Aetiology
Empyema represents the most severe end of the spectrum of pleural inflammation in response to infection.[1] Initially, inflammation of the pleural space leads to a simple, free-flowing parapneumonic effusion. In most cases, this resolves with antibiotic treatment, but approximately 7% become infected, leading to the development of a complicated parapneumonic effusion (CPE).[17] If the CPE is undertreated, an empyema may form.
The majority of pleural infections follow bacterial pneumonia.[8] Pleural inflammation leads to the development of a parapneumonic effusion and invasion of the pleural space by bacteria. Therefore, risk factors for pneumonia, including aspiration (e.g., following a stroke, in the presence of a nasogastric or endotracheal tube), presence of an immunocompromised state (e.g., due to haematological disease, chemotherapy, HIV, or malnutrition), alcohol abuse, and intravenous drug use are also risk factors for empyema. Other causes of empyema include bronchogenic carcinoma, oesophageal rupture, blunt or penetrating chest trauma, mediastinitis with pleural extension, infected congenital cysts of the airway and oesophagus, extension from sources below the diaphragm, cervical and thoracic spine infections, and post-surgical aetiologies.[8] Less common causes include subphrenic abscesses, extensions of mediastinal or chest wall infections, and bacteraemia.
Although empyema usually develops following pneumonia, the microbiology of empyema differs from that of pneumonia. Empyema is frequently polymicrobial, and an organism is only identified in approximately 60% of pleural infections.[18] The organisms cultured in empyema following community-acquired pneumonia are significantly different from those which develop following hospital-acquired pneumonia or iatrogenic aetiologies. In community-acquired infection, gram-positive aerobic bacteria are most common, particularly the Streptococcus milleri group, Streptococcus pneumoniae, and staphylococci.[18] The latter is particularly prominent in the paediatric population, where 87% of infections are caused by aerobic gram-positive cocci.[19] Gram-negative bacteria are less commonly cultured in community-acquired infection, but anaerobes are often seen both in isolation and co-infection with aerobic organisms, although they are difficult to culture so may be involved in a greater percentage of cases.[8][18] In hospital-acquired infection, staphylococci (particularly MRSA) are the most commonly cultured pathogen, though there has also been an emergence of gram-negative bacteraemia.[18][20] Due to this, different antibiotics should be used in patients with community- and hospital-acquired infections, and broader-spectrum antibiotics are required for the empirical treatment of empyema than those used in the treatment of pneumonia.[8]
Pathophysiology
Empyema represents the end-stage of a progressive process evolving from a small amount of free-flowing, non-infected pleural fluid to a large amount of frank pus that can become loculated and result in thick pleural peel.
The formation of empyema is classically divided into 3 stages: exudative stage, fibrinopurulent stage, and organisational stage. During the exudative stage (Stage 1), sterile pleural fluid accumulates in the pleural space secondary to inflammation and increased permeability of the visceral pleura. The fibrinopurulent stage (Stage 2) commences with bacterial invasion of the pleural space and is characterised by the deposition of fibrin on visceral and parietal pleural membranes and the formation of fibrinous septae, loculations, and adhesions. The high metabolic activity leads to a fall in pleural fluid glucose concentration and pH, and neutrophil lysis leads to an increase in lactate dehydrogenase levels. If the infection progresses, the empyema becomes organised (Stage 3), with the formation of thick, non-elastic pleural peel and dense fibrinous septations that inhibit lung expansion as a result of fibroblast proliferation, causing a condition known as trapped lung.[21]
Classification
American College of Chest Physicians[1]
Parapneumonic effusions are subdivided into 4 categories.
Category 1: Simple parapneumonic effusion
Small free-flowing pleural effusion.
Category 2: Simple parapneumonic effusion
Small to moderate (i.e., less than half of the haemithorax) free-flowing effusion
Gram stain and culture of the pleural fluid negative, pleural fluid pH >7.2, and glucose >3.3 mmol/L (60 mg/dL).
Category 3: Complicated parapneumonic effusion (must have at least one of the following)
Size of effusion: more than half of the haemithorax, loculated or associated with a thickened parietal pleura
Gram stain or culture positive
Pleural fluid pH <7.2 or glucose <3.3 mmol/L (60 mg/dL).
Category 4: Empyema
Pus present in the pleural space.
Light's classification of pleural effusions[2]
Class 1: Non-significant
Thickness of the fluid on the decubitus chest x-ray <10 mm.
Class 2: Typical parapneumonic
Thickness of the fluid on the decubitus chest x-ray >10 mm, pleural fluid pH >7.2, and glucose >2.2 mmol/L (40 mg/dL).
Class 3: Borderline complicated
Pleural fluid pH 7.0 to 7.2 or LDH >1000 IU/L, Gram stain and culture negative.
Class 4: Simple complicated
Pleural fluid pH <7.0, Gram stain or culture positive, not loculated, no frank pus present.
Class 5: Complex complicated
Pleural fluid pH <7.0, Gram stain or culture positive, multiple loculated.
Class 6: Simple empyema
Presence of frank pus, single locule, or free-flowing effusion.
Class 7: Complex empyema
Presence of frank pus and multiple loculations.
Community- versus hospital-acquired empyema[3]
Community-acquired empyema
Empyema that develops following community-acquired pneumonia.
Hospital-acquired empyema
Empyema following hospital-acquired pneumonia, surgery, or iatrogenic intervention in the pleural space.
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