Diseases of the Pleura

Overview

Pleural disease = inflammatory effusions (pleuritis), non-inflammatory fluid collections, pneumothorax. Mostly SECONDARY to underlying pulmonary/systemic disease.

Pleuritis (classified by exudate)

1. Serous/fibrinous/serofibrinous — mostly infective (TB, pneumonia, pulmonary infarct, lung abscess, bronchiectasis); also RA/SLE, uraemia, pleural mets, tumour irradiation, systemic infection. Pleuritic pain+friction rub. Usually resorbs; repeated attacks→fibrous adhesions.

2. Suppurative (empyema thoracis) — infection converts serofibrinous→pus, mostly direct spread from lung; also subdiaphragmatic/liver abscess, penetrating injury. Yellow-green creamy pus→granulation/fibrous tissue→tough adhesions (±calcification)→restricts lung expansion.

3. Haemorrhagic — has inflammatory/tumour cells (unlike simple haemothorax). Causes: pleural mets, bleeding disorders, rickettsial disease.

Non-inflammatory effusions

1. Hydrothorax — non-inflammatory serous fluid. Commonest cause (often bilateral): CHF; also renal failure, cirrhosis, Meig’s syndrome, pulmonary oedema, lung tumours. TRANSUDATE: clear/straw, SG<1.012, protein<1g/dl, few cells. <300mL: asymptomatic (obliterated costophrenic angle only). Large: opaque hemithorax, contralateral tracheal shift, dyspnoea — relieved by drainage.

2. Haemothorax — pure blood. Causes: chest/visceral trauma, ruptured aortic aneurysm. Evacuate promptly — else clots/organises→fibrous adhesions.

3. Chylothorax — uncommon, milky lymphatic fluid (fat-rich). From thoracic duct rupture (trauma) or obstruction (mostly LYMPHOMA). More often LEFT-sided.

Pneumothorax

Air in pleural cavity, 3 settings:

Spontaneous — alveolar rupture in underlying disease (emphysema, asthma, TB commonest; also chronic bronchitis, bronchiectasis, infarction, bronchial cancer). Young patients: recurrent subpleural bleb rupture, no cause = spontaneous IDIOPATHIC pneumothorax
Traumatic — chest/lung trauma, ruptured oesophagus/stomach, thoracic surgery
Therapeutic (artificial) — historic TB treatment, deliberate lung collapse

Effects: small volume resorbs. Larger → dyspnoea, chest pain, lung collapse, CONTRALATERAL mediastinal shift. Flap-valve defect (air in on inspiration, can’t exit on expiration) = TENSION PNEUMOTHORAX — emergency, urgent decompression needed.

Clinical relevance

Transudate vs exudate distinction (hydrothorax’s low SG/protein/cells) = most practically important pleural fluid lab distinction — separates systemic pressure/oncotic causes (CHF, cirrhosis, renal failure) from local causes needing explanation (infection, malignancy, infarction). Empyema’s natural history (pus→adhesions→calcification) = why drainage is time-sensitive — delay converts treatable infection into fixed restrictive process. Tension pneumothorax’s flap-valve mechanism converts mechanical problem (collapse) into circulatory emergency — rising pressure compresses great veins, impairs venous return not just ventilation — demands emergency decompression. Chylothorax’s left-sided predominance+lymphoma link follow from thoracic duct anatomy (ascends left side of mediastinum, courses through nodal territory).

Overview

Pleural disease spans inflammatory effusions (pleuritis), non-inflammatory fluid collections, and pneumothorax — most are secondary to underlying pulmonary or systemic disease rather than primary pleural conditions.

Pleuritis (Inflammatory Effusions)

Inflammation of the pleura, classified by exudate character.

1. Serous/fibrinous/serofibrinous pleuritis — from acute pleural inflammation; mostly infective, especially intrapulmonary (TB, pneumonia, pulmonary infarct, lung abscess, bronchiectasis); also collagen disease (RA, SLE), uraemia, pleural metastasis, tumour irradiation, systemic infection (typhoid, tularaemia, blastomycosis, coccidioidomycosis). Produces pleuritic chest pain and an audible friction rub. Usually minimal exudate that resorbs; repeated attacks can organise into fibrous adhesions obliterating the pleural cavity.

2. Suppurative pleuritis (empyema thoracis) — bacterial/fungal infection converting a serofibrinous effusion into frank pus, most often by direct spread from the lung; also subdiaphragmatic/liver abscess extension or penetrating chest injury, occasionally haematogenous/lymphatic. Yellow-green creamy pus, large volume; eventually replaced by granulation and fibrous tissue, producing tough fibrocollagenic adhesions (later calcification), causing serious restriction of pulmonary expansion.

3. Haemorrhagic pleuritis — distinguished from simple haemothorax by containing inflammatory or exfoliated tumour cells in the exudate. Causes: pleural metastasis, bleeding disorders, rickettsial disease.

Non-Inflammatory Pleural Effusions

1. Hydrothorax — non-inflammatory serous fluid accumulation, uni- or bilateral. Commonest cause (often bilateral): congestive heart failure; also renal failure, liver cirrhosis, Meig’s syndrome, pulmonary oedema, primary/secondary lung tumours. A genuine transudate: clear, straw-coloured, specific gravity <1.012, protein <1 g/dl, minimal cellularity. Under 300 mL (normal <15 mL): asymptomatic, seen only as an obliterated costophrenic angle on erect CXR. Larger collections: opaque hemithorax, contralateral tracheal deviation, dyspnoea — promptly relieved by drainage.

2. Haemothorax — pure blood in the pleural cavity; commonest causes: chest/thoracic visceral trauma, ruptured aortic aneurysm. Prompt evacuation is important — retained blood clots and organises into fibrous adhesions obliterating the cavity.

3. Chylothorax — uncommon, milky lymphatic fluid (high emulsified fat content) in the pleural cavity, most often from thoracic duct rupture (trauma) or obstruction (most often malignant lymphoma). More often left-sided.

Pneumothorax

Air in the pleural cavity, in three settings:

Spontaneous — from spontaneous alveolar rupture in underlying lung disease, most commonly emphysema, asthma, TB; also chronic bronchitis (elderly), bronchiectasis, pulmonary infarction, bronchial cancer. In young patients, recurrent rupture of peripheral subpleural blebs without identifiable cause produces spontaneous idiopathic pneumothorax.
Traumatic — chest wall/lung trauma, ruptured oesophagus/stomach, thoracic surgery.
Therapeutic (artificial) — historically used in chronic pulmonary TB treatment, deliberately collapsing the lung to limit respiratory movement.

Effects: small air volumes resorb spontaneously; larger volumes cause dyspnoea, chest pain, lung collapse, and contralateral mediastinal shift. A flap-valve defect that admits air on inspiration but prevents its escape on expiration produces tension pneumothorax — a genuine emergency requiring urgent pressure relief to prevent severe dyspnoea and circulatory collapse.

Clinical Relevance

Hydrothorax’s transudate characteristics (low specific gravity, low protein, minimal cells) versus an exudative effusion is the single most practically important laboratory distinction in pleural fluid analysis, since it immediately separates “systemic pressure/oncotic” causes (heart failure, cirrhosis, renal failure) from causes requiring a local pleural or pulmonary explanation (infection, malignancy, infarction).
Empyema’s natural history — pus organising into tough fibrocollagenic adhesions that eventually calcify — is why drainage is time-sensitive; delay allows the exudate to progress past the point where simple thoracentesis can resolve it, converting a treatable infection into a fixed restrictive process.
Tension pneumothorax’s flap-valve mechanism (air enters on inspiration, cannot exit on expiration) is what converts a mechanical problem (lung collapse) into a circulatory emergency — progressively rising intrapleural pressure eventually compresses the great veins and impairs venous return, not just ventilation, which is why it demands emergency decompression rather than routine management.
Chylothorax’s left-sided predominance and lymphoma association follow directly from thoracic duct anatomy — the duct ascends on the left side of the mediastinum before draining into the venous system, so its rupture or obstruction naturally produces a left-sided effusion, and its course through mediastinal nodal territory explains the lymphoma link.