DEFINITIONS
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According to the Global Initiative for Chronic Obstructive Lung Disease (GOLD), “Chronic Obstructive Pulmonary Disease (COPD) is a preventable and treatable disease with some significant extrapulmonary effects… Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases.”
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COPD has many phenotypes related to varying degrees of small airway disease and emphysema, each of which may prove to have a distinct pathogenesis and clinical course.
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Emphysema, which represents a specific phenotype of COPD is defined as “ . . a condition of the lung characterized by abnormal, permanent enlargement of airspaces distal to the terminal bronchiole, accompanied by the destruction of their walls, and without obvious fibrosis.”
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Patients with emphysema typically have loss of lung elastic recoil, leading to airflow limitation, lung hyperinflation, and air trapping. Destruction of alveolar-capillary membranes leads to reduction in diffusion capacity.
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Cigarette smoking accounts for the majority of cases of emphysema (80%–90%), however, other etiologies including α 1 -antitrypsin deficiency, occupational exposures, environmental pollution, female gender, childhood infections, and poor socioeconomic status have also been implicated.
PHYSIOLOGIC CONSIDERATIONS
Loss of elastic recoil: A key component in pathogenesis of emphysema is a loss of lung elastic recoil. Abnormally reduced recoil leads to airway collapse and is likely a major determinant of flow limitation in the airways. Expiratory airflow limitation in the setting of poor elastic recoil then leads to gas trapping, the phenomenon of “auto-peep,” and ultimately hyperinflation.
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Hyperinflation: Abnormal lung elastic recoil and parenchymal lung destruction with bulla formation typically seen in emphysema ultimately lead to pulmonary hyperinflation. Hyperinflation impairs proper diaphragmatic function and may result in abnormal hemodynamics related to alterations in intrathoracic pressure and “auto-peep.”
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Airflow obstruction: The severity of airflow obstruction, as measured by the forced expiratory time in 1 second (FEV 1 ), has been shown to be inversely proportional to survival. The underlying mechanism of increased airflow resistance is variable and ultimately related to the predominant COPD phenotype (i.e., emphysema versus chronic bronchitis). Mechanisms include mucus hypersecretion, airway inflammation, and airway collapse due to loss of recoil.
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Dynamic hyperinflation: Increases in minute ventilation that occur normally in response to exercise is accompanied by an increase in gas trapping, hyperinflation, and hemodynamic derangements in many patients with COPD. The phenomenon of “breath stacking” is often sited as a likely mechanism of exercise limitation in this patient population. In fact, a decreased ratio of the inspiratory capacity to total lung capacity (IC/TLC), a sensitive predictor of the development of dynamic hyperinflation during exercise, inversely correlates with mortality and exercise capacity. Additionally, IC/TLC may signal those at risk for cardiac dysfunction as measured by the oxygen pulse, a noninvasive estimate of stroke volume.
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Gas exchange abnormalities: Both hypoxemia and hypercapnea are common in severe emphysema and loosely correlate with severity of airflow obstruction.
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Pulmonary vascular disease: Mild to moderate and rarely severe pulmonary hypertension has been associated with severe emphysema. Possible mechanisms include chronic hypoxia, mechanical obstruction of small pulmonary arteries from hyperinflation, vascular inflammation, and destruction of the pulmonary vascular bed.
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Diaphragm dysfunction: Inspiratory muscle function, in particular diaphragm function, can be severely limited in patients with emphysema and lung hyperinflation. Diaphragm flattening and thus, shortening of diaphragmatic muscle fibers, creates a mechanically disadvantageous condition resulting in reduced inspiratory force generation. Additionally, the development of intrinsic positive end-expiratory pressure creates increased load on the muscles of ventilation.
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Systemic disease: COPD is now well known to have systemic manifestations in addition to its debilitating effects on the lungs. Weight loss, cardiovascular disease, skeletal muscle dysfunction, depression, osteoporosis, sleep disorders, and sexual dysfunction are all common in patients with COPD.
RATIONALE FOR LUNG VOLUME REDUCTION SURGERY
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Improved lung elastic recoil
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May lead to improvements in peak expiratory flow and FEV 1
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Variable effects on airway resistance
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Does not explain improvements observed in vital capacity
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Improved lung volumes
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Although both total lung capacity (TLC) and residual volume (RV) are increased in patients with emphysema, there is a disproportionate increase in RV, thus resulting in a significant increase in RV/TLC.
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Lung volume reduction surgery (LVRS) decreases RV moreso than TLC, resulting in an overall decrease in RV/TLC
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Attempts made at time of surgery to remove only severely emphysematous lung that is unlikely to participate in significant gas exchange and functions primarily to compress potentially viable lung tissue.
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Improved diaphragm function
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LVRS results in an overall lengthening of the diaphragm, thus improving diaphragmatic force generation and improving maximal inspiratory and transdiaphramatic pressures.
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Acute histologic changes in the diaphragm after LVRS, in contrast, have shown evidence of sarcolemmal injury, suggesting no improvement in contractile qualities of individual muscle fibers.
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SELECTION OF THE CANDIDATE LUNG VOLUME REDUCTION SURGERY
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History of LVRS
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Early attempts that predate modern LVRS at reducing thoracic volume have included:
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Phrenectomy
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Whole lung radiation
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Abdominal binders
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Induction of pneumoperitoneum
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Modern LVRS
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First reported in a study in 1959 by Otto Brantigan in which most severely affected lung tissue on one side was removed with hilar denervation. The procedure was repeated on the contralateral side if symptoms persisted. Despite reports of symptomatic improvement, the procedure was largely abandoned, primarily for its high mortality rate.
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In 1994, Cooper et al. published a series of 20 patients who underwent bilateral LVRS via median sternotomy. Significant improvements in pulmonary function testing included a 22% decrease in TLC, a 39% decrease in RV, and an 82% increase in FEV 1 .
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Cooper’s report of significant physiologic improvements, improved symptoms, with no deaths after 15 months after LVRS led to a renewed interest and popularity in the procedure.
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Optimal techniques for LVRS were defined with several studies:
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A randomized, prospective comparison of laser versus resection with staples showed that the staple procedure provided greater average improvement, improvement in a higher number of patients, and longer duration of benefit.
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A bilateral procedure, compared with a unilateral procedure, showed greater benefit, with no increased morbidity or mortality.
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Several small randomized, prospective, placebo controlled studies comparing lung volume reduction surgery to standard medical therapy with pulmonary rehabilitation showed variable benefits of LVRS.
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In 1996, pressured by the enormous potential cost of Medicare reimbursement for LVRS, a joint venture sponsored by the Health Care Financing Administration and the National Heart, Lung, and Blood Institute was initiated to study the efficacy, safety, and cost effectiveness of LVRS.
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Eighteen institutions were chosen to participate in the National Emphysema Treatment Trial (NETT), which was a prospective multicentered, placebo-controlled study comparing LVRS with maximal medical therapy.
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The primary outcome measures for NETT were survival and maximal exercise capacity.
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Entry criteria for the NETT (summary)
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Evidence of bilateral emphysema on high-resolution CT chest (HRCT)
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Body mass index (BMI) ≤ 31.1 kg/m (men) or ≤ 32.3 kg/m (women)
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Taking 20 mg prednisone daily
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FEV 1 ≤ 45% predicted, TLC ≥s 100% predicted, RV ≥ 150% predicted
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PCO 2 ≤ 60 mm Hg, PO 2 ≥ 45 mm Hg on room air
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Postrehabilitation 6-minute walk test ≥ 140 meters
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Nonsmoker for 4 months before initial interview and throughout screening, verified with plasma cotinine levels
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Completion of a formal pulmonary rehabilitation program
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Exclusion criteria for NETT (Summary)
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Prior thoracic surgery (lung transplant, LVRS, median sternotomy, lobectomy)
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Significant cardiac arrhythmias
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Exercise induced syncope
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Myocardial infarction (MI) within 6 months with left ventricular ejection fraction less than 45%
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Congestive heart failure
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Uncontrolled hypertension
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Recurrent pulmonary infections
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Significant bronchiectasis
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Pleural or interstitial pulmonary disease that precludes surgery
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Pulmonary nodule requiring surgery
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Giant bullae (>1/3 volume of lung) discussed separately later in chapter
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Pulmonary hypertension (peak systolic ≥ 45 mm Hg or mean ≥ 35 mm Hg)
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Right-sided heart catheterization required if peak systolic pulmonary artery pressure on echocardiogram ≥ 45 mm Hg
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>6 L/min oxygen requirement
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Computed tomographic (CT) evidence of diffuse emphysema
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Unexplained weight loss
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Systemic or oncologic illness with expected survival <5 years
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6-minute walk distance ≤140 meters after rehabilitation
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SURGICAL TECHNIQUE
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LVRS involves resection of approximately 30% of the apices of both lungs for upper lobe disease and the lower lobes (possibly sparing the superior segments) for lower lobe disease.
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The lung tissue does not hold sutures or staples well, so the staples are buttressed with bovine pericardium.
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The procedure may be performed through either VATS or a median sternotomy.
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Results are comparable for the two surgical approaches.
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VATS is associated with shorter length of stay, quicker return to independent existence and less total cost of all health care services for the 6 months that follow LVRS.
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POSTOPERATIVE CARE
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Patients are almost always extubated in the operating room after LVRS.
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Early ambulation and aggressive pulmonary toilet are critical to minimize postoperative complications.
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Mortality rate for LVRS is less than 5%.
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Complications are seen in Table 15-1 .
TABLE 15-1 ▪
▪SHOWS COMPLICATION RATES AFTER LUNG VOLUME REDUCTION SURGERY BY MEDIAN STERNOTOMY (MS) OR VIDEO-ASSISTED THORACIC SURGERY (VATS)
Postoperative Complications
MS (%)
VATS (%)
P value
None
41
48
0.06
Atrial fibrillation
3
1
0.68
Arrhythmias
22
20
0.43
Failure of early extubation
3
6
0.30
Tracheostomy
10
6
0.33
Failure to wean
6
3
0.06
Prolonged air leak
1
1
0.62
Reoperation for air leak
2
6
0.05
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Interim analysis of NETT
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In 2001, an interim analysis of the NETT identified a subgroup of patients who were at an unacceptably high risk of death after undergoing LVRS.
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Patients with an FEV 1 ≤ 20% predicted and had either a homogenous distribution of emphysema on CT or a carbon monoxide diffusing capacity (DLCO) ≤ 20% predicted had a 30-day mortality rate after surgery of 16% compared with 0% in the medical arm.
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Patients meeting these criteria were excluded from further enrollment in the NETT and should not be considered for LVRS in clinical practice.
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NETT OUTCOMES
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Survival benefit
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Overall 90-day mortality rate in the LVRS group was 7.9%, compared with 1.3% in the medical group ( P < 0.001).
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The mortality rate for all patients in the NETT, which was based on a mean follow-up of 29.2 months, was identical in the surgical and medical arms (0.11 death/person-year)
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Patients in the previously described high-risk group (see earlier) had a 28.6% 90-day mortality rate with surgery compared with 0% for medical therapy ( P < 0.001)
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Surgical patients who were identified as having low exercise capacity and upper lobe predominant emphysema had a significant improvement in total mortality when compared with medical treatment (0.07 versus 0.15 death/person-year [risk ratio 0.47], P < 0.005)
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Low exercise: < 40 watts exercise capacity for men, <25 watts for women.
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Upper lobe predominant emphysema: Each lung divided into three zones on HRCT (apical, middle, lower) and assigned a grade 0 (no emphysema) to 4 (>75% emphysema). A difference of 2 or more in grade among the three zones in one lung was indicative of heterogeneous disease and, if most predominant, in upper zone defined as upper lobe predominant ( Fig. 15-1 ).
Figure 15-1
Examples of qualitative grading of emphysema severity. 0: no emphysema, 1: 1% to 25%, 2: 26% to 50%, 3: 51% to 75%, 4: 76% to 100%. A difference in grading of 2 or more in one lung is indicative of heterogeneous emphysema.
Rights were not granted to include this figure in electronic media. Please refer to the printed book.
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Long-term outcomes based on a median follow-up of 4.3 years actually revealed a small but significant reduction in total mortality rate for all patients in the surgical arm versus medical arm (0.11 versus 0.13 deaths/person-year, P = 0.02) and the benefit was even more pronounced in the low exercise/upper lobe predominant group (relative risk [RR] = 0.57, P = 0.01).
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Quality of life (QOL) and physiologic benefits ( Fig. 15-2 )
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QOL
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There was a significant overall benefit in health-related QOL at 24 months as defined by a decrease of 5 points or more on the St. George’s Respiratory Questionnaire (SGRQ) in patients receiving LVRS (33% vs. 9%, P < 0.01).
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Significant improvements in the SGRQ in patients undergoing LVRS were also observed for all patients when stratified by preoperative predictors (baseline exercise capacity and pattern of emphysema) with the exception of patients with high-baseline exercise capacity and non–upper lobe emphysema as well as patients at high risk for death as defined earlier.
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Physiologic benefits
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More patients randomized to LVRS had improvements in exercise capacity of 10 W or more than patients randomized to medical treatment at 6, 12, and 24 months (28%, 22%, and 15% vs. 4%, 5%, and 3%; P < 0.001 for each time point)
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Improvements in lung function as measured by FEV 1 were observed at 6, 12, and 24 months, with 65%, 56%, and 43% showing improvement with LVRS as opposed to 27%, 26%, and 19% in the medical arm ( P < 0.001 for each time point)
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Subgroup analysis revealed significant improvements at all time points in exercise capacity for patients with upper lobe–predominant emphysema regardless of baseline exercise capacity, although benefits were more pronounced in those with lower exercise capacity.
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Patients with non–upper lobe–predominant emphysema showed a significant improvement in exercise capacity only at 6 months and only for those with low baseline exercise.
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Long term benefits for LVRS up to 3 years for exercise capacity and lung function were sustained for both the group as a whole as well as for non–high-risk patients with upper lobe–predominant emphysema.
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