patients with ALI/CPE was significantly higher in the first 2 years after hospital discharge but essentially converged by 5 years (Table 5).

Table Graphic Jump Location
TABLE 5 ]  Probability of Death During the First 5 Y After Hospital Discharge in the Cohort of All Hospital Survivors (Observed) Compared With the US Population Matched by Age and Sex (Expected)
a 

During each year some patients were lost to follow-up.

The main findings of this study are that (1) patients with ALI have a significantly higher risk of death during hospitalization than those with CPE, but if discharged alive the long-term survival in both patient groups is similar; (2) the same applies to the subset of patients with ALI meeting the criteria for ARDS based on the Berlin definition, although the difference in hospital mortality compared with patients with CPE may be even more pronounced; (3) compared with the general population, patients (ALI or CPE) discharged from the hospital are at high risk of death during the first 2 years, after which their life expectancy starts to assimilate; (4) there seem to be no subgroups among patients with ALI or patients with CPE in whom hospital/long-term mortality differs (except for possibly the ARDS and ALI + CPE subgroups among ALI, which may have a higher hospital mortality); (5) independent predictors of hospital mortality are age, severity of illness, and possibly history of CAD and recent chemotherapy, whereas age and possibly smoking and recent chemotherapy are independently associated with higher long-term mortality.

The difference in hospital mortality in ALI/ARDS vs CPE is plausible, given the differences in underlying pathophysiology (decreased vs intact capacity to reabsorb fluid from the alveolar space in ALI/ARDS vs CPE, respectively).4 Further, our findings are consistent with other studies reporting a 40% to 60% hospital/short-term mortality in patients with ALI/ARDS1419 and 12% hospital mortality along with a 40% 1-year mortality among (predominantly) patients with CPE.20 However, to our knowledge this is the first study explicitly comparing outcomes between these two distinct patient groups, especially regarding long-term prognosis.

One of the strengths of this study is that patients were exclusively from the well-characterized Olmsted County population.24,25 These patients receive virtually all of their health care at our institution (or its local outposts), which uses a hospital-wide unified electronic medical record system linked to our ICU database.21 This infrastructure allowed us to closely follow patients over an extensive period of time, as demonstrated by a median (interquartile range) follow-up among long-term survivors of 5.2 (4.3-6.6) years.

One of the limitations of this study is that generalizability may be limited, since Olmsted County patients are less ethnically diverse, wealthier, and more highly educated than the national average.25 Further, Olmsted County patients may also have access to high-quality health care more readily than elsewhere. Another limitation of this study is that the gold standard diagnosis had been established based on the ALI definition3 before it was replaced by the Berlin definition of ARDS.2 The main difference is the newly introduced requirement of a PEEP of ≥ 5 cm H2O.2 However, the Berlin definition does not specify the time frame within which this criterion has to be met. In this study, the majority of patients with ALI fulfilled this criterion within 12 to 72 h, and results were similar when comparing these subsets of patients with ALI against CPE (with the difference in hospital mortality possibly being even more pronounced), suggesting that the results apply equally to patients with ARDS vs patients with CPE.

Although we addressed in our analysis many potential confounding variables (using different approaches), as in all observational studies we cannot exclude the possibility of residual unmeasured confounding. The main limitation in this regard is that we could not control for the number of previous episodes of acute pulmonary edema. Particularly in patients with CPE, the duration of the underlying heart failure as indicated by the number of previous episodes is likely an independent risk factor for death. Given that for each enrolled patient we only included the first episode during the accrual period, patients with CPE may have been on average at an earlier stage of heart failure, so that we may have overestimated their survival time to some extent.

Furthermore, for assessing the gold standard diagnosis of ALI vs CPE, experts previously reviewed patients’ medical records after death or hospital discharge, also taking into account patients’ clinical course (especially response to therapy). Therefore, we cannot exclude the possibility that experts were more likely to classify patients who died during hospitalization as having ALI rather than CPE. However, assessment was based on definitions including multiple components,7 and our results are consistent with those from other reports, thus making it unlikely that ascertainment bias was a major issue.

Another limitation is that power to detect a difference in long-term mortality between patients with ALI/ARDS and patients with CPE may have been limited, but based on the relatively small effect estimate (which is less affected by sample size and event rate) it is unlikely that there is a clinically significant difference between these two groups. Similarly, we did not identify any subgroups of patients with ALI/ARDS and patients with CPE in whom mortality differs, but power to detect such interactions is generally low.26

Although some studies in the past indicated improvements in incidence27 and mortality19 of these syndromes over time, our results suggest that mortality in patients with ALI/ARDS and patients with CPE is still high and did not change substantially over the past decade(s).1420 Future research should, thus, continue to focus on prevention and treatment of these syndromes.

Although hospital mortality is higher in patients with ALI/ARDS compared with patients with CPE, long-term survival is not significantly different in hospital survivors from both groups. Age and severity of illness are independent predictors of hospital mortality, whereas age is the only significant independent predictor of long-term mortality among hospital survivors. Patients with either syndrome who survive the first couple of years after hospital discharge appear to have eventually a similar long-term prognosis as the general population.

Author contributions: C. N. S. serves as the guarantor of the paper as a whole. C. N. S. contributed to designing the study, obtaining and analyzing data, and drafting and critically revising the manuscript; M. B. and O. G. contributed to designing the study and critically revising the manuscript; and G. A. W. contributed to obtaining the data and critically revising the manuscript.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Other contributions: We thank L. Renfro, PhD, who provided methodologic support during the initial phases of the study.

Additional information: The e-Figure can be found in the Supplemental Materials section of the online article.

ALI

acute lung injury

APACHE

Acute Physiology and Chronic Health Evaluation

CAD

coronary artery disease

CPE

cardiogenic pulmonary edema

HR

hazard ratio

PEEP

positive end-expiratory pressure

Vincent JL, Akça S, De Mendonça A, et al; SOFA Working Group. Sequential organ failure assessment. The epidemiology of acute respiratory failure in critically ill patients. Chest. 2002;121(5):1602-1609. [CrossRef] [PubMed]
 
Ranieri VM, Rubenfeld GD, Thompson BT, et al; ARDS Definition Task Force. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012;307(23):2526-2533. [PubMed]
 
Bernard GR, Artigas A, Brigham KL, et al. The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med. 1994;149(3 pt 1):818-824. [CrossRef] [PubMed]
 
Ware LB, Matthay MA. Clinical practice. Acute pulmonary edema. N Engl J Med. 2005;353(26):2788-2796. [CrossRef] [PubMed]
 
Rana R, Vlahakis NE, Daniels CE, et al. B-type natriuretic peptide in the assessment of acute lung injury and cardiogenic pulmonary edema. Crit Care Med. 2006;34(7):1941-1946. [CrossRef] [PubMed]
 
Ware LB, Fremont RD, Bastarache JA, Calfee CS, Matthay MA. Determining the aetiology of pulmonary oedema by the oedema fluid-to-plasma protein ratio. Eur Respir J. 2010;35(2):331-337. [CrossRef] [PubMed]
 
Schmickl CN, Shahjehan K, Li G, et al. Decision support tool for early differential diagnosis of acute lung injury and cardiogenic pulmonary edema in medical critically ill patients. Chest. 2012;141(1):43-50. [CrossRef] [PubMed]
 
Lin Q, Fu F, Chen H, Zhu B. Copeptin in the assessment of acute lung injury and cardiogenic pulmonary edema. Respir Med. 2012;106(9):1268-1277. [CrossRef] [PubMed]
 
Komiya K, Ishii H, Teramoto S, et al. Diagnostic utility of C-reactive protein combined with brain natriuretic peptide in acute pulmonary edema: a cross sectional study. Respir Res. 2011;12:83. [CrossRef] [PubMed]
 
Herasevich V, Yilmaz M, Khan H, Hubmayr RD, Gajic O. Validation of an electronic surveillance system for acute lung injury. Intensive Care Med. 2009;35(6):1018-1023. [CrossRef] [PubMed]
 
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Figures

Figure Jump LinkFigure 1 –  Study flowchart. ALI = acute lung injury; CPE = cardiogenic pulmonary edema.Grahic Jump Location
Figure Jump LinkFigure 2 –  Kaplan-Meier plot: long-term survival in patients with ALI (solid black line) vs patients with CPE (dotted gray line) after the onset of acute pulmonary edema. Visually, patients with ALI died faster than patients with CPE (diverging survival curves) during the first 50 to 100 d, after which the mortality rate appeared to be similar (parallel survival curves).Grahic Jump Location
Figure Jump LinkFigure 3 –  Kaplan-Meier plot: long-term survival after hospital discharge in patients with ALI (solid black line) vs patients with CPE (dotted gray line). Log-rank test P = .50.Grahic Jump Location

Tables

Table Graphic Jump Location
TABLE 1 ]  Patient Characteristics

Data are presented as median (interquartile range) or % (No.). ALI = acute lung injury; APACHE = Acute Physiology and Chronic Health Evaluation; CAD = coronary artery disease; CPE = cardiogenic pulmonary edema; na = not applicable; PEEP = positive end-expiratory pressure.

Table Graphic Jump Location
TABLE 2 ]  Risk of Death in Patients With ALI vs Patients With CPE During and After Hospitalization

HR = hazard ratio. See Table 1 legend for expansion of other abbreviations.

a 

Adjusted for age, APACHE III score, history of coronary artery disease, and chemotherapy.

b 

Adjusted for age, smoking, and chemotherapy.

Table Graphic Jump Location
TABLE 3 ]  Independent Predictors of Hospital and Long-term Mortality (in Hospital Survivors)

See Table 1 and 2 legends for expansion of abbreviations.

a 

After adjusting for ALI vs CPE diagnosis.

Table Graphic Jump Location
TABLE 4 ]  Sensitivity Analyses

See Table 1 and 2 legends for expansion of abbreviations.

Table Graphic Jump Location
TABLE 5 ]  Probability of Death During the First 5 Y After Hospital Discharge in the Cohort of All Hospital Survivors (Observed) Compared With the US Population Matched by Age and Sex (Expected)
a 

During each year some patients were lost to follow-up.

References

Vincent JL, Akça S, De Mendonça A, et al; SOFA Working Group. Sequential organ failure assessment. The epidemiology of acute respiratory failure in critically ill patients. Chest. 2002;121(5):1602-1609. [CrossRef] [PubMed]
 
Ranieri VM, Rubenfeld GD, Thompson BT, et al; ARDS Definition Task Force. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012;307(23):2526-2533. [PubMed]
 
Bernard GR, Artigas A, Brigham KL, et al. The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med. 1994;149(3 pt 1):818-824. [CrossRef] [PubMed]
 
Ware LB, Matthay MA. Clinical practice. Acute pulmonary edema. N Engl J Med. 2005;353(26):2788-2796. [CrossRef] [PubMed]
 
Rana R, Vlahakis NE, Daniels CE, et al. B-type natriuretic peptide in the assessment of acute lung injury and cardiogenic pulmonary edema. Crit Care Med. 2006;34(7):1941-1946. [CrossRef] [PubMed]
 
Ware LB, Fremont RD, Bastarache JA, Calfee CS, Matthay MA. Determining the aetiology of pulmonary oedema by the oedema fluid-to-plasma protein ratio. Eur Respir J. 2010;35(2):331-337. [CrossRef] [PubMed]
 
Schmickl CN, Shahjehan K, Li G, et al. Decision support tool for early differential diagnosis of acute lung injury and cardiogenic pulmonary edema in medical critically ill patients. Chest. 2012;141(1):43-50. [CrossRef] [PubMed]
 
Lin Q, Fu F, Chen H, Zhu B. Copeptin in the assessment of acute lung injury and cardiogenic pulmonary edema. Respir Med. 2012;106(9):1268-1277. [CrossRef] [PubMed]
 
Komiya K, Ishii H, Teramoto S, et al. Diagnostic utility of C-reactive protein combined with brain natriuretic peptide in acute pulmonary edema: a cross sectional study. Respir Res. 2011;12:83. [CrossRef] [PubMed]
 
Herasevich V, Yilmaz M, Khan H, Hubmayr RD, Gajic O. Validation of an electronic surveillance system for acute lung injury. Intensive Care Med. 2009;35(6):1018-1023. [CrossRef] [PubMed]
 
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