Introduction

Pleural empyema is a purulent pleural effusion, typically occurring after pneumonia, thoracic surgery, penetrating thoracic injury or mediastinal oesophageal perforation. Less frequently, pleural empyema can occur from respiratory or gastric aspiration (more common in the elderly) or by haematogenous spread from another focus of infection (eg. liver abscess).  Overall mortality is around 20%. However, there is a marked variation in the aggressiveness of empyema and advanced multilocular empyema inadequately treated initially can have a mortality of up to 50%.

Aetiology of pleural empyema

The aetiology reflects the initiating event and therefore a wide range of organisms can be involved, including Gram-positive and Gram-negative aerobes and anaerobes. Pleural empyemas are often polymicrobial.

Diagnosis of pleural empyema

Aspiration of fluid for:

• Cytology
• Gram stain may show organisms.  Anaerobes may not be evident on Gram stain
• Microscopy. Neutrophils are seen in bacterial effusions. Lymphocytes are seen if TB involved. TB can be demonstrated by the use of acid-fast stain
• Culture.

Can be difficult to differentiate pleural empyema from pleural effusion in the absence of a positive Gram stain or bacterial culture. If neither Gram stain nor culture are positive, the following parameters are highly indicative of empyema:

• Grossly purulent pleural fluid
pH £7.2
• WBC >50,000 cells/mm³ (or polymorphonuclear leukocyte count of 1,000 IU/dL)
• Pleural glucose <60 mg/dL
• Lactate dehydrogenase >1,000 IU/mL.

Management of empyema

Antibiotics alone cannot resolve the infection: drainage or other surgical intervention is required for cure.

Specimens of aspirated pus, when available, (ideally at an early stage) should be submitted for culture and sensitivity.

Treatment objectives are:

• To sterilise the pleural space
• To obliterate the cavity with lung expansion, surgical decortication or enzymatic debridement.

Antibiotic rationale

The aetiology of the empyema, together with the patient’s previous treatment history and condition, will influence the choice of antibiotic therapy.

In the early stages, combinations of antibiotics may be necessary to provide effective activity against the wide range of potential pathogens including aerobic Gram-positive cocci, Gram-negative bacilli and anaerobes.

Diffusion of antibiotics into both infected and uninfected pleural fluid is generally good, but there may be limited penetration if a thickened pleural membrane has been established. Fluoroquinolones and macrolides achieve tissue concentrations many times higher than their plasma concentrations. While the reverse is true for most beta-lactams, cefuroxime achieves concentrations in bronchial mucosa equivalent to those achieved in plasma.

Antibiotics can be diluted in pleural fluid and so should be given in high-doses.

Pathological factors will also influence the choice of antibiotic.

Certain antibiotics may be inactive in the conditions of gross puss or inside an abscess;

• Aminoglycosides can be inactivated by low pH
• Some samples of pus have been seen to inactivate penicillin and ampicillin in the absence of detectable, extracellular beta-lactamases.

In addition, many of the potential pathogens have beta-lactamase producing strains.

The chosen antibiotics should be administered intravenously in high-doses and may need to be continued for an extended period.

Empirical therapy

Regimens which provide the broad-spectrum required, together with beta-lactamase stability, and would be suitable for empirical therapy include:

• A combination of a second-generation cephalosporin such as cefuroxime plus metronidazole

or alternatively

• co-amoxiclav monotherapy
• In penicillin-allergic patients: clindamycin
• Culture and sensitivity results from any aspirated pus samples can be used to guide future therapy
• CRP should be monitored to follow the resolution of inflammation.

It is important to check that re-accumulation of empyema has not occurred.