This document discusses pleural effusions, which occur when fluid accumulates in the pleural space between the lungs and chest wall. A small amount of fluid is normal but excess fluid can accumulate if the rate of fluid formation exceeds drainage by lymphatics. Effusions are classified as transudative or exudative based on their protein content and cell characteristics. Common causes of transudative effusions include heart failure and cirrhosis, while exudative effusions have infectious or inflammatory causes like pneumonia or cancer. Diagnosis involves physical exam, imaging like chest x-ray, and analyzing pleural fluid obtained via thoracentesis.

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.

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.

16. USG THORAX

17. CT CHEST

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.