Pleural Effusion 31.10.14

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PLEURAL EFFUSION

Dr. Ahbab Hussain


Assistant Professor
Department of Respiratory Medicine
Learning Objectives
• Pleural anatomy
• Physiology
• Pathogenesis of pleural effusion
• Clinical features
• Causes
• Investigations
• Treatment
Introduction
• Excessive accumulation of pleural fluid in
pleural space.

• Imbalance between production and clearance.

• Pathology can be in lung, pleura or systemic.


Pleural anatomy
• The pleura consists of two membranes:
- Visceral pleura
- Parietal pleura

• Pleural space: the potential space between


parietal and visceral pleura
• Contains tiny amount of pleural fluid ~0.3
ml/kg
• Pleura lines not only the surfaces of the lung
that are in direct contact with the chest wall
but also the diaphragmatic and mediastinal
borders of the lung.
• Two apposing visceral surfaces form fissures.

• Lining of the pleurae formed by mesothelial


cells.
• On the parietal pleura there are openings in
the mesothelial cells called as stomata (only
on parietal pleura).

• These stomata leads to lymphatic channels,
allowing passage way for liquid from pleural
space to the lymphatic system.
PHYSIOLOGY
• Pleural space normally contains small amount
of fluid (10 ml).
• Formation of fluid is ongoing primarily from
the parietal pleural surface, and fluid is
resorbed through the stomata into the
lymphatic channels of the parietal pleura.

• Normally rate of formation = absorption.
PHYSIOLOGY
• Pleural fluid is the ultra filtrate from the
pleural capillaries.
• There are counteracting forces which are
responsible for transport of fluid, these are
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.
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.
PATHOGENESIS
• There are mainly two categories of change

1. Alteration of the permeability (i.e. 2. Alteration in the driving pressure,


change in the filtration coeff K)& encompassing a change in the
permeability to protein -reflection hydrostatic pressure or COP of the
coeff. parietal or visceral pleura without any
change in the permeability.
Pleura becomes more permeable to
the fluid and Large mol weight Accumulated fluid  Transudative
components of blood.

Changes seen most commonly in CHF


Accumulated fluid  Exudative or hypoproteinemia.

Changes seen most commonly in


inflammatory and neoplastic diseases
ETIOLOGY
• Major causes of Pleural effusion
Transudate:
• Increased hydrostatic pressure; “overflow
of liquid from the lung interstitium-CHF
• Decreased plasma oncotic pressure
Nephrotic syndrome
• Movement of transudative ascitic fluid
through Diaghphram.
EXUDATE
Inflammatory
• Infection (TB, bacterial pneumonia)
• Pulmonary embolus
• Connective tissue dis (lupus, RA)
• Adjacent to subdiaphragmatic diseases (pancreatitis,
subphrenic abscess)
Malignant
Others
benign ovarian tumors (Meig’s syndrome)
asbestos exposure
hypothyroidism
CLINICAL FEATURES
SYMPTOMS:
• Symptoms depend on the size of effusion and
nature of underlying process.
• Inflammatory process present with Pleuritic
chest pain.
• When effusion is large pt present with dyspnea.
• Small or moderate size effusion with otherwise
normal lung does not have dyspnea.
• If nature is inflammatory or is infected fever is
commonly present.
• A h/o cardiac, renal or liver impairment can
suggest transudative effusion.
• Old age, wt. loss, and a h/o smoking point
towards MPE.
• Trauma may result in hemothorax.
• Patient presenting with fever, dyspnea and
pleuritic chest pain up to 03 wks following
cardiac surgery.
• History and findings s/o CTD( connective tissue
disorder)
CLINICAL FEATURES
PHYSICAL EXAMINATION:
• Movement will be diminished, fullness of the
intercostal space, Trail sign may be +ve on opposite
side.
• Trachea, apex beat may be shifted depending on the
amount of fluid. Vocal fremitus –nt.
• Region overlying fluid is dull. (dull note)
• Delayed shifting dullness may be present. Absent in
massive and loculated effusion.
• Breathsounds-decreased.
INVESTIGATIONS: Imaging Studies
• Chest X-ray
Chest X-ray

Classical homogenous opacity with curved upper border, i.e. the Ellis S-
shaped curve.
Ultrasonography thorax
• This helps in detecting even the small amount
of fluid.
• USG is helpful in cases of loculated PE for
confirmation of the diagnosis and for making a
site for aspiration.
• Helps in differentiating fluid filled and solid
lesions.
• Also helps in detecting subpulmonic effusion
from sub diaphragmatic collection.
CT thorax
• Used to assess the complex situation in which
anatomy is not fully assessed by plain
radiography or USG.
• Helps in selecting drainage site in empyema.
• Differentiates loculated empyema from lung
abscess.
Exudate Vs Transudate
• Light’s criteria for exudative PE
– Pleural fluid protein divided by serum protein> 0.5
– Pleural fluid LDH divided by serum LDH >0.6
– Pleural fluid LDH more than 2/3rd the upper limit
of normal serum LDH
• Sensitivity-98%, specificity-74%
• A total nucleated cell count of >1000/ml is
exudate.
TREATMENT
• Depend on the nature of underlying cause.
• Drainage of fluid, pleurodesis and surgical
management are the therapeutic options for
pleural effusion.
THANKS

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