Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Effusion”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources

Pleural fluid characteristics of patients with symptomatic pleural effusion after coronary artery bypass graft surgery.

BACKGROUND: This study describes the pleural fluid characteristics of patients who develop symptomatic pleural effusions after coronary artery bypass graft surgery (CABG). METHODS: Post-CABG patients who underwent a therapeutic thoracentesis for a symptomatic pleural effusion were included unless another explanation for the pleural effusion was present. RESULTS: During the study, 71 patients (mean age, 61 years) were identified; 49 were men and 22 were women. All patients underwent internal mammary artery grafting. Early effusions (<30 days after CABG) occurred in 45 patients (63%) and late effusions (>/=30 days after CABG) developed in 26 (37%). Early effusions were bloody (median red blood cell count, 706 x 10(12)/L [706,000 mm(3)])with a high eosinophil count (median, 0.385), whereas effusions that occurred in the late period were yellow exudates with predominant lymphocytes (median, 0.68) and monocytes (median, 0.20). The mean pleural fluid level of lactate dehydrogenase was more than 3 times the upper limit of the reference range in serum in early effusions, whereas late effusions had significantly lower lactate dehydrogenase levels. CONCLUSIONS: Characteristics of early and late effusions differ significantly, suggesting a different pathogenesis of the effusions. Patients who develop a symptomatic pleural effusion after CABG should undergo a therapeutic thoracentesis; however, further investigations are warranted only in patients who have pleural fluid characteristics different from those described.

Aged↗

Evaluation of CT findings for diagnosis of pleural effusions.

Computed tomography studies are usually used to assess patients with pleural effusions, and radiologists should be aware of the significance of different CT findings for the diagnosis of the effusion. The purpose of this study was to evaluate CT findings for etiological diagnosis of pleural effusions. Contrast-enhanced CT of the chest of 211 patients with pleural effusion of definite diagnosis were evaluated. The CT images were evaluated for the presence and extent of pleural effusion, thickening or nodules, extrapleural fat and other changes in the mediastinum or lung. The CT scans were read by two independent observers and correlation between them was evaluated. Comparison of CT findings between benign and malignant effusions, between exudates and transudates, and between empyemas and the other parapneumonic effusions were carried out. Kappa values for most CT findings were > 0.85. Loculation, pleural thickening, pleural nodules, and extrapleural fat of increased density were only present in exudative effusions. Multiple pleural nodules and nodular pleural thickening were the only pleural findings limited to malignant pleural effusions. The signs were also more frequently seen in empyemas than in other parapneumonic effusions. Computed tomography findings can help to distinguish between transudates and exudates. Although there is some overlap between benign and malignant pleural effusions, pleural nodules and nodular pleural thickening were present almost exclusively in the latter. Although differences between CT findings of empyemas and the other parapneumonic effusions exist, there is no finding which can definitely differentiate between them.

Adolescent↗

Incidence and management of pleural effusions after diaphragm peritonectomy or resection for advanced mullerian cancer.

OBJECTIVES: Diaphragm peritonectomy or resection is an effective way to cytoreduce diaphragm disease but frequently results in sympathetic pleural effusions. Our objective was to determine the incidence and management of effusions that developed after diaphragm surgery in patients with advanced mullerian cancer. METHODS: We reviewed the records of all patients with stage IIIC-IV epithelial ovarian, fallopian tube, or peritoneal cancer who had diaphragm peritonectomy or resection as part of optimal primary cytoreduction at our institution from 2000-2003. All patients had preoperative and serial postoperative chest X-rays to detect and follow pleural effusions. Factors evaluated included the presence and size of preoperative and postoperative effusions, their laterality, and subsequent need for thoracentesis and/or chest tube placement for symptomatic effusions. RESULTS: Of the 215 patients who had primary cytoreduction during the study period, 59 (27%) underwent diaphragm peritonectomy or resection. In addition to standard cytoreduction, 31 (53%) of these 59 patients had diaphragm surgery alone, while 28 (47%) had diaphragm surgery in combination with other upper abdominal resections. Laterality of diaphragm surgery was as follows: right only, 43 (73%); left only, 2 (3%); and bilateral, 14 (24%). Intraoperative chest tubes were placed in 7 (12%) patients. In the remaining 12 patients with preoperative effusions, postoperative effusions on the same side as the diaphragm surgery increased in 6 patients (50%), and 3 patients (25%) required postoperative thoracentesis or chest tube. In the remaining 40 patients without preoperative effusions, ipsilateral effusions developed in 24 patients (60%), and 5 patients (13%) required postoperative chest tubes. The overall rate of new or increased ipsilateral effusions was 58%; the overall rate of postoperative thoracentesis or chest tube placement was 15%. In 75% of the patients, thoracentesis or chest tubes were placed within 5 days of surgery (median, 3 days; range, 2-24). CONCLUSIONS: More than half of patients developed ipsilateral pleural effusions after diaphragm peritonectomy for cytoreduction. Most were managed conservatively without requiring a chest tube or thoracentesis. The incidence of symptomatic effusions was not high enough to recommend routine chest tube placement at the time of diaphragm peritonectomy or resection.

Adult↗

Rapid diagnosis of infectious pleural effusions by use of reagent strips.

Reagent strips have not yet been tested for use in the diagnosis of infectious pleural effusions. A reagent strip was used to evaluate 82 patients with pleural effusions: 20 patients had transudative effusions, 35 had infectious exudative effusions (empyema in 14 and parapneumonic effusion in 21), and 27 had noninfectious exudative effusions. Pleural fluid protein, as evaluated by the reagent strip, proved accurate for the detection of exudative effusions (sensitivity, 93.1%; specificity, 50%; positive predictive value, 84.3%; negative predictive value, 71.5%; odds ratio [OR], 6.77; and 95% confidence interval [CI], 1.87-24). The reagent strip leukocyte esterase test effectively detected infectious exudative effusions (sensitivity, 42.8%; specificity, 91.3%; positive predictive value, 88.2%; negative predictive value, 51.2%; OR, 4.46; and 95% CI, 1.2-16.4). Pleural pH was significantly predicted by the reagent strip but was of no assistance in categorization of exudative effusions as infectious or noninfectious. Compared with physical, laboratory, and microbiological data, the reagent strip was as accurate for estimation of percentages of infectious and noninfectious exudative effusions. Thus, reagent strips may be a rapid, easy-to-use, and inexpensive technique for discriminating transudative from exudative pleural effusions and for categorizing exudative pleural effusions as infectious or noninfectious.

Adult↗

New formula for quantification of pleural effusions from computed tomography.

The authors develop a method to accurately and easily estimate the volume of pleural effusions with computed tomography (CT). In 15 patients with either simple or loculated pleural effusions (14 right-sided and 11 left-sided), routine helical CT examinations of the thorax were obtained. Two experienced radiologists visually estimated the volume of the effusions. Three-dimensional reconstructions of the pleural effusions were performed from the helical CT examinations, and the volumes of the effusions were calculated. Effusion volumes were also estimated using the formula d2 x l (d = greatest depth of the effusion on a single CT image, l = greatest length of the effusion). The computer calculated the estimated volumes and they were then statistically compared. The coefficient of correlation between the estimation by measurement and calculated volumes of all effusions was 0.908 (p<0.0001) for the right side, and 0.849 for the left side (p<0.002). Excluding the loculated effusions, the coefficient of correlation was 0.969 for the right side and 0.949 for the left side (p<.001). The volume estimation by visual inspection was also correlated to the calculated volumes (0.84 on the left and 0.85 on the right, p<0.008), but resulted in a consistent overestimation by 300 ml to 500 ml. Although pleural effusion volumes can be estimated by visual inspection with good correlation, some overestimation is consistently seen. Use of the formula d2 x l readily enables estimation of pleural effusion volume from CT, from two simple measurements. This formula-based method of volume estimation provides an accurate and easily measured means of estimation that is readily obtained from routine CT of the chest.

Humans↗

Pleural effusions in systemic amyloidosis.

PURPOSE OF REVIEW: Large, recurrent pleural effusions in systemic amyloidoses are rare but clinically challenging events predominantly affecting patients with primary systemic amyloidosis. Examining the mechanisms by which these effusions form and persist offers perspective on the pathophysiology and basis for therapeutic interventions. RECENT FINDINGS: Between 1977 and 2003, the literature consisted of approximately 21-25 case reports on pleural effusions in systemic amyloidosis. In 2003, Boston University published a retrospective single-center analysis of 35 primary systemic amyloidosis patients with large, refractory pleural effusions. To define the role of cardiomyopathy in large, refractory pleural effusions, the Boston University Amyloid Program compared demographics, pleural fluid chemistries, echocardiographic indices, and renal function measures of the pleural effusion group with data from 120 primary systemic amyloidosis cardiomyopathy patients with no pleural effusions. Neither cardiomyopathy nor nephrotic syndrome explained pleural effusions in primary systemic amyloidosis patients. The large number of exudative effusions supported primary disruption of the pleural surface and its function by amyloid. Disease mechanisms, natural history, and management options are discussed here. SUMMARY: Large pleural effusions in systemic amyloidosis occur most often in primary systemic amyloidosis, predominantly resulting from direct infiltration of the parietal pleural surface. Left atrial hypertension from primary systemic amyloidosis cardiomyopathy contributes to but is not sufficient to form and sustain these effusions. Untreated patients have a median survival of 1.6 months. Secondary, familial, and senile systemic amyloidosis do not infiltrate the pleural surfaces or induce pleural effusions in a clinically significant fashion.

Amyloidosis↗

Prevalence and characteristics of pleural effusions in superior vena cava syndrome.

OBJECTIVE AND BACKGROUND: The prevalence and characteristics of pleural effusions occurring in adults with the superior vena cava (SVC) syndrome are unknown. The purpose of the present study was to characterize these pleural effusions. METHODS: Charts of patients diagnosed with SVC syndrome at a tertiary care referral centre were reviewed. Radiographs were evaluated for the presence and size of pleural effusions, presence and location of masses and mediastinal width. If a pleural effusion was present, the patient's chart and a pre-existing database on pleural effusions were searched to determine whether the effusion was sampled and the results of any laboratory investigations on the fluid. RESULTS: The SVC syndrome occurred in 78 patients. Malignancy was the aetiology in 60% of the cases and bronchogenic carcinoma was the most common malignancy. An intravascular device was the aetiology in the majority of benign cases. Pleural effusion was found in 70% of patients with a malignant aetiology and 58% of those with a benign cause (P=0.345). The mean size of the effusions was larger in malignant cases (P=0.012). Of the 44 effusions 22 were sampled (17 in malignancy and five with benign processes); none was transudates, 20 (91%) were exudative (four of these were chylous) and the remaining two were reported as exudates but did not have pleural chemistries documented. CONCLUSIONS: More than half of patients with SVC syndrome have pleural effusions, regardless of the aetiology. However, the effusions are larger when associated with malignancy. The majority of these effusions are exudative and occasionally chylous. None was transudates.

Adult↗

Lipoprotein analysis in a chyliform pleural effusion: implications for pathogenesis and diagnosis.

A chyliform effusion is an uncommon high lipid pleural effusion that does not result from a leakage of the thoracic duct. Characteristically, it emerges from chronic pleurisy and contains high levels of cholesterol. The origin of this cholesterol is unknown, but it is often attributed to the degeneration of red and white blood cells. In this study we have carried out detailed lipoprotein analyses in a chyliform effusion, a chronic tuberculous effusion and three inflammatory effusions of recent onset, in an attempt to elucidate the process of cholesterol accumulation and possible lipoprotein alterations. Mean cholesterol was 92 mg/dl in the inflammatory exudates and 1,237 mg/dl in the chyliform effusion. In inflammatory effusions of recent onset most cholesterol was bound to low density lipoprotein (LDL) with corresponding apoprotein B levels. The chronic tuberculous exudate showed a shift of cholesterol binding towards high density lipoprotein (HDL). In the chyliform effusion most cholesterol was found in the HDL region. Our results suggest that in acute inflammation, the pleural barrier opens to plasma LDL. We hypothesize that in chronicity this cholesterol becomes trapped in the pleural space and undergoes a change in lipoprotein binding characteristics. In a chyliform effusion, cholesterol further accumulates and builds complexes containing triglycerides and proteins. In clinical routine, total cholesterol values above 200 mg/dl strongly suggest a chyliform effusion. Since triglyceride values may be as high as in chylous effusions (greater than 110 mg/dl), the diagnostic routine in all suspected high lipid effusions should involve cholesterol and triglyceride measurements.

Aged↗

Pericardial effusion in AIDS. Incidence and survival.

BACKGROUND: Although pericardial effusion is known to be common among patients infected with HIV, the incidence of pericardial effusion and its relation to survival have never been described. METHODS AND RESULTS: To evaluate the incidence of pericardial effusion and its relation to mortality in HIV-positive subjects, 601 echocardiograms were performed on 231 subjects recruited over a 5-year period (inception cohort: 59 subjects with asymptomatic HIV, 62 subjects with AIDS-related complex, and 74 subjects with AIDS; 21 HIV-negative healthy gay men; and 15 subjects with non-HIV end-stage medical illness). Echocardiograms were performed every 3 to 6 months (82% had follow-up studies). Sixteen subjects were diagnosed with effusions (prevalence of effusion for AIDS subjects entering the study was 5%). Thirteen subjects developed effusions during follow-up; 12 of these were subjects with AIDS (incidence, 11%/y). The majority of effusions (80%) were small and asymptomatic. The survival of AIDS subjects with effusions was significantly shorter (36% at 6 months) than survival for AIDS subjects without effusions (93% at 6 months). This shortened survival remained significant (relative risk, 2.2, P = .01) after adjustment for lead time bias and was independent of CD4 count and albumin level. CONCLUSIONS: There is a high incidence of pericardial effusion in patients with AIDS, and the presence of an effusion is associated with shortened survival. The development of an effusion in the setting of HIV infection suggests end-stage HIV disease (AIDS).

AIDS-Related Complex↗

Bloody pericardial effusion in patients with cardiac tamponade: is the cause cancerous, tuberculous, or iatrogenic in the 1990s?

STUDY OBJECTIVES: The decrease in incidence of tuberculosis, along with the increase in invasive cardiovascular procedures, may have changed the frequency of causes of bloody pericardial effusion associated with cardiac tamponade, although this is not yet recognized by medical textbooks. We analyzed the causes of bloody pericardial effusion in the clinical setting of cardiac tamponade in the 1990s; patients' survival; the effect of laboratory results on discharge diagnosis; and how often bloody pericardial effusion is a presenting manifestation of a new malignancy or tuberculosis. DESIGN: Retrospective, observational, single-center study. SETTING: A community hospital. PATIENTS: The charts of all patients who underwent pericardiocentesis for cardiac tamponade and had bloody pericardial effusion were retrospectively reviewed. RESULTS: Of 150 patients who had pericardiocentesis for relieving cardiac tamponade, 96 patients (64%) had a bloody pericardial effusion. The most common cause of bloody pericardial effusion was iatrogenic disease (31%), namely, secondary to invasive cardiac procedures. The other common causes were malignancy (26%), complications of atherosclerotic heart disease (11%), and idiopathic disease (10%). Tuberculosis was detected as a cause of bloody pericardial effusion in one patient and presumed to be the cause in another patient. Bloody pericardial effusion was found to be a presenting manifestation of a newly diagnosed malignancy in two patients. The patients in the idiopathic and iatrogenic groups were all alive and had no recurrence of pericardial effusion at 24 +/- 27 and 33 +/- 21 months after hospital discharge, respectively, whereas 80% of patients with malignancy-related bloody effusions died within 8 +/- 6 months. CONCLUSIONS: In a patient population that is reasonably representative of that in most community hospitals in the United States, the most common cause of bloody pericardial effusion in patients with signs or symptoms of cardiac tamponade is now iatrogenic disease. Of the noniatrogenic causes, malignancy, complications of acute myocardial infarction, and idiopathic disease predominated. Hemorrhagic tuberculous pericardial effusions are uncommon and may likely reflect a low incidence of cardiac tuberculosis in community hospitals in the United States.

Adult↗

Pleural fluid pH in parapneumonic effusions.

The pH and carbon dioxide tension were measured in 24 consecutive parapneumonic effusions, along with the leukocyte count, leukocytic differential count, and levels of glucose and protein. Three categories of parapneumonic effusions were characterized: (1) empyemas; (2) benign (nonloculated) effusions; and (3) loculated effusions. A pH greater than 7.30 was present in all ten benign effusions, and spontaneous resolution occurred in each case. All ten empyemas and the four loculated effusions had a pH less than 7.30. All four loculated effusions required drainage with a chest tube for resolution. The pH of the pleural fluid alone separated the empyemas and loculated effusions from benign effusions. The early separation of parapneumonic effusions on the basis of the pleural fluid appears useful. If the pH is greater than 7.30, a benign effusion is present, and spontaneous resolution is likely. If the pH is less than 7.30, loculation of the pleural space may occur regardless of whether the effusion fulfills the criteria for empyema.

Drainage↗

Eosinophilic pleural effusion in adults at Srinagarind Hospital.

The presence of pleural eosinophilia remains a controversy in etiology and prognosis. We conducted this study to evaluate the etiology of eosinophilic pleural effusion and to define the factors that determine malignancy in eosinophilic pleural effusion. Between 1 August 1994 and 1 July 2000, 50 patients were diagnosed with eosinophilic pleural effusion; 35 men and 15 women averaging 56.4 years of age. Most (96%) had exudative pleural effusion. Malignancy was the most common (46%) established cause followed by tuberculosis (10%), parapneumonic effusion (8%), and empyema thoracis (2%). We encountered only one case of pneumothorax and parasitic pleural effusion (from Strongyloides stercoralis). Unknown causes constituted 22% of cases. The etiology of those who had previously undergone thoracocentesis did not differ from those having their first thoracocentesis. Patients with malignant pleural effusion had significant longer duration of clinical symptoms (> or = 1 month) and weight loss than benign pleural effusion. The median duration of symptoms in benign pleural effusion was 14 days. Fever was more characteristic in patients with benign than in those with malignant pleural effusion. The percentage of eosinophils in pleural fluid and blood did not differ between the two groups. Pleural fluid eosinophils in malignant vs benign pleural effusion were 26.6% (range 10% to 63%), and 30.6% (range 10% to 93%), respectively. We concluded that, pleural eosinophilia did not indicate benign conditions which would spontaneously resolve. Malignant pleural effusion should be considered especially in areas malignancy is prevalent.

Adolescent↗

Benign and malignant pleural effusions in former Wittenoom crocidolite millers and miners.

Serial plain chest radiographs taken between 1943 and 1982 for 280 claimants for compensation for asbestosis and 32 claimants for malignant pleural mesothelioma from the Wittenoom asbestos industry were reviewed by two observers to identify diffuse pleural thickening and pleural effusion. A pleural effusion which appeared and resolved within two years without radiographic or clinical evidence of underlying malignancy, infection or cardiac failure was seen in 15 cases by reader 1 and 24 cases by reader 2. Eighteen cases of effusion, determined from clinical records to be caused by malignant pleural mesothelioma, were seen by reader 1 and 20 by reader 2. The latent periods between commencing work and the first radiograph showing effusion were much shorter for subjects with benign asbestos pleural effusion than for subjects with effusion due to malignant pleural mesothelioma, although there was considerable overlap in the range. The longest latent period for benign asbestos pleural effusion was 22 years and the shortest period for effusion due to malignant pleural mesothelioma was 12 years. The latent period for benign asbestos pleural effusion was inversely related to total cumulative exposure, whereas that for effusion due to malignant pleural mesothelioma was significantly shorter for subjects who had worked in the mill than for those who had worked in the mine. A long latent period and a history of working in the mill were significant discriminators for a malignant as opposed to a benign basis for an effusion. The appearance of a benign asbestos pleural effusion appeared to be a risk factor for the severity of subsequent diffuse pleural thickening.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Eosinophilic pleural or peritoneal effusions in dogs and cats: 14 cases (1986-1992).

Case records of 9 dogs and 5 cats with eosinophilic effusions were reviewed. The animals ranged from 11 months to 13 years old. Seven animals had pleural effusions, 5 had peritoneal effusions, and 2 had pleural and peritoneal effusions. Neoplasia was confirmed in 6 animals and suspected in 1. Eosinophilic pleural effusion was diagnosed 2 days after pneumothorax developed as a consequence of thoracic tube placement in a cat, and pneumothorax was diagnosed in another cat with eosinophilic peritoneal effusion. Other abnormalities seen in 1 or 2 animals associated with eosinophilic effusion were radiographic signs of interstitial or peribronchial pulmonary infiltrates, a history of allergic respiratory tract and skin disease, intestinal lymphangiectasia and lung lobe torsion, chylothorax, bite wounds causing intestinal perforation, and feline leukemia virus infection. Based only on the protein concentration of the effusion, 7 effusions were classified as transudates and 7 were classified as exudates. Five of the 14 animals had eosinophilia (> 1,200 eosinophils/microliters); 3 of these animals had neoplastic disease. Mean eosinophil count in blood samples was not significantly different between animals with neoplasia and those without. Eosinophil counts in blood samples were not linearly related to counts in effusions; however, in some animals the number of eosinophils in the effusion was much higher than the eosinophil count in blood, suggesting concentration of eosinophils in the effusion.

Animals↗

Vascular endothelial growth factor concentrations in body cavity effusions in dogs.

Vascular endothelial growth factor (VEGF) has potent angiogenic, mitogenic, and vascular permeability enhancing properties specific for endothelial cells. VEGF is present in high concentrations in inflammatory and neoplastic body cavity effusions and has been implicated in the pathogenesis of neoplastic and inflammatory effusion formation. In this study, VEGF was quantitated by solid-phase enzyme-linked immunoadsorbent assay (ELISA) in samples of pericardial, pleural, and peritoneal effusions (N = 38) from dogs (N = 35) with neoplastic and non-neoplastic diseases. VEGF was detected in 37 of 38 effusions (median, 754; range, 18-3,669 pg/mL) and was present in much higher concentrations than in previously established normal concentrations for canine plasma (median, < 1 pg/mL; range, < 1-18 pg/mL) or in those previously noted in the plasma of dogs with hemangiosarcoma (HSA; median, 17 pg/mL; range, < 1-67 pg/mL). In 4 dogs with HSA, the concurrent plasma VEGF concentration was much lower than in the abdominal effusion (P = .029). No significant correlation was demonstrated between VEGF effusion concentration and effusion total protein content or nucleated cell count. Mean VEGF concentrations were significantly higher in pericardial (median, 3,533; range, 709-3,669 pg/mL) and pleural effusions (median, 3,144; range, 0-3,663 pg/mL) compared to peritoneal effusions (median, 288; range, 18-2,607 pg/mL; P < .05). There was no marked difference demonstrated between effusions associated with malignant and nonmalignant diseases. Further studies are necessary to elucidate the role of VEGF in body cavity effusion formation in dogs.

Animals↗

MR imaging of the knee: can changes in the intracapsular fat pads be used as a sign of synovial proliferation in the presence of an effusion?

OBJECTIVE: Synovial proliferation is difficult to detect on MR images when joint effusions are present. The objective of this study was to assess the efficacy of MR changes in intracapsular fat pads (prefemoral, quadriceps, Hoffa's) as a sign of synovial proliferation in patients with knee effusions. MATERIALS AND METHODS: MR images were obtained in 70 patients with knee effusions. An effusion was considered present if the suprapatellar bursa was distended 1 cm in anterior to posterior diameter on T2-weighted sagittal images. The experimental group consisted of 32 patients with proliferative effusions (effusions associated with synovial proliferation) diagnosed on the basis of histologic or microbiologic data or strict rheumatologic criteria. This group comprised 11 patients with pigmented villonodular synovitis, six with rheumatoid arthritis, one with psoriatic arthritis, three with hemosideric arthritis, and 11 with septic arthritis. The control group comprised 38 subjects with knee effusions who had no arthroscopic evidence of synovial proliferation. After determining the MR criteria of proliferative effusion, two observers who had no knowledge of these cases evaluated abnormalities of the intracapsular fat pads seen on sagittal intermediate-weighted midline MR images. RESULTS: Characteristic changes in the fat pads were noted on MR images in patients with proliferative synovial effusions. Scalloping or truncation of the prefemoral fat pad was 77% sensitive and 95% specific as a predictor of proliferative effusion. Defects and displacement of Hoffa's fat pad had a sensitivity of 57% and a specificity of 99%, and nonvisualization or irregular margins of the quadriceps fat pad had a sensitivity of 61% and a specificity of 100%. CONCLUSION: Characteristic changes in intracapsular fat pads seen on MR images of patients with proliferative effusions can help distinguish these patients from those with effusions without synovial proliferation.

Adipose Tissue↗

Serous effusions in malignant lymphomas: a review.

Serous effusions are a common complication of lymphomas. Although the frequency of pleural effusion is 20-30% in non-Hodgkin's lymphoma (NHL) and Hodgkin's disease (HD), the involvement of peritoneal and pericardial cavities is uncommon. Among lymphoma subtypes, T-cell neoplasms, especially the lymphoblastic lymphomas, more frequently involve the serous fluids. The thoracic duct obstruction and impaired lymphatic drainage appear to be the primary mechanism for pathogenesis of pleural effusion in HD and direct pleural infiltration is the predominant cause in NHL. There is wide variation in rate of positive cytologic findings of NHL in pleural effusion (22.2-94.1%). Cytologic features of specific lymphoma subtypes such as lymphoblastic lymphoma, follicular center cell lymphoma, including Burkitt-type lymphoma, marginal zone lymphoma, MALT lymphoma, and anaplastic large-cell lymphoma, etc., have been described in the literature. The differential diagnostic problems of lymphomas in serous effusions include reactive lymphocytoses, early involvement by lymphomatous process, small round-cell tumors (SRCT), and presence of look-alike of Reed-Sternberg cells. To overcome these difficulties, various ancillary studies, including immunocytochemistry (ICC), morphometry, flow cytometry (FCM), and cytogenetics/molecular genetics (PCR, in-situ hybridization, and Southern blotting), have been performed on effusion specimens. ICC not only distinguishes lymphomas from reactive lymphocytoses and SRCTs, it significantly modifies the morphologic diagnosis to achieve a better classification of lymphomas. Combined morphology and immunophenotyping by FCM, has a sensitivity as well as specificity of 100%. Morphometry also distinguishes reactive lymphocytoses from malignant lymphoma with a high degree of sensitivity (>85%) and specificity (>95%). Limitations of individual ancillary techniques can be overcome by using multiple parameters. Although lymphomas rarely present as serous effusions without the involvement of other thoracic and extrathoracic sites, a small group of lymphomas called primary effusion lymphomas (PEL) exhibit exclusive or dominant involvement of serous cavities, without a detectable solid tumor mass. This body cavity based lymphoma (BCBL) is a distinct clinicopathologic entity and is found predominantly in AIDS patients with preexisting Kaposi sarcoma. In the absence of obstructive or infiltrative tumor mass, its pathogenesis has been attributed to stimulation by vascular endothelial growth factor (VEGF)/vascular permeability factor (VPF), leading to vascular leakage. Cytomorphologically, PEL is usually a large-cell lymphoma, which appears to bridge features of large-cell immunoblastic and anaplastic large-cell lymphoma (ALCL). Most of these cases comprise a unique subgroup of B-cell lymphoma, with features of both high-grade anaplastic and B-immunoblastic lymphoma, but T-cell and/or natural killer cell immunophenotypes are described. Its association with various viral DNAs has been studied in detail by molecular techniques. Pleural effusion due to lymphomas, either primary or otherwise, is considered as one of the factors adversely influencing overall survival. The presence of pleural effusion at the time of presentation is not only associated with extremely poor outcome of lymphomas, it is also a predictor of disease relapse after chemotherapy and decreased survival. When the patients of lymphomatous pleural effusions with and without mediastinal mass present in respiratory distress, thoracocentesis is the initial diagnostic and therapeutic choice in these patients. In such situations, cytology along with ancillary studies not only gives a quick diagnosis of lymphoma, but also offers prognostically significant information such as classification of lymphomas, its grade and immunophenotype, and presence/absence of viral DNAs and tumor lysis syndrome.

Ascitic Fluid↗

Tumor-associated antigens in effusions of malignant and benign origin.

We determined the concentration and effusion/serum ratio of mucin-like carcinoma-associated antigen (MCA) in comparison to carcinoembryonic antigen, carbohydrate antigen 19-9, cancer antigen 125, and cancer antigen 15-3 in 80 sera and 99 effusions from 64 patients with histologically confirmed malignancies (4 patients out of this group showed various effusions simultaneously, which were analyzed separately) and 31 patients with various nonneoplastic diseases. Tumor cells were detected by cytological examination in 41 effusions (60.3%) from patients with neoplastic diseases, while in another 27 cases this method failed to demonstrate the malignant origin of the effusion. Of the cytological "positive" malignant effusions 90% were also correctly identified by an elevated MCA concentration at a cutoff level of 10 U/ml, whereas only one effusion of benign origin (3%) showed a slightly elevated MCA concentration of 10.5 U/ml. In 33% of cytologically "negative" effusions of patients with neoplastic diseases, the MCA concentration was also elevated, with a maximum of 453 U/ml. Increased MCA levels in cytologically confirmed malignant effusions were not restricted to metastatic breast cancer. All 17 cytologically "positive" "non-breast cancer" effusions were correctly identified by their MCA concentrations. None of the other tumor markers reached this high sensitivity at the same level of specificity. The ratio of effusion/serum concentration of all tumor markers as well as the concentration of cancer antigen 125 in effusions was of little diagnostic value. Our results indicate that the MCA concentration in an effusion correlates very closely with its malignant origin and is superior to all the other antigens tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, Neoplasm↗