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Correspondence |

Postobstructive Pulmonary Edema Response: A Case for Hydrostatic Mechanisms FREE TO VIEW

Petros Kopterides, MD; Iraklis Tsangaris, MD; Apostolos Armaganidis, MD
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Affiliations: Medical School of Athens University, Athens, Greece,  Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN,  Cardiovascular Research Institute,  Department of Medicine, University of California San Francisco, San Francisco, CA

Correspondence to: Petros Kopterides, MD, 68 Kamaterou St, Kamatero 13451, Athens, Greece; e-mail: petkop@ath.forthnet.gr



Chest. 2007;132(6):2056-2057. doi:10.1378/chest.07-1650
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Published online

We read with interest the hypothesis-generating study by Fremont et al in a recent issue of CHEST (June 2007)1in which the authors, based on the observation that patients identified as having postobstructive pulmonary edema had a lower mean edema fluid/plasma protein ratio, concluded that “postobstructive pulmonary edema is a form of hydrostatic pulmonary edema.” Even though the assumption may eventually be proven to be true, we think it is currently based on a tenuous laboratory abnormality, the low pulmonary edema fluid/plasma protein ratio. The dramatic clinical presentation of a patient with upper airway obstruction and postobstructive pulmonary edema forces the attending physicians to use, in a knee-jerk fashion, nebulized salbutamol or racemic epinephrine and IV dexamethasone in a desperate attempt to avoid reintubation. However, experimental studies in animal and ex vivo human lungs4 have demonstrated that therapy with β-agonists can accelerate the rate of alveolar fluid clearance within hours of starting treatment via an increase in intracellular cyclic adenosine monophosphate that results in increased Na+ transport across type II alveolar cells through up-regulation of the apical sodium and chloride channels and Na+/K+-ATPase. In addition, a single dexamethasone injection has been shown to modulate lung epithelial Na+ channels and Na+/K+-ATPase and to increase alveolar fluid clearance, thereby accelerating recovery from pulmonary edema.5 Therefore, the medications used in the management of patients with presumed postobstructive pulmonary edema may facilitate the reabsorption of edema fluid and lead to an erroneously high edema fluid/plasma protein ratio.

From our point of view, the edema fluid/plasma protein ratio may be confounded by the medical treatment that is instituted and potentially can lead to the misclassification of the etiology of pulmonary edema in selected cases. A retrospective analysis of the authors’ extensive databank of patients with pulmonary edema would provide an excellent opportunity to refute or validate this statement.

The authors have not reported to the ACCP any conflicts of interest.

The authors have no conflicts of interest to disclose.

Fremont, RD, Kallet, RH, Matthay, MA, et al (2007) Postobstructive pulmonary edema: a case for hydrostatic mechanisms.Chest131,1742-1746. [PubMed] [CrossRef]
 
Sakuma, T, Okaniwa, G, Nakada, T, et al Alveolar fluid clearance in the resected human lung.Am J Respir Crit Care Med1994;150,305-310. [PubMed]
 
Sakuma, T, Folkesson, HG, Suzuki, S, et al β-Adrenergic agonist stimulated alveolar fluid clearance inex vivohuman and rat lungs.Am J Respir Crit Care Med1997;155,506-512. [PubMed]
 
McAuley, DF, Frank, JA, Fang, X, et al Clinically relevant concentrations of beta2-adrenergic agonists stimulate maximal cyclic adenosine monophosphate-dependent airspace fluid clearance and decrease pulmonary edema in experimental acid-induced lung injury.Crit Care Med2004;32,1470-1476. [PubMed]
 
Noda, M, Suzuki, S, Tsubochi, H, et al Single dexamethasone injection increases alveolar fluid clearance in adult rats.Crit Care Med2003;31,1183-1189. [PubMed]
 
To the Editor:

We thank Dr. Kopterides and colleagues for their comments on our study of edema fluid-to-plasma protein ratios in patients with postobstructive pulmonary edema. The authors question whether the use of medications known to increase the rate of alveolar fluid clearance (β-agonists and corticosteroids)12 has led to misclassification of the etiology of postobstructive pulmonary edema in our study.3We agree that alveolar epithelial fluid transport can increase the edema fluid-to-plasma protein ratio through the more rapid clearance of fluid and solute compared to protein.4 Misclassification would be most likely to occur if substantial time had elapsed between the onset of acute pulmonary edema and sampling of the edema fluid and plasma. In our study, the median time to fluid collection was very short, 1.5 h (interquartile range, 0.5 to 5 h).3 Furthermore, rapid alveolar fluid clearance could only lead to misclassification of patients with underlying hydrostatic pulmonary edema, who might be misclassified as having increased permeability edema because of an elevated edema fluid-to-plasma protein ratio; patients with increased permeability pulmonary edema would not be misclassified. In our study, 7 of 10 patients had edema fluid-to-plasma protein ratios in the hydrostatic range (< 0.65). Two patients had levels that were slightly above this cutoff point at 0.66 and 0.69, still suggesting a predominant hydrostatic mechanism. One patient had an initial ratio of 0.80, suggesting either a nonhydrostatic mechanism or the possibility that sampling of the edema fluid took place after alveolar epithelial fluid transport had begun. Thus, among the 10 patients studied, only 1 patient had the potential to be misclassified. Furthermore, only a minority of patients received β-agonists or corticosteroids during the study period: one patient received albuterol, two patients received epinephrine, and four patients received corticosteroids. In summary, the available evidence including the low edema fluid-to-plasma protein ratio in the majority of the patients despite intact alveolar fluid clearance strongly supports a hydrostatic mechanism of edema fluid formation in postobstructive pulmonary edema.

References
Sakuma, T, Folkesson, HG, Suzuki, S, et al β-Adrenergic agonist stimulated alveolar fluid clearance inex vivohuman and rat lungs.Am J Respir Crit Care Med1997;155,506-512. [PubMed]
 
Noda, M, Suzuki, S, Tsubochi, H, et al Single dexamethasone injection increases alveolar fluid clearance in adult rats.Crit Care Med2003;31,1183-1189. [PubMed] [CrossRef]
 
Fremont, RD, Kallet, RH, Matthay, MA, et al Postobstructive pulmonary edema: a case for hydrostatic mechanisms.Chest2007;131,1742-1746. [PubMed]
 
Matthay, MA, Folkesson, HG, Clerici, C Lung epithelial fluid transport and the resolution of pulmonary edema.Physiol Rev2002;82,569-600. [PubMed]
 

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Tables

References

Fremont, RD, Kallet, RH, Matthay, MA, et al (2007) Postobstructive pulmonary edema: a case for hydrostatic mechanisms.Chest131,1742-1746. [PubMed] [CrossRef]
 
Sakuma, T, Okaniwa, G, Nakada, T, et al Alveolar fluid clearance in the resected human lung.Am J Respir Crit Care Med1994;150,305-310. [PubMed]
 
Sakuma, T, Folkesson, HG, Suzuki, S, et al β-Adrenergic agonist stimulated alveolar fluid clearance inex vivohuman and rat lungs.Am J Respir Crit Care Med1997;155,506-512. [PubMed]
 
McAuley, DF, Frank, JA, Fang, X, et al Clinically relevant concentrations of beta2-adrenergic agonists stimulate maximal cyclic adenosine monophosphate-dependent airspace fluid clearance and decrease pulmonary edema in experimental acid-induced lung injury.Crit Care Med2004;32,1470-1476. [PubMed]
 
Noda, M, Suzuki, S, Tsubochi, H, et al Single dexamethasone injection increases alveolar fluid clearance in adult rats.Crit Care Med2003;31,1183-1189. [PubMed]
 
Sakuma, T, Folkesson, HG, Suzuki, S, et al β-Adrenergic agonist stimulated alveolar fluid clearance inex vivohuman and rat lungs.Am J Respir Crit Care Med1997;155,506-512. [PubMed]
 
Noda, M, Suzuki, S, Tsubochi, H, et al Single dexamethasone injection increases alveolar fluid clearance in adult rats.Crit Care Med2003;31,1183-1189. [PubMed] [CrossRef]
 
Fremont, RD, Kallet, RH, Matthay, MA, et al Postobstructive pulmonary edema: a case for hydrostatic mechanisms.Chest2007;131,1742-1746. [PubMed]
 
Matthay, MA, Folkesson, HG, Clerici, C Lung epithelial fluid transport and the resolution of pulmonary edema.Physiol Rev2002;82,569-600. [PubMed]
 
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