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Pleural effusion


Essentials

  • 1

    In the majority of patients, a posteroanterior and lateral chest x-ray will confirm and localize an effusion. Ultrasound, lateral decubitus films and computed tomography scanning are more sensitive in diagnosing and localizing small effusions.

  • 2

    Pleural fluid analysis is the principal method of determining the underlying cause of an effusion.

  • 3

    Ultrasound-guided thoracocentesis is the recommended method for diagnostic or therapeutic fluid drainage.

  • 4

    Treatment is dependent on the underlying disease. Large pleural effusions with cardiorespiratory compromise should be aspirated to provide symptomatic relief.

  • 5

    Transudates generally respond to treatment of the underlying condition. Exudates usually require further investigative procedures and specific treatments.

Introduction

A pleural effusion is an accumulation of fluid in the pleural space caused by a disruption of the homoeostatic forces that control normal flow. Massive pleural effusions may produce significant cardiorespiratory compromise requiring urgent attention in the emergency department. However, many are asymptomatic or produce minimal disturbance. In this latter group, the role of emergency department care is assessment to ascertain the aetiology of the effusion, as this dictates the most appropriate treatment. Information regarding the likely cause can be obtained by a thorough history and physical examination. Important adjuvant investigations include chest x-ray (CXR), ultrasound, examination of pleural fluid and biopsies obtained during thoracocentesis. Bronchoscopy and thoracoscopy have a role to play in the small group of patients in whom the mentioned procedures fail to establish a cause; however, their use is beyond the scope of initial emergency department assessment and stabilization.

Aetiology, pathogenesis and pathology

Pathology and pathogenesis

The pleural cavity is normally a small space bordered by the visceral and parietal pleura, both of which are composed of mesothelial lining cells. In normal conditions it contains approximately 0.25 mL/kg of low-protein liquid. The pleura act as semipermeable membranes and fluid movement is determined principally by capillary pressure, plasma oncotic pressure and capillary permeability, governed by the Starling law. The parietal pleura appear to be the more important surface for pleural liquid turnover in the normal physiological state. Current evidence suggests that most pleural fluid drainage occurs via pleuro-lymphatic communications or stomas, augmented by respiratory muscle action and intrinsic lymphatic vessel contractility. Overall absorptive capacity can exceed production by a factor of 10 to 20, allowing maintenance of pleural fluid volume in most cases. Pleural effusions occur due to one of the following:

  • Disturbances in the hydrostatic-osmotic pressure gradients, resulting in a transudate

  • Pleural inflammation with loss of semipermeable membrane function, resulting in a protein-rich exudate

  • Lymphatic obstruction (usually producing a transudate)

Transudates are ultrafiltrates of plasma and arise as a result of relatively few conditions. Exudates are produced by a wider variety of inflammatory conditions and often require more extensive investigation.

Aetiology

Box 6.7.1 lists the causes of transudative and exudative pleural effusions. The commonest causes are congestive cardiac failure, pneumonia, malignancy and pulmonary embolus.

Box 6.7.1
Causes of transudative and exudative pleural effusions

Effusions always transudative

  • Congestive cardiac failure

  • Cirrhosis

  • Nephrotic syndrome

  • Peritoneal dialysis

  • Hypoalbuminaemia

  • Urinothorax

  • Atelectasis

  • Constrictive pericarditis

  • Superior vena caval obstruction

  • Cerebrospinal fluid leaks (trauma, surgery, Ventriculoperitoneal (VP) shunts)

  • Glycinothorax

‘Classic’ exudates that can be transudates

  • Malignancy

  • Pulmonary embolism

  • Sarcoidosis

  • Hypothyroidism

Exudates

  • Infectious

    • Bacterial pneumonia

    • Tuberculosis

    • Parasites

    • Fungal disease

    • Atypical pneumonia

    • Nocardia, actinomyces

    • Subphrenic abscess

    • Hepatic abscess

    • Splenic abscess

    • Hepatitis

    • Spontaneous oesophageal rupture

Iatrogenic

  • Drug-induced (amiodarone, phenytoin, nitrofurantoin, β-blockers, dantrolene sodium, methysergide maleate, procarbazine HCl, methotrexate, medications causing drug-induced lupus syndrome: procainamide HCl, hydralazine HCl, quinidine)

  • Oesophageal perforation

  • Oesophageal sclerotherapy

  • Central venous catheter migration

  • Enteral feeding

  • Post–coronary artery bypass graft

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