体位改变对单侧胸腔积液患者气体交换的影响

目的　观察单侧胸腔积液患者患侧和健侧卧位对动脉血氧分压的影响以及体位对气体交换的影响与肺功能之间的关系。方法 采用自身对照设计、显著性检验和直线相关分析等方法。结果 53例单侧胸腔积液患者患侧卧位时PaO₂(PaO₂-E)为67.8±15.3mmHg,健侧卧位时(PaO₂-N)为79.9±13.8mmHg,二者差值在2.3～26.4mmHg之间,平均12.1±6.9mmHg,差异有显著性意义(P<0.001)。其中40例PaO₂-N高于PaO₂-E,13例PaO₂-N低于PaO₂-E。X线胸片上积液量的多少及肺功能指标与ΔPaO₂N-E之间无明显的相关。结论 体位变化对单侧胸腔积液患者的气体交换确实存在一定的影响。尽管大多数患者健侧卧位时血气交换状况改善,但并不呈一致性变化,健侧和患侧卧位血气的变化与患者的肺功能指标F-EV1及FVC也没有显著的相关。     

Body positional effect on gas exchange in unilateral pleural effusion

The positional effect on gas exchange was studied in eight patients who had unilateral pleural fluid without clinical or radiologic evidence of parenchymal lung disease. In all eight patients, PaO2 values were higher when the lung with the pleural fluid was uppermost. The mean PaO2 in this position was 71.9 +/- 9.3 mm Hg (mean +/- SE) compared with 66.7 +/- 8.7 mm Hg in the lateral decubitus position with the pleural fluid lowermost. The mean difference in PaO2 between the two positions was 5.1 +/- mm Hg (p less than 0.005). Larger positional differences were found in the patients with the smallest pleural effusions. These results are probably due to perfusion of areas of unventilated lung, accentuated by gravity with a consequent increase in shunting. A large effusion also causes a decrease in perfusion, so that ventilation-perfusion mismatching is decreased and the positional effect on gas exchange diminished.     

Effect of thoracentesis on arterial blood gas tension

The effect of thoracentesis on arterial blood gas tension was studied in 30 patients with unilateral free pleural effusions of various causes. Arterial blood gases were measured before thoracentesis and at 20 minutes, two hours after the procedure. P(A-a)O2 was determined at the same time. The PaO2, PaCO2 and HCO3 showed significant decrease but the concurrent significant increase of the P(A-a)O2 before thoracentesis. The PaO2 showed increase and P(A-a)O2 decrease but the PaCO2 not changes after thoracentesis 20 minutes and two hours. The results suggested that pleural effusion might result in hypoxaemia and chronic compensated alkalosis.     

The effect of positional changes on oxygenation in patients with pleural effusions

In unilateral parenchymal pulmonary disease, arterial oxygenation decreases when the patient is positioned such that the abnormal lung is dependent; however, few studies have evaluated the effect of the body position on oxygenation in patients with unilateral or asymmetric pleural effusions. To our knowledge, no previous study has evaluated the possible transient effects of changing position on the level of arterial oxygen saturation (SaO2) in such patients. Accordingly, we studied ten normoxic patients spontaneously breathing room air, who had asymmetric pleural effusions as documented by chest x-ray film and physical examination. We monitored pulse, respiratory rate, and blood pressure every five minutes and SaO2 by ear oximetry continuously while patients were in the following positions: sitting; supine; and left and right lateral decubitus. The mean SaO2 was 95 percent and 94.3 percent in the sitting and supine positions, respectively. Mean SaO2 fell to 93.4 percent when the patients were positioned so that the side with the largest pleural effusion was dependent. When the side with the pleural effusion was down, the mean SaO2 was significantly lower than in either the sitting position or with the side with the pleural effusion up. We could find no significant relationship between the size of the pleural effusion and the amount of arterial oxygen desaturation. We conclude that there is a decrease in SaO2 in normoxic patients when the side with the larger pleural effusion is dependent; however, this decreased SaO2 does not appear to be clinically significant in patients with normal SaO2.     

Serum levels of vascular endothelial growth factor dependent on the stage progression of lung cancer

STUDY OBJECTIVE: In lung cancer, vascular endothelial growth factor (VEGF) is an important cytokine and is correlated with tumor vessel density, malignant pleural effusions, and coagulation-fibrinolysis factors in vitro. We investigated the correlation between serum VEGF level and stage progression in lung cancer to study the predicted value of VEGF level. We also studied whether coagulation-fibrinolysis factors and PaO(2) levels, which are also important factors for the prediction of the clinical course, are correlated with VEGF. METHODS: Forty-nine patients with lung cancer were investigated prospectively. VEGF levels of sera and malignant effusions, and plasma concentrations of coagulation-fibrinolysis factors were measured by enzyme-linked immunosorbent assay. We measured PaO(2) levels in all patients at rest. RESULTS: Serum levels of VEGF were increased significantly according to stage progression. Additionally, plasma concentrations of D dimer, thrombin-antithrombin complex (TAT), and tissue plasminogen activator/plasminogen activator inhibitor type I complex were elevated significantly according to stage progression. The serum VEGF level had a significant positive correlation with the TAT and D dimer levels. Serum VEGF levels had a significant negative correlation with PaO(2) levels. The incidence of cerebral vascular disorder was significantly higher in the patients with systemic hypoxemia than in those without (p<0.05). Mean VEGF levels in malignant effusions in eight patients (five with pleural effusions, two with pericardial effusions, and one with both) were extremely high, especially in pericardial effusions ([mean +/- SD] pleural effusions, 531.9+/-285.4 pg/mL; pericardial effusion, 3,071.6+/-81.3 pg/mL). CONCLUSION: We predict that in lung cancer, VEGF production and the abnormality of the coagulation-fibrinolysis system differ depending on the stage of progression of disease. Serum VEGF levels would be affected by PaO(2) levels in lung cancer.     

A comparative study of the effects of almitrine bismesylate and lateral position during unilateral bacterial pneumonia with severe hypoxemia.

The management of patients with unilateral pneumonia and severe hypoxemia often represents a therapeutic challenge. Mechanical ventilation with the diseased lung uppermost may improve gas exchange, but it is not devoid of adverse effects. No hemodynamic measurements have been reported in patients ventilated in this manner; therefore, whether or not the improvement in PaO2 is counterbalanced by hemodynamic deterioration remains unknown. Almitrine bismesylate is a drug that seems able to improve gas exchange in patients with chronic obstructive pulmonary disease or the adult respiratory distress syndrome. The increase in PaO2 after its administration has been attributed to an improvement in ventilation-perfusion relationships. Its use has never been reported during unilateral pneumonia with severe hypoxemia. We therefore compared its effects with those of lateral position in eight consecutive mechanically ventilated patients with unilateral pneumonia. Blood gas and hemodynamic measurements were performed both at maintenance FIO2 and at an FIO2 of 1.0. Almitrine (1 mg/kg over 1 h) had no effect on PaO2 under either FIO2 condition. Cardiac output remained unchanged, but mean pulmonary artery pressure increased from 22.5 +/- 1.2 to 26.5 +/- 1.3 mm Hg (p < 0.02). By contrast, lateral position had striking effects on PaO2, which increased from 100 +/- 14 mm Hg in supine position to 156 +/- 23 mm Hg (p < 0.01) when the abnormal lung was placed uppermost at maintenance FIO2 and from 207 +/- 21 (supine) to 300 +/- 28 mm Hg (lateral) (p < 0.01) at FIO2 1.0.(ABSTRACT TRUNCATED AT 250 WORDS)     

The prone position in ARDS patients. A clinical study

The gas exchange and hemodynamics were evaluated before, during, and after a two-hour period of prone position in 13 moderate-severe ARDS patients. Lung computerized tomography was obtained in both the supine and prone positions in two of these patients. Average arterial oxygenation improved after prone positioning (p less than 0.01). A PaO2 improvement of at least 10 mm Hg after 30 minutes of prone position was used as a criterion to discriminate between responders and nonresponders to the postural change. Eight patients met the "responders" group criterion, and in the five nonresponder patients, the PaO2 did not change significantly throughout the study. Computerized tomograms in the prone position showed disappearance of posterobasal densities and appearance of new densities in the anterior regions, in both patients studied. One of these was a responder, the other a nonresponder. A brief test period in prone position is indicated in ARDS patients to identify those who may benefit from this postural treatment. The definite mechanism of the arterial oxygenation improvement observed remains to be clarified.     

Effect of thoracentesis on respiratory mechanics and gas exchange in the patient receiving mechanical ventilation

BACKGROUND: This study reports the effect of thoracentesis on respiratory mechanics and gas exchange in patients receiving mechanical ventilation. Study design: Prospective. SETTING: University hospital. PATIENTS: Eight patient receiving mechanical ventilation with unilateral (n = 7) or bilateral (n = 1) large pleural effusions. INTERVENTION: Therapeutic thoracentesis (n = 9). MEASUREMENTS: Resistances of the respiratory system measured with the constant inspiratory flow interrupter method measuring peak pressure and plateau pressure, effective static compliance of the respiratory system (Cst,rs), work performed by the ventilator (Wv), arterial blood gases, mixed exhaled Pco2, and pleural liquid pressure (Pliq). RESULTS: Thoracentesis resulted in a significant decrease in Wv and Pliq. Thoracentesis had no significant effect on dynamic compliance of the respiratory system; Cst,rs; effective interrupter resistance of the respiratory system, or its subcomponents, ohmic resistance of the respiratory system and additional (non-ohmic) resistance of the respiratory system; or intrinsic positive end-expiratory pressure (PEEPi). Indices of gas exchange were not significantly changed by thoracentesis. CONCLUSIONS: Thoracentesis in patients receiving mechanical ventilatory support results in significant reductions of Pliq and Wv. These changes were not accompanied by significant changes of resistance or compliance or by significant changes in gas exchange immediately after thoracentesis. The reduction of Wv after thoracentesis in patients receiving mechanical ventilation is not accompanied by predictable changes in inspiratory resistance and static compliance measured with routine clinical methods. The benefit of thoracentesis may be most pronounced in patients with high levels of PEEPi.     

Sustained effects of thoracocentesis on oxygenation in mechanically ventilated patients

Background and objective: No consensus exists as to the benefit of pleural drainage in mechanically ventilated patients with conflicting data concerning the effects on gas exchange. We determined the effects on gas exchange over a 48‐hour period of draining, by thoracocentesis, large volume pleural effusions. Methods: A total of 15 thoracocenteses were performed in 10 mechanically ventilated patients with ultrasound evidence of pleural effusions predicted to be greater than 800 mL in volume. Gas exchange, mixed expired CO2, dynamic lung compliance, ventilator settings before procedure and at 30 min, 4, 8, 24 and 48 h were determined. Data were analysed using paired t‐tests and repeated‐measure anova . Results: Following thoracocentesis there was a 40% increase in the PaO₂ from 82.0 ± 10.6 mm Hg to 115.2 ± 31.1 mm Hg (P < 0.05) with a 34% increase in the P:F ratio from 168.9 ± 55.9 mm Hg to 237.8 ± 72.6 mm Hg (P < 0.05). These effects were maintained for a period of 48 h. There was a correlation between the amount of fluid drained and the effects on oxygenation with an increase in the PaO₂ of 4 mm Hg for each 100 mL of pleural fluid drained. A‐a gradients continued to improve over the course of the study together with a reduction in the dead space fraction and improved dynamic compliance. Conclusions: Drainage of large pleural effusions in mechanically ventilated patients leads to a significant improvement in gas exchange, and these effects are sustained for 48 h after the procedure supporting a role in the discontinuation of mechanical ventilation.     

Effect of posture on arterial oxygenation in patients with chronic obstructive pulmonary disease.

We studied 117 patients with chronic obstructive pulmonary disease (COPD) to evaluate (1) the frequency and magnitude of postural changes in resting arterial oxygenation and (2) the relationship of these changes to other measures of pulmonary function and exercise arterial blood gases. Compared to the supine measurement, room air PaO2 measured while standing increased more than 3 mm Hg in 28 patients (group 1), did not change (+/- 3 mm Hg) in 57 patients (group 2), and decreased more than 3 mm Hg in 32 patients (group 3) (range = 31 mm Hg increase to 20 mm Hg decrease). Patients in group 1 had significantly less severe disease than patients in the other two groups. There were no significant pulmonary function differences between groups 2 and 3. Supine PaO2 was similar for all groups, suggesting that standing PaO2 accounted for the postural change in PaO2. Because of unpredictable postural changes in PaO2 in patients with COPD, we believe that body position should be noted for arterial blood gas measurements and should be kept constant for valid comparison of serial measurements. These findings may also be important for other diffuse lung diseases.     

Pleural effusion in patients with pulmonary embolism

Background and objective: It has been suggested that pulmonary embolism (PE) is an under‐recognized cause of pleural effusion. This study aimed to (i) establish the incidence and clinical relevance of pleural effusion in patients with pulmonary emboli; and (ii) determine if there is a relationship between development of pleural effusions and the location of emboli and number of pulmonary arteries involved. Methods: A retrospective analysis of all CT pulmonary angiograms (CTPA) performed over 12 months on adult patients with clinically suspected PE in a hospital which used CTPA as first‐line imaging investigation for PE. Results: Of 285 CTPA, 60 patients (21%) had evidence of pulmonary emboli (38 had both central and peripheral clots and 22 peripheral emboli only). Emboli were bilateral in 39 cases and unilateral in 21 cases. Pleural effusion was present in almost one half (n = 29, 48%) of the patients with pulmonary emboli. Patients with pulmonary emboli were more likely to have a pleural effusion (OR 2.2 (95% CI: 1.1–4.7), P < 0.05) than patients without PE; however, the effusions were generally very small. Most (86%) of the effusions were present on the same side as the emboli. The location of emboli and number of arteries involved did not predict the presence of pleural effusions. Conclusions: Pleural effusion is common in patients with pulmonary emboli demonstrated on CTPA. These effusions are small and seldom alter clinical management. Clinicians should therefore have a high threshold of suspicion in attributing large or contralateral pleural effusions to embolic diseases without excluding alternative diagnoses.     

Pleural fluid levels of interleukin-5 and eosinophils are closely correlated

BACKGROUND: The mechanisms responsible for the accumulation of eosinophils in pleural fluid are not fully understood. The purpose of this study was to evaluate the relationship between eosinophil accumulation and the levels of interleukin (IL)-5, IL-3, and granulocyte/macrophage colony-simulating factor (GM-CSF) in pleural effusions. METHODS: We evaluated 30 patients with eosinophilic pleural effusions (eosinophil count > 10% nucleated cells in pleural fluid) and 10 patients with noneosinophilic pleural effusions. The patients with eosinophilic pleural effusions included 22 patients with post-coronary artery bypass graft surgery pleural effusions and 8 patients with eosinophilic pleural effusions caused by other causes. IL-5, IL-3, and GM-CSF in all pleural fluids were measured using enzyme-linked immunosorbent assay kits. RESULTS: The mean level of IL-5 in eosinophilic pleural effusions (283.1 +/- 341.6 pg/mL) was significantly (p < 0.025) higher than that in the noneosinophilic effusions (28.2 +/- 19.0 pg/mL). The absolute eosinophil count and percentage correlated significantly with the level of IL-5 in all patients (r = 0.55, p < 0.001, and r = 0.54, p < 0.001, respectively). There was no significant correlation between IL-5 levels and RBC counts in all patients (r = 0.24, p > 0.05). GM-CSF and IL-3 levels were below the detectable range in all pleural fluids. CONCLUSION: There is a significant relationship between the levels of IL-5 in pleural fluid and the total number and percentage of eosinophils in the pleural fluid. IL-5 seems to be related to the eosinophil accumulation associated with blood or air in the pleural space and other eosinophilic pleural effusions.     

Effect of body position on arterial oxygen tension in the elderly

BACKGROUND: It is well known that body position can have an effect on gas exchange though the magnitude of this effect has not been studied thoroughly in the elderly. OBJECTIVES: This study analyzes the effect body position change has on arterial oxygen tension (PaO(2)) and arterial carbon dioxide tension (PaCO(2)) in healthy elderly. METHODS: We tested 46 "lung-healthy" elderly, including 30 women and 16 men, 67-88 years of age. Blood was drawn from the radial artery first in the sitting position and subsequently in the supine position. Spirometry was performed. RESULTS: Mean (SD) sitting PaO(2) was 10.53 kPa (1.22), whereas mean supine PaO(2) was 9.85 kPa (1.33). The difference between sitting and supine PaO(2) was 0.68 kPa (0.86) and was statistically significant. Sitting PaCO(2) was 5.06 kPa (0.47) and supine PaCO(2) was 5.05 kPa (0.54). The difference between sitting and supine PaO(2) correlated positively with FEV(1)/FVC %, negatively with the corresponding difference between sitting and supine PaCO(2), and negatively with BMI. CONCLUSIONS: We conclude that the significant difference in PaO(2) in sitting and supine positions clearly shows that the position needs to be considered both when attempting to establish reference values and when evaluating gas exchange in elderly persons. The positional changes in oxygenation are related to the corresponding change in PaCO(2), and to FEV(1)/FVC % and BMI.     

Analysis of pleural effusions in acute pulmonary embolism: radiological and pleural fluid data from 230 patients

BACKGROUND AND OBJECTIVE: The aims of this study were to describe the frequency and radiographical characteristics of pleural effusions in a large population of patients with acute pulmonary embolism (PE) and characterize the pleural fluid biochemistry in those patients who underwent diagnostic thoracentesis. METHODS: This was a retrospective observational single-centre study. A total of 230 consecutive patients with a diagnosis of PE over a 9-year period were enrolled. Spiral CT pulmonary angiography (52%) and high-probability ventilation and perfusion scans (42%) were used as the main reference methods. RESULTS: Pleural effusions were observed in 32% and 47% of patients by CXR and CT, respectively. Typically, pleural effusions were small (90% occupied less than one third of the hemithorax) and unilateral (85%), but occasionally they reached more than a half of the hemithorax. On CT, 21% of pleural effusions showed loculation. In patients with loculated pleural fluid the diagnosis of PE had been delayed for a mean of 12.2 days after symptoms developed. The presence of pleural fluid was not related to infarction. Twenty-six of 93 (28%) patients with effusions on imaging underwent thoracentesis. All the fluids met Light's criteria for exudate, 58% contained erythrocyte counts >10,000/microL and 46% showed neutrophilic predominance. CONCLUSIONS: Small pleural effusions, mostly unsuitable for diagnostic thoracentesis, were present in about one third of patients with PE. All the pleural effusions due to PE were exudates. If PE diagnosis was delayed the pleural effusion tended to become loculated.     

Modification of pleural fluid pH by local anesthesia.

BACKGROUND: It is a common practice to anesthetize patients before performing a thoracentesis. We postulated that this technique may cause a clinically significant difference in the pH of the pleural fluid. METHODS: We compared two methods of determining pleural fluid pH. Fifty patients undergoing diagnostic or therapeutic thoracentesis were enrolled. Two 4-mL aliquots of pleural fluid were anaerobically collected into blood gas syringes containing heparin, one before (group A) and the other after (group B) anesthetizing the patient with 5 mL of 2% mepivacaine. pH was then determined on both samples using an arterial blood gas machine. Agreement analysis was performed overall and in subcategories of pH used to define complicated (<7.1), borderline (7.1 to 7.3), or uncomplicated (>7.3) parapneumonic effusions. We analyzed these same data stratified by the volume of pleural fluid in relationship to the size of the hemithorax (<15% and >15%). RESULTS: There was a statistical difference between the mean pH in both groups (group A, 7.32; group B, 7.28; p<0.0001). There was a significant correlation between the two measures (r = 0.97; p<0.0001). Using the pH subcategories, there was 45% discordance in classification for patients with parapneumonic effusions. The pH values obtained in group B wrongly predicted whether the patient required a chest tube in two of four cases (50%). In patients with effusions that occupied <15% of the affected hemithorax, there was an 80% discordance in classification for patients with parapneumonic effusions, and the pH values obtained in group B wrongly predicted whether the patient required a chest tube in two of two cases (100%). CONCLUSIONS: Local anesthesia is typically used before thoracentesis is performed. However, in cases of suspected parapneumonic effusions that occupy <15% of the affected hemithorax, pH results may be significantly altered by use of local mepivacaine anesthesia.     

Pleural effusions after coronary artery bypass graft surgery

After coronary artery bypass graft surgery, most patients will have a small, unilateral, left-sided pleural effusion, and approximately 10% of patients will have a larger effusion. These large effusions can be separated into (1) early effusions occurring within the first 30 days of surgery that are bloody exudates with a high percentage of eosinophils, and (2) late effusions occurring more than 30 days after surgery that are clear yellow lymphocytic exudates. The primary symptom of pleural effusion after coronary artery bypass graft surgery is dyspnea; chest pain and fever are uncommon. Most patients with large pleural effusions after coronary artery bypass graft surgery are treated successfully with one to three therapeutic thoracenteses.     

Relationship of pleural effusions to pulmonary hemodynamics in patients with congestive heart failure

On the basis of both experimental and clinical studies it is not clear whether left, right, or biventricular heart failure are necessary for the formation of pleural effusions. In order to study the relationship of pulmonary hemodynamics and the presence of pleural effusions in patients with congestive heart failure, we prospectively evaluated 37 patients admitted to the coronary care unit with congestive heart failure secondary to ischemic heart disease or a cardiomyopathy. We used real-time ultrasonography to document the presence of pleural effusions. We found that 19 of the 37 patients with heart failure had pleural effusions. Mean pulmonary artery wedge pressure was 24.1 +/- 1.3 mmHg (SE) in the 19 patients with pleural effusions versus 17.2 +/- 1.5 mmHg (SE) (p less than 0.001) in the 18 patients without pleural effusions. Pulmonary artery pressure was also higher in patients with pleural effusions with a mean value of 38.0 +/- 1.5 mmHg (SE) versus 30.7 +/- 2.1 mmHg (SE) (p less than 0.05) in the patients without pleural effusions. In contrast, mean right atrial pressure was not different between patients with pleural effusions (12.6 +/- 1.5 mmHg) (SE) versus those without pleural effusions (9.8 +/- 1.0 mmHg) (SE) (p = NS). In addition, there was no difference in cardiac output, pulmonary vascular resistance, or total protein concentrations between patients with and without pleural effusions. We conclude that, in patients with congestive heart failure, an elevated left atrial pressure is closely correlated with the presence of pleural effusions, while concurrent elevation of right atrial pressure is not associated with the presence of pleural effusions.     

The pathogenesis of low glucose, low pH malignant effusions

Possible mechanisms to explain the finding of a low pH, low glucose, malignant pleural effusion include: use of glucose and acid production by pleural fluid constituents including leukocytes and free malignant cells; pleural membrane metabolism, especially by malignant cells; abnormal transfer of glucose, carbon dioxide, and hydrogen ion across a diseased pleural membrane. To determine the pathogenesis of low glucose, low pH effusions, we performed incubation and glucose and gas transport studies in 5 patients with malignant effusions, 3 with a low pH (less than 7.30) and 2 with a pH greater than 7.30 (control patients). After 24 h of incubation, there was no significant difference in the metabolic activity of pleural fluid between low pH fluids and control fluids. Transport studies confirmed impaired glucose transfer both into and out of the pleural space and impaired efflux of CO2 from the pleural space in patients with low pH effusions, whereas control patients demonstrated free transfer across the pleural membrane. It appears that an abnormal pleural membrane (tumor or fibrosis), rather than increased acid production, results in a low glucose concentration from impaired glucose transfer from blood to pleural fluid and a low pH from impaired hydrogen ion efflux in some malignant effusions.     

Metalloproteinases and tissue inhibitors of metalloproteinases in exudative pleural effusions.

The aim of this study was to assess the expression of several metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in exudative pleural effusions, and their relationship with inflammatory and fibrinolytic mediators in parapneumonic effusions. The study included 51 parapneumonic effusions (30 empyema or complicated parapneumonic, 21 noncomplicated parapneumonic), 28 tuberculous, 30 malignant and 30 transudates. Inflammatory markers (tumour necrosis factor-alpha, interleukin-8, polymorphonuclear elastase), fibrinolytic system variables (tissue plasminogen activator (PA), urokinase PA (u-PA), plasminogen activation inhibitor (PAI)-1, PAI-2), and several MMPs (MMP-1, MMP-2, MMP-8, MMP-9) and TIMPs (TIMP-1, TIMP-2) were determined by ELISA in plasma and pleural fluid. Elevated MMP-2 and TIMP-1 concentrations were observed in all the pleural fluid samples studied. The group of empyema or complicated parapneumonic effusions showed higher MMP-1, MMP-8 and MMP-9 concentrations than the remaining exudates. There was no correlation between MMP and TIMP levels in plasma and pleural fluid in this group of effusions. In parapneumonic effusions, MMP-1, MMP-8 and MMP-9 showed a positive correlation with the inflammatory markers and with u-PA and PAI-1. Moreover, there was a relationship between MMP-8 concentration in pleural fluid and pleural thickening at the end of treatment. In conclusion, elevated metalloproteinase-1, -8 and -9 expression was found in parapneumonic pleural effusions. These metalloproteinases could be implicated in the local inflammatory response existing in this group of effusions.     

Pleural effusions on the intensive care unit; Hidden morbidity with therapeutic potential

Despite 50–60% of intensive care patients demonstrating evidence of pleural effusions, there has been little emphasis placed on the role of effusions in the aetiology of weaning failure. Critical illness and mechanical ventilation lead to multiple perturbations of the normal physiological processes regulating pleural fluid homeostasis, and consequently, failure of normal pleural function occurs. Effusions can lead to deleterious effects on respiratory mechanics and gas exchange, and when extensive, may lead to haemodynamic compromise. The widespread availability of bedside ultrasound has not only facilitated earlier detection of pleural effusions but also safer fluid sampling and drainage. In the majority of patients, pleural drainage leads to improvements in lung function, with data from spontaneously breathing individuals demonstrating a consistent symptomatic improvement, while a meta‐analysis in critically ill patients shows an improvement in oxygenation. The effects on respiratory mechanics are less clear, possibly reflecting heterogeneity of underlying pathology. Limited data on clinical outcome from pleural fluid drainage exist; however, it appears to be a safe procedure with a low risk of major complications. The current level of evidence would support a clinical trial to determine whether the systematic detection and drainage of pleural effusions improve clinical outcomes.