What every physician needs to know:
Trapped lung syndrome refers to a condition in which the lung does not fully expand during pleural drainage to oppose the chest wall. This form of non-expandable lung is the sequela of prior pleural inflammation that results in the creation of a fibrous peel on the visceral pleura. The resulting negative pleural pressure causes a pleural effusion ex-vacuo. As hydrostatic forces are the sole cause of increased pleural fluid formation, pleural fluid analysis will reveal a transudative effusion.
It is important to differentiate trapped lung from entrapped lung (also known as lung entrapment). Like trapped lung, lung entrapment refers to a lung that will not fully expand with pleural drainage. The major difference is that lung entrapment may result from either pleural or non-pleural causes, while trapped lung results from pleural causes only. Patients with active pleural inflammation can have thickening of the visceral pleura, causing non-expandable lung, especially toward the end of pleural drainage. Non-pleural causes of lung entrapment include diseases that increase the elastic recoil pressures of the lung, such as endobronchial obstruction causing atelectasis or interstitial disease, such as lymphangitic carcinomatosis.
Are you sure your patient has trapped lung syndrome? What should you expect to find?
As patients with trapped lung do not have active pleural inflammation, they are usually asymptomatic, and the effusion is often found incidentally on physical exam or chest imaging. If the effusion is sampled, pleural fluid analysis will reveal a transudate. Pleural manometry (measuring pleural pressure during thoracentesis) is simple to perform and is extremely useful in diagnosing patients with trapped lung.
Under normal conditions, if one were to add fluid to a closed system (the thorax), the pressure would rise; and as the fluid is removed, the pressure would fall until a steady state is reached. In the chest, the pleural pressure at functional residual capacity (FRC) is normally slightly negative (-3 to -5 cmH20) because the balance of forces of the chest have a tendency to expand, and the lung’s elastic recoil results in a tendency for the lung to collapse.
In the setting of trapped lung, despite the presence of a pleural effusion, the pleural pressure is low, and it drops significantly with the removal of fluid. This high pleural elastance (change in pressure/change in volume) is a hallmark of trapped lung.
Beware: there are other diseases that can mimic trapped lung syndrome:
Patients with lung entrapment are usually symptomatic from their effusion, as there is typically some active pleural inflammation, and pleural fluid analysis will demonstrate an exudative effusion. Common causes of lung entrapment include malignant pleural effusions, complicated parapneumonic effusions, and endobronchial obstruction that causes a post-obstructive pneumonia with atelectasis.
Pleural manometry in patients with lung entrapment can show a normal pleural elastance during the initial removal of fluid; however, as more fluid is removed and the lung does not fully expand, the slope of the elastance curve increases.
It has been shown that the development of a vague type of chest discomfort during thoracentesis is likely due to dropping pleural pressures and the operator should consider discontinuing drainage. In this setting, some authors advocate that atmospheric air be allowed to enter the pleural space in order to bring the pleural pressure back to a more physiologic range so as to diminish the patient’s discomfort. A chest CT scan can be obtained to demonstrate visceral pleural thickening and non-expandable lung (Figure 1).
How and/or why did the patient develop trapped lung syndrome?
Pleural effusions resolve when the underlying disease that has caused the imbalance in hydrostatic or oncotic (or both) pressures has resolved. If a patient with lung entrapment has resolution of the active pleural inflammation, and the pleura heals without the development of thickening of the visceral pleura, the pleural physiology will return to normal. Examples of this process include patients who have completely recovered from an episode of community-acquired pneumonia with a parapneumonic effusion or patients who develop a pleural effusion after cardiac surgery.
However, the same patient’s pleura may heal such that a visceral peel develops, and despite the lack of residual pleural inflammation, a pleural effusion persists due to the negative pleural pressure created by the visceral peel. In this example, the fluid early in the course of the patient’s illness would be exudative, and the elastance curve consistent with lung entrapment. Later in the resolution and healing process, it would be a transudate and the elastance curve would be consistent with trapped lung.
Which individuals are at greatest risk of developing trapped lung syndrome?
It is unclear why some patients form a visceral pleural peel while others heal their pleural space with no residual visceral pleural thickening.
What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?
Patients with a trapped lung have a transudative effusion, whereas those with an entrapped lung have an exudative effusion. It is important to review the pleural elastance curves to distinguish between these two syndromes. The pleural fluid analysis and physiology can then be put into clinical context, as there may be overlap between lung entrapment and trapped lung during the healing phase of the disease.
What imaging studies will be helpful in making or excluding the diagnosis of trapped lung syndrome?
In both causes of non-expandable lung, post-drainage imaging may reveal a pneumothorax. The cause of pneumothorax in these patients may be likened to pouring milk out of a bottle. As the milk pours out, a vacuum is created in the bottle and air enters. Similarly, in the setting of non-expandable lung, as fluid is removed, pleural pressure drops and eventually air has to enter the pleural cavity. Though the air may enter from the atmosphere (i.e., between the catheter and skin), it is likely that local deformation forces develop and create small tears in the visceral pleura.
Unlike spontaneous or traumatic pneumothorax that are often localized to the apex on an upright chest x-ray, pneumothorax attributable to non-expandable lung may be located at the base, as the dependent part of the lung may fail to expand fully. If a chest CT is obtained after drainage, visceral pleural thickening can be readily identified. Visceral pleural thickening may also be identified on ultrasound prior to pleural drainage, and should alert the physician that the lung may not fully expand with drainage.
What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of trapped lung syndrome?
Pleural manometry is easily performed at the bedside during thoracentesis, but it is necessary to use the syringe-pump method as opposed to a vacuum bottle if pleural pressure is to be measured. Although pleural manometry may add five minutes to the procedure, the information gained about the underlying pleural physiology is well worth the time and effort.
The simplest way to measure pleural pressure is by using the drainage tubing as a U-shaped water manometer. With the tubing connected to the catheter in the patient’s chest and the collection bag. The syringe is removed, and the difference in height from catheter insertion site to where drainage ceases is the pressure in the pleural space at the level of the catheter’s entry into the chest. For example, if fluid stops draining with the tubing 6cm above the catheter insertion site, the pleural pressure is +6 cmH20. If the fluid stops flowing with the tubing 16cm below the skin insertion site, the pleural pressure is -16 cmH20. Pressures are measured at regular intervals (e.g., every 240 mL, or four pumps of a 60 mL syringe), then plotted to obtain the pleural elastance curve (change in pressure on the Y axis vs. change in volume on the X axis). Recent studies, however, suggest that disposable digital manometers are more accurate than the “poor-man’s U-shaped manometer”.
The pressure curve of lung entrapment starts out with a normal and relatively flat pressure-volume curve with little change in pressure for any change in volume. As the terminal part of the lung fails to expand with continued drainage, the pressure drops additionally with any given change in volume, and the curve steepens. The pressure curve of trapped lung typically starts out at zero or slightly negative and drops precipitously during the initial withdrawal of pleural fluid.
What diagnostic procedures will be helpful in making or excluding the diagnosis of trapped lung syndrome?
As pleural manometry is easy to perform and does not add additional risk or cost to the procedure, it should be performed during every thoracentesis. The air-contrast chest CT scan and sometimes chest ultrasonography may show visceral pleural thickening.
What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis of trapped lung syndrome?
If you decide the patient has trapped lung syndrome, how should the patient be managed?
Dyspnea in patients with pleural effusion is due to the chest wall (primarily diaphragm) operating at a disadvantageous position on its length-tension relationship rather than from either hypoxemia or lung collapse. As such, dyspnea secondary to lung entrapment (such as from malignant pleural effusions) can be relieved by implantation of a tunnelled pleural catheter. Despite the lung’s not expanding, their dyspnea improves because the diaphragm can now function more effectively.
As the large majority of patients with trapped lung are asymptomatic, treatment of their pleural effusion is not necessary. However, some patients may be dyspneic from a restrictive ventilatory defect and may benefit from decortication. It is important to make sure the patient’s dyspnea is due to the non-expandable lung and not another underlying cardiopulmonary condition before sending the patient for decortication.
What is the prognosis for patients managed in the recommended ways?
Patients with trapped lung have a good prognosis as they are typically asymptomatic and do not require treatment. The most important consideration is to avoid unnecessary interventions (that may result in iatrogenic injury) such as inappropriate hospitalization and chest tube placement after thoracentesis when in the setting of ex-vacuo pneumothorax (basal pneumothorax on frontal chest x-ray after drainage). It is not likely that the lung will re-expand with chest tube drainage, and unless the patient becomes symptomatic, it may be better to simply allow the pleural fluid to re-accumulate.
What other considerations exist for patients with trapped lung syndrome?
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- What every physician needs to know:
- Are you sure your patient has trapped lung syndrome? What should you expect to find?
- Beware: there are other diseases that can mimic trapped lung syndrome:
- How and/or why did the patient develop trapped lung syndrome?
- Which individuals are at greatest risk of developing trapped lung syndrome?
- What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?
- What imaging studies will be helpful in making or excluding the diagnosis of trapped lung syndrome?
- What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of trapped lung syndrome?
- What diagnostic procedures will be helpful in making or excluding the diagnosis of trapped lung syndrome?
- What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis of trapped lung syndrome?
- If you decide the patient has trapped lung syndrome, how should the patient be managed?
- What is the prognosis for patients managed in the recommended ways?
- What other considerations exist for patients with trapped lung syndrome?