Ann Thorac Surg 2005;80:1933-1934
© 2005 The Society of Thoracic Surgeons
Case report
New Treatment Method for Reexpansion Pulmonary Edema: Differential Lung Ventilation
Sang Rock Cho, MD
a
,
*
,
Jeong Sang Lee, MD
a
,
Mun Soo Kim, MD
b
a Department of Thoracic and Cardiovascular Surgery, Seoul City Boramae Hospital, Seoul
b Center for Lung Cancer, National Cancer Center, Goyang Si, South Korea
Accepted for publication June 4, 2004.
* Address correspondence to Dr Cho, Utah Center for Advanced Imaging Research, University of Utah, 729 Arapeen Dr, Salt Lake City, UT 84108 (Email: csr0404{at}ucair.med.utah.edu).
 |
Abstract
|
|---|
Reexpansion pulmonary edema (REPE) is an iatrogenic complication that develops in a lung rapidly reinflated after varied periods of collapse. Though infrequent, it is often lethal. Measures to prevent REPE are well known and mild cases may be reversed with conventional ventilator therapy and medication; however, there is no definitive treatment for this condition in its severest forms. Asynchronous differential lung ventilation is a relatively new therapeutic modality for preoperative, intraoperative, or postoperative treatment of respiratory failure secondary to ventilation-perfusion mismatch. Successful treatment of severe REPE in a 29-year-old male patient is described, using asynchronous differential lung ventilation.
|
Introduction
|
|---|
Reexpansion pulmonary edema (REPE) is an iatrogenic complication which develops in a lung that has been rapidly reinflated after varied periods of collapse secondary to a pneumothorax or a pleural effusion of large volume. Its incidence is relatively low, but mortality is up to 21% [1]. Methods to prevent this disease are well known, and conventional ventilator therapy with administration of some medications may be used for treatment of mild cases. However, there is no definitive treatment method for severe cases. This report describes a successful rescue from severe iatrogenic (thoracostomy-induced) REPE by asynchronous differential lung ventilation.
A 29-year-old man was transferred to the emergency room with a history of mild right chest pain for 1 week. Clinical examination and chest radiography confirmed nearly complete collapse of the right lung but other laboratory data including arterial blood gas analysis were within normal limits. Closed thoracostomy was performed in the emergency room and negative pressure was routinely applied to the pleural space (20 cm H2O through a two bottle system). After 2 hours the patient showed severe respiratory difficulty, cyanosis and coughing with a large amount of frothy secretion, tachypnea (44/min), and tachycardia (120/min). Wet rales were heard loudly over the right whole chest on auscultation, and the chest radiograph indicated unilateral pulmonary edema (Fig 1). After transfer to the intensive care unit, the patient suffered a decrease in blood pressure and loss of consciousness. Arterial blood gas analysis showed severe respiratory acidosis (pH: 7.14; partial pressure of carbon dioxide [PCO
2]: 73 mm Hg; partial pressure of oxygen [PO
2] mm Hg: 67; bicarbonate: 24 mEq/L). The amount of frothy secretion was not changed in spite of conventional ventilator therapy (7200 series, Puritan-Bennet Corp of California, CA). The endotracheal tube was replaced with a double-lumen endobronchial tube to prevent secretions from flowing over to the left lung. Conventional ventilator therapy was continued and a hyperosmolar agent, inotropics, diuretics, bronchodilator, and steroids were infused. However, the patient's condition did not change and the amount of frothy bronchial secretion did not decrease. An endobronchial suction catheter for the double-lumen endobronchial tube was placed in the endobronchial tube to the affected side and ventilator therapy was changed to unilateral ventilator therapy on the unaffected left lung (tidal volume: 400 mL; frequency: 20/min; fraction of inspired oxygen [FIO
2]: 1.0). Nonetheless, respiratory acidosis remained severe in spite of overcorrection of hypoxemia (pH: 7.18; PCO
2: 61; PO
2: 237; bicarbonate: 24) and the patient remained unconscious. Tachycardia and hypotension worsened to 160 per min and 60 mm Hg (systole), respectively. After 40 minutes under unilateral ventilator therapy hypoxemia recurred (pH: 7.22; PCO
2: 63; PO
2: 34; bicarbonate: 25), the total volume of bronchial secretion reached 700 mL and urine output approached zero. Another ventilator of the same brand was then attached to the affected right lung with readjustment of the ventilator settings after removal of the endobronchial suction tube. Tidal volume, respiratory rate, and FIO
2 were 350 mL, 25 per min, and 1.0, respectively. Positive end-expiratory pressure (5 cm H2O) was applied to the right side only. At that time right and left peak inspiratory pressures were 27 and 15 cm H2O. As soon as this asynchronous differential lung ventilation was applied, the vital signs of the patient began to stabilize. Blood in the syringe for arterial blood gas analysis changed from dark red to bright red and the results of arterial blood gas analysis (pH: 7.40; PCO
2: 39; PO
2: 100; bicarbonate: 23) confirmed the correction. Urination restarted. The tidal volume of the left side was then readjusted to 300 mL because chest radiography showed that the mediastinum was still shifted to the right side. Hypotension, tachycardia, and oliguria normalized after 3 hours of asynchronous ventilation and arterial blood gas analysis showed respiratory alkalosis and hyperoxemia (pH: 7.55; PCO
2: 24; PO
2: 345; bicarbonate: 21). Ventilator settings were therefore readjusted. The patient then began to recover consciousness, but full sedation was maintained to prevent displacement of the double-lumen endobronchial tube. Chest radiography at 10 hours posttreatment showed that the pulmonary edema in the right lung had gradually decreased (Fig 2). At 48 hours peak inspiratory pressures equalized (20 cm H2O) so the double-lumen endobronchial tube was changed to a single-lumen endotracheal tube and conventional ventilator therapy was restarted. Pneumonia by Pseudomonas aeruginosa occurred in the right lung but was cured by a tracheostomy and antibiotic therapy after a sensitivity test. Ventilator therapy was discontinued on day 6, as the patient was conscious. The patient was transferred to a ward on day 13 and antibiotic therapy was stopped on day 19. Three months after discharge, a bulla on the apex of the right lung was resected by video-assisted thoracoscopic surgery.
|
Comment
|
|---|
In severe cases ventilation-perfusion mismatch is worsened by conventional ventilator therapy, because the affected lung is in a state of hyperperfusion and poor compliance, while the unaffected lung is in a state of hypoperfusion and comparatively better compliance. Methods to prevent iatrogenic REPE are well known [2]; however, a definitive treatment method has not been described for (thoracostomy-induced) severe iatrogenic REPE although there is a case report using high frequency jet ventilation [3]. In this report we show that when this iatrogenic disease occurs, negative pressure applied to the pleural space should be stopped immediately. If the condition of the patient does not improve with such management, asynchronous differential lung ventilation is the definitive treatment of choice because this method can completely reverse the pathophysiologic course.
|
References
|
|---|
- Mahfood S, Hix WR, Aaron BL, Blaes P, Watson DC. Reexpansion pulmonary edema Ann Thorac Surg 1988;45:340-345.[Abstract]
- Light RW. PneumothoraxIn: Murray JF, Nadel JA, editors. Textbook of respiratory medicine. 2nd ed. Philadelphia, PA: WB Saunders; 1994. pp. 2193-2210.
- Waga M, Sanagawa Y, Okamoto Y. A case of anesthetic management for re-expansion pulmonary edema of the dependent lung saved by superimposed HFJV during one lung ventilation for the thoracoscopic operation associated with bilateral pneumothorax Masui 2000;49:643-645.[Medline]
This article has been cited by other articles:
|
|
|
|
 
N. Barbetakis, G. Samanidis, D. Paliouras, and C. Tsilikas
Re-expansion pulmonary edema following video-assisted thoracic surgery for recurrent malignant pleural effusion
Interactive CardioVascular and Thoracic Surgery,
June 1, 2008;
7(3):
532 - 534.
[Abstract]
[Full Text]
[PDF]
|
|
|
Top
Abstract
Introduction
