Pleural & Oesophageal Disease

🫁 Pleural & Oesophageal Disease

Light’s criteria, pleural effusion, empyema staging, pneumothorax management, pleurodesis, and Boerhaave’s syndrome — the MRCS pleural and oesophageal essentials.

Pleural Effusion & Light’s Criteria

A pleural effusion is an abnormal accumulation of fluid in the pleural space. The first priority is classifying it as a transudate (low protein — systemic cause) or exudate (high protein — local cause). This is achieved using Light’s Criteria, which are highly sensitive for exudates.

Light’s Criteria

An effusion is an exudate if it meets ANY ONE of the following three criteria. If none are met, it is a transudate.

🧠 Light’s Criteria — “The Three Ratios”

An effusion is an EXUDATE if ANY ONE of these is true:

1. Pleural fluid protein / serum protein > 0.5
2. Pleural fluid LDH / serum LDH > 0.6
3. Pleural fluid LDH > ⅔ of the upper limit of normal serum LDH

Sensitivity ~98% for exudates. Specificity ~75% (misclassifies ~25% of transudates — especially in diuretic-treated heart failure, where protein is concentrated). If criteria met but clinically looks like transudate: use serum-effusion albumin gradient (>12 g/L = transudate).

Transudate

Protein <30 g/L — systemic cause

Mechanism: Increased hydrostatic pressure OR decreased oncotic pressure → fluid leaks across normal pleural membranes.

Cardiac failure — most common cause overall. Bilateral. Raised hydrostatic pressure in pulmonary capillaries. Usually right-sided or bilateral.
Liver failure / cirrhosis — hypoalbuminaemia (↓ oncotic pressure) + portal hypertension. May have ascites (hepatic hydrothorax via diaphragmatic defects).
Nephrotic syndrome — massive proteinuria → hypoalbuminaemia → ↓ oncotic pressure
Hypothyroidism — myxoedema → reduced lymphatic drainage
Meigs syndrome — ovarian fibroma + ascites + pleural effusion (right-sided)
Peritoneal dialysis
Constrictive pericarditis — elevated systemic venous pressure

Exudate

Protein >30 g/L — local/pleural cause

Mechanism: Increased capillary permeability (inflammation, malignancy, infection) → protein-rich fluid leaks into pleural space.

Malignancy — lung cancer (most common malignant cause), mesothelioma, pleural metastases (breast, ovary, lymphoma). Haemorrhagic effusion (blood-stained). M1a stage in NSCLC.
Infection / parapneumonic effusion — commonest exudate overall. Can progress to empyema.
Tuberculosis — lymphocyte-predominant exudate. High ADA (adenosine deaminase). Pleural biopsy diagnostic.
Pulmonary embolism — can be transudate or exudate (haemorrhagic). Small, unilateral.
Rheumatoid arthritis / SLE — autoimmune pleuritis. Low glucose in RA effusion (classic).
Post-CABG (Dressler’s syndrome) — autoimmune pericarditis/pleuritis after cardiac surgery or MI.
Pancreatitis — high amylase in effusion. Left-sided (left pleural space adjacent to pancreatic tail).
Oesophageal rupture (Boerhaave’s) — high amylase (salivary), low pH, food particles.

Additional Pleural Fluid Analysis

Test	Finding	Interpretation
pH	<7.2	Empyema, malignancy (poor prognosis), oesophageal rupture, TB, RA. pH <7.2 in parapneumonic = needs drainage.
Glucose	<2.2 mmol/L	Empyema, malignancy, TB, RA (especially RA — very low glucose). Normal pleural fluid glucose ~ serum.
LDH	Very high	Empyema, malignancy. LDH is a marker of cell turnover and inflammation.
Amylase	High	Pancreatitis (pancreatic amylase), oesophageal rupture (salivary amylase), malignancy.
Cytology	Malignant cells	Positive in ~60% of malignant effusions. Repeat if negative (false negative common). Mesothelioma may require biopsy.
Microscopy + culture	Organisms	Parapneumonic / empyema. Send for Gram stain, C&S, AFB (TB).
Differential WBC	Neutrophils dominant	Parapneumonic / acute infection / PE
Differential WBC	Lymphocytes dominant	TB, malignancy, lymphoma, post-CABG
Appearance	Milky/turbid	Chylothorax (thoracic duct injury — post-surgery, trauma, lymphoma). Triglycerides >1.24 mmol/L confirms chyle.
Haematocrit	Pleural fluid Hct >50% of blood Hct	Haemothorax (trauma, malignancy, pulmonary infarction)
ADA (adenosine deaminase)	>40 U/L	Tuberculosis (high sensitivity in lymphocyte-predominant exudate).

Management of Pleural Effusion

Diagnostic thoracocentesis: Aspirate 20–50 mL for analysis. USS guidance mandatory (BTS guidelines). Reduces complications (pneumothorax, visceral injury).
Therapeutic thoracocentesis: Drain up to 1.5 L per session (avoid re-expansion pulmonary oedema). Repeat if needed.
Intercostal chest drain (ICD): For empyema, haemothorax, large symptomatic effusions.
Pleurodesis: For recurrent malignant effusion (see below).
Indwelling pleural catheter (IPC): Tunnelled pleural catheter for malignant effusions — patient self-drains at home. Alternative to pleurodesis. AMPLE trial: IPC vs pleurodesis — equivalent symptom relief, IPC preferred if trapped lung or non-expanded lung.
Treat underlying cause: Diuretics for cardiac failure, chemotherapy for malignant effusion.

Pleurodesis — Mechanism & Agents

Pleurodesis is the chemical or mechanical obliteration of the pleural space to prevent recurrence of effusion or pneumothorax. A sclerosing agent is instilled via chest drain, causing inflammation → fibrosis → visceral and parietal pleura fuse together, eliminating the space.

Talc (talc poudrage via thoracoscopy, or talc slurry via drain): Most effective agent. Talc poudrage (VATS) preferred — higher success rate (~90%). Talc slurry via drain is simpler but slightly less effective. Risk: acute respiratory distress (use graded talc, <5 micron particles removed).
Tetracycline / doxycycline: Chemical pleurodesis via drain. Less effective than talc. Used when talc unavailable.
Bleomycin: Chemotherapy agent used as pleurodesing agent in malignant effusions. Expensive.
Lung must be fully expanded before pleurodesis — otherwise the pleural surfaces cannot appose and pleurodesis fails (“trapped lung” = relative contraindication → use IPC instead).

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