ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Ann Thorac Surg 2007;84:1656-1661. doi:10.1016/j.athoracsur.2007.06.038
© 2007 The Society of Thoracic Surgeons
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow CME: Take the activity for this article:
 Large-Volume Thoracentesis and the Ri...
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Armin Ernst
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Feller-Kopman, D.
Right arrow Articles by Ernst, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Feller-Kopman, D.
Right arrow Articles by Ernst, A.
Related Collections
Right arrow Pleura
Right arrowRelated Article

Original Articles: General Thoracic

Large-Volume Thoracentesis and the Risk of Reexpansion Pulmonary Edema

David Feller-Kopman, MDa,*, David Berkowitz, MDa, Phillip Boiselle, MDb, Armin Ernst, MDa

a Department of Interventional Pulmonology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts
b Department of Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts

Accepted for publication June 13, 2007.

* Address correspondence to Dr Feller-Kopman, Interventional Pulmonology, Johns Hopkins Hospital, 1830 East Monument St, Fifth Floor, Baltimore, MD 21205 (Email: dfellerk{at}jhmi.edu).


General thoracic surgery: The Annals of Thoracic Surgery CME Program is located online at http://cme.ctsnetjournals.org. To take the CME activity related to this article, you must have either an STS member or an individual non-member subscription to the journal.

 

   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 References
 
Background: To avoid reexpansion pulmonary edema (RPE), thoracenteses are often limited to draining no more than 1 L. There are, however, significant clinical benefits to removing more than 1 L of fluid. The purpose of this study was to define the incidence of RPE among patients undergoing large-volume (≥1 L) thoracentesis.

Methods: One hundred eighty-five patients undergoing large-volume thoracentesis were included in this study. The volume of fluid removed, absolute pleural pressure, pleural elastance, and symptoms during thoracentesis were compared in patients who did and did not experience RPE.

Results: Of the 185 patients, 98 (53%) had between 1 L and 1.5 L withdrawn, 40 (22%) had between 1.5 L and 2 L withdrawn, 38 (20%) had between 2 L and 3 L withdrawn, and 9 (5%) had more than 3 L withdrawn. Only 1 patient (0.5%, 95% confidence interval: 0.01% to 3%) experienced clinical RPE. Four patients (2.2%, 95% confidence interval: 0.06% to 5.4%) had radiographic RPE (diagnosed only on postprocedure imaging without clinical symptoms). The incidence of RPE was not associated with the absolute change in pleural pressure, pleural elastance, or symptoms during thoracentesis.

Conclusions: Clinical and radiographic RPE after large-volume thoracentesis is rare and independent of the volume of fluid removed, pleural pressures, and pleural elastance. The recommendation to terminate thoracentesis after removing 1 L of fluid needs to be reconsidered: large effusions can, and should, be drained completely as long as chest discomfort or end-expiratory pleural pressure less than –20 cm H2O does not develop.

Pleural effusions are a common problem, with more than 1.3 million cases occurring each year in the United States [1]. As such, therapeutic thoracentesis is one of the most commonly performed medical procedures. Although complete drainage is generally desirable to maximize the improvement in a patient’s symptoms, to minimize the potential for subsequent procedures, to predict the success of pleurodesis for malignant pleural effusions, and to optimize postdrainage chest imaging, expert consensus suggests limiting drainage in one setting to 1 L to avoid reexpansion pulmonary edema (RPE) [1].

Reexpansion pulmonary edema is a potentially life-threatening complication of lung reexpansion after thoracentesis or tube thoracostomy. Reexpansion pulmonary edema was first described by Pinault in 1853 as a complication of thoracentesis [2]. It was not until 1958, however, that RPE was documented after treatment of a pneumothorax [3]. Despite being described more than 150 years ago, the incidence of RPE remains unknown. In the comprehensive review by Mahfood and colleagues [4], only 47 cases of RPE had been reported between 1958 and 1987. Since then, a few small case series have reported the incidence to be anywhere from 0.2% to 14% [5–8]. However, the mortality rate associated with RPE can be as high as 20% [4].

The clinical presentation of RPE can vary widely. The onset of symptoms usually occurs within several hours after pleural drainage, although it can occur anytime within 24 hours [5]. Symptoms consist of chest discomfort, persistent cough (with or without bloody, frothy sputum), dyspnea, tachypnea, respiratory failure, and hemodynamic instability. The management of these patients is supportive; diuresis, steroids, inotropic agents, and the use of continuous positive airway pressure have all been suggested [7].

Asymptomatic cases of RPE ("radiographic RPE") have also been described. These cases are diagnosed only by postprocedure imaging [8].

The risk of RPE is thought to be minimal if pleural pressure is maintained above –20 cm H2O throughout the thoracentesis [6]. If pleural pressure is not monitored, an arbitrary cut-off of 1 L has been suggested to prevent RPE from developing [1, 4, 9]. Draining an effusion completely has many potential benefits, so draining only an arbitrary, partial amount, can negatively impact a patient by reducing the benefits of therapeutic thoracentesis.

In this study, we sought to determine the incidence of RPE after large-volume thoracentesis and its relationship to the volume of pleural fluid removed, pleural pressures, and symptoms experienced during thoracentesis.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 References
 
The study protocol was approved by the Internal Review Board of Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts. Informed consent was not required as the study entailed solely a review of medical records.

Patients
Data were collected prospectively during thoracenteses performed by or supervised by the section of Interventional Pulmonology at Beth Israel Deaconess Medical Center between August 2001 and June 2005. All thoracenteses on the medical inpatient service are supervised by Interventional Pulmonology, and most outpatient medical thoracenteses are performed by one of two Interventional Pulmonology attendings or by an Interventional Pulmonology fellow. All consecutive thoracenteses with volumes of 1 L or more were included in the analysis if pleural manometry was also performed.

Thoracentesis
As is our standard of practice, all thoracenteses were performed under ultrasonography guidance using the SonoSite 180 Plus (SonoSite, Bothell, Washington) and a Pleura-Seal thoracentesis kit, using the syringe-pump method (Arrow-Clark, Reading, Pennsylvania). Pleural pressures were measured either by a simple water manometer or by an electronic transducer system (Biobench; National Instruments, Austin, Texas). Doelkin and coworkers [10] found high correlations between measurements made by these two systems (r = 0.97, p < 0.001).

Data Collection
End-expiratory pleural pressures were recorded after withdrawing 5 mL fluid (opening pressure) and every 240 mL thereafter until (1) there was no more fluid present (as confirmed by ultrasonography), (2) the patient experienced chest discomfort, or (3) pleural pressure was less than –20 cm H2O (closing pressure) as previously described [11]. The last recorded pressure was defined as the closing pressure, and the thoracentesis was terminated. The sensation of vague chest discomfort is distinct from a sensation of ipsilateral sharp pain, which is often located over the scapula and may be related to irritation of the diaphragm by the thoracentesis catheter. If the patient had the sharp pain, an attempt at repositioning the catheter was made and additional fluid was removed. If the pain continued, the procedure was terminated. For patients with the vague chest discomfort, a closing pleural pressure was recorded and the procedure was terminated. It has previously been shown that the sensation of chest discomfort correlates to the development of dropping pleural pressures [11].

Elastance of the pleural space was calculated as the change in pressure (opening pressure minus closing pressure) divided by the total volume of fluid removed.

The indication for thoracentesis, pleural fluid results, volume of fluid withdrawn, and complications were evaluated by medical record review, physical examination, and analysis of postthoracentesis radiographs.

Diagnostic Criteria for Reexpansion Pulmonary Edema
A diagnosis of RPE was made on a clinical or radiographic basis. Clinical criteria included at least two of the following: a new cough (lasting more than approximately 20 minutes), worsening dyspnea, hypoxia, tachypnea, or hemodynamic instability. As many patients will have cough after the removal of pleural fluid, an arbitrary cut-off of a cough lasting more than approximately 20 minutes was used to help define clinical RPE [11]. Radiographic criteria included a chest radiograph or computed tomography scan with a new finding of focal ground-glass opacities in a vascular distribution, in the absence of another clinical explanation. A radiographic diagnosis of RPE was made only after review by both an attending radiologist who was blinded as to the clinical status of the patient, and an attending pulmonologist who concurred on the diagnosis. These inclusion criteria were left intentionally broad so as to include as many patients with clinically significant and radiographic RPE as possible. All hospitalized patients were followed for at least 48 hours, and outpatients were contacted by phone the day after the thoracentesis.

Statistical Methods
Owing to the small sample size and nonnormal distributions within the data, nonparametric Wilcoxon rank sum tests with a two-tailed alpha level of 0.05 were used to compare patients with and without RPE. Hodges-Lehmann point estimator and the two-sample Moses confidence interval methods were used for the median difference between samples on the main outcomes [12, 13]. Statistical analysis was performed by Michelle Secic, MS (Secic Statistical Consulting, Chardon, Ohio).


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 References
 
In all, 185 patients (mean age, 68 years; SD, 15; 107 men [58%]) had at least 1 L pleural fluid removed at a single thoracentesis with concomitant pleural manometry. Thoracentesis was performed on the left lung in 78 patients (42%). The maximum volume of fluid removed was 6.55 L; mean (SD) volume was 1.67 L (0.76L; Fig 1).


Figure 1
View larger version (80K):
[in this window]
[in a new window]

  		Fig 1. Volume histogram, showing volume of pleural fluid removed (in mL) per thoracentesis in consecutive patients.

 
Thoracentesis was most often terminated when no more fluid could be removed (Table 1). Diagnoses were made by pleural fluid analysis and patient history (Table 2), and have a similar distribution to results of pleural fluid analyses in other studies [11]. In all, 164 patients (89%) had postthoracentesis imaging. The most common complication was pneumothorax, which occurred in 9 patients (5%). Only 1 of these patients required a tube thoracostomy for definitive management. Another patient had a malignant pleural effusion with physiology consistent with lung entrapment and subsequently had a chronic indwelling pleural catheter (PleurX; Denver Biomedical, Denver, Colorado) placed for recurrence of her dyspnea and effusion.


View this table:
[in this window]
[in a new window]

  		Table 1 Reason for Terminating Large-Volume Thoracentesis in 185 Patients
 

View this table:
[in this window]
[in a new window]

  		Table 2 Diagnoses for 185 Patients Undergoing Large-Volume Thoracentesis
 
There was only 1 case (0.5%, 95% confidence interval [CI]: 0.01% to 3%) of clinical RPE. This patient experienced worsening dyspnea and developed a new, nonproductive cough, toward the end of the procedure. New airspace disease in the partially reexpanded left lower lobe was evident on postthoracentesis imaging. Her pulse oximetry (breathing room air) also dropped from 95% to 90% approximately 20 minutes after the termination of the thoracentesis. The total volume of pleural fluid removed was 1.4 L. The patient was treated with intravenous diuretics, improved over 48 hours, and was discharged to home in stable condition, off supplemental oxygen. This patient’s pleural fluid was exudative, and cytology confirmed pleural involvement from the patient’s underlying mantle-cell lymphoma.

A radiographic diagnosis of RPE (without clinical symptoms) was made in 4 patients (2.2%, 95% CI: 0.06% to 5.4%; Fig 2). Three of the patients with radiographic-only RPE had malignant pleural effusions (all exudates), and 1 had a parapneumonic effusion that was a transudate. All 4 patients with radiographic-only RPE reported improvement in dyspnea after the thoracentesis and therefore did not require therapy for RPE. If the patient who had clinical RPE is grouped with those who had radiographic RPE, patients with RPE had significantly higher volumes removed than did patients without RPE (medians with and without RPE, respectively: 2,400 cc and 1,420 cc, p = 0.02; median difference, 800 cc; 95% CI: 100 to 1,250). As only 1 patient had clinically significant RPE, one can not conclude that there is a statistical association between clinical RPE and volume of fluid removed.


Figure 2
View larger version (133K):
[in this window]
[in a new window]

  		Fig 2. Chest roentgenogram and computed tomography (CT) examples of patients with radiographic-only reexpansion pulmonary edema from our study. (A) The x-ray film on the left reveals a moderate-large right effusion. (B) After complete drainage, the x-ray film on the right reveals a hazy ground-glass infiltrate in the right lower-lobe. A follow-up roentgenogram 1 day later revealed complete clearing radiographic resolution of this opacity. (C) The chest CT scan on the left reveals a large left pleural effusion with contralateral shift of the mediastinum and total left lung atelectasis. (D) The CT scan on the right reveals ground-glass airspace opacities in the left upper and lower lobes. These had completely resolved on a follow-up chest CT scan 2 weeks later.

 
Neither pleural pressures nor pleural elastance were associated with RPE (Fig 3). There was, however, a trend toward a higher opening pressure when comparing the 5 patients who had either clinical or radiographic RPE with patients who did not (medians 10 and 3.8 cm H2O respectively, p = 0.06; median difference, 5 cm H2O; 95% CI: 0 to 10). There were no statistically significant differences between the samples of patients with and without RPE with respect to closing pressures (p = 0.58) or elastance (p = 0.59). In studies with small samples, nonsignificant findings beg the question of whether or not the samples are really "not different" or if there simply is not enough power to detect the observed differences as statistically significant. In this case, however, we believe the nonsignificant results coordinate with clinically insignificant findings. Specifically, median closing pressures were –8.7 and –10.6 cm H2O, and median elastances were 7.8 and 9.5 for patients with and without RPE, respectively.


Figure 3
View larger version (97K):
[in this window]
[in a new window]

  		Fig 3. Results of pleural manometry. There were no significant differences in opening or closing pressures, total change in pleural pressure (Ppl), or pleural elastance (Epl) among patients who developed reexpansion pulmonary edema (RPE; dark gray bars), clinical or radiographic, compared with patients who did not (no RPE; light gray bars). Data are represented as medians with interquartile ranges.

 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
References
 
In the largest series of patients undergoing large-volume thoracentesis published to date, we found that RPE is in fact rare. Additionally, we believe that a radiographic diagnosis of RPE is clinically insignificant because dyspnea actually improved in our 4 patients with radiographic RPE. This belief is supported by other studies reporting that patients with radiographic RPE were asymptomatic and did not require specific therapy [8, 14].

The actual incidence of radiographic RPE may even be higher than our finding of 2.2% because postprocedure imaging is not required in all patients who undergo thoracentesis [15–18]. Postprocedure radiographs are obtained in our practice when there is operator suspicion of a pneumothorax, when we need to confirm full lung reexpansion before attempts are made to achieve pleurodesis, and when further assessment of the underlying lung parenchyma/pleura is clinically indicated. Although our 1 patient with clinical RPE improved with relatively noninvasive therapy (intravenous diuretics), the clinical manifestation of RPE should not be understated because more severe outcomes have been reported [4].

When pleural pressures are not being monitored during large-volume thoracentesis, expert opinion (level C evidence) suggests terminating the thoracentesis at 1 L [1]. This arbitrary cut-off was based on experimental evidence indicating that an operator cannot "feel" a sudden change in pleural pressure. On many occasions, however, more than 1 L of fluid needs to be removed. The benefits of removing all the fluid from the pleural space, which is often more than 1 L, include maximizing symptomatic improvement, optimizing postprocedural imaging, predicting lung reexpansion before attempting pleurodesis, and avoiding the risks of repeated procedures.

The physiology underlying RPE is not completely understood. Proposed mechanisms include the generation of excessive negative pleural pressure [4, 6, 19, 20], an increase in pulmonary capillary permeability [21, 22], and reperfusion injury with the release of inflammatory mediators, possibly resulting from hypoxic injury to the atelectatic lung [14, 23, 24] as well as hypoxic injury to the atelectatic lung. Alterations in lymphatic clearance and increased alveolar surface tension from alterations in surfactant have also been suggested [19].

On the basis of animal models, Light and colleagues [6] and others [25, 26] have suggested that thoracentesis should be terminated when pleural pressures drop below –20 cm H2O. In our study, 28 patients (15%) had closing pressures that were –20 cm H2O or less, and none experienced either clinical or radiographic RPE. As mentioned above, mean closing pressures did not differ significantly between the 5 patients with RPE and those without. This finding should not be taken to mean that negative pleural pressure is not related to RPE; however, it does raise the possibility that negative pleural pressure may not contribute as much as once believed. This finding may also suggest that a closing pressure of –20 cm H2O is too conservative because during full inspiration to total lung capacity with an open glottis, a healthy person can generate –30 cm H2O pressure without adverse outcomes. In the initial animal studies by Pavlin and colleagues [19], RPE developed when –40 mm Hg (–54 cm H2O) was applied to the pleural space of lungs that had been collapsed by an artificial pneumothorax for more than 7 days. A pressure of –20 mm Hg (–27 cm H2O) did not result in RPE [19].

The rate at which the pleural space is evacuated may also be important in the development of RPE, as may be the duration of lung collapse [19]. Anecdotal reports suggest a higher incidence of RPE among patients who receive tube thoracostomy or who undergo vacuum bottle drainage of their effusion.

The technique used to monitor pleural pressure is quite simple and has been recently reviewed [27]. As a standard thoracentesis kit or simple drainage tubing can be used as a U-shaped water manometer, pleural manometry should not add to the cost of the procedure. That being said, measuring pressures during a large volume thoracentesis can add 5 to 10 minutes to the procedure, depending on the volume of fluid removed.

Limitations of the Study
Some limitations of our study deserve comment. Firstly, though we have previously shown that the development of chest discomfort during therapeutic thoracentesis correlates with dropping pleural pressures [11], we made formal measurements of pleural pressures in this study and these results may not be able to be extrapolated to patients who undergo large-volume thoracenteses in whom pressures are not measured, even if chest discomfort is used as a signal to terminate the thoracentesis. The risk of RPE when pressures are not measured will require further study, as at this time we can not conclude that pleural manometry itself serves to minimize the risk of RPE. In fact, Jones and colleagues [8] reported only 2 patients who developed radiographic-only RPE (0.2%) after the removal of 1,000 mL and 1,200 mL. That study, however, did not attempt to correlate RPE with volume, pressure, or pleural elastance, and they were unable to identify any patient or procedural risk factors that could predict the development of RPE. Additionally, they suggest their relatively low incidence of RPE could be because they stopped the procedure if any symptoms developed, whereas our goal was to remove as much pleural fluid as possible.

As mentioned above, because postprocedure imaging was not obtained in all cases, the incidence of radiographic RPE may be higher than our 2.2%. Given the lack of clinical significance of radiographic RPE, we do not encourage postprocedure imaging solely to rule out this diagnosis. Our study was at a tertiary medical center, and the distribution of diagnoses listed in Table 2 may not reflect those of other academic medical centers or the community in general. Likewise, all procedures were performed by or supervised by the Interventional Pulmonology service, which may have contributed to the overall safety of the procedure. Additionally, as we universally used the syringe-pump method for removing pleural fluid, it is possible that the use of a vacuum bottle may result in a higher rate of RPE. The use of a vacuum bottle has been associated with a higher incidence of pneumothorax [16], likely secondary to the fact that the vacuum bottle continued to remove fluid despite the creation of significantly negative pleural pressures. Lastly, our study does not address the incidence of RPE among patients treated for pneumothorax.

In conclusion, clinical and radiographic RPE after large-volume thoracentesis is rare and independent of fluid volume removed, pleural pressures, and pleural elastance. Radiographic RPE does not require treatment. As it is currently impossible to predict who will develop RPE, and as the development of RPE is not related to the volume of fluid removed, the recommendation to terminate thoracentesis after removing 1 L of fluid needs to be reconsidered: large effusions can be drained completely with good clinical results.

We believe that pleural effusions should be "drained dry" unless manometry results are consistent with lung entrapment or a trapped lung or, if manometry is not being used, patients experience chest discomfort—a sign that has been correlated with a drop in pleural pressure [11]. Future studies will hopefully define the pathophysiology of RPE, identify factors that predict RPE, and verify whether a pleural pressure of –20 cm H2O should be the lower threshold for termination or whether a lower pressure would still be safe.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

  1. Light RW. Pleural diseasesPhiladelphia: Lippincott Williams & Wilkins; 2001.
  2. Pinault H-A. Considérations cliniques sur la thoracentèse 1853These de Paris, (in French).
  3. Carlson RI, Classen KL, Gollan F, et al. Pulmonary edema following the rapid reexpansion of a totally collapsed lung due to a pneumothorax: a clinical and experimental study Surg Forum 1958;9:367-371.[Medline]
  4. Mahfood S, Hix WR, Aaron BL, et al. Reexpansion pulmonary edema Ann Thorac Surg 1988;45:340-345.[Abstract]
  5. Trachiotis GD, Vricella LA, Aaron BL, et al. As originally published in 1988: reexpansion pulmonary edema. Updated in 1997 Ann Thorac Surg 1997;63:1206-1207.[Free Full Text]
  6. Light RW, Jenkinson SG, Minh VD, et al. Observations on pleural fluid pressures as fluid is withdrawn during thoracentesis Am Rev Respir Dis 1980;121:799-804.[Medline]
  7. Matsuura Y, Nomimura T, Murakami H, et al. Clinical analysis of reexpansion pulmonary edema Chest 1991;100:1562-1566.[Medline]
  8. Jones PW, Moyers JP, Rogers JT, et al. Ultrasound-guided thoracentesis: is it a safer method? Chest 2003;123:418-423.[Medline]
  9. Sautter RD, Dreher WH, MacIndoe JH, et al. Fatal pulmonary edema and pneumonitis after reexpansion of chronic pneumothorax Chest 1971;60:399-401.[Medline]
  10. Doelken P, Huggins JT, Pastis NJ, et al. Pleural manometry: technique and clinical implications Chest 2004;126:1764-1769.[Medline]
  11. Feller-Kopman D, Walkey A, Berkowitz D, et al. The relationship of pleural pressure to symptom development during therapeutic thoracentesis Chest 2006;129:1556-1560.[Medline]
  12. Monahan J. Algorithm 616: fast computation of the Hodges-Lehmann location estimator ACM Transact Mathemat Software 1984;10:265-270.
  13. Hollander M, Wolfe DA. Nonparametric statistical methodsNew York: John Wiley and Sons; 1973.
  14. Mahajan VK, Simon M, Huber GL. Reexpansion pulmonary edema Chest 1979;75:192-194.[Medline]
  15. Doyle JJ, Hnatiuk OW, Torrington KG, et al. Necessity of routine chest roentgenography after thoracentesis Ann Intern Med 1996;124:816-820.[Abstract/Free Full Text]
  16. Petersen WG, Zimmerman R. Limited utility of chest radiograph after thoracentesis Chest 2000;117:1038-1042.[Medline]
  17. Capizzi SA, Prakash UB. Chest roentgenography after outpatient thoracentesis Mayo Clin Proc 1998;73:948-950.[Medline]
  18. Aleman C, Alegre J, Armadans L, et al. The value of chest roentgenography in the diagnosis of pneumothorax after thoracentesis Am J Med 1999;107:340-343.[Medline]
  19. Pavlin J, Cheney Jr FW. Unilateral pulmonary edema in rabbits after reexpansion of collapsed lung J Appl Physiol 1979;46:31-35.[Abstract/Free Full Text]
  20. Miller WC, Toon R, Palat H, et al. Experimental pulmonary edema following re-expansion of pneumothorax Am Rev Respir Dis 1973;108:654-656.[Medline]
  21. Suzuki S, Tanita T, Koike K, et al. Evidence of acute inflammatory response in reexpansion pulmonary edema Chest 1992;101:275-276.[Medline]
  22. Sprung CL, Loewenherz JW, Baier H, et al. Evidence for increased permeability in reexpansion pulmonary edema Am J Med 1981;71:497-500.[Medline]
  23. Nakamura H, Ishizaka A, Sawafuji M, et al. Elevated levels of interleukin-8 and leukotriene B4 in pulmonary edema fluid of a patient with reexpansion pulmonary edema Am J Respir Crit Care Med 1994;149:1037-1040.[Abstract]
  24. Sivrikoz MC, Tuncozgur B, Cekmen M, et al. The role of tissue reperfusion in the reexpansion injury of the lungs Eur J Cardiothorac Surg 2002;22:721-727.[Abstract/Free Full Text]
  25. Villena V, Lopez-Encuentra A, Pozo F, et al. Measurement of pleural pressure during therapeutic thoracentesis Am J Respir Crit Care Med 2000;162:1534-1538.[Abstract/Free Full Text]
  26. Lan RS, Lo SK, Chuang ML, et al. Elastance of the pleural space: a predictor for the outcome of pleurodesis in patients with malignant pleural effusion Ann Intern Med 1997;126:768-774.[Abstract/Free Full Text]
  27. Feller-Kopman D. Therapeutic thoracentesis: the role of ultrasound and pleural manometry Curr Opin Pulm Med 2007;13:312-318.[Medline]

Related Article

Invited commentary
Mark S. Soberman
Ann. Thorac. Surg. 2007 84: 1661-1662. [Extract] [Full Text] [PDF]



This article has been cited by other articles:


Home page
 ICVTSHome page
E. Apostolakis and I. Koniari
Re-expansion pulmonary oedema: is its prevention possible?
Interactive CardioVascular and Thoracic Surgery, June 1, 2008; 7(3): 489 - 490.
[Full Text] [PDF]

Home page
 ICVTSHome page
C. Echevarria, D. Twomey, J. Dunning, and B. Chanda
Does re-expansion pulmonary oedema exist?
Interactive CardioVascular and Thoracic Surgery, June 1, 2008; 7(3): 485 - 489.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
M. S. Soberman
Invited commentary
Ann. Thorac. Surg., November 1, 2007; 84(5): 1661 - 1662.
[Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow CME: Take the activity for this article:
 Large-Volume Thoracentesis and the Ri...
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Armin Ernst
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Feller-Kopman, D.
Right arrow Articles by Ernst, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Feller-Kopman, D.
Right arrow Articles by Ernst, A.
Related Collections
Right arrow Pleura
Right arrowRelated Article

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS