1. Pleural Effusion

1.1 Epidemiology

• Pleural disease is common worldwide, affecting ~3000 people per million annually.
• Pleural effusion (fluid in the pleural space) is among the most frequent pleural disorders.
• Most effusions are either transudates, parapneumonic/infected effusions, or malignant effusions.

1.2 Aetiology

A pleural effusion arises when fluid accumulates in the pleural space – underlying mechanisms differ between transudate and exudate:

1. Transudate Effusions (often bilateral)
   • Usually due to systemic factors (e.g. increased hydrostatic pressure, decreased oncotic pressure)
   • Common causes:
     • Cardiac failure
     • Renal failure
     • Liver cirrhosis (hypoalbuminaemia)
     • Nephrotic syndrome
     • Hypothyroidism (rare)
2. Exudate Effusions (usually unilateral)
   • Result from pleural disease or inflammation altering capillary permeability or lymphatic drainage
   • Common causes:
     • Infection (parapneumonic effusions, empyema, tuberculosis)
     • Malignancy (lung cancer, breast cancer, mesothelioma)
     • Pulmonary embolism
     • Rheumatoid arthritis or SLE (connective tissue disease)
     • Pancreatitis (high amylase effusions)

1.3 Risk Factors

• Cardiac disease (heart failure, constrictive pericarditis)
• Chronic liver disease (cirrhosis)
• Chronic kidney disease (nephrotic syndrome, renal failure)
• Infections (pneumonia, tuberculosis)
• Malignancy (primary or metastatic)
• Connective tissue diseases (e.g. rheumatoid arthritis, SLE)

1.4 Clinical Features

• Breathlessness (dyspnoea) as fluid accumulates:
  • Rate of fluid build-up influences symptom severity.
• Pleuritic chest pain may occur if the pleura are inflamed (e.g. parapneumonic effusion) or infiltrated by malignancy.
• On examination:
  • Reduced chest expansion on the affected side
  • Stony dullness to percussion
  • Quiet or diminished breath sounds
  • Possible bronchial breathing above large effusions (where lung is compressed).

1.5 Diagnostic Approach

1. Chest X-ray
   • Confirms presence of fluid (blunting of costophrenic angles, fluid level).
   • Large effusions appear as water-dense shadows with a meniscus sign.
2. Blood Tests
   • Routine: FBC, U&E, LFTs.
   • Additional tests depending on clinical suspicion: e.g. tumour markers, rheumatoid factor, ANA, etc.
3. Pleural Aspiration (Ultrasound-guided)
   • At least 50 mL of fluid taken for:
     • Protein, LDH, glucose, pH
     • Microbiological tests (culture, acid-fast bacilli if TB suspected)
     • Cytology (malignant cells)
   • Light’s criteria differentiate exudates from transudates.
4. Further Imaging
   • Pleural ultrasound: detects loculations, guiding aspiration/drain placement.
   • CT thorax (especially if exudate): identifies pleural thickening, nodularity, or a suspicious lung lesion.
5. Pleural Biopsy
   • Required if a cause remains unclear after fluid analysis (particularly if malignancy or tuberculosis is suspected).
   • Can be done via image-guided (US/CT) needle biopsy or thoracoscopy.

1.6 Immediate Management

1. Symptomatic Relief
   • Drain large effusions if they cause significant breathlessness. Typically remove fluid slowly (0.5–1.5 L/24 h) to prevent re-expansion pulmonary oedema.
2. Address Underlying Causes
   • Diuretics for fluid overload (cardiac/renal).
   • Antibiotics if infection is suspected.
   • Therapeutic aspiration may temporarily relieve symptoms while awaiting definitive diagnosis.

1.7 Long-Term Management

• Treat the underlying disease: e.g. optimising heart failure, controlling liver disease, managing malignancy.
• Recurrent Effusions (especially malignant):
  • Repeated aspirations for symptomatic relief.
  • Pleurodesis (e.g. talc insufflation) or pleurectomy to obliterate the pleural space and prevent fluid reaccumulation.

1.8 Prognosis / Complications

• Prognosis depends heavily on the underlying cause.
• Malignant effusions have poor outcomes as they indicate advanced disease.
• Infective causes (e.g. empyema) need prompt drainage to avert complications like sepsis or persistent pleural thickening.
• Uncontrolled effusions can severely reduce quality of life due to dyspnoea.

2.1 Epidemiology

• Pneumothorax refers to air in the pleural space, causing partial or complete lung collapse.
• Incidence of primary spontaneous pneumothorax is higher in males (about 2–3 times more common) and typically peaks in the early 20s.

2.2 Aetiology

Pneumothoraces are generally classified into:

1. Primary Spontaneous Pneumothorax
   • Occurs without underlying lung disease.
   • Commonly in tall, thin, young men; risk increased by smoking or inhalation of recreational drugs.
   • Often due to subpleural blebs/bullae rupture.
   • Associations: Marfan’s syndrome, Ehlers–Danlos syndrome.
2. Secondary Spontaneous Pneumothorax
   • Occurs with pre-existing lung disease (e.g. COPD, cystic fibrosis, advanced fibrotic conditions).
   • Even a small pneumothorax can be severe or life-threatening in patients with limited respiratory reserve.
3. Tension Pneumothorax
   • Air enters the pleural space on inspiration but cannot escape on expiration.
   • Intrapleural pressure builds, compressing mediastinal structures.
   • Presents with hypotension, tracheal deviation away from the affected side, and severe respiratory distress.
   • Medical emergency (see below).
4. Traumatic Pneumothorax
   • Caused by penetrating or blunt chest trauma, including iatrogenic injuries (e.g. central line placement, pleural biopsy).

2.3 Risk Factors

• Smoking (major risk factor for subpleural blebs).
• Underlying lung disease (COPD, cystic fibrosis, interstitial lung disease).
• Connective tissue disorders (Marfan’s, Ehlers–Danlos).
• Mechanical ventilation (high airway pressures).
• Chest trauma (accidental or iatrogenic).

2.4 Clinical Features

• Sudden onset of pleuritic chest pain and/or breathlessness.
• Small pneumothoraces may be asymptomatic (especially in young, otherwise healthy individuals).
• Severe dyspnoea if the patient has poor respiratory reserve (as in COPD).
• Physical exam:
  • Reduced chest expansion on the affected side
  • Hyperresonance to percussion
  • Diminished or absent breath sounds
• Tension pneumothorax: Hypotension, distended neck veins, tracheal deviation away from the pneumothorax.

2.5 Diagnostic Approach

1. Clinical Suspicion
   • Differentiate from pulmonary embolism or acute severe asthma/COPD exacerbation.
2. Chest X-ray
   • Demonstrates a visible pleural line with no lung markings peripheral to it.
   • Tension pneumothorax: mediastinal shift away from the affected side.
3. Further Imaging
   • CT chest: Used if a small pneumothorax is suspected but not clearly visible, or to distinguish large bullae from pneumothorax.

2.6 Immediate Management

2.6.1 Tension Pneumothorax

• Do not investigate – treat with immediate decompression using a large-bore needle (2nd intercostal space, mid-clavicular line) before obtaining a chest X-ray.
• Follow with chest drain insertion.

2.6.2 Spontaneous Pneumothorax

• Primary spontaneous (in otherwise healthy individuals):
  • Small and asymptomatic: often observed; may resolve spontaneously.
  • Larger or symptomatic: aspirate pleural air.
    • If aspiration fails, insert chest drain.
• Secondary spontaneous (associated with lung disease):
  • More likely to require chest drain.
  • Even small pneumothoraces can cause severe compromise.

2.6.3 Traumatic Pneumothorax

• Chest drain typically indicated, especially if large (i.e. >2cm) or symptomatic.
• Manage associated injuries (rib fractures, vascular trauma).

2.7 Long-Term Management

• Chest drain care:
  • Monitor for continuous air leak (bubbling in the drain).
  • Failure of lung re-expansion or persistent air leak > 5–7 days may require surgical intervention (e.g. pleurectomy, bullae resection).
• Preventive measures for recurrent pneumothoraces:
  • Pleurodesis or pleurectomy in cases of repeated episodes (bilateral or same-side recurrence), or for individuals with high-risk occupations (pilots, divers).
  • Smoking cessation.

2.8 Prognosis / Complications

• Recurrence rate after a first primary spontaneous pneumothorax can be up to 50%, usually within 2 years.
• Recurrence is higher for secondary pneumothoraces.
• Smoking strongly increases recurrence risk.
• Tension pneumothorax is life-threatening without rapid decompression.

3. Benign Pleural Thickening

3.1 Epidemiology

• Benign pleural thickening is common and frequently asymptomatic.
• Often detected incidentally on clinical examination or imaging.

3.2 Aetiology

Benign pleural thickening typically arises from previous pleural injury or non-malignant inflammatory processes. Common causes include:

1. Post-Infection
   • Previous empyema (often basolateral thickening ± calcification).
   • Post-tuberculosis (‘apical capping’, can become calcified).
   • Chronic or persistent infection (e.g. non-tuberculous mycobacteria, aspergillosis).
2. Inflammatory/Other Causes
   • Asbestos exposure (plaques ± diffuse pleural thickening).
   • Post-pleurodesis (deliberate induction of pleural adhesions).
   • Post-haemothorax (often basolateral thickening ± calcification).
   • Certain drugs (e.g. methysergide, bromocriptine) can cause diffuse changes.
3. Benign after Trauma or Surgical Intervention
   • Scarring from chest trauma or interventional procedures.

3.3 Clinical Features

• Generally asymptomatic and discovered incidentally.
• On clinical examination:
  • Dullness to percussion
  • Quiet or diminished breath sounds over the thickened area
• On imaging (e.g. chest X-ray):
  • Areas of pleural opacity; can be localised or diffuse
  • Possible calcification (especially post-infective or after haemothorax)
• In extensive cases:
  • Restrictive lung defect on pulmonary function testing
  • Dyspnoea if large pleural areas are thickened

3.4 Diagnostic Approach

1. Clinical History
   • Previous infections (tuberculosis, empyema), trauma, asbestos exposure.
2. Imaging
   • Chest X-ray: May show plaques, calcification, or thickened pleura (basal or apical).
   • CT scan: Better characterises the extent of thickening, possible calcifications, and differentiates from malignancy.
   • Features suspicious for malignancy (e.g. mesothelioma) include nodular or circumferential thickening and mediastinal pleural involvement.
3. Exclusion of Pleural Malignancy
   • If there is progressive thickening, nodularity, or involvement of the mediastinal pleura, further investigations (biopsy) may be required.

3.5 Management

• Typically no active intervention is required if the patient is asymptomatic and imaging suggests stable benign thickening.
• Surgical pleurectomy (removal of pleura) is considered only in severe cases where extensive pleural thickening causes debilitating restrictive defects and dyspnoea.
  • This procedure carries significant morbidity and mortality.

3.6 Prognosis / Complications

• Usually stable and does not progress if the inciting cause is removed or resolved (e.g. treated infection, avoidance of asbestos).
• Differential diagnosis: Pleural malignancy (e.g. mesothelioma) can mimic benign thickening. Ongoing monitoring or investigation may be necessary if there is any suspicion of malignancy.