Differentiation of Cardiac from Noncardiac Pleural Effusions in Cats using Second-Generation Quantitative and Point-of-Care NT-proBNP Measurements

BACKGROUND: Pleural effusion is a common cause of dyspnea in cats. N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP) measurement, using a first‐generation quantitative ELISA, in plasma and pleural fluid differentiates cardiac from noncardiac causes of pleural effusion. HYPOTHESIS/OBJECTIVES: To determine whether NT‐proBNP measurements using second‐generation quantitative ELISA and point‐of‐care (POC) tests in plasma and pleural fluid distinguish cardiac from noncardiac pleural effusions and how results compare to the first‐generation ELISA. ANIMALS: Thirty‐eight cats (US cohort) and 40 cats (UK cohort) presenting with cardiogenic or noncardiogenic pleural effusion. METHODS: Prospective cohort study. Twenty‐one and 17 cats in the US cohort, and 22 and 18 cats in the UK cohort were classified as having cardiac or noncardiac pleural effusion, respectively. NT‐proBNP concentrations in paired plasma and pleural fluid samples were measured using second‐generation ELISA and POC assays. RESULTS: The second‐generation ELISA differentiated cardiac from noncardiac pleural effusion with good diagnostic accuracy (plasma: sensitivity, 95.2%, specificity, 82.4%; pleural fluid: sensitivity, 100%, specificity, 76.5%). NT‐proBNP concentrations were greater in pleural fluid (719 pmol/L (134–1500)) than plasma (678 pmol/L (61–1500), P = 0.003), resulting in different cut‐off values depending on the sample type. The POC test had good sensitivity (95.2%) and specificity (87.5%) when using plasma samples. In pleural fluid samples, the POC test had good sensitivity (100%) but low specificity (64.7%). Diagnostic accuracy was similar between first‐ and second‐generation ELISA assays. CONCLUSIONS AND CLINICAL IMPORTANCE: Measurement of NT‐proBNP using a quantitative ELISA in plasma and pleural fluid or POC test in plasma, but not pleural fluid, distinguishes cardiac from noncardiac causes of pleural effusion in cats

Dynamic and volumetric variables reliably predict fluid responsiveness in a porcine model with pleural effusion

Background: The ability of stroke volume variation (SVV), pulse pressure variation (PPV) and global end-diastolic volume (GEDV) for prediction of fluid responsiveness in presence of pleural effusion is unknown. The aim of the present study was to challenge the ability of SVV, PPV and GEDV to predict fluid responsiveness in a porcine model with pleural effusions. Methods: Pigs were studied at baseline and after fluid loading with 8 ml kg−1 6% hydroxyethyl starch. After withdrawal of 8 ml kg−1 blood and induction of pleural effusion up to 50 ml kg−1 on either side, measurements at baseline and after fluid loading were repeated. Cardiac output, stroke volume, central venous pressure (CVP) and pulmonary occlusion pressure (PAOP) were obtained by pulmonary thermodilution, whereas GEDV was determined by transpulmonary thermodilution. SVV and PPV were monitored continuously by pulse contour analysis. Results: Pleural effusion was associated with significant changes in lung compliance, peak airway pressure and stroke volume in both responders and non-responders. At baseline, SVV, PPV and GEDV reliably predicted fluid responsiveness (area under the curve 0.85 (p<0.001), 0.88 (p<0.001), 0.77 (p = 0.007). After induction of pleural effusion the ability of SVV, PPV and GEDV to predict fluid responsiveness was well preserved and also PAOP was predictive. Threshold values for SVV and PPV increased in presence of pleural effusion. Conclusions: In this porcine model, bilateral pleural effusion did not affect the ability of SVV, PPV and GEDV to predict fluid responsiveness

Myelomatous Pleural Effusion

ABSTRACT Multiple myeloma (MM) is a common hematologic malignancy. Pleural effusion is a rare presenting feature of multiple myeloma which carries a poor prognosis. Few cases of multiple myeloma with pleural involvement have been reported in the medical literature. We report a patient with MM diagnosed by cytologic examination of pleural fluid. Our patient was a 64- year old man with multiple myeloma who was receiving chemotherapy. He had developed dry coughs and exertional dyspnea about a month prior to the admission. Radiographic examination showed left pleural effusion with mediastinal shift to the opposite side. Diagnostic thoracentesis of pleural fluid was performed for the patient. Pathologic examination of pleural fluid showed plasmocytes and plasmablast type mononuclear cells with atypical nuclei, consistent with the diagnosis of pleural effusion due to multiple myeloma. In view of multiple etiologies of pleural effusion in malignant diseases, rare etiologies should also be considered in order to treat the effusion appropriately. (Tanaffos 2007; 6(2): 68-72) Key words: Multiple myeloma, Pleural effusion, Plasmablas

Bacterial Infection Elicits Heat Shock Protein 72 Release from Pleural Mesothelial Cells

Heat shock protein 70 (HSP70) has been implicated in infection-related processes and has been found in body fluids during infection. This study aimed to determine whether pleural mesothelial cells release HSP70 in response to bacterial infection in vitro and in mouse models of serosal infection. In addition, the in vitro cytokine effects of the HSP70 isoform, Hsp72, on mesothelial cells were examined. Further, Hsp72 was measured in human pleural effusions and levels compared between non-infectious and infectious patients to determine the diagnostic accuracy of pleural fluid Hsp72 compared to traditional pleural fluid parameters. We showed that mesothelial release of Hsp72 was significantly raised when cells were treated with live and heat-killed Streptococcus pneumoniae. In mice, intraperitoneal injection of S. pneumoniae stimulated a 2-fold increase in Hsp72 levels in peritoneal lavage (p<0.01). Extracellular Hsp72 did not induce or inhibit mediator release from cultured mesothelial cells. Hsp72 levels were significantly higher in effusions of infectious origin compared to non-infectious effusions (p<0.05). The data establish that pleural mesothelial cells can release Hsp72 in response to bacterial infection and levels are raised in infectious pleural effusions. The biological role of HSP70 in pleural infection warrants exploration

Is Adenosine Deaminase in Pleural Fluid a Useful Marker for Differentiating Tuberculosis from Lung Cancer or Mesothelioma in Japan, a Country with Intermediate Incidence of Tuberculosis?

The objective of this study was to evaluate the utility of the determination of adenosine deaminase (ADA) level in pleural fluid for the differential diagnosis between tuberculous pleural effusion (TPE) and malignant pleural effusion (MPE) in Japan, a country with intermediate incidence of tuberculosis (TB). We retrospectively reviewed the clinical records of 435 patients with pleural effusion and investigated their pleural ADA levels as determined by an auto analyzer. ROC analysis was also performed. The study included patients with MPE (n＝188), TPE (n＝124), benign nontuberculous pleural effusion (n＝94), and pleural effusion of unknown etiology (n＝29). The median ADA level in the TPE group was 70.8U/L, which was significantly higher than that in any other groups (p＜0.05). The area under the curve (AUC) in ROC analysis was 0.895. With a cut-off level for ADA of 36U/L, the sensitivity, specificity, positive predictive value, and negative predictive value were 85.5%, 86.5%, 69.7%, and 93.6%, respectively. As many as 9% of patients with lung cancer and 15% of those with mesothelioma were false-positive with this ADA cutoff setting. Although the ADA activity in pleural fluid can help in the diagnosis of TPE, it should be noted that some cases of lung cancer or mesothelioma show high ADA activity in geographical regions with intermediate incidence of TB, in contrast to high prevalence areas

Role of Pleural Fluid Cholesterol in Pleural Effusion

Pleural effusion occurs when formation and accumulation of pleural fluid exceeds its absorption. It indicates an imbalance between pleural fluid formation and its removal. Pleural fluid accumulates in settings of increased hydrostatic pressure, increased vascular permeability, decreased oncotic pressure, increased intrapleural negative pressure and decreased lymphatic drainage. On the basis of pathophysiology, pleural effusion can be transudates or exudates. It is important to establish an accurate etiological diagnosis so that the patient may be treated in a rational manner. Using Light’s criteria may need other extra investigations to differentiate transudates and exudates but using pleural fluid cholesterol (pCHOL) will help to diagnose them with only the pleural fluid analysis. Moreover the albumin or protein gradient will need serum as well as the pleural fluid investigations and will have more financial burden than just investigating pleural fluid cholesterol. Pleural cholesterol is thought to be derived from degenerating cells and vascular leakage from increased permeability. Thus pleural fluid cholesterol is one of the important investigations that can distinguish exudates from transudates. Routine use of pleural fluid cholesterol for classifying pleural effusion should be encouraged to improve the accuracy, sensitivity and specificity

Microbiome profile associated with malignant pleural effusion.

INTRODUCTION:There is ongoing research into the development of novel molecular markers that may complement fluid cytology malignant pleural effusion (MPE) diagnosis. In this exploratory pilot study, we hypothesized that there are distinct differences in the pleural fluid microbiome profile of malignant and non-malignant pleural diseases. METHOD:From a prospectively enrolled pleural fluid biorepository, samples of MPE were included. Non-MPE effusion were included as comparators. 16S rRNA gene V4 region amplicon sequencing was performed. Exact Sequence Variants (ESVs) were used for diversity analyses. The Shannon and Richness indices of alpha diversity and UniFrac beta diversity measures were tested for significance using permutational multivariate analysis of variance. Analyses of Composition of Microbiome was used to identify differentially abundant bacterial ESVs between the groups controlled for multiple hypothesis testing. RESULTS:38 patients with MPE and 9 with non-MPE were included. A subgroup of patients with metastatic adenocarcinoma histology were identified among MPE group (adenocarcinoma of lung origin (LA-MPE) = 11, breast origin (BA-MPE) = 11). MPE presented with significantly greater alpha diversity compared to non-MPE group. Within the MPE group, BA-MPE was more diverse compared to LA-MPE group. In multivariable analysis, ESVs belonging to family S24-7 and genera Allobaculum, Stenotrophomonas, and Epulopiscium were significantly enriched in the malignant group compared to the non-malignant group. CONCLUSION:Our results are the first to demonstrate a microbiome signature according to MPE and non-MPE. The role of microbiome in pleural effusion pathogenesis needs further exploration

Pneumothorax, pneumomediastinum and subcutaneous emphysema following closed percutaneous pleural biopsy: a case report

Minimally invasive investigations, such as pleural fluid cytological assessment and closed percutaneous pleural biopsy, are often performed first in the investigation of suspected malignant pleural effusions. Malignant pleural effusions can be diagnosed with pleural fluid cytology alone in most cases; however, closed pleural biopsy is performed to increase the diagnostic yield when pleural fluid cytology is negative. This additional yield is at the expense of increased complication rates. We report a 64-year old man with a negative pleural fluid cytology but suspected malignant pleural effusion who underwent a closed pleural biopsy, which was complicated by pneumothorax, pneumomediastinum and severe subcutaneous emphysema. Pulmonary laceration by the pleural biopsy needle is the most likely aetiology of these complications. Our case report highlights an infrequent but significant complication of closed percutaneous pleural biopsy

Report of results of pleural biopsy (Needle biopsy and open biopsy) in 108 cases and 245 biopsies

1. The results of 245 pleural biopsies perfomed in 108 patients including 219 pleural needle biopsies and 26 pleural open biopsies were reported. The method of pleural biopsy seems to be superior to any other currently available diagnostic procedures for the etiological diagnosis of pleurisy. 2. When the pleural needle biopsy is compared with the pleural open biopsy, the former method has definite advantages over the open biopsy. The pleural needle biopsy is simple, repeatable and has almost no complication. The method of pleural needle biopsy is the initial method of choice as Donohoe correctly stated and should be employed in every cases of the pleurisy to confirm the etiological diagnosis. The open biopsy should be reserved only for those cases in whom the needle biopsy had not proved satisfactory. 3. Utilizing the method of needle biopsy, the pathological diagnosis was made in 86 per cent of our cases at the initial biopsy. By repeated needle biopsies, the results have improved to 91-92 per cent. 4. Most of the failures of the pleural needle biopsy were noted at the early stage of the study due to the unfamiliarity of the biopsy technique and later due to the incooperation of the patients. 5. The presence of the free pleural fluid serves as a convenient guide for the performance of the needle biopsy but successful needle biopsy was easily done without presence of pleural fluid when there is adequate pleural thickening. 6. 63-75 per cent of our diagnosed cases were proved to have granulomatous pleuritis, 13-31 per cent non-specific pleuritis and 5.4-5.8 per cent eosinophilic pleuritis due to paragonomiasis. The distribution of this pathological diagnosis seems to reflect quite well the actual picture of incidences of pleurisy of various different etiology in young adults in Korea. 7. The relationship of the success in obtaining adequate tissue by needle biopsy and interval between onset of symptom and biopsy was discussed. It was found that the interval has no significant effect on the production of adequate tissue by needle biopsy if the time elapsed is 4 weeks or more from the onset of symptom. 8. The significance of the pathological findings of ranulomatous pleuritis at one biopsy and non-specific pleuritis at another biopsy in the same patient was discussed. It is concluded that the single finding of nonspecific pleuritis at one needle biopsy cannot rule out the presence of granulomatous pleuritis and it is recommended that pleural biopsy be repeated whenever necessary. 9. The diagnostic significance of the chemical analysis of the pleural fluid was discussed in correlation with the results of the pleural needle biopsies. It is concluded that the number of examinations are not quite sufficient to draw any definite conclusion at the present stage of our study. 10. The finding of sanguinous pleural fluid in the patient of granulomatous pleuritis is quite high (72.7 %) and it was found that the sanguinous pleural fluid was most frequently found in the patients with granulomatous pleuritis in non-cancerous age. 11. Two groups of pleurisy patients with or without parenchymal lung lesion on chest X-ray were discussed in correlation with the results of the needle biopsy. It was found that the incidence of the pathological evidence of granulomatous inflammation on the biopsy specimens in these two groups is almost the same regardless of the presence of the demonstrable parenchymal lung lesion. 12. Histopathological finding of granulomatous pleuritis was discussed in conjunction with the significance of two types of tubercles, the soft tubercles and hard tubercles. In all specimens diagnosed as granulomatous pleuritis granulomas were demonstrated ranging from large, conglomerate tubercles with central caseation or giant cells to small granulomas without central caseation or Langhans' giant cells. 13. Histopathological significance of the finding of non-specific pleuritis on the biopsy specimens was discussed and the existence of a specific entity of &#34;non-specific pleuritis&#34; which is equivalent to the non-specific inflammation of the pericardium. 14. Cases of pleurisy due to paragonomiasis were discussed and the need of specific attention for search of new cases was emphasized.</p