Abstract

This case report describes a 61-year-old man who developed reexpansion pulmonary edema (RPE) of the collapsed left lung after video-assisted thoracoscopic surgery because of left thoracic empyema, complicated with secondary contralateral pulmonary edema later. The left lung was gently reexpanded after surgery under one-lung ventilation anesthesia for 2.5 hours. The patient developed RPE of the left lung immediately after surgery, and required mechanical ventilation with positive end-expiratory pressure support. RPE was resolved within 24 hours. Nevertheless, delayed onset of contralateral pulmonary edema manifested on chest radiography 4 days later without clinical symptoms such as tachypnea or dyspnea. There was no evidence of pulmonary infection, fluid overload, postoperative renal insufficiency or cardiogenic onslaught. Late manifestation of contralateral pulmonary edema in the wake of previous left-sided RPE was suspected from exclusion of possible culprits. Response to steroid therapy made inflammation-related pulmonary edema a likely diagnosis. This case demonstrates that delayed contralateral pulmonary edema with only radiographic evidence can emerge 4 days after resolution of RPE of a collapsed lung. Methods to prevent RPE and management of one-lung ventilation are described.

Keywords

postoperative complications; pulmonary edema, reexpansion; pulmonary ventilation, one-lung; thoracic surgery, thoracoscopy;

1. Introduction

Reexpansion pulmonary edema (RPE) is a potentially life-threatening complication of reexpansion of a collapsed lung following treatment of pleural effusion, pneumothorax and even after a short period of one-lung ventilation (OLV) for video-assisted thoracoscopic surgery (VATS).¹⁻⁶ It is more likely to occur after reexpansion of a chronically collapsed lung or drainage of a large amount of pleural fluid or air. The reported incidence of RPE ranges from 0.9%⁷ to 14%,² and the mortality rate associated with RPE can be as high as 20%.³ Mostly, it occurs in chronic collapsed lungs after rapid reexpansion. While bilateral RPE is common, the occurrence of unilateral RPE, though rare, has also been reported.⁸⁻¹⁰ We present a case of unilateral RPE that occurred immediately after VATS for thoracic empyema. Unexpectedly, contralateral pulmonary edema of delayed onset emerged on radiography 4 days after the resolution of RPE of the diseased lung, without clinical symptoms such as tachypnea or dyspnea.

2. Case Report

A 61-year-old man weighing 72 kg underwent VATS for decortication because of left thoracic empyema. He had initially presented with persistent fever and productive cough for 2 weeks. Left pleural effusion was noted on chest radiography, which could not be controlled by antibiotic treatment or by drainage with an intrapleural catheter. His medical history was remarkable for type II diabetes mellitus of 5 years’ duration, properly controlled with oral hypoglycemic medication. Preoperative chest radiography showed a moderate amount of pleural effusion and partial lung collapse in the left hemithorax (Figure 1A). Laboratory examination revealed leukocytosis with a shift to the left (leukocyte count, 17,130/μL; neutrophil, 95.3%). Bacterial culture of pleural effusion was positive for group A streptococcal infection.

General anesthesia was induced with intravenous fentanyl 100 μg and etomidate 20 mg. After neuromuscular blockade with cisatracurium 10 mg, a 37-Fr left-sided, double-lumen endobronchial tube (Broncho-Cath^TM Left; Mallinckrodt Medical, Dublin, Ireland) was placed. The correct position of the endobronchial tube was confirmed by both chest auscultation of breath sounds and fiberoptic bronchoscopic examination. Anesthesia was maintained with 6−8% desflurane in oxygen. Standard monitoring was applied, including electrocardiography, pulse oximetry, direct arterial blood pressure and capnography during operation.

The surgery was performed uneventfully in the right lateral decubitus position, taking 2.5 hours. OLV was achieved mechanically at a pressure of 25 cmH₂O and a tidal volume of around 500 mL. Intraoperative arterial blood gas analysis revealed a PaO₂ of 110 mmHg and a PaCO₂ of 41 mmHg under pure oxygen ventilation. The amount of blood loss during operation was 400 mL. Pus accumulating over the left costophrenic angle and 500 mL of turbid and yellowish pleural fluid were evacuated. Restricted administration of perioperative fluid was adopted according to our institute’s policy for thoracic surgery. Balanced fluid with 1200 mL of crystalloid and 500 mL of synthetic colloid fluid (hydroxyethyl starch, 200/0.5) was administered over a period of 3 hours with stable hemodynamics and adequate urine output (> 1 mL/kg/hr). Before closure of the open hemithorax, the collapsed left lung was manually and gently insufflated to prevent atelectasis and to check for leakage at the peak inspiratory pressure of 20 cmH₂O. A chest tube was placed and connected to the underwater-seal drainage bottle without suction. The patient was then extubated when awake after reversal of neuromuscular blockade. However, minimal straw-colored bronchial secretions appeared in the left bronchial lumen of the double-lumen tube and an episode of severe coughing with physical effort was noted after extubation.

The patient was transferred to the postoperative care area but became progressively tachypneic, dyspneic and severely hypertensive (noninvasive blood pressure, 230/110 mmHg). Pulse oximetry revealed oxygen saturation < 75% with oxygen supplement of 8 L/min via a facemask. He was conscious and cooperative but his breathing was strenuous. The drainage from the chest tube was clean without negative pressure applied. Chest auscultation revealed wet rales over the left hemithorax and clear breath sounds over the right. Repeated arterial blood gas analysis revealed severe respiratory hypoxemia with normocapnia (PaO₂ of 45.7 mmHg, PaCO₂ of 44.4 mmHg) under oxygen supplement of 10 L/min via a facemask. Reintubation was performed 30 minutes after extubation. Chest X-ray was then taken and showed diffuse opacity of the left hemithorax (Figure 1B). Fiberoptic bronchoscopy revealed copious straw-colored secretion flowing out from the left main bronchus. One-hundred milliliters of clear, yellowish proteinaceous fluid was aspirated during bronchoscopy

Under the diagnosis of RPE based on clinical picture and unilateral presentation of pulmonary fluid, the patient was mechanically ventilated with positive end-expiratory pressure (PEEP) support at 5 cmH₂O. He had an uneventful intensive care unit course. The trachea was extubated on the following day after the patient’s condition became better with fluid restriction and diuretic treatment.

Nevertheless, an inhomogeneous infiltrate appeared in the right lung (Figure 1C) on the 4th postoperative day. The general condition of the patient was good except for coughing while lying supine. He had no fever or productive cough. Sputum staining and blood culture for bacterial growth were negative. Laboratory examinations showed decreasing leukocyte count (10,940/μL) and normal kidney function (blood urea nitrogen, 21 mg/dL; creatinine, 0.9 mg/ dL). Postoperatively, daily intake/output was balanced and daily urine output was 1200−1500 mL. There was no evidence of aspiration or physical and radiological signs of heart failure. A tentative diagnosis of right-sided pulmonary edema secondary to previous left RPE and involvement of systemic inflammation was made by exclusion of other causes.^9,10 Intravenous methylprednisolone, 40 mg every 8 hours, was administered and tapered off in 5 days. Subsequent chest X-ray showed that the rightsided pulmonary edema had resolved (Figure 1D). The patient was discharged on the 14^th postoperative day without respiratory complaints.

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Figure 1 Chest films show: (A) preoperative accumulation of pleural effusion and reduction of lung volume in the left hemithorax; (B) pulmonary edema limited to the left lung after reexpansion; (C) appearance of infiltrates in the right lung on the 4th postoperative day; (D) resolution of right lung infiltrates after steroid therapy.

3. Discussion

In this case report, we described delayed onset of contralateral pulmonary edema following RPE of a collapsed diseased lung subjected to VATS. Although RPE is a well-known complication of lung reexpansion after treatment of pleural effusion, pneumothorax, or OLV for VATS, our case was unusual because delayed contralateral pulmonary edema emerged 4 days after the preceding RPE of a collapsed lung. The contralateral pulmonary edema was benign, manifesting on chest radiography with the finding of increased infiltrates, which responded well to steroid therapy. There was no fever, leukocytosis, or positive culture for pathogens, and its response to steroid therapy rendered the diagnosis of pneumonia unlikely. In addition, by careful exclusion, lack of evidence of aspiration, fluid overload, postoperative renal insufficiency and signs of heart failure led to the diagnosis of inflammation-related pulmonary edema secondary to previous RPE. Resolution after steroid therapy explained the nature of the contralateral pulmonary edema in this patient.

The severity of RPE can range from showing only subclinical radiographic signs¹¹ to life-threatening hypoxemia or even circulatory insufficiency¹² with a high mortality rate of 20%.³ Several hypotheses have been proposed to explain the different mechanisms of RPE. Previous studies suggest increased endothelial permeability as a result of combined alveolar-capillary membrane disruption and ischemia− reperfusion injury of hypoxic lung.¹³⁻¹⁶ Increases in reactive oxygen species, lipid and polypeptide mediators and immune complexes during reperfusion lead to endothelial damage.¹⁴⁻¹⁶ In addition, hydrostatic forces in the lung microcirculation, generated by rapid reexpansion of the collapsed lung, may also contribute to RPE.¹⁷ As the pathophysiological processes implicate, duration of collapse > 3 days, severity of collapse > 30%, and technique used for reexpansion, such as negative pressure suction and rapid inflation with positive pressure or large effusion volume evacuated, are more likely to result in RPE.^3,13

The onset of RPE usually occurs within several hours after reexpansion, although it can occur anytime within 24 hours.¹³ Mostly, it occurs in the ipsilateral collapsed lung after reexpansion. Involvement of the contralateral non-collapsed lung, though rare, is also a possible manifestation of RPE. Activation of proinflammatory cytokines from reperfusion and/or reoxygenation injury as a result of reexpansion are believed to be the causes of contralateral RPE.^3,13 Contralateral RPE, especially concomitantly, was reported to be associated with more severe symptoms and higher rate of mortality.^3,13 It is similar to acute respiratory distress syndrome in the manifestation of multiorgan dysfunction. Nevertheless, if contralateral RPE occurs after resolution of RPE of the collapsed hypoxic lung, it is usually milder and can be cleared faster than that of the causal collapsed hypoxic lung.⁸ It is possible that the contralateral lung is injured through a leukocytemediated mechanism, when all the airways are flooded with edematous fluid which is extravasated through the injured capillaries with inflammatory mediators.^10,18 Unlike previous reports in the literature, our case is different in its delayed presentation of contralateral pulmonary edema on chest radiography, which occurred 4 days after RPE of the collapsed hypoxic lung had been resolved. The patient was symptomless and the contralateral pulmonary edema responded to steroid therapy. Data that would have been useful to further exclude cardiogenic pulmonary edema, such as pulmonary capillary wedge pressure and cardiac output, were not obtained because they were not considered to be clinically justifiable as the patient had no history, physical finding or radiographic evidence to suggest fluid overload or cardiogenic pulmonary edema.

OLV has become a common procedure for thoracoscopic surgery. Lung collapse and its reinflation in OLV, in addition to surgical manipulation of the nondependent lung, can contribute to the development of RPE.^6,19 Short-period OLV is sufficient to induce proinflammatory cytokine expression in animal model despite the lack of physiological lung injury (> 60 minutes),¹⁹ and in a patient compromised by immediate RPE without history of chronic collapsed lung (> 90 minutes).⁶ Methods to prevent lung injury or iatrogenic RPE after thoracic surgery and OLV are well-known,²⁰ including low ventilatory strategies and use of PEEP to avoid ventilatorassociated lung injury, fluid restriction, alveolar recruitment strategies, and lower fraction of oxygen if possible. After OLV, the nondependent lung should be gently and slowly reexpanded without negative pressure applied to the pleural space, especially in high-risk patients with a collapsed lung before surgery. However, if RPE still occurs, treatment remains supportive, including positive-pressure mechanical ventilation, application of PEEP, steroid administration, diuresis, and inotropic support in severe cases.²

In summary, it is important that when caring for patients with a collapsed lung, physicians are aware of RPE and its various manifestations. Management of OLV should be exercised to avoid further lung injury after thoracic surgery. These measures will facilitate prevention of RPE, but prompt treatment should be executed if it does occur.