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Joseph et al have made a valuable contribution to the evaluation of pleural effusions.1 However, we would like to sound a note of caution. Throughout all the literature, including the study by Joseph et al, one message remains the same: no single test is diagnostic for transudates or exudates.2 Thus, overreliance on such a test can be very misleading and lead to either under or over-investigation.
Rarely in the literature is there any discussion regarding the place of pleural fluid protein or lactate dehydrogenase (LDH) estimation. Specifically, how does it alter management? Does the finding of a transudate obviate the need for further investigation? The main problem is that a significant number of malignant effusions are classified as transudates, whichever method is used.
The cause of a transudate is usually clinically obvious. If, however, there is no obvious underlying cause, surely cytological and/or histological examination should still be sought, as for an exudate?
Estimation of pleural fluid protein or LDH is also irrelevant if the fluid is bloodstained, as here further investigation for possible malignancy is warranted anyway.
We propose that the principal use for pleural fluid protein or LDH measurement is when a probable underlying cause for a transudative effusion is apparent, such as heart failure or hypoalbuminaemia, and the fluid is not bloodstained. In this situation the finding of a transudate may help to reassure that no further investigation is necessary except observation, and that a trial of treatment with, for example, diuretics may be of help.
We appreciate the comments by Quantrill and Dabal on our recent paper1 and would like to clarify the issues raised by them. By definition, when the pleural fluid is classified as a transudate, it indicates that a pathological process does not involve the pleural surface and that an effusion is formed because of a hydrostatic imbalance. If the pleural fluid is bloodstained, it therefore suggests disruption of the pleural membrane by an inflammatory or malignant process and hence cannot be classified as a transudate, which obviates the need for estimation of fluid LDH or protein estimation for diagnostic classification. However, as suggested by Quantrill and Dabal, an occasional malignancy may present as a transudate, in which case the mechanism is usually an effusion from collapse of a lobe causing an increase in the negative pleural pressure. Whatever the mechanism, if clinical suspicion for malignancy is high, further appropriate investigations need to be carried out.
Furthermore, Quantrill and Dabal state that hypoalbuminaemia is an apparent cause for transudative effusions.2 However, recent literature shows that hypoalbuminaemia per se may not cause pleural effusions.3 In our paper we have provided the positive likelihood ratios of the various tests so a clinician armed with the pretest probability for any individual patient and the positive likelihood ratio can work out the post-test probability using a standard nomogram.4,5 In light of the above, we suggest that fluid LDH and total protein ratio are useful in the diagnostic separation of pleural effusions.