Effusions from parapneumonic

infections and empyema

AGENDA
The clinical importance of
infection in the pleural space
Historical perspective
The epidemiology of pleural
infection
The pathophysiology of pleural
infection
Bacteriology
The diagnosis and clinical
asessment of pleural infection

Differential diagnosis
Predictors of clinical outcome in
pleural infection
Radiology
Antibiotics
Chest catheter drainage
Intrapleural fibrinolytics
Future directions

NICK A MASKELL AND ROBERT JO DAVIES

TEXTBOOK OF PLEURAL DISEASE

The clinical importance of infection in the pleural space

Frank purulent pleural empyema has an overall mortality up
to 20%, which rise further to about 35% in the
immunocompromised host.
The actual mortality rise from empyema is substantially
influenced by the presence of co-morbid disease.
In addition to this mortality, up to 40% of patients will fail
treatment which chest tube drainage and antibiotics alone
and still require surgical drainage of their pleural collection.
Simple parapneumonic effusions arise in up to 57% of cases
of pneumonia.
NICK A MASKELL AND ROBERT JO DAVIES
TEXTBOOK OF PLEURAL DISEASE

The clinical importance of infection in the pleural space

Parapneumonic effusion occurred in 20 to 40% of
patients who are hospitalized with pneumonia.
The mortality in patients with parapneumonic
effusion is higher than that in patients with
pneumonia without a parapneumonic effusion.
Some of the excess mortality is due to mismanagement
of the parapneumonic effusion.
Light RW. Pleural diseases, 4th ed. Baltimore: Lippincott,
Williams and Wilkins; 2001.

Definition
Parapneumonic effusion is any pleural effusion
secondary to pneumonia ( bacterial or viral ) or lung
abscess.
Empyema is , by definition, pus in the pleural space.
A complicated parapneumonic effusion is a
parapneumonic pleural effusion for which an invasive
procedure is necessary for its resolution, or a
parapneumonic effusion on which the bacterial
cultures are positive.
Light RW. Pleural diseases, 4th ed. Baltimore: Lippincott,
Williams and Wilkins; 2001.

Historical perspective
500BC. Hippocrates: open thoracic drainage.
1876-1891: chest tube and under water seal.
1919 First World War: open early surgical drainage, mortality as high
as 70%.
Hewitt and Bulau: adequate pus drainage with a closed chest tube,
avoidance of early open drainage, obliteration of the pleural space,
proper nutritional support. Reduced the mortality to 4.3%.
1940s: Penicillin
1940s Tillett: intrapleural fibrinolytic therapy; frequent antigenic side
effects
1897 Estlander and 1890 Schede: thoracoplasty
19th Century end Fowler and Beck: decortication of the pleura
Video assisted thoracoscopic surgery ( VATS)
NICK A MASKELL AND ROBERT JO DAVIES
TEXTBOOK OF PLEURAL DISEASE

The epidemiology of pleural infection

More common in the elderly and childhood.
Men are affected twice as often as women.
Higher in those with diabetes, alcoholism and
substance abuse, rheumatoid arthritis and chronic
lung disease.
Poor dentition and risk factors for aspiration are
associated with an increase prevalence of anaerobic
infection.
NICK A MASKELL AND ROBERT JO DAVIES
TEXTBOOK OF PLEURAL DISEASE

Parapneumonic effusion

70%

post bacterial pneumonia

hospital acquired pneumonia
Primary empyema

4%

Post operative

12%

Traumatic

3%

blunt trauma
penetrating trauma
Iatrogenic

4%

e.g. post chest tube insertion

Abdominal infection

2%

e.g. subphrenic abscess

Miscellaneous

3%

esophageal perforation
bacteremia
rupture of lung abscess into pleural cavity
intravenous drug abuse ( contaminated needles )
NICK A MASKELL AND ROBERT JO DAVIES
TEXTBOOK OF PLEURAL DISEASE

35%
Streptococcus milleri

30%

Other

25%

Proteus

20%

Enterobacteriacea

15%

H influenzae
Anaerobic

10%

Staphylococcus

5%
0%

Pneumococcus
Other streoptcoccus
Community acquired
NICK A MASKELL AND ROBERT JO DAVIES
TEXTBOOK OF PLEURAL DISEASE

30%
MRSA

25%

Enterobacteriacea
20%

Entercocci
Staphylococci

15%

Pseudomonas
Streoptococci

10%

Anaerobes
5%
0%

Others
S. milleri
Hospital-acquired
NICK A MASKELL AND ROBERT JO DAVIES
TEXTBOOK OF PLEURAL DISEASE

The pathophysiology of pleural infection

Development of the initial pleural effusion: the
exudative phase
The evolution of infection: the fibropurulent phase
Natural healing: the organizing stage

Andrews NC, Parker EF, Shaw RR, Wilson NJ, Webb WR.
Management of nontuberculous empyema. Am Rev Respir Dis
1962;85:935936.

Development of the initial pleural effusion: the exudative phase

There is rapid outpouring of fluid into the pleural space.
Most of the fluid is due to increased pulmonary interstitial
fluid traversing the pleura to enter the pleural space but some
of this is due to increased permeability of the capillaries in
the pleural space.
The pleural fluid in this stage is characterized by negative
bacterial studies, a glucose level above 60 mg/dl, a pH above
7.20, and a lactic acid dehydrogenase (LDH) level of less
than three times the upper normal limit of serum.
If the patient does not see a physician or receives the wrong
antibiotic, the effusion may proceed to the second stage,
which is the fibropurulent stage.
The Proceedings of the American Thoracic Society 3:75-80 (2006)

The evolution of infection: the fibropurulent phase

The pleural fluid in this stage is characterized by positive
bacterial studies, a glucose level below 60 mg/dl, a pH below
7.20, and a pleural fluid LDH more than three times the
upper normal limit for serum.
In this stage, the pleural fluid becomes infected and
progressively loculated.
The pleural fluid needs to be drained in this stage and
drainage becomes progressively difficult as more loculations
form.
If a stage 2 effusion is not drained, the effusion may progress
to the third stage.
The Proceedings of the American Thoracic Society 3:75-80 (2006)

Natural healing: the organizing stage

Fibroblasts grow into the pleural fluid from both the
visceral and parietal pleurae, producing a thick
pleural peel.
The peel over the visceral pleura prevents the lung
from expanding.
Because the pleural space must be eradicated if a
pleural infection is going to be eliminated, this peel
must be removed if the infection is going to be cured.
The Proceedings of the American Thoracic Society 3:75-80 (2006)

Lights classification of parapneumonia effusions and empyema

Class1-Non significant

Small<10mm thick on decubitus

No thoracentesis needed

Class2-Typical parapneumonic

>10mm thick
Glucose>40, pH>7.2, Gram stain
and culture negative

Class3-Borderline complicated

pH 7.0-7.2 or LDH>1000
Gram stain and culture negative

Class4-Simple complicated

pH<7.0 , Gram stain and culture

positive, no loculated or frank pus

Class5-Complex complicated

pH<7.0, Gram stain and culture

positive, multiple loculation

Class 6-Simple empyema

Frank pus, single locule or free

Class 7-Complex empyema

Frank pus, multiple loculations

Aerobic and gram positive (180)

Viridan streptococcus

46

48%

S milleri group

44

Staphylococcus group

39

S pneumonia

31

Other streptococcus spp.

14

Enterococcus spp.

Aerobic gram-negative (101)

Klebsiella pneumonia

43

27%

Pseudomonas spp.

15

Escherichia coli

14

Haemophilus spp.

10

Enterobacter spp.

Proteus mirabilis

E. Corrodens

Salmonella spp.

Anaerobes (86 )

Peptostreptococcus spp.

24

23%

Bacteroides spp.

23

Fusobacterium spp.

18

Prevotella spp.

Veillonella spp.

Porphyromonas spp.

Actinomycetes spp

anaerobes mixed
Miscellaneous/ Others (8 ) 2%

Bacteriology
Aerobic organisms are the most frequent organisms identified
from infected pleural fluid.
These are most commonly Gram-positive organisms from
Streptococcal species, followed by Staphylococcus aureus.
Gram-negative empyema is more frequent in patients with
underlying diseases, especially those with diabetes and
alcoholism.
Staphylococcus aureus and Gram-negative enteric bacteria
such as Klebsiella pneumonia have a particular propensity to
cause pleural infection.
NICK A MASKELL AND ROBERT JO DAVIES
TEXTBOOK OF PLEURAL DISEASE

History, examination and CXR

The diagnosis and clinical asessment of pleural infection

Measure pleural fluid pH
Request fluid Grams stain and culture

Pleural effusion and evidence for infection

Yes
No

Grams stain positive

Or culture positive
Or pH<7.2

Start antibiotics
Perform diagnostic pleural aspiration
With image guidance if required

No
Frank purulent pleural fluid?

Yes

Pleural infection unlikely

Treat with antibiotics provided
Clinical progress is good

Yes
Pleural infection likely
Proceed to chest drainage

Flow diagram describing a diagnostic pathway for

patients with possible pleural infection

Differential diagnosis
Pleural involvement occurs in up to 5% of
patients with rheumatoid arthritis.
Pleural malignancy
Chylothorax and pseudochylous effusion
Pulmonary embolism
Esophageal rupture
NICK A MASKELL AND ROBERT JO DAVIES
TEXTBOOK OF PLEURAL DISEASE

Predictors of clinical outcome in pleural infection

Pleural infection has a high mortality and morbidity
and presents a clinical challenge in the timing of
surgical intervention.
Frankly purulent pleural fluid, co-morbid diabetes,
delayed referral and pleural drainage, the presence of
fluid loculation and a low pleural fluid white count
may predict a poor outcome.
NICK A MASKELL AND ROBERT JO DAVIES
TEXTBOOK OF PLEURAL DISEASE

Radiology
The presence of fever, pulmonary infiltrates and fluid
should always alert clinician to the possibility of a
parapneumonic collection.
Ultrasound is good visualizing septations within
loculations that are not usually seen on CT images,
but may not identify some separate fluid loculations
in inaccessible areas of the thorax.
NICK A MASKELL AND ROBERT JO DAVIES
TEXTBOOK OF PLEURAL DISEASE

Five basic ultrasound patterns of pleural effusions

Tu, C.-Y. et al. Chest 2004;126:1274-1280

Five basic ultrasound patterns of pleural effusions

Top left, I = anechoic pattern: no echogenic density within the
effusion
Top right, IIB = complex nonseptated and relatively nonhyperechoic
pattern: some visible bright spots as echogenic density within the
effusion, and the echogenic shape changed with respiration
Center left, IIA = complex nonseptated and relatively hyperechoic
pattern: predominant hyperechoic spots visible within the effusion,
and the echogenic shape not changed with respiration
Center right, III = complex septated pattern: prominent fibrinous
septation visible within the effusion
Bottom, IV = homogenously echogenic pattern: echogenic spots
density evenly distributed within the effusion
Tu, C.-Y. et al. Chest 2004;126:1274-1280

Pleural Effusions in Febrile Medical ICU Patients*

Chest Ultrasound Study
Chih-Yen Tu, MD (Chest. 2004;126:1274-1280.)

Antibiotics
Antibiotics
40% culture negative
It is not uncommon to need at least 2 weeks of
therapy and some times longer.
Decisions on the length of treatment can be guided by
repeated measurements of serum CRP.

NICK A MASKELL AND ROBERT JO DAVIES

TEXTBOOK OF PLEURAL DISEASE

Mark Cohen and Steven A. Sahn Chest, May 2001; 119: 1547.

Chest catheter drainage

Optimal size of catheter?
Excellent outcomes may be achieved with such small catheter especially
when combined with fibrinolytic therapy.
Drainage may fail if the fluid is of high viscosity and direct blocks the
tube.
The balance of forces drawing it down the tube is inadequate.
If the fluid is partitioned by fibrinous septaeFig.ppt.
The rapidity of chest tube drainage might be improved by increasing the
drain size, but the successful drainage is unchanged.
Here again, provide that the catheter is patent, its bore is irrelevant.
NICK A MASKELL AND ROBERT JO DAVIES
TEXTBOOK OF PLEURAL DISEASE

Intrapleural fibrinolytics

1949 Tillet and Sherry: partial purified streptococcal fibrinolysin

Highly purified streptokinase: 250000IU
Urokinase: 100000IU
It form a complex with plasminogen that converts additional
circulating plasminogen to plasmin. Plasmin lyses fresh fibrin clot and
digests prothrobin and fibrinogen.
Improvement in the chest radiograph and greater volume pleural
drainage, not outcome of mortality, surgical frequency, or hospital stay.
Tube drainage with streptokinase and early surgical intervention
showed reduced length of hospitalization
Potential side effect: hemorrhage, pleuritic pain and fever
NICK A MASKELL AND ROBERT JO DAVIES
TEXTBOOK OF PLEURAL DISEASE

Surgery for pleural infecetion

No definite data that define the point at which a patient
with empyema should proceed to surgical intervention.
Open thoracotomy with decortication
Mini-thoracotomy
Video-assisted thoracoscopic surgery (VATS)
Rib resection with open drainage
VATS: reduced hospital inpatient time, postoperative
complications and length of operating time
VATS: failures are with empyema in the organizing stage of
the disease
NICK A MASKELL AND ROBERT JO DAVIES
TEXTBOOK OF PLEURAL DISEASE

Figure 2 Surgical scars: open decortication.

Jaffe, A et al. Arch Dis Child 2003;88:839-841

Copyright 2003 BMJ Publishing Group Ltd.

Figure 1 Surgical scars: VATS.

Jaffe, A et al. Arch Dis Child 2003;88:839-841

Copyright 2003 BMJ Publishing Group Ltd.

Luh, S.-P. et al. Chest 2005;127:1427-1432

Future Directions
Increasing resistant micro-organism
intrapleural fibrinolytics still no know if they
actually reduce mortality and need for surgical
intervention.
Comparing the use of intrapleural fibrinolytics with
early VATS

NICK A MASKELL AND ROBERT JO DAVIES

TEXTBOOK OF PLEURAL DISEASE

THANKS FOR YOUR ATTENTION