Pleural empyema

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

An empyema is a collection of pus within a pre-existing body cavity. It must be differentiated from an abscess, which is a collection of necrotic and suppurated tissue located in the parenchyma of an organ.^[1] Empyema is most commonly used to refer to pus collection in the pleural cavity although several other organs can be affected example brain, gallbladder, joint and urinary bladder. Thoracic empyema arises from an infection within the lung, often associated with parapneumonic effusions. Parapneumonic effusions may be uncomplicated or complicated effusions. Complicated parapneumonic effusion results when bacteria invade the pleural space with a resultant formation of an empyema.

Pleural infection was first described by Hippocrates as far back as 460-370 B.C.^[2] During this time open chest drainage was the sole treatment modality and was associated with high mortality. In 1873, Playfair gave the first description of a water-seal chest drainage system in the treatment of a child with thoracic empyema.^[3] In 1875, Gotthard Bülau a German Internist described the use of closed water-seal chest drainage to treat an empyema, as an alternative to the standard rib resection and open tube drainage. He punctured the pleural membrane with trocar and introduced a rubber catheter into the pleural cavity. The free end of the catheter inserted in a bottle one-third full of solution allowing pus to flow freely from the chest into the bottle.^[4][5] Closed chest tube drainage was experimentally practiced during the influenza epidemic in 1917–19 when open surgical drainage was associated with a high mortality rate. This coincided with world war I and the resultant crisis of streptococcal pneumonia and empyema.^[6] Closed chest tube drainage became the standard of treatment from late 1950.^[7]

Pleural empyema may be classified according to the etiology and pathological course of the disease.^[8] Primary thoracic empyema occurs most commonly as iatrogenic empyema without associated pneumonia whereas secondary empyema happens more commonly secondary to pneumonia. Empyema necessitans is a spontaneous discharge of an empyema that has burrowed through the parietal pleura into the chest wall to form a subcutaneous abscess that may eventually rupture through the skin.^[9][10] Tuberculous empyema is the most common cause of empyema necessitans with majority of affected patients being immunocompromised.^[11][12] There are 3 stages of empyema which are important in terms of the laboratory findings. These are exudative, fibrinopurulent and organizing.^[13]

The process leading to the formation of empyema involves migration of organisms into the pleural cavity. Lung parenchymal infection stimulates local pleural immune activation, neutrophil migration and release of inflammatory cellular components and toxic oxygen species, such as IL-6, IL-8 and tumour necrosis factor (TNF)-α.^[14][15][16] These mediators promotes endothelial injury resulting in increased pleural membrane permeability and increased osmotic pressure.^[13] With persistent inflammation, increased permeability of vascular and mesothelial membranes results in increased plasma leakage into the pleural cavity. Coagulation cascade when activated within the pleural cavity contributes to the development of a “fibrinopurulent” or “complicated” parapneumonic effusion. Fibrin is deposited over the pleural surfaces with fibrinous septae producing loculated effusions.^[17][18]

Streptococcus pneumoniae was the most common bacteria found in empyemas before the development of antibiotics. More recently, however, anaerobes have become the predominant organism in culture positive empyemas (and therefore careful anaerobic cultures should always be sent when working up parapneumonic effusions). Mixed aerobic and anaerobic infections are also common. In general any bacteria can cause an empyema, however different bacteria are associated with different rates of empyema formation.^[19] Some of the common bacteria causes include; bacteroides, fusobacterium, haemophilus influenzae, pneumococcal infections, staphylococcus aureus, streptococcus, and TB.

Empyema must be diffrentiated from pneumonia, lung abscess, lung cancer and parapneumonic effusions on the basis of the presentation, physical examination findings, chest xray, ultrasound and CT scan findings. For instance on ultrasound, empyema is positive for suspended microbubble sign, air fluid level, curtains sign and loss of gliding sign but these are negative in a lung abscess.

Again empyema is differentiated from a lung abscess in that empyema on CT scan is seen as a lung mass whose cavity is regular with smooth well-defined boundary and shape changes with change in patient’s position.^[20] Mass may resolve on antibiotics. The split pleura sign is present^[21] (most reliable sign to differentiate empyema from lung abscess).^[22]

The incidence and prevalence of empyema has been increasing over the past 15 years. More than 40% of patients have preexisting comorbidities.^[23] There have been a 26% increase in age and sex-standardized incidence rate from 8.7 per 100,000 person-years in 1997 to 11.8 per 100,000 person in 2011.^[23] This increment is most notably among older people aged ≥ 80 years (87.3% [from 20.4 per 100,000 in 1997 to 38.2 per 100,000 in 2011]) compared with people aged 40 to 64 years (27.8% [from 10.7 per 100,000 in 1997 to 12.6 per 100,000 in 2011]).^[23] Men are more commonly affected with empyema than women. The male to female ratio is approximately 1.7- to 3.1-fold higher in men than in women.^[23] The rate of patients with empyema requiring hospitalization appear to be increasing in western populations, however updated population-based data are scanty. The few available data on adult empyema have reported increase between 30% and 97% over the past 15 years in the United States and Canada.^[23][24] There is however a decreasing trend in the median days of hospital stay from 22 days 17 days.^[23]

Common risk factors in the development of empyema include:^[25] Bacterial pneumonia, thoracic surgery^[26] NSAIDs use during acute viral infection is associated with an increased risk of empyema in children,^[27] Lung abscess, chest trauma,^[28] and post-thoracostomy drainage.^[29]

There is no established screening modality for empyema however, lateral chest x-ray is the initial imaging of choice in patients with pneumonia. It is superior in detecting parapneumonic effusions compared to anteroposterior chest x ray.^[30]

If left untreated 40% of complicated pneumonia results in effusion with 60% resulting in the formation of empyema.^[31] Empyema may result in the following complications; empyema necessitans,^[10] imparired perfusion and ventilation of lungs as a result of pleural thickening and reduced lung function, necrotizing fasciitis of the chest wall,^[12] bronchopulmonary fistula or alveolar-pleural fistula,^[12][32] The prognosis of empyema after treatment is good however, the risk of permanent lung damage and mortality increase when empyema complicates pneumonia.^[23][33] Advanced age and comorbidity are strong prognostic factors. Thirty-day mortality rate ranges from 1.2% in patients aged 15 to 39 years to 20.2% in those aged ≥ 80 years. Mortality also varies substantially according to level of comorbidity.^[23]

Symptoms of empyema may vary in severity. Most patients with empyema may prersent with fever and chills, cough, shortness of breath, pleuritic chest pain, anaerobic infections however, can be more indolent, with up to 70% of patients having symptoms for more than 1 week.^[34][1] Additionally, these patients tend to have more constitutional symptoms including; excessive night sweating, weight loss

On examination, the following findings may be seen:^[34][9][35] lateral chest wall swelling and tenderness, clubbing of the fingernails, dull percussion note, reduced breath sounds on the affected side of the chest, egophony, coarse crackles, increased fremitus, mediastinal shift to opposite side with large empyema

Diagnosis is confirmed by thoracentesis. Aspiration of the purulent fluid is necessary especially when condition is not resolving on antibiotics. The pleural fluid typically has a low pH (<7.20), low glucose (<60 mg/dL), and contains infectious organisms. Although the presence of pus or organisms on gram stain is extremely helpful in making a diagnosis of empyema, a positive bacteria culture from pleural fluid is not needed before diagnosis of empyema is comfirmed.^[36][31]

Chest radiography is the initial imaging modality in evaluation of pleural disease.^[37] Lateral view is superior in detecting parapneumonic effusions and empyema compared to anteroposterior chest x ray.^[30] Chest X ray of empyema shows air-fluid level with continuous homogenous pattern from the mediastinum to the chest wall forming and obtuse angle with the lung parenchyma. Thoracic ultrasound have greater sensitivity in detecting pleural effusions than clinical examination or chest radiographs (AP or lateral).^[38] Thoraxic ultrasound is the next prefered imaging test after chest xray.^[39][38] Ultrasound in empyema is positive for suspended microbubble sign, air fluid level, curtains sign and loss of gliding sign.^[40] Thoracic MRI may show an internally septated, thick wall, and heterogeneous mass especially in empyema necessitans^[9] On Computed tomographic scan, empyema is seen as a lung mass whose cavity is regular with smooth and regular lumen and well-defined boundary. The shape changes with change in patient’s position.^[20] Mass on CT scan may resolve on antibiotics. The split pleura sign on CT scan is present (most reliable sign to differentiate empyema from lung abscess where it is absent).^[21][22]

Leucocytosis as well as increased levels of pleural adenosine deaminase and pleural lactate dehydrogenase (usually above 1000) may provide additional diagnostic feature for empyema.^[41]

The mainstay of therapy for empyema includes:^[42] controlling the infectious focus, drainage of fluid and pus, re-expansion of the lung. This involves the use of antimicrobial agents, thrombolytics,^[43][44] and drainage of the pleural space.^[45][8][46] Pharmacologic therapies for acute empyema include either Ceftriaxone, Nafcillin or Oxacillin, Vancomycin or Linezolid, or TMP-SMX. The preferred regimen for subacute and chronic empyema is a combination of Clindamycin and Ceftriaxone.

Definitive surgical treatment for empyema entails drainage of the infected pleural fluid. A chest tube may be inserted, often using ultrasound guidance. Intravenous antibiotics are given. If this is insufficient, surgical debridement of the pleural space may be required.^[42][46][45] Management strategies of empyema necessitans with pulmonary involvement and lung abscess may involve thoracotomy with pulmonary resection in addition to extended duration antimicrobial therapy.^[34][9]

Early and efficient treatment of pleural effection have been found to prevent the development of empyema.^[23][33]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Pleural infection was first described by Hippocrates as far back as 460-370 B.C.^[1] During this time open chest drainage was the sole treatment modality and was associated with high mortality. In 1873, Playfair gave the first description of a water-seal chest drainage system in the treatment of a child with thoracic empyema.^[2] In 1875, Gotthard Bülau a German Internist described the use of closed water-seal chest drainage to treat an empyema, as an alternative to the standard rib resection and open tube drainage. He punctured the pleura membrane with trocar and introduced a rubber catheter into the pleural cavity. The free end of the catheter inserted in a bottle one-third full of solution allowing pus to flow freely from the chest into the bottle.^[3][4] Closed chest tube drainage was experimentally practised during the influenza epidemic in 1917–19 when open surgical drainage was associated with a high mortality rate. This coincided with world war I and the resultant crisis of streptococcal pneumonia and empyema.^[5] Closed chest tube drainage became the standard of treatment from late 1950.^[6]

• Pleural infection was first described by Hippocrates as far back as 460-370 B.C.^[7] During this time open chest drainage was the sole treatment modality and was associated with high mortality.
• In 1300s, Guy de Chauliac also called Guido or Guigo de Cauliaco, a surgeon of medieval France, commented with surprise on the lack of ancient writings concerning thoracic wounds and the disagreements on the treatment of these wounds. Lanfranc of Paris, William of Bologna, and Roland of Parma advocated that open treatment of penetrating thoracic wounds using tents and drains allow blood and decaying organic materials to escape however, Henri de Mondeville was of different opinion that immediate closure of wounds helps to prevent heat loss and air entry.^[8]
• During the early 1500s, Giovanni da Vigo, an Italian surgeon and physician of Pope Julius II, was one of the first surgeons to discuss firearm wounds to the chest.^[8]
• IN 1873, Playfair gave the first description of a water-seal chest drainage system in the treatment of a child with thoracic empyema.^[2]
• In 1875, Gotthard Bülau a German Internist described the use of closed water-seal chest drainage to treat an empyema, as an alternative to the standard rib resection and open tube drainage. He punctured the pleura membrane with trocar and introduced a rubber catheter into the pleural cavity. The free end of the catheter inserted in a bottle one-third full of solution allowing pus to flow freely from the chest into the bottle.^[3][4]
• Closed chest tube drainage was experimentally practised during the influenza epidemic in 1917–19 when open surgical drainage was associated with a high mortality rate. This coincided with world war I and the resultant crisis of streptococcal pneumonia and empyema.^[5]
• In 1950, Vincenzo Monaldi an Italian pulmonologist suggested draining the thoracic cavity with a more superior approach at the second or third intercostal space.^[9]
• The modern three chamber thoracic drainage system was first described by Howe in 1952 but not widely employed at the time.^[10]
• Closed chest tube drainage became the standard of treatment from late 1950.^[6]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Empyema may be classified according to the etiology, anatomical location, and pathological course of the disease.^[1] Primary thoracic empyema occurs most commonly as iatrogenic empyema without associated pneumonia whereas secondary empyema happens more commonly secondary to pneumonia. Empyema necessitans is a spontaneous discharge of an empyema that has burrowed through the parietal pleura into the chest wall to form a subcutaneous abscess that may eventually rupture through the skin.^[2][3] Empyema is mostly caused by bacteria. It may be tuberculous or nontuberculous. Tuberculous empyema is the most common cause of empyema necessitans with majority of affected patients being immunocompromised.^[4][5] There are 3 stages of empyema which are important in terms of the laboratory findings. These are exudative, fibrinopurulent and organizing.^[6]

Empyema may be classified according to the etiology, anatomical location/organ, and pathological course of the disease as follows:^[1]

Primary empyema occurs most commonly as iatrogenic empyema without associated pneumonia whereas secondary empyema happens more commonly secondary to pneumonia.

Empyema necessitans is a spontaneous discharge of an empyema that has burrowed through the parietal pleura into the chest wall to form a subcutaneous abscess that may eventually rupture through the skin.^[2][3]

Tuberculous empyema is the most common cause of empyema necessitans. This disease can be found in patients with impaired immunity or who are immunocompetent however majority of patients affected are immunocompromised.^[4][5]

Empyema may be classified according to the stage of the disease as follows:^[7]

• Exudative

In the exudative stage, the pus accumulates, and initial sterile fluid becomes infected with fluid characteristics of;

• • Glucose>60
  • pH>7.2
  • LDH<500

• Fibrinopurulent

During this stage, bacteria multiplies with increase in polymorphs and fibrin deposition on both pleural surfaces with fluid characteristics of;

• • glucose<40
  • pH <7.2
  • LDH>1000

• Organizing

This stage is characterized by loculations, inelastic membranous peel, and lung entrapment as a result of scarring of the pleural space.^[6]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

The process leading to the formation of empyema involves migration of organisms into the pleural cavity. Lung parenchymal infection stimulates local pleural immune activation, neutrophil migration and release of inflammatory cellular components and toxic oxygen species, such as IL-6, IL-8 and tumour necrosis factor (TNF)-α.^[1][2][3] These mediators promotes endothelial injury resulting in increased pleural membrane permeability and increased osmotic pressure.^[4] With persistent inflammation, increased permeability of vascular and mesothelial membranes results in increased plasma leakage into the pleural cavity. Coagulation cascade when activated within the pleural cavity contributes to the development of a “fibrinopurulent” or “complicated” parapneumonic effusion. Fibrin is deposited over the pleural surfaces with fibrinous septae producing loculated effusions.^[5][6]

The process leading to the formation of empyema involves migration of organisms into the pleural cavity. This may be via direct extension/contiguous route. Lung parenchymal infection stimulates local pleural immune activation, neutrophil migration and release of inflammatory cellular components and toxic oxygen species, such as IL-6, IL-8 and tumour necrosis factor (TNF)-α.^[1][2][3] These mediators promotes endothelial injury resulting in increased pleural membrane permeability and increased osmotic pressure.^[4] The resultant empyema may spontaneously burrowed through the parietal pleura into the chest wall to form a subcutaneous abscess that may eventually rupture through the skin leading to formation of empyema necessitans.^[7] Mesothelial cells release TNF-α and concurrently antifibrinolytic mediator function is enhance, example plasminogen activator inhibitor-1 and -2^[8].

Mycobacteria bacille Calmette–Guerin infection of pleural cells lead to enhanced VEGF release.^[5] Mycobacteria bacille Calmette–Guerin (BCG) and S. aureus infections increase permeability across the mesothelial membrane, partly via downregulation of β-catenin. ^[5][6]

S. aureus infection of the pleura have been found to result in pleural mesothelial cells expression of early response genes c-fos and c-jun, followed by the expression of pro-apoptotic genes Bak and Bad during later stage of infection.^[9] This results in apoptosis of mesothelial tissue and impaired membrane integrity, which may contribute to loss of the normal fibrinolytic function of the pleura.

With persistent inflammation, increased permeability of vascular and mesothelial membranes results in increased plasma leakage into the pleural cavity. Coagulation cascade when activated within the pleural cavity contributes to the development of a “fibrinopurulent” or “complicated” parapneumonic effusion. Fibrin is deposited over the pleural surfaces with fibrinous septae producing loculated effusions.^[5][6]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ogheneochuko Ajari, MB.BS, MS [2] Prince Tano Djan, BSc, MBChB [3]

Streptococcus pneumoniae was the most common bacteria found in empyema before the development of antibiotics. More recently, however, anaerobes have become the predominant organism in culture positive empyema (and therefore careful anaerobic cultures should always be sent when working up parapneumonic effusions). Mixed aerobic and anaerobic infections are also common. In general any bacteria can cause an empyema, however different bacteria are associated with different rates of empyema formation.^[1] Some of the common bacteria causes include; bacteroides, fusobacterium, haemophilus influenzae, pneumococcal infections, staphylococcus aureus, streptococcus, and TB.

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. There are no life-threatening causes of empyema, however complications resulting from untreated empyema is common.

The following are common causes of empyema:^[1]

• Bacteroides
• Fusobacterium
• Haemophilus influenzae
• Pneumococcal infections
• Staphylococcus aureus
• Streptococcus
• Streptococcus pyogenes
• TB^[2]

Less common causes of empyema include:

• Actinomyces^[3]
• Proteus^[4]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Empyema must be diffrentiated from pneumonia, lung abscess, lung cancer and parapneumonic effusions on the basis of the presentation, physical examination findings, chest xray, ultrasound and CT scan findings. For instance on ultrasound, empyema is positive for suspended microbubble sign, air fluid level, curtains sign and loss of gliding sign but these are negative in a lung abscess.

Again empyema is differentiated from a lung abscess in that empyema on CT scan is seen as a lung mass whose cavity is regular with smooth well-defined boundary and shape changes with change in patient’s position.^[1] Mass may resolve on antibiotics. The split pleura sign is present^[2] (most reliable sign to differentiate empyema from lung abscess).^[3]

Empyema must be diffrentiated from pneumonia, lung abscess, lung cancer and parapneumonic effusions as shown below:

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

The incidence and prevalence of empyema has been increasing over the past 15 years. More than 40% of patients have preexisting comorbidities.^[1] There have been a 26% increase in age and sex-standardized incidence rate from 8.7 per 100,000 person-years in 1997 to 11.8 per 100,000 person in 2011.^[1] This increment is most notably among older people aged ≥ 80 years (87.3% [from 20.4 per 100,000 in 1997 to 38.2 per 100,000 in 2011]) compared with people aged 40 to 64 years (27.8% [from 10.7 per 100,000 in 1997 to 12.6 per 100,000 in 2011]).^[1] Men are more commonly affected with empyema than women. The male to female ratio is approximately 1.7- to 3.1-fold higher in men than in women.^[1] The rate of patients with empyema requiring hospitalization appear to be increasing in western populations, however updated population-based data are scanty. The few available data on adult empyema have reported increase between 30% and 97% over the past 15 years in the United States and Canada.^[1][2] There is however a decreasing trend in the median days of hospital stay from 22 days 17 days.^[1]

The incidence and prevalence of empyema has been increasing over the past 15 years. More than 40% of patients have preexisting comorbidities.^[1]

There have been a 26% increase in age and sex-standardized incidence rate from 8.7 per 100,000 person-years in 1997 to 11.8 per 100,000 person-years in 2011.^[1] This increment is most notably among older people aged ≥ 80 years (87.3% [from 20.4 per 100,000 in 1997 to 38.2 per 100,000 in 2011]) compared with people aged 40 to 64 years (27.8% [from 10.7 per 100,000 in 1997 to 12.6 per 100,000 in 2011])^[1]

Empyema is increases with increasing age. Elderly patients >64 years are most commonly affected.^[1]

Men are more commonly affected with empyema than women. The male to female ratio is approximately 1.7- to 3.1-fold higher in men than in women.^[1]

The rate of patients with empyema requiring hospitalization appears to be increasing in western populations, however updated population-based data are scanty. The few available data on adult empyema have reported increases between 30% and 97% over the past 15 years in the United States and Canada.^[1][2]

There is however a decreasing trend in the median days of hospital stay from 22 days 17 days.^[1]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

There is no established screening modality for empyema however, lateral chest x-ray is the initial imaging of choice in patients with pneumonia. It is superior in detecting parapneumonic effusions compared to anteroposterior chest x ray.^[1]

There is no established screening modality for empyema however, lateral chest x-ray is the initial imaging of choice in patients with pneumonia. It is superior in detecting parapneumonic effusions compared to anteroposterior chest x ray.^[1]

Template:WS Template:WH

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Common risk factors in the development of empyema include:^[1] Bacterial pneumonia, thoracic surgery^[2] NSAIDs use during acute viral infection is associated with an increased risk of empyema in children,^[3] Lung abscess, chest trauma,^[4] and post-thoracostomy drainage.^[5]

Common risk factors in the development of empyema include:^[1]

• Bacterial pneumonia
• Lung abscess
• Thoracic surgery^[2]
• NSAIDs use during acute viral infection is associated with an increased risk of empyema in children^[3][6]
• Chest trauma^[4]
• Following tube thoracostomy drainage^[5]
• Poor dental hygiene individuals^[7]
• Alcoholics^[7]
• Unconciousness leading to aspiration of gastric contents^[7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

If left untreated 40% of complicated pneumonia results in effusion with 60% resulting in the formation of empyema.^[1] Empyema may result in the following complications; empyema necessitans,^[2] imparired perfusion and ventilation of lungs as a result of pleural thickening and reduced lung function, necrotizing fasciitis of the chest wall,^[3] bronchopulmonary fistula or alveolar-pleural fistula,^[3][4] The prognosis of empyema after treatment is good however, the risk of permanent lung damage and mortality increase when empyema complicates pneumonia.^[5][6] Advanced age and comorbidity are strong prognostic factors. Thirty-day mortality rate ranges from 1.2% in patients aged 15 to 39 years to 20.2% in those aged ≥ 80 years. Mortality also varies substantially according to level of comorbidity.^[5]

If left untreated 40% of complicated pneumonia results in effusion with 60% resulting in the formation of empyema.^[1]

Cpmlications of empyema include:

• Empyema necessitans^[2]
• Imparired perfusion and ventilation of lungs as a result of pleural thickening and reduced lung function.
• Necrotizing fasciitis of the chest wall^[3]
• Bronchopulmonary fistula or alveolar-pleural fistula^[3][4]

Majority of people fully recover from empyema after treatment. However the risk of permanent lung damage and mortality increase when empyema complicates pneumonia.^[5][6] “If an empyema does not rupture, death will occur” – Hippocrates. Advanced age and comorbidity are strong prognostic factors, and empyema remains a serious condition requiring a long hospital stay. Thirty-day mortality rate ranges from 1.2% in patients aged 15 to 39 years to 20.2% in those aged ≥ 80 years with age-adjusted adjusted 30-day mortality rate of 0.69. Mortality also varies substantially according to level of comorbidity.^[5]

The prognosis risk of empyema may be stratified using the RAPID score as shown below:^[7][8]

Interpretation of score:

Low risk: 0-2

Medium risk: 3-4

High risk: 5-7

The following co-morbid factors have been found to be associated with high-risk scores:^[7]

• Gram-negative rod infections
• Heart disease
• Diabetes
• Cancer
• Lung disease
• Increased length of hospital stay

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