ALOK SINHADepartment of Medicine

Manipal College of Medical SciencesPokhara, Nepal

Negative intrapleural pressure: ~ 5mm

PLEURISY

Disease process involving the pleura and giving rise to • pleuritic pain • evidence of pleural friction

Common feature of • Pulmonary infection • Infarction• Malignancy

Primary pleural involvement – in T.B.

Clinical features

Characteristic symptom – Pleural pain On examination: Rib movement restricted – reduced chest

expansion Pleural rub may be present

• may only be heard in deep inspiration near pericardium - pleuro-pericardial rub

Loss of the pleural rub and diminution in the chest pain indicate • Either recovery

or • development of a pleural effusion

Normal X-ray does not exclude pulmonary cause for pleurisy• pulmonary infection which may not have

been severe enough • may have resolved before the chest X-ray

was taken

The accumulation within the pleural space of

Serous fluid -

Frank pus -

Blood -

pleural effusion

empyema

haemothorax

Pleural fluid accumulates

increased hydrostatic & decreased osmotic pressure – ‘Transudate’

Increased microvascular pressure due to disease of pleural surface or injury in the adjacent lung ‘Exudate’

Common causes Tuberculosis Pneumonia ('para-pneumonic effusion') Cardiac failure Pulmonary infarction Malignant disease Subdiaphragmatic disorders - subphrenic abscess - pancreatitis etc Hypoproteinaemia

Nephrotic syndrome Liver failure Malnutrition

Uncommon causes Connective tissue diseases systemic lupus erythematosus rheumatoid arthritis Acute rheumatic fever Post-myocardial infarction syndrome Meigs' syndrome (ovarian tumour + pleural effusion) Myxoedema Uraemia Asbestos-related benign pleural effusion

Transudate Congestive heart failure Cirrhosis (hepatic hydrothorax) Hypoalbuminemia Nephrotic syndrome Myxedema Constrictive pericarditis

Tuberculous Parapneumonic

causes Malignancy

(carcinoma, lymphoma,mesothelioma)

Pulmonary embolism

Pancreatitis Collagen-vascular conditions

(rheumatoid arthritis, SLE) Asbestos exposure   Trauma

Postcardiac injury (Dressler’s) syndrome

Esophageal perforation Radiation pleuritis Drug use   Chylothorax Meigs syndrome Sarcoidosis Yellow nail syndrome

Exudate

Clinical assessment

Symptoms and signs of pleurisy often precede the development of an effusion in patients with• Tuberculosis• underlying pneumonia • pulmonary infarction • connective tissue disease

Particular attention should be paid to a recent history of • contact with tuberculosis• respiratory infection• presence of heart disease• liver or renal disease • occupation (e.g. exposure to asbestos)• risk factors for thromboembolism

BREATHLESSNESS - only symptom related to effusion and its severity depends on the • size • rate of accumulation

Clinical features

Manifest when pleural effusions >300 mL

On inspection: Fullness of chest on affected side Reduced expansion of chest Tracheal shift with Trail’s sign - observed

with effusions  of > 1000 mL• Prominence of lower part of

sternocleidomastoid due to tracheal deviation

On palapation

Trachea & apex beat shifted to opposite side

Decreased tactile fremitus

• Displacement toward the side of the effusion is an important clue to obstruction of a lobar bronchus

Percussion: Dullness on percussion- stony dull

• obliteration of tympanitic percussion note over Traube’s space in left sided effusion

Level of dullness goes up in axilla Dullness over grocco’s triangle

surface markings • left sixth rib• left midaxillary line• left costal margin

Traube's space

Grocco’s triangle

XII th rib

Upper margin of fluid

Grocco's Paravertebral Triangle

Triangular area of dullness at the back of chest on the healthy side

Base – horizontally along the XII th rib Apex – at the level of upper margin of fluid on

diseased side Internally – vertebral line Externally – line joining the apex and lateral

base

Ascultation

Decreased or absent breath sounds

Pleural friction rub may be present ONLY WHEN EFFUSION IS SMALL

compressed lung

zone of compensatory emphysema

Findings at the upper level of moderate effusion

Skodaic resonance – percussion

Dull on percussionAbsent Br sound

Increased VF, egophony & bronchial breath sounds

Egophony: high-pitched nasal or bleating quality sound

Possible findings at the upper level of dullness in case of moderate pleural effusion:

1. lung is compressed Increased vocal fremitus & aegophony –

nasal quality of sounds transmitted Bronchial breath sound2. there may be a zone of compensatory

emphysema above it Skodaic resonance on percussion

INVESTIGATIONS

1.Chest X ray

P A view: minimum of 200cc of fluid required to produce blunting of costophregnic angles in

Lateral view: 60 ml lateral decubitus Xray: 10 ml

200 ml fluid required to produce this shadow60 ml in lateral view10 ml in decubitus Xray

X ray tube

X rays

Some atypical pleural effusions

Localised effusions: previous scarring or adhesions in the pleural space

Subpulmonary effusion: Pleural fluid localised below the lower lobe simulates an elevated hemidiaphragm

Fluid localised within an oblique fissure may produce a rounded opacity simulating a tumour

Subpulmonic effusion - Rt

Phantom tumor-Pleural effusion inInterlobar fissure

2. Ultra sonography of thorax

2. USG of thorax:

• Can detect even less than 10 ml• Can differentiate between pleural thickening

& effusion• USG guided needle aspiration in small effusion

3. Diagnostic aspiration of pleural fluid

1. Protein2. L.D.H.

3. Sugar – low in bacterial infections & Rh. arthritis4. A.D.A – high (>42) in T.B. & some fungal

infections5. Amylase – high in pancreatitis, oesophageal

rupture, malignancy

Required for calculating LIGHT’S CRITERIA

1.Biochemical analysis

6.pH • Low pH suggests

infection rheumatoid arthritis ruptured oesophagus advanced malignancy

(FOR DISTINGUISHING PLEURAL TRANSUDATE FROM EXUDATE)

Pleural fluid is an EXUDATE if one or more of theFollowing criteria are met:

1. Pleural fluid protein:serum protein ratio > 0.5

2. Pleural fluid LDH: serum LDH ratio > 0.6

3. Pleural fluid LDH > two-thirds of the upper limit of normal serum LDH

2. Microscopic examinationPredominant cell type

• provides useful information and cytological examination is essential

Polymorphs suggest bacterial infection

Lymphocytes: tuberculous High ADA + Pl. fluid lymphocyte/neutrophil > 0.75 – Highly diagnostic of tuberculous pleural effusion

Malignant cells ma be seen in malignancy

3.Gram stain • may suggest parapneumonic effusion

4.ELISA or

PCR• Helpful in diagnosing T.B. if acid-fast bacilli

are not seen

5. Cultures: positive in 30 to 70%

(Enzyme-linked immunosorbent assay)

(Polymerase chain reaction)

May be required if all fails With all methods combined yield is close

to 95%

4. Pleural biopsy

Combining pleural aspiration with biopsy increases the diagnostic yield

Ultrasound or CT guided biopsy with Abrams needle is most frequently employed

Pleural aspiration and biopsy Abrams needle

If all of them unhelpful:

5. Throcacoscopy

6. HRCT

THORACOSCOPY

Summary of Investigations X ray USG thorax Pleural fluid examination

• Biochemical• Microscopic• Gram staining• Culture

PCR or ELISA Pleural biopsy Thoracoscopy HRCT

Cardiacfailure*

Serous,Strawcoloured

Transudate Few serosal cells Other evidence of leftventricular failure.Response to diuretics.

PLEURAL EFFUSION: MAIN CAUSES & FEATURES

Cause

Appearance offluid

Type offluid

Predominantcells in fluid

Other diagnostic features

Tuberculosis Serous,UsuallyAmbercoloured

Exudate Lymphocytes(occasionallypolymorphs)

+ tuberculin testIsolation of M.tuberculosis frompleural fluid (20%)Positive pleural biopsy(80%)

Malignantdisease

Serous,OftenBloodstained

Exudate Serosal cells &LymphocytesOften clumps ofmalignant cells

Positive pleural biopsy(40%)Evidence of malignantdisease elsewhere

Pulmonaryinfarction

Serous or blood-stained

Exudate(rarelytransudate

Red bloodCellsEosinophils

Evidence ofPulmonaryInfarction.Source ofEmbolism.Factorspredisposingto venousthrombosi

Rheumatoid disease

SerousTurbid ifchronic

Exudate Lymphocyte(occasionalpolymorphs)

Rheumatoid arthritis; rheumatoid factor in serum.Cholesterol in chronic effusion; very low glucose in pleural fluid

SystemicLupuserythematosus

(SLE)

Serous Exudate Lymphocytesand serosalcells

• OtherManifestationsof SLE• Antinuclearfactor or AntiDNA in Serum(Ds DNA)

Acutepancreatitis

Serous orBloodstained

Exudate No cellspredominate

High amylasein pleural fluid(greater thanin serum)

Obstruction ofthoracic duc

Milky Chyle(Chylous Effusion)

None Chylomicrons

Hemorrhagic Chylous- thoracic duct obstruction

Transudate in CCF

Presence of blood is consistent with Pulmonary infarction Malignancy Tuberculosis Traumatic Anticoagulation Mesothelioma

Result from: Hypersensitivity reaction to Mycobacterium

Microbial invasion of the pleura (less common)

• acid-fast bacillus stains of pleural fluid are rarely diagnostic (<10-20 % of cases)

• pleural fluid cultures grow Mycobacterium tuberculosis in less than 65% of cases

Tuberculous pleural effusion

Effusion may accompany1.Primary T. B.

• commonly unilateral, and results from a hypersensitivity phenomenon

• May recover without treatment, but in close to two thirds active tuberculosis develops within 5 years

2. Post primary T. B.: Subpleural T B focus

ruptures into the pleural space Clinically presentation as

• acute • subacute • chronic form

With fever, nonproductive cough or chest pain

Diagnosed on the basis of: Microscopy + Adenosine deaminase

(ADA) activity ADA > 43 U/mL in pleural fluid supports

the diagnosis of TB pleuritis. sensitivity - 78%

ADA + Pl. fluid lymphocyte/neutrophil > 0.75 – Highly diagnostic of tuberculous pleural effusion

Other investigation

Chest radiography: • shows a small to moderate effusion (only

4% are large)• Parenchymal disease is seen in a third

of cases

• Enzyme-linked immunosorbent assay(ELISA) • Polymerase Chain Reaction (PCR)

may be helpful diagnostically Provide a more rapid diagnosis in the

more than 90% of cases in which acid-fast bacilli are not seen on smear

Cultures: positive in 30 to 70% - results take a long time

Treatment

Fever resolves within 2 weeks of instituting category I ATT • may persist for 6 or 8 weeks

The effusion usually resolves by 6 weeks • may persist for 3 to 4 months

Very ill patients may be helped by short-term corticosteroid treatment

ADA can be +in: Fungal infections like coccidomycosis & HistoplasmosisSome cases of malignancy & connective tissue disorder

Malignant

P l e u r a l e f f u s i o n

CausesMost malignant effusions are metastatic

Investigations

Pleural fluid cytology CT chest with pleural contrast

• Nodular, mediastinal, or circumferential pleural thickening on CT-highly specific for malignant disease

Treatment options Therapeutic pleural aspiration

Intercostal chest drainage pleurodesis - seal the visceral to the

parietal pleura to prevent pleural fluid accumulating

commonly used agents are sterile talc, tetracycline, and bleomycin • Corticosteroids should be discontinued

beforehand