We present the case of a 64-year-old female patient who presented to our service complaining of progressive shortness of breath over a period of 1 month. Physical examination showed that the patient was afebrile and had signs of a right-sided pleural effusion, which was confirmed radiologically. Her routine laboratory tests were within normal values, with an erythrosine sedimentation rate of 47 out of 63 and a white blood cell count of 7.800 cells/mm3. A diagnostic thoracentesis was performed and showed a straw-colored exudate according to Light's criteria,1 with a pleural fluid/serum protein ratio of 0.65, a pleural fluid/serum lactate dehydrogenase ratio of 0.55, and a pleural fluid lactate dehydrogenase of 180 IU/L (upper limit of normal for serum 200 IU/L). The pleural fluid, adenosine deaminase, was 57 IU. No growth of bacteria was found from cultures of the pleural fluid, and the smear for acid-fast bacilli was negative. Cytologic examination showed a predominantly lymphocytic exudate (70%) with no malignant cells or markers of specific infections or granulomas.
After the nonconclusive results of pleural fluid analysis, a therapeutic thoracentesis was performed and 1.5 L of pleural fluid was drained. Repeat cytologic examination was also nondiagnostic and the patient was scheduled for medical thoracoscopy.
Medical thoracoscopy using local anesthesia and conscious sedation with midazolam was performed. The procedure was performed in the left lateral decubitus position through 2 ports in the right fifth intercostal space, 1 in the anterior axillary line and the second in the posterior axillary line. Two liters of fluid were removed. The visceral pleura were normal, overlying a heavily anthracotic lung, whereas the parietal pleura were markedly congested but no nodules or masses were visualized (Fig. 1). After the fluid was removed and air was allowed into the pleural space, the parietal pleura became more edematous and roughened by dots of mucosal swellings that became more evident as time passed (Fig. 2). During the process of biopsy-taking, the parietal pleura were markedly edematous (Fig. 3). Biopsy results also showed mucosal edema and chronic pleuritis.
The evolution of the roughened pleura suggested a pathophysiologic explanation for recurrent pleural effusion. In healthy humans, fluid moves from the capillaries in the parietal pleura to the pleural space, resulting in a small volume of normal pleural fluid.2 In this case, the permeability of the capillaries in the parietal pleura seemed to be markedly increased (for whatever reason), and this appeared to be responsible for the exudation of fluid into the pleural space. We hypothesize that the pleural fluid continued to increase until it reached a volume large enough to elevate the pleural pressure and to produce a state of pressure equilibrium between the pleural capillary and the pleural pressure. It is known that the presence of pleural fluid leads to elevated pleural pressure.3 When the pleural fluid was suddenly removed during the thoracoscopy procedure, the pleural pressure became atmospheric with the development of an open pneumothorax. As a result, the hydrostatic gradient between the capillaries in the parietal pleura and the pleural space was increased. This resulted in increased fluid leakage from the parietal pleural capillaries and in the formation of submesothelial edema, which gave the pleura its bizarre appearance, which we termed “goose-skin pleura.” This observation confirms visually that the mechanism of the formation of the pleural fluid was leakage of fluid from the capillaries in the parietal pleura.4,5
We did not notice a specific distribution of the small dimples of swollen pleura either in the cephalad or caudad portions of the parietal pleura, in contrast with what was suggested earlier, that the pleural fluid was filtered more cephalad than caudad.6 However, no specific distribution would be expected with a pneumothorax as the hydrostatic gradient between the capillaries in the parietal pleura and the pleural space should be the same throughout the hemithorax. The cause of the unilaterally increased leakage of the fluid from the capillaries in the parietal pleura, which eventually contributed to the formation of the pleural effusion, remains unknown.
This phenomenon could as well be one of the causes of recurrence of pleural effusions after a large-volume thoracentesis.
1. Light RW, MacGregor MT, Luchsinger PC, et al. Pleural effusions
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2. Light RW. Physiology of the pleural space Pleural Diseases: Fifth Edition. Baltimore: Lippincott Williams & Wilkins; 2007:7–16.
3. Light RW, Jenkinson SG, Minh VD, et al. Observations on pleural fluid pressures as fluid is withdrawn during thoracentesis. Am Rev Respir Dis. 1980;121:799–804.
4. Miserocchi G, Negrini D. Pleural space: pressure and fluid dynamics. In: Crystal RG, West JB, eds. The Lung: Scientific Foundations. Philadelphia: Lippincott-Raven; 1997;1217–1225.
5. Miserocchi G. Physiology and pathophysiology of pleural fluid turnover. Eur Respir J. 1997;10:219–225.
6. Negrini D, Miserocchi G. Size-related differences in parietal extrapleural and pleural liquid pressure distribution. J Appl Physiol. 1989;67:1967–1972.