Approximately 1 million patients develop parapneumonic effusions (PPEs) annually in the United States. The outcome of these effusions is related to the interval between the onset of clinical symptoms and presentation to the physician, comorbidities, and timely management. Early antibiotic treatment usually prevents the development of a PPE and its progression to a complicated PPE and empyema. Pleural fluid analysis provides diagnostic information and guides therapy. If the PPE is small to moderate in size, free-flowing, and nonpurulent (pH, 17.30), it is highly likely that antibiotic treatment alone will be effective. Prolonged pneumonia symptoms before evaluation, pleural fluid with a pH !7.20, and loculated pleural fluid suggest the need for pleural space drainage. The presence of pus (empyema) aspirated from the pleural space always requires drainage. Fibrinolytics are most likely to be effective during the early fibrinolytic stage and may make surgical drainage unnecessary. If pleural space drainage is ineffective, video-assisted thoracic surgery should be performed without delay.Parapneumonic effusion (PPE; i.e., pleural fluid that results from pneumonia or lung abscess) is the most common cause of an exudative pleural effusion. PPE may be the consequence of either community-acquired or nosocomial pneumonia. Between 20% and 57% of the 1 million patients hospitalized yearly in the United States with pneumonia develop a PPE [1][2][3]. Although PPEs are relatively common, empyema (i.e., the accumulation of pus in the pleural space) is less common, occurring in 5%-10% of patients who experience PPE [4]. In a review of 14 studies of empyema that involved a total of 1383 patients, 70% of PPEs were secondary to pneumonia (figure 1) [4]. CLASSIFICATIONA practical, clinical classification of PPE is as follows: (1) an uncomplicated parapneumonic effusion (UPPE) resolves with antibiotic therapy alone, without pleural space sequelae; (2) a complicated parapneumonic effusion (CPPE) requires pleural space drainage to resolve pleural sepsis and prevent progression to an empyema; and (3) empyema, the end stage of a PPE, occurs. Empyema is defined by its appearance; it is an opaque, whitish-yellow, viscous fluid that is the result of serum coagulation proteins, cellular debris, and fibrin deposition. Empyemas develop primarily because of delayed presentation by the patient with advanced pneumonia and progressive pleural infection and, less often, from inappropriate clinical management. Early antibiotic treatment prevents progression of pneumonia and the development of a PPE. Early antibiotic treatment will prevent development of an UPPE and progression to empyema. Risk factors for empyema include age (empyemas occur most frequently among children and elderly persons), debilitation, male sex, pneumonia requiring hospitalization, and comorbid diseases, such as bronchiectasis, chronic obstructive pulmonary disease, rheumatoid arthritis, alcoholism, diabetes, and gastroesophageal reflux disease [5]. Bacterial pneumonia, pneumon...

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Pleural effusions associated with malignancy (either malignant or paramalignant) pose diagnostic and therapeutic dilemmas for the clinician. This article reviews the common causes of malignant and paramalignant pleural effusions, pathogenesis, clinical presentation, chest radiography, pleural fluid characteristics, diagnosis, prognosis, and treatment.Talc, used either by poudrage or slurry, is the most effective agent used for pleurodesis. Talc, which needs to be sterilized, has no clinically important immediate, short-term or long-term adverse effects.

All-cause mortality rate in patients with idiopathic pulmonary fibrosis. Implications for the design and execution of clinical trials.King TE Jr 1 , Albera C, Bradford WZ, Costabel U, du Bois RM, Leff JA, Nathan SD, Sahn SA, Valeyre D, Noble PW. La versione definitiva è disponibile alla URL:http: //www.atsjournals.org/doi/abs/10.1164 Rationale: FVC has emerged as a standard primary endpoint in clinical trials evaluating novel therapies for patients with idiopathic pulmonary fibrosis (IPF). However, it has recently been proposed that all-cause mortality or a composite comprised of all-cause mortality and all-cause nonelective hospitalization be adopted as the standard primary endpoint for IPF clinical trials.Objectives: To conduct a comprehensive evaluation of mortality in three phase 3 clinical trials and evaluate the feasibility of mortality trials in patients with IPF. Methods:The study population included 622 patients randomized to placebo in the CAPACITY studies evaluating pirfenidone (n = 347) or the INSPIRE study evaluating interferon-γ1b (n = 275). The Kaplan-Meier estimate of 2-year survival was fit to the exponential distribution and used to calculate sample size requirements for a mortality study with 90% power to detect a 25% reduction in all-cause mortality with a two-sided α of 0.05. Modeling analyses were used to assess the effects of selected variables on sample size and study design. Measurements and Main Results:A total of 73 deaths occurred during the period of observation (mean duration of follow-up, 80.1 wk). The all-cause mortality rate was 6.6% at 1 year and 13.7% at 2 years. Based on the observed 2-year mortality rate, a total of 508 events would be required to detect a significant treatment benefit in a two-arm trial with 90% power to detect a 25% reduction in all-cause mortality. The estimated sample size for a trial enrolled over 3 years with a maximum follow-up period of 5 years is 2,582 patients. Conclusions:The all-cause mortality rate is relatively low in patients with IPF with mild to moderate impairment in lung function. Accordingly, the necessary size, duration, and cost of allcause mortality trials in this population are substantial and likely prohibitive.

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1. Hypoxic and hypercapnic ventilatory drives were measured in eight healthy male subjects before and after ingestion of ethanol, in a dose of 17 mmol/kg body weight. 2. A significant decrease in hypoxic ventilatory drive was observed at 20 min after ethanol (P less than 0.05). A significant depression in hypercapnic drive was observed at 70 min after indigestion of ethanol (P less than 0.05). The mean peak blood ethanol (24mmol/1) occurred at 20 min, at which time the lowest mean hypoxic drive was recorded. 3. Ethanol in moderate doses produced a depression of both hypoxic and hypercapnic ventilatory drives in normal subjects. This suggests that ethanol may play a role in the precipitation of acute respiratory failure in certain patients in whom the ventilatory drive is already impaired, as in chronic airways obstruction.

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Protected transbronchial needle aspiration (PTBNA) of pneumonic lung theoretically could bypass dislodged upper respiratory tract flora, a potential source of contamination of protected specimen brush (PSB) cultures. To evaluate the usefulness of PSB and PTBNA in establishing the etiology of pneumonia, we prospectively studied 20 patients with acute bacterial pneumonia not receiving antibiotics. After informed consent, patients had fiberoptic bronchoscopy under fluoroscopy to localize the pneumonia, and specimens were obtained by the PSB. The protective plug of a specially devised needle for PTBNA was pneumatically dislodged and aspiration was performed within the infiltrate under fluoroscopy. Quantitative cultures were plated immediately for aerobes, anaerobes, and Legionella. Greater than 4 X 10(3) organisms/brush or 1 X 10(4) organisms/ml needle aspirate were considered to be consistent with infection. The results using PSB and PTBNA were compared in 15 of 20 patients in whom a definitive diagnosis (positive blood or pleural fluid culture) or presumptive diagnosis (expectorated sputum culture, clinical characteristics, and response to specific therapy) was established. The PSB and PTBNA cultures on uninfected control subjects (n = 5) being bronchoscoped for other reasons were negative. The PSB and PTBNA were each diagnostic in 2 of the 5 patients with definitive diagnoses. In the group with a presumptive diagnosis (n = 10), PSB was diagnostic in 7 of 10 and PTBNA in 9 of 10. The overall (definitive plus presumptive) diagnostic yield was 60% for PSB and 73% for PTBNA. Multiple organisms were isolated in high concentrations in 53% of the patients. The most common organisms recovered in addition to the primary pathogen was alpha hemolytic streptococci.(ABSTRACT TRUNCATED AT 250 WORDS)