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PLEURAL EFFUSION 
Dr Nirav Dhinoja
INTRODUCTION 
 There is normally a very thin layer of fluid (from 2 to 
10 μm thick) between the two pleural surfaces, the 
parietal pleura and visceral pleura. 
 The pleural space and the fluid within it are not 
under static conditions. 
 During each respiratory cycle the pleural pressures 
and the geometry of the pleural space fluctuate 
widely. Fluid enters and leaves the pleural space 
constantly.
 The serous membrane 
covering the lung 
parenchyma is called the 
visceral pleura. 
 The remainder of the lining of 
the pleural cavity is the 
parietal pleura. 
 The parietal pleura receives 
its blood supply from the 
systemic capillaries. 
 The visceral pleura is 
supplied predominantly by 
branches of the bronchial 
artery in humans
The lymphatic vessels in the parietal 
pleura are in direct 
communication with the pleural space by 
means of stomas. 
These stomas are the only route through 
which cells and large particles can leave 
the pleural space. 
Although there are abundant lymphatics 
in the visceral pleura, these lymphatics 
do not appear to participate in the 
removal of particulate matter from the 
pleural space.
MECHANISM OF PLEURAL FLUID TURNOVER 
Dependent on the hydrostatic and oncotic pressures across membranes. 
When the capillaries in the parietal pleura are considered, it can be seen that the 
net hydrostatic pressure favoring the movement of fluid from these capillaries to 
the pleural space 
is the systemic capillary pressure (30cm H2O) minus the 
negative pleural pressure (-5cm H2O) or 35cm H2O. 
Opposing this is the oncotic pressure in the blood (34cm H2O) minus the oncotic 
pressure in the pleural fluid (5 cm H2O), or 29cm H2O. 
The resulting net pressure differences of 6 cm H2O (35-29) favors movement of 
fluid from the parietal pleura into the pleural space.
Parietal Pleura Visceral 
Pleura Space Pleura 
Hydrostatic Pressure 
+30 - 5 + 24 
35 29 
6 0 
Net 
29 29 
+ 34 + 5 +34 
Oncotic Pressure
NORMAL COMPOSITION PLEURAL FLUID 
 Volume 0.2 mL/kg 
 Cells/ mm3 1000 – 5000 
 Mesothelial cells 60% 
 Monocytes 30% 
 Lymphocytes 5% 
 PMN’s 5% 
 Protein 1-2 g/dL 
 LDH <50% plasma level 
 Glucose  plasma level 
 pH ≥ plasma level
PATHOPHYSIOLOGY 
 Pleural fluid will accumulate when the rate of 
pleural fluid formation is greater than the rate of 
pleural fluid removal by the lymphatics. 
 Pleural effusions have classically been divided into 
 Transudative 
 Exudative
 A transudative pleural effusion occurs when 
alterations in the systemic factors that influence 
pleural fluid movement result in a pleural effusion. 
Ex. Heart failure, nephrotic syndrome, hepatic 
cirhosis. 
 Exudative pleural effusions occur when the pleural 
surfaces are altered. Ex. Pleurisy.
ETIOLOGY 
Elevated pleural capillary pressure : 
Congestive heart failure, pericardial disease. 
Elevated pleural permeability : 
Pleural inflammation, neoplastic pleural disease 
(metastatic disease or mesotheliomas), pulmonary emboli, 
systemic lupus erythematosus (SLE). 
Decreased serum oncotic pressure : 
Cirrhosis, nephrotic syndrome, myxedema. 
Dysfunction of parietal pleura lymphatics drainage. 
Trauma, such as esophageal perforation, post-cardiac injury 
syndrome.
CLINICAL FEATURES 
Many patients have no symptoms due to the 
effusion when effusion is small. 
Pleuritic chest pain is the usual symptom of 
pleural inflammation. 
Irritation of the pleural surfaces may also result in a 
dry, nonproductive cough. 
With larger effusions, dyspnea results from lung 
compression.
PHYSICAL EXAMINATION 
 Signs are proportional to amount of effusion. 
 Fullness of intercostal spaces. 
 Decreased or absent tactile fremitus. 
 Dullness to percussion. 
 Diminished breath sounds over the site of the effusion. 
 Change in findings with change in position. 
 Signs of pneumonia like bronchial breathing,crackles 
etc.
CHEST XRAY 
The first fluid accumulates in the lowest portion of the thoracic 
cavity, which is the posterior costophrenic angle. 
The earliest radiologic sign of a pleural effusion is blunting of 
the posterior costophrenic angle on the lateral chest 
radiograph. 
If a posteroanterior radiograph is obtained with the patient 
lying on the affected side, free pleural fluid will gravitate 
inferiorly and a pleural fluid line will be visible.
Pleural fluid is loculated when it does not shift freely 
in the pleural space as the patient’s position is 
changed. 
Loculated pleural effusions occur when there are 
adhesions between the visceral and parietal 
pleurae. 
Both ultrasound and computed tomography (CT) 
have useful in making this differentiation.
USG THORAX
CT CHEST
 Should thoracentesis be performed? 
 If thoracentesis is done 
 Is the fluid a transudate or exudate? 
 If the fluid is an exudate 
 What is the etiology?
SHOULD THORACENTESIS BE PERFORMED? 
Most patients should be tapped 
 Newly recognized effusion. 
Two exceptions 
 Small Effusions ( < 1 cm on decubitus) 
 Congestive Heart Failure 
 Thoracentesis only if bilateral effusions not equal. 
 Fever. 
 Pleuritic chest pain. 
 Impending respiratory faillure.
Is The Fluid A Transudate Or Exudate? 
Transudative Effusions 
 Mechanical 
 No capillary leak or cytokine activation 
 Excessive formation or impaired absorption 
 Limits the differential with no additional workup 
 CHF, Cirrhosis, or Nephrotic Syndrome 
 If Exudative, more investigation required 
 Method: LIGHT’s Criteria
LIGHT’S CRITERIA (EXUDATE) 
 Pleural fluid total protein/ serum protein >0.5 
 Pleural total protein > 3g/dl. 
 Pleural fluid LDH/serum LDH > 0.6 
 Pleural fluid LDH > 200 IU/l. 
 Pleural fluid LDH level > 2/3 of upper normal 
level of serum LDH.
EFFUSIONS 
Transudate Exudate 
 Congestive Heart 
Failure 
 Nephrotic syndrome 
 Cirrhosis 
 Meig’s Syndrome 
 Hydronephrosis 
 Peritoneal Dialysis 
 Parapneumonic 
 Malignancy 
 Pulmonary Embolism 
 Tuberculosis 
 Traumatic 
 Collagen Vascular (SLE, 
RA) 
 Drug induced, Uremia, 
Dressler’s syndrome
OTHER USEFUL TESTS 
 Brain Natriuretric Peptide (N<1000 pg/mL) 
 > 1000 in CHF 
 Glucose < 60 mg/dL 
 Empyema or Rheumatoid Arthritis 
 pH < 7.2 Empyema 
 Triglycerides > 110 mg/dL 
 Chylothorax 
 Amylase 
 Malignancy, Pancreatic disease.
OTHER USEFUL TESTS 
 Pleural to blood Hct > 0.5 
 Hemothorax 
 Cell Count 
 PMN predominate in parapneumonic pneumonia. 
 Lymphocyte predominate in malignancy, Tb, CABG. 
 The pleural fluid ADA level above 45 IU/L - tuberculous pleuritis. 
 Fluid Culture 
 Grams stain, bacterial culture, acid fast bacilli smear and culture, 
and fungal culture. 
 Cytology for malignancy.
PLEURAL FLUID MANAGEMENT 
 Observation 
 Defervesce quickly 
 Uncomplicated pleural effusion 
 Therapeutic drainage (thoracentesis) 
 Early exudative phase 
 Tube thoracostomy 
 Complex pleural fluid spaces 
 VATS (Video assisted thoracoscopic surgery) 
 Poor clinical response to above interventions 
 Decortication: removal of pleural peel
 Parapneumonic effusion 
 Any pleural effusion associated with bacterial or 
viral pneumonia 
 Loculated parapneumonic effusion 
 Not free flowing 
 Multiloculated parapneumonic effusion 
 Noncommunicating compartments 
Empyema (fibrosuppurative exudate) 
 Pus in the pleural space. 
 pH < 7.2, Glucose < 60 mg/dL, High LDH.
EMPYEMA 
 Empyema is an accumulation of pus in the pleural 
space. 
 It is most often associated with pneumonia. 
 It can also be produced by : 
 Rupture of a lung abscess into the pleural space. 
 Contamination introduced from trauma or thoracic 
surgery. 
 Mediastinitis or the extension of intra-abdominal 
abscesses.
ETIOLOGY EMPYEMA 
 Infectious Pneumonias 
 Staph aureus 
 Strep pneumonia 
 Gram negative bacilli 
 Tuberculous pleuritis 
Thoracic trauma 
 Severe Sepsis
NATURAL HISTORY EMPYEMA 
 Exudative stage 
 Rapid accumulation of inflammatory fluid 
 Normal pH, Glucose, and LDH level 
 Antibiotics effective 
 Fibropurulent stage 
 PMN’s, Fibrin deposition, loculations occur 
 Low pH and glucose, high LDH 
 Organization stage (fibrothorax) 
 Fibroblast proliferation between pleural layers 
 Pleural peel develops, decortication required
CLINICAL FEATURES 
 Primary signs & symptoms of pneumonia. 
 Most patients are febrile, develop increased work of 
breathing or respiratory distress, and often appear 
more ill. 
 Physical findings are similar to effusion.
DIAGNOSIS 
 Similar to other effusion radiologically. 
 Pleural fluid analysis is must to differentiate. 
 Characteristic of pus : 
 Bacteria are present on Gram staining. 
 pH is <7.20. 
 >100,000 neutrophils/μL. 
 Pleural fluid culture & PCR analysis to identify 
organism.
TREATMENT 
 Systemic antibiotics. 
 Depends on culture & sensitivity report. 
 2 weeks of IV antibiotics.(in staphylococci infection 
response is very slow so required for 3-4wks.) 
 Closed tube drainage. 
 VATS 
 Open decortication.
TREATMENT 
 In the child who remains febrile and dyspneic >72 
hr after initiation of therapy with intravenous 
antibiotics and thoracostomy tube drainage, 
surgical decortication via VATS or open 
thoracotomy may speed recovery. 
 If pneumatoceles form, no attempt should be made 
to treat them surgically or by aspiration, unless they 
reach cause respiratory embarrassment or become 
secondarily infected.
COMPLICATIONS 
 Local 
 Bronchopleural fistula. 
 Pyopneumothorax. 
 Purulent pericarditis. 
 Pulmonary abscesses. 
 Peritonitis from extension 
through the diaphragm. 
 Osteomyelitis of the ribs. 
 Systemic 
 Septicemia. 
 Meningitis 
 Arthritis. 
 Osteomyelitis.
Dr Dhinoja's Guide to Pleural Effusion Diagnosis & Treatment

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Dr Dhinoja's Guide to Pleural Effusion Diagnosis & Treatment

  • 1. PLEURAL EFFUSION Dr Nirav Dhinoja
  • 2. INTRODUCTION  There is normally a very thin layer of fluid (from 2 to 10 μm thick) between the two pleural surfaces, the parietal pleura and visceral pleura.  The pleural space and the fluid within it are not under static conditions.  During each respiratory cycle the pleural pressures and the geometry of the pleural space fluctuate widely. Fluid enters and leaves the pleural space constantly.
  • 3.  The serous membrane covering the lung parenchyma is called the visceral pleura.  The remainder of the lining of the pleural cavity is the parietal pleura.  The parietal pleura receives its blood supply from the systemic capillaries.  The visceral pleura is supplied predominantly by branches of the bronchial artery in humans
  • 4. The lymphatic vessels in the parietal pleura are in direct communication with the pleural space by means of stomas. These stomas are the only route through which cells and large particles can leave the pleural space. Although there are abundant lymphatics in the visceral pleura, these lymphatics do not appear to participate in the removal of particulate matter from the pleural space.
  • 5. MECHANISM OF PLEURAL FLUID TURNOVER Dependent on the hydrostatic and oncotic pressures across membranes. When the capillaries in the parietal pleura are considered, it can be seen that the net hydrostatic pressure favoring the movement of fluid from these capillaries to the pleural space is the systemic capillary pressure (30cm H2O) minus the negative pleural pressure (-5cm H2O) or 35cm H2O. Opposing this is the oncotic pressure in the blood (34cm H2O) minus the oncotic pressure in the pleural fluid (5 cm H2O), or 29cm H2O. The resulting net pressure differences of 6 cm H2O (35-29) favors movement of fluid from the parietal pleura into the pleural space.
  • 6. Parietal Pleura Visceral Pleura Space Pleura Hydrostatic Pressure +30 - 5 + 24 35 29 6 0 Net 29 29 + 34 + 5 +34 Oncotic Pressure
  • 7. NORMAL COMPOSITION PLEURAL FLUID  Volume 0.2 mL/kg  Cells/ mm3 1000 – 5000  Mesothelial cells 60%  Monocytes 30%  Lymphocytes 5%  PMN’s 5%  Protein 1-2 g/dL  LDH <50% plasma level  Glucose  plasma level  pH ≥ plasma level
  • 8. PATHOPHYSIOLOGY  Pleural fluid will accumulate when the rate of pleural fluid formation is greater than the rate of pleural fluid removal by the lymphatics.  Pleural effusions have classically been divided into  Transudative  Exudative
  • 9.  A transudative pleural effusion occurs when alterations in the systemic factors that influence pleural fluid movement result in a pleural effusion. Ex. Heart failure, nephrotic syndrome, hepatic cirhosis.  Exudative pleural effusions occur when the pleural surfaces are altered. Ex. Pleurisy.
  • 10. ETIOLOGY Elevated pleural capillary pressure : Congestive heart failure, pericardial disease. Elevated pleural permeability : Pleural inflammation, neoplastic pleural disease (metastatic disease or mesotheliomas), pulmonary emboli, systemic lupus erythematosus (SLE). Decreased serum oncotic pressure : Cirrhosis, nephrotic syndrome, myxedema. Dysfunction of parietal pleura lymphatics drainage. Trauma, such as esophageal perforation, post-cardiac injury syndrome.
  • 11. CLINICAL FEATURES Many patients have no symptoms due to the effusion when effusion is small. Pleuritic chest pain is the usual symptom of pleural inflammation. Irritation of the pleural surfaces may also result in a dry, nonproductive cough. With larger effusions, dyspnea results from lung compression.
  • 12. PHYSICAL EXAMINATION  Signs are proportional to amount of effusion.  Fullness of intercostal spaces.  Decreased or absent tactile fremitus.  Dullness to percussion.  Diminished breath sounds over the site of the effusion.  Change in findings with change in position.  Signs of pneumonia like bronchial breathing,crackles etc.
  • 13. CHEST XRAY The first fluid accumulates in the lowest portion of the thoracic cavity, which is the posterior costophrenic angle. The earliest radiologic sign of a pleural effusion is blunting of the posterior costophrenic angle on the lateral chest radiograph. If a posteroanterior radiograph is obtained with the patient lying on the affected side, free pleural fluid will gravitate inferiorly and a pleural fluid line will be visible.
  • 14.
  • 15. Pleural fluid is loculated when it does not shift freely in the pleural space as the patient’s position is changed. Loculated pleural effusions occur when there are adhesions between the visceral and parietal pleurae. Both ultrasound and computed tomography (CT) have useful in making this differentiation.
  • 18.  Should thoracentesis be performed?  If thoracentesis is done  Is the fluid a transudate or exudate?  If the fluid is an exudate  What is the etiology?
  • 19. SHOULD THORACENTESIS BE PERFORMED? Most patients should be tapped  Newly recognized effusion. Two exceptions  Small Effusions ( < 1 cm on decubitus)  Congestive Heart Failure  Thoracentesis only if bilateral effusions not equal.  Fever.  Pleuritic chest pain.  Impending respiratory faillure.
  • 20. Is The Fluid A Transudate Or Exudate? Transudative Effusions  Mechanical  No capillary leak or cytokine activation  Excessive formation or impaired absorption  Limits the differential with no additional workup  CHF, Cirrhosis, or Nephrotic Syndrome  If Exudative, more investigation required  Method: LIGHT’s Criteria
  • 21. LIGHT’S CRITERIA (EXUDATE)  Pleural fluid total protein/ serum protein >0.5  Pleural total protein > 3g/dl.  Pleural fluid LDH/serum LDH > 0.6  Pleural fluid LDH > 200 IU/l.  Pleural fluid LDH level > 2/3 of upper normal level of serum LDH.
  • 22. EFFUSIONS Transudate Exudate  Congestive Heart Failure  Nephrotic syndrome  Cirrhosis  Meig’s Syndrome  Hydronephrosis  Peritoneal Dialysis  Parapneumonic  Malignancy  Pulmonary Embolism  Tuberculosis  Traumatic  Collagen Vascular (SLE, RA)  Drug induced, Uremia, Dressler’s syndrome
  • 23. OTHER USEFUL TESTS  Brain Natriuretric Peptide (N<1000 pg/mL)  > 1000 in CHF  Glucose < 60 mg/dL  Empyema or Rheumatoid Arthritis  pH < 7.2 Empyema  Triglycerides > 110 mg/dL  Chylothorax  Amylase  Malignancy, Pancreatic disease.
  • 24. OTHER USEFUL TESTS  Pleural to blood Hct > 0.5  Hemothorax  Cell Count  PMN predominate in parapneumonic pneumonia.  Lymphocyte predominate in malignancy, Tb, CABG.  The pleural fluid ADA level above 45 IU/L - tuberculous pleuritis.  Fluid Culture  Grams stain, bacterial culture, acid fast bacilli smear and culture, and fungal culture.  Cytology for malignancy.
  • 25. PLEURAL FLUID MANAGEMENT  Observation  Defervesce quickly  Uncomplicated pleural effusion  Therapeutic drainage (thoracentesis)  Early exudative phase  Tube thoracostomy  Complex pleural fluid spaces  VATS (Video assisted thoracoscopic surgery)  Poor clinical response to above interventions  Decortication: removal of pleural peel
  • 26.  Parapneumonic effusion  Any pleural effusion associated with bacterial or viral pneumonia  Loculated parapneumonic effusion  Not free flowing  Multiloculated parapneumonic effusion  Noncommunicating compartments Empyema (fibrosuppurative exudate)  Pus in the pleural space.  pH < 7.2, Glucose < 60 mg/dL, High LDH.
  • 27. EMPYEMA  Empyema is an accumulation of pus in the pleural space.  It is most often associated with pneumonia.  It can also be produced by :  Rupture of a lung abscess into the pleural space.  Contamination introduced from trauma or thoracic surgery.  Mediastinitis or the extension of intra-abdominal abscesses.
  • 28. ETIOLOGY EMPYEMA  Infectious Pneumonias  Staph aureus  Strep pneumonia  Gram negative bacilli  Tuberculous pleuritis Thoracic trauma  Severe Sepsis
  • 29. NATURAL HISTORY EMPYEMA  Exudative stage  Rapid accumulation of inflammatory fluid  Normal pH, Glucose, and LDH level  Antibiotics effective  Fibropurulent stage  PMN’s, Fibrin deposition, loculations occur  Low pH and glucose, high LDH  Organization stage (fibrothorax)  Fibroblast proliferation between pleural layers  Pleural peel develops, decortication required
  • 30. CLINICAL FEATURES  Primary signs & symptoms of pneumonia.  Most patients are febrile, develop increased work of breathing or respiratory distress, and often appear more ill.  Physical findings are similar to effusion.
  • 31. DIAGNOSIS  Similar to other effusion radiologically.  Pleural fluid analysis is must to differentiate.  Characteristic of pus :  Bacteria are present on Gram staining.  pH is <7.20.  >100,000 neutrophils/μL.  Pleural fluid culture & PCR analysis to identify organism.
  • 32. TREATMENT  Systemic antibiotics.  Depends on culture & sensitivity report.  2 weeks of IV antibiotics.(in staphylococci infection response is very slow so required for 3-4wks.)  Closed tube drainage.  VATS  Open decortication.
  • 33. TREATMENT  In the child who remains febrile and dyspneic >72 hr after initiation of therapy with intravenous antibiotics and thoracostomy tube drainage, surgical decortication via VATS or open thoracotomy may speed recovery.  If pneumatoceles form, no attempt should be made to treat them surgically or by aspiration, unless they reach cause respiratory embarrassment or become secondarily infected.
  • 34. COMPLICATIONS  Local  Bronchopleural fistula.  Pyopneumothorax.  Purulent pericarditis.  Pulmonary abscesses.  Peritonitis from extension through the diaphragm.  Osteomyelitis of the ribs.  Systemic  Septicemia.  Meningitis  Arthritis.  Osteomyelitis.