Diagnosis and Management of Trapped Lung

By Peter Doelken, MD, FCCP; and Steven A. Sahn, MD, FCCP

Print This | TOC | Previous | Next

Objectives

  1. Describe visceral pleural restriction as part of the differential diagnosis of unexpandable lung.
  2. Describe trapped lung as a clinical entity consisting of chronic pleural effusion caused by visceral pleural restriction and absent active pleural disease.
  3. Describe the cause of persistence of pleural fluid in trapped lung as local deformation forces exceeding fluid removal forces.
  4. Distinguish trapped lung from active pleural disease with coexisting lung entrapment.
  5. Identify the patient with trapped lung who is a candidate for therapeutic intervention.

Key words

decortication; diagnostic pneumothorax; lung entrapment; pleural manometry; trapped lung; unexpandable lung

Abbreviation

CABG = coronary artery bypass grafting

Trapped lung is a persistent, benign pleural effusion with no apparent cause for the persistence of fluid other than mechanical restriction of the visceral pleura preventing lung expansion.1 Trapped lung is thus a diagnosis to be considered during evaluation of the unexpandable lung. Failure of the lung to expand fully when subjected to negative pressure in the physiologic range may be caused by endobronchial, parenchymal, or pleural disease. Although the pleural effusion, if present, may be transudative in the unexpandable lung due to endobronchial or parenchymal disease, the fluid is exudative when associated with active pleural disease. Therefore, trapped lung is a diagnosis of exclusion and rests on the demonstration of a visceral pleural-restricting membrane in the absence of endobronchial, severe parenchymal, and active pleural disease.

Definition of Terms

A number of conditions may mechanically prevent the lung from expanding. Among them are malignancy involving the visceral pleura or the fibrinous peel of pleuritis itself. These conditions are distinguished from trapped lung by the presence of an active pleural process, which may either progress or resolve, spontaneously or with specific therapy. The mechanism of pleural fluid accumulation in active inflammatory or malignant conditions associated with lung entrapment also differs from the mechanism in trapped lung. In the latter, there is no alternate explanation other than mechanical restriction of lung expansion for the persistence of pleural effusion, whereas intense inflammation or malignancy are sufficient to cause effusion even in the absence of entrapment. The mechanical restriction of the visceral pleura from any cause will be called lung entrapment throughout this manuscript, whereas trapped lung will refer solely to the chronic condition previously described. Trapped lung is considered an outcome of fibrinous or granulomatous pleuritis. The value of this precise definition of trapped lung for the clinician is that the diagnosis describes a clinical entity for which therapy is not necessarily required but spontaneous improvement is not expected.

History

Trapped lung was recognized as a complication of pneumothorax therapy for tuberculosis. Approximately 5% of patients treated with therapeutic pneumothoraces developed an unexpandable lung characterized by the failure to expand between therapeutic refills. In some patients, failure to expand was related to fibrosis and scarring of the lung; in others, it was due to the formation of scar tissue on the visceral pleura. Manometry performed during refills revealed more negative pressure and increased elastance of the pleural space. Left untreated, the pressure in the persistent pleural space became more negative and an effusion ex vacuo developed.sup2/sup With abandonment of therapeutic pneumothorax, the most common cause of trapped lung today probably is a remote complicated parapneumonic effusion or empyema that was insufficiently drained. In 1954, Stead and colleaguessup1 published a case series of 24 patients with presumed tuberculous pleurisy who underwent thoracotomy for a variety of reasons. For nine of the 24 patients (38%), there was no histologic evidence of tuberculosis in the operative specimens. Two of the nine had large amounts of fibrous tissue completely obliterating the pleural space; the remaining seven cases shared the findings of a chronic pleural effusion, a thin fibrous pleural peel preventing expansion of the affected lung, and nonspecific fibrous pleuritis on histology. Of those seven patients, organizing pneumonitis was found in four, multiple subpleural bullae in one (the authors speculated a spontaneous pneumothorax might have resulted in pleural inflammation), and histoplasmosis in one; in one patient, the diagnosis was unclear. The authors invoked a mechanical cause for the persistence of pleural fluid in all seven cases.

In another case series of 21 patients who underwent thoracotomy for undiagnosed pleural effusions, nonspecific fibrous pleuritis was the only finding in three patients.3 Two other patients had nonspecific fibrinous pleuritis, and the authors suggested viewing fibrinous pleuritis and fibrous pleuritis as different stages of the same process. Of the five patients with either fibrinous or fibrous pleuritis in this series, only two had a history suggestive of antecedent infection; one had a remote lung abscess and the other had experienced fever and chills several months earlier. No cause for the pleuritis was evident in the remaining three.

In 1966, Moore and Thomas4 reported an additional four cases of persistent pleural effusions attributed to nonspecific pleuritis and lung entrapment. Two of the four patients had a history suggestive of pneumonia, one had a pneumothorax, and one had a history of chest trauma.

A case series of persistent pleural effusions after coronary artery bypass grafting (CABG) requiring surgical decortication has been reported.5 As the precise time of the initial injury is known in postcardiac surgery patients, the authors were able to correlate histologic findings with the temporal relationship to the injury. The investigators found diminishing cellularity and increasing fibrosis of the pleural peel as time elapsed from CABG. It appears that trapped lung can be a late sequela of cardiac surgery if a persistent pleural effusion after surgery is not treated appropriately while still in the fibrinous inflammatory stage.

Pathophysiology and Technical Considerations

The pleural fluid in trapped lung exists in hydrostatic equilibrium with oncotic gradients intact.6 The persistence of a pleural space under these conditions requires a mismatch of the shape of the thoracic contents and the chest wall or a size mismatch resulting in deformation forces exceeding the hydrostatic and oncotic forces that favor fluid removal from the pleural space. Similar conditions are found in the normal pleural space, along the lobar margins, where increased deformation forces result in a thicker pleural liquid layer, a steeper pressure gradient, and more negative pressures.7,8

When pleural liquid pressure is measured, the initial mean pressure has been shown to be negative in trapped lung and to drop sharply upon fluid withdrawal. However, in malignant effusion, negative initial mean pressures and rapid decreases may also be encountered.9-12 This is likely related to coexistent malignant lung entrapment or other malignancy-related causes of unexpandable lung. Therefore, the demonstration of negative initial pleural liquid pressure or increased elastance of the pleural space is not sufficient to establish the diagnosis of trapped lung. In contrast, positive initial mean pleural pressure virtually excludes trapped lung as the sole cause of a pleural effusion. On occasion, a patient with trapped lung may experience pain after only a small amount of fluid has been withdrawn; this is usually accompanied by excessively negative pressure, and the pain may be alleviated by opening the thoracentesis system to the atmosphere. Similarly, patients with lung entrapment associated with malignancy or other causes may experience sudden onset of pain coincident with a sharp decrease in pleural pressure. In these patients, considerable amounts of fluid may already have been withdrawn prior to the onset of pain. Again, alleviating the negative pressure usually results in immediate relief. Thoracostomy with small-bore catheters and a standard drainage system (controlled suction and gravity drainage) has the advantage of not resulting in excessively negative pressure. Small-bore tube thoracostomy may be the method of choice for demonstration of lung entrapment when pleural space manometry is not available during thoracentesis. However, thoracostomy tubes in conjunction with one-way valve drainage systems do not allow the free exchange of air and fluid and should not be used if lung entrapment is suspected.

Causes of Trapped Lung

Trapped lung is a residual condition resulting from a remote inflammatory pleural process. The responsible process must have caused a pleural effusion that persisted long enough for a mature fibrous membrane to develop over the visceral pleura. This membrane prevents pleural apposition after eventual resolution of the inflammatory process. Among the causes of trapped lung are uremic pleuritis, complicated parapneumonic effusion, postcardiac surgery, postcardiac injury syndrome, hemothorax, rheumatoid pleuritis, and tuberculous pleurisy.2,13-20 Obviously, appropriate management, including drainage and/or specific therapy during the acute stage of these conditions, may prevent the development of trapped lung. However, in some cases the process may have been subclinical or the patient may have never sought medical attention.

Presentation

Trapped lung commonly presents as an asymptomatic, chronic, unilateral pleural effusion. It is a diagnostic dilemma rather than a condition requiring treatment. Occasionally, patients present with dyspnea, restrictive dysfunction on pulmonary function testing, and no other apparent cause of their dyspnea. The patient may recall a remote episode of pleurisy or pneumonia, or report a history of CABG, end-stage renal disease, or other rarer conditions associated with the development of trapped lung.1,4

Diagnosis of Trapped Lung

The diagnosis of trapped lung requires the exclusion of other causes of unexpandable lung after thoracentesis. The causes of unexpandable lung include airway obstruction resulting in atelectasis, severe parenchymal disease, and visceral pleural restriction. All of these conditions may coexist. If pleural pressure is measured, a sharp drop in pressure is usually evident. However, the sharp decrease may not be seen until a significant amount of fluid has been withdrawn; this usually indicates that something other than a purely mechanical cause is responsible for pleural fluid formation. If the fluid is an exudate, active pleural disease is usually present. If the fluid is a transudate, either systemic or local hydrostatic conditions cause pleural fluid formation. Negative initial pleural pressure and an immediate sharp pressure drop favor mechanical restriction as the sole cause of persistence of pleural effusion.9-11 The pleural fluid usually has low levels of protein and lactate dehydrogenase under these circumstances. A CT scan obtained with negative pleural pressure and preferably air contrast may demonstrate a visceral pleural membrane, severe parenchymal disease, or an endobronchial lesion. Subpleural atelectasis may be seen and does not represent relaxation atelectasis in the presence of negative pleural pressure. Negative pressure in the pleural space is assured if a functioning thoracostomy tube is in place with suction. If the examination is to follow a thoracentesis, fluid may be exchanged with air and the negative pressure can be established just prior to removal of the drainage catheter. However, if pleural pressure measurement is not available, a small-bore thoracostomy tube with drainage system should be placed.

If the lung does not expand after drainage of an effusion with low lactate dehydrogenase and protein levels, a visceral pleural membrane is present, and endobronchial disease and severe parenchymal disease are absent, a presumptive diagnosis of trapped lung can be established. Initially negative pleural pressure (usually < ­5 cm H2O) supports the diagnosis. However, trapped lung can only be diagnosed with certainty with successful decortication, which is not indicated in many patients.

Prevention and Management

It is likely that the development of trapped lung can be prevented with appropriate management of the pleural space during the acute inflammatory phase of most contributing conditions.13 Fortunately, trapped lung is relatively uncommon as a result of the rapid resolution of pleural effusions or lack of reaccumulation after thoracentesis while specific therapy is administered.21 Trapped lung in the asymptomatic patient does not require therapy, and the patient can be reassured about the benign nature of the condition. Occasionally, trapped lung may lead to physiologic impairment when substantial amounts of lung are involved. Pulmonary function testing usually reveals restrictive dysfunction in these patients. Before recommending decortication, the physician should try to exclude other causes of dyspnea because decortication is associated with morbidity. In particular, in patients who experience relief after thoracentesis, other causes of transudative effusion, such as congestive heart failure, should be suspected. Only if all other causes of dyspnea have been excluded or successfully treated should decortication be considered. A CT scan may demonstrate coexisting severe parenchymal disease in the lung affected by the restricting visceral pleural membrane and may demonstrate scar tissue extending into the lung parenchyma, making decortication technically difficult. The ideal candidate for decortication is the patient in good general health with only a visceral pleural membrane involving a substantial part of the lung. Subpleural atelectasis may be expected to resolve after decortication. Patients with complete atelectasis of a lobe due to trapped lung present a more difficult situation because the atelectatic lung cannot be assessed by CT preoperatively.

References

  1. Stead WW, Eichenholz A, Stauss H-K. Operative and pathologic findings in twenty-four patients with syndrome of idiopathic pleurisy with effusion, presumably tuberculous. Am Rev Tuberc Pulm Dis 1955; 71:473­502
  2. Farber JE, Lincoln NS. The unexpandable lung. Am Rev Tuberc 1939; 40:704­709
  3. Douglass BE, Carr DT, Bernatz PE. Diagnostic thoracotomy in the study of “idiopathic” pleural effusion. Am Rev Tuberc Pulm Dis 1956; 74:954­957
  4. Moore PJ, Thomas PA. The trapped lung with chronic pleural space, a cause of recurring pleural effusion. Milit Med 1967; 132:998­1002
  5. Lee YCG, Vaz MAC, Ely KA, et al. Symptomatic persistent post-coronary artery bypass graft pleural effusions requiring operative treatment: clinical and histologic features. Chest 2001; 119:795­800
  6. Black LF. The pleural space and pleural fluid. Mayo Clin Proc 1972; 47:493­506
  7. Lai-Fook SJ. Mechanics of the pleural space: fundamental concepts. Lung 1987; 165:249­267
  8. Boggs DS, Kinasewitz GT. Pathophysiology of the pleural space. Am J Med Sci 1995; 309:53­59
  9. Light RL, Jenkinson SG, Minh V, et al. Observations on pleural fluid pressures as fluid is withdrawn during thoracentesis. Am Rev Respir Dis 1980; 121:799­804
  10. Light RW, Stansbury DW, Brown SE. The relationship between pleural pressures and changes in pulmonary function after therapeutic thoracentesis. Am Rev Respir Dis 1986; 133:658­661
  11. Villena V, Lopez-Encuentra A, Pozo F, et al. Measurement of pleural pressures during therapeutic thoracentesis. Am J Respir Crit Care Med 2000; 162:1534­1538
  12. Lan R, Singh KL, Chuang M, et al. Elastance of the pleural space: a predictor for the outcome of pleurodesis in patients with malignant effusion. Ann Intern Med 1997; 126:768­774
  13. Young D, Simon J, Pomerantz M. Current indications for and status of decortication for “trapped lung.” Ann Thorac Surg 1972; 14:631­634
  14. Kollef MH, Peller T, Knodel A, et al. Delayed pleuropulmonary complications following coronary artery revascularization with the internal mammary artery. Chest 1988; 94:68-­71
  15. Kollef MH. Chronic pleural effusion following coronary artery revascularization with the internal mammary artery. Chest 1990; 97:750­751
  16. Kollef MH. Symptomatic pleural effusion after coronary artery revascularization: unsuspected pleural injury from internal mammary artery resection. South Med J 1993; 86:585­588
  17. Rodelas R, Rakowski TA, Argy WP, et al. Fibrosing uremic pleuritis during hemodialysis. JAMA 1980; 243:2424­2425
  18. Berger HW, Rammohan G, Neff MS, et al. Uremic pleural effusion: a study in 14 patients on chronic dialysis. Ann Intern Med 1975; 82:362­364
  19. Yarbrough JW, Sealy WC, Miller JA. Thoracic surgical problems associated with rheumatoid arthritis. J Thorac Cardiovasc Surg 1975; 69:347­354
  20. Brunk JR, Drash EC, Swineford O. Rheumatoid pleuritis successfully treated with decortication: report of a case and review of the literature. Am J Med Sci 1966; 251:545­551
  21. Cohen M, Sahn SA. Resolution of pleural effusions. Chest 2001; 119:1547­1562

Copyright ©2003 American College of Chest Physicians