FAILURE OF TALC PLEURODESIS IS ASSOCIATED WITH INCREASED PLEURAL FIBRINOLYSIS

Diffuse pleural inflammation and fibrin deposition following the insti llation of the sclerosing agent is considered necessary for a successf ul pleural symphysis. We hypothesized that an impairment in fibrin for mation or an increased endopleural fibrinolysis would lead to failure of pleurodesis. To investigate changes in the pleural coagulation/fibr inolysis balance, we studied 75 consecutive patients who underwent tho racoscopy. Fifty-four of these patients with malignant pleural effusio ns and four with a benign recurrent effusion underwent thoracoscopic t alc pleurodesis. Another four patients with malignancy and 13 with ben ign effusions had no talc poudrage performed and were included as a co ntrol group. Serial determinations of thrombin-antithrombin III comple x (TAT), plasminogen activator inhibitor (PAI), and D-dimer were made in pleural fluid samples taken at the beginning of thoracoscopy (basel ine), immediately after thoracoscopic biopsies had been done (postbiop sy), 3 h after thoracoscopy-either with; talc poudrage or without-and 24 and 48 h after the procedure, as well as in cases of recurrence of effusions (farline). Successful pleurodesis was obtained in 42 of 52 p atients who could be evaluated (81%), and failure was seen in 10. Stro ng activation of coagulation and production of PAI was observed in all groups, including the control (no talc) group. Fibrinolytic activity (as expressed by D-dimer levels) showed a clear decline 24 h after tal c poudrage in patients with a good outcome of pleurodesis, as opposed to those with bad results and to the control group, and returned to th e baseline by 15 d. We conclude that increased pleural fibrinolytic ac tivity is associated with failure of pleurodesis, despite significant inhibitory activity of PAI in all groups.