Parapneumonic effusions account for about one third of all pleural effusions. Approximately 40% of patients with pneumonia develop a concomitant effusion, which is associated with an increased morbidity and mortality.In order to select the most appropriate therapy for the individual patient, the effusion should be categorized as being in the exudative, fibropurulent, or organizational stage, and all necessary information should be compiled to decide whether the effusion is likely to take an uncomplicated or a complicated course. There is a considerable variation in the aggressiveness and course of parapneumonic effusions, and, therefore, the spectrum of the appropriate therapy may vary from a conservative approach in uncomplicated effusions to aggressive surgical intervention in advanced multiloculated empyemas. This review discusses current diagnostic and therapeutic options and offers guidelines for treating the various stages of parapneumonic effusions and empyemas. Eur Respir J 1997; 10: 1150-1156 Definitions "Pleurisy" (syn. pleuritis) is best defined as an inflammatory process of the pleura, which can be caused either by a variety of infectious microorganisms or by other inflammatory mechanisms. It is usually associated with localized chest pain that is synchronous with the respiratory cycle and is often manifested as a pleural rub on auscultation. It may induce an exudative pleural effusion. The pain and the rub sometimes subside when an effusion develops.A "parapneumonic effusion" is an accumulation of exudative pleural fluid associated with an ipsilateral pulmonary infection."Uncomplicated parapneumonic effusions" are not infected and do not usually need tube thoracostomy."Complicated parapneumonic effusions" are usually associated with the pleural invasion of the infectious agent and require tube thoracostomy and sometimes decortication for their resolution.An effusion is called an "empyema" when the concentration of leucocytes becomes macroscopically evident as a thick and turbid fluid (pus). In more than 50% of cases, it is of parapneumonic origin. Other common causes include surgical procedures (mainly thoracic surgery), traumas and oesophageal perforation. PathophysiologyParapneumonic effusions and empyemas usually develop along the following lines. The pleuritis sicca stageThe inflammatory process of the pulmonary parenchyma extends to the visceral pleura, causing a local pleuritic reaction. This leads to a pleural rub and the characteristic pleuritic chest pain, which originates from the sensitive innervation of the adjacent parietal pleura. A significant number of patients with pneumonia report pleuritic chest pain without developing a pleural effusion [1], suggesting that the involvement of the pleura may be limited to this stage in many cases of pneumonia. The exudative stageThe ongoing inflammatory process leads to a mediator-induced increased permeability of local tissue and of regional capillaries. The subsequent accumulation of fluid in the pleural space is probably the combined ...

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There is no clear evidence as to how maximal inspiratory mouth pressure (PI,max) should be measured, although plateau pressures sustained for 1 s and measured at residual volume (RV) are usually recommended.Peak and plateau PI,max were measured at RV and at functional residual capacity (FRC) in 533 healthy subjects (aged 10-90 yrs) in order to comparably test all PI,max measurements for their predictors, reproducibility and normal values.Plateau pressures accounted for 82.0-86.3% of peak pressures. Peak and plateau pressures measured at FRC accounted for 84.3-90.5% of pressures at RV, and were highly correlated. Age was negatively predictive and weight and body mass index positively predictive of PI,max, but regression parameters were low. All PI,max measurements were comparable when calculating regression parameters, between-subject variability and reproducibility.In conclusion, peak and plateau maximal inspiratory mouth pressure are comparably useful for the assessment of inspiratory muscle strength and can be reliably measured at functional residual capacity and at residual volume. Regression equations are of low impact in predicting normal values due to the weak influence of demographic and anthropometric factors and to the high unexplained between-subject-variability. Agerelated 5th percentiles can indicate the lower limit of the normal range. Eur Respir J 2004; 23: 708-713.

SUMMARYThe pathogenesis of pulmonary sarcoidosis has been related to an increased production of Th1-like cytokines. However, cytokine expression in sarcoidosis has not been systematically studied at a singlecell level. We therefore investigated the expression of IL-2, IL-4, IL-13, tumour necrosis factor-alpha (TNF-a ) and interferon-gamma (IFN-g) intracellularly in bronchoalveolar lavage (BAL) and peripheral blood CD31 T lymphocytes from patients with pulmonary sarcoidosis (radiologic stage II±III, n 8) and normal controls (n 9) by flow cytometry. In contrast to IL-4 and IL-13, the percentage of T lymphocytes expressing intracellular IL-2 (49´3^21´3% versus 14´5^15´6%), IFN-g (75´5^14´9% versus 32´6^18´7%) and TNF-a (68´3^18´7% versus 36´8^20´8%) was significantly higher in patients with sarcoidosis than in normal controls (each P , 0´005). In contrast to BAL lymphocytes, expression of these cytokines in peripheral blood lymphocytes did not differ between patients with sarcoidosis and normal controls. Close correlations were observed between the percentages of BAL lymphocytes expressing intracellular IL-2, IFN-g and TNF-a , but not for IL-4 or IL-13. Analysis of the expression of these cytokines in T lymphocyte subsets revealed IL-2, IFN-g, and TNF-a in CD41 as well as CD8 1 T lymphocytes, suggesting a contribution of TC1 cells to the production of proinflammatory cytokines in sarcoidosis. We conclude that a Th1-like cytokine pattern can be observed in CD41 as well as in CD8 1 BAL T lymphocytes in patients with pulmonary sarcoidosis.

Hypercapnia has been accepted during nasal intermittent positive pressure ventilation (nIPPV) and during subsequent spontaneous breathing in patients with chronic hypercapnic respiratory failure (HRF) due to COPD. We tested the hypothesis that nIPPV aimed at normalizing PaCO2 will reduce PaCO2 during subsequent spontaneous breathing. For that purpose 14 consecutive inpatients (age 61.4 +/- 9.9 years) with chronic HRF due to COPD were established on passive pressure-controlled nIPPV in a stepwise approach. Assisted ventilation with supplemental oxygen to reach normoxemia was started followed by passive ventilation with a stepwise increment in the inspiratory pressure and finally by a stepwise increase in the respiratory rate to establish normocapnia. Baseline pulmonary function parameters were: FEV1 0.97 +/- 0.43 l, PaCO2 59.5 +/- 8.4 mmHg, PaO2 49.9 +/- 7.8 mmHg, HCO3- 35.6 +/- 5.2 mmol/l, pH 7.39 +/- 0.04. Normoxemia as well as normocapnia was thus established by decreasing PaCO2 by 19.5 +/- 7.0 mmHg during nIPPV within 8.8 +/- 3.8 days (P < 0.001) (inspiratory pressure 29.8 +/- 3.8 mmHg, respiratory rate 22.9 +/- 1.9 BPM). Spontaneous PaCO2 measured 4 h after cessation of nIPPV decreased to 46.0 +/- 5.5 mmHg (P < 0.001), and HCO3- decreased to 27.2 +/- 3.0 mmol/l (P < 0.001). At 6 months of follow-up, II patients continued nIPPV with stable blood gases and with a decrease of P0.1/Plmax from 9.4 +/- 4.3% to 5.9 +/- 2.0% (P < 0.005). In conclusion, normalization of PaCO2 by passive nIPPV in patients with HRF due to COPD is possible and leads to a significant reduction of PaCO2 during subsequent spontaneous breathing and is associated with improved parameters of respiratory muscle function.