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Lung volume reduction surgery in COPD

Lung volume reduction surgery in COPD
Literature review current through: Jan 2024.
This topic last updated: Mar 15, 2023.

INTRODUCTION — Emphysema is a form of chronic obstructive pulmonary disease (COPD) that is defined by abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles and is associated with destruction of the alveolar walls. Emphysema causes dyspnea through airflow limitation, hyperinflation, and loss of gas exchanging surfaces in the lungs (also known as increased physiologic dead space).

Lung volume reduction surgery (LVRS, also called reduction pneumoplasty or bilateral pneumectomy) is a surgical technique that may be beneficial for some patients with advanced emphysema who have poor control of their disease despite maximal medical therapy. LVRS entails reducing the lung volume by wedge excision of emphysematous tissue [1]. Subsequent modifications to LVRS include nonresectional lung volume reduction [2-5].

The indications, contraindications, technique, and outcomes of LVRS will be reviewed here. The general management of chronic obstructive pulmonary disease, the evaluation and management of giant bullae, and the role of lung transplantation in end-stage emphysema are discussed separately. (See "Management of refractory chronic obstructive pulmonary disease" and "Bronchoscopic treatment of emphysema" and "Evaluation and medical management of giant bullae" and "Lung transplantation: General guidelines for recipient selection".)

RATIONALE OF LVRS — The mechanisms by which lung volume reduction surgery (LVRS) might provide benefit are not known with certainty. It has been suggested that LVRS reduces the size mismatching between the hyperinflated lungs and the chest cavity, thereby restoring the outward circumferential pull on the bronchioles (ie, increasing elastic recoil) and improving expiratory airflow [6-12]. As an example, in a study of 20 patients undergoing volume reduction surgery, 16 experienced an increase in elastic recoil [13]. The patients with improved elastic recoil had a significantly greater increase in exercise capacity than the four without increased elastic recoil.

Other postulated mechanisms for clinical benefit include:

Improvement in the mechanical function of the diaphragm and intercostal muscles by decreasing the functional residual capacity (FRC; the amount of air left in the lungs after exhalation of a tidal volume breath) and returning the diaphragm to a more normal curved and lengthened configuration (figure 1) [14,15]. In a study that examined the relative contribution of the thoracic (intercostal and scalene muscles) and abdominal (diaphragm) compartments to tidal volume breaths, an increase in the abdominal contribution was noted after LVRS, suggesting improved diaphragmatic function [16]. In addition, improved synchrony of the diaphragm with other inspiratory muscles was noted, suggesting a reduction in respiratory muscle fatigue following LVRS. Improved chest wall asynchrony has also been suggested [17].

Improved left ventricular filling, end-diastolic dimension, and cardiac index due to decreased intrathoracic pressure [18].

Reduction in lung volumes during exercise (ie, reduced dynamic hyperinflation), which is associated with reduced exertional dyspnea [10]. (See "Dynamic hyperinflation in patients with COPD".)

Improved endothelial function and blood pressure [19].

Decreased circulating inflammatory markers (tumor necrosis factor [TNF]-alpha, interleukin [IL]-6, and IL-8) but improved alpha-1 antitrypsin levels [20].

LVRS CLINICAL TRIALS — Several randomized trials and a systematic review have examined the efficacy and safety of LVRS [2,21-29]. LVRS modestly improves spirometry, lung volumes, exercise capacity, dyspnea, and quality of life and may improve long-term survival among highly selected patients. Certain clinical features appear to influence the degree of risk and benefit.

A systematic review identified 11 studies (1760 participants), of which almost 70 percent were from the National Emphysema Treatment Trial (NETT) [29]. Short-term mortality was higher with LVRS (odds ratio [OR] 6.16, 95% CI 3.22-11.79, 1489 participants), while long-term mortality favored LVRS (OR 0.76, 95% CI 0.61-0.95, 1280 participants). Participants with upper lung zone predominant emphysema and poor exercise tolerance appeared to have a better outcome, as described below. (See 'Subgroup analysis' below.).

National Emphysema Treatment Trial — NETT is the largest randomized trial of LVRS [27].

Trial design — NETT compared the benefits of LVRS versus maximal medical therapy in 1218 patients with advanced emphysema [27]. Following a baseline assessment, the patients underwent 6 to 10 weeks of mandatory pulmonary rehabilitation and were then randomly assigned to LVRS or continued medical therapy. LVRS was performed by thoracotomy in 70 percent and by video-assisted thoracoscopy in 30 percent.

Primary endpoints — The primary endpoints of NETT were mortality and maximal exercise capacity at 24 months [27].

Early in the trial, a high risk of death (16 percent versus 0 percent for the medical therapy group) was identified in a subgroup of patients with a forced expiratory volume in one second (FEV1) of 20 percent predicted or less AND either homogeneous emphysema or a diffusing capacity for carbon monoxide (DLCO) that was 20 percent predicted or less [30]. Patients with these characteristics were subsequently excluded from enrollment in NETT and LVRS is contraindicated in such patients.

Among patients without these high-risk characteristics, the 30-day mortality rate was 2.2 percent in the LVRS group, compared with 0.2 percent in the medical therapy group (p<0.001). At two years, total mortality among non-high-risk patients did not differ between the LVRS and medical therapy groups (0.09 versus 0.10 deaths per person-year).

Improvement in exercise capacity was defined as an increase in the maximal workload of more than 10 watts at 24 months compared with the post-rehabilitation baseline [27]. Excluding the high-risk group, exercise capacity improved by more than 10 watts in 16 percent of LVRS patients and 3 percent of medical therapy patients. In a separate analysis, the mean difference in maximal workload between the two groups was 10.9 watts, favoring LVRS, with 10 watts being the minimal clinically important difference in patients with severe emphysema [31]. Thus, the effects of LVRS on exercise capacity were modest, but statistically and clinically significant.

A separate analysis of NETT data using longitudinal data methodology confirms that surgical therapy compared with nonsurgical therapy results in improved lung function which gradually decreases over five years [32].

Subgroup analysis — A subgroup analysis of NETT results was performed to assess whether particular patient characteristics would lead to differential risks or benefits [27]. In addition to the high-risk group (called group A) described above (see 'Primary endpoints' above), the response of four additional subgroups to LVRS versus medical therapy was assessed. The subgroups were not prespecified, so the analyses should be viewed with caution.

Patients with upper lobe predominant emphysema and a low exercise capacity comprised 24 percent of all patients and were designated group B (figure 2 and table 1). Low exercise capacity was defined as less than the sex-specific 40th percentile (40 watts in males and 25 watts in females). Among this group, surgery did not affect 90 day mortality (2.9 versus 3.3 percent), but it reduced long-term mortality (risk ratio 0.47, p = 0.005) (figure 2) [27,33]. Surgery was significantly more likely to lead to short-term and long-term improvement of exercise capacity and health-related quality of life.

Patients with upper lobe predominant emphysema and high exercise capacity comprised 34 percent of all patients and were designated group C (figure 2 and table 1). Surgery did not impact the 90 day, short-term, or long-term mortality of this group (risk ratio 0.98, p = 0.70) (figure 2) [27,33]. Surgery improved both exercise capacity and quality of life, and the improvements were sustained through three and four years of follow-up, respectively. High exercise capacity was defined as greater than the sex-specific 40th percentile (40 watts in males and 25 watts in females).

Patients with non-upper lobe predominant emphysema and low exercise capacity comprised 12 percent of all patients and were designated group D (figure 2 and table 1). Among this group, LVRS slightly increased 90 day mortality, but did not affect mortality at 24 months (figure 2). Limited short-term improvement of exercise capacity was noted in this group; however, this advantage disappeared by the long-term follow-up [27,33].

Patients with predominantly non-upper lobe emphysema and high exercise capacity comprised 18 percent of all patients and were designated group E (figure 2 and table 1). Among this group, LVRS increased 90-day mortality (10.1 versus 0.9 percent), and slightly increased long-term mortality (risk ratio 2.06, p = 0.02) [27,34,35]. These patients had little short-term or long-term functional improvement with either type of therapy (figure 2 and table 1).

PATIENT SELECTION — The National Institute for Heath and Care Excellence (NICE) suggests a stepwise approach for identifying potentially eligible patients for LVRS. At the completion of pulmonary rehabilitation when medications for COPD have been optimized, patients with a forced expiratory volume in one second (FEV1) <50 percent predicted and persistent limiting breathlessness without an obvious contraindication should be further evaluated for potential lung volume reduction (surgical or bronchoscopic) [36].

Evaluation — Consideration for lung volume reduction surgery (LVRS) includes a thorough assessment of both cardiopulmonary function and the severity and distribution of emphysema. Testing typically includes pulmonary function tests, a six-minute walk test, arterial blood gas, electrocardiogram, echocardiogram with measurement of pulmonary artery pressures, a cardiopulmonary exercise test, and high resolution computed tomography (HRCT). The results of this assessment are used to determine the patient's candidacy for LVRS.

HRCT has several roles in the evaluation of patients for possible LVRS: to confirm the presence of emphysema, quantitate the amount of lung affected, assess the anatomic distribution, and identify other conditions that may preclude LVRS. As an example, patients with a diffuse and homogeneous distribution of emphysema on HRCT are less likely to benefit from LVRS than patients with a heterogeneous distribution of emphysema, particularly those with upper lobe predominant disease [27,30] (see 'Subgroup analysis' above).

Quantitative assessment of emphysema severity and distribution are weak predictors of physiological and clinical outcomes after LVRS [37]. A prospective, single-center study of 250 patients undergoing LVRS examined results of thoracoscopic resection as a function of emphysema distribution [38]. In the 138 patients with homogenous emphysema and FEV1 and diffusing capacity for carbon monoxide (DLCO) >20 percent predicted, perioperative and one-year mortality were similar to the 112 patients with heterogeneous emphysema, although patients with heterogeneous emphysema experienced a slightly better chance of long-term survival without need for lung transplantation. Spirometric and walk distance was generally similar, although improvement was numerically lesser in patients with homogeneous emphysema.

In the National Emphysema Treatment Trial (NETT), HRCT identified other diseases that precluded LVRS on the scans of 174 patients (eg, pulmonary nodules, bronchiectasis, pleural disease, interstitial lung disease, giant bullae). (See "Diagnostic evaluation of the incidental pulmonary nodule" and "Evaluation and medical management of giant bullae".)

Indications — The indications for LVRS in patients with emphysema are generally derived from the entry criteria for NETT and the results of that trial (table 2) [27].

Appropriate candidates for LVRS typically have the following features:

Age less than 75 years [39].

Severe dyspnea despite optimal medical therapy and maximal pulmonary rehabilitation [27,40].

Longer than six months of smoking cessation [27,40].

Marked airflow obstruction on spirometry (forced expiratory volume in one second [FEV1] less than 45 percent predicted), consistent with the diagnosis of advanced chronic obstructive pulmonary disease (COPD) [40].

A DLCO that is NOT less than 20 percent predicted [27].

Lung volume measurements showing air trapping (eg, residual volume [RV] greater than 150 percent predicted, total lung capacity [TLC] greater than 100 percent predicted, an increased RV/TLC ratio). An increased RV/TLC ratio correlates with improved forced vital capacity (FVC) following LVRS [7,34,40,41].

Computed tomography findings of hyperinflation and heterogeneously distributed emphysema with some areas having better preserved lung tissue [35,38,42-46]. Patients with predominantly upper lung zone emphysema are more likely to benefit.

Post-rehabilitation, a six-minute walk distance greater than 140 meters, but a low maximal achieved cycle ergometry (eg, less than 40 watts for men or 25 watts for women while breathing supplemental oxygen at 30 percent) [27,40].

Contraindications — The contraindications to LVRS for emphysema are generally derived from the exclusion criteria used for NETT and from the results of that trial and other studies (table 2) [27,40,47], although some of these criteria have been expanded subsequently:

Age greater than 75 [40].

Cigarette smoking within the prior six months [27].

A comorbid illness that would increase surgical mortality (eg, significant coronary heart disease, heart failure with a left ventricular ejection fraction less than 40 percent) [27,40].

Severe cachexia or obesity (eg, 31.1 kg/m2 for men and 32.3 kg/m2 for women) [27,40].

Inability to complete a 6 to 10 week program of pulmonary rehabilitation [27,40].

A chest wall deformity, previous pleurodesis, or thoracotomy that would preclude surgery [27,40].

A chest HRCT scan that shows minimal emphysema or shows homogeneously distributed emphysematous changes without areas of preserved lung tissue, particularly if the FEV1 is less than 20 percent predicted [27].

Findings on HRCT that would be considered a contraindication for LVRS (eg, giant bulla, interstitial lung disease, pulmonary nodule) [27].

Markedly abnormal alveolar gas exchange with a DLCO less than 20 percent of predicted, an arterial partial pressure of carbon dioxide (PaCO2) >60 mmHg, or an arterial partial pressure of oxygen (PaO2) <45 mmHg [40].

Pulmonary hypertension (pulmonary artery systolic pressure >45 mmHg, mean pulmonary artery pressure >35 mmHg) [40]. Echocardiographically estimated systolic arterial pulmonary artery pressure >35 mmHg was not associated with impaired LVRS outcome in a single case series of patients with heterogeneous emphysema [48].

Patients with severe alpha-1 antitrypsin deficiency appear less likely to benefit from LVRS than patients with emphysema who are alpha-1 antitrypsin replete, although alpha-1 antitrypsin deficiency was not an absolute contraindication in NETT. (See "Treatment of alpha-1 antitrypsin deficiency", section on 'Lung volume reduction surgery'.)

Indications for unilateral LVRS — Unilateral LVRS is sometimes performed instead of bilateral LVRS, when a patient has one or more of the following: unilateral or severely asymmetric emphysema, contralateral pleurodesis, contralateral thoracotomy, hemodynamic instability or massive air leak during the first side of a planned bilateral LVRS, or severe native lung hyperinflation after single lung transplantation for emphysema [49,50]. Some groups have successfully utilized staged bilateral procedures with the timing of the contralateral procedure dependent on evidence of deterioration in improvement after the first procedure [2,51].

Successful unilateral, repeat LVRS via video-assisted thoracoscopic surgery (VATS) or thoracotomy has been performed after initial bilateral thoracoscopic LVRS [52,53]. In the largest series of 22 carefully selected, the indications included utilizing LVRS as a bridge to transplantation and resection of newly diagnosed intrapulmonary nodules.

ANESTHETIC MANAGEMENT — Patients with advanced chronic obstructive pulmonary disease (COPD) who undergo lung volume reduction surgery (LVRS) are at increased risk for perioperative complications and require careful preoperative assessment and targeted adjustments to perioperative management [50,54].

Preoperative evaluation — Preoperative assessment typically includes ensuring that medical therapy for COPD is optimized and that comorbid illnesses (eg, coronary heart disease, heart failure) have been evaluated and treated, as necessary [54]. Preoperative management of patients with COPD is reviewed separately. (See "Evaluation of perioperative pulmonary risk" and "Evaluation of cardiac risk prior to noncardiac surgery" and "Strategies to reduce postoperative pulmonary complications in adults" and "Anesthesia for patients with chronic obstructive pulmonary disease".)

Monitoring — Standard monitoring during the procedure includes blood pressure, pulse oximetry, capnography, core temperature, and continuous electrocardiogram [55]. Generally, an arterial line is placed for blood pressure monitoring and serial assessment of arterial blood gases [56]. Central venous pressure monitoring is frequent, but not universal; pulmonary artery catheter placement has not been found to provide additional benefit [56,57]. (See "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults", section on 'Respiratory effects'.)

Antimicrobial prophylaxis — Antimicrobial prophylaxis is administered within 60 minutes prior to the skin incision. The choice of antimicrobial therapy is discussed separately. (See "Antimicrobial prophylaxis for prevention of surgical site infection in adults", section on 'Thoracic surgery'.)

Anesthesia — LVRS is typically performed under general anesthesia; short-acting anesthetic agents are preferred over longer-acting agents to enable early extubation. Intravenous agents are typically used for induction of anesthesia, as severe bullous disease may make the uptake and distribution of inhalational agents unpredictable [56]. A thoracic epidural catheter is usually placed for administration of epidural anesthetic agents during and/or after surgery. (See "Evaluation of perioperative pulmonary risk", section on 'General anesthesia versus neuraxial or regional anesthesia'.)

A potential alternative may be to perform awake thoracoscopic LVRS with thoracic epidural anesthesia [3]. Patients should meet NETT criteria and have no radiological evidence of extensive pleural adhesions (eg, pleural thickening and calcifications), unfavorable anatomy, previous surgery of the cervical or upper thoracic spine, compromised coagulation, or a bleeding disorder [3]. Thoracic epidural anesthesia provided somatosensory and motor block at the T1 to T8 level to secure motor block of the intercostal muscles while preserving diaphragmatic respiration. During the procedure, patients breathed O2 through a venturi facemask to keep oxygen saturation above 90 percent.

Single lung ventilation — After induction of anesthesia, appropriate positioning and sterile draping, a double-lumen endotracheal tube (or other endotracheal tube that will allow isolation of ventilation to one lung) is placed to administer single lung ventilation to the nonoperative lung and to enable deflation of the operative lung [56]. Correct placement of the endotracheal tube is confirmed bronchoscopically. Deflation of the operative lung may be slow due to the underlying obstructive airways disease and may require gentle suctioning and external pressure.

During single lung ventilation, patients with advanced COPD may develop air trapping and hyperinflation, causing hemodynamic instability. Ventilatory techniques, such as using low tidal volumes (eg, 5 mL/kg), lower respiratory rates, and longer expiratory times (eg, an inspiratory to expiratory ratio of 1:3 or 1:5), can help to prevent this complication. Lowering minute ventilation in this way may lead to alveolar hypoventilation and elevation in the arterial partial pressure of carbon dioxide (PaCO2). Accepting deliberate alveolar hypoventilation to mitigate auto-positive end-expiratory pressure (auto-PEEP) is known as permissive hypercapnic ventilation (PHV). With this technique, the pH is allowed to drop gradually into the range of 7.35 to 7.2. (See "One lung ventilation: General principles" and "Permissive hypercapnia during mechanical ventilation in adults".)

If the strategies of permissive hypercapnia cause the pH to drop below 7.2, strategies such as a cautious increase in ventilatory rate, suctioning of airway secretions, optimizing muscle relaxation, and administering inhaled bronchodilator therapy, should help to improve alveolar ventilation [56].

If a patient should develop hyperinflation and hemodynamic instability despite measures to minimize air trapping and auto-PEEP, transient disconnection of the endotracheal tube from the ventilator usually leads to resolution over several seconds [50].

TECHNICAL ASPECTS — Several different surgical approaches and techniques for volume reduction are used to perform lung volume reduction surgery (LVRS) [47].

Thoracotomy versus thoracoscopy — Bilateral LVRS may be performed through a median sternotomy, staged anterolateral thoracotomies, or video-assisted thoracoscopy. When bilateral LVRS is planned, most experts operate on the more severely affected side first. Unilateral LVRS is typically performed through a lateral thoracotomy or a video-assisted thoracoscopic approach.

The decision about whether to perform LVRS via thoracotomy or thoracoscopy depends in large part on the surgical and institutional expertise [50]. In a nonrandomized analysis of National Emphysema Treatment Trial (NETT) data, morbidity and mortality were similar when LVRS was performed via thoracotomy or thoracoscopy [58]. Thoracoscopic LVRS was associated with lower costs and shorter hospitalizations (9 versus 10 days) than median sternotomy.

An additional modification uses a single thoracoscopic access route to plicate the targeted emphysematous lung (without resection) [4]. Initial studies suggest improved perioperative morbidity and similar physiological and symptomatic outcomes compared with more traditional nonawake resectional LVRS, as described below. (See 'Nonresectional lung volume reduction' below.)

Lung volume reduction technique — Volume reduction is generally achieved by making a series of wedge excisions in areas where the emphysematous changes are most marked. Typically, the amount of lung resected is 20 to 35 percent of each lung or as much as 60 percent of the total thoracic volume [27,50]. The goal is to remove as much diseased lung as possible, while preserving the greatest amount of functioning lung.

Buttressed staple sutures are typically employed to close the resultant defects and prevent air leaks. Bovine pericardial strips and/or other materials (eg, polytetrafluoroethylene strips) may be used to buttress the suture line and reduce the incidence of postoperative air leaks [50,59-63]. Less than 5 percent of patients in NETT had unbuttressed suture lines, so insufficient data are available to compare results with and without buttressed sutures [64].

After completion of the wedge resections, two chest tubes are placed in the chest cavity, the clamp or bronchial blocker is removed from that side of the endotracheal tube, and mechanical ventilation is resumed to the deflated lung. Gradual reinflation is preferred to aggressive efforts at reinflation [50].

An investigative technique plicates the most emphysematous area of lung tissue rather than resecting it, as described below. (See 'Nonresectional lung volume reduction' below.)

POSTOPERATIVE MANAGEMENT — Immediately postoperatively, patients are assessed for anemia due to excessive intraoperative blood loss, cardiac ischemia, electrolyte abnormalities, hypercapnia, hypoxemia, and inadequate lung re-expansion (eg, due to air leak, suboptimal function of chest tubes). If these factors are all acceptable, the patient is extubated. The majority of patients are extubated in the operating room to minimize the duration of positive pressure ventilation [50].

Postextubation respiratory insufficiency can result from bronchoconstriction from the underlying chronic obstructive pulmonary disease (COPD), atelectasis, pneumothorax, hypoventilation due to postoperative pain, or pneumonia. For awake patients with a rising arterial partial pressure of carbon dioxide (PaCO2) despite prompt attention to these factors, noninvasive positive pressure ventilation may be used to avoid reintubation. (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications".)

Due to the high proportion of patients with air leaks, careful attention to the proper function of the chest tubes is key to prevent development of a pneumothorax and consequent respiratory insufficiency. Brief kinking or blockage of a chest tube can lead to rapid accumulation of a pneumothorax and cardiopulmonary decompensation. A chest radiograph is obtained daily to confirm full lung re-expansion. Chest tubes are generally left in place until the lung is fully re-expanded and there is no evidence of air leak. The procedure for chest tube removal is described separately. (See "Thoracostomy tubes and catheters: Indications and tube selection in adults and children".)

Management of postoperative pain usually involves a combination of regional and systemic agents to enable early mobilization of the patient and effective cough [56]. (See "Strategies to reduce postoperative pulmonary complications in adults", section on 'Postoperative strategies' and "Approach to the management of acute pain in adults".)

Prevention of deep venous thrombosis and pulmonary embolism is discussed separately. (See "Prevention of venous thromboembolic disease in adult nonorthopedic surgical patients".)

COMPLICATIONS — Major short-term complications of lung volume reduction surgery (LVRS) include death, reintubation, arrhythmias, mechanical ventilation for more than two days, pneumonia, and persistent air leak.

Major morbidity and mortality — Among the 511 non-high-risk patients in the National Emphysema Treatment Trial (NETT) who underwent LVRS, the operative mortality rate was 6 percent, major pulmonary morbidity 30 percent, and major cardiovascular morbidity 20 percent [65].

In a review of the Society of Thoracic Surgeons Database of 538 patients who underwent LVRS subsequent to NETT (2003 to 2011), the 30 day mortality rate was 5.6, slightly higher than the 2.2 percent mortality among non-high-risk patients in NETT (difference 3.4, 95% CI 1-5) [66]. It would be helpful for future studies to provide information about mortality at later time points. Missing data on 14 percent of patients may affect the outcomes reported.

A review of the Nationwide Inpatient Sample (NIS) database suggested that the number of LVRS procedures declined from 2000 to 2010; the in-hospital mortality was 6 percent and did not change significantly over time [67]. Age >65 was the strongest predictor for in-hospital mortality; the presence of interstitial lung disease and malnutrition were also independent predictors. An analysis of NIS from 2007 to 2013 revealed an increase in the total number of procedures performed (from 320 in 2007 to 605 in 2013) [68]. The total hospital mortality was 5.5 percent. A higher number of comorbidities and the presence of secondary pulmonary hypertension were associated with increased mortality.

A review of the Society of Thoracic Surgeons (STS) General Thoracic Database identified 1617 patients who underwent LVRS at 165 North American hospitals between 2001 and 2017 [69]. Since 2011, national utilization has increased with decreasing mortality rates. Multivariable analysis suggested that older age, male sex, underweight body mass index, and an Easter Clinical Oncology Group score >4 were associated with major morbidity or mortality.

Air leaks — Air leak following LVRS is frequent. In NETT, approximately 90 percent of patients had an air leak within 30 days of LVRS; the mean duration of air leak was seven days [64]. Patients with a low DLCO, upper lobe predominant emphysema, and pleural adhesions were more likely to have a persistent air leak and to experience prolonged leakage. In addition, White patients, patients using inhaled glucocorticoids, and patients with a low forced expiratory volume in one second (FEV1) tended to have a protracted duration of air leak.

In a separate series, among 250 consecutive patients who underwent LVRS, persistent air leaks lasting over seven days occurred in 45 percent; re-exploration for air leaks or bleeding was needed in 3 and 1 percent, respectively. Postoperative reintubation and mechanical ventilation were necessary in 7 percent [70].

Other complications — In the NETT trial, the most common complications were reintubation (22 percent), arrhythmias (19 percent), pneumonia (18 percent), and mechanical ventilation for more than two days (13 percent) [71]. Less common complications included intraoperative myocardial infarction, deep venous thrombosis, pulmonary embolism, and wound infection [50].

The NIS database analysis found a higher number of comorbidities and the presence of secondary pulmonary hypertension were associated with a greater likelihood of tracheostomy during the admission for LVRS [68].

LONG-TERM OUTCOMES — The effect of lung volume reduction surgery (LVRS) on several long-term outcomes such as degree of dyspnea, quality of life, oxygenation, the BODE index, and cost effectiveness has been assessed.

One single center experience reported survival estimates of 0.99 at one year, 0.97 at two years, and 0.78 at five years [72].

A separate single center report noted 2.2 percent 90-day mortality and 0.94 one-year, 0.91 two-year, and 0.71 five-year survival estimates after LVRS [73].

Dyspnea — Relief of dyspnea after LVRS has been examined in nonrandomized series and in the National Emphysema Treatment Trial (NETT) as a secondary endpoint [21,27,70]. In a series of 250 consecutive patients, dyspnea scores were improved over baseline in 88 percent, 79 percent, and 40 percent of patients at six months, one year, and five years following LVRS (figure 3) [70].

In NETT (see 'National Emphysema Treatment Trial' above), patients who underwent LVRS had a significantly greater improvement in dyspnea scores, as assessed by changes in the University of California San Diego (UCSD) Shortness of Breath Questionnaire, than those in the medical therapy group [27]. A subsequent analysis of the NETT data using longitudinal data analysis techniques confirmed improved dyspnea scores after LVRS out to five years [32].

Quality of life — Quality of life before and after LVRS has been examined in a number of studies (table 1) [32,33,39,70,74,75]. In a follow-up to NETT (see 'National Emphysema Treatment Trial' above), health-related quality of life was assessed using the St. George's Respiratory Questionnaire (SGRQ) [33]. Patients with upper lobe predominant disease and a low exercise capacity demonstrated improvement in SGRQ that lasted through five years of follow-up (p<0.001 years 1 to 3, p = 0.01 year 5). Patients with upper lobe predominant disease and a high exercise capacity also had an improved SGRQ, although the degree of significance was less. (See 'Subgroup analysis' above.)

In a separate series of 250 patients who underwent LVRS at a single center, significant improvement in the quality of life was noted compared with values prior to surgery (figure 4A-B) [70].

Unilateral LVRS has also been associated with improved quality of life in selected patients. As an example, in a series of 97 patients with asymmetric emphysema who underwent unilateral LVRS, significant improvement that persisted at least 36 months was noted in the Short Form-36 Quality of Life questionnaire [39].

Lung function — Among NETT participants, forced expiratory volume in one second (FEV1) improved after LVRS (approximately 24 to 32 percent predicted) compared with no change in the medical treatment arm, but then declined gradually to baseline over approximately five years [32]. Residual volume RV, as a measure of air trapping, decreased from approximately 220 to 165 percent predicted after LVRS and approached the baseline after five years.

Oxygenation — In NETT, resting arterial partial pressure of oxygen (PaO2) was more likely to increase and both treadmill and self-reported oxygen use (during rest, exercise, and sleep) were more likely to decrease with LVRS compared to medical therapy [76]. Improvement in oxygenation was predominantly seen in patients with upper lobe predominant emphysema. In a long-term analysis, after the initial improvement, differences in oxygenation between LVRS and medical therapy were no longer statistically significant after five years [32].

BODE index — Changes in the multidimensional index known as the BODE index have been assessed following LVRS (calculator 1). In a retrospective cohort study of 186 patients with severe COPD who underwent LVRS, the postoperative, but not the preoperative BODE, correlated with five year survival [77]. A decrease to a lower BODE score class was associated with reduced mortality (hazard ratio 0.50, 95% CI 0.38-0.66). In NETT, patients undergoing LVRS exhibited a significant improvement in BODE compared with medically treated patients (figure 5) [78]. Furthermore, those who exhibited a one point decrease in BODE (improvement) after six months experienced a significantly better long term survival compared with those that experienced a one point rise (worsening) (figure 6). (See "Chronic obstructive pulmonary disease: Prognostic factors and comorbid conditions", section on 'BODE index'.)

Cost-effectiveness — The cost effectiveness of LVRS was assessed using the results of NETT described above [27,79-83] (see 'National Emphysema Treatment Trial' above). Not including high-risk patients, the cost-effectiveness of LVRS versus medical therapy was USD $140,000 per quality-adjusted life-year (QALY) gained (95% CI, $40,155 to $239,359) at 5 years, and was projected to be $54,000 per QALY gained at 10 years [83]. Thus, LVRS is substantially more costly than medical therapy.

LVRS AND LUNG TRANSPLANTATION — When emphysema is advanced, both lung volume reduction surgery (LVRS) and lung transplantation are often considered.

Comparison — A retrospective series compared functional outcomes (pulmonary function tests, arterial blood gas analysis, six-minute walk distance) in 33 patients who underwent LVRS versus 39 patients who had single lung transplantation and 27 patients who had bilateral sequential lung transplantation [84]. The patients were evaluated before the operation and at 3, 6, and 12 months after surgery. The following results were noted:

The mean FEV1 improved by 79 percent at six months and 82 percent at 12 months in the LVRS group, 231 and 212 percent in the single lung transplant group, and 498 and 518 percent in the bilateral lung transplant group (figure 7).

The six-minute walk distance at six months after surgery improved by 28 percent in the LVRS group, 47 percent in the single lung transplant recipients, and 79 percent in the bilateral lung transplant recipients (figure 8).

All lung transplant recipients required supplemental oxygen before surgery, whereas none needed oxygen at rest or during exercise after the transplant. Eighty-eight percent of the patients who underwent LVRS required oxygen before surgery, and only 5.5 percent were oxygen-dependent during exercise and none at rest after LVRS.

Thus, while LVRS results in substantial improvements, single and bilateral lung transplantation result in superior lung function. Interpretation of these results must be cautious given the retrospective nature of the study and the baseline differences in age and pulmonary physiology between the groups.

Bridging procedure — Patients who undergo LVRS are not automatically excluded from undergoing lung transplantation. Limited experience with patients who initially undergo LVRS suggests that subsequent successful transplantation is possible. In one prospective study, LVRS prior to lung transplantation improved symptoms and lung function enough to delay lung transplantation for a median of 33 months in 8 of 58 potential lung transplant candidates, while not impairing recovery or survival after transplantation [85]. Outcomes of lung transplantation following LVRS are discussed separately. (See "Lung transplantation: General guidelines for recipient selection", section on 'Chronic obstructive pulmonary disease (COPD)'.)

BRONCHOSCOPIC LUNG VOLUME REDUCTION — Lung volume reduction surgery (LVRS) is associated with significant perioperative mortality, even when performed thoracoscopically. Bronchoscopic lung volume reduction (bLVR) using endobronchial valves allows clinicians to reduce lung volume in selected patients via a flexible bronchoscope and eliminate the need for surgery. Bronchoscopic lung volume reduction is discussed separately. (See "Bronchoscopic treatment of emphysema", section on 'Endobronchial valves' and "Management of refractory chronic obstructive pulmonary disease", section on 'Bronchoscopic lung volume reduction'.)

INVESTIGATIVE TECHNIQUES

Nonresectional lung volume reduction — Nonresectional lung volume reduction utilizes unilateral or staged thoracoscopic procedures where the most emphysematous target areas of the lung are visualized and introflexed while redundant lung edges are grasped with ring forceps and the lung plicated without resecting the lung [2-5]; approximately 50 percent of the upper lobe lung volume is reduced without resection. In small case series with nonrandomized controls, this approach has been associated with favorable physiological and symptomatic outcomes but lesser perioperative morbidity and lower costs compared with traditional resectional LVRS [2-4].

Additional modifications include the use of a single thoracoscopic access route with near complete plication of the targeted emphysematous lung without resection (Quasilobar minimalist LVRS, QLM) with improved perioperative morbidity and similar physiological and symptomatic outcomes to the more traditional nonawake resectional LVRS [4] and awake, nonresectional LVRS [4].

A separate group confirmed an improved BODE index (decreased) following staged bilateral awake nonresectional LVRS and nonawake resectional LVRS; benefit persisted for up to two years [2].

In comparison to contemporary patients undergoing unilateral resectional LVRS, patients undergoing awake nonresectional LVRS experienced shorter anesthesia time, operative time, and global operating room time [3]. Intraoperatively, PaCO2 was higher in the awake group, although there was no difference in PaO2/FiO2. A subsequent randomized trial compared unilateral thoracoscopic nonresectional LVRS in awake patients with resectional LVRS under general anesthesia [51]. Awake patients had a shorter length of stay (6 versus 7.5 days) and a greater proportion were discharged within six days but with transient permissive hypercarbia; lung function and symptomatic improvement was similar between the two groups through two years of follow-up. Thoracoscopic lobar plication in QLM is associated with shorter duration of air leaks than resectional LVRS [4].

Laser ablation — Laser ablation has been compared to stapler resection in patients undergoing unilateral LVRS [86-89], but the laser technique has been abandoned due to adverse effects. In individual studies, increased mortality, an increase in the frequency of late pneumothorax, and decreased improvement in forced expiratory volume in one second (FEV1) at six months were associated with laser ablation [86,88].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Chronic obstructive pulmonary disease".)

SUMMARY AND RECOMMENDATIONS

Lung volume reduction surgery (LVRS), also called reduction pneumoplasty, is a surgical technique that involves reducing the lung volume by multiple wedge excisions in areas where emphysematous changes are most marked. Typically, the amount of tissue resected is 20 to 35 percent of the volume of each lung. Nonresectional LVRS achieves similar benefits with plication of emphysematous lung. (See 'Introduction' above.)

LVRS modestly improves spirometry, lung volumes, exercise capacity, dyspnea, and quality of life and may improve long-term survival among highly selected patients. Certain clinical features appear to influence the degree of risk and benefit. (See 'National Emphysema Treatment Trial' above.)

Potential complications of LVRS include persistent air leak, intraoperative myocardial infarction, reintubation, prolonged mechanical ventilation, pneumonia, wound infection, arrhythmias, deep venous thrombosis, pulmonary embolism, and death. (See 'Complications' above.)

A reasonable approach to identifying patients for possible LVRS is to evaluate patients at the completion of pulmonary rehabilitation when medications for COPD have been optimized. Patients with a forced expiratory volume in one second (FEV1) <50 percent predicted and persistent limiting breathlessness without an obvious contraindication should be further evaluated for potential lung volume reduction. (See 'Patient selection' above.)

We recommend not performing LVRS in high-risk patients (FEV1 of 20 percent predicted or less and either a diffusing capacity [DLCO] of 20 percent predicted or less or homogeneous emphysema on chest computed tomography) (Grade 1B). (See 'National Emphysema Treatment Trial' above.)

For patients who have advanced emphysema that is upper lobe predominant, who have a low post-rehabilitation exercise tolerance despite maximal medical therapy for COPD, and who meet the inclusion criteria established by the National Emphysema Treatment Trial (NETT), we suggest performing LVRS rather than continuing with medical therapy alone (Grade 2B). For all other patients with advanced emphysema, the decision to perform LVRS should be made on a case-by-case basis, with careful consideration of the patient's values and preferences. (See 'National Emphysema Treatment Trial' above and 'Long-term outcomes' above.)

Patients with severe alpha-1 antitrypsin deficiency appear less likely to benefit from LVRS than patients with emphysema who are alpha-1 antitrypsin replete. (See "Treatment of alpha-1 antitrypsin deficiency", section on 'Lung volume reduction surgery'.)

Patients with advanced COPD are at increased risk for perioperative complications. All patients being considered for LVRS require careful preoperative assessment to ensure that medical therapy for COPD has been optimized and that any comorbid illnesses have been identified and treated, as needed. (See 'Preoperative evaluation' above.)

The choice of whether to perform LVRS via thoracotomy or thoracoscopy is usually based on the surgical and institutional expertise and preference. (See 'Thoracotomy versus thoracoscopy' above.)

The majority of patients are extubated in the operating room. Management of postoperative pain usually involves a combination of regional and systemic agents to enable early mobilization of the patient and effective cough. Due to the high frequency of air leaks, careful attention to the proper function of the chest tubes is essential. (See 'Postoperative management' above.)

LVRS does not automatically exclude a patient from undergoing lung transplantation. Limited experience with patients who initially undergo LVRS suggests that subsequent successful transplantation is possible. (See 'LVRS and lung transplantation' above.)

  1. BRANTIGAN OC, MUELLER E, KRESS MB. A surgical approach to pulmonary emphysema. Am Rev Respir Dis 1959; 80:194.
  2. Pompeo E, Mineo TC. Two-year improvement in multidimensional body mass index, airflow obstruction, dyspnea, and exercise capacity index after nonresectional lung volume reduction surgery in awake patients. Ann Thorac Surg 2007; 84:1862.
  3. Mineo TC, Pompeo E, Mineo D, et al. Awake nonresectional lung volume reduction surgery. Ann Surg 2006; 243:131.
  4. Pompeo E, Elkhouly A, Rogliani P, et al. Quasilobar minimalist lung volume reduction surgery. Eur J Cardiothorac Surg 2021; 60:598.
  5. Pompeo E, Tacconi F, Mineo TC. Comparative results of non-resectional lung volume reduction performed by awake or non-awake anesthesia. Eur J Cardiothorac Surg 2011; 39:e51.
  6. Fessler HE, Permutt S. Lung volume reduction surgery and airflow limitation. Am J Respir Crit Care Med 1998; 157:715.
  7. Fessler HE, Scharf SM, Ingenito EP, et al. Physiologic basis for improved pulmonary function after lung volume reduction. Proc Am Thorac Soc 2008; 5:416.
  8. Ingenito EP, Loring SH, Moy ML, et al. Interpreting improvement in expiratory flows after lung volume reduction surgery in terms of flow limitation theory. Am J Respir Crit Care Med 2001; 163:1074.
  9. Ingenito EP, Loring SH, Moy ML, et al. Comparison of physiological and radiological screening for lung volume reduction surgery. Am J Respir Crit Care Med 2001; 163:1068.
  10. Martinez FJ, de Oca MM, Whyte RI, et al. Lung-volume reduction improves dyspnea, dynamic hyperinflation, and respiratory muscle function. Am J Respir Crit Care Med 1997; 155:1984.
  11. Keller CA, Ruppel G, Hibbett A, et al. Thoracoscopic lung volume reduction surgery reduces dyspnea and improves exercise capacity in patients with emphysema. Am J Respir Crit Care Med 1997; 156:60.
  12. Sciurba FC. Early and long-term functional outcomes following lung volume reduction surgery. Clin Chest Med 1997; 18:259.
  13. Sciurba FC, Rogers RM, Keenan RJ, et al. Improvement in pulmonary function and elastic recoil after lung-reduction surgery for diffuse emphysema. N Engl J Med 1996; 334:1095.
  14. Lando Y, Boiselle PM, Shade D, et al. Effect of lung volume reduction surgery on diaphragm length in severe chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1999; 159:796.
  15. Gorman RB, McKenzie DK, Butler JE, et al. Diaphragm length and neural drive after lung volume reduction surgery. Am J Respir Crit Care Med 2005; 172:1259.
  16. Bloch KE, Li Y, Zhang J, et al. Effect of surgical lung volume reduction on breathing patterns in severe pulmonary emphysema. Am J Respir Crit Care Med 1997; 156:553.
  17. Zoumot Z, LoMauro A, Aliverti A, et al. Lung Volume Reduction in Emphysema Improves Chest Wall Asynchrony. Chest 2015; 148:185.
  18. Jörgensen K, Houltz E, Westfelt U, et al. Effects of lung volume reduction surgery on left ventricular diastolic filling and dimensions in patients with severe emphysema. Chest 2003; 124:1863.
  19. Clarenbach CF, Sievi NA, Brock M, et al. Lung Volume Reduction Surgery and Improvement of Endothelial Function and Blood Pressure in Patients with Chronic Obstructive Pulmonary Disease. A Randomized Controlled Trial. Am J Respir Crit Care Med 2015; 192:307.
  20. Mineo D, Ambrogi V, Cufari ME, et al. Variations of inflammatory mediators and alpha1-antitrypsin levels after lung volume reduction surgery for emphysema. Am J Respir Crit Care Med 2010; 181:806.
  21. Yusen RD, Lefrak SS, Gierada DS, et al. A prospective evaluation of lung volume reduction surgery in 200 consecutive patients. Chest 2003; 123:1026.
  22. Lederer DJ, Thomashow BM, Ginsburg ME, et al. Lung-volume reduction surgery for pulmonary emphysema: Improvement in body mass index, airflow obstruction, dyspnea, and exercise capacity index after 1 year. J Thorac Cardiovasc Surg 2007; 133:1434.
  23. Geddes D, Davies M, Koyama H, et al. Effect of lung-volume-reduction surgery in patients with severe emphysema. N Engl J Med 2000; 343:239.
  24. Hillerdal G, Löfdahl CG, Ström K, et al. Comparison of lung volume reduction surgery and physical training on health status and physiologic outcomes: a randomized controlled clinical trial. Chest 2005; 128:3489.
  25. Miller JD, Berger RL, Malthaner RA, et al. Lung volume reduction surgery vs medical treatment: for patients with advanced emphysema. Chest 2005; 127:1166.
  26. Miller JD, Malthaner RA, Goldsmith CH, et al. A randomized clinical trial of lung volume reduction surgery versus best medical care for patients with advanced emphysema: a two-year study from Canada. Ann Thorac Surg 2006; 81:314.
  27. Fishman A, Martinez F, Naunheim K, et al. A randomized trial comparing lung-volume-reduction surgery with medical therapy for severe emphysema. N Engl J Med 2003; 348:2059.
  28. Lammi MR, Marchetti N, Barnett S, Criner GJ. Heterogeneity of lung volume reduction surgery outcomes in patients selected by use of evidence-based criteria. Ann Thorac Surg 2013; 95:1905.
  29. van Agteren JE, Carson KV, Tiong LU, Smith BJ. Lung volume reduction surgery for diffuse emphysema. Cochrane Database Syst Rev 2016; 10:CD001001.
  30. National Emphysema Treatment Trial Research Group, Fishman A, Fessler H, et al. Patients at high risk of death after lung-volume-reduction surgery. N Engl J Med 2001; 345:1075.
  31. Sutherland ER, Make BJ. Maximum exercise as an outcome in COPD: minimal clinically important difference. COPD 2005; 2:137.
  32. Lim E, Sousa I, Shah PL, et al. Lung Volume Reduction Surgery: Reinterpreted With Longitudinal Data Analyses Methodology. Ann Thorac Surg 2020; 109:1496.
  33. Naunheim KS, Wood DE, Mohsenifar Z, et al. Long-term follow-up of patients receiving lung-volume-reduction surgery versus medical therapy for severe emphysema by the National Emphysema Treatment Trial Research Group. Ann Thorac Surg 2006; 82:431.
  34. Ingenito EP, Evans RB, Loring SH, et al. Relation between preoperative inspiratory lung resistance and the outcome of lung-volume-reduction surgery for emphysema. N Engl J Med 1998; 338:1181.
  35. Hunsaker A, Ingenito E, Topal U, et al. Preoperative screening for lung volume reduction surgery: usefulness of combining thin-section CT with physiologic assessment. AJR Am J Roentgenol 1998; 170:309.
  36. Hopkinson NS. Lung volume reduction for emphysema comes of age. BMJ 2021; 372:n14.
  37. Washko GR, Martinez FJ, Hoffman EA, et al. Physiological and computed tomographic predictors of outcome from lung volume reduction surgery. Am J Respir Crit Care Med 2010; 181:494.
  38. Weder W, Tutic M, Lardinois D, et al. Persistent benefit from lung volume reduction surgery in patients with homogeneous emphysema. Ann Thorac Surg 2009; 87:229.
  39. Hamacher J, Büchi S, Georgescu CL, et al. Improved quality of life after lung volume reduction surgery. Eur Respir J 2002; 19:54.
  40. American Thoracic Society, European Respiratory Society. Standards for the diagnosis and management of patients with COPD. http://www.thoracic.org/clinical/copd-guidelines/index.php (Accessed on March 29, 2010).
  41. Fessler HE, Scharf SM, Permutt S. Improvement in spirometry following lung volume reduction surgery: application of a physiologic model. Am J Respir Crit Care Med 2002; 165:34.
  42. Cederlund K, Tylén U, Jorfeldt L, Aspelin P. Classification of emphysema in candidates for lung volume reduction surgery: a new objective and surgically oriented model for describing CT severity and heterogeneity. Chest 2002; 122:590.
  43. Flaherty KR, Kazerooni EA, Curtis JL, et al. Short-term and long-term outcomes after bilateral lung volume reduction surgery : prediction by quantitative CT. Chest 2001; 119:1337.
  44. McKenna RJ Jr, Brenner M, Fischel RJ, et al. Patient selection criteria for lung volume reduction surgery. J Thorac Cardiovasc Surg 1997; 114:957.
  45. Slone RM, Pilgram TK, Gierada DS, et al. Lung volume reduction surgery: comparison of preoperative radiologic features and clinical outcome. Radiology 1997; 204:685.
  46. Washko GR, Hoffman E, Reilly JJ. Radiographic evaluation of the potential lung volume reduction surgery candidate. Proc Am Thorac Soc 2008; 5:421.
  47. Martinez FJ, Chang A. Surgical therapy for chronic obstructive pulmonary disease. Semin Respir Crit Care Med 2005; 26:167.
  48. Caviezel C, Aruldas C, Franzen D, et al. Lung volume reduction surgery in selected patients with emphysema and pulmonary hypertension. Eur J Cardiothorac Surg 2018; 54:565.
  49. Pompeo E, Marino M, Nofroni I, et al. Reduction pneumoplasty versus respiratory rehabilitation in severe emphysema: a randomized study. Pulmonary Emphysema Research Group. Ann Thorac Surg 2000; 70:948.
  50. Boasquevisque CH, Yildirim E, Waddel TK, Keshavjee S. Surgical techniques: lung transplant and lung volume reduction. Proc Am Thorac Soc 2009; 6:66.
  51. Pompeo E, Rogliani P, Tacconi F, et al. Randomized comparison of awake nonresectional versus nonawake resectional lung volume reduction surgery. J Thorac Cardiovasc Surg 2012; 143:47.
  52. Kostron A, Horn-Tutic M, Franzen D, et al. Repeated lung volume reduction surgery is successful in selected patients. Eur J Cardiothorac Surg 2015; 48:710.
  53. Tacconi F, Pompeo E, Forcella D, et al. Lung volume reduction reoperations. Ann Thorac Surg 2008; 85:1171.
  54. DeCamp MM Jr, Lipson D, Krasna M, et al. The evaluation and preparation of the patient for lung volume reduction surgery. Proc Am Thorac Soc 2008; 5:427.
  55. Hillier J, Gillbe C. Anaesthesia for lung volume reduction surgery. Anaesthesia 2003; 58:1210.
  56. Brister NW, Barnette RE, Kim V, Keresztury M. Anesthetic considerations in candidates for lung volume reduction surgery. Proc Am Thorac Soc 2008; 5:432.
  57. Buettner AU, McRae R, Myles PS, et al. Anaesthesia and postoperative pain management for bilateral lung volume reduction surgery. Anaesth Intensive Care 1999; 27:503.
  58. McKenna RJ Jr, Benditt JO, DeCamp M, et al. Safety and efficacy of median sternotomy versus video-assisted thoracic surgery for lung volume reduction surgery. J Thorac Cardiovasc Surg 2004; 127:1350.
  59. Fischel RJ, McKenna RJ Jr. Bovine pericardium versus bovine collagen to buttress staples for lung reduction operations. Ann Thorac Surg 1998; 65:217.
  60. Hazelrigg SR, Boley TM, Magee MJ, et al. Comparison of staged thoracoscopy and median sternotomy for lung volume reduction. Ann Thorac Surg 1998; 66:1134.
  61. Swanson SJ, Mentzer SJ, DeCamp MM Jr, et al. No-cut thoracoscopic lung plication: a new technique for lung volume reduction surgery. J Am Coll Surg 1997; 185:25.
  62. Vaughn CC, Wolner E, Dahan M, et al. Prevention of air leaks after pulmonary wedge resection. Ann Thorac Surg 1997; 63:864.
  63. Moser C, Opitz I, Zhai W, et al. Autologous fibrin sealant reduces the incidence of prolonged air leak and duration of chest tube drainage after lung volume reduction surgery: a prospective randomized blinded study. J Thorac Cardiovasc Surg 2008; 136:843.
  64. DeCamp MM, Blackstone EH, Naunheim KS, et al. Patient and surgical factors influencing air leak after lung volume reduction surgery: lessons learned from the National Emphysema Treatment Trial. Ann Thorac Surg 2006; 82:197.
  65. Naunheim KS, Wood DE, Krasna MJ, et al. Predictors of operative mortality and cardiopulmonary morbidity in the National Emphysema Treatment Trial. J Thorac Cardiovasc Surg 2006; 131:43.
  66. Decker MR, Leverson GE, Jaoude WA, Maloney JD. Lung volume reduction surgery since the National Emphysema Treatment Trial: study of Society of Thoracic Surgeons Database. J Thorac Cardiovasc Surg 2014; 148:2651.
  67. Ahmad S, Taneja A, Kurman J, et al. National trends in lung volume reduction surgery in the United States: 2000 to 2010. Chest 2014; 146:e228.
  68. Attaway AH, Hatipoğlu U, Murthy S, Zein J. Lung Volume Reduction Surgery in the United States From 2007 to 2013: Increasing Volumes and Reason for Caution. Chest 2019; 155:1080.
  69. Abdelsattar ZM, Allen M, Blackmon S, et al. Contemporary Practice Patterns of Lung Volume Reduction Surgery in the United States. Ann Thorac Surg 2021; 112:952.
  70. Ciccone AM, Meyers BF, Guthrie TJ, et al. Long-term outcome of bilateral lung volume reduction in 250 consecutive patients with emphysema. J Thorac Cardiovasc Surg 2003; 125:513.
  71. DeCamp MM Jr, McKenna RJ Jr, Deschamps CC, Krasna MJ. Lung volume reduction surgery: technique, operative mortality, and morbidity. Proc Am Thorac Soc 2008; 5:442.
  72. Ginsburg ME, Thomashow BM, Bulman WA, et al. The safety, efficacy, and durability of lung-volume reduction surgery: A 10-year experience. J Thorac Cardiovasc Surg 2016; 151:717.
  73. Horwood CR, Mansour D, Abdel-Rasoul M, et al. Long-Term Results After Lung Volume Reduction Surgery: A Single Institution's Experience. Ann Thorac Surg 2019; 107:1068.
  74. Mineo TC, Ambrogi V, Pompeo E, et al. Impact of lung volume reduction surgery versus rehabilitation on quality of life. Eur Respir J 2004; 23:275.
  75. Kaplan RM, Sun Q, Ries AL. Quality of well-being outcomes in the National Emphysema Treatment Trial. Chest 2015; 147:377.
  76. Snyder ML, Goss CH, Neradilek B, et al. Changes in arterial oxygenation and self-reported oxygen use after lung volume reduction surgery. Am J Respir Crit Care Med 2008; 178:339.
  77. Imfeld S, Bloch KE, Weder W, Russi EW. The BODE index after lung volume reduction surgery correlates with survival. Chest 2006; 129:873.
  78. Martinez FJ, Han MK, Andrei AC, et al. Longitudinal change in the BODE index predicts mortality in severe emphysema. Am J Respir Crit Care Med 2008; 178:491.
  79. Wise RA, Drummond MB. The role of NETT in emphysema research. Proc Am Thorac Soc 2008; 5:385.
  80. Ault A. US government to pay for lung volume reduction surgery. Lancet 2003; 362:712.
  81. Drazen JM, Epstein AM. Guidance concerning surgery for emphysema. N Engl J Med 2003; 348:2134.
  82. Ramsey SD, Berry K, Etzioni R, et al. Cost effectiveness of lung-volume-reduction surgery for patients with severe emphysema. N Engl J Med 2003; 348:2092.
  83. Ramsey SD, Shroyer AL, Sullivan SD, Wood DE. Updated evaluation of the cost-effectiveness of lung volume reduction surgery. Chest 2007; 131:823.
  84. Gaissert HA, Trulock EP, Cooper JD, et al. Comparison of early functional results after volume reduction or lung transplantation for chronic obstructive pulmonary disease. J Thorac Cardiovasc Surg 1996; 111:296.
  85. Tutic M, Lardinois D, Imfeld S, et al. Lung-volume reduction surgery as an alternative or bridging procedure to lung transplantation. Ann Thorac Surg 2006; 82:208.
  86. Keenan RJ, Landreneau RJ, Sciurba FC, et al. Unilateral thoracoscopic surgical approach for diffuse emphysema. J Thorac Cardiovasc Surg 1996; 111:308.
  87. Little AG, Swain JA, Nino JJ, et al. Reduction pneumonoplasty for emphysema. Early results. Ann Surg 1995; 222:365.
  88. McKenna RJ Jr, Brenner M, Gelb AF, et al. A randomized, prospective trial of stapled lung reduction versus laser bullectomy for diffuse emphysema. J Thorac Cardiovasc Surg 1996; 111:317.
  89. Meyers BF, Sultan PK, Guthrie TJ, et al. Outcomes after unilateral lung volume reduction. Ann Thorac Surg 2008; 86:204.
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References

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