Diagnoses: Panacinar emphysema. Pleural bleb. Chronic necrotizing pulmonary aspergillosis.

Follow-up--Comparison of pre-operative and post-operative PFTs: By 3 mo after the operation, FEV1 had increased by 22%.

Date

FEV1(L)/FVC (L)--% (N >70%)

TLC (L)

DLCO (ml/mn/mmHg)

2/99

1.1/3.2--34%

--

--

9/98

0.9 /3.6--25%

7.1

11 (40% predicted)

10/91

1.7 /4--42%

--

15


Lung Volume Reduction Surgery (LVRS) in Emphysema

Introduction: Chronic obstructive pulmonary disease, defined as the presence of chronic bronchitis/small airways disease &/or emphysema, often leads to airflow insufficiency. Some patients also have reactive airways disease. COPD is caused principally by cigarette smoking, although emphysema also occurs in persons with alpha-1-antitrypsin deficiency. Only some of the people with either of these risk factors develop the disease. COPD is common in adults (4-6% of adult white men and 1-3% of adult white women). It has prolonged morbidity and causes or contributes to death in over 8% of the population, usually in persons over age 55 [1].

Clinical features: Patients with the chronic bronchitic form of COPD have the insidious onset of sputum-producing cough, wheezing, increasing dyspnea, and increasing frequency of chest illnesses. Sputum is grossly purulent during exacerbations and mucoid in between. Some patients develop hypoxemia, hypercapnia, erythrocytosis, and right heart failure. Patients with primarily emphysema develop gradual onset of dyspnea on exertion. Cough and wheezing are infrequent; chest auscultation typically reveals distant breath sounds. Hyperinflation with enlargement of the chest cavity and flattening of the diaphragm may develop. Arterial blood gases usually remain within normal limits until the disease is advanced [1].

Pulmonary function tests: With airflow limitation, PFTs show a decrease in the FEV1 and the ratio of FEV1/FVC. Serial measurements show a more rapid decline in FEV1 than that which occurs with aging. There may be a modest response to bronchodilators. In patients with pulmonary emphysema, TLC and lung compliance are increased, and DLCO is decreased [1].

Diagnosis: A combination of clinical history, radiographic findings, and PFTs are used to make the diagnosis. The course is followed by PFTs and blood gases.

Histopathology--Definitions:

Types of emphysema:

Histologic changes: A 3-dimensional view of emphysema shows development of holes in alveolar walls [3]. In 2-dimensional histologic sections, emphysema is diagnosed by finding segments of isolated alveolar walls. Normally, all alveolar walls are connected and remain so even when the lung is distended. The finding of isolated portions of walls defines emphysema in distended and non-distended specimens. Occasionally, increased numbers of PMNs, accompanied by microscopic hemorrhages, can be seen in the alveolar walls.

Other lesions expected in LVRS [4,5]

Treatment: Besides treatment of airflow limitation with bronchodilators, infections with antibiotics, hypoxemia with oxygen, and pressing for smoking cessation, transplantation has been used for the late stages of disease. Recently, lung reduction procedures have been shown to increase function in certain persons with predominant emphysema [9].

Rationale for LVRS: Popularized by Cooper in 1995, LVRS aims to restore radial traction on bronchi and vessels, reduce expiratory airflow obstruction, and relieve dyspnea by reducing lung volume, thereby increasing elastic recoil. Although optimal criteria are not yet well-defined [9-12], appropriate patient selection, near perfect operation, and expert perioperative management are required to prevent prohibitive morbidity [13]. Preoperative pulmonary rehabilitation seems to improve the outcome of LVRS [14]. When LVRS is combined with wedge resection for carcinoma, it may increase the operability of patients with emphysema without significantly increasing morbidity [4].

Outcome: Mild degrees of COPD decrease life expectancy only slightly compared to smokers without it, but severe degrees (FEV1 <0.75 L) are associated with 30% mortality at 1 y and 95% at 10 y. Causes of death include infection, pneumonia, pneumothorax, cardiac arrhythmias, and pulmonary embolism. Many die of lung cancer. Cessation of smoking and optimal medical management prolong life [1]. Benefits of LVRS have been maintained for up to 3 years [15].

Pathogenesis: The proteinase-antiproteinase theory of development of emphysema proposes that a predominance of proteinases accounts for lung destruction. It was initially thought that the excess proteinases attacked the alveolar wall from within the alveolus. More recently, the PMN in the blood has come under scrutiny. Support for the new theory includes recruitment of PMNs to, and slowing of transit through, the capillaries of the upper lung zones, and activation of a PMN adhesion molecule (CD11/CD18) more in the upper, than lower, zones. This activation is especially prominent in pocket areas between PMNs and endothelium, where high concentrations of PMN proteinases can then digest elastin/collagen. The theory does not explain the different types of emphysema, or the predominance of emphysema in lower lobes in alpha-1-antitrypsin deficiency, in which other other proteinases and intermittent infections may play a role. Other factors favoring upper lobe disease include preferential distribution of smoke to upper lobes and slow clearance of toxic smoke products from upper lobes [16-18].

References

1. Snider G, Faling L, Rennard S. Chronic bronchitis and emphysema. In: J Murray, J Nadel (eds.): Textbook of Respiratory Medicine, 2nd ed. Philadelphia, WB Saunders, 1994, pp 1331-1397.

2. Snider G. Reduction pneumoplasty for giant bullous emphysema. Implications for surgical treatment of nonbullous emphysema. Chest 1996; 109:540-548.

3. Nagai A, Thurlbeck W. Scanning electron microscopic observations of emphysema in humans. A descriptive study. Am Rev Respir Dis 1991; 144:901-908.

4. Ojo T, Martinez F, Paine III R, Christensen P, Curtis J, Weg J, Kazerooni E, et al. Lung volume reduction surgery alters management of pulmonary nodules in patients with severe COPD. Chest 1997; 112:1494-1500.

5. Duarte I, Gal A, Mansour K, Lee R, Miller J. Pathologic findings in lung volume reduction surgery. Chest 1998; 113:660-664.

6. Pigula F, Keenan R, Ferson P, Landreneau R. Unsuspected lung cancer found in work-up for lung reduction operation. Ann Thorac Surg 1996; 61:174-176.

7. McKenna Jr R, Fischel R, Brenner M, Gelb A. Combined operations for lung volume reduction surgery and lung cancer. Chest 1996; 110:885-888.

8. Zulueta J, Bloom S, Rozansky M, White A. Lung cancer in patients with bullous disease. Am J Respir Crit Care Med 1996; 154:519-522.

9. Sciurba F, Rogers R, Keenan R, Slivka W, Gorscan III J, Ferson P, Holbert J, et al. Improvement in pulmonary function and elastic recoil after lung-reduction surgery for diffuse emphysema. N Engl J Med 1996; 334:1095-1099.

10. Cooper J, Lefrak S. Is volume reduction surgery appropriate in the treatment of emphysema? Yes. Am J Respir Crit Care Med 1996; 153:1201-1204.

11. Make B, Fein A. Is volume reduction surgery appropriate in the treatment of emphysema? No. Am J Respir Crit Care Med 1996; 153:1205-1207.

12. Weinmann G, Hyatt R. Evaluation and research in lung volume reduction surgery. Am J Respir Crit Care Med 1996; 154:1913-1918.

13. Naunheim K, Ferguson M. The current status of lung volume reduction operations for emphysema. Ann Thorac Surg 1996; 62:601-612.

14. Moy M, Ingenito E, Mentzer S, Evans R, Reilly Jr J. Health-related quality of life improves following pulmonary rehabilitation and lung volume reduction surgery. Chest 1999; 115:383-389.

15. Pohl M, Lefrak S, Yusen R, Davis G, Patterson G, Meyers B, Cooper J. Functional results of 200 consecutive bilateral lung volume reduction surgery patients. Am J Respir Crit Care Med 1999; 159:A924.

16. Hogg J. The traffic of polymorphonuclear leukocytes through pulmonary microvessels in health and disease. AJR 1994; 163:769-775.

17. Klut M, Doerschuk C, van Eeden S, Burns A, Hogg J. Activation of neutrophils within pulmonary microvessels of rabbits exposed to cigarette smoke. Am J Respir Cell Mol Biol 1993; 9:82-89.

18. Terashima T, Klut M, English D, Hards J, Hogg J, van Eeden S. Cigarette smoking causes sequestration of polymorphonuclear leukocytes released from the bone marrow in lung microvessels. Am J Respir Cell Mol Biol 1999; 20:171-177.

Clinical summary

Comments: mw6825@itsa.ucsf.edu

Table of Contents

Last revised 4/8/99

Copyright 1999 by Martha L. Warnock. All rights reserved.