Reply to Zisis and Stratakos

We thank Dr Zisis and Dr Stratakos for their attention to our work and for the interesting arguments raised for our consideration. The first point of the LTTE is to express disagreement to Argon Beam Coagulation (ABC) and pleural abrasion as adequate surgical techniques to induce pleurodesis. The results of our study no doubt justify Dr Zisis’ word of caution regarding the use of ABC; however, in patients being treated with pleural abrasion an overall recurrence rate of 3.4% was noted [1]. Such results are in concordance with others previously reported and, in 2001, the ACCP Delphi Consensus Conference quoted pleural abrasion with a slightly superior consensus than apical pleurectomy in the case of PSP [2]. However, if ‘a significant part of the extrapleural layer remains intact after apical pleurectomy’, as stated by Dr Zisis, we can consider pleural abrasion and apical pleurectomy as surgical procedures inducing almost similar patho-physiologic changes to the apex of the pulmonary cavity and as such they should not be cause for controversy. The second point is whether Vanderschueren classification should be part of the decision-making in the surgical treatment of PSP. In this sense the work of Dr Ayed is noteworthy for its goal of stratifying the course of PSP with histo-pathological and clinical findings [3]. The recurrence rate observed in this study by performing lung apex resection and pleurectomy is 3.1% and, in a preceding report, the same author reported a recurrence rate of 5.5% by performing apical resection and pleural abrasion [4]. In both studies PSP recurrence was more frequently encountered in patients with Type 1 Vanderschueren findings: two out of three cases in the group treated with pleurectomy and three out of four cases in the group treated with pleural abrasion. Thus, patients with Type 1 PSP appear to be exposed to a higher risk of recurrence, independently of the type of surgical pleurodesis performed. Such results underline the evidence that PSP cannot always be relayed to blebs/bullae perforation, and strengthen the hypothesis of the presence of alternative routes to air accumulation in the pleural cavity, such as the so-called theory of ‘enhanced pleural porosity’ or the possibility of air transmigration via the peribronchial interstitium [5]. At this point, Dr Zisis’ question as to whether we know the ideal surgical treatment for PSP is entirely justified, revealing our poor judgement in performing the same surgical treatment for a non-uniform pathology. In the face of such uncertainty in the pathogenesis of PSP I would stress the importance of taking advantage of VATS as a diagnostic tool. In this sense I would underline the importance of repeated manoeuvres of lung exclusion/ ventilation to completely reveal the distribution of subpleural paraseptal emphysema, whether associated or not with the presence of extrinsic blebs/bullae. I interpret in this light the interesting findings of Dr Noppen on the distribution of lung abnormalities revealed by autofluorescence during medical thoracoscopy [5]. I would also point out the importance of VATS to exclude the presence of diaphragmatic abnormalities secondary to endometriosis implants which could be considered a classic case of misdiagnosed Type 1 Vanderschueren PSP. Ultimately, VATS furnishes useful specimens for the immuno-histochemical detection of those diffuse interstitial lung diseases in which pneumothorax could be the first clinical sign.