Sachin Venugopal Menon1, Rahul Abbas2, Suresh Padmini3, Rakesh Pulichikkat4
BACKGROUND
In patients with pleural effusion, irrespective of aetiology, the alterations in physiological states leading to restrictive lung functions and hypoxemia. In this study, we have aimed to study the effects of tuberculous pleural effusion on the pulmonary function and the predictive value of the initial severity of pleural effusion on chest x-ray and the residual pleural thickening in the severity of the restrictive abnormality. Also, we have compared the various pleural fluid characteristics in predicting the restrictive abnormality in tuberculous pleural effusion.
MATERIALS AND METHODS
The patients selected for the study, were initially subjected to diagnostic and therapeutic pleural tap on admission. They were then put on standard DOTS therapy. Their PFT was done on admission, then at one month, then two months and at the end of therapy at six months. Their chest X-ray was taken at monthly intervals and the residual pleural thickening was estimated. The resultant data was analysed statistically by ANOVA test, paired-t test and by Pearson’s correlation.
RESULTS
In our study, we have found a significant restrictive abnormality in lung function testing in our selected patients of tuberculous pleural effusion. They had a FVC% value of less than 80%. An interesting finding in our study was that, there was an element of small airway disease in our patients. This was manifested as an abnormal FET 25-75%. Also, we have found no relationship of the initial severity of pleural effusion with the final restrictive abnormality.
Also, we found no correlation between the pleural fluid characteristics and the RPT. We had compared the protein concentration, ADA and lymphocyte counts with the RPT. There was no statistical difference in the group with RPT and the group without any RPT as far as these parameters is applied. So, the finding from our study does support the theory of increased hypersensitivity as the origin of RPT.
In our patients, we have done therapeutic thoracocentesis on admission. PFT done immediately after this found a significant restrictive abnormality though the patients had a subjective relief of dyspnoea. On follow-up, subsequent PFTs revealed that there was significant improvement in all the parameters of PFT.
All values showed statistically significant improvement after six months of treatment.
The small airway obstruction is a significant finding in our study. This compels us to speculate about its pathogenesis. So far in literature no clear-cut explanation has been offered. However, endobronchial fibrosis in small airways as a result of tubercular parenchymal disease may be responsible for this. This suggests that tuberculous pleural effusion is no more a compartmentalized affection of the pleura, but also has some parenchymal component difficult to demonstrate clinically and radiologically.
CONCLUSION
a. Tuberculous pleural effusion causes a restrictive abnormality and small airway obstruction.
b. These abnormalities improve gradually over a period of six months when the patient is on AKT.
c. These abnormalities have no relation with the pleural fluid cytochemical and biochemical characteristics.
d. These abnormalities also have no relationship with the initial severity of the pleural effusion or the RPT.
As we can see that, one of the highlights of this study was small airway obstruction, shown uniformly in all the thirty study subjects. The mechanism of which is difficult to explain and definitely needs undertaking of further long-term and large-scale studies.
