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 Table of Contents  
Year : 2017  |  Volume : 3  |  Issue : 3  |  Page : 59-62

Reexpansion pulmonary edema

1 OPUS 12 Foundation, Bethlehem, PA, USA
2 Department of Surgery, Division of Traumatology and Surgical Critical Care, University of Pennsylvania, School of Medicine, Philadelphia, PA, USA

Date of Web Publication21-Apr-2017

Correspondence Address:
Stanislaw P Stawicki
Department of Research and Innovation, St. Luke's University Health Network, EW2 Research Administration, 801 Ostrum Street, Bethlehem, Pennsylvania 18015
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/IJAM.IJAM_98_16

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Key points: (a) Reexpansion pulmonary edema-RxPE– is a rare form of acute lung injury, with an incidence of approximately 1% following evacuation of a pneumothorax; (b) RxPE usually follows rapid reinflation of collapsed lung parenchyma; (c) The most common factor associated with RxPE is the duration of lung collapse– more than 3 days seems to be the critical amount of time; (d) The pathophysiologic changes associated with RxPE are complex and not yet fully understood; (e) The pathologic process results from a combination of rapid pulmonary reexpansion with concurrent mechanical alveolar injury, decrease in surfactant and regional lung tissue hypoxemia, inflammatory cell migration and release of inflammatory mediators, and the resulting changes in capillary-alveolar barrier occurring concurrently with increased capillary/hydrostatic pressures; (f) Clinical manifestations of RxPE vary from minimal symptoms to life-threatening hypoxia and cardio-respiratory collapse; (g) The patient may experience dyspnea, thoracic pain, cough with or without pink/foamy sputum, cyanosis, rales and stertors on auscultation. Other clinical symptoms may include fever, nausea, vomiting, tachycardia, and hypotension; (h) The symptoms of RxPE usually appear within the first two hours following pulmonary reexpansion, but may be delayed by as many as 24-48 h; (i) RxPE usually lasts clinically for as long as 1-2 days, but may take anywhere from 5 to 7 days to resolve; (j) Critical care practitioners should be familiar with the most common factors involved in the pathogenesis of RxPE; (k) The knowledge of these predisposing factors and the ability to effectively treat RxPE are important to prevention and treatment of this potentially fatal condition.
The following core competencies are addressed in this article: Medical knowledge, Patient care.
Republished with permission from: Stawicki SP, Sarani B, Braslow BM. Reexpansion pulmonary edema. OPUS 12 Scientist2008;2(2):29-31.

Keywords: Acute lung injury, diagnosis and treatment, lung reinflation, morbidity and mortality, reexpansion pulmonary edema, risk factors

How to cite this article:
Stawicki SP, Sarani B, Braslow BM. Reexpansion pulmonary edema. Int J Acad Med 2017;3, Suppl S1:59-62

How to cite this URL:
Stawicki SP, Sarani B, Braslow BM. Reexpansion pulmonary edema. Int J Acad Med [serial online] 2017 [cited 2022 Dec 8];3, Suppl S1:59-62. Available from: https://www.ijam-web.org/text.asp?2017/3/3/59/204979

  Introduction Top

Reexpansion pulmonary edema (RxPE) is a rare form of acute lung injury.[1],[2],[3] It usually follows rapid reinflation of collapsed lung parenchyma, with an incidence up to 1%, following evacuation of a pneumothorax or pleural effusion. Although RxPE was known as a clinical entity since at least the 1850s, its pathophysiologic mechanism remains to be fully elucidated.[1],[2],[3],[4],[5] Because of the associated significant mortality (as high as 21%), the most effective clinical approach to RxPE is prevention.[1],[6]

  Reexpansion Pulmonary Edema: Risk Factors Top

The phenomenon of RxPE is multifactorial [Table 1][1],[2],[3],[5],[7],[8],[9]. Pulmonary collapse lasting for over 72 h is the single most important factor associated with the genesis of RxPE. RxPE may also be related to (a) the volume of the intrathoracic space occupied by fluid, air, or a mass lesion; (b) clinical variables associated with pulmonary reexpansion technique or procedure; (c) presence of bronchial obstruction; (d) application of excessive suction to the tracheobronchial tree during bronchoscopy and/or suctioning with a tracheal suction catheter; (e) alteration of the pulmonary artery pressure; and (f) removal of large extrathoracic lesions (i.e., giant abdominal masses that exert compression on the thoracic cavity). Echevarria et al.[4] postulate that younger patient age may also be associated with greater propensity to develop RxPE.
Table 1: Summary of risk factors associated with reexpansion pulmonary edema

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It has also been suggested that one-lung ventilation during anesthesia may alter the distribution of blood flow between the nondependent and dependent lungs, potentially predisposing to RxPE. In addition, Yanagidate et al.[10] speculate that thoracic epidural anesthetic administration may affect the sympathetic control of pulmonary circulation.

Of interest, a study of RxPE in a primate model by Miller et al.[11] found that evacuating a large pneumothorax of 3 days duration using suction of − 10 cm H2O versus no suction resulted in 100% incidence of RxPE in the suction group versus 0% incidence in the no suction group.

  Pathophysiology Top

The pathophysiology of RxPE is complex and involves several simultaneously occurring processes [Figure 1]. RxPE can be unilobar or multilobar, depending on the degree of preexisting atelectasis. A study by Mahfood et al.[8] described 93% of the cases being unilateral, with 6.7% being bilateral and <1% being contralateral.
Figure 1: Proposed pathophysiologic mechanism of reexpansion pulmonary edema[6]

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It has been proposed that rapid lung expansion, following prolonged (3–7 days) pulmonary collapse, contributes to increased pulmonary vascular permeability, loss of surfactant, and increased production of oxygen free radicals. When subjected to sudden reexpansion, the lung experiences simultaneous rapid increase in blood inflow and concurrent alveolar distention. This leads to increase in pulmonary capillary pressure, hydrostatic pressure, pressure-induced mechanical alveolar–capillary disruption, increased capillary permeability and transudation of fluid into the lung, overflow of fluid and protein contributing to the development of pulmonary edema, and finally hypoxia and hypoxic-induced cardiac dysfunction.[3],[6],[7],[12],[13],[14],[15],[10]

Simultaneously, increased blood flow and rapid alveolar distention lead to alterations in the alveolar–capillary barrier and alveolar injury secondary to the reopening of atelectatic segments of the lung. Hydrostatic pressure elevations seen in RxPE are likely associated with elevations of various selectin proteins (E-selectin, L-selectin, and P-selectin). This is then associated with the recruitment of neutrophils, release of neutrophil granular contents, and elevations in interleukin-8, monocyte chemoattractant protein-1, nitric oxide, and free radical concentrations in the lung. These changes, in turn, exacerbate the imbalances in pulmonary fluid-protein homeostasis, leading to further worsening of pulmonary edema.[3],[6],[7],[12],[13],[14],[15],[10]

  Diagnosis Top

The clinical diagnosis of RxPE is difficult. When making the diagnosis, it is important to carefully consider the clinical history, clinical presentation, and radiographic evidence. Clinical history often features prolonged nature (3–7 days) of the thoracic space-occupying lesion and rapid removal of more than 1.5 L of extrapulmonary thoracic contents (i.e., effusion, pneumothorax, mass). The symptoms of RxPE usually appear within the first 2 h following pulmonary reexpansion but may be delayed by 24–48 h. RxPE usually lasts clinically for as long as 1–2 days but may take anywhere from 5 to 7 days to resolve.[6],[7],[8],[13],[15],[10]

The symptoms of RxPE vary from minimal or no symptoms (i.e., radiographic pulmonary edema only) to life-threatening hypoxia, hemodynamic instability, and death. The patient may experience dyspnea, thoracic pain, cough with or without pink/foamy sputum, cyanosis, rales, and stertors on auscultation. Other clinical symptoms may involve fever, nausea, vomiting, tachycardia, and hypotension. The evolution of RxPE is highly variable and often takes an unpredictable path, from spontaneous resolution to fatal respiratory failure.[6],[7],[8],[13],[15],[10]

Radiography will demonstrate pulmonary edema with interstitial opacities, pulmonary consolidations, air bronchograms, pulmonary clefts, and Kerley's “B” lines. Because of the variability in both clinical and radiologic features of RxPE, the differential diagnosis should include cardiogenic pulmonary edema, pulmonary infection, and pneumonitis.[16]

  Treatment Top

The treatment of RxPE consists of a combination of (a) administration of supplemental oxygen, (b) ventilatory support (invasive versus noninvasive), (c) appropriate hemodynamic monitoring, (d) vasopressor and/or inotropic agent use, and (e) careful diuresis. Clinical maneuvers that may be helpful in the setting of RxPE include (a) lateral decubitus position with the affected side facing up – this maneuver may reduce intrapulmonary shunting and improve oxygenation, (b) avoidance of application of excessive ventilatory pressures, and (c) occlusion of the pulmonary artery with a balloon catheter on the affected side – this maneuver is not routinely performed and should be used with extreme caution. In addition, negative pressure applied to the pleural space may need to be reduced or turned off (provided that any reduction in negative pressure would not lead to creation of intrathoracic tension physiology).[6],[7],[8],[13],[15],[10]

Several options may be entertained if the patient requires ventilatory support. Many patients do not exhibit significant increases in oxygen demand, and nasal cannula or face mask oxygen supplementation may be the only interventions needed. Some patients who do not need tracheal intubation benefit from continuous positive airway pressure or bilevel positive airway pressure delivered through specialized facial mask. In severe cases, patients may require tracheal intubation and application of positive end-expiratory pressure. In the setting of refractory pulmonary failure, differential two-lung ventilatory strategies have been described.[2],[6],[7],[8],[17],[13],[15]

  Prevention Top

Careful performance of pleural drainage procedures may be the key in preventing RxPE. It is crucial that the provider placing the pleural catheter is aware of the chronicity of the space-occupying pulmonary process. Over 80% of RxPE cases occur in patients with prolonged duration of lung collapse (3–7 days being the critical time frame).[2],[3],[6],[15],[10]

It is also important to try to estimate the volume of the space-occupying process, which may be important when performing a gradual, staged drainage. For example, in the setting of preexisting pulmonary hypertension or severe hypoxemia, it is recommended that slow evacuation of the space-occupying process is performed under careful clinical monitoring conditions.[2],[6],[7],[8],[17],[13],[15]

The proposed amount of intrathoracic volume that can be safely withdrawn varies from study to study. Most authors recommend that each drainage procedure or “step” should not evacuate more than 1000 mL at a time, especially if the evolution of the space-occupying process took longer than 72 h. Some have suggested that 1500 mL may represent a safe limit. A strategy of carefully monitoring the pleural pressure during thoracic drainage procedure has also been described, with larger volumes (up to 5000 mL) being able to be evacuated without the development of RxPE as long as the pleural pressures do not exceed − 20 cm H2O.[2],[6],[7],[8],[17],[13],[14],[15],[10]

  Conclusions Top

Over 80% of RxPE cases occur in patients with prolonged duration of lung collapse (3–7 days being the critical time frame). The etiology of RxPE is multifactorial. Because of potentially high mortality, the best clinical approach to RxPE is prevention. Careful performance of pleural drainage procedures may be the key in preventing RxPE. It is crucial that the provider placing the pleural catheter or surgically removing a mass lesion is aware of the chronicity of the space-occupying pulmonary process. If clinical signs of RxPE become apparent, prompt recognition and institution of supportive measures are important. Appropriate monitoring, hemodynamic support, and ventilatory assistance may be necessary.


Justifications for re-publishing this scholarly content include: (a) The phasing out of the original publication after a formal merger of OPUS 12 Scientist with the International Journal of Academic Medicine and (b) Wider dissemination of the research outcome(s) and the associated scientific knowledge.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Barbetakis N, Samanidis G, Paliouras D, Tsilikas C. Re-expansion pulmonary edema following video-assisted thoracic surgery for recurrent malignant pleural effusion. Interact Cardiovasc Thorac Surg 2008;7:532-4.  Back to cited text no. 1
Conen A, Joos L, Bingisser R. Ipsilateral reexpansion pulmonary edema after drainage of a spontaneous pneumothorax: A case report. J Med Case Rep 2007;1:107.  Back to cited text no. 2
Contralateral Reexpansion Pulmonary Edema. Available from: http://www.medscape.com/viewarticle/410615_3. [Last accessed on 2008 Apr 14].  Back to cited text no. 3
Echevarria C, Twomey D, Dunning J, Chanda B. Does re-expansion pulmonary oedema exist? Interact Cardiovasc Thorac Surg 2008;7:485-9.  Back to cited text no. 4
Fremont RD, Kallet RH, Matthay MA, Ware LB. Postobstructive pulmonary edema: A case for hydrostatic mechanisms. Chest 2007;131:1742-6.  Back to cited text no. 5
Genofre EH, Vargas FS, Teixeira LR, Vaz MA, Marchi E. Reexpansion pulmonay edema. J Pneumol 2003;29:101-6.  Back to cited text no. 6
Mahajan VK, Simon M, Huber GL. Reexpansion pulmonary edema. Chest 1979;75:192-4.  Back to cited text no. 7
Mahfood S, Hix WR, Aaron BL, Blaes P, Watson DC. Reexpansion pulmonary edema. Ann Thorac Surg 1988;45:340-5.  Back to cited text no. 8
Mihara T, Kurahashi K. Re-expansion pulmonary edema (RPE) during surgery for intraabdominal giant tumor. Masui 2008;57:191-6.  Back to cited text no. 9
Yanagidate F, Dohi S, Hamaya Y, Tsujito T. Reexpansion pulmonary edema after thoracoscopic mediastinal tumor resection. Anesth Analg 2001;92:1416-7.  Back to cited text no. 10
Miller WC, Toon R, Palat H, Lacroix J. Experimental pulmonary edema following re-expansion of pneumothorax. American Review of Respiratory Disease. 1973 Sep; 108(3):664-6.  Back to cited text no. 11
Neustein SM. Reexpansion pulmonary edema. J Cardiothorac Vasc Anesth 2007;21:887-91.  Back to cited text no. 12
Otomo A, Kawatani M, Morikawa T, Nakazawa K, Makita K. Reexpansion pulmonary edema after removal of a giant thoracic tumor associated with long-time lung collapse and mediastinal shift. Masui 2004;53:291-3.  Back to cited text no. 13
Sue RD, Matthay MA, Ware LB. Hydrostatic mechanisms may contribute to the pathogenesis of human re-expansion pulmonary edema. Intensive Care Med 2004;30:1921-6.  Back to cited text no. 14
Tariq SM, Sadaf T. Images in clinical medicine. Reexpansion pulmonary edema after treatment of pneumothorax. N Engl J Med 2006;354:2046.  Back to cited text no. 15
Gluecker T, Capasso P, Schnyder P, Gudinchet F, Schaller MD, Revelly JP, et al. Clinical and radiologic features of pulmonary edema. Radiographics 1999;19:1507-31.  Back to cited text no. 16
McCoskey EH, McKinney LM, Byrd RP Jr., Roy TM. Re-expansion pulmonary edema following puncture of a giant bulla. J Am Osteopath Assoc 2000;100:788-91.  Back to cited text no. 17


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  [Table 1]

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