ETIOLOGY
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The pleural space exists between the parietal and visceral pleura. This space has a small amount of fluid, the purpose of which is to lubricate the parietal and visceral pleura to assist with lung mechanics.
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The amount of pleural fluid within each pleural space at any given time is <1 ml. The rate of pleural fluid production is approximately 0.01 mL/kg/h. The route of pleural fluid egress is through parietal pleural lymphatics normally at a rate 28 times faster than production.
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In diseased states, either the egress or production of pleural fluid results in pathologic states of pleural fluid accumulation. There are several factors that can cause an increase in pleural fluid.
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Increase in hydrostatic pressure (i.e., congestive heart failure)
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Decrease in oncotic pressure (i.e., malnourished patients)
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Increase in the space available for pleural fluid accumulation (lung collapse)
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Increase in the permeability of the microvascular circulation secondary to inflammatory mediators
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Inadequate egress of pleural fluid through lymphatics secondary to obstruction from tumor or fibrosis
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Transdiaphragmic movement of ascitic fluid into the pleural space
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Increased production of fluid by intrathoracic malignancy
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CLINICAL FEATURES
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An extensive history including prior surgery, medications, connective tissue disorders, past hospitalization, and social history can assist with focusing the differential diagnosis in a patient presenting with a pleural effusion.
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Dyspnea is the predominant complaint and is more prominent with activity.
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Other symptoms include cough and chest pressure.
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Physical examination findings include
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Decreased breath sounds on the affected side
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Dullness to percussion
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Decreased fremitus.
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DIAGNOSIS
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Imaging studies
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Plain chest radiographs.
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There is typically blunting of the costophrenic angle, and when apparent, a meniscus on the chest x-ray study signifying a pleural effusion.
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Chest x-ray is not helpful in diagnosing pleural effusions until the amount in the thoracic space exceeds 500 mL.
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To determine how loculated the effusion appears, a decubitus film is helpful to visualize the fluid layering on the lateral chest wall or mediastinum.
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Pleural effusions in conjunction with other radiographic findings can help with determining the etiology of the effusion.
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Complete opacification of the hemithorax with contralateral shift of the mediastinum is usually the result of malignancy, or other cause of a massive effusion.
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Bilateral effusion in the presence of a large cardiac silhouette is typically suggestive of congestive heart failure being the cause of the effusions. Other etiologies for bilateral effusions with a normal cardiac silhouette include systemic illnesses such as lupus erythematosus, renal failure, or cirrhosis.
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Ultrasound
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This can detect effusions as small as 50 mL.
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This mode of imaging helps to determine whether the fluid is loculated and assist with localization of the fluid for thoracentesis.
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Computer tomography
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This mode of imaging may be helpful in determining the etiology of the pleural effusion, assessing if the effusion is loculated, and assisting with treatment plans ( Fig. 47-1 ).
Figure 47-1
A and B , Computed tomography scan evaluation of patient after double lung transplant with large bilateral pleural effusions and compressive atelectasis.
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Thoracentesis
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The initial step in evaluating the patient with a pleural effusion is determining if the effusion is transudative or exudative.
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Transudate pleural effusion usually results from an increase in hydrostatic pressure or a decrease in oncotic pressure ( Table 47-1 ).
TABLE 47-1▪
CAUSES OF TRANSUDATIVE EFFUSIONS
Congestive heart failure
Cirrhosis
Nephrotic syndrome
Peritoneal dialysis
Atelectasis
Myxedema
Pulmonary edema
Hypoalbuminemia
Constrictive pericarditis
Malignancy
Sarcoidosis
Pulmonary embolism
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Exudative effusion results from an increase in permeability ( Table 47-2 ).
TABLE 47-2▪
CAUSES OF EXUDATIVE PLEURAL EFFUSIONS
Malignancy
Lung
Lymphoma
Mesothelioma
Metastatic disease
Infectious
Parapneumonic condition
Tuberculosis
Fungal infection
Viral infection
Parasitic
Abdominal abscess
Hepatitis
Noninfectious Gastrointestinal
Pancreatitis
Esophageal rupture
Abdominal surgery
Variceal sclerotherapy
Collagen Vascular Disease
Lupus erythematosus
Rheumatoid arthritis
Wegener’s granulomatosis
Churg-Strauss syndrome
Familial Mediterranean fever
Sjögren’s syndrome
Immunoblastic lymphadenopathy
Other
Pulmonary embolism
Dressler’s syndrome
Asbestos
Uremia
Trapped lung
Radiation therapy
Meig’s syndrome
Trauma
Lymphatic Disease
Chylothorax
Lymphangioleiomyomatosis
Yellow nail syndrome
Drug Induced
Drug-induced lupus erythematosus
Nitrofurantoin
Dantrolene
Amiodarone
Methysergide
Procarbazine
Practolol
Bromocriptine
Minoxidil
Bleomycin
Methotrexate
Methysergide
Mitomycin
Adapted from Bartter T, Santarelli R, Akers SM, Pratter MR. The evaluation of pleural effusion. Chest 1994;106:1209-1214 (with permission).
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This procedure can be both diagnostic and therapeutic ( Figs. 47-2 and 47-3 ).
Figure 47-2
A and B , Patient after coronary artery bypass graft surgery with moderate-size left pleural effusion.
Figure 47-3
A and B , Same patient in Figure 47-2 after complete thoracentesis and medical therapy of heart failure.
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This will assist in determining the characteristics of the effusion (transudate versus exudates) and will determine if the lung will re-expand and replace the space initially occupied by the pleural effusion.
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There are no absolute contraindications for thoracentesis.
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Relative contraindications are coagulopathy, an uncooperative patient, and cutaneous disease such as herpes zoster infection at the needle entry site.
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Not all pleural effusions need to be analyzed if the etiology of the effusion is known (e.g., postsurgical changes after thoracic or abdominal surgery or related to congestive heart failure). But if the cause or etiology is unclear, diagnostic thoracentesis should be performed.
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Diagnostic thoracentesis should be performed when a clinically suspected pleural effusion has been confirmed on chest x-ray study and remains undiagnosed.
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Therapeutic thoracentesis is performed to relieve symptoms associated with large pleural effusions such as dyspnea.
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Lung volumes increase by about one third of the volume of fluid withdrawn, but arterial blood gases usually show little change.
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Chest x-ray study should be performed following successful and unsuccessful thoracentesis.
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Complications associated with thoracentesis include
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Pneumothorax
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The incidence of pneumothorax varies between 3% and 20%. Thoracentesis can be performed on patients receiving artificial ventilation. The incidence of pneumothorax in this patient population has been reported to be 6%.
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Pneumothorax following ultrasound-guided thoracentesis may be due to the generation of nonuniform pressure gradients over the visceral pleura, producing stress failure and microfistulae. This scenario would occur particularly if the lung cannot conform to a new geometric chest configuration with large volume drainage. Thus, in some cases, pneumothorax may be unavoidable and unrelated to inadvertent lung puncture.
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Pain at the site of the procedure
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Vasovagal reaction
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Re-expansion pulmonary edema
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Rare complication. Reported in 1% to 2% of patients ; likely less
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More likely to occur with prolonged lung collapse
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Pathogenesis is not well characterized. Edema fluid analysis compatible with permeability edema. Mechanical stress failure of alveolar-capillary membranes due to high negative pleural pressures or reperfusion, or both, are likely mechanisms.
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Clinical features include acute dyspnea, cough, pink frothy sputum (sometimes copious), signs of respiratory distress, and cyanosis, which can progress over several hours to 1 to 2 days.
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Chest x-ray study shows unilateral pulmonary edema; can be bilateral on occasion ( Fig. 47-4 ).
Figure 47-4
Chest x-ray study depicting re-expansion pulmonary edema ( A ) following large volume pleural fluid removal. The patient is now intubated. ( B , Baseline film showing large pleural effusion.)
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Treatment: supportive
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Prevention: Do not remove >1 liter of fluid unless monitoring pleural pressures. With chest tube insertion, connect to underwater-seal, not negative pressure.
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Outcome: up to 20% mortality rate reported, but the rate is likely lower with current treatment approaches for adult respiratory distress syndrome.
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Subcutaneous hematoma
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Pleural infection.
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EVALUATION OF PLEURAL EFFUSIONS
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Before sending the pleural effusion to the laboratory for evaluation, the bedside visual inspection of the fluid may assist in determining a diagnosis.
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Grossly bloody effusions: trauma or malignancy
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Whitish fluid/milky: chylothorax or pseudochylous effusion
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Foul odor and/or pus: empyema
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Food particles within the fluid: esophageal rupture.
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Brown/“anchovy paste”: amebic liver abscess with rupture into pleural cavity
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Yellow/green with or without debris: rheumatoid arthritis
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Black: Aspergillus niger empyema
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Viscous: mesothelioma
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Ammonia odor: urinothorax
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Light’s criteria is still the standard with which other diagnostic tests are compared to evaluate pleural fluid. Performed by simultaneously measuring the lactate dehydrogenase levels (LDH) and protein in the serum and pleural fluid.
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Exudate . One or more of the following
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Pleural fluid/serum LDH greater than 0.6
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Pleural fluid/serum protein greater than 0.5
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Pleural fluid LDH greater than two thirds of upper normal limits for serum
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A pleural fluid/serum cholesterol greater than 0.3 is a new addition.
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Transudate . None of the above-mentioned criteria are met.
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Other studies ordered at the time of the thoracentesis include ( Table 47-3 ):
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pH
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Decreased pH (<7.20) in pleural effusions is related to increased acid production by cells and organisms and due to impaired efflux from the pleural space due to pleuritis or pleural effusions. Causes include complicated parapneumonic effusion and empyema, effusions associated with esophageal rupture, malignant effusions; occasionally, rheumatoid and tuberculous effusions.
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Glucose
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Decreased glucose (<60 mg/dl) is due to decreased transport of glucose from the blood to the pleural fluid (impact on glucose transporters), as well as increased utilization by polymorphonuclear leukocytes, malignant cells, and bacteria. The differential diagnosis of low glucose, low pH effusions are seen in Table 47-4 .
TABLE 47-4▪
CAUSES OF LOW GLUCOSE, LOW pH EFFUSIONS
Rheumatoid pleurisy
Empyema
Esophageal rupture
Malignancy
Tuberculosis
Lupus pleuritis
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Cell count and differential
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Leukocyte count: greater than 50,000/μL complicated parapneumonic effusion/empyema; greater than 10,000/μL indicates significant inflammation; transudates usually less than 1000/μL
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Lymphocye-predominant: tuberculosis (also absence of reactive mesothelial cells); lymphoma main considerations
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Eosinophils: mainly associated with hemothorax, prior thoracentesis, pneumothorax, pulmonary infarction and parasitic disease. Note: more than 30% is idiopathic.
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Basophils: more than 10% can occur with leukemia
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Plasma cells: myeloma and related conditions
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Cytology
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When appropriate, also include
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Gram’s stain and culture
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Triglycerides and cholesterol if chylothorax or pseudochylous effusion suspected
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Amylase (and serum amylase) if pancreatitis, pancreatic pseudocyst, malignancy, and esophageal rupture are considered.
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Antinuclear antibody (ANA), rheumatoid factor, lupus erythematosis (LE) cells
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TABLE 47-3▪
EXUDATIVE PLEURAL FLUID ANALYSIS
Low Glucose (<60)
Complicated parapneumonic effusion
Rheumatoid
Malignant
Tuberculous
Low pH (<7.2)
Empyema
Complicated parapneumonic effusion
Rheumatoid
Malignant
Tuberculous
Esophageal rupture
Elevated Amylase
Esophageal rupture
Pancreatitis
Malignancy
Elevated RBCs (>100,000/mm 3 )
Trauma
Malignancy
Pulmonary embolism
Hemothorax
Elevated Lymphocytes
Lymphoma
Other malignancy
Chronic infection
Tuberculosis
Fungi
Postpericardiotomy syndrome
Sarcoidosis
Eosinophils
Hemothorax
Pneumothorax
Thoracentesis
Parasitic disease
Pulmonary infarction
Drug induced
Asbestos
Malignancy
RBCs, red blood cells.
Adapted from Bartter T, Santarelli R, Akers SM, Pratter MR. The evaluation of pleural effusion. Chest 1994;106:1209-1214 (with permission).
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Transudate effusion
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Secondary to imbalances in the hydrostatic or oncotic pressures, or a movement of fluid from the peritoneal cavity.
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The most common etiology is congestive heart failure, with the other etiologies being those seen in Table 47-1 .
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Exudate effusion
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The differential diagnosis of exudative effusion is significantly larger than that of transudate effusion, as seen in Table 47-2 .
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Table 47-4 narrows the differential diagnosis based on characteristics from the pleural effusion analysis.
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PARAPNEUMONIC EFFUSION AND EMPYEMA
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Definition, incidence and importance:
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Parapneumonic effusion is an effusion accompanying pneumonia and is not limited solely to bacterial pathogens (can include atypical and viral pneumonias).
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Occurs in 20% to 57% of hospitalized patients with bacterial pneumonia.
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Presence of a parapneumonic effusion is associated with higher mortality rates for pneumonia. It can become complicated, increasing morbidity, added interventions, hospital stay, costs, and the mortality rate.
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Can progress very rapidly and become loculated very quickly, so diagnosis and drainage is very important.
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An empyema is classically defined by the presence of pus on aspiration of the pleural space. The presence of organisms on Gram’s stain of aspirated pleural fluid has also been included in the definition.
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Pathogenetic classification and risk stratification
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Divided into three stages
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The stages represent a continuum, with no well-defined temporal sequences (i.e., patient, clinical setting, organism specific).
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Stage 1: Uncomplicated parapneumonic effusion due to movement of fluid from the lung, together with increased permeability of pleural capillaries in the presence of limited capacity to efficiently resorb the fluid. The fluid is exudative, sterile, and free flowing, and resolves with resolution of the pneumonia.
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Stage 2: Complicated parapneumonic effusion due to fibroproliferation, resulting in loculations, bacterial invasion, influx of neutrophils, pleural fluid acidosis (pH, 7.2), low glucose (<60 mg/dL) and higher LDH (3 times upper limit of normal serum value).
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Negative bacterial studies in the presence of a complicated parapneumonic effusion are common and can be due to: antibiotic therapy, sampling error due to a missing infected loculation, clearance of organisms from pleural space, and the presence of fastidious organisms that are difficult to culture, such as anaerobes.
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Loculations and visceral peel are flimsy and easily lysed.
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Stage 3: Empyema : Fulfills above-mentioned definition. Associated with progressive locuation and the proliferation of fibroblasts, resulting in visceral and parietal pleural peel that can prevent full lung expansion (trapped lung)
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Risk Stratification for parapneumonic effusion and empyema: An evidence-based approach was developed by the American College of Chest Physicians (ACCP) Concensus Panel. This is depicted in Table 47-5 .
TABLE 47-5▪
CATEGORIZING RISK FOR POOR OUTCOME IN PATIENTS WITH PARAPNEUMONIC EFFUSIONS
Pleural Space Anatomy
Pleural Fluid Bacteriology
Pleural Fluid Chemistry
Category
Risk of Poor Outcome
Drain
A0
Minimal, free-flowing (<10 mm on lateral decubitus film)
AND
Bx
Culture and Gram’s AND stain results unknown
AND
Cx
pH unknown
1
Very low
No
A1
Small to moderate free-flowing effusion (>10 mm and <1/2 hemithorax)
AND
B0
Neg culture and Gram’s stain
OR
C0
pH ≥ 7.20
2
Moderate
No
A2
Large, free-flowing (≥ 1/2 hemithorax) loculated effusion, or effusion with thickened parietal pleura
OR
B1
Positive culture or Gram’s stain
OR
C1
pH < 7.20
3
Moderate
Yes
B2
pus
4
High
Yes 
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