Diagnosis and Management of Trapped Lung

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

Print This | TOC | Previous | Next

---

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.

---

Print This | TOC | Previous | Next

3300 Dundee Road • Northbrook, Illinois 60062-2348 • (847) 498-1400 • (800) 343-2227
Copyright ©1999-2008 American College of Chest Physicians. All Rights Reserved.
ACCP Privacy Policy | ACCP Web Site Terms of Use