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PubMed2005

Etiology and prognostic significance of massive pleural effusions.

It has been stated that malignancy is the most common aetiology of massive pleural effusions. To determine the most frequent causes of massive pleural effusions and to assess the diagnostic yield of different diagnostic procedures and survival, we prospectively studied 1084 patients with pleural effusion. Massive pleural effusions were identified in 121 of 1084 patients (11.2%). Compared with non-massive pleural effusions, massive pleural effusions were significantly more likely to be malignant (53.7% vs. 38.3%, P=0.03) or secondary to cirrhosis (9.9% vs. 2.6%, P=0.0000). On the other hand, massive pleural effusions were significantly less likely to be secondary to infection (10.7% vs. 19.2%, P=0.003) or congestive heart failure (0.8% vs. 6.7%, P=0.03). There was a significant increase in the yield of diagnostic studies in patients with massive malignant pleural effusions (56.9% for cytological studies and 36.9% for biopsies). On the other hand, there was no difference in the diagnostic yield of microbiological and histological studies in the group of tuberculous pleural effusions. In our study population, patients with non-massive malignant pleural effusions had a significantly better survival than those with massive malignant pleural effusions, with a median survival of 8 months (95% confidence interval, 7-9) compared with 5 months (95% confidence interval, 4-6) (P=0.0009). We conclude that malignancy is the most common cause of a massive exudative effusion. Massive malignant pleural effusions are associated with worse survival, independent of age and histologic subgroup, than are non-massive malignant pleural effusions.

Adult↗
PubMed2000

E-cadherin and alpha-, beta-, and gamma-catenin protein expression is up-regulated in ovarian carcinoma cells in serous effusions.

The aims of this study were firstly, to investigate the expression of E-cadherin complex proteins in ovarian carcinoma cells in serous effusions and in primary and metastatic lesions; and secondly to study the value of these four proteins and calretinin, a mesothelial marker, in the differential diagnosis of ovarian carcinoma cells from reactive mesothelial cells in effusions. Sixty-seven malignant effusions and 97 corresponding primary (n=36) and metastatic (n=61) lesions were immunohistochemically stained for E-cadherin and alpha-, beta-, and gamma-catenin. Staining extent and intensity were scored. Effusion specimens were additionally analysed for calretinin immunoreactivity. Membrane immunoreactivity for E-cadherin and alpha-, beta-, and gamma-catenin was detected on carcinoma cells in the majority of the effusions, but rarely on reactive mesothelial cells (p<0.001 for all markers). Calretinin immunoreactivity was confined to mesothelial cells (p<0.001). An association was seen between E-cadherin and alpha-catenin expression, in both effusions and solid tumours, and for beta-catenin in solid tumours (range p<0. 001 to p=0.014). Up-regulation of all four cadherin complex proteins was seen in carcinoma cells in effusions, when compared with corresponding primary tumours (range p<0.001 to p=0.028). As with effusions, metastatic lesions showed up-regulation of alpha-, beta-, and gamma-catenin when compared with primary carcinomas (p=0.002-0. 015). Carcinoma cells in effusions showed in addition elevated levels of E-cadherin when compared with metastatic lesions (p<0.001). Staining results in effusions showed no association with effusion site, tumour type or histological grade. Immunoblotting on 29 malignant effusions confirmed the presence of all four proteins in the majority of samples and co-precipitation of E-cadherin and beta-catenin was seen in ten specimens examined. E-cadherin complex proteins are widely expressed in ovarian carcinoma cells. Together with calretinin, they form a powerful battery of markers for the cytological diagnosis of carcinoma cells in effusions. The up-regulation of E-cadherin complex proteins in serous effusions and metastatic lesions may mark an early metastatic phenotype and possibly mediates survival of tumour cells at these sites through the inhibition of apoptosis.

Ascitic Fluid↗
PubMed1991

Assessment of experimental pericardial effusion using nuclear magnetic resonance imaging techniques.

An experimental canine model of pericardial effusion was designed to validate previous clinical nuclear magnetic resonance imaging (NMR) studies. Saline (n = 7), serum (n = 4), blood (10% hematocrit [n = 5]; 20% hematocrit [n = 5]), and lipid (n = 4) effusions were chosen to resemble: (1) transudative/exudative, (2) nonhemorrhagic/hemorrhagic, and (3) chylous effusions, respectively. There was a linear correlation between the infused volume and the pericardial/epicardial distance measurements on the nuclear magnetic resonance images. Hemorrhagic and nonhemorrhagic exudative effusions were distinguished from transudative effusions by the low signal intensity of transudative effusions images obtained at a TR (repetition time) of 400 and 800 msec. Nonhemorrhagic effusions had significantly lower effusion-to-myocardial signal intensity ratio at TR of 400 msec than did hemorrhagic effusions. Differences in hematocrit were not appreciated qualitatively or quantitatively. Compared with other effusion types, only chylous effusions were hyperintense to myocardium at a TR of 400 msec. Chylous effusions were further uniquely characterized by a decreasing effusion-to-myocardial signal intensity ratio with increasing TR. These experimental findings corroborate the findings of earlier clinical reports and suggest that NMR can provide important assistance in the evaluation of pericardial effusions.

Animals↗
PubMed1990

Pericardial effusion after cardiac surgery in children and effects of aspirin for prevention.

Seventy-four children aged 0.3 to 21.4 years (median 4.0) were followed echocardiographically on days 4, 7, 14 and 28 (+/- 2 days) after cardiac surgery to evaluate the incidence of postoperative pericardial effusion, to identify the patients at greatest risk of developing an effusion and to evaluate the use of aspirin as prophylaxis against pericardial effusion. Pericardial effusion was graded relative to the size of the aortic root from grade 0 (no effusion) to grade 5 (larger than the aortic root dimension). Patients were randomly divided into 2 groups: group 1 (32 patients) received aspirin 60 mg/kg/day for 7 days starting on the third postoperative day; group 2 (42 patients) received no aspirin. Forty-eight patients (65%) developed an effusion during the study period, 3 required pericardiocentesis and 1 died of tamponade. All patients with tamponade had a grade 4 effusion. Age or type of operation did not alter the cumulative incidence of significant effusion. No patient with a grade 0 effusion on the first echocardiogram developed a grade 4 or 5 effusion. Results in groups 1 and 2 were similar. Pericardial effusions are common in the first month after cardiac surgery. Patients with no effusion in the immediate postoperative period appear to be at lesser risk of developing a grade 4 effusion in the first month after operation. Finally, aspirin prophylaxis against postoperative pericardial effusions did not significantly alter the outcome in this small series of patients.

Adolescent↗
PubMed1997

Trace elements in pleural effusions.

When the secretion of pleural fluids exceeds their resorption, liquid (pleural effusion ) will accumulate between the visceral and parietal pleura. Pleural effusions derived from the liquid components of blood are expected to contain trace elements and may, as a sink for trace elements, deprive the body of needed essential elements upon their removal by medical intervention. Consequently, patients may be at risk of drifting into trace-element deficiencies. Because the literature is almost devoid of data about trace elements in effusions, the concentrations of 14 trace elements (Ba, Ca, Cd, Co, Cs, Cu, Mg, Mn, Mo, Pb, Rb, Sn, Sr, Zn) were determined simultaneously by inductively-coupled argon-plasma mass spectrometry (ICP-MS) in effusions from 17 patients. The median values for the concentrations of Rb (209 microgram/kg, range 104-334 microgram/kg) and Cs (1.5 micrograms/kg, range 0.8-2.4 microgram/kg) in the effusions were almost the same as in the sera. The concentrations of Mg (range 15-22 mg/kg), Ca range 52-91 mg/kg), Sr (range 12-37 micrograms/kg), and Ba (range 1.4-18.2 micrograms/kg) were consistently lower in the effusions than in the sera by 18% for Mg, 26% Ca 14% for Sr, and 88% for Ba (percentages based on median in serum as 100%). The concentrations of the essential trace elements Co (range 0.16-0.5 microgram/kg), Cu (130-902 micrograms/kg), Mn (0.2-2.2 micrograms/kg), Mo (0.4-1.5 micrograms/kg), Sn (0.4-1.2 micrograms/kg), and Zn (27-1931 micrograms/kg) in the effusions are generally lower (25-55% based on median) than in the corresponding sera, although a few effusions have higher concentrations of Co, Mn Mo, or Zn than in the sera. The concentrations of Cd (range 0.2-0.5 microgram/kg) in the effusions were approximately the same as in the sera for three patients, considerably lower than in the sera for four patients, and considerably higher for three patients. The concentrations for lead (range 0.6-45 micrograms/kg) in the effusions were generally much higher than in the sera. The effusions were not significantly contaminated with lead-rich erythrocytes. The concentrations of Ca, Cu, and Zn in the effusions correlated positively with the protein concentrations in the effusions. One kilogram of the effusions contain from 10-30% of the trace elements present in the entire volume of serum in circulation.

Adult↗
PubMed2004

Altered expression and activation of the nerve growth factor receptors TrkA and p75 provide the first evidence of tumor progression to effusion in breast carcinoma.

The aim of this study was to characterize phenotypic alterations along the progression of breast carcinoma from primary tumor to pleural effusion through analysis of the expression of nerve growth factor (NGF) and its receptors phospho-TrkA (p-TrkA activated receptor) and p75. Sections from 42 malignant pleural effusions from breast cancer patients and 65 corresponding solid tumors (34 primary, 31 metastatic) were evaluated for protein expression of the activated p-TrkA receptor. The majority of lesions were additionally studied for NGF and p75 expression. Six effusions and four breast carcinoma cell lines were studied for expression of p-TrkA using immunoblotting (IB). Membrane expression of p-TrkA was high in carcinoma cells in effusions (39/42, 93%) and locoregional recurrences (12/13, 92%), with significantly lower expression in both primary tumors (14/34, 41%) and lymph node metastases (8/18, 44%), respectively (p < 0.001 for effusions vs. primary tumors; p = 0.001 for effusions vs. lymph nodes). In contrast, p75 expression was less frequent in effusions compared to both primary tumors and lymph node metastases, significantly so for the latter (p = 0.019). NGF expression was comparable at all sites, but its expression in tumor cells in effusions (7/21 cases) was limited to cases in which time to progression (TTP) to effusion occurred within 5 years or less from primary operation. In univariate analysis of survival, mean and median TTP were 6.3 and 6 years for NGF-negative effusions, compared to 3 and 4 years for NGF-positive cases (p = 0.013). IB confirmed expression of p-TrkA in five of six effusions, while all four breast cancer cell lines were p-TrkA-negative. Our data provide the first documented evidence of molecular events that occur along tumor progression of breast carcinoma from primary tumors to effusion. The almost universal expression of p-TrkA in cancer cells in effusions and late recurrences is in full agreement with our recent report linking this factor with poor prognosis in ovarian cancer. Furthermore, the rapid progression to effusion in cases showing NGF expression in tumor cells underscores the aggressive clinical behavior of tumors that are able to utilize this pathway in an autocrine manner.

Adult↗
PubMed2003

Infection of mesothelial cells with human herpes virus 8 in human immunodeficiency virus-infected patients with Kaposi's sarcoma, Castleman's disease, and recurrent pleural effusions.

Recurrent pleural effusions are common complications of hospitalized patients with human immunodeficiency virus (HIV) infection and may pose difficult diagnostic dilemmas. A common cause of recurrent pleural effusions in up to 30% of HIV-seropositive patients is pulmonary involvement by Kaposi's sarcoma, a human herpesvirus 8 (HHV 8)-related neoplasm. The pathogenesis of these effusions is unclear. These recurrent effusions, although benign, have shown significant mesothelial atypia/reactive changes of uncertain etiology. We attempted to evaluate these effusions morphologically and molecularly for the presence of HHV 8, with particular attention to mesothelial cells. All recurrent pleural effusions, as defined by any effusion tapped for cytological examination on more than two occasions, in HIV-positive patients at the National Institutes of Health were examined from 1998 to the present. Cases were stratified according to patients with and without histologically confirmed HHV 8 disease manifestations. Five patients with HHV 8 diseases (four with disseminated Kaposi's sarcoma and one with Castleman's disease) were identified. As a control group, five effusions from HIV-seropositive patients without known HHV 8-related diseases were identified. Cytological examination of effusions in patients with HHV 8-related diseases demonstrated atypical/markedly reactive mesothelial cells accompanied by a polymorphous background of lymphocytes. Molecular studies for B- and T-cell clonality in microdissected whole samples showed no definitive clones in these cases. Conversely, polymerase chain reaction (PCR) studies for the HHV 8 virus was positive in these samples. PCR studies on pure populations of microdissected mesothelial cells from the HHV 8-related effusions were positive for HHV 8 sequences, whereas those from HIV patients with non-HHV 8 related diseases were negative. Immunohistochemistry for HHV 8 (monoclonal antibody to latent nuclear antigen (LNA-1; ORF-73) on cellblock material demonstrated scattered positive mesothelial cells in three of the five cases of HHV 8-associated effusions. HHV 8 has been recently implicated in the pathogenesis of Kaposi's sarcoma and primary effusion lymphoma. Mesothelial cells in recurrent pleural effusions from patients with Kaposi's sarcoma and Castleman's disease appear to be infected with HHV 8. Additional studies need to be done to define the role of mesothelial cell infection in the pathogenesis of these HHV 8-associated effusions and define the prognostic significance.

B-Lymphocytes↗
PubMed1996

Analysis of pleural effusions using flow cytometry.

Flow cytometry allows a rapid and accurate analysis of the cells in serous fluids. The aim of this study was to evaluate the use of flow cytometric analysis in malignant pleural effusions. 26 patients (13 females, 13 males; mean age 52 +/- 19 years; range 16-82) were included in the study. 15 had malignant pleural effusions (7 adenocarcinoma, 2 lymphoma, 2 chronic myeloid leukemia, 1 ovarian carcinoma, 1 small cell lung carcinoma, 1 squamous cell lung carcinoma and empyema, and 1 malignant mesothelioma) with positive cytology. 2 had benign effusions associated with malignancy (1 squamous cell lung carcinoma and congestive heart failure, and 1 neuroblastoma and hypoproteinemia). 9 had benign effusions (3 tuberculosis, 1 congestive heart failure, 3 parapneumonic pleural effusion, 1 benign mesothelioma, and 1 pulmonary embolism). Flow cytometric analysis of pleural effusions revealed an increased DNA index in malignant effusions: 1.32 +/- 0.44 versus 0.88 +/- 0.23 in benign effusions (p < 0.04). The cell cycle distribution of cells such as G1/G0 and S in malignant effusions did not differ from that of benign pleural effusions; however G2+M increased significantly in malignant effusions (p < 0.03). Using analysis of mononuclear immunophenotyping, CD3+, CD4+, and CD8+ cells did not show any significant difference between the two groups. The lymphocyte activation marker CD38 was positive in 57.6 +/- 11.5% of malignant fluid cells and 38.5 +/- 6.2% of benign fluid cells (p < 0.04). The mean carcinoembryonic antigen levels in malignant and benign pleural effusions were 98.7 +/- 157.3 and 0.9 +/- 1.2 ng/ml, respectively (p < 0.03). In conclusion, the results of our study indicate that finding cells with an abnormal DNA content strongly supports the diagnosis of malignant pleural effusions. Additionally, mononuclear cell phenotypes have to be taken into consideration for malignant pleural effusions, particularly activated T cells. We recommend that flow cytometry should be performed if the cytology is equivocal.

Adolescent↗
PubMed1993

Electrocardiographic changes in pericardial effusion.

OBJECTIVE: To investigate the association between ECG changes and the presence of pericardial effusion. BACKGROUND: The ECG changes associated with pericardial effusion described in textbooks are based only on small series of human cases and data from animals. These changes include low QRS voltage, electrical alternans, P wave changes, and T wave inversion. METHODS: All patients who had undergone 2 temporally separate echocardiographic and ECG examinations, with 1 echocardiographic examination indicating the presence and the other indicating the absence of pericardial effusion were identified (n = 46). These patients were age- and sex-matched to 46 patients without effusion (control subjects). Pericardial effusion was classified echocardiographically as small (n = 28), moderate (n = 13), and large (n = 5). The ECG variables were independently measured by two investigators blinded to effusion status. RESULTS: When 2 temporally separate ECGs for 46 patients were obtained in a repeated-measures fashion (1 obtained during the absence and the other during the presence of effusion; median time interval, 1.24 months), only the mean heart rate in patients with sinus rhythm (98 beats per minute increasing to 106 beats per minute) and the percentage of patients with QRS voltage of less than 0.5 mV (10 percent increasing to 22 percent) were associated with the development of effusion. A weak correlation (r = 0.296) was noted between QRS voltage and effusion size. Electrical alternans occurred only in one of the five patients with a large effusion but in no others. In addition, when the ECGs indicating effusion from the 46 patients were compared with the ECGs from their age- and sex-matched control subjects, differences in heart rate (106 beats per minute vs 80 beats per minute, respectively) and small changes in QRS voltage were associated with effusion status. No ECG variable was sensitive for the detection of pericardial effusion. CONCLUSIONS: In both repeated-measures and case-control comparisons, ECG findings are two few, subtle, insensitive, and nonspecific to be useful as indicators of the presence of pericardial effusion.

Adult↗
PubMed1999

Large pleural effusions occurring after coronary artery bypass grafting. Cardiovascular Surgery Associates, PC.

BACKGROUND: Large pleural effusions sometimes occur after coronary artery bypass grafting (CABG), but their characteristics and clinical course are largely unknown. OBJECTIVE: To describe the clinical course and pleural fluid findings in patients with large pleural effusions occurring after CABG. DESIGN: Retrospective case series. SETTING: Tertiary care, university-affiliated, nonprofit teaching hospital. PATIENTS: 3707 patients who had CABG between 1 February 1996 and 1 August 1997. MEASUREMENTS: Chest radiographs were reviewed, and information on pleural fluid findings, pleural effusion treatment, and cardiac surgery was obtained from medical records and a cardiac surgery database. RESULTS: Pleural effusions that occupied more than 25% of the hemithorax were found in 29 patients (0.78%). Seven of the effusions were attributed to congestive heart failure, 2 were attributed to pericarditis, and 1 was attributed to pulmonary embolism. The explanation for the remaining 19 effusions was unclear. All but 2 effusions were predominantly left-sided. Of these 19 effusions, 8 were bloody and 11 were nonbloody. Bloody effusions usually occurred earlier, contained higher lactic acid dehydrogenase levels, and were frequently eosinophilic. Nonbloody effusions tended to be more difficult to manage. CONCLUSIONS: Large pleural effusions may develop in a small proportion of patients after CABG. The cause of many of these effusions is unclear. Most bloody effusions can be managed with one to three therapeutic thoracenteses. Resolution of nonbloody effusions may require anti-inflammatory agents, tube thoracostomy, or intrapleural injection of sclerosing agents.

Aged↗
PubMed2000

Sonography for hip joint effusion in adults with hip pain.

OBJECTIVE: To study the prevalence of ultrasonic hip joint effusion and its relation with clinical, radiological and laboratory (ESR) findings in adults with hip pain. METHODS: Patients (n = 224) aged 50 years or older with hip pain, referred by the general practitioner for radiological investigation, underwent a standardised examination. The distance between the ventral capsule and the femoral neck, an increase in which represents joint effusion, was measured sonographically. Joint effusion was defined in three different ways: "effusion" according to Koski's definition, "major effusion", and "asymmetrical effusion" based on only individual side differences. RESULTS: "Effusion" was present in 80 (38%), "major effusion" in 20 (9%), and "asymmetrical effusion" in 47 (22%) patients. Pain in the groin or medial thigh, pain aggravated by lying on the side, decreased extension/internal rotation/abduction/flexion, painful external rotation, and pain on palpation in the groin showed a significant relation (adjusted for age and radiological osteoarthritis of the hip) with ultrasonic hip joint effusion. "Major effusion" showed a significant relation with an increased ESR. When patients with bilateral pain and increased ESR were excluded, a side difference in the range of motion of extension of the hip was shown to be a good predictor for "asymmetrical effusion" (positive predictive value: 71%, negative predictive value: 80%). CONCLUSION: This study showed a relatively high prevalence of ultrasonic joint effusion in adults with hip pain in general practice. Furthermore the results indicate a relation between joint effusion and clinical signs.

Aged↗
PubMed1997

Pleural effusions in the medical ICU: prevalence, causes, and clinical implications.

OBJECTIVE: To determine the prevalence and causes of pleural effusions in patients admitted to a medical ICU (MICU). DESIGN: Prospective. SETTING: MICU in a tertiary care hospital. PATIENTS: One hundred consecutive patients admitted to the MICU at the Medical University of South Carolina whose length of stay exceeded 24 h had chest radiographs reviewed daily and chest sonograms performed within 10 h of their latest chest radiograph. RESULTS: The prevalence of pleural effusions in 100 consecutive MICU patients was 62%, with 41% of effusions detected at admission. Fifty-seven of 62 (92%) pleural effusions were small. Causes of pleural effusions were as follows: heart failure, 22 of 62 (35%); atelectasis, 14 of 62 (23%); uncomplicated parapneumonic effusions, seven of 62 (11%); hepatic hydrothorax, five of 62 (8%); hypoalbuminemia, five of 62 (8%); malignancy, two of 62 (3%); and unknown, three of 62 (5%). Pancreatitis, extravascular catheter migration, uremic pleurisy, and empyema caused an effusion in one instance each. Heart failure was the most frequent cause of bilateral effusions (13/34 [38%]). When compared with patients who never had effusions during their MICU stay, patients with pleural effusions were older (54+/-2 years, mean+/-SEM, vs 47+/-2 years [p=0.04]), had lower serum albumin concentration (2.4+/-0.1 vs 3.0+/-0.01 g/dL [p=0.002]), higher acute physiology and chronic health evaluation II scores during the initial 24 h of MICU stay (17.2+/-1.1 vs 12+/-1.2 [p=0.010]), longer MICU stays (9.8+/-1.0 vs 4.6+/-0.7 days [p=0.0002]), and longer mechanical ventilation (7.0+/-1.3 vs 1.9+/-0.7 days [p=0.004]). No patient died as a direct result of his or her pleural effusion. Chest radiograph readings had good correlation with chest sonograms (p<0.0001). CONCLUSION: Pleural effusions in MICU patients are common, and most are detected by careful review of chest radiographs taken with the patient in erect or semierect position. When clinical suspicion for infection is low, observation of these effusions is warranted initially, because most are caused by noninfectious processes that should improve with treatment of the underlying disease.

Age Factors↗
PubMed1998

Effusion cytology of renal cell carcinoma.

BACKGROUND: Effusions in patients with renal cell carcinoma are rare; the clinicopathologic features of these patients have not been described fully. METHODS: All effusions from patients with renal cell carcinoma obtained between 1986 and 1997 at the study institution were reviewed. RESULTS: Twelve effusions from 9 patients were benign, and 8 effusions from 7 patients were malignant. Patients with sarcomatoid tumors presented early with benign effusions, and patients with papillary tumors presented later with malignant effusions. Patients with clear cell tumors were intermediate. The majority of patients who developed malignant effusions had tumors that were classified as T3 or higher (according to the American Joint Committee on Cancer) at the time of resection. Tumor cells had abundant clear to vacuolated cytoplasm, large nuclei, and prominent nucleoli. Cells from clear cell and papillary tumors could not be distinguished in effusion specimens unless papillae were present. At last follow-up 13 of 15 patients were dead of disease within 2 years of the onset of effusion (median 24 weeks; range, 1-93 weeks), including 7 of 9 patients with benign effusions. CONCLUSIONS: Malignant effusions due to renal cell carcinoma most commonly occur in patients with papillary and clear cell tumors. Malignant effusions from these two tumor types are difficult to distinguish unless papillae are present. Effusions associated with renal cell carcinoma confer a poor prognosis.

Aged↗
PubMed2006

D-dimer levels in pleural effusions.

INTRODUCTION: D-dimer is a degradation product of cross-linked fibrin. We hypothesized that hemorrhagic pleural effusions would have greater D-dimer levels than non-hemorrhagic pleural effusions, and that persistently bloody effusions would be distinguishable from thoracentesis-induced bloody effusions by the D-dimer level. METHODS: Forty pleural effusions were studied. D-dimer levels (measured by ELISA), red blood cell (RBC) count, white blood cell (WBC) count, lactate dehydrogenase (LDH), and protein level was measured for each effusion. Ten effusions, five non-bloody, and five bloody were studied for each of the following disease states: parapneumonic effusion, congestive heart failure, post-coronary artery bypass grafting, and lung cancer. RESULTS: No significant difference of the D-dimer level was noted between bloody and non-bloody effusions of different disease states (P=0.286). There was no significant difference in the median D-dimer levels between all the bloody and all the non-bloody effusions (P=0.88). There was no significant difference (P=0.51) in D-dimer levels between five diseases groups when the bloody and non-bloody fluids were combined. The D-dimer levels did not correlate with the RBC count (r=0.11, P=0.48), WBC count (r=0.13, P=0.53), LDH (r=0.01, P=0.93), or protein levels (r=-0.01, P=0.93) in any of the groups. CONCLUSION: Measurement of pleural fluid D-dimer levels does not distinguish persistently bloody effusions from non-bloody effusions, and does not aid in narrowing the differential diagnosis of an effusion.

Coronary Artery Bypass↗
PubMed2000

Clinical clues to the causes of large pericardial effusions.

PURPOSE: To examine whether the size of the effusion, the presence of tamponade, and inflammatory signs are useful in determining the causes of moderate or severe pericardial effusions. SUBJECTS AND METHODS: All echocardiograms performed at a general hospital between January 1990 and April 1996 were screened for pericardial effusion. Patients with moderate (echo-free space of 10 to 20 mm during diastole) or severe (echo-free space >20 mm) effusions were studied. RESULTS: We identified 322 patients (166 [52%] men, mean [+/- SD] age 56 +/- 17 years [range 15 to 88 years]), 132 (41%) with moderate and 190 (59%) with severe pericardial effusion. The most frequent etiologic diagnoses were acute idiopathic pericarditis (n = 66 [20%]), iatrogenic effusions (n = 50 [16%]), cancer (n = 43 [13%]), and chronic idiopathic pericardial effusion (n = 29 [9%]). In 192 (60%) of the patients, the cause of the effusion was a known medical condition. In the 130 other patients, inflammatory signs were associated with acute idiopathic pericarditis (likelihood ratio = 5. 4, P < 0.001), severe effusions without inflammatory signs or tamponade were associated with chronic idiopathic pericardial effusion (likelihood ratio = 20, P < 0.001), and tamponade without inflammatory signs was associated with malignant effusions (likelihood ratio = 2.9, P < 0.01). CONCLUSIONS: In many patients, pericardial effusions are due to a known underlying disease or condition. In patients without underlying diseases, inflammatory signs, the size of effusion, and the presence or absence of cardiac tamponade can be helpful in establishing cause.

Acute Disease↗
PubMed2003

Transforming growth factor beta-1 level in pleural effusion.

OBJECTIVE: Transforming growth factor-beta1 is an important immunomodulator. The diagnostic role of TGF-beta1 has not been systematically investigated in pleural effusion. METHODOLOGY: A prospective clinical study of 45 patients (23 men, 22 women; mean age 49 +/- 21 years) with pleural effusion was performed. Of these patients, 19 had malignant pleural effusion, 14 had tuberculous pleural effusion, seven had empyema/parapneumonic pleural effusion, and five had transudative pleural effusion due to congestive heart failure. The concentrations of TGF-beta1 were measured by ELISA in all pleural fluid samples and in serum samples only from patients with malignant and tuberculous pleural effusions. RESULTS: The median TGF-beta1 levels of malignant, tuberculous and empyema/parapneumonic pleural effusions were 7.25 ng/mL, 7.81 ng/mL, and 9.75 ng/mL, respectively. There was no significant difference between them. The median TGF-beta1 level was 5.62 ng/mL in the transudate pleural effusion group and it was significantly lower than that in the empyema/parapneumonic group (P < 0.05). The pleural fluid TGF-beta1 levels did not correlate with cell profiles of the pleural fluid. The median serum TGF-beta1 levels in malignant and tuberculous pleural effusion groups were 7.38 ng/mL and 7.38 ng/mL, respectively. There was no significant difference between the levels of TGF-beta1 in paired samples of serum and pleural fluid. CONCLUSIONS: This study shows that TGF-beta1 concentrations in exudative pleural effusions are higher than those in transudative effusions secondary to congestive heart failure but TGF-beta1 concentrations do not assist in differentiating exudative effusions.

Adult↗
PubMedDate not supplied

The bacteriology and cytology of chronic otitis media with effusion.

The bacteriology and cytology of middle ear effusion from 729 children with persistent otitis media with effusion were studied. Thirty-five percent of these chronic effusions were culture-positive. Type b and non-type b Haemophilus influenzae, Streptococcus pneumoniae, Neisseria sp. and Staphylococcus epidermidis were the predominant isolates. Serous and mucoid effusion cultures yielded bacteria more often in younger than in older children. In addition bacteria were seen in 17% of the Gram-stained smears of the sterile effusions; Gram-positive cocci predominated in these effusions. Disparate effusion culture results were obtained in 32% of bilateral otitis media cases. Effusions which yielded H. influenzae and S. pneumoniae on culture had more polymorphonuclear leukocytes than did effusions which yielded S. epidermidis or Neisseria or were sterile. Phagocytic cells were equally prevalent in sterile effusions with or without bacteria on Gram stain. Phagocytic cells were seen less often in mucoid effusions from antibiotic-treated patients than in mucoid effusions from untreated patients. The results suggest that certain bacteria in chronic middle ear effusion contribute to the pathogenesis of this condition by eliciting a local inflammatory cell response.

Age Factors↗
PubMed2005

Distribution of pleural effusion in congestive heart failure: what is atypical?

OBJECTIVES: This study was performed to determine the distribution of pleural effusion between the right and left hemithorax in patients with uncomplicated congestive heart failure, and to determine whether left-sided pleural effusion actually constitutes an atypical distribution in congestive heart failure. METHODS: The study group consisted of 120 consecutive patients with both clinical and radiographic evidence of uncomplicated congestive heart failure, and whose chest radiographs at the time of presentation also showed evidence of pleural effusion. The presence or absence of pleural effusion in the right and left hemithorax was recorded for each case, as was the size of each pleural effusion, and the distribution of pleural effusion in these 120 patients was entered into a 2 x 2 table and analyzed by chi2 analysis. RESULTS: There were 207 total pleural effusions, with 105 on the right and 102 on the left. Isolated right-sided pleural effusions occurred in 18 patients, there were bilateral pleural effusions larger on the right than the left in 25, there were bilateral pleural effusions of roughly equal size on each side in 36, there were bilateral pleural effusions larger on the left side than the right in 26, and there were isolated left-sided pleural effusions in 15. The difference was not statistically significant (chi2 = 0.316; P < or = 1.0). CONCLUSIONS: Left-sided pleural effusion is not an atypical finding in congestive heart failure and is not, in and of itself, an indication for further clinical or imaging evaluation.

Adult↗