This document provides information on pleural effusion and thoracic empyema. It begins with objectives and introductions. It then covers anatomy and physiology of the pleura, pathogenesis and causes of pleural effusion and empyema. It discusses the classification of transudative versus exudative effusions. It also covers clinical presentation, complications, and treatment options for pleural effusion, empyema and malignant pleural effusions. Treatment methods discussed include thoracentesis, tube thoracostomy, drainage-based methods, and obliteration of the pleural space.

1. 5/17/2023 MUHAS, Department of Surgery 1
(1.5 hours)
PLEURAL EFFUSION
& THORACIC EMPYEMA

2. Objectives
By the end of this session, students should be able
to,
1) Elaborate the pathophysiology and causes of
pleural effusion and empyema thoracis
2) Identify a patient with pleural effusion/empyema
thoracis based on clinical presentation
3) Investigate a patient and come to a final
diagnosis
4) Manage a patient with pleural effusion, thoracic
empyema and their complications.
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3. INTRODUCTION
•Excessive accumulation of pleural fluid.
•Imbalance between production and
clearance.
•PE is not a specific disease but it is a
reflection of underlying pathology.
•Pathology can be in the lungs, pleura or
systemic.
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4. Pleural anatomy
•The pleura consists
of two membranes:
- Visceral pleura
- Parietal pleura
•At hilum; parietal
pleura is continuous
with the visceral
pleura
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5. Anatomy cont.
Normally the pleural space contains:
 Clear pleural fluid ~0.3 ml/kg
 Low protein content
 Small number of mononuclear cells
 Pleural fluid glucose equal to serum
glucose level.
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6. Anatomy cont.
•Pleural lining is formed by mesothelial cells.
•Below the mesothelial lining is a thin
connective tissue lining which has Blood
vessels and lymphatics which are important in
dynamics of pleural fluid formation.
•Parietal pleura has stomata allowing
passageway for liquid from pleural space to
the lymphatic system.
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7. Anatomy cont.
•Sensory nerve endings are there in the parietal
and diaphragmatic pleura.
•Blood vessels supplying parietal pleural
surface originate from the systemic arterial
circulation-primarily Inter Costal Arteries.
•Venous blood from the parietal pleura drains
to systemic venous system.
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8. Anatomy cont.
•Visceral pleura is also supplied primarily by systemic
arteries, specifically branches of bronchial arterial
circulation, but the venous drainage is in to
pulmonary venous system.
•The Lymphatic vessels that drain the pleural surfaces
transport their fluid contents to different lymph
nodes.
•Ultimately the fluid is transported to the right
lymphatic or thoracic ducts, which empty in to the
systemic venous circulation
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9. Physiology
•Pleural space normally contains small amount
of fluid (10 ml).
•As per recent concept, formation of fluid is
ongoing primarily from the parietal pleural
surface, and fluid is reabsorbed through the
stomata into the lymphatic channels of the
parietal pleura.
•Normally rate of formation = absorption;
about 0.02 ml/kg/hour.
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10. Physiology cont.
•Pleural fluid is the ultra filtrate from the
pleural capillaries.
•There are counteracting forces which are
responsible for transport of fluid; Hydrostatic
pressure - P, and Colloid oncotic pressure -
COP.
•‘P’ promotes movement of fluid out of the
capillaries and COP prohibits the movement
from the capillaries.
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11. Physiology cont.
Fluid movement = K[(Pc –Pis ) – σ(COPc –COPis )]
Starlings equationcan be
applied to parietal pleura:
Pc = 30 cm H2 O,
Pis (mean intrapleural pressure)=
- 5 cm H2 O,
COPc = 32 cm H2 O,
COPis = 6 cm H2 O,
=1, K=1
Fluid movement at parietal
pleura = [30-(-5)]-1(32-6)
= 9 cm H2 O
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12. Pathogenesis
•A change in the magnitude of any of the
factors in the Starling equation can cause
sufficient imbalance in the pleural fluid
dynamics resulting in pleural fluid
accumulation.
•Interference with resorptive process like
blockage of lymphatic drainage as occurs
when tumor cells invade the lymphatic
channels or the draining LN.
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13. Pathogenesis cont.
•There are mainly two
categories of change
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14. Transudate vs. Exudate
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15. Aetiology
Causes of Transudative
Effusions
•Congestive heart failure
•Cirrhosis
•Nephrotic syndrome
•Hypoalbuminemia
•Fluid retention/overload
•Pulmonary embolism
•Lobar collapse
•Meigs’ syndrome
note
•Transudative effusions
occur because of
increased hydrostatic
pressure or decreased
oncotic pressures
•The etiology of pleural
effusion remains unclear in
nearly 20% of cases
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16. Aetiology cont.
Causes of Exudative Effusions
• Malignant
• Primary lung, pleural, or
metastatic carcinoma
• Lymphoma
• Mesothelioma
• Infectious
• Bacterial (parapneumonic)/
Empyema
• Tuberculosis
• Fungal
• Viral
• Parasitic
• Collagen-Vascular Disease related
• Rheumatoid arthritis
• Wegener’s granulomatosis
• Systemic lupus erythematosus
• Churg-Strauss syndrome
• Abdominal and Gastrointestinal
Disease–related
• Esophageal perforation
• Subphrenic abscess
• Pancreatitis, pancreatic
pseudocyst
• Meigs’ syndrome
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17. Aetiology cont.
Causes of Exudative Effusions
•Others
•Chylothorax
•Uremia
•Sarcoidosis
•After coronary artery bypass grafting
•Radiation / Trauma
•Dressler’s syndrome
•Pulmonary embolism with infarction
•Asbestosis related
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18. Pleural Empyema/ Pyothorax/ Purulent
Pleuritis/ Empyema Thoracis
•Accumulation of Pus in the Pleural cavity
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19. Other descriptions
Weese et al. defined an empyema as pleural fluid with
• a sp. Gravity >1.018,
• a WBC count >500 cells/mm3 or
• a protein level >2.5g/dl.
Vianna defined an empyema as pleural fluid on which
• the bacterial cultures are positive or
• the WBC count is > 15,000/mm3 and
• the protein level is >3.0g/dl.
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20. Thoracic Empyema
•Empyema is different from an abscess because the
later is the formation and collection of pus in a
newly formed cavity within the lung parenchyma.
•Any pleural effusion associated with bacterial
pneumonia, lung abscess or bronchiectasis is a
parapneumonic effusion.
•Many complicated parapneumonic effusions are
empyemas.
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21. Aetiology- Thoracic empyema
NON-TRAUMATIC
• Direct extension from an
adjacent site :lung
infection
• Aspiration pneumonia
• Post-obstructive
pneumonia
• Bronchiectasis, lung
abscess
TRAUMATIC
• Instrumentation and rupture of esophagus
• Leakage of an esophageal anastomosis after
resection
• Development of a bronchopleural fistula
following pneumonectomy
• Pleural aspiration/ tube drainage
Non- surgical trauma:
• Abdominal sepsis: subphrenic abscess , liver
abscess
• Sepsis in the pharynx, thoracic spine or chest
wall may extend into the pleura via tissue
planes or mediastinum
• Gun shot wounds, blast injuries and stab
wounds.
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23. Aetiology - Bacteriology
•Streptococcus pneumonia: 15 – 20%
•Staphylococcus spp: 15 – 30%
•Streptococcus spp
•Gram Negatives: 20 – 50%
•Klebsiella, Enterobacter, pseudomonas,
Haemophilus, E. coli
•Anaerobes
•Fusobacterium, Bacteroides fragilis
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24. Pathology- Thoracic empyema
(1) Exudative STAGE (approx. 7days)
 Once infected by pathogenic organisms, the
connective tissue layers within the pleural
membranes become edematous and produce an
exudation of sterile proteinaceous fluid that starts
to fill the pleural cavity.
 At this stage, the pleural fluid is thin with a relatively
low white cell count and the visceral pleura and
underlying lung remain mobile.
 Fluid at this stage is having a low WBC count, low
LDH level and a normal glucose level and pH.
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25. Pathology cont.
(2) Fibrinopurulent STAGE
•Transitional stage, from 7 to 21 days
•Newly formed layers of fibrin become laid down on the
epithelial surface within the pleural cavity, particularly
on the pleural cavity.
• The empyema fluid now becomes more thicker and
more turbid, containing, a higher white cell count.
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26. Pathology cont.
Fibrinopurulent STAGE…
•With the deposition of fibrin on both pleural
surfaces, lung movements in this stage may
become increasingly restricted.
•The pleural fluid ph and glucose levels becomes
progressively lower and LDH level becomes
progressively higher.
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27. Pathology cont.
(3) Organizational STAGE
•Thickened fibrinous layers organize as collagen and
become vascularized by an ingrowth of capillaries.
•This stage may begin within two weeks but usually
takes 4-6 weeks to develop to a point at which the
empyema cavity becomes surrounded by a cortex,
peel or rind that may be more than 2 cm thick.
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28. Pathology cont.
Organizational STAGE…
• This inelastic pleural peel encases the lung and renders
it virtually functionless.
• By this time the empyema contains frank pus, which
may be viscid.
• Ultimately, an inadequately treated empyema cavity
may become obliterated and its rind may calcify,
producing a so-called fibrothorax, particularly in case
of old tuberculous pleural infection.
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29. Pathology cont.
Organizational STAGE…
•The inner layers of the thickened empyema cortex
continue to show a considerable inflammatory cell
infiltrate and
•The fibrous outermost layers exert an increasingly
restrictive effect, both compressing the underlying
lung (the so called “trapped lung” effect) and also
tending to draw the overlying ribs together,
ultimately producing a chest deformity with a dorsal
scoliosis that is concave towards the affected side.
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30. Pathology cont.
Organizational STAGE…
•Dry “sicca” pleuritis stage, the inflammatory
process of the pulmonary parenchyma extends to
the visceral pleura, causing a local pleuritic
reaction.
•This leads to a pleural rub and a characteristic
pleuritic chest pain which originates from the
sensitive innervations of the adjacent parietal
pleura.
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31. Clinical presentation
•Depends on the nature of infecting organism.
•Competence of patients immune system.
•Ranges from complete absence of symptoms
to a severe illness with all usual manifestations
of toxicity.
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32. Clinical presentation cont.
•Acute empyema:
•Fever, cough with pleuritic pain
•Features of fluid in pleural space
•Decreased chest expansion
•Stony dullness with decreased VF and VR
•Absent breath sounds
•Features of the underlying condition
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33. Clinical presentation cont.
•Sub acute and chronic empyema:
•Less severe presentation as patient often has
been on antibiotics
•Slow convalescence after a pneumonic illness
•Clinical features of fluid as above
•Features of the underlying condition; eg
bronchiectasis, lung abscess, osteomyelitis of
ribs
•Features of bronchopleural fistula or empyema
necessitans
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34. Causes of Chronicity
•Inadequate Tube Drainage.
•Chronic pulmonary Disease (TB or Fungal
Infection)
•Immunosuppressed patients.
•Presence of Foreign body within the pleural space.
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35. Complications
•Spread to the subcutaneous tissue:
•Dissection through chest wall; Empyema Necessitans
•Dissection into abdominal cavity.
•Septicaemia & septic shock.
•Pleural thickening
•Chest deformity- scoliosis
•Rupture into the lung:
 Dissection into lung parenchyma
 BronchoPleural fistula & pyopneumothorax
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36. Treatment Benign pleural
effusion
•Transudative pleural effusions are managed by
treatment of the underlying disease and usually
resolve after it has been controlled.
•Occasionally, additive intervention is required,
either because the effusion is symptomatic or
because the underlying medical problem is
refractory to maximal medical treatment

37. Treatment- malignant PE
•The optimal treatment for malignant pleural
effusion is controversial
•malignant disease of long duration can
prevent full lung expansion because of;
 visceral pleural restriction
endobronchial obstruction
 parenchymal fibrosis
replacement by tumor.

38. •Treatment options
Drainage alone
Obliteration of pleural space

39. Drainage-Based Methods of Malignant
Effusion Control
• Serial thoracenteses appropriately control malignant
pleural effusions for some patients
temporarily relief, for poor prognosis pts.
• Occasionally, thoracentesis creates a hydropneumothorax
because of poor compliance or entrapment of the
ipsilateral lung.
• It can be achieved through;
1. serial percutaneous aspiration
2. Implantation of a long-term pleural catheter or
placement of a percutaneous medium durability pleural
catheter

40. THORACOCENTESIS
•Can be dose using large bore needle
•Applicable and curative in children
•May be sufficient in exudative phase
Limitation
•Thick pus
•Organized phase
•multiloculation
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41. Closed tube thoracostomy
•First step in adult
•Useful for fibrinopurulent and exudative stages
•Insert a thoracic catheter (relatively large 28 to
36F) tubes in 6th or 7th ICS between anterior and
posterior axillary lines and connect to UWSD
bottle
• Track above superior border of a rib to avoid damage to
neurovascular bundle
•Continuous controlled suction; reduce drainage
duration
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42. Closed tube thoracostomy…
•Limitation
•Tube blockage
•Multiloculation lead to inadeguate
drainage
•Presence of bronchopleural fistula
•Thick fibrous cortex limit lung expansion
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44. Indications for removal of tube
•Volume of the pleural drainage is less than 50ml for
24 hrs and until the draining fluid becomes clear
yellow.
•The amount of sediment (representing WBCs and
debris) in the collection system should not be more
than 5ml.
•Tube ceases to work
Because it serves no useful purpose rather it as a
conduit for pleural super-infection.
NB; daily monitoring
Drainage fluid; colour, volume, patency and gas
bubbles
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45. Sclerosis-Based Pleural Effusion
Management
•accelerating the process of pleurodesis
•a substance that increases the inflammatory
response and thus causes intense adhesions
within the pleural envelope
•Examples talc, Cycline Drugs and Bleomycin

46. PROGNOSIS
•Favourable in patients started on
appropriate antibiotic.
•Early chest tube drainage is beneficial.
•Decortication or open drainage has
decreased mortality and morbidity.
•Mortality 6-12%
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47. References
•A Manual of Clinical Surgery by S. Das. 9th Edition
•Manipal Manual of Surgery by K. Rajgopal Shenoy
4th Edition
•Schwartz’s Principles of Surgery, 11th Edition
•www.uptodate.com
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