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Postural changes in pleural fluid constituents.

Measurement of pleural fluid constituents (pH, PCO2, protein, lactic dehydrogenase [LDH], glucose, red blood cells [RBC], and white blood cells [WBC]) are of value in the diagnosis of pleural effusions and in the separation of exudates from transudates. The position of the patient (sitting or lying) prior to thoracentesis may result in differences in the measurement of these constituents. We found significant postural changes (p < 0.05) in the measurement of pH, protein, LDH, and RBCs in all exudative effusions (n = 12) in the upright sitting position compared with the supine position. No postural changes were noted in the transudative effusions (n = 6). The location of basal pleural tumors and the molecular weight of certain constituents may explain this postural sedimentary effect. Repeated thoracentesis after 30 min in the sitting position may result in exudative values when borderline transudates are found in a patient previously in a supine position.

Aged↗

[Advantages and limitations of chemicomorphological study of pleural fluid].

A chemical-physical and morphological examination of 109 pleural samples taken from 66 patients showed that the most reliable laboratory tests for discriminating between an exudate and transudate were specific gravity, total effusion protein content and the effusion/serum protein ratio, while LDH and cell number seem less important. In the differential diagnosis of pleuritis, pleural fluid amylase assays are important only if certain well-defined diseases are suspected (particularly pancreatitis). In this case the assay is irreplaceable. Glucose assay may be carried out for a wider range of complaints although a review of the literature shows it to be always below 30 mg, particularly in cases of rheumatoid arthritis. A cytological examination offers a pathognomonic guide in the case of tumours and as a back-up to other checks for many other complaints.

Adult↗

Reinvestigation of clinical value of Rivalta reaction of puncture fluid.

Rivalta reaction is still used as a puncture fluid test for differentiation of exudate and transudate. However, the test method of Rivalta reaction has not been standardized, or positive precipitates for the reaction have not been investigated. Thus, we clarified the measurement method, and investigated Rivalta reaction-positive proteins. Rivalta reaction-positive punctuates converted to negative when pH increased to 4.6 or higher, showing the necessity of pH adjustment of acetic acid solution to 3.6-4.2 in Rivalta reaction. Using pH 4.0 acetic acid solution, 8 types of proteins were identified in Rivalta reaction-positive turbid precipitates: C-reactive protein (CRP), alpha1-antitrypsin (alpha1-AT), alpha1-acid glycoprotein (alpha1-AG), haptoglobin (Hp), transferrin (Tf), ceruloplasmin (Cp), fibrinogen (Fg), and hemopexin (Hpx). Since these are acute reactive proteins, or proteins increased in malignant tumors and infections, positivity for Rivalta reaction at the specified pH may suggest pathological inflammation.

C-Reactive Protein↗

[Pleural effusion of non-neoplastic etiology in a patient with a rare form of myeloma].

Pleural effusions can be a manifestation of several nosological entities. Etiologic diagnosis involves a good clinical history, followed by thoracocentesis with pleural biopsy and eventually bronchoscopy or thoracoscopy. The differentiation between transudates and exudates, by the biochemical characteristics of the pleural effusions, can orientate the underlying disorder. It is known that there are more than 35 different etiological entities of exudative pleural effusions. However, pneumonia, malignancies, pulmonary embolism, abdominal disease and tuberculosis are the major causes (around 90%). Transudative effusions are more frequently due to congestive heart failure, renal or hepatic failure. The AA present a clinical situation of pleural effusion, the etiology of which was initially attributed to congestive heart failure, with a good response, clinical and radiological response to the treatment established. However the laboratory alteration persisted (anaemia, renal failure, acute inflammation). The subsequent study showed the existence of a rare syndrome, a Myeloma Ig M lambda that can lead to differential diagnosis with Waldenström's Macroglobulinemia, about which the authors make some theoretical considerations showing the difficulty in etiologic diagnosis of some pleural effusions.

Aged↗

Management of pleural effusions.

This review summarizes current strategies in the treatment of patients with pleural effusion. To determine whether a patient has a transudative or exudative pleural effusion, Light's criteria should be applied to measure the concentrations of protein and lactate dehydrogenase (LDH) in the pleural fluid and serum. If the effusion is transudative, therapy should be directed toward the underlying congestive heart failure, cirrhosis, or nephrosis. Consideration should be given to pleurodesis with a sclerosant if patients with recurrent transudative effusion have severe dyspnea due to their effusion. If the effusion is exudative, attempts should be made to define the etiology. The diagnosis of pleural malignancy is most easily established via pleural fluid cytology. If this is negative and the patient is suspected of having pleural malignancy, thoracoscopy is indicated. The concentrations of adenosine deaminase and gamma-interferon in pleural fluid are useful in the diagnosis of pleural tuberculosis. Patients with pneumonia and pleural effusion should undergo therapeutic thoracentesis; the pleural fluid should be Gram-stained and cultured, and the differential cell count, glucose and LDH concentration, and pH should be determined. Indicators of a poor prognosis include the presence of frank pus, a positive Gram-stain, a pleural glucose concentration of less than 2.2 mmol/L, a pH less than 7.00, the presence of pleural loculations, and an LDH concentration greater than three times the upper limit of normal in serum. If the pleural fluid cannot be completely evacuated because of loculations, intrapleural thrombolytic therapy should be considered. If thrombolytics are ineffective, thoracoscopy or thoracotomy with decortication should be performed. Dyspneic patients with malignant pleural effusions whose dyspnea is relieved with therapeutic thoracentesis should be considered for pleurodesis using a tetracycline derivative. Talc is not recommended because it induces acute respiratory distress syndrome in about 5% of patients, with an overall mortality of 1%.

Biopsy, Needle↗

Diagnostic principles in pleural disease.

When a patient with an undiagnosed pleural effusion is evaluated, the first question to answer is whether the patient has a transudate or an exudate. This is best done using Light's criteria, but these criteria occasionally misidentify a transudate as an exudate. If the patient's pleural fluid meets exudative criteria, but the patient appears clinically to have a transudative effusion, then the serum-pleural fluid albumin gradient should be measured. If this is greater than 1.2 g-dL-1, the patient probably does have a transudative effusion. If the patient has an exudative pleural effusion, additional tests are indicated to determine the aetiology of the effusion. The gross appearance and the odour of the pleural fluid should be noted and samples of all exudates should be sent for bacterial cultures. Laboratory tests that are useful in the differential diagnosis of exudative pleural effusions include: differential white cell count of the pleural fluid; cytology of the pleural fluid; and levels of adenosine deaminase, glucose, amylase and lactate dehydrogenase in the pleural fluid. If pleural tuberculosis is suspected, a needle biopsy of the pleura is indicated. Thoracoscopy is very efficient at diagnosing malignant pleural effusion and tuberculosis pleuritis, but rarely establishes any other diagnosis.

Biopsy, Needle↗

Plasma exudation. Correlation between Evans blue dye and radiolabeled albumin in guinea pig airways in vivo.

We quantified the tissue exudation and luminal transudation of two plasma markers, Evans blue (EB) dye and [125I]-human serum albumin (HSA), into the airways of the anesthetized guinea pig in response to platelet activating factor (PAF). There was a highly significant correlation between the tissue content of EB and [125I]-HSA in all airways studied. Significant correlation for transudation of the two markers was limited to high rates of plasma leakage. [125I]-HSA was the more sensitive marker for the association between exudation and transudation and the effect of PAF on transudation. EB was the better marker for assessing the relationship between the dose of PAF and plasma exudation.

Animals↗

Enhancement of ascites on MRI following intravenous administration of Gd-DTPA.

OBJECTIVE: The enhancement of ascites following intravenous administration of Gd-DTPA on MRI was investigated. MATERIALS AND METHODS: Magnetic resonance imaging was performed in 20 patients with ascites (8 peritoneal carcinomatosis, 2 tuberculous peritonitis, 8 liver cirrhosis, 1 nephrotic syndrome, 1 peritoneal adhesion), and T1-weighted SE images were obtained before and 15-20 min following intravenous administration of Gd-DTPA (0.1 mmol/kg). RESULTS: There were 10 exudative ascites and 10 transudative ascites. Eight of 10 exudative ascites showed enhancement, in contrast to none of 10 transudative ascites. The precontrast signal intensity ratios (SIRs) of exudative ascites were significantly higher (p < 0.05) than those of transudative ascites, and the postcontrast SIRs of exudative ascites were significantly higher (p < 0.01) than those of transudative ascites. This difference was thought to be caused by increased peritoneal permeability and higher protein concentration in the cases with exudative ascites in this study. CONCLUSION: It is concluded that enhancement of ascites on MRI obtained 15-20 min after intravenous administration of Gd-DTPA is not an uncommon finding in exudative ascites (especially associated with peritoneal carcinomatosis).

Ascites↗