Fig. 55.1
Pleural elastance curves. Open circle = normal elastance, closed circle = lung entrapment, x = trapped lung (Reprinted with permission of the American Thoracic Society. Copyright © American Thoracic Society. Light RW, Jenkinson SG, Minh VD, George RB. Observations on pleural fluid pressures as fluid is withdrawn during thoracentesis. Am Rev Respir Dis. 1980;121:799–804, Official Journal of the American Thoracic Society, Diane Gern, publisher)
Though confusing terms, “lung entrapment” and “trapped lung” describe different pathophysiology. Lung entrapment describes an inability of the lung to fully reexpand during thoracentesis and can be due to visceral pleural thickening, parenchymal disease, or airway obstruction. Parenchymal diseases such as interstitial lung disease and lymphangitic carcinomatosis lead to an increase in the elastic recoil of the lung and may inhibit full lung reexpansion. Likewise, endobronchial obstruction can cause atelectasis and a drop in Ppl. Patients often present with dyspnea related to the effusion as well as with signs and symptoms related to the underlying disease. Chest discomfort or other signs of pleural inflammation may also be present. The effusion associated with lung entrapment is typically exudative, due to active pleural inflammation. The initial Ppl is usually positive and drops steeply toward the terminal portion of the thoracentesis, as a result of the lung not fully expanding. With normal healing of the underlying process, the effusion may completely resolve without any resultant thickening of the visceral pleura.
Trapped lung, on the other hand, represents the sequelae of prior pleural inflammation resulting in visceral pleural thickening. This creates negative pressure in the pleural space and results in an “effusion ex vacuo” – the negative Ppl is the cause of the effusion. Since there is no active pleural inflammation, patients typically present with a chronic, and asymptomatic, effusion that is identified on routine physical exam or chest X-ray. As the effusion is due to an excess of negative pleural pressure, it is rare to see contralateral mediastinal shift on a chest radiograph, even in the presence of a moderate–large effusion. Likewise, as the effusion is due to an imbalance of hydrostatic forces, it is almost always transudative in nature. Since the large majority of these patients are asymptomatic, therapy aimed at the pleural effusion is usually not required. The rare patient with trapped lung who is dyspneic from the effusion typically has a restrictive ventilatory defect, and decortication may be required to expand the underlying lung.
Lung entrapment and trapped lung are part of a continuum of the natural healing process of the underlying disease. As such, one may occasionally obtain pleural fluid results that fall in the exudative range in the setting of trapped lung physiology, depending on when the thoracentesis is performed in the healing process. Likewise, if a patient has multiple problems, such as pneumonia with high pleural elastance and congestive heart failure, transudative fluid may be obtained with lung entrapment physiology. Additionally, especially in the setting of lung entrapment, one should evaluate the different phases of pleural elastance. Though overall/mean elastance can be low, especially if the majority of fluid is removed in the setting of a normal elastance, the terminal part of the curve will have high elastance, and this can be overlooked if pressures are not measured frequently enough. We typically measure a Ppl once a fluid column is obtained (opening pressure) and every 240 cc. If pressures are falling (i.e., the slope of the elastance curve is changing) or the patient develops chest discomfort, we measure pressure more frequently. It is therefore crucial to interpret Ppl and elastance within the specific clinical context.
PPL and Pneumothorax
Though the mechanisms of pneumothorax in the setting of nonexpandable lung are not fully understood, it is likely that with a reduction in Ppl, atmospheric air either enters the pleural space around the catheter/via the catheter tract or the drop in Ppl causes local deformation forces that cause a small tear in the visceral pleura. The use of vacuum bottles to drain fluid has been associated with a higher incidence of pneumothorax. Unlike using a syringe pump system and intermittently measuring Ppl, it is likely that the vacuum bottles continue to drain fluid even when the lung is not able to expand, creating a vacuum in the pleural space itself.
Techniques of Measuring Pleural Pressure
Pleural pressure can be measured via in several ways, including using a U-shaped water manometer, an “overdamped” water manometer, or sophisticated electronic transducer systems. A benefit of the U-shaped manometer is the fact that it is relatively inexpensive. A disadvantage, however, is the fact that it may be difficult to accurately record values due to the inspiratory and expiratory pleural pressure swings. Doelken et al. have recently described their use of an overdamped water manometer that uses a 22-ga needle as a resistor and have shown excellent correlation to the electronic system (r = 0.97). The benefits of this system are that it is relatively easy to set up, and that it also provides real-time mean Ppl without the large respirophasic swings that are encountered with systems that are not damped. Electronic transducer systems can be configured to standard intensive care unit (ICU) monitors; however, as these monitors are not calibrated to measure negative pressure, one needs to calibrate an “offset.” Additionally, ICU hemodynamic transducers report data in mmHg, as compared to the standard cmH20 typically used for Ppl measurements. This problem is easily resolved by using the conversion factor of 1 mmHg = 1.36 cmH20. A clear advantage of using an electronic transducer system is the ability to review the Ppl curves after the data has been collected and analyze pressure anywhere in the respiratory cycle (i.e., end-inspiratory, end-expiratory, as well as mean Ppl). Most authors currently report mean or end-expiratory (i.e., FRC) Ppl. It may be, however, that end-inspiratory pressure is most related to the development of pressure-related complications such as chest discomfort and reexpansion pulmonary edema.
PPL and Symptoms
Careful attention should always be paid to patient symptoms during the removal of pleural fluid, especially when formal pressure measurements are not being obtained. Whereas sharp pain, typically felt over the ipsilateral shoulder, may be due to diaphragmatic irritation by the catheter, a more vague chest discomfort has been shown to correlate with potentially dangerous drops in Ppl. Interestingly, in this study, there was a trend toward a lower pleural elastance in the patients who developed cough, possibly suggesting that cough is due to normal expansion of the lung/resolution of atelectasis as the pleural fluid is removed, and one need not terminate a thoracentesis solely for the development of cough. It should also be noted that nearly 9% of patients in this study had Ppl < −20 cmH20 without any symptoms, and it is therefore not uncommon to see patients who have a basilar pneumothorax with visceral pleural thickening after a large-volume thoracentesis who have nonexpandable lung and normal pleural elastance.
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