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]
Summary
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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