Suspicion is very high for tuberculous pleural effusion, in a young patient from an area with a high rate of TB, a lymphocytic exudate pointing to TB, lymphoma or tumor. Tumor unlikely due to age, negative cytology. Lymphoma could be but no evidence of associated nodal pathology. High adenosine deaminase in LP would point with great certainty to a pleural TB although it would be advisable to confirm the diagnosis with a pleural biopsy since it can also occur in lymphomas and empyemas of other origin.

A 32-year-old man from Cameroon consults for fever cough and left hemithorax pain of 1 month of evolution. He took amoxicillin-clavulanic acid for 1 week without improvement of symptoms. A blood test showed a white blood cell count of 8000/microL and a hemoglobin of 12.8 g/dL. Chest X-ray shows a loculated left pleural effusion occupying one third of the hemithorax. A thoracentesis shows a yellowish fluid with the following features: red blood cells 2000/µL, leukocytes 2500/µL with 90% lymphocytes, protein 4.9 g/dL, lactate dehydrogenase 550 VIL, glucose 67 mg/dL, and absence of malignant cells on cytologic study. Which of the following tests would be most useful in diagnosing the cause of the pleural effusion?

A thoracic computed tomography (CT) scan.

Measurement of pleural fluid adenosine deaminase.

[Cuttoff values of biochemical tests on pleural fluid: their usefulness in differential diagnosis of 1,040 patients with pleural effusion].

The aim of biochemical pleural fluid testing is to reach an etiological diagnosis of the pleural effusion. We assessed the utility of considering cuttoff points for the wide range of analytes used to investigate pleural fluid. Among 1,040 patients with pleural effusion, we sought the etiologies of those fluids which showed any of the following characteristics: red blood cell count = 10 x 109/L, leukocytes = 10 x 109/L, percentage of neutrophils or lymphocytes >50%, protein = 50 g/L, glucose = 60 mg/dL, pH = 7.2, lactate dehydrogenase = 1,000 U/L, adenosine deaminase = 40 U/L, amylase = 100 U/L or cholesterol = 60 mg/dL. Some of the more prominent findings were: a) a sixth of transudates were blood-tinged or contained predominantly neutrophils; b) a groosly bloody fluid suggests malignant disease, trauma, or pulmonary embolization; c) nearly 90% of fluids containing = 10 x 10(9) leukocytes/L were parapneumonics; d) 73% of tuberculous pleural fluids had protein > or = 50 g/L, e) tuberculosis and parapneumonics explained more than 90% of fluids with high adenosine deaminase content; f) one third of amylase-rich pleural effusions were malignant; g) a low pleural glucose or pH levels indicate that patient probably has a parapneumonic, tuberculous or malignant etiology; y h) the diagnostic yield of pleural fluid cytology in malignant effusions was 57%, a percentage which raised to 94% in those with low glucose fluid level. Cuttof values of biochemical pleural fluid tests may greatly support particular causes of pleural effusions.

The clinical manifestations of the tuberculous pleural effusion in adult patients.

The clinical data of 52 patients with tuberculous pleural effusion were analyzed. Their average age was 48 years old. Thirty two (62%) of them were sick for less than one week. Fever, chest pain and cough were the predominant pictures. Six of the 52 patients had coexisting disease. Intermediate strength protein purified derivative (PPD) test was found to be positive in 14 out of 31 (45%) patients. Their pleural effusions were usually unilateral, right-sided, and nearly half of them occupied more than half of the hemithorax. One third of these patients and concomitant pulmonary tuberculosis and pleural effusion. None of the patients had grossly bloody effusion. All of the effusions were exudative, and the glucose levels in the pleural fluid were invariably above 60 mg/dl. Presence of mesothelial cells in the pleural fluid was found in 28% of them, but none of the patients presented with significant eosinophils in the pleural fluid. Pleural fluid and sputum cultures for Mycobacterium tuberculosis usually reveal a negative study unless a concomitant pulmonary lesion was present. Combined antituberculosis and prednisolone treatment decreased the duration of constitutional symptoms and hastened the resolution of pleural effusion. In conclusion, tuberculous pleural effusion should be considered in elderly patients presenting with massive exudative pleural effusion even with a negative PPD study. Cultures of sputum and pleural fluid are less helpful in patients without parenchymal disease. Prednisolone is recommended in extremely ill patients.

Explosive pleuritis.

The objective of the present paper is to describe the clinical and computed tomography features of 'explosive pleuritis', an entity first named by Braman and Donat in 1986, and to propose a case definition. A case report of a previously healthy, 45-year-old man admitted to hospital with acute onset pleuritic chest pain is presented. The patient arrived at the emergency room at 15:00 in mild respiratory distress; the initial chest x-ray revealed a small right lower lobe effusion. The subsequent clinical course in hospital was dramatic. Within 18 h of admission, he developed severe respiratory distress with oxygen desaturation to 83% on room air and dullness of the right lung field. A repeat chest x-ray, taken the morning after admission, revealed complete opacification of the right hemithorax. A computed tomography scan of the thorax demonstrated a massive pleural effusion with compression of pulmonary tissue and mediastinal shift. Pleural fluid biochemical analysis revealed the following concentrations: glucose 3.5 mmol/L, lactate dehydrogenase 1550 U/L, protein 56.98 g/L, amylase 68 U/L and white blood cell count 600 cells/mL. The pleural fluid cultures demonstrated light growth of coagulase-negative staphylococcus and viridans streptococcus, and very light growth of Candida albicans. Cytology was negative for malignant cells. Thoracotomy was performed, which demonstrated a loculated parapneumonic effusion that required decortication. The patient responded favourably to the empirical administration of intravenous levofloxacin and ceftriaxone, and conservative surgical methods in the management of the empyema. This report also discusses the patient's rapidly progressing pleural effusion and offers a potential case definition for explosive pleuritis. Explosive pleuritis is a medical emergency defined by the rapid development of a pleural effusion involving more than 90% of the hemithorax over 24 h, which causes compression of pulmonary tissue and mediastinal shift to the contralateral side.

Etiology and pleural fluid characteristics of large and massive effusions.

To report the etiology of large and massive pleural effusions, and to compare their biochemical fluid characteristics with those of smaller size, and between malignant and nonmalignant conditions. Retrospective chart review of all patients undergoing thoracentesis at an academic medical center in Lleida, Spain, during a 10-year period. Posteroanterior chest radiographs were available in 766 patients during the study period. Large pleural effusions (ie, two thirds or more of the hemithorax without its complete obliteration) were identified in 70 patients (9%), and massive pleural effusions (ie, hemithorax was completely opacified) were identified in 93 patients (12%). A similar etiologic spectrum between large and massive pleural effusions was observed. The most frequent cause of these pleural effusions was malignancy (89 patients; 55%), followed by complicated parapneumonic or empyema (36 patients; 22%), and tuberculosis (19 patients; 12%). Compared with nonmalignant pleural effusions, patients with large or massive malignant pleural effusions were more likely to have pleural fluids with higher RBC counts (18.0 x 10(9) cells/L vs 2.7 x 10(9) cells/L, respectively; p < 0.001) and lower adenosine deaminase (ADA) activity (11.5 vs 31.5 U/L, respectively; p < 0.001), which were the two parameters that were selected by a stepwise logistic-regression model as independent predictors of malignancy. In addition, large/massive malignant pleural effusions showed higher median RBC counts (18.0 x 10(9) cells/L vs 4.3 x 10(9) cells/L, respectively; p < 0.001), higher lactate dehydrogenase levels (641 vs 409 U/L, respectively; p = 0.001), lower pH (7.39 vs 7.42, respectively; p = 0.006) content, but similar cytologic yield (63% vs 53%, respectively; p = 0.171) than smaller malignant pleural effusions. The presence of a large or massive pleural effusion enables the clinician to narrow the differential diagnosis of pleurisy, since most effusions are secondary to malignancy or infections (either bacterial or mycobacterial). Bloody pleural fluid with low ADA content favors a malignant condition.

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.

Responsive treatment of pleural effusion due to probable tuberculosis infection.

Early diagnosis of Mycobacterium tuberculosis disease is crucial for initiating treatment and interrupting disease transmission. In keeping with the pathophysiology of disease, bacteriological evidence in extra-pulmonary tuberculosis proves to be difficult. Clinical judgment and radiographic findings are important to establish diagnosis and to evaluate treatment response. A case of 27 year-old-male with shortness of breath and associated TB symptoms is reported. The tuberculin test was highly positive and chest X-ray showed massive right-lung pleural effusion. Pleural analysis showed exudates with high mononuclear cells (98%), protein level of 5.0 g/dL, glucose level of 87 mg/dL, and high LDH level (1240 IU/L). The acid-fast bacilli (AFB) tests were negative for pleural fluid and sputum. Cultures of fluid and sputum were also negative. After being treated adequately with non-specific treatment, which showed no improvement and having undergone pleural puncture for his treatment and diagnosis, the patient started to have antituberculosis treatment. His condition was improved significantly as shown by a serial of chest X-ray follow-up.

Management of parapneumonic effusions.

When a patient with a parapneumonic pleural effusion is first evaluated, a therapeutic thoracentesis should be performed if more than a minimal amount of pleural fluid is present. Fluid obtained at the therapeutic thoracentesis should be gram-stained and cultured and analyzed for glucose, pH, LDH, white blood cells, and differential cell count. If the fluid cannot be drained because of loculations, a chest tube should be inserted and thrombolytic agents administered. If the pleural fluid recurs after the initial therapeutic thoracentesis but the patient is doing well clinically and the initial pleural fluid glucose was greater than 60 mg/dL; the pH, greater than 7.2; the LDH, less than three times the upper normal limit for serum and the cultures are negative; he or she can be observed. If one or more of the aforementioned criteria are not met, a second therapeutic thoracentesis should be performed, with repeat diagnostic evaluations of the pleural fluid. If the fluid recurs a second time, a small chest tube should be placed if the pleural fluid glucose and pH were lower and the LDH higher on the second thoracentesis than on the first thoracentesis. Patients with loculated-parapneumonic effusions should be treated with tube thoracostomy and thrombolytic agents. If drainage is incomplete, thoracoscopy, with breakdown of adhesions and debridement of the pleural space, is indicated. If thoracoscopy is unsuccessful, then thoracotomy, with decortication, is indicated unless the patient is too debilitated.

Clinical and laboratory parameters in the differential diagnosis of pleural effusion secondary to tuberculosis or cancer.

To evaluate the clinical and laboratory characteristics of pleural effusions secondary to tuberculosis (TB) or cancer (CA). A total of 326 patients with pleural effusion due to TB (n=182) or CA (n=144) were studied. The following parameters were analyzed: patient gender, age and pleural effusion characteristics (size, location, macroscopic fluid aspect, protein concentration, lactate dehydrogenase (DHL) and adenosine deaminase activity (ADA) and nucleated cell counts). Young male patients predominated in the tuberculosis group. The effusions were generally moderate in size and unilateral in both groups. Yellow-citrine fluid with higher protein (p < 0.001) levels predominated in effusions from the tuberculosis group (5.3 + 0.8 g/dL) when compared to the CA group (4.2 +/- 1.0 g/dL), whereas DHL levels were more elevated in CA (1,177 +/- 675 x 1,030 +/- 788 IU; p = 0.003) than in TB. As expected, ADA activity was higher in the TB group (107.6 +/- 44.2 x 30.6 +/- 57.5 U/L; p < 0.001). Both types of effusions presented with high nucleated cell counts, which were more pronounced in the malignant group (p < 0.001). TB effusion was characterized by a larger percentage of leukocytes and lymphocytes (p < 0.001) and a smaller number of mesothelial cells (p = 0.005). Lymphocytes and macrophages were the predominant nucleated cell in neoplastic effusions. Our results demonstrate that in lymphocytic pleural exudate obtained from patients with clinical and radiological evidence of tuberculosis, protein and ADA were the parameters that better characterize these effusions. In the same way, when the clinical suspicion is malignancy, serous-hemorrhagic lymphocytic fluid should be submitted to oncotic cytology once this easy and inexpensive exam reaches a high diagnostic performance (approximately equal 80%). In this context, we suggest thoracocentesis with fluid biochemical and cytological examination as the first diagnostic approach for these patients.

Does pleural fluid appearance really matter? The relationship between fluid appearance and cytology, cell counts, and chemical laboratory measurements in pleural effusions of patients with cancer.

Previous reports have suggested that the appearance of pleural effusions (i.e., the presence or absence of blood) might help to establish the etiology of the effusions. This study explores the relationship between pleural fluid appearance and the results of chemical and cytological analyses in a group of patients with recurrent symptomatic pleural effusions and a diagnosis of cancer. Medical records were reviewed from all 390 patients who were diagnosed with cancer, who underwent thoracentesis before placement of an intrapleural catheter (IPC) between April 2000 and January 2006. Adequate information for data analysis was available in 365 patients. The appearance of their pleural fluid was obtained from procedure notes dictated by the pulmonologists who had performed the thoracenteses. The patients were separated into 2 groups based on fluid appearance: non-bloody and bloody. Group differences in cytology interpretation were compared by using the chi square test. Cellular counts, chemical laboratory results, and survival after index procedure were compared by using the student's t test. Pleural fluid cytology was positive on 82.5% of the non-bloody effusions and on 82.4% of the bloody ones. The number of red blood cells (220.5 x 103/microL vs. 12.3 x 103/microL) and LDH values (1914 IU/dl vs. 863 IU/dl) were statistically higher in bloody pleural effusions. The presence or absence of blood in pleural effusions cannot predict their etiology in patients with cancer and recurrent symptomatic pleural effusions.

Pleural effusion

The sensitivity and specificity of Light's criteria for detection of exudates have been measured in many studies and are usually reported to be around 98% and 80%, respectively. This means that although Light's criteria are relatively accurate, twenty percent of patients that are identified by Light's criteria as having exudative pleural effusions actually have transudative pleural effusions. Therefore, if a patient identified by Light's criteria as having an exudative pleural effusion appears clinically to have a condition that usually produces transudative effusions, additional testing is needed. In such cases, albumin levels in blood and pleural fluid are measured. If the difference between the albumin level in the blood and the pleural fluid is greater than 1.2 g/dL (12 g/L), this suggests that the patient has a transudative pleural effusion. However, pleural fluid testing is not perfect, and the final decision about whether a fluid is a transudate or an exudate is based not on

Pleural effusion

When a pleural effusion has been determined to be exudative, additional evaluation is needed to determine its cause, and amylase, glucose, pH and cell counts should be measured. Red blood cell counts are elevated in cases of bloody effusions (for example after heart surgery or hemothorax from incomplete evacuation of blood). Amylase levels are elevated in cases of esophageal rupture, pancreatic pleural effusion, or cancer. Glucose is decreased with cancer, bacterial infections, or rheumatoid pleuritis. pH is low in empyema (<7.2) and maybe low in cancer. If cancer is suspected, the pleural fluid is sent for cytology. If cytology is negative, and cancer is still suspected, either a thoracoscopy, or needle biopsy of the pleura may be performed. Gram staining and culture should also be done.

Pearls and myths in pleural fluid analysis.

Virtually all patients with a newly discovered pleural effusion should undergo thoracentesis to aid in diagnosis and management. The routine pleural fluid (PF) evaluation usually includes the following: cell count and differential; tests for protein, LDH, glucose, adenosine deaminase, cytology and, if infection is a concern, pH and bacterial and mycobacterial cultures. Distinguishing transudates from exudates with Light's criteria is a pragmatic first step. If the effusion is an exudate, various PF tests have proven diagnostic utility: adenosine deaminase levels >35 IU/L usually indicate tuberculosis in lymphocyte-predominant PF; pH < 7.2 or glucose less than 60 mg/dL allow the clinician to identify complicated parapneumonic effusions; and conventional cytology may reveal malignant cells in 60% of the patients with malignant effusions. A number of optional PF tests may complement the diagnostic approach to an undiagnosed pleural effusion. For example, natriuretic peptide assays significantly improve the accuracy of a diagnosis of cardiac pleural effusion, whereas PF mesothelin levels greater than 20 nmol/L are highly suggestive of mesothelioma.

Thoracentesis

pH Normal pleural fluid pH is approximately 7.60. A pleural fluid pH below 7.30 with normal arterial blood pH has the same differential diagnosis as low pleural fluid glucose. Triglyceride and cholesterol Chylothorax (fluid from lymph vessels leaking into the pleural cavity) may be identified by determining triglyceride and cholesterol levels, which are relatively high in lymph. A triglyceride level over 110 mg/dl and the presence of chylomicrons indicate a chylous effusion. The appearance is generally milky but can be serous. The main cause for chylothorax is rupture of the thoracic duct, most frequently as a result of trauma or malignancy (such as lymphoma). Cell count and differential The number of white blood cells can give an indication of infection. The specific subtypes can also give clues as to the type on infection. The amount of red blood cells are an obvious sign of bleeding.

IgG4-related pleural effusion with high adenosine deaminase levels: A case report and literature review.

Levels of pleural fluid adenosine deaminase (ADA), a useful marker for the diagnosis of tuberculous pleurisy, are elevated in some reports of immunoglobulin G4 (IgG4)-related pleural effusion. We describe a patient with IgG4-related pleural effusion who exhibited a high concentration of ADA. Furthermore, we reviewed the literature to compare patients with IgG4-related pleural effusion and tuberculous pleurisy. A 75-year-old male patient had dyspnea for 1 month with a left pleural effusion that was exudative, lymphocyte dominant. The pleural fluid test results revealed a total protein (TP) concentration of 6.60 g/dl, a lactate dehydrogenase (LDH) level of 383 IU/dl, and an ADA concentration of 54.5 U/L. An interferon gamma release assay showed a negative result. Histological analysis of the thoracoscopic pleural biopsy revealed lymphoplasmacytic infiltration, with 80 IgG4-positive plasma cells/high-power field, and an IgG4/IgG ratio of approximately 40% to 50%. Other diseases were ruled out based on symptoms, negative autoimmune antigen results, and histopathologic findings. Thus, he was diagnosed with IgG4-related pleural effusion. He received 15 mg of prednisolone as therapy. His pleural effusion and symptoms improved gradually within several months, and prednisolone was tapered to 6 mg daily. It is important to distinguish between IgG4-related pleural effusion and tuberculous pleurisy. Therefore, we compared 22 patients with IgG4-related pleural effusion from PubMed and the Japan Medical Abstracts Society to 40 patients with tuberculous pleurisy at Fukujuji Hospital from January 2017 to May 2019. According to thoracentesis findings, 14 of 18 patients with IgG4-related pleural effusion had high ADA more than 40 U/L. The pleural effusion of patients with IgG4-related pleural effusion showed higher TP levels (P < .001) and lower LDH (P < .001) and ADA levels (P = .002) than those with tuberculous pleurisy. Moreover, the pleural fluid ADA/TP ratio was a good predictor for differentiating IgG4-related pleural effusion and tuberculous pleurisy (area under the receiver operating characteristic curve of 0.909; 95% confidence level: 0.824-0.994).

[A case of tuberculous pleurisy developing contralateral effusion during anti-tuberculosis chemotherapy].

A 55-year-old woman was admitted to our hospital because of chest pain, fever, and right pleural effusion that was exudative and lymphocyte-dominant with a high level of adenosine deaminase (ADA). Since her blood QuantiFERON-TB 3G test (QFT) was positive, she was diagnosed with tuberculous pleurisy. After initiation of anti-tuberculosis chemotherapy with isoniazid, rifampicin, ethambutol, and pyrazinamide, her symptoms improved. Later, liquid culture of the pleural effusion turned positive for Mycobacterium tuberculosis. On the 18th day of treatment, her chest X-ray and computed tomography exhibited pleural effusion in a moderate amount in the left thorax, with subsiding pleural effusion in the right thorax. Thoracocentesis demonstrated that the left thorax effusion was also exudative and lymphocyte-dominant, with elevated QFT response and high ADA concentration, suggesting tuberculous pleurisy. Mycobacterium tuberculosis was detected in the culture of a left pleural biopsy specimen obtained by thoracoscopy. We assumed that the left pleural effusion was due to paradoxical worsening because (1) on admission no effusion or lung parenchymal lesion was detected in the left hemithorax, (2) on the 14th day of treatment she was afebrile without pleural effusion on both sides, and (3) the bacilli were sensitive to the drugs she had been taking regularly. We performed drainage of the left effusion and continued the same anti-tuberculosis drugs, which led to the elimination of all her symptoms and of the pleural effusion on both sides. In conclusion, paradoxical worsening should be included in the differential diagnosis when contralateral pleural effusion is detected during the treatment of tuberculosis.

[Clinical analysis of lymphoma with chest involvement: report of 25 cases].

To study clinical characteristics and diagnostic methods of lymphoma with chest involvement. Twenty-five lymphoma patients with chest involvement were retrospectively analysed, they were all diagnosed in Peking University Third Hospital during 2000 to 2007. The data were collected including clinical manifestations, blood examinations, chest X-ray and CT scan, diagnostic methods and pathologic diagnosis. The median age of the 25 patients was 46 years old. Pyrexia (13 cases), weight loss over 10 percent in 6 months (11 cases), cough (10 cases), shortness of breath (9 cases) and painless enlargement of the peripheral lymph nodes (16 cases) were common manifestations. Erythrocyte sedimentation rate and serum lactate dehydrogenase (LDH) level were increased in 72.7% and 81% patients, respectively. The enlargement of mediastinum lymph nodes (16 cases, 64%) was the most common presentation of chest radiography, followed by pulmonary involvement (15 cases, 60%) including infiltration or pulmonary consolidation, mass, multiple nodules, diffuse ground-glass shadow, miliary lesion. There were also presentations of pleural effusion (10 cases, 40%), pericardial effusion (4 cases, 16%), chest wall mass (2 cases, 8%). Eighteen patients (72%) had at least two kinds of these presentations. The appearance of pleural effusion were yellow turbid, bloody or chyliform. Rivalta tests were all positive. The median value of pleural effusion examinations were listed as follows: specific gravity 1.031, total cells 9800 x 10(6)/L, WBC 6.72 x 10(9)/L, lymphocyte 86%, neutrophil 14%, protein 31.4 g/L, LDH 296 U/L, adenosine deaminase (ADA) 67.4 U/L. Most patients (16 cases) were diagnosed by surgical biopsy, especially peripheral lymph nodes biopsy (12 cases). Other patients were diagnosed by ultrasound or CT-guided biopsy (5 cases), video-assisted thoracoscopic pleural biopsy (1 case), video-mediastinoscopic mediastinum lesion biopsy (1 case), bronchial mucosa biopsy through bronchoscope (1 case), bone marrow examination (1 case). All the cases were non-Hodgkin lymphoma except one. There was no specific clinical manifestation for lymphoma with chest involvement, but in almost half of patients there were enlargement of not only peripheral but also mediastinum lymph nodes. And there were some characteristics in serum, pleural effusion, chest X-ray and CT scan. Surgical biopsy of peripheral lymph nodes was a simple and convenient method for diagnosis. Micro-invasive biopsy had good diagnostic value for lymphoma with chest involvement, including ultrasound- or CT-guided biopsy for superficial mass, pleura, lung, liver, spleen and deep lymph nodes, video-assisted thoracoscopic and video-mediastinoscopic biopsy for pleura, lung and mediastinum lesions. But bronchial mucosa and lung biopsy during bronchoscopy had a low diagnostic rate for lymphoma.

Malignant pleural effusion

Diagnosis Clinical evaluation Clinical factors predicting the diagnosis of malignant pleural effusions are symptoms lasting more than 1 month and the absence of fever. Imaging This is needed to confirm the presence of a pleural effusion. Chest radiograph is usually performed first and may demonstrate an underlying lung cancer as well as the pleural effusion. Ultrasound has a sensitivity of 73% and specificity of 100% at distinguishing malignant pleural effusions from other causes of pleural effusion, based on the presence of visible pleural metastases, pleural thickening greater than 1 cm, pleural nodularity, diaphragmatic thickening measuring greater than 7mm and an echogenic swirling pattern visible in the pleural fluid. Biochemical analysis Malignant pleural effusions are exudates. A low pleural fluid pH is associated with poorer survival and reduced pleurodesis efficacy.

Serial pleural fluid analysis in a new experimental model of empyema.

Prior attempts to create an animal model of empyema by direct inoculation of bacteria alone into the pleural space have been unsuccessful. The animals either died of overwhelming sepsis or cleared the infection from the pleural space without development of an empyema. We hypothesized that injection of bacteria with a nutrient agar into the pleural space would allow the bacteria to remain in the pleural space for an extended time period, permitting an empyema to develop. The bacterium Pasteurella multocida in brain heart infusion (BHI) agar was injected into the right hemithorax of 12 New Zealand white male rabbits. Our preliminary studies showed that the animals died in less than 7 days if they were not given parenteral antibiotics. For this reason, the rabbits were given penicillin, 200,000 U, IM, every 24 h starting 24 h after bacterial injection. Pleural fluid was sampled by thoracentesis at 12, 24, 48, 72, and 96 h after bacterial injection. Pleural fluid pH, glucose, lactate dehydrogenase (LDH), leukocyte count, and Gram's stain and culture (in one half of the animals) were obtained at each time point. Pleural biopsy specimens were obtained at autopsy after 96 h. The mean pleural fluid pH reached a nadir of 7.01 at 24 h and remained less than 7.1 throughout the experiment. The mean pleural fluid glucose level reached a nadir of 10 mg/dL at 24 h. The mean pleural fluid LDH peaked at 21,000 IU/L at 24 h and the mean pleural fluid leukocyte count peaked at 12 h with a value of 67,000 cells per cubic millimeter. Gram's stains revealed organisms and cultures were positive for growth in all animals at 12 and 24 h. Some animals had positive Gram's stains and growth on cultures up to 72 h after bacterial injection. At autopsy, all rabbits injected with bacteria had gross pus in the right pleural space and had developed a thick pleural peel. Microscopic specimens of the pleura revealed large numbers of leukocytes (primarily polymorphonuclear lymphocytes) with invasion of the adjacent lung and chest wall. In conclusion, this model more closely mimics the empyema that occurs in humans, relative to previous animal models. This model appears appropriate for additional randomized studies in which different methods for the treatment of empyema can be evaluated.

[Clinical analysis of 20 cases with Streptococcus pneumoniae necrotizing pneumonia in China].

Streptococcus pneumoniae necrotizing pneumonia (SPNP) was reported elsewhere but not in China yet. Inappropriate treatment due to poor recognition of this disease could influence its prognosis. This paper presents the clinical characteristics, diagnosis and treatment of SPNP hoping to elevate pediatrician's recognition level for this disease. Clinical manifestations, radiological findings, treatment and prognosis of 20 patients (9 boys, 11 girls) who had been hospitalized with SPNP in Beijing Children's Hospital from 2004-2011 were retrospectively analyzed. The patients included in this study aged from 9 months to 6 years [(27.9 ± 15.8) m] and were healthy before admission. They were febrile for 8 to 50 days [(27.7 ± 13.5) d] and hospital day was 24 - 55 days [(36.5 ± 8.3) d]. The general condition of all subjects was relatively poor and they all had fever and cough. One child had moderate fever and nineteen children had high fever. Dyspnea was found in sixteen children. Fine rales were found on auscultation in 18 children, among whom diffuse wheeze appeared in 4 children, and wheezy phlegm was found in two children. Signs of pleural effusion were discovered in all cases by physical examination and chest X-ray. White blood cell (WBC) count was 16.2 - 60.95×10(9)/L and neutrophil was 70.5% - 80.2% in peripheral blood routine test. Erythrocyte sedimentation rate (ESR) was 44 - 109 mm/h [(69.6 ± 16) mm/h]and C-reactive protein (CRP) was 80 - > 160 mg/L. The pleural effusion biochemistry and routine test revealed a WBC count of 6400×10(6)/L-too much to count, polykaryocyte of 51% - 90%, glucose of 0.02 - 1.8 mmol/L, protein of 32 - 51 g/L and LDH of 5475 IU/L-or higher. Pleural effusion culture in all cases and blood culture in 2 cases was positive for Streptococcus pneumoniae. Chest X-ray or CT revealed high density and well-distributed lobar consolidation in one lung or two lungs initially. Single or multiple low density lesions in the area of lobar consolidation were found a week later, accompanied by multiple cystic shadow or cavity at the same time or afterwards. Bulla of lung appeared later. Pleural effusions were found in all patients. Seven cases complicated with hydropneumothorax, two with otitis media, one with heart failure, one with cardiac insufficiency. Seventeen patients were treated with vancomycin or teicoplanin or linezolid two with amoxicillin and clavulanate potassium. Other two patients had been treated with meropenem and cephalosporin antibiotics respectively before admission, and they had been at recovery stage when they were hospitalized. Thoracic close drainage and thoracoscopy were performed respectively in 18 cases and 3 cases, respectively. After a follow up of more than 6 months, chest CT showed that almost all lesions in lungs recovered during 4-6 months. No one received pneumonectomy. SPNP has special manifestations. The incidence in infants is higher. Patients' general condition is poor and febrile course is relatively long. All patients manifested fever and cough, with a presence of dyspnea in most of them. WBC, neutrophil and CRP elevated apparently. The characteristic of pleural effusion indicates empyema. In early stage, the chest X-ray and CT showed high-density lobar lesions, followed by low-density lesions and cyst gradually. Bulla of lung and/or hydropneumothorax may appear at the late stage. But if diagnosed and treated promptly, the prognosis of SPNP was relatively good.

Pleural fluid pH: diagnostic, therapeutic, and prognostic value.

Measurement of pleural fluid pH has diagnostic, therapeutic, and prognostic implications in exudative pleural effusions (Table II). A parapneumonic effusion with a pleural fluid pH below 7.2 indicates an empyema is forming which necessitates chest tube drainage in all patients, whereas a pleural fluid pH over 7.3 does not require drainage. If the pH of a parapneumonic effusion is 7.2 to 7.3, serial pleural fluid pH measurements with clinical observation will help to determine the need for chest tube drainage. A pleural fluid glucose level of below 60 mg/dl and a lactic dehydrogenase level over 1,000 IU/dl in conjunction with a pleural fluid pH of 7.2 to 7.3 indicate an impending empyema. These findings are consistent with our clinical experience in patients with parapneumonic effusion. Tuberculous pleural effusions had a pleural fluid pH below 7.4 in all reported patients. This pH may be of value in distinguishing tuberculous pleural effusions from recent malignant effusions, which tend to have a higher pleural fluid pH, particularly if used in conjunction with other pleural fluid values, cell counts, and other clinical parameters. In patients with malignant pleural effusions, a pH of less than 7.3 is usually seen in those effusions present for several months and is associated with a lower glucose level and a higher white cell count and lactic dehydrogenase level. Results of cytologic study of the pleural fluid and pleural biopsy are often positive, there is poor response to sclerosing agents, and the prognosis is poor. A rheumatoid pleural effusion most often has a pleural fluid pH below 7.3. A pleural fluid pH below 6 is seen almost exclusively in esophageal rupture but rarely with empyemas, whereas a pleural fluid pH below 7 occurs in esophageal rupture, empyema, and rheumatoid pleural effusions. In pleural effusions secondary to congestive heart failure, the pH is almost always greater than 7.4 unless systemic acidemia coexists, in which case the pleural fluid pH is within 0.04 units of the simultaneous arterial pH. The major value of pleural fluid pH is to determine the need for chest tube drainage in parapneumonic effusions and to determine the response to sclerosing agents in patients with malignant pleural effusions. As with all diagnostic tests, the results should be interpreted in the context of other diagnostic tests of the pleural fluid and clinical aspects before diagnostic or therapeutic decisions are made.

Clinical and laboratory parameters of pleural tuberculosis.

This prospective observational clinical study was done to find out the clinical and laboratory parameters of pleural tuberculosis patients, to find out a sensitive and specific tool for diagnosis and to see the effectively of a standard anti-TB regime Isoniazide, Rifampicine, Pyrazinamide, Ethambutol, (2HRZE/4HR) for treatment of pleural tuberculosis in an adult medicine unit, department of Medicine, Chittagong Medical College Hospital, Chittagong, Bangladesh. A series of total thirty-three consecutive pleural tuberculosis patients admitted in that unit over a period of 6 months were enrolled. All thirty-three pleural tuberculosis patients were observed for their demographic and clinical parameters and undergone some relevant investigations like complete blood count, Mantoux test, pleural fluid study and pleural histopathological study. Later on, they were put on anti-tuberculosis therapy without steroid and followed their response after one month. All patients of pleural tuberculosis presented in this medicine unit had fever and cough associated with chest pain (87.9%), dysnoea (42.4%), haemoptysis (9.1%), weight loss (84.4%), anorexia (90.9%). Age of presentation was 34.1+/-16.2 years and of them, 60.7% patients were below 30. Mean Erythrocyte Sedimentation Rate (ESR) was 97.04 mm in 1st hour and 57.6% cases had ESR more than 100. 63.6% had Mantoux Test (MT) positive (>10 mm). Only 6.1% had hemorrhagic effusion and others had straw colored fluid. Mean pleural fluid protein is 5.9 gram/L and sugar 65.7 mg/dl. No Acid Fast Bacilli (AFB) was seen on microscopy in pleural fluid. Pleural biopsy revealed 54.5% granulomatous lesion with or without caseation and another 24.2% shows chronic inflammation. Seventy seven percentage (77%) patients were attended follow-up clinic after 1 month and all patients (100%) were improved with this anti-TB therapy. Of the total patient treated with anti TB drug, 53.5% had no pleural effusion, other had minimum effusion. Only 6.06% require subsequent steroid addition and other measures. Pleural biopsy is the investigations of choice for pleural tuberculosis especially in resource poor countries. Pleural tuberculosis can be treated with a standard anti-TB regime successfully without steroid.

Malignant Pleural Effusion -- Evaluation -- Histopathological Diagnosis

Pleural Fluid Analysis - Normal physicochemical characteristics include pH between 7.60 and 7.64, protein levels of less than 2 percent (2 gm/dl), less than 100 WBC’s per cubic millimeter, Glucose content similar to that of plasma, LDH level less than half of that present within the plasma. The following parameters can be used in making a diagnosis of malignant etiology underlying the accumulation of pleural fluid – pH less than 7.30, LDH levels greater than 1000 U/l, reduced pleural fluid glucose concentration (30 to 50 mg/dl), lymphocyte values greater than 50 to 70%. [109] [115]

[Pleural mesothelioma: experience with 62 cases in 9 years].

To describe the diagnostic approach, clinical and radiological characteristics, and survival of patients with pleural mesothelioma treated in our hospital over a 9-year period. All patients with a diagnosis of pleural mesothelioma diagnosed in our hospital from January 1992 through December 2000 were studied. Sixty-two patients (49 men) with a mean age of 65 years (range, 45-85) were diagnosed. Probable or known contact with asbestos was established for 41 patients (66%). Ninety-four percent of the patients had chest pain or dyspnea at the onset of clinical assessment. The tumor was situated in the right hemithorax in 33 patients; 59 patients had pleural effusion, and 3 only had pleural thickening. The pleural fluid was bloody in 19% of patients, glucose levels were less than 60 mg/dL in 44%, and the pH of pleural fluid was less than 7.20 in 19%. The diagnosis was established by pleural biopsy for 52%, and by thoracoscopy or thoracotomy for 44%. The median survival was 11 months (95% confidence interval, 8-15); the probability of survival was 0.22 after 2 years, and 0.09 after 5. For the subgroup of patients with epithelial tumors the probability of survival was 0.31 after 2 years and 0.16 after 5 years. In the univariate analysis the predictors of survival were general clinical status (Karnofsky scale), platelet count, serum albumin level, pleural pH, glucose and lactate dehydrogenase levels, and histological type. The clinical, radiological, and biochemical characteristics of the pleural fluid from patients with pleural mesothelioma and their survival rate were described.

Urinothorax

Diagnosis Due to the main symptoms typically being urological rather than respiratory, the condition requires exclusion of other conditions and the identification of specific symptoms before diagnosis. Pleural fluid analysis is one way to diagnose the condition. The pleural fluid is most often straw-colored, and it has a distinct smell like ammonia. The fluid usually has a nucleated cell count between 50 and 1500 per cm3. The pH of the fluid is usually between 5 and 7. Primary factors for diagnosing urinothorax by pleural fluid include low protein and high lactate dehydrogenase content. Low glucose levels and acidity are also described, but are not reliable ways to diagnose or rule out urinothorax. The most important chemical diagnostic factor of the fluid is that the ratio of creatinine to serum is more than 1 and usually more than 10.

Pleurisy

Sometimes an x-ray is taken while lying on the painful side. This may show fluid, as well as changes in fluid position, that did not appear in the vertical x-ray. Blood test Blood tests can detect bacterial or viral infections, pneumonia, rheumatic fever, a pulmonary embolism, or lupus. ECG Electrocardiography test can determine if a heart condition contributes to the symptoms. Ultrasound Ultrasonography uses sound waves to create an image. It may show where fluid is located in the chest. It also can show some tumors. Although ultrasound may detect fluid around the lungs, also known as a pleural effusion, sound waves are scattered by air. Therefore, an actual picture of the lungs cannot be obtained with ultrasonography. Computed tomography (CT) scan A CT scan provides a computer-generated picture of the lungs that can show pockets of fluid. It also may show signs of pneumonia, a lung abscess, or a tumor.

Hemothorax

Although imaging techniques can demonstrate that fluid is present within the pleural space, it may be unclear what this fluid represents. To establish the nature of the fluid, a sample can be removed by inserting a needle into the pleural cavity in a procedure known as a thoracentesis or pleural tap. In this context, the most important assessment of the pleural fluid is the percentage by volume that is taken up by red blood cells (the hematocrit) A hemothorax is defined as having a hematocrit of at least 50% of that found in the affected person's blood, although the hematocrit of a chronic hemothorax may be between 25 and 50% if additional fluid has been secreted by the pleura. Pleural fluid can dilute hemothoraces in as low as 3–4 days. The red blood cells in the effusion spontaneously break down. Distinguishing the pleural fluid from blood by colour is impossible when the hematocrit value is over 5%. For these reasons, even if there is a hematocrit value under 50%, further

[Case of tuberculous pleurisy with eosinophilic pleural effusion and hematological eosinophilia].

A 30-year-old man suffered from a chest-pain on his left side and was also having a low-grade fever though he actually neglected these symptoms for a while. Later, he was referred to our hospital due to the detection of chest abnormal shadows through the mass examination of chest X-ray taken on 18th October, 2005. His chest X-ray showed bilateral pleural effusion and it was confirmed that the right pleural effusion was encapsulated by his chest CT. The patient's hematological examination performed during his initial visit, showed an increased level of WBC with blood eosinophilia. He also had a puncture of pleural effusion at the time of admission to the center. Moreover, pleural effusion on both sides was exudative and elevations of ADA and eosinophil count as well were traced. In the patient's right pleural effusion, mycobacterium tuberculosis direct (MTD) test was positive. As there were no findings suggesting collagen disease, malignancy, parasite infection, and other complications, he was diagnosed as tuberculous pleurisy with eosinophilic pleural effusion and blood eosinophilia. He was treated with four antitubercular agents, namely, INH, RFP, EB and PZA. As the result, his pleural effusion and blood eosinophil counts were decreased along with an improvement in inflammatory reaction. The most common conditions associated with eosinophilic pleural effusion are described as malignancy, collagen disease, paragonimiasis, drug induced pleurisy, asbestosis, pneumothorax, and trauma, while there are only a few reports about such eosinophilic pleural effusion caused by tuberculous pleurisy. In this case, he also showed blood eosinophilia. Based on these findings, we finally came to the conclusion that the case is a very rare and significantly unique case of eosinophilic pleurisy with blood eosinophilia.

Pleural effusion

Chemical composition including protein, lactate dehydrogenase (LDH), albumin, amylase, pH, and glucose Gram stain and culture to identify possible bacterial infections White and red blood cell counts and differential white blood cell counts Cytopathology to identify cancer cells, but may also identify some infective organisms Other tests as suggested by the clinical situation – lipids, fungal culture, viral culture, tuberculosis cultures, lupus cell prep, specific immunoglobulins Light's criteria Definitions of the terms "transudate" and "exudate" are the source of much confusion. Briefly, transudate is produced through pressure filtration without capillary injury while exudate is "inflammatory fluid" leaking between cells.

Bornholm disease

Physical exam findings In a studied case of Bornholm disease the chest pain was unable to be reproduced on palpation and failed to improve with changes in position. The pain was made worse during deep inhalation. A pleural rub was present, however lung auscultation was clear and rashes were absent. Laboratory findings and imaging In a prior case of Bornholm disease the laboratory results showed the white blood cell count, hemoglobin, hematocrit, creatinine, liver function test (LFT), troponin, and creatine kinase (CK) were all within normal limits. The chest x-ray showed bilateral pleural effusions which resolved after infection. The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels were found to be elevated. The electrocardiogram (EKG) did not show any abnormalities related to ischemia.

InternalMed_Harrison

The fluid is straw colored and at times hemorrhagic; it is an exudate with a protein concentration >50% of that in serum (usually ~4–6 g/dL), a normal to low glucose concentration, a pH of ~7.3 (occasionally <7.2), and detectable white blood cells (usually 500–6000/μL). Neutrophils may predominate in the early stage, but lymphocyte predominance is the typical finding later. Mesothelial cells are generally rare or absent. AFB are rarely seen on direct smear, and cultures often may be falsely negative for M. tuberculosis; positive cultures are more common among postprimary cases. Determination of the pleural concentration of adenosine deaminase (ADA) may be a useful screening test, and TB may be excluded if the value is very low. Lysozyme is also present in the pleural effusion. Measurement of IFN-γ, either directly or through stimulation of sensitized T cells with mycobacterial antigens, can be helpful. Needle biopsy of the pleura is often required for diagnosis and is recommended over

Pleural effusion

Thoracentesis Once a pleural effusion is diagnosed, its cause must be determined. Pleural fluid is drawn out of the pleural space in a process called thoracentesis, and it should be done in almost all patients who have pleural fluid that is at least 10 mm in thickness on CT, ultrasonography, or lateral decubitus X-ray and that is new or of uncertain etiology. In general, the only patients who do not require thoracentesis are those who have heart failure with symmetric pleural effusions and no chest pain or fever; in these patients, diuresis can be tried, and thoracentesis is avoided unless effusions persist for more than 3 days. In a thoracentesis, a needle is inserted through the back of the chest wall in the sixth, seventh, or eighth intercostal space on the midaxillary line, into the pleural space. The use of ultrasound to guide the procedure is now standard of care as it increases accuracy and decreases complications. After removal, the fluid may then be evaluated for:

Ascites

Classification Ascites exists in three grades: Grade 1: mild, only visible on ultrasound and CT Grade 2: detectable with flank bulging and shifting dullness Grade 3: directly visible, confirmed with the fluid wave/thrill test Pathophysiology Ascitic fluid can accumulate as a transudate or an exudate. Amounts of up to 35 liters are possible. Roughly, transudates are a result of increased pressure in the hepatic portal vein (>8 mmHg, usually around 20 mmHg (e.g., due to cirrhosis), while exudates are actively secreted fluid due to inflammation or malignancy. As a result, exudates are high in protein and lactate dehydrogenase and have a low pH (<7.30), a low glucose level, and more white blood cells. Transudates have low protein (<30 g/L), low LDH, high pH, normal glucose, and fewer than 1 white cell per 1000 mm3. Clinically, the most useful measure is the difference between ascitic and serum albumin concentrations. A difference of less than 1 g/dl (10 g/L) implies an exudate.