Abstract

Background: Tuberculous, parapneumonic and traumatic loculated pleural-effusions pose therapeutic challenges due to resultant pleural-thickening and compromised lung-function for life. Tuberculosis is widely prevalent in developing countries, necessitating appropriate, effective, and economical treatment for loculated pleural-effusion to reduce the burden and sequelae. Objective: An uncontrolled and blind before-after intervention study to determine the effectiveness of intrapleural fibrinolytic therapy (IPFT) using urokinase in loculated pleural effusions was conducted at a tertiary-care respiratory center after obtaining approval and written informed consent. Methods: Fifty-one patients with loculated pleural effusion were administered with repeated cycles of three doses of 1 Lakh IU of urokinase intrapleurally until complete drainage of pleural fluid. Pre- and post-IPFT clinical and radiological responses were compared using removal of fluid, ultrasound, and chest radiography were compared. The Kolmogorov-Smirnov test and paired t test with significance at a P value less than 0.05 were applied to test statistically significant differences in proportions and means, respectively. Results: Tuberculosis was the most common etiology leading to loculated pleural effusion (80%), and 82.4% of tuberculosis patients required at least two cycles of IPFT. Complete resolution in chest radiograph after IPFT was observed in 80.4% of patients. Chest pain (13.7%) and fever (9.8%) were the most common undesired effects associated with IPFT. A statistically significant reduction in mean intrapleural fluid levels pre- and post-IPFT from 184±81 ml to 67±52 ml was observed. Conclusion: IPFT with urokinase is an effective treatment modality in patients with post-tubercular loculated pleural effusions. IPFT has minimal and tolerable undesired effects and prevents sequelae such as pleural thickening and consequent compromise of respiratory function.

Highlights

  • Tuberculous, parapneumonic and traumatic loculated pleural-effusions pose therapeutic challenges due to resultant pleural-thickening and compromised lung-function for life

  • Loculated pleural effusions usually occur as a result of adhesions and sequelae of complicated tuberculosis, parapneumonic effusion, empyema, haemothorax and malignant effusions.[1,2]

  • Delayed hypersensitivity responses to Mycobacterium tuberculosis is implicated in the causation of pleural effusion in tuberculosis.[3,4,5]

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Summary

Introduction

Tuberculous, parapneumonic and traumatic loculated pleural-effusions pose therapeutic challenges due to resultant pleural-thickening and compromised lung-function for life. Methods: Fifty-one patients with loculated pleural effusion were administered with repeated cycles of three doses of 1 Lakh IU of urokinase intrapleurally until complete drainage of pleural fluid. Delayed hypersensitivity responses to Mycobacterium tuberculosis is implicated in the causation of pleural effusion in tuberculosis.[3,4,5] The presence of septae lead to formation of loculi resulting in poor drainage despite appropriately positioned patent intercostal tube, thereby increasing the susceptibility to device-associated secondary infections by emerging multidrug resistant organisms acquired in the hospital environment.[6,7,8,9] The consequential fibrosis of pleural cavity leads to pleural thickening and compromised pulmonary function, posing a therapeutic challenge for life.

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