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Background: Over 30% of adult patients with pleural infection either die and/or require surgery. There is no robust means of predicting at baseline presentation which patients will suffer a poor clinical outcome. A validated risk prediction score would allow early identification of high-risk patients, potentially directing more aggressive treatment thereafter., Objectives: To prospectively assess a previously described risk score (the RAPID (Renal (urea), Age, fluid Purulence, Infection source, Dietary (albumin)) score) in adults with pleural infection., Methods: Prospective observational cohort study that recruited patients undergoing treatment for pleural infection. RAPID score and risk category were calculated at baseline presentation. The primary outcome was mortality at 3 months; secondary outcomes were mortality at 12 months, length of hospital stay, need for thoracic surgery, failure of medical treatment and lung function at 3 months., Results: Mortality data were available in 542 out of 546 patients recruited (99.3%). Overall mortality was 10% at 3 months (54 out of 542) and 19% at 12 months (102 out of 542). The RAPID risk category predicted mortality at 3 months. Low-risk mortality (RAPID score 0-2): five out of 222 (2.3%, 95% CI 0.9 to 5.7%); medium-risk mortality (RAPID score 3-4): 21 out of 228 (9.2%, 95% CI 6.0 to 13.7%); and high-risk mortality (RAPID score 5-7): 27 out of 92 (29.3%, 95% CI 21.0 to 39.2%). C-statistics for the scores at 3 months and 12 months were 0.78 (95% CI 0.71-0.83) and 0.77 (95% CI 0.72-0.82), respectively., Conclusions: The RAPID score stratifies adults with pleural infection according to increasing risk of mortality and should inform future research directed at improving outcomes in this patient population., Competing Interests: Conflict of interest: J.P. Corcoran reports grants from the UK Medical Research Council (MRC; grant number G1001128), during the conduct of the study. Conflict of interest: I. Psallidas reports grants from the UK MRC (grant number G1001128), during the conduct of the study, as well as grants and personal fees from the European Respiratory Society (ERS), outside the submitted work. Conflict of interest: S. Gerry has nothing to disclose. Conflict of interest: F. Piccolo has nothing to disclose. Conflict of interest: C.F. Koegelenberg has nothing to disclose. Conflict of interest: T. Saba has nothing to disclose. Conflict of interest: C. Daneshvar has nothing to disclose. Conflict of interest: I. Fairbairn has nothing to disclose. Conflict of interest: R. Heinink has nothing to disclose. Conflict of interest: A. West has nothing to disclose. Conflict of interest: A.E. Stanton has nothing to disclose. Conflict of interest: J. Holme has nothing to disclose. Conflict of interest: J.A. Kastelik has nothing to disclose. Conflict of interest: H. Steer has nothing to disclose. Conflict of interest: N.J. Downer has nothing to disclose. Conflict of interest: M. Haris has nothing to disclose. Conflict of interest: E.H. Baker has nothing to disclose. Conflict of interest: C.F. Everett has nothing to disclose. Conflict of interest: J. Pepperell has nothing to disclose. Conflict of interest: T. Bewick has nothing to disclose. Conflict of interest: L. Yarmus has nothing to disclose. Conflict of interest: F. Maldonado has nothing to disclose. Conflict of interest: B. Khan has nothing to disclose. Conflict of interest: A. Hart-Thomas has nothing to disclose. Conflict of interest: G. Hands has nothing to disclose. Conflict of interest: G. Warwick has nothing to disclose. Conflict of interest: D. De Fonseka has nothing to disclose. Conflict of interest: M. Hassan reports grants from the UK MRC (grant number G1001128), during the conduct of the study. Conflict of interest: M. Munavvar has nothing to disclose. Conflict of interest: A. Guhan has nothing to disclose. Conflict of interest: M. Shahidi has nothing to disclose. Conflict of interest: Z. Pogson has nothing to disclose. Conflict of interest: L. Dowson has nothing to disclose. Conflict of interest: N.D. Popowicz has nothing to disclose. Conflict of interest: J. Saba has nothing to disclose. Conflict of interest: N.R. Ward has nothing to disclose. Conflict of interest: R.J. Hallifax reports grants from the UK MRC (grant number G1001128), during the conduct of the study. Conflict of interest: M. Dobson reports grants from the UK MRC (grant number G1001128), during the conduct of the study. Conflict of interest: R. Shaw reports grants from the UK MRC (grant number G1001128), during the conduct of the study. Conflict of interest: E.L. Hedley reports grants from the UK MRC (grant number G1001128), during the conduct of the study. Conflict of interest: A. Sabia reports grants from the UK MRC (grant number G1001128), during the conduct of the study. Conflict of interest: B. Robinson reports grants from the UK MRC (grant number G1001128), during the conduct of the study. Conflict of interest: G.S. Collins has nothing to disclose. Conflict of interest: H.E. Davies has nothing to disclose. Conflict of interest: L-M. Yu has nothing to disclose. Conflict of interest: R.F. Miller has nothing to disclose. Conflict of interest: N.A. Maskell has nothing to disclose. Conflict of interest: N.M. Rahman reports grants from the UK MRC (grant number G1001128), during the conduct of the study, as well as personal fees from the UK National Institute for Health Research (NIHR) Oxford Biomedical Research Centre, outside the submitted work., (Copyright ©ERS 2020.)

Background: More than 30% of patients with pleural infection either die or require surgery. Drainage of infected fluid is key to successful treatment, but intrapleural fibrinolytic therapy did not improve outcomes in an earlier, large, randomized trial., Methods: We conducted a blinded, 2-by-2 factorial trial in which 210 patients with pleural infection were randomly assigned to receive one of four study treatments for 3 days: double placebo, intrapleural tissue plasminogen activator (t-PA) and DNase, t-PA and placebo, or DNase and placebo. The primary outcome was the change in pleural opacity, measured as the percentage of the hemithorax occupied by effusion, on chest radiography on day 7 as compared with day 1. Secondary outcomes included referral for surgery, duration of hospital stay, and adverse events., Results: The mean (±SD) change in pleural opacity was greater in the t-PA-DNase group than in the placebo group (-29.5±23.3% vs. -17.2±19.6%; difference, -7.9%; 95% confidence interval [CI], -13.4 to -2.4; P=0.005); the change observed with t-PA alone and with DNase alone (-17.2±24.3 and -14.7±16.4%, respectively) was not significantly different from that observed with placebo. The frequency of surgical referral at 3 months was lower in the t-PA-DNase group than in the placebo group (2 of 48 patients [4%] vs. 8 of 51 patients [16%]; odds ratio for surgical referral, 0.17; 95% CI, 0.03 to 0.87; P=0.03) but was greater in the DNase group (18 of 46 patients [39%]) than in the placebo group (odds ratio, 3.56; 95% CI, 1.30 to 9.75; P=0.01). Combined t-PA-DNase therapy was associated with a reduction in the hospital stay, as compared with placebo (difference, -6.7 days; 95% CI, -12.0 to -1.9; P=0.006); the hospital stay with either agent alone was not significantly different from that with placebo. The frequency of adverse events did not differ significantly among the groups., Conclusions: Intrapleural t-PA-DNase therapy improved fluid drainage in patients with pleural infection and reduced the frequency of surgical referral and the duration of the hospital stay. Treatment with DNase alone or t-PA alone was ineffective. (Funded by an unrestricted educational grant to the University of Oxford from Roche UK and by others; Current Controlled Trials number, ISRCTN57454527.).

Background: Intrapleural fibrinolytic agents are used in the drainage of infected pleural-fluid collections. This use is based on small trials that did not have the statistical power to evaluate accurately important clinical outcomes, including safety. We conducted a trial to clarify the therapeutic role of intrapleural streptokinase., Methods: In this double-blind trial, 454 patients with pleural infection (defined by the presence of purulent pleural fluid or pleural fluid with a pH below 7.2 with signs of infection or by proven bacterial invasion of the pleural space) were randomly assigned to receive either intrapleural streptokinase (250,000 IU twice daily for three days) or placebo. Patients received antibiotics and underwent chest-tube drainage, surgery, and other treatment as part of routine care. The number of patients in the two groups who had died or needed surgical drainage at three months was compared (the primary end point); secondary end points were the rates of death and of surgery (analyzed separately), the radiographic outcome, and the length of the hospital stay., Results: The groups were well matched at baseline. Among the 427 patients who received streptokinase or placebo, there was no significant difference between the groups in the proportion of patients who died or needed surgery (with streptokinase: 64 of 206 patients [31 percent]; with placebo: 60 of 221 [27 percent]; relative risk, 1.14 [95 percent confidence interval, 0.85 to 1.54; P=0.43), a result that excluded a clinically significant benefit of streptokinase. There was no benefit to streptokinase in terms of mortality, rate of surgery, radiographic outcomes, or length of the hospital stay. Serious adverse events (chest pain, fever, or allergy) were more common with streptokinase (7 percent, vs. 3 percent with placebo; relative risk, 2.49 [95 percent confidence interval, 0.98 to 6.36]; P=0.08)., Conclusions: The intrapleural administration of streptokinase does not improve mortality, the rate of surgery, or the length of the hospital stay among patients with pleural infection., (Copyright 2005 Massachusetts Medical Society.)