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Ann Thorac Surg 1997;63:1206-1207
© 1997 The Society of Thoracic Surgeons

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Update

Reexpansion Pulmonary Edema

As Originally Published in 1988:

Updated in 1997 by Gregory D. Trachiotis, MD, Luca A. Vricella, MD, Benjamin L. Aaron, MD, and William R. Hix, MD

Division of Cardiothoracic Surgery, Department of Surgery, The George Washington University Medical Center, Washington, DC

Reexpansion pulmonary edema (RPE) remains a rare complication that occurs when a collapsed lung is rapidly reexpanded by evacuation of air or fluid. Since our review of the reported world experience with 47 cases of RPE between 1958 and 1987 [1], we have seen about 1 case per 2 years at our institution. Eighty-three percent of cases of RPE are a result of a chronically collapsed lung from a pneumothorax, and 83% are on the affected side; 6.7% are bilateral, and a few can occur in the contralateral lung. The onset of RPE occurs as rapidly as 1 hour in 64% of cases, and uniformly results in 24 hours. Although it is likely that rapid reexpansion by application of negative pressure contributes to RPE, it can occur in more than 33% of cases when reexpansion is allowed without pleural suction. The mortality remains about 20%, and seems to be associated with bilaterality and sudden onset of RPE [1].

The pathophysiology of RPE remains undefined, although there have been thoughtful reports in the experimental and clinical arenas [2–5]. The common end-point in the pathological process likely results from enhanced endothelial permeability [4,5]. This destructive process is thought to be a result of combined alveolar-capillary membrane disruption and ischemia-reperfusion–mediated injury. These processes are likely to be initiated by the stretching or distention and increased pulmonary flow that occur during pulmonary reexpansion [5]. Once there is microvascular injury, the pathologic process is believed to propagate and worsen by local cellular imbalances in nitric oxide levels and by-products [4], neutrophil aggregation and degranulation [2,3], and free-radical–mediated tissue necrosis. The pathologic mechanism premised to be the basis of RPE is similar to that observed in the adult respiratory distress syndrome [4,5], postpneumonectomy pulmonary edema [5], and after pulmonary reimplantation.

The mainstay in therapy for RPE remains oxygenation, a low threshold for mechanical ventilation with positive end-expiratory pressure, diuresis, and hemodynamic support. With the recent data regarding the pathologic processes occurring in RPE, we have used the prostaglandin analogue misoprostil and ibuprofin or indocin suppositories once the diagnosis is suspected and early in therapy. The rationale for the use of these agents is based on either their cytoprotective or their antiinflammatory actions. Perhaps even more therapeutic is positioning the patient in the lateral decubitus position with the affected side up. This position may help reduce edema and intrapulmonary shunting. We continue to allow gradual lung expansion on underwater seal, and apply pleural suction once the lung is nearly expanded. Reexpansion pulmonary edema usually resolves in 24 to 72 hours.

In patients with bullous disease or young patients with a difficult recovery, there should be consideration of bullectomy or pleurodesis. We have also observed an increasing number of patients with acquired immunodeficiency syndrome–related pneumothoraces that are at risk for RPE. These patients are best managed with tube thoracostomy or a Heimlich valve [6].

Reexpansion pulmonary edema can occur unexpectedly and dramatically. Physicians who are called to treat a pneumothorax or hydrothorax should be aware of this phenomenon. Efforts should be made to reduce its occurrence or ameliorate the pathologic responses. Despite a growing understanding of the pathologic mechanism involved in RPE, a 20% mortality can be expected.

Footnotes

Address reprint requests to Dr Trachiotis, Division of Cardiothoracic Surgery, George Washington University Medical Center, 2150 Pennsylvania Ave, NW, Washington, DC 20037

References

1. Mahfood S, Hix WR, Aaron BL, Blaes P, Watson DC. Reexpansion pulmonary edema. Ann Thorac Surg 1988;45:340–5.[Abstract]
2. Suzuki S, Tatsuo T, Koike K, Fujimura S. Evidence of acute inflammatory response in reexpansion pulmonary edema. Chest 1992;101:275–6.[Abstract/Free Full Text]
3. Nakamura H, Ishizaka A, Sasafuji M, et al. Elevated levels of interleukin-8 and leukotriene B4 in pulmonary fluid of a patient with reexpansion pulmonary edema. Am J Respir Crit Care Med 1994;149:1037–40.[Abstract]
4. Williams EA, Evans TW, Goldstraw P. Acute lung injury following lung resection: is one lung anaesthesia to blame? Thorax 1996;51:114–6.[Abstract/Free Full Text]
5. Trachiotis GD, Hix WR. Postpneumonectomy pulmonary edema. Hosp Phys 1995;31:30–6.
6. Trachiotis GD, Vricella LA, Alyono D, Aaron BL, Hix WR. Management of AIDS-related pneumothorax. Ann Thorac Surg 1996;62:1608–13.[Abstract/Free Full Text]

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This Article Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): William R. Hix Donald C. Watson Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by mahfood, S. Articles by Watson, D. C. Search for Related Content PubMed PubMed Citation Articles by mahfood, S. Articles by Watson, D. C.