Diseases of Pleura ALOK SINHA Department of Medicine

Diseases of Pleura ALOK SINHA Department of Medicine

Diseases of Pleura ALOK SINHA Department of Medicine Manipal College of Medical Sciences Pokhara, 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 PLEURAL EFFUSION The accumulation within the pleural space of

pleural effusion Serous fluid - Frank pus - Blood - haemothorax

empyema Pleural fluid accumulates increased increased hydrostatic hydrostatic & & decreased decreased osmotic osmotic pressure

pressure Transudate 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 Exudate Tuberculous

Parapneumonic causes Malignancy (carcinoma, lymphoma,mesothelioma) Pulmonary embolism

Pancreatitis Collagen-vascular conditions (rheumatoid arthritis, SLE) Asbestos exposure Trauma

Postcardiac injury (Dresslers) syndrome Esophageal perforation Radiation pleuritis

Drug use Chylothorax Meigs syndrome Sarcoidosis Yellow nail syndrome

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 Trails 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 Traubes space in left sided effusion Level of dullness goes up in axilla Dullness over groccos triangle surface markings

left sixth rib left midaxillary line left costal margin Traube's space Upper margin of fluid Groccos triangle XII th rib 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

Findings at the upper level of moderate effusion zone of compensatory emphysema compressed lung Skodaic resonance percussion Increased VF, egophony & bronchial breath sounds Dull on percussion

Egophony: high-pitched nasal or bleating quality sound Absent Br 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 sound 2. there may be a zone of compensatory

emphysema above it Skodaic resonance on percussion INVESTIGATIONS 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 shadow 60 ml in lateral view 10 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 Subpulmon ic effusion Rt Phantom tumor -Pleural effusion in Interlobar 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.Biochemical analysis 1. Protein 2. L.D.H.

Required for calculating LIGHTS CRITERIA 3. Sugar low in bacterial infections & Rh. arthritis 4. A.D.A high (>42) in T.B. & some fungal infections 5. Amylase high in pancreatitis, oesophageal rupture, malignancy 6.pH Low pH suggests

infection rheumatoid arthritis ruptured oesophagus advanced malignancy LIGHT'S CRITERIA (FOR DISTINGUISHING PLEURAL TRANSUDATE FROM EXUDATE) Pleural fluid is an EXUDATE if one or more of the Following 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 examination Predominant 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 PCR (Enzyme-linked immunosorbent assay) or (Polymerase chain reaction) Helpful in diagnosing T.B. if acid-fast bacilli are not seen 5. Cultures: positive in 30 to 70%

4. Pleural biopsy May be required if all fails With all methods combined yield is close to 95% Combining pleural aspiration with biopsy increases the diagnostic yield

Ultrasound or CT guided biopsy with Abrams needle is most frequently employed Abrams needle Pleural aspiration and biopsy 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 PLEURAL EFFUSION: MAIN CAUSES & FEATURES Cause Tuberculosis Appear

ance of Type of fluid fluid Serous, Usually Amber coloured Exudate Other diagnostic cells in fluid features

Predominant Lymphocytes (occasionally polymorphs) + tuberculin test Isolation of M. tuberculosis from pleural fluid (20%) Positive pleural biopsy (80%) Malignant

disease Serous, Often Blood stained Exudate Cardiac failure* Serous,

Straw coloured Transudate Serosal cells & Lymphocytes Often clumps of malignant cells Positive pleural biopsy Few serosal cells

Other evidence of left ventricular failure. Response to diuretics. (40%) Evidence of malignant disease elsewhere Pulmonary infarction

Serous or Exudate blood- (rarely stained transudate Red blood Cells Eosinophils Rheumatoid disease Serous Turbid if

chronic Lymphocyte (occasional polymorphs) Exudate Evidence of Pulmonary Infarction. Source of Embolism.

Factors predisposing to venous thrombosi Rheumatoid arthritis; rheumatoid factor in serum. Cholesterol in chronic effusion; very

low glucose in pleural fluid Systemic Serous Lupus erythematosus (SLE) Exudate Lymphocytes and serosal

cells Other Manifestations of SLE Antinuclear factor or Anti DNA in Serum (Ds DNA) Acute pancreatitis

Serous or Blood stained Exudate No cells predominate High amylase in pleural fluid (greater than in serum)

Obstruction of thoracic 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 Tuberculous pleural effusion 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 Effusion may accompany 1.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 acidfast 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 & Histoplasmosis Some cases of malignancy & connective tissue disorder M a l i g n a

n t P P ll e eu u rr a a ll e e ff ff u u ss ii o on n

Causes Most 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

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