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Ann Thorac Surg 2000;70:669-671
© 2000 The Society of Thoracic Surgeons

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Case report

Reexpansion pulmonary edema after VATS successfully treated with continuous positive airway pressure

^a Division of Pulmonary and Critical Care Medicine, Long Island Jewish Medical Center, New Hyde Park, New York, USA
^b Department of Medicine, Long Island Jewish Medical Center, New Hyde Park, New York, USA
^c Division of Cardiothoracic Surgery, Long Island Jewish Medical Center, New Hyde Park, New York, USA

Address reprint requests to Dr Rossoff, Division of Pulmonary and Critical Care Medicine, Long Island Jewish Medical Center, Room C-20, 270-05 76th Ave, New Hyde Park, NY 11042
e-mail: miqbal{at}dnamail.com

	Abstract

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Reexpansion pulmonary edema is a well-described complication of treatment for pleural effusion and pneumothorax. It is very rarely described in association with anesthesia and video-assisted thoracoscopic surgery. The etiology is unclear but several mechanisms have been proposed. We report a case of reexpansion pulmonary edema after video-assisted thoracoscopic surgery treated successfully with continuous positive airway pressure.

	Introduction

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Reexpansion pulmonary edema (RPE) is a well-known complication of drainage of pneumothoraces and pleural effusions [1, 2]. In a unilateral intervention RPE can occur ipsilaterally, contralaterally, or bilaterally. Video-assisted thoracoscopic surgery (VATS) is being used more often for both diagnostic and therapeutic interventions with a low rate of complication [3]. We report an interesting case of unilateral RPE after VATS pleurodesis for recurrent malignant pleural effusion. We could find only three similar cases in the medical literature [3]. Our case is unique in that the patient’s hypoxemia was successfully treated with continuous positive airway pressure (CPAP).

A 67-year-old African American woman with a history of metastatic uterine adenocarcinoma was admitted with a recurrent left-sided malignant pleural and dyspnea. The left pleural cavity was sclerosed 8 months before by tube thoracostomy but the fluid returned after 6 months. She denied all other complaints aside from hypertension controlled on lisinopril and hydrochlorthiazide.

Chest roentgenogram revealed a large left pleural effusion and she underwent VATS with insufflated talc and mechanical pleurodesis. Approximately 3,000 mL of serosanguinous fluid was evacuated and two separately placed chest tubes connected to -20 cm H₂O suction. She was extubated rapidly but within a few hours developed dyspnea and hypoxemia on pulse oximetry. Her pulse was 120 bpm, blood pressure 180/110 mm Hg, and respiratory rate was 34 breaths/min. Chest auscultation revealed diffuse rhonchi and crackles localized to the left upper hemithorax. A chest roentgenogram (Fig 1A) revealed a left mid-lung zone inhomogeneous infiltrate, which rapidly progressed to florid unilateral left pulmonary edema (Fig 1B). Arterial blood gas revealed a pH of 7.30, PCO₂ of 56 mm Hg, and PO₂ of 68 mm Hg on FiO₂ of 1.0. She was treated with CPAP of 5 cm H₂O by full-face mask and intravenous diuretics. She improved over the next 6 to 8 hours with pulse oximetry consistently above 95% on 100% oxygen and CPAP. She diuresed more than a liter in the first 2 hours with continued decrease in oxygen requirements. A follow-up chest roentgenogram revealed virtual clearing of the edema (Fig 2). The CPAP mask was discontinued after 2 days and chest tubes after 4 days. Repeat arterial blood gas improved with a pH of 7.41, PO₂ of 115 mm Hg, and PCO₂ of 45 mm Hg on 2 L O₂ via nasal cannula.

View larger version (85K): [in this window] [in a new window]   Fig 1. (A) Four hours after extubation showing early infiltrates in the left upper lobe. (B) Twelve hours after extubation showing full-blown left-sided reexpansion pulmonary edema with air bronchgrams.

View larger version (119K): [in this window] [in a new window]   Fig 2. Resolution of left-sided pulmonary edema 48 hours after treatment.

	Comment

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Reexpansion pulmonary edema can range from a simple radiologic curiosity to life threatening hypoxemia with a mortality rate as high as 20% [2]. Video-assisted thoracoscopic surgery used increasingly in the treatment of recurrent pleural effusion and pneumothorax, has few reported complications with RPE reported only twice [3]. The edema is usually seen within 2 hours, occasionally delayed by 24 to 48 hours, of reexpansion of a lung collapsed for at least 72 hours [1]. The RPE can be lobar or multilobar, probably related to the prior degree of atelectasis [2]. Reexpansion pulmonary edema is usually short lived but rarely, as in this case, it can become life threatening and persist for up to a week.

Different mechanisms of edema formation have been proposed. The edema fluid to serum protein ratio in some of the cases has demonstrated increased vascular permeability in the reexpanded lung [4]. Negative pressure pleural suction and mechanical stress on the lung may contribute by altering regional perfusion [5]. Another possible mechanism is the vascular endothelial damage of a reperfusion injury in the areas of previous hypoxic vasoconstriction with resultant reactive oxygen species altering permeability of vascular endothelium [2, 6]. Decreased surfactant and lymph flow in the collapsed lung may also play a role [1, 5]. Lymphatic drainage in malignant pleural effusions, as in our case, may be further compromised. Additional stress by mechanical forces (stretch of the collapsed lung, surgical manipulation, and change from positive pressure to spontaneous respiration) may have contributed to the RPE.

Different strategies for prevention of RPE have been proposed. Although RPE has been reported without negative pressure suction, reduced levels (less than -10 cm of water) have been recommended [7]. Reducing the rate of fluid or air withdrawal has also been recommended [1]. The utility of CPAP in both cardiac and noncardiac pulmonary edema has been widely touted [8]. Although theoretically contraindicated in a unilateral process our patient improved, suggesting possible occult bilateral involvement. Although other treatment modalities were used the improvement most closely coincided with CPAP application.

In conclusion, the possibility of RPE should be considered in patients undergoing VATS. Continuous positive airway pressure may be a useful first line of treatment in severe cases, possibly avoiding the need for endotracheal intubation and positive pressure ventilation.

	References

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1. Mahajan V.K., Simon M., Guber G.L. Reexpansion pulmonary edema. Chest 1979;75:192-194.[Abstract/Free Full Text]
2. Mahfood S., Hix W.R., Aaron B.L., et al. Reexpansion pulmonary edema. Ann Thorac Surg 1988;45:340-345.[Abstract]
3. Yim A.P.C., Liu H.P. Complications and failures of video-assisted thoracic surgery. Ann Thorac Surg 1996;61:538-541.[Abstract/Free Full Text]
4. Sprung C., Lowenberz J., Baier H., et al. Evidence for increased permeability in RPE. Am J Med 1981;71:497-500.[Medline]
5. Ziskind M.M., Weill H., George R.A. Acute pulmonary edema following the treatment of spontaneous pneumothorax with excessive negative intrapleural pressure. Am Rev Respir Dis 1965;92:632-636.[Medline]
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8. Wysock M., Tric L., Wreff M.A., Millet H., Herman B. Noninvasive pressure support ventilation in patients with acute respiratory failure. Chest 1995;107:761-768.[Abstract/Free Full Text]

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This Article Abstract Full Text (PDF) 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): Rudy P. Lackner Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Iqbal, M. Articles by Lackner, R. P. Search for Related Content PubMed PubMed Citation Articles by Iqbal, M. Articles by Lackner, R. P.