Terry Baker (Dr.

PLEURAL EFFUSION Pulmonologist and Internist

Senior Medical Officer, NCH
Assistant Lecturer, Dept. of Medicine, UWI
 CASE: JB
65 year old man
Known to have diabetes and hypertension > 8 years
Retired teacher, Lived in India for 2 years teaching English
Previous smoker – stopped 8 years ago
Complains of worsening SOB x 6/52 with right –sided chest pain
On further questioning admits to anorexia x 3/12 , with unintentional weight loss of approximately 8 kg/2 months, occ.
fever
On Examination
MM pale but moist, R supraclavicular LN , No clubbing, No oedema. Saturation 90 % on RA
BP 114/72, PR 118/min, regular
RR 32/min, trachea central, stony dullness R mid-lower zones with reduced breath sounds om auscultation
Abdominal and CNS examinations unremarkable
INVESTIGATIONS
Blood studies :
CBC- HB 9.5, WBC 13.6, Platelets 592
Electrolytes : NA 128 MMOL/L, K 4.2, CL 108, CO2 18

Chest X-ray
Ultrasound of the Chest
CASE: AC
32 year old woman
Sudden onset of R sided pleuritic chest pain and SOB
? Viral illness – having headache, cough, fever with loss of appetite x 3/7 prior to
admission
Delivered infant boy via emergency caesarean section 2/52 prior to presentation
On Examination
MM pink sl dry. Saturation 93% RA, oedema of lower limbs R>L, tender R calf
Chest : RR 28 breaths/min R chest crackles on auscultation with reduced breath sounds
PR 112/min BP 128/84
Next Step?
CTPA IMAGE
 Pathological accumulation of fluid in the pleural
PLEURAL EFFUSION space, most common manifestation of pleural disease
Causes of vary widely, ranging from fairly harmless
effusions accompanying viral pleuritis to
prognostically highly relevant ones due to congestive
heart failure or cancer
The normal pleural space contains approximately 10
mL of fluid (0.13 ml/kg)
Mean rate of production and the absorption of
pleural fluid is normally 0.2 mL/kg/hr which implies
that the entire volume of the pleural fluid normally
turns over within one hour
 Pleura effusion develops when more fluid enters the
pleural space than is removed.
 The parietal pleura accounts for most of the
PLEURAL EFFUSION production of pleural fluid, and for most of its
resorption

Pleural effusion due to left-heart failure is an

exception, in which the fluid comes from the visceral
pleura

Most common causes of a pleural effusion in adults are

Heart failure
 Malignancy
 Pneumonia
 Tuberculosis
 Pulmonary embolism
Pneumonia is the leading etiology in children
PLEURAL EFFUSION- MECHANISMS
Increased permeability (pneumonia)
Decreased intra-pleural pressure (atelectasis)
Decreased plasma oncotic pressure (hypoalbuminemia)
Increased pleural membrane permeability
Obstructed lymphatic flow (pleural malignancy or infection);
Increased interstitial fluid in the lungs secondary to increased pulmonary capillary
pressure (heart failure)
Diaphragmatic defects (hepatic hydrothorax)
Thoracic duct rupture (chylothorax)
EVALUATION OF PATIENT WITH PLEURAL EFFUSION
 EVALUATION OF PATIENT WITH PLEURAL EFFUSION
Complete history and physical examination should be performed

.Signs and symptoms of an effusion vary depending on the underlying disease

Dyspnea, cough, and pleuritic chest pain are common.

Chest examination of a patient with pleural effusion :

• dullness (stony) to percussion,
• decreased or absent tactile fremitus,
• decreased breath sounds
• no voice transmission.
• egophony

.
IMAGING INVESTIGATIONS
Chest X-ray
 Unilateral vs Bilateral Pleural Effusions
 A posterior-anterior view reveals effusions of volume 200 mL or larger
 A lateral decubitus view reveals effusions of volume 50 mL or larger. A lateral
decubitus view can be used to confirm the free flow of the effusion around the lung

Thoracic Ultrasound
Chest ultrasound is very useful
Especially important if multiple punctures are needed. Ultrasound-assisted
pleural puncture markedly lowers the risk of iatrogenic pneumothorax,
CHEST X-RAY
Left Pleural Effusion Loculated Pleural Effusion
CHEST X-RAY –PA AND LATERAL DECUBITUS
IMAGING INVESTIGATIONS
Thoracic Ultrasound
Chest ultrasound is very useful
Especially important if multiple punctures are needed. Ultrasound-assisted
pleural puncture markedly lowers the risk of iatrogenic pneumothorax
Chest CT
 Reveals pleural effusions that cannot be seen on conventional chest x-rays.
 It can distinguish pleural fluid from pleural tissue proliferation, and
 It provides clues to the potential causes of the effusion(pneumonia, cancer,
pulmonary embolism).
 If possible it should be performed after an initial puncture
THORACOCENTESIS
THORACOCENTESIS
A diagnostic thoracocentesis of a pleural effusion to obtain a small quantity
of fluid is indicated when the cause of the effusion is unclear.

Thoracocentesis to obtain larger volumes is indicated to relieve effusion

related symptoms such as dyspnea

1.5 L of effusion fluid is the maximum amount recommended to be

removed at one time.

Timely thoracentesis or the insertion of a pleural drain is necessary if a

pleural effusion is large and leads to respiratory or cardiac
decompensation.
 THORACOCENTESIS
Punctures or drain insertions that do not have to be performed on an emergency basis should be carried out in the
setting of an INR that is less than 1.5.

 A current chest x-ray should be available

The intervention should be performed under ultrasonographic guidance.

 The puncture is performed under aseptic technique, generally with a 21-gauge needle and a 50 mL syringe outfitted
with a three-way stopcock.

Except in emergency situations (marked dyspnea, suspected pleural empyema), punctures for pleural effusion should
be carried out during normal working hours

Punctures at other times are associated with higher procedure-related risks (pneumothorax, infection)
THORACOCENTESIS IN TRANSUDATIVE EFFUSIONS
Patients with bilateral pleural effusions do not always need to have a diagnostic or
therapeutic tap

Patients with pulmonary embolism and a pleural effusion usually do not need thoracocentesis

The underlying disease that has been identified (congestive heart failure, nephrotic syndrome,
pulmonary embolism) should be treated.

A diagnostic thoracocentesis is indicated if the patient has pleuritic chest pain, symptoms that
are out of proportion to the size of the effusion, fever, an unexplained lack of response to
treatment, or the patient has a unilateral effusion or effusions of markedly disparate size
 COMPLICATIONS OF THORACOCENTESIS
Usually well tolerated procedure complications may increase morbidity/mortality
 Iatrogenic Pneumothorax : most common complication of thoracentesis, with historical incidence
rates as high as 19%. Use of ultrasound reduces risk of pneumothorax
Bleeding
puncture site bleeding,
chest wall hematoma
 haemothorax : rare, should be suspected when a patient develops vital sign instability, a drop
in hematocrit, or rapid pleural fluid reaccumulation following thoracentesis
Re-expansion Pulmonary Oedema :uncommon complication is characterized by the development of
hypoxemia and new alveolar infiltrates within 24h of pleural fluid drainage
Infection
Loculation of pleural effusion with repeat thoracocentesis
POST THORACOCENTESIS
Chest radiography is not necessary after thoracentesis as long as no new symptoms
arise
Symptoms of concern post procedure:
Air is obtained during the procedure

Dyspnea, cough, chest pain, hypoxia

Tactile fremitus is lost over the upper part of the aspirated haemithorax
PLEURAL FLUID ANALYSIS
ANALYSIS – MACROSCOPIC APPEARANCE
The gross appearance of the fluid may provide clues to the diagnosis.

Milky fluid is typical of chylothorax

Pus is proof of empyema, and a bloody effusion

Bloody effusion more common when a malignancy is the cause.

Chylothorax can be distinguished from empyema by centrifugation: chylous fluid remains

milky, but empyema fluid displays a clear supernatant
 TRANSUDATES VS EXUDATES
Important to differentiate transudates from exudates

With a transudative pleural effusion, only necessary to treat the cause of the effusion
such as heart failure or cirrhosis.

However, if it is an exudative effusion, more investigation is indicated to identify the

local problem

Exudative effusions can be separated effectively from transudative effusions

using Light’s criteria
TRANSUDATIVE PLEURAL EFFUSIONS
Result from imbalances in hydrostatic and oncotic forces
Caused by a limited number of recognized clinical conditions
 * Heart failure
 * Cirrhosis.
 Nephrotic syndrome
 Atelectasis
 Peritoneal dialysis
 Constrictive pericarditis
 Superior vena caval obstruction
Urinothorax /Glycinothorax
Myxedema

Transudative effusions usually respond to treatment of the underlying condition

 EXUDATIVE PLEURAL EFFUSION
 Exudates present more of a diagnostic dilemma.

 Exudates occur when the local factors influencing the accumulation of pleural fluid are
altered; pleural surfaces or the capillaries in the location where the fluid originates are
altered

 Most common causes:

 Pneumonia (parapneumonic)
 Malignancy
 Thromboembolism
EXUDATIVE PLEURAL EFFUSION
LIGHT’S CRITERIA
Richard Light, MD, professor of Medicine in the Division of Allergy, Pulmonary and
Critical Care
Light’s Criteria
Classify an effusion as exudate if one or more of the following are present:
(1) the ratio of pleural fluid protein to serum protein is greater than 0.5,
(2) the ratio of pleural fluid lactate dehydrogenase (LDH) to serum LDH is greater
than 0.6
(3) The pleural fluid LDH level is greater than two thirds of the upper limit of normal
for serum LDH.
 LIGHT’S CRITERIA
Light’s criteria are nearly 100 (99.5%) percent sensitive at identifying exudates

Can tell the difference between a transudate and an exudate in 93–96% of cases

Approximately 20% of patients with pleural effusion caused by heart failure may fulfill the
criteria for an exudative effusion.

Diuretic drugs given to treat congestive heart failure can elevate the concentrations of protein,
LDH, and lipids in a pleural effusion

Obtaining effusion fluid by pleural tap after cardiac decompensation has already occurred
can lead to the incorrect identification of an exudate
ALTERNATE CRITERIA
Difference between protein levels in the serum and the pleural fluid i >3.1 g/dL, the
patient should be classified as having a transudative effusion

A serum-effusion albumin gradient >1.2 g/dL also can indicate that the pleural
effusion is most likely a true transudate

Neither protein nor albumin gradients alone should be the primary test used to
distinguish transudative effusions from exudative effusions - they result in the incorrect
classification of a significant number of exudates
MICROBIOLOGY
Gram staining can help identify the underlying pathogen.
The microbiological identification of a pathogenic organism in a non-purulent
parapneumonic effusion succeeds in only 25% of cases
Application of the polymerase chain reaction (PCR) improves sensitivity compared to
conventional culture techniques
If tuberculous pleuritis is suspected, microbiological examination and culture should be
performed
Microbiological examination has less than 5% sensitivity for the detection of acid-fast
bacilli; culture yields a somewhat higher sensitivity of 10–20 %
Adenosine deaminase plays an important role in lymphoid cell differentiation. A pleural
fluid ADA level greater than 40 U per L has a sensitivity of 90 to 100 percent and a
specificity of 85 to 95 percent for the diagnosis of tuberculous pleurisy
 CYTOLOGY
In approximately 50% of lung cancers and 60% of all cancers taken together the
malignant nature of a pleural effusion can be confirmed cytologically.

Negative test results are related to factors such as the type of tumor (e.g., commonly
negative with mesothelioma, sarcoma, and lymphoma) and the tumor burden in the
pleural space

The diagnostic yield may be improved by additional pleural taps

Therapeutic puncture is usually followed by recurrence of the effusion

PH VALUES
Pleural fluid acidosis is found in complicated pleural infections, tuberculosis,
rheumatoid arthritis, and malignant effusions
In patients with malignant effusions, acidosis of the effusion fluid is correlated with
shorter survival
These patients generally have more extensive disease and a lower chance of
successful pleurodesis
Low pH is the best indicator of a complicated course of parapneumonic pleural
effusion.
If the pH is less than 7.2, a pleural drain should be inserted without delay
GLUCOSE AND AMYLASE
Glucose
The glucose concentration is normally the same in pleural fluid as in the blood.
A low glucose concentration in a pleural effusion is found in empyema, tuberculosis,
malignancy, and rheumatoid arthritis

Amylase
One in two patients with acute pancreatitis has a pleural effusion with an elevated
amylase concentration
OTHER INVESTIGATIONS
Differential Blood-Cell Count
can further narrow down the differential diagnosis.
An elevated concentration of neutrophils is often seen in acute processes, such as para-
pneumonic effusion, empyema, and effusion due to pulmonary embolism.
A predominantly lymphocytic picture is more common in tuberculosis, longstanding pleural
effusions, congestive heart failure, or malignant etiology
N-terminal pro-B-type natriuretic peptide, or NTproBNP
 sensitive biomarker for systolic and diastolic heart failure,
 its concentrations in the blood and in pleural effusion fluid are very closely correlated.
Rheumatoid Factor

Tumour Markers
MEDICAL TREATMENT OF PLEURAL EFFUSION
TREATMENT
Treatment of underlying condition

Diuretics

Antibiotics

Repeated Thoracocentesis
NON-MEDICAL MANAGEMENT OF PLEURAL EFFUSION
INDICATIONS FOR CHEST TUBE IN PATIENTS WITH
PLEURAL EFFUSIONS
Infected effusion (complicated para-pneumonic effusion, empyema, pleural
pH <7.2, positive culture)

Malignant or benign effusions requiring bedside pleurodesis

Haemothorax

Chylothorax
 PLEURODESIS
Instillation of an irritant (pleurodetic) into the pleural space to cause inflammatory changes
Inflammation results in bridging fibrosis between the visceral and parietal pleural surfaces,
effectively obliterating the potential pleural space.
Most often used for recurrent malignant effusions, such as in patients with lung cancer or
metastatic disease.
Patients often have limited life expectancy and the goal of therapy is to palliate symptoms
while minimizing patient discomfort, hospital length of stay, and overall costs
Pleurodesis is likely to be successful only if the pleural space is drained completely before
pleurodesis and if the lung is fully re-expanded to appose the visceral and parietal pleura
after sclerosis
Patients with lung entrapment from malignant effusions are not good candidates for pleurodesis,
as the visceral and parietal pleural surfaces cannot stay apposed to allow the bridging fibrosis
 SCLEROSING AGENTS
Various agents, can be employed to sclerose the pleural space and effectively prevent
recurrence of the malignant pleural effusion.
Talc
Doxycycline
Bleomycin sulfate (Blenoxane)
Zinc sulfate
Quinacrine hydrochloride

Talc is the most effective sclerosing agent and can be administered as slurry through chest
tubes or pleural catheters or direct insufflation via thorascopy

All sclerosing agents can produce fever, chest pain, and nausea.

 Talc rarely causes more serious adverse effects, such as empyema and acute lung injury
 Valid alternative for pleurodesis in malignant and some
INDWELLING TUNNELLED benign recurrent effusions.

PLEURAL CATHETERS
Can be inserted as an outpatient procedure and be
intermittently drained at home, minimizing the amount of
time spent in the hospital for patients with short prognoses.
After catheter insertion, the pleural space should be
drained three times a week.

No more than 1,000 mL of fluid should be removed at a

time—or less if drainage causes chest pain or cough
secondary to trapped lung

Can be used for patients with recurrent effusions and

trapped lungs

Contraindicated in patients with uncontrolled coagulopathy,

multi-loculated pleural effusions, or extensive malignancy in
the skin
INDWELLING TUNNELLED PLEURAL CATHETERS
Complications reported from use of TPC include:

Malfunction of the catheter (9.1%)

 Clogging (3.7%)

 Pain (5.6%)

 Infection (2.8%)

Tumor invasion of the catheter track (less than 1%

 CASE JB
65 year old man
Known to have diabetes and hypertension > 8 years
Retired teacher, Lived in India for 2 years teaching English
Previous smoker – stopped 8 years ago
Complains of worsening SOB x 6/52 with right –sided chest pain
On further questioning admits to anorexia x 3/12 , with unintentional weight loss of approximately 8 kg/2 months, occ.
fever
On Examination
MM pale but moist, R supraclavicular LN , No clubbing, No oedema. Saturation 90 % on RA
BP 114/72, PR 118/min, regular
RR 32/min, trachea central, stony dullness R mid-lower zones with reduced breath sounds om auscultation
Abdominal and CNS examinations unremarkable
CASE AC
32 year old woman
Sudden onset of R sided pleuritic chest pain and SOB
? Viral illness – having headache, cough, fever with loss of appetite x 3/7 prior to
admission
Delivered infant boy via emergency caesarean section 2/52 prior to presentation
On Examination
MM pink sl dry. Saturation 93% RA, oedema of lower limbs R>L, tender R calf
Chest : RR 28 breaths/min R chest crackles on auscultation with reduced breath sounds
PR 112/min BP 128/84
CT PA IMAGE