Culture-Negative Septic Shock Compared With Culture-Positive Septic Shock: A Retrospective Cohort Study.

OBJECTIVES: To determine the clinical characteristics and outcomes of culture-negative septic shock in comparison with culture-positive septic shock. DESIGN: Retrospective nested cohort study. SETTING: ICUs of 28 academic and community hospitals in three countries between 1997 and 2010. SUBJECTS: Patients with culture-negative septic shock and culture-positive septic shock derived from a trinational (n = 8,670) database of patients with septic shock. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Patients with culture-negative septic shock (n = 2,651; 30.6%) and culture-positive septic shock (n = 6,019; 69.4%) were identified. Culture-negative septic shock compared with culture-positive septic shock patients experienced similar ICU survival (58.3% vs 59.5%; p = 0.276) and overall hospital survival (47.3% vs 47.1%; p = 0.976). Severity of illness was similar between culture-negative septic shock and culture-positive septic shock groups ([mean and SD Acute Physiology and Chronic Health Evaluation II, 25.7 ± 8.3 vs 25.7 ± 8.1]; p = 0.723) as were serum lactate levels (3.0 [interquartile range, 1.7-6.1] vs 3.2 mmol/L [interquartile range, 1.8-5.9 mmol/L]; p = 0.366). As delays in the administration of appropriate antimicrobial therapy after the onset of hypotension increased, patients in both groups experienced congruent increases in overall hospital mortality: culture-negative septic shock (odds ratio, 1.56; 95% CI [1.47-1.66]; p < 0.0001) and culture-positive septic shock (odds ratio, 1.65; 95% CI [1.59-1.71]; p < 0.0001). CONCLUSIONS: Patients with culture-negative septic shock behave similarly to those with culture-positive septic shock in nearly all respects; early appropriate antimicrobial therapy appears to improve mortality. Early recognition and eradication of infection is the most obvious effective strategy to improve hospital survival.

Identifying Malignant Pleural Effusion by A Cancer Ratio (Serum LDH: Pleural Fluid ADA Ratio).

AIM: We studied the diagnostic potential of serum lactate dehydrogenase (LDH) in malignant pleural effusion. METHODS: Retrospective analysis of patients hospitalized with exudative pleural effusion in 2013. RESULTS: Serum LDH and serum LDH: pleural fluid ADA ratio was significantly higher in cancer patients presenting with exudative pleural effusion. In multivariate logistic regression analysis, pleural fluid ADA was negatively correlated 0.62 (0.45-0.85, p = 0.003) with malignancy, whereas serum LDH 1.02 (1.0-1.03, p = 0.004) and serum LDH: pleural fluid ADA ratio 0.94 (0.99-1.0, p = 0.04) was correlated positively with malignant pleural effusion. For serum LDH: pleural fluid ADA ratio, a cut-off level of >20 showed sensitivity, specificity of 0.98 (95 % CI 0.92-0.99) and 0.94 (95 % CI 0.83-0.98), respectively. The positive likelihood ratio was 32.6 (95 % CI 10.7-99.6), while the negative likelihood ratio at this cut-off was 0.03 (95 % CI 0.01-0.15). CONCLUSION: Higher serum LDH and serum LDH: pleural fluid ADA ratio in patients presenting with exudative pleural effusion can distinguish between malignant and non-malignant effusion on the first day of hospitalization. The cut-off level for serum LDH: pleural fluid ADA ratio of >20 is highly predictive of malignancy in patients with exudative pleural effusion (whether lymphocytic or neutrophilic) with high sensitivity and specificity.

Spatial modulation microscopy for real-time imaging of plasmonic nanoparticles and cells.

Spatial modulation microscopy (SMM) is a technique originally developed for quantitative spectroscopy of individual nano-objects. Here, a parallel implementation of the SMM technique is demonstrated based on a line detector capable of demodulation at kHz frequencies. The capabilities of the imaging system are shown using an array of plasmonic nanoantennas and dendritic cells incubated with gold nanoparticles.

Characterization of oil bodies in adlay (Coix lachryma-jobi L).

Oil bodies were observed in cells of both embryo and aleurone layers of mature adlay grains (Coix lachryma-jobi L. var. ma-yuen Stapf). Stable oil bodies were successfully isolated from the adlay grains. Thin-layer chromatography revealed that the contents stored in the adlay oil bodies were mainly neutral lipids (>90% triacylglycerols and about 5% diacylglycerols). The integrity of the isolated oil bodies was presumably maintained via electronegative repulsion and steric hindrance provided by their surface proteins. Immunological cross-recognition using antibodies against sesame oil-body proteins indicated that two oleosin isoforms (termed oleosin-H and oleosin-L) and one caleosin were present in the adlay oil bodies. Full-length cDNA fragments encoding these three unique oil-body proteins were obtained by PCR cloning. MALDI-MS analyses confirmed that the three full-length cDNA fragments encoded the two oleosin isoforms and one caleosin observed in the oil bodies isolated from the adlay grains.

Lysozyme, a mediator of sepsis that intrinsically generates hydrogen peroxide to cause cardiovascular dysfunction.

In septic shock, cardiovascular collapse is caused by the release of inflammatory mediators. We previously found that lysozyme (Lzm-S), released from leukocytes, contributed to the myocardial depression and arterial vasodilation that develop in canine models of septic shock. To cause vasodilation, Lzm-S generates hydrogen peroxide (H(2)O(2)) that activates the smooth muscle soluble guanylate cyclase (sGC) pathway, although the mechanism of H(2)O(2) generation is not known. To cause myocardial depression, Lzm-S binds to the endocardial endothelium, resulting in the formation of nitric oxide (NO) and subsequent activation of myocardial sGC, although the initial signaling event is not clear. In this study, we examined whether the myocardial depression produced by Lzm-S was also caused by the generation of H(2)O(2) and whether Lzm-S could intrinsically generate H(2)O(2) as has been described for other protein types. In a canine ventricular trabecular preparation, we found that the peroxidizing agent Aspergillus niger catalase, that would breakdown H(2)O(2), prevented Lzm-S- induced decrease in contraction. We also found that compound I, a species of catalase formed during H(2)O(2) metabolism, could contribute to the NO generation caused by Lzm-S. In tissue-free experiments, we used a fluorometric assay (Ultra Amplex red H(2)O(2) assay) and electrochemical sensor techniques, respectively, to measure H(2)O(2) generation. We found that Lzm-S could generate H(2)O(2) and, furthermore, that this generation could be attenuated by the singlet oxygen quencher sodium azide. This study shows that Lzm-S, a mediator of sepsis, is able to intrinsically generate H(2)O(2). Moreover, this generation may activate H(2)O(2)-dependent pathways leading to cardiovascular collapse in septic shock.

Incidence and aetiology of eosinophilic pleural effusion.

Although eosinophilic pleural effusion (EPE) has been a subject of numerous studies, its clinical significance still remains unclear. The aim of our study was to evaluate: 1) the relative incidence and aetiology of EPE; 2) the predictors of malignancy in patients with EPE; and 3) the relationship between repeated thoracentesis and pleural fluid eosinophilia. A retrospective analysis of 2,205 pleural fluid samples from 1,868 patients treated between 1995 and 2007 was performed. We identified 135 patients with EPE (7.2% of all patients with pleural effusion) and 153 EPE samples. The most common condition associated with EPE was malignancy (34.8%) followed by infectious (19.2%), unknown (14.1%), post-traumatic (8.9%) and miscellaneous (23.0%) pleural effusions. The incidence of malignancy was significantly higher in patients with a lower (< or =40%) pleural fluid eosinophil percentage. 40 patients with EPE underwent a second thoracentesis. In 16, eosinophilia was present in both pleural fluid samples, 14 revealed pleural fluid eosinophilia only after the second thoracentesis and 10 had eosinophilia only in the first pleural fluid sample. Pleural fluid eosinophilia should not be regarded as a predictor of nonmalignant aetiology. Probability of malignancy is lower in effusions with a high eosinophil percentage. The incidence of EPE in patients undergoing second thoracentesis is not different to that found during the first thoracentesis.

N,N'-diacetylchitobiose, an inhibitor of lysozyme, reverses myocardial depression and lessens norepinephrine requirements in Escherichia coli sepsis in dogs.

Cardiovascular dysfunction in septic shock (SS) is ascribed to the release of inflammatory mediators. Norepinephrine (NE) is often administered to treat low MAP in SS. We recently found that lysozyme c (Lzm-S) released from leukocytes was a mediator of myocardial depression in an Escherichia coil model of SS in dogs. This effect can be blocked in an in vitro preparation by chitobiose, a competitive inhibitor of Lzm-S. In the present study, we examined whether chitobiose treatment can reverse myocardial depression and obviate NE requirements in two respective canine E. coli preparations. In a 6-h study, we administered chitobiose after 3.5 h of E. coli bacteremia and compared stroke work (SW) and MAP at 6 h with a sepsis control group. In a 12-h study, we determined whether chitobiose treatment can reduce the need for NE requirements during 12 h of bacteremia. In the latter study, either chitobiose or NE was given when MAP decreased approximately 20% from the presepsis value in respective groups. In anesthetized, mechanically ventilated dogs, we monitored hemodynamic parameters during continuous E. coli infusion. In the 6-h study, chitobiose improved SW and MAP at the 6-h period as compared with the nontreated sepsis group. In the 12-h study, SW and MAP increased after chitobiose without the necessity of NE administration. These results suggest that inhibitors of Lzm-S such as chitobiose may improve myocardial depression and reduce the need for NE requirements in SS.

Clinical practice guidelines for hospital-acquired pneumonia and ventilator-associated pneumonia in adults.

Hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP) are important causes of morbidity and mortality, with mortality rates approaching 62%. HAP and VAP are the second most common cause of nosocomial infection overall, but are the most common cause documented in the intensive care unit setting. In addition, HAP and VAP produce the highest mortality associated with nosocomial infection. As a result, evidence-based guidelines were prepared detailing the epidemiology, microbial etiology, risk factors and clinical manifestations of HAP and VAP. Furthermore, an approach based on the available data, expert opinion and current practice for the provision of care within the Canadian health care system was used to determine risk stratification schemas to enable appropriate diagnosis, antimicrobial management and nonantimicrobial management of HAP and VAP. Finally, prevention and risk-reduction strategies to reduce the risk of acquiring these infections were collated. Future initiatives to enhance more rapid diagnosis and to effect better treatment for resistant pathogens are necessary to reduce morbidity and improve survival.

Successful factor XIII treatment of refractory chylothorax in tuberous sclerosis complex-associated lymphangioleiomyomatosis, multifocal multinodular pneumocyte hyperplasia and mediastinal lymphadenopathy.

Tuberous sclerosis complex (TSC) or Bourneville disease is a rare autosomal dominant neurocutaneous disorder that affects various organs. Pulmonary involvement in TSC may consist of lymphangioleiomyomatosis (LAM) and multifocal micronodular pneumocyte hyperplasia (MMPH), occurring together or alone. In patients with TSC-LAM, chylous pleural effusion (CPE) is a rare, though well-recognized, complication with an unpredictable clinical course. In refractory or persistent CPE, optimal management remains a clinical challenge. We report the unique case of a 29-year-old Caucasian female, neversmoker, with definite TSC since infancy, characterized by seizures, facial angiofibromas ("adenoma sebaceum"), bilateral renal angiomyolipomas, hepatic angiomyolipomas, subcortical/cortical tubers, and subependymal nodules. At 27 years old, due to bleeding from the renal angiomyolipomas, she underwent nephrectomy, first of the right, and then a year and 9 months later, of the left kidney. She was hemodialysis dependent for the next five years until cadaveric kidney transplantation. The medical history was also remarkable for recurrent exudative lymphocytic PE despite repeated therapeutic thoracenteses, with first presentation at 23.5 years of age. Chylothorax was initially diagnosed at 24 years and 8 months old (PE triglycerides 4.53 mmol/L), and reconfirmed at age 29 (PE triglycerides 12.46-15.30 mmol/L). Computerized tomography scan of the thorax showed a large encapsulated PE in the left lung field, multiple thin walled cysts (≤ 5 mm in diameter) in the lung parenchyma bilaterally, and mediastinal lymphadenopathy - all prominent features of LAM - as well as nodular pulmonary lesions (≤ 3 mm in diameter) consistent with MMPH. Given the persistent nature of the CPE, a five-day course of recombinant human factor XIII (FXIII) was administered intravenously. The chylothorax completely resolved within three months. There has been no recurrence of CPE on follow-up chest X-rays (i.e., total follow-up period of 53 months). This report suggests that the transglutaminase FXIII, a blood coagulation factor, may have an important clinical benefit in treating recurrent or thoracentesis-refractory CPE in TSC-LAM. To our knowledge, this is the first known case in the literature describing the successful treatment of CPE with FXIII in TSC-LAM. Because CPE is rare and there is currently no gold standard for its management, regardless of etiology, further research is warranted to investigate the potential clinical use of FXIII as an effective and safe treatment strategy in selected patients.

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.

Routine use of pleural fluid cultures. Are they indicated? Limited yield, minimal impact on treatment decisions.

In pleural infection, it has been recommended that Gram stain and cultures should be obtained on a routine basis. However, this recommendation has not been tested prospectively. We evaluated the yield of microbiological studies in 259 patients with parapneumonic pleural effusion. Microbiological studies were positive on the pleural fluid of 50 patients (19.3%). In 48 of the 50 patients with positive microbiological results (96%), the need for pleural drainage was correctly predicted by pleural fluid parameters. There were no differences in hospital stay (9.5+/-2.5 days versus 9.9+/-3.2 days, P=0.68) or in mortality (2 deaths in each group, P=0.58) between the group of patients in which antibiotic treatment was changed according to microbiological results and the group of patients in which it is not. In conclusion, this study demonstrates that, at least in our institution, routine microbial investigation of pleural fluid adds very little to the standard management of parapneumonic effusions.

Differentiating Malignant from Tubercular Pleural Effusion by Cancer Ratio Plus (Cancer Ratio: Pleural Lymphocyte Count).

Background. We performed prospective validation of the cancer ratio (serum LDH : pleural ADA ratio), previously reported as predictive of malignant effusion retrospectively, and assessed the effect of combining it with "pleural lymphocyte count" in diagnosing malignant pleural effusion (MPE). Methods. Prospective cohort study of patients hospitalized with lymphocyte predominant exudative pleural effusion in 2015. Results. 118 patients, 84 (71.2%) having MPE and 34 (28.8%) having tuberculous pleural effusion (TPE), were analysed. In multivariate logistic regression analysis, cancer ratio, serum LDH : pleural fluid lymphocyte count ratio, and "cancer ratio plus" (ratio of cancer ratio and pleural fluid lymphocyte count) correlated positively with MPE. The sensitivity and specificity of cancer ratio, ratio of serum LDH : pleural fluid lymphocyte count, and "cancer ratio plus" were 0.95 (95% CI 0.87-0.98) and 0.85 (95% CI 0.68-0.94), 0.63 (95% CI 0.51-0.73) and 0.85 (95% CI 0.68-0.94), and 97.6 (95% CI 0.90-0.99) and 94.1 (95% CI 0.78-0.98) at the cut-off level of >20, >800, and >30, respectively. Conclusion. Without incurring any additional cost, or requiring additional test, effort, or time, cancer ratio maintained and "cancer ratio plus" improved the specificity of cancer ratio in identifying MPE in the prospective cohort.

Management and Outcomes of Acute Respiratory Distress Syndrome Caused by Blastomycosis: A Retrospective Case Series.

Acute respiratory distress syndrome (ARDS) is an uncommon, highly fatal, and poorly understood manifestation of blastomycosis. Optimal management remains unknown, including the roles of adjunctive corticosteroids and extracorporeal membrane oxygenation (ECMO).We conducted a retrospective chart review of patients with ARDS caused by blastomycosis, managed in intensive care units in Manitoba, Canada, from 1992 to 2014. ARDS was defined using the Berlin definition. Corticosteroid therapy was defined as ≥150 mg cortisol equivalent in 24 hours. Logistic regression was used to identify determinants of a fatal outcome, and bootstrap resampling was used to assess sample size requirements.Forty-three patients with ARDS caused by blastomycosis were identified. ARDS was mild, moderate, and severe in 2 (5%), 12 (28%), and 29 (67%) patients, respectively. Management included amphotericin B (n = 42, 98%), vasopressors (n = 36, 84%), corticosteroids (n = 22, 51%), renal replacement (n = 13, 30%), and ECMO (n = 4, 11%). Seventeen patients (40%) died. All patients treated with ECMO survived (P = 0.14). Corticosteroids were not associated with survival benefit in univariate (P = 0.43) or multivariate analyses (odds ratio 0.52, 95% confidence interval 0.11-2.34). Bootstrap studies indicated that almost 500 patients would be needed to confirm a significant reduction in mortality from corticosteroids (type I error = 0.05, power = 80%).Blastomycosis is an uncommon, albeit important, cause of ARDS in this geographic area. Given the rarity of disease and the large cohort needed to demonstrate mortality benefit, the role of adjunctive therapies, including corticosteroids and ECMO, may remain unconfirmed, and clinical judgment should guide management decisions.

Characterization of membrane N-glycan binding sites of lysozyme for cardiac depression in sepsis.

PURPOSE: In sepsis, reversible myocardial depression has been ascribed to the release of mediators of inflammation. We previously found that lysozyme released from leukocytes from the spleen and other organs mediated myocardial depression in an Escherichia coli model of septic shock in dogs. We hypothesize that lysozyme binds to or cleaves a cardiac surface membrane N-glycoprotein to cause depression. The objectives of the present study were: 1) to determine whether the binding of lysozyme is reversible; 2) to assess the N-glycan structure to which lysozyme binds; 3) to examine whether nonenzymatic proteins, termed lectins, with a binding specificity similar to that of lysozyme could also cause depression; and 4) to assess whether the membrane to which lysozyme binds is affected by the enzymes protease type XIV and collagenase A, that are used to prepare single cell myocyte experiments. METHODS: We measured isometric contraction in a right ventricular trabecular preparation. RESULTS: We found that lysozyme binds in a reversible manner to the Man beta(1-4) GlcNAc beta(1-4)GlcNAc moiety in the tri-mannosyl core structure of high mannose/hybrid and tri-antennary carbohydrate classes where GlcNAc is N-acetylglucosamine and Man is mannose. Lectins with a specificity similar to that of lysozyme also caused depression, and lysozyme's depressant activity was eliminated by protease type XIV and collagenase A. CONCLUSIONS: These results indicate that lysozyme reversibly binds to a membrane glycoprotein to cause myocardial depression in sepsis. We further localize its binding site to a variant of the chitotriose structure in the tri-mannosyl core of the membrane glycoprotein.

Serial pulmonary function in patients with acute heart failure.

This study delineates the effects of congestive heart failure on routine pulmonary function tests and assesses the changes in pulmonary function as congestive heart failure was treated. Twenty-eight patients had spirometry, lung volumes, and diffusing capacity measurements initially and at frequent intervals after their initial hospitalization for congestive heart failure. Initially the patients had both obstructive (mean forced expiratory volume in 1 s [FEV1], 48.2% +/- 13% predicted) and restrictive (mean forced vital capacity [FVC], 5.6% +/- 15.7% predicted) ventilatory dysfunction, but a normal carbon monoxide diffusing capacity. With treatment, pulmonary function rapidly improved initially and there was no further significant improvements in the mean pulmonary function after two weeks of treatment. However, there was marked interindividual variability and several patients took months to reach their best level of pulmonary function. Even with treatment, the patients retained evidence of obstructive ventilatory dysfunction and at the time of their best spirometry 53% (8/15) of nonsmokers still had an abnormally low FEV1/FVC ratio.

Albuterol and isoproterenol in bronchial asthma. Efficacy and toxicity of drugs administered via intermittent positive pressure breathing.

This study compared the efficacy and side effects of 1.25, 2.5, 5, 10, and 15 mg of albuterol and isoproterenol hydrochloride administered by intermittent positive pressure breathing (IPPB) to 12 patients with reversible airway obstruction. Equal doses of the two medications induced similar peak increases in pulmonary function, but the increase following albuterol persisted longer. The degree of bronchodilation was impressive; 15 mg of albuterol induced a mean increase over six hours of 82% in the forced expiratory volume in one second. Significant cardiovascular side effects were more common after isoproterenol than after albuterol. Albuterol is superior to isoproterenol as a bronchodilator when administered by IPPB because, for a given peak bronchodilation, cardiovascular side effects are fewer and bronchodilation persists longer with albuterol. The optimal dose of isoproterenol hydrochloride is 2.5 to 5.0 mg and the optimal dose of albuterol is 10 mg when these drugs are given by IPPB.

Trimethoprim alone in the treatment and prophylaxis of urinary tract infection.

Trimethoprim was used alone to treat urinary tract infections in 20 women who were unable to tolerate sulfonamides. Of ten acute symptomatic urinary tract infections, four were cured, three were not, and three cases could not be evaluated. Two other women received trimethoprim for suppression of infection complicating stag-horn calculi. The conditions of both patients improved clinically but the urine remained infected. Eight women treated prophylactically with low-dose trimethoprim for recurrent urinary tract infection accumulated a total of 16 patient-years of prophylaxis. During treatment, the incidence of infection was 0.56 per patient-year compared with 4.25 infections in the year preceding study. Adverse reactions occurred in eight of 20 patients and administration of the drug had to be stopped in five cases. Trimethoprim alone is effective for the treatment and prophylaxis of urinary tract infections, but may cause a high incidence of adverse reactions in patients known to be sensitive to sulfonamides.

Doxepin treatment of depressed patients with chronic obstructive pulmonary disease.

During each of two six-week treatment periods, 12 depressed outpatients with chronic obstructive pulmonary disease received increasing doses of doxepin hydrochloride or a placebo as tolerated. The mean maximal doses of doxepin hydrochloride and placebo were 105 and 128 mg, respectively. Three of the 12 patients dropped out because of doxepin's side effects. The depression and anxiety scores at the end of the treatment periods were virtually identical and not significantly different from baseline scores. Changes in the 12-minute walking distance were more closely correlated with changes in the depression and anxiety scores than with changes in the forced expiratory volume in 1 s or forced vital capacity. Thus, doxepin is ineffective in treating depressed patients with chronic obstructive pulmonary disease; improvements in the 12-minute walking distance were closely correlated with improvements in the depression or anxiety scores.

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.