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BACKGROUND - Although recent reports suggest that the incidence of parapneumonic empyema has increased in several regions of the USA, national trends in disease burden are unknown. National trends in the incidence of parapneumonic empyema hospitalisations and changes in empyema by associated pathogens were examined.
METHODS - National hospitalisation data (1996-2008) were analysed and rates estimated using census estimates as denominators. Incidence rate ratios (IRR) compared 2008 with 1996 rates. Discharge diagnosis codes were used to characterise pathogens associated with empyema hospitalisations.
RESULTS - Overall, national parapneumonic empyema-related hospitalisation rates increased from 3.04 per 100,000 in 1996 to 5.98 per 100,000 in 2008, a 2.0-fold increase (95% CI 1.8 to 2.1). The increases were observed among children (IRR 1.9 (95% CI 1.4 to 2.7)) and adults aged 18-39, 40-64 and ≥65 years (IRR 1.8 (95% CI 1.5 to 2.1), 2.0 (95% CI 1.6 to 3.1) and 1.7 (95% CI 1.5 to 2.0), respectively). Overall, pneumococcal empyema rates remained relatively stable in all age groups whereas streptococcal- (non-pneumococcal) and staphylococcal-related empyema rates increased 1.9-fold and 3.3-fold, respectively, with consistent increases across age groups. The overall in-hospital case fatality ratio for parapneumonic empyema-related hospitalisations was 8.0% (95% CI 6.4% to 9.5%) in 1996 and 7.2% (95% CI 6.3% to 8.1%) in 2008 (p=0.395). Of the empyemas where study pathogens were listed (37.6%), staphylococcal-related empyema had the largest absolute increases across age groups and was associated with longer hospital stay and higher in-hospital mortality than other empyemas.
CONCLUSIONS - Although parapneumonic empyema-related hospitalisations remained relatively rare, they increased substantially during the study period. A number of pathogens, especially staphylococcus, contributed to this increase.
Intrapleural fibrin deposition and subsequent fibrosis characterize evolving empyema and contribute to the morbidity associated with this condition. Single-chain urokinase (scuPA) is proenzyme form of the urokinase plasminogen activator, which has recently been shown to effectively clear intrapleural loculation in tetracycline-induced pleurodesis in rabbits. The authors therefore hypothesized that scuPA could likewise improve intrapleural injury associated with empyema. The authors used a rabbit model of empyema induced by intrapleural administration of Pasturella multocida to test this hypothesis and determined the effects of intrapleural scuPA on pleural fluids indices of inflammation and intrapleural fibrosis. The authors found that intrapleural administration of scuPA was well tolerated, generated readily detectable fibrinolytic activity in the empyema fluids and did not induce intrapleural or systemic bleeding. Pleural fluid volume, intrapleural protein, and D-dimer concentrations were increased at 24 and 48 hours (P < .01, respectively) after induction of empyema. Intrapleural loculation did not occur in the scuPA- or vehicle control-treated animals and there was no significant change in the pleural empyema or thickening scores. These findings confirm that intrapleural scuPA generates fibrinolysis in empyema fluids but does not alter fibrotic repair at the pleural surface or the intensity of intrapleural inflammation in this empyema model.