• Pleural effusion is extremely common — estimated 1.5 million new cases per year in the United States alone ^[3]
• The most common causes worldwide are congestive heart failure (CHF), pneumonia (parapneumonic effusions), and malignancy ^[3]

• Tuberculosis (TB) remains a highly prevalent cause of exudative pleural effusion in Hong Kong, unlike in Western countries where it is uncommon. Hong Kong's TB notification rate remains around 50-60 per 100,000 population (one of the highest in the developed world) ^[1][3]
• Malignant pleural effusion (MPE): Lung cancer is the leading cause of cancer death in Hong Kong, and it is the most common malignancy causing pleural effusion locally. Breast cancer, lymphoma, and mesothelioma are other important causes ^[1]
• Heart failure: The ageing population in Hong Kong means CHF-related transudative effusions are extremely common on medical wards
• Hepatic hydrothorax: Given the high prevalence of chronic hepatitis B in Hong Kong, cirrhosis-related pleural effusions (hepatic hydrothorax) are seen more frequently than in Western populations

Risk factors are essentially those of the underlying conditions:

• Transudative: Heart failure, cirrhosis (HBV-related in HK), nephrotic syndrome, renal failure
• Exudative: TB exposure, smoking (lung cancer), occupational asbestos exposure (mesothelioma), pneumonia, autoimmune disease (SLE, RA), prior thoracic surgery

The pleura consists of two continuous serous membranes:

1. Visceral pleura: Covers the lung parenchyma, dips into the fissures. It receives its blood supply from the bronchial circulation (systemic) and drains into the pulmonary veins. It has no somatic pain fibres — this is why disease affecting only the visceral pleura is painless.

2. Parietal pleura: Lines the inner surface of the chest wall, diaphragm, and mediastinum. It receives its blood supply from the intercostal arteries (systemic) and drains into the intercostal veins (→ azygos system). It is innervated by the intercostal nerves (costal and peripheral diaphragmatic portions) and the phrenic nerve (central diaphragmatic and mediastinal portions). This is why:

   • Costal pleural irritation → well-localized, sharp chest pain
   • Central diaphragmatic irritation → referred pain to the ipsilateral shoulder tip (via phrenic nerve → C3, C4, C5)

3. Pleural space: A potential space between the two layers, normally containing 5–15 mL of fluid with protein content ~1.5 g/dL. The intrapleural pressure is normally slightly sub-atmospheric (about −5 cmH₂O at end-expiration), which helps keep the lung expanded against the chest wall.

Understanding fluid dynamics is key to understanding why effusions form. Think of it as a balance:

Fluid INTO the pleural space comes from:

• Parietal pleural capillaries (systemic circulation, higher hydrostatic pressure ~30 cmH₂O)
• The hydrostatic pressure gradient pushes fluid from the capillaries through the parietal pleura into the pleural space

Fluid OUT of the pleural space goes via:

• Reabsorption at the venous end (lower hydrostatic pressure) driven by oncotic pressure
• Lymphatic drainage via stomata (pores) on the parietal pleura — these drain into the mediastinal lymph nodes. Lymphatic drainage accounts for the majority of pleural fluid clearance and can handle up to ~700 mL/day

The four determinants of pleural fluid volume are ^[1][2]:

1. Hydrostatic pressure (at the arterial end) — pushes fluid OUT of capillaries
2. Oncotic pressure (at the venous end) — pulls fluid BACK into capillaries
3. Capillary permeability — determines how leaky the vessels are
4. Lymphatic drainage capacity — the main exit route for pleural fluid

This is the most fundamental classification. Every pleural effusion should be categorized as transudative or exudative because it completely changes your differential and management ^[1][2].

The Light's criteria remain the gold standard to distinguish transudative from exudative effusions ^[1][2]:

An effusion is exudative if any ONE of the following is met:

If none of the above are met → transudative

This is a key classification for management decisions (particularly whether to insert a chest drain):

Why does pH drop? Bacteria metabolize glucose anaerobically → produce lactic acid and CO₂ → ↓pH. Neutrophils also consume glucose and release LDH. So low pH + low glucose + high LDH = bacterial activity within the pleural space.

The classical examination findings of a pleural effusion form a recognizable pattern. Understanding why each sign occurs is essential:

Always look for clues to the aetiology — this is what examiners want to see:

More sensitive than CXR. Can detect as little as 20 mL of fluid. Key advantages:

• Differentiates effusion from pleural thickening (fluid is anechoic/hypoechoic; thickening is echogenic and does not flow)
• Identifies loculations and septations
• Assesses echogenicity: echogenic or complex fluid suggests exudate; anechoic fluid can be either
• Guides drainage and biopsy → ↓complication rate of procedures

Reserved for uncertain diagnosis or complex cases:

• Precisely determines location, size, and nature of effusion
• Identifies pleural thickening, enhancement (suggests empyema or malignancy), and pleural nodularity (malignancy)
• Detects underlying parenchymal disease (pneumonia, mass, PE)
• Guides biopsy targeting

• Do NOT tap if the effusion is bilateral, small-moderate, and the clinical picture is clearly transudative (e.g., known CHF with bilateral effusions and good response to diuretics) ^[1]
• DO tap (diagnostic thoracocentesis) if:
  • Unilateral effusion
  • Bilateral but asymmetric or atypical features
  • Fever, pleuritic pain, or concern for infection/malignancy
  • New effusion of unclear cause
  • Failure to respond to treatment of presumed cause

Indicated when pleural fluid analysis is non-diagnostic, especially in suspected TB or malignancy:

• Definition: Pleural effusion with malignant cells identified in pleural fluid cytology or pleural biopsy
• Most common causes: Lung (most common), breast, lymphoma, ovarian, gastric ^[1]
• Mechanism: Direct tumour invasion of pleura → ↑permeability + impaired lymphatic drainage. Also mediastinal nodal involvement blocking lymphatic outflow
• Features: Often large, rapidly re-accumulating, may be haemorrhagic
• Significance: Indicates advanced (usually incurable) disease. Median survival with MPE from lung cancer is ~4–6 months

• Mechanism: TB bacilli reach the pleural space (usually from a subpleural caseous focus rupturing into the pleural space) → triggers a strong delayed-type hypersensitivity (Type IV) response → lymphocyte-rich exudative effusion. Importantly, the effusion is often the immune response — actual organisms may be scarce (AFB smear positive in < 10%, culture positive in ~30%)
• Typical profile: Young patient in HK, unilateral, lymphocytic exudate, ADA > 30, low glucose, high protein
• Key investigation: Pleural biopsy (Abram's needle) is first-line because TB granulomas are diffusely distributed → good yield even with blind biopsy ^[1]

• Definition: Pleural effusion in a patient with cirrhosis and portal hypertension, in the absence of primary cardiac or pulmonary disease
• Mechanism: Ascitic fluid passes through congenital diaphragmatic defects (small fenestrations, usually on the right) into the pleural space, driven by the positive intra-abdominal pressure and negative intrapleural pressure. This is why it is almost always right-sided (~85%)
• Note: It is classified as a transudate even though the patient has liver disease — the fluid itself crosses passively through the diaphragmatic defects

• Definition: Accumulation of chyle in the pleural space
• Mechanism: Disruption of the thoracic duct → chyle (rich in dietary long-chain triglycerides absorbed by intestinal lacteals) leaks into the mediastinum and then into the pleural space
• Causes: Trauma/surgical (most common — post-oesophagectomy, post-cardiac surgery), lymphoma (most common non-traumatic cause), other malignancies, sarcoidosis
• Diagnostic: Pleural fluid triglycerides > 1.24 mmol/L (110 mg/dL), milky appearance, chylomicrons present on lipoprotein analysis

The pleural surfaces are normal. The fluid accumulates because Starling forces are deranged systemically. Usually bilateral ^[1][2][3].

Light's criteria classify a pleural effusion as exudative if it meets any ONE of the following three conditions ^[1][2][3]:

If none of the three criteria are met → transudative.

Must-know principle: Pleural fluid biochemistry should always be sent together with a paired serum sample (serum protein + serum LDH) drawn at the same time. Without the serum values, you cannot calculate the ratios ^[3].

Think about what LDH and protein tell you:

• Protein: Reflects capillary permeability. Normal capillaries leak very little protein into the pleural space. If the pleural fluid protein is high relative to serum → the capillaries are leaky → inflammation → exudate.
• LDH (lactate dehydrogenase): LDH is an intracellular enzyme released when cells are damaged or dying. High pleural fluid LDH reflects active cellular turnover/necrosis within the pleural space — whether from bacteria, tumour cells, inflammatory cells, or mesothelial cell injury. The more active the disease process, the higher the LDH.

Why use ratios rather than absolute values? Because a patient with very high serum protein (e.g., multiple myeloma with serum protein of 100 g/L) might have pleural fluid protein of 40 g/L that looks "high" in absolute terms but is actually low relative to serum — it's a transudate. Ratios normalise for the patient's own serum values.

Light's criteria tend to overdiagnose exudative fluid, especially if the patient is on chronic diuretics ^[1].

Why? Diuretics remove free water → serum proteins and LDH become concentrated → pleural fluid ratios approach exudative thresholds even though the underlying process is transudative (e.g., CHF patient on furosemide).

The fix: If Light's criteria suggest exudate but the clinical picture strongly suggests transudate → calculate the serum-to-pleural-fluid albumin gradient:

Another complementary check mentioned in the senior notes ^[1]: serum-pleural fluid protein difference < 3.1 g/dL → likely exudative (i.e., the protein levels are close together → high permeability → true exudate).

Pro tip: The moment you aspirate frank pus, you don't even need to wait for biochemistry — the diagnosis is empyema and you should insert a chest drain immediately ^[1].

The first-line investigation. Always start here.

Projections:

• PA erect → higher quality, accurate heart size assessment. Minimum ~175 mL of fluid to detect (blunting of CP angle) ^[1][5]
• AP (portable) → lower quality, exaggerates heart size and mediastinal contour; used for bed-bound patients ^[5]
• Lateral decubitus → patient lies on the affected side → free-flowing fluid layers dependently. Minimum ~100 mL detectable. Detects loculations (fluid does NOT redistribute on position change) ^[1]

Key CXR findings in pleural effusion ^[1][3][5]:

Additional features to examine on CXR (looking for the CAUSE) ^[4]:

• Lung fields: masses, consolidation, cavitation → malignancy, pneumonia, TB
• Hilum: hilar enlargement → lymphoma, lung cancer, sarcoidosis
• Heart: cardiomegaly → CHF
• Bones: lytic lesions → metastatic disease
• Upper lobe venous diversion + Kerley B lines → pulmonary venous congestion (CHF) ^[6]

More sensitive than CXR — can detect as little as ~20 mL of fluid. Increasingly used as the first-line bedside tool.

Reserved for complex or uncertain cases. Provides the most comprehensive anatomical information.

Radiological approach to pleural shadows on CT ^[4]:

• Colour/density: effusion = darker than chest wall muscle; thickening = same density; plaques = very bright white
• Contour: smooth → fluid, thickening, or plaques; lobulated → malignancy
• Distribution: diffuse → benign thickening or malignant pleural disease; patchy → pleural plaques
• Enhancement: enhanced → empyema

A dedicated imaging technique worth understanding in detail:

• Technique: Patient lies on the affected side (side of effusion down) for a lateral decubitus film
• Purpose: Free-flowing fluid layers along the dependent chest wall. This allows you to:
  1. Confirm the effusion is free-flowing (fluid redistributes with gravity)
  2. Identify loculations (if fluid does NOT redistribute → loculated, may need different drainage strategy)
  3. Assess tappability: > 1 cm fluid thickness on decubitus film → suitable for safe thoracocentesis ^[1]
• Contrast with pneumothorax: For suspected pneumothorax, the patient lies with the suspected side UP on a lateral decubitus film (air rises, making it visible). This is the opposite orientation to effusion assessment.

Pleural fluid by pleural tapping is not required if bilateral effusion is strongly suggestive of transudative cause ^[1][2][3].

This applies when:

• Bilateral, symmetric effusions
• Clear clinical diagnosis (e.g., decompensated CHF with cardiomegaly, ↑JVP, bilateral oedema, ↑BNP)
• Response to treatment (e.g., effusion shrinks with diuresis)

BUT tap if: asymmetric, unilateral, febrile, fails to respond to treatment, or atypical features present.

• Pleural fluid haematocrit > 50% of peripheral blood haematocrit → confirmed haemothorax
• This is distinct from a "bloody" effusion (which can occur in malignancy, TB, PE) where the haematocrit is much lower
• A true haemothorax requires chest tube drainage ± surgical consultation, not just diagnostic evaluation

• Clinical context: Cirrhosis with ascites + right-sided pleural effusion (usually without primary cardiopulmonary disease)
• Confirmation: Pleural fluid analysis shows transudate. If ascites is present, can demonstrate the diaphragmatic defect by injecting 99mTc-sulphur colloid into the peritoneal cavity → radiotracer appears in the pleural space within hours = pleuroperitoneal communication
• Do NOT insert a chest tube for hepatic hydrothorax → may cause massive protein/electrolyte depletion, infection, renal failure, and bleeding ^[7]

TB pleuritis is one of the most important diagnoses to make in Hong Kong ^[1][2][3]. The challenge is that:

• AFB smear of pleural fluid is positive in < 10% (organisms are scarce)
• TB culture of pleural fluid is positive in only ~30% (better but still low)
• ADA > 30–40 IU/L with lymphocytic predominance has sensitivity ~90% and specificity ~92% → highly useful screening tool ^[1][2]
• Pleural biopsy (Abrams needle) is first-line ^[1][3] because TB granulomas are diffusely distributed → sensitivity ~80% with histology + culture of biopsy tissue

The combined sensitivity of pleural fluid ADA + culture + biopsy histology + biopsy culture approaches 95%.

• Cytology (20 mL × 3) is the initial diagnostic step — sensitivity ~60-75% ^[1][3]
• If cytology negative → CT thorax with contrast to identify pleural thickening/nodularity, lung masses, lymphadenopathy
• If CT suspicious → pleural biopsy via medical thoracoscopy (sensitivity > 90%) ^[1]
• PET-CT for staging and identifying occult primary
• For lymphoma: pleural fluid cytology may not be diagnostic → send for flow cytometry (identifies clonal B-cell or T-cell populations)

• When the underlying cause cannot be eradicated (e.g., incurable malignancy) ^[3]
• Preferred when pleural fluid accumulates slowly ^[3]
• Symptomatic relief of dyspnoea in any large effusion
• As a temporising measure while definitive treatment is initiated

The procedure follows a strict protocol:

1. Review CXR to confirm diagnosis, location, and extent ^[2]
2. Position patient: (1) 45° semi-supine with hand behind head; or (2) sitting up leaning over table with padding ^[2]
3. USG guidance if available — significantly reduces pneumothorax rate (~0.5% vs 5–15% blind) ^[2]
4. Aseptic technique throughout
5. Puncture site: safety triangle — bounded by the lateral edge of pectoralis major, lateral edge of latissimus dorsi, 5th ICS and base of axilla along the mid or posterior axillary line, immediately above a rib (to avoid the intercostal neurovascular bundle which runs along the inferior border of each rib) ^[2]
6. Anaesthetise all layers of the thoracic wall down to pleura ^[2]
7. Diagnostic tap: withdraw 20–50 mL → send for LDH, protein, cell count/diff, cytology, Gram/C&ST, AFB ± pH/glucose ^[2]
8. Therapeutic tap: connect 3-way tap → aspirate slowly and repeatedly
   • Avoid pushing aspirated content back into pleural cavity ^[2]
   • Avoid aspirating > 1–1.5 L per procedure → to prevent re-expansion pulmonary oedema (RPO) ^[2]
9. Post-procedure CXR and close monitoring for complications ^[2]

Why does re-expansion pulmonary oedema (RPO) occur? ^[8] When a lung has been compressed for a prolonged period ( > 3 days), the pulmonary capillary endothelium is damaged by ischaemia and oxidative stress. When the lung suddenly re-expands, blood flow returns to these damaged capillaries → protein-rich fluid leaks into the alveoli → unilateral pulmonary oedema. Risk factors include lung collapse > 3 days, high-volume drainage, and early suction use ^[8]. Signs: cough, SOB, desaturation that improves upon clamping the drain. CXR: alveolar shadowing. Management: supportive + clamp drain ^[8].

Chest tube drainage is a more definitive drainage modality than simple thoracocentesis. The key question is: when do you escalate from a simple tap to a chest drain?

Chest drain (large-bore) is indicated if ^[1]:

Clinical indications:

• Respiratory distress ^[1]
• Sepsis ^[1]

Radiological indications:

• Large non-purulent effusion (≥ 40% of hemithorax) ^[1]
• Loculation on CXR/USG ^[1]
• Pleural thickening with contrast enhancement on CT thorax ^[1]

Pleural fluid indications (complicated effusion or empyema):

• Appearance: overtly purulent (empyema) ^[1]
• Biochemical: pH < 7.2 or glucose < 2.2 mmol/L ^[1]
• Microbiology: positive Gram stain ± culture ^[1]

• Principle: use negative pressure to suck effusion out ^[3]
• Inserted in the safety triangle (same landmarks as thoracocentesis)
• Connected to an underwater seal drainage system — the water seal acts as a one-way valve, allowing fluid/air out but preventing air from re-entering the pleural space
• The water column oscillates ("swings") with respiration — this confirms the tube is in the pleural space and patent

• Daily monitoring of drain output volume and character
• Serial CXR to assess lung re-expansion
• Remove drain when output is minimal (< 150–200 mL/day) and lung is re-expanded on CXR

• Always treat the underlying infection with appropriate antibiotics
• Duration: 1–2 weeks for uncomplicated parapneumonic effusion; 4–6 weeks for empyema ^[1]
• Cover anaerobes + typical organisms ^[2]: common pathogens include Streptococci milleri group, Strep pneumoniae, S. aureus, and anaerobes (e.g., Bacteroides) ^[1]
• Empirical regimens typically include a beta-lactam/beta-lactamase inhibitor (e.g., amoxicillin-clavulanate) or a carbapenem, with metronidazole added for anaerobic cover if not already provided
• Chest physiotherapy + mobilisation ^[1] — aids sputum clearance and prevents deconditioning

As stated above (see Section D.1). To emphasise the key decision points:

Frank pus or turbid/cloudy pleural fluid on sampling → mandates drain insertion ^[2]

pH < 7.2 or glucose < 2.2 mmol/L or positive Gram stain → mandates drain insertion ^[1]

Large effusion (≥ 40% hemithorax), loculation, or sepsis → drain insertion ^[1]

If none of the above: antibiotics alone with close monitoring + repeat imaging.

When chest drain drainage is inadequate (persistent sepsis, loculated collections not draining, trapped lung), escalate in this order:

• MPE occurs in 50% of all metastatic malignancy (especially NSCLC) ^[10]
• Mechanism: direct invasion from neighbouring structures, haematogenous spread, lymphatic obstruction ^[10]
• Treatment is determined by:
  1. Symptoms — is the patient dyspnoeic?
  2. Rate of re-accumulation — does it come back quickly after tapping?
  3. Lung expandability — can the lung re-expand fully after drainage?
  4. Performance status and life expectancy — can the patient tolerate procedures?

PleurX drain: long-term drainage for recurrent pleural effusion ^[11] — this is the brand name commonly used in Hong Kong for the IPC.

Indications for pleurodesis ^[10]:

• Pneumothorax: SSP; PSP (recurrent, synchronous bilateral, persistent air leak, high-risk professions, pregnancy)
• Pleural effusion: recurrent malignant pleural effusion, chylothorax with failed conservative treatment
• Post-op: persistent output after pericardial window surgery

Contraindications: parapneumonic effusion / empyema (because it makes subsequent drainage and decortication difficult) ^[10]

Why is empyema a contraindication for pleurodesis? Because pleurodesis obliterates the pleural space with adhesions. If there is active infection (empyema), obliterating the space traps the infected material — you create an undrained abscess. You need to drain the infection first, not seal it in.

Absolute prerequisite: Lung must be fully expanded to allow pleural apposition ^[2] — if the lung is trapped (non-expandable), the two pleural surfaces cannot come into contact, and pleurodesis will fail.

Preferred in recurrent MPE or surgically unfit patients ^[10].

Principle: Irritation to stimulate chronic inflammation → adhesion and fibrosis formation → obliteration of pleural space ^[3]

Agents ^[2][10]:

Procedure ^[10]:

1. Adequate analgesia ± sedation — pleurodesis causes significant pleuritic pain (the inflammation is intentional)
2. Connect chest drain, then apply sclerosing agent via drain when lung re-expanded
3. Clamp chest drain for 1–2 hours to hold the sclerosant in contact with the pleural surfaces
4. If co-existing pneumothorax / bubbling chest drain → do NOT clamp drain → instead hang up drain to ~50 cm above patient to drain air but retain the sclerosant ^[10]
5. Continue drainage until drain output < 150 mL/day × 2 days + CXR shows lung re-expanded ^[10]

Complications ^[10]:

• Pain (most common) — avoid NSAIDs because the inflammatory action of pleurodesis is essential for success ^[10]. Use opioids or paracetamol instead
• Fever — expected inflammatory response
• Recurrence — 3% with surgical pleurodesis ^[10]; higher with chemical pleurodesis (~10–20%)
• Rare: cardiac arrhythmia, respiratory failure (especially with talc poudrage using non-graded talc → can cause ARDS)

First-line in pneumothorax ^[10], also considered for MPE in patients with good performance status.

Techniques ^[10]:

• VATS (video-assisted thoracoscopic surgery) — more common
• Open thoracotomy — rarely needed, higher morbidity

Surgical methods for creating pleural adhesion ^[10]:

• Stapling / resection of blebs / bullae (for pneumothorax)
• Mechanical abrasion by dry gauze — physically scrubs the parietal pleural surface to denude the mesothelium → triggers inflammation and fibrosis
• Pleurectomy — stripping of the parietal pleura entirely → raw surface adheres to visceral pleura
• Talc poudrage — direct application of talc powder under thoracoscopic vision

Recurrence rate: ~3% with surgical pleurodesis vs ~10–20% with chemical pleurodesis ^[10].

An IPC (commonly PleurX drain ^[11]) is a tunnelled, semi-permanent catheter placed in the pleural space, with a one-way valve on the external end. The patient or a carer can connect a drainage bottle at home and drain the effusion as needed — typically every 1–3 days.

• Rapidly reaccumulating pleural effusion without effective treatment ^[3]
• Malignant pleural effusion with short life expectancy ^[10]
• Trapped lung / non-expandable lung — where pleurodesis is not possible because the lung cannot appose the chest wall ^[10]
• Patient preference (avoids repeated hospital admissions)

• ↓ Length of hospital stay ^[2]
• ↓ Need for repeated interventions ^[2]
• Chance of spontaneous pleurodesis (up to 40%) ^[2] — the chronic irritation from the catheter can induce pleural adhesion even without a sclerosant
• Further ↑ (51%) if talc pleurodesis performed via the indwelling catheter ^[2] — you can instil talc through the IPC to enhance the pleurodesis rate

• ↑ Complication rate including:
  • Infection (empyema, cellulitis at insertion site) — the most feared complication
  • Blockage (protein/fibrin clots occlude the catheter)
  • Tract metastasis — tumour cells seed along the catheter tract ^[2]
• Protein and electrolyte depletion (with frequent large-volume drainage)
• Catheter dislodgement

• Do NOT put in chest tube ^[7]
• Management: diuretics, Na restriction, ± thoracocentesis or TIPS ^[7]
• Consider liver transplantation for definitive cure in appropriate candidates
• Refractory cases: consider TIPS (transjugular intrahepatic portosystemic shunt) → ↓portal pressure → ↓ascites → ↓fluid crossing diaphragmatic defects

• Anti-TB chemotherapy is the primary treatment (standard RIPE regimen × 6–9 months)
• Most TB effusions resolve with anti-TB treatment alone without drainage
• Therapeutic thoracocentesis only if large and symptomatic
• Corticosteroids: controversial; some evidence for ↓residual pleural thickening and ↓time to symptom resolution, but not routinely recommended
• Pleural biopsy (Abram's needle) is first-line diagnostic investigation in HK ^[1] (as discussed in prior section)

This applies specifically to parapneumonic effusions and represents the natural progression of untreated pleural infection ^[1][2]:

This is one of the most important chronic complications:

Distinction to understand ^[10]:

• Lung entrapment: lung cannot expand fully because of an active disease (e.g., active malignancy encasing the lung); the pleural fluid is exudative
• Trapped lung: lung cannot expand fully because of a remote inflammatory condition that left behind a fibrous peel; the pleural fluid is transudative (the inflammation is gone, but the scar remains)
• These represent a continuum of the same disease process: the active disease resolves, leaving behind fibrosis ^[10]

These can occur during thoracocentesis, chest drain insertion, or pleural biopsy: