pleural effusion

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PLEURAL EFFUSION Dr Nirav Dhinoja

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Page 1: Pleural effusion

PLEURAL EFFUSION

Dr Nirav Dhinoja

Page 2: Pleural effusion

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.

Page 3: Pleural effusion

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

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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.

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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 oncoticpressure 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.

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Parietal Pleura Visceral

Pleura Space Pleura

Hydrostatic Pressure

+30 - 5 + 24

35 29

6 0

Net

29 29

+ 34 + 5 +34

Oncotic Pressure

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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

Page 8: Pleural effusion

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

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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.

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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.

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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.

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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,cracklesetc.

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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.

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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.

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USG THORAX

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CT CHEST

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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?

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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.

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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

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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.

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EFFUSIONS

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

Transudate Exudate

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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.

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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.

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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

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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.

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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.

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ETIOLOGY EMPYEMA

Infectious Pneumonias

Staph aureus

Strep pneumonia

Gram negative bacilli

Tuberculous pleuritis

Thoracic trauma

Severe Sepsis

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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

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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.

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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.

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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.

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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.

Page 34: Pleural effusion

COMPLICATIONS

Local

Bronchopleural fistula.

Pyopneumothorax.

Purulent pericarditis.

Pulmonary abscesses.

Peritonitis from extension

through the diaphragm.

Osteomyelitis of the ribs.

Systemic

Septicemia.

Meningitis

Arthritis.

Osteomyelitis.

Page 35: Pleural effusion